Diseases, Nurse's Quick Check - 2nd Ed

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Nurses
Quick
Check
Diseases
Second Edition
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STAFF
Executive Publisher
Judith A. Schilling McCann, RN, MSN
Editorial Director
H. Nancy Holmes
Clinical Director
Joan M. Robinson, RN, MSN
Art Director
Elaine Kasmer
Editorial Project Manager
Ann E. Houska
Clinical Project Manager
Janet Rader Clark, RN, BSN
Editor
Kimberly A.J. Bilotta
Clinical Editors
Collette Bishop Hendler, RN, BS, MS, CCRN;
Anita Lockhart, RN, MSN; Dorothy P. Terry, RN
Copy Editors
Leslie Dworkin, Jeannine Fielding, Linda Hager
Designer
Joseph John Clark
Digital Composition Services
Diane Paluba (manager), Joyce Rossi Biletz,
Donald G. Knauss, Donna S. Morris
Associate Manufacturing Manager
Beth J. Welsh
Editorial Assistants
Karen J. Kirk, Jeri OShea, Linda K. Ruhf
Indexer
Dianne Schneider
The clinical treatments described and recommended in

this publication are based on research and consultation
with nursing, medical, and legal authorities. To the best
of our knowledge, these procedures reflect currently
accepted practice. Nevertheless, they cant be considered
absolute and universal recommendations. For individual
applications, all recommendations must be considered in
light of the patients clinical condition and, before
administration of new or infrequently used drugs, in light
of the latest package-insert information. The authors and
publisher disclaim any responsibility for any adverse
effects resulting from the suggested procedures, from any
undetected errors, or from the readers misunderstanding
of the text.
2009 by Lippincott Williams & Wilkins. All rights
reserved. This book is protected by copyright. No part of
it may be reproduced, stored in a retrieval system, or
transmitted, in any form or by any meanselectronic,
mechanical, photocopy, recording, or otherwise
without prior written permission of the publisher, except
for brief quotations embodied in critical articles and
reviews and testing and evaluation materials provided by
the publisher to instructors whose schools have adopted
its accompanying textbook. Printed in China. For
information, write Lippincott Williams & Wilkins, 323
Norristown Road, Suite 200, Ambler, PA 19002-2756.
NQCD2010408
Library of Congress Cataloging-in-Publication Data
Nurses quick check. Diseases. 2nd ed.
p. ; cm.
Includes bibliographical references and index.
1. DiseasesHandbooks, manuals, etc. 2. Nursing
Handbooks, manuals, etc. I. Lippincott Williams & Wilkins.
[DNLM: 1. DiseaseHandbooks. 2. Nursing Care
Handbooks. 3. TherapeuticsHandbooks.
WY 49 N9742 2008]
RT65.N78 2008
616dc22
ISBN-13: 978-0-7817-8940-0 (alk. paper)
ISBN-10: 0-7817-8940-0 (alk. paper) 2007049036
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Contents
Contributors and consultants vii
Diseases (in alphabetical order)
Less common diseases 922

Selected references
933
Web resources 935

Index 937
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Contributors
and consultants
Beverly Anderson, RN, MSN, MOT
Kendra S. Seiler, RN, MSN
Associate Professor
Malcolm X College
Chicago
Nursing Instructor
Rio Hondo College
Whittier, Calif.
Elizabeth A. Archer, RN, EdD
LaDelle Smothers, RN, BSN, MS
Associate Professor
Baptist College of Health Sciences
Memphis
RN Consultant (traveling)
Britthaven, Inc.
Kinston, N.C.
Julie A. Calvery, RN, MS
Rita M. Wick, RN, BSN
Instructor
University of Arkansas
Fort Smith
Education Specialist
Berkshire Health Systems
Pittsfield, Mass.
Kim Cooper, RN, MSN

Nursing Department Chair
Ivy Tech Community College
Terre Haute, Ind.
Lillian Craig, RN, MSN, FNP-C

Adjunct Faculty
Oklahoma Panhandle State University
Goodwell
Shelley Yerger Hawkins, APRN-BC, DSN, FNP, GNP,

FAANP
Post Doctoral Fellow

University of North Carolina
Chapel Hill
Elizaveta House, RN, BSN

Procurement Coordinator
LifeChoice Donor Services, Inc.
Windsor, Conn.
Angela R. Irvin, RN, MSN, ARNP, NP-C

Nurse Practitioner
University of Louisville (Ky.) Family & Geriatric Medicine
Vanessa Kramasz, RN, MSN, FNP

Lead Faculty & Nurse Practitioner
Gateway Technical College
Burlington, Wis.
vii
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Nurses
Quick
Check
Diseases
Second edition
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Abortion, spontaneous
Overview
Description
H Also known as miscarriage

H Expelled products of conception from the uterus be-
fore fetal viability (see Types of spontaneous abortion)
Pathophysiology
H Abortion may result from fetal, placental, or maternal
factors.
Fetal factors
H Fetal factors usually cause abortion to occur between
9 and 12 weeks gestation.
H Spontaneous abortion may result from defective embryologic development.
H Faulty implantation of a fertilized ovum may cause
the ovum to be rejected.
H Abortion may also result from failure of the endometrium to accept the fertilized ovum.
Placental factors
H Placental factors usually cause abortion to occur
around 14 weeks gestation when the placenta takes
over the hormone production necessary to maintain
pregnancy. These factors include:
premature separation of a normally implanted
placenta
abnormal placental implantation
abnormal platelet function.
Maternal factors
H Maternal factors usually cause abortion to occur
between 11 and 19 weeks gestation.
Causes
Spontaneous abortion
H Fetal factors
H Placental factors
H Maternal infection
H Severe malnutrition
H Abnormalities of the reproductive organs
H Thyroid gland dysfunction
H Lowered estriol secretion
H Diabetes mellitus
H Trauma
H Surgery that necessitates manipulation of the pelvic
organs
H Blood group incompatibility and Rh isoimmunization
H Illicit drug use
H Environmental toxins
H Incompetent cervix
Incidence
H Percentage of all pregnancies that end in miscar-
riage: up to 15%
H First pregnancies that end in miscarriage: about 30%
H Miscarriages that occur during the first trimester: at
least 75%
Common characteristics
H Pink discharge for several days before cramping
H Scant brown discharge for several weeks before
cramping
H Abdominal cramps
H Vaginal bleeding
Complications
H Infection
H Hemorrhage
H Anemia
H Coagulation defects
H Disseminated intravascular coagulation
H Psychological issues of loss and failure
Assessment
History
H Pink discharge for several days or scant brown dis-
charge for several weeks before onset of cramps and

increased vaginal bleeding
H Cramps that appear for a few hours, intensify, then
occur more frequently
H Continued cramps and bleeding if any uterine contents remain (cramps and bleeding may subside if
entire contents expelled)
Physical findings
H Vaginal bleeding
H Cervical dilation
H Passage of nonviable products of conception
Test results
Laboratory
H Serum human chorionic gonadotropin levels are
decreased, suggesting spontaneous abortion.
H Cytologic analysis shows evidence of products of
conception.
H Serum hemoglobin level and hematocrit are decreased due to blood loss.
Imaging
H Presence or absence of fetal heart tones or empty
amniotic sac is revealed by ultrasound examination.
Treatment
General
H Accurate evaluation of uterine contents before plan-
ning treatment
H Progression of spontaneous abortion unpreventable,
except in cases caused by an incompetent cervix

H Hospitalization to control severe hemorrhage
H Possible bed rest
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Medications
H Transfusion with packed red blood cells or whole
blood (severe bleeding)

H I.V. oxytocin (stimulates uterine contractions)
H Rho(D) immune globulin for an Rh-negative female
with a negative indirect Coombs test
Surgery
H Dilatation and curettage or dilatation and evacuation,
if remnants remain in the uterus

H Surgical reinforcement of the cervix (cerclage) to
prevent abortion
Nursing considerations
Key outcomes
The patient will:
H exhibit no signs and symptoms of infection
H communicate feelings about the current situation
H express feelings of having greater control over the
current situation
H use available support systems, such as family and
friends, to aid in coping.
Nursing interventions
H Do not allow bathroom privileges because the pa-
tient may expel uterine contents without knowing it.

H Inspect bedpan contents carefully for intrauterine
material.
H Save all sanitary pads for evaluation.
H Give prescribed drugs.
H Provide perineal care.
H Provide emotional support and counseling.
H Encourage expression of feelings.
H Help the patient develop effective coping strategies.
Monitoring
H Amount, color, and odor of vaginal bleeding
H Vital signs
H Intake and output
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment
H vaginal bleeding or spotting
H bleeding that lasts longer than 8 days or excessive
bleeding
H importance of reporting signs of bright red blood
immediately
H signs of infection, such as fever and foul-smelling
vaginal discharge
H gradual increase of daily activities
H schedule for returning to work (normally within 1
to 4 weeks)
H abstinence from intercourse for 1 to 2 weeks
H prevention of spontaneous abortion
Types of spontaneous abortion

Depending on clinical findings, a spontaneous abortion
(miscarriage) may be threatened or inevitable, incomplete
or complete, or missed, habitual, or septic. Heres how the
seven types compare.
Threatened abortion
Bloody vaginal discharge occurs during the first half of
pregnancy. About 20% of pregnant women have vaginal
spotting or actual bleeding early in pregnancy; of these,
about 50% abort.
Inevitable abortion
The membranes rupture and the cervix dilates. As labor
continues, the uterus expels the products of conception.
Incomplete abortion
The uterus retains part or all of the placenta. Before 10
weeks gestation, the fetus and placenta are usually expelled together; after the 10th week, theyre expelled separately. Because part of the placenta may adhere to the
uterine wall, bleeding continues. Hemorrhage is possible
because the uterus doesnt contract and seal the large
vessels that feed the placenta.
Complete abortion
The uterus passes all the products of conception. Minimal
bleeding usually accompanies complete abortion because
the uterus contracts and compresses the maternal blood
vessels that feed the placenta.
Missed abortion
The uterus retains the products of conception for 2
months or more after the death of the fetus. Uterine
growth ceases; uterine size may even seem to decrease.
Prolonged retention of the dead products of conception
may cause coagulation defects such as disseminated intravascular coagulation.
Habitual abortion
Spontaneous loss of three or more consecutive pregnancies constitutes habitual abortion.
Septic abortion
Infection accompanies abortion. This may occur with
spontaneous abortion, but usually results from an illegal
abortion or from the presence of an intrauterine device.
H contraceptive information
H avoidance of tampons for 1 to 2 weeks
H follow-up examination.
Discharge planning
H Refer the patient for professional counseling, if
indicated.
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Abruptio placentae
Overview
Description
H Disseminated intravascular coagulation (DIC)

H Maternal death
H Fetal death
Assessment
H Premature separation of the placenta from the uter-
History
ine wall
H Usually occurs after 20 weeks gestation, most commonly during the third trimester
H Common cause of bleeding during the second half of
pregnancy
H Fetal prognosis depending on gestational age and
amount of blood lost
H Good maternal prognosis if hemorrhage can be controlled
H Classified according to degree of placental separation
and severity of maternal and fetal symptoms (see Degrees of placental separation in abruptio placentae)
H Also called placental abruption
Mild abruptio placentae (marginal

separation)
H Mild to moderate vaginal bleeding
H Vague lower abdominal discomfort
H Mild to moderate abdominal tenderness
Moderate abruptio placentae (about 50%
placental separation)
H Continuous abdominal pain
H Moderate dark red vaginal bleeding
H Severe or abrupt onset of symptoms
Severe abruptio placentae (70% placental
separation)
H Abrupt onset of agonizing, unremitting uterine pain
H Moderate vaginal bleeding
Pathophysiology
Physical findings
H Spontaneous rupture of blood vessels at the placental
Mild abruptio placentae

H Fetal monitoring possibly indicating uterine irritability
H Strong and regular fetal heart tones
Moderate abruptio placentae
H Vital signs possibly indicating impending shock
H Tender uterus remaining firm between contractions
H Barely audible or irregular and bradycardic fetal
heart tones
H Labor that usually starts within 2 hours and proceeds
rapidly
Severe abruptio placentae
H Vital signs that indicate rapidly progressive shock
H Absence of fetal heart tones
H Tender uterus with boardlike rigidity
H Possible increased uterine size in severe concealed
abruptions
bed may be due to lack of resiliency or to abnormal

changes in uterine vasculature.
H State may be complicated by hypertension or by an
enlarged uterus that cant contract sufficiently to seal
off the torn vessels.
H Bleeding continues unchecked, possibly shearing off
the placenta partially or completely.
Causes
H Exact cause unknown
H Traumatic injury
H Amniocentesis
H Chronic or gestational hypertension
H Multiparity
H Short umbilical cord
H Dietary deficiency
H Smoking
H Advanced maternal age
H Pressure on the vena cava from an enlarged uterus
H Diabetes mellitus
Test results
Laboratory
H Serum hemoglobin level and platelet counts are decreased.
H Progression of abruptio placentae and detection of
DIC is shown by fibrin split products.
Imaging
H Pelvic examination under double setup (preparations
for an emergency cesarean delivery) and ultrasonography may rule out placenta previa.
H Vaginal bleeding
H Abdominal discomfort
H Abdominal tenderness
Treatment
Complications
General
H Hemorrhage
H Shock
H Renal failure
H Blood loss evaluated and controlled

H Viable infant delivered
H Coagulation disorders prevented
Incidence
H Most common in multigravida women older than
age 35, women with gestational hypertension, and

women who use cocaine
Abruptio placentae
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Degrees of placental separation in abruptio placentae

Mild separation
Moderate separation
Severe separation
Internal bleeding between the placenta

and uterine wall characterizes mild
separation.
In moderate separation, external hemorrhage occurs through the vagina.
External hemorrhage is also characteristic in severe separation.
H For severe placental separation with no signs of fetal
life, vaginal delivery unless contraindicated by uncontrolled hemorrhage or other complications
ALERT
Because of possible fetal blood loss through the placenta, a pediatric team should be ready at delivery
to assess and treat the neonate for shock, blood
loss, and hypoxia.
ALERT
Complications of abruptio placentae require
prompt appropriate treatment. With a complication such as DIC, the patient needs immediate intervention with platelets and whole blood, as ordered, to prevent exsanguination.
H Nothing to eat or drink until delivery of the fetus
H Bed rest until delivery of the fetus
H Obtain blood samples for hemoglobin level and
hematocrit, coagulation studies, and type and crossmatching, as ordered.

H Provide emotional support during labor.
H Provide information of progress and condition of
fetus during labor.
H Encourage verbalization of feelings.
H Help develop effective coping strategies.
H Administer I.V. fluids and blood products.
Monitoring
H Maternal vital signs
H Central venous pressure
H Intake and output
H Vaginal bleeding
H Fetal heart rate (electronically)
H Progression of labor
Patient teaching
Be sure to cover:
H signs of placental abruption
H possibility of an emergency cesarean delivery
H possibility of the delivery of a premature neonate
H changes to expect in the postpartum period
H possibility of neonatal death
H factors affecting survival of the neonate
H importance of frequent monitoring and prompt
management to reduce the risk of death.
Key outcomes
Discharge planning
The patient will:

H maintain stable vital signs
H maintain balanced fluid volume
H express feelings of increased comfort
H communicate feelings about the situation
H use available support systems to aid in coping.
H Refer the patient for professional counseling, if
Medications
H I.V. fluid infusion (by large-bore catheter) as
ordered
Surgery
H Cesarean delivery if the fetus is in distress
indicated.
H Insert an indwelling urinary catheter.
Abruptio placentae
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Accelerationdeceleration injuries
Physical findings
Overview
H Neck muscle asymmetry

H Reduced neck mobility
H Gait disturbances
H Rigidity or numbness in the arms
H Tenderness at the exact location of the injury
H Decreased active and passive range of motion
Description
Test results
H Injury resulting from sharp hyperextension and flex-
Imaging
H Full cervical spine X-rays rule out cervical fracture.
ion of the neck that damages muscles, ligaments,

disks, and nerve tissue
H Excellent prognosis; symptoms usually subside with
symptomatic treatment
H Also called whiplash
Pathophysiology
H Unexpected force causes the head to jerk back and
then forward.
H The neck bones snap out of position, causing injury.
H Irritated nerves can interfere with blood flow and
transmission of nerve impulses.

H Pinched nerves can affect certain body part functions.
Causes
Treatment
General
H Soft cervical collar (see Applying a cervical collar)
H Ice packs
H Physical therapy
H Limited activity during the first 72 hours after the in-
jury
H Limited neck movement
H Limited strenuous activities, such as lifting and con-
tact sports, until full recovery has been established

(which may take more than 2 years)
H Motor vehicle accident

H Sports accident
H Fall
H Assault, including shaking a child
Medications
Risk factors
H Corticosteroids
H Absence of head restraint in automobile

H Osteoporosis
H Driving under the influence of alcohol or drugs
Surgery
Incidence
H 1,000,000 cases each year in the United States
H Average age of patient with acceleration-deceleration
injury: the late 40s
H Nuchal rigidity
H Neck muscle asymmetry
Complications
H Temporomandibular disorder
H Oral analgesics, such as acetaminophen, non-
steroidal anti-inflammatory drugs, and opioids

H Muscle relaxants, such as baclofen, carisoprodol,
and cyclobenzaprine
H Surgical stabilization possible in severe cervical
acceleration-deceleration injuries
Key outcomes
The patient will:
H identify factors that intensify pain
H modify behavior to limit movement and avoid extended injury
H develop effective coping mechanisms
H attain the highest degree of mobility possible
H state feelings and fears about the injury.
Assessment
History
H Provide protection of the spine during all care.

H Apply a soft cervical collar.
H Mechanism of injury
H Pain initially minimal, but increases 12 to 72 hours
after the accident

H Dizziness
H Headache
H Back pain
H Shoulder pain
H Vision disturbances
H Tinnitus
Acceleration-deceleration injuries
Monitoring
H Pain control
H Response to medications
H Complications
H Neurologic status
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Applying a cervical collar

Cervical collars are used to support an injured or weakened cervical spine and to maintain alignment during
healing.The soft cervical collar, made of spongy foam,
provides gentler support and reminds the patient to avoid
cervical spine motion.
Patient teaching
Be sure to cover:
H activity restrictions
H proper application of soft cervical collar
H medication administration, dosage, and possible
adverse effects
H instructions regarding driving and the use of alcohol
while taking opioids.
Acceleration-deceleration injuries
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Acne vulgaris
Overview
Description
H Inflammatory disorder of the sebaceous gland con-
tiguous with a hair follicle (pilosebaceous follicle)

H Possibly developing in distinctive pilosebaceous units
(sebaceous follicles)
H Acne lesions: inflammatory (pustules, papules, and
nodules) and noninflammatory (closed and open

comedones) lesions
H Good prognosis with treatment
Pathophysiology
H Acne begins with sebum accumulation that obstructs
the pilosebaceous unit.

H The mass of accumulated keratinous sebaceous ma-
terial and bacteria within the pilosebaceous follicle

causes inflammation when its exposed to the dermis
with rupture of a follicle.
H The Propionibacterium acnes bacteria produce
substances that promote inflammation.
H In noninflammatory acne, the comedones are open,
called blackheads, or closed, called whiteheads; accumulated material causes distention of the follicle
and thinning of follicular canal walls.
H Inflammatory acne develops in closed comedones
when the follicular wall ruptures, expelling sebum
into the surrounding dermis and initiating inflammation.
H Pustules form when the inflammation is close to the
surface; papules and cystic nodules can develop
when the inflammation is deeper, causing mild to
severe scarring.
Causes
H Follicular hyperkeratinization
H Excessive sebum production
H Proliferation of P. acnes
H Hormonal dysfunction
Causes of acne flare-ups

H Menstrual cycle
H Stress
H Trauma
H Tropical climates
H Rubbing from tight clothing
H Environmental exposure to coal tar derivatives, certain chemicals, cosmetics, or hair pomades
H Hormonal contraceptives containing norethindrone
and norgestrel; testosterone
H Anabolic agents
H Corticotropin, gonadotropins, corticosteroids (prolonged use)
H Iodine- or bromine-containing drugs
H Trimethadione
H Phenytoin
H Isoniazid
8
Acne vulgaris
H Lithium
H Halothane
Incidence
H Affects nearly 75% of adolescents, although lesions
can appear as young as age 8

H Affects males more commonly and more severely
H Occurs in females at an earlier age and tends to
affect them for a longer time, sometimes into adulthood

H Tends to be familial
H Pustules, papules, nodules
H Closed and open comedones
H Follicles located primarily on face and upper parts of
chest and back
Complications
H Deep cystic process
H Gross inflammation
H Abscess formation
H Secondary bacterial infection
H Acne scars
Assessment
History
H Presence of one or more predisposing factors
H Seasonal or monthly eruption patterns
H Pain and tenderness around area of infected follicle
Physical findings
H Acne lesions, typically located on the face, neck,
shoulders, chest, and upper back

H Red, swollen area around the infected follicle
H Acne plugs that appear as closed or open comedones
H Oily and thickened skin
H Visible scars
Test results
Laboratory
H Culture and sensitivity of pustules or abscesses shows
causative organism of secondary bacterial infection.
Treatment
General
H Treatment of causative factors
H Well-balanced diet
H Regular exercise
Medications
H Topical
Antibiotics, including erythromycin, clindamycin,

and sodium sulfacetamide
Keratolytics, including benzoyl peroxide, azelaic
acid, and salicylic acid
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Retinoids, including adapalene, tretinoin, and

tazarotene
H Systemic
Antibiotics, such as tetracycline, erythromycin, and
clindamycin
Diuretics such as spironolactone
Oral hormonal contraceptives
Retinoids, including isotretinoin
Surgery
H Comedo extraction
H Intralesional steroids such as triamcinolone
H Cryosurgery
H Dermabrasion
Special populations
Tetracycline is contraindicated during pregnancy
and childhood because it may cause permanent
discoloration of teeth (in children younger than
age 8), enamel defects, and bone growth retardation. Erythromycin is an alternative for these patients.
H Sensitivity reactions
H GI disturbances
H Liver dysfunction
H Response to treatment
H Skin and mucous membranes
Patient teaching
Be sure to cover:
H the disorder and treatment
H medications and possible adverse reactions
H when to notify the physician
H signs and symptoms of infection
H causative factors associated with acne flare-up
H well-balanced diet
H adequate rest
H stress management.
ALERT
Because oral tretinoin is known to cause birth defects, the manufacturer, with Food and Drug Administration approval, recommends pregnancy
testing before dispensing, dispensing only a 30-day
supply, repeat pregnancy testing throughout the
treatment period, effective contraception during
treatment, and informed consent of the patient or
parents regarding the danger of the drug.
Key outcomes
The patient will:
H exhibit improved or healed wounds or lesions
H demonstrate the recommended skin care regimen
H verbalize feelings about body image
H verbalize understanding of the condition and treatment.
H Assist the patient in identifying and eliminating pre-
disposing factors.
H Encourage good personal hygiene and the use of oil-
free skin care products.

H Discourage picking or squeezing the lesions.
H Encourage the patient to verbalize his feelings.
H Encourage patient to develop interests that support a
positive self-image and de-emphasize appearance.
Monitoring
H Liver function studies, serum triglyceride levels, and
pregnancy testing with tretinoin use

H Complications
Acne vulgaris
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Acquired
immunodeficiency
syndrome and human
immunodeficiency virus
Assessment
Overview
Physical findings
Description
H Persistent generalized adenopathy

H Nonspecific symptoms (weight loss, fatigue, night
H Human immunodeficiency virus (HIV) type 1; retro-
virus causing acquired immunodeficiency syndrome

(AIDS)
H Causes patients to become susceptible to opportunistic infections, unusual cancers, and other abnormalities
H Marked by progressive failure of the immune system
H Transmitted by contact with infected blood or body
fluids and associated with identifiable high-risk behaviors
Pathophysiology
H HIV strikes helper T cells bearing the CD4 antigen.
H The antigen serves as a receptor for the retrovirus
and lets it enter the cell.

H After invading a cell, HIV replicates, leading to cell
death, or becomes latent.
H HIV infection leads to profound pathology, either
directly, through destruction of CD4+ cells, other
immune cells, and neuroglial cells, or indirectly,
through the secondary effects of CD4+ T-cell dysfunction and resultant immunosuppression.
History
H Mononucleosis-like syndrome after high-risk expo-
sure and inoculation; then may remain asymptomatic

for years
H Laboratory evidence of seroconversion only sign in
latent stage
sweats, fevers)
H Neurologic symptoms resulting from HIV encepha-
lopathy
H Opportunistic infection or cancer (Kaposis sarco-
ma)
Special populations
Children show a higher incidence of bacterial
infections.
Test results
Laboratory
H CD4+ T-cell count of at least 200 cells/ml confirms
HIV infection.
H Screening test enzyme-linked immunosorbent assay
and confirmatory test (Western blot) detect the presence of HIV antibodies, which indicate HIV infection.
Treatment
Causes
General
H Infection with HIV, a retrovirus
H Variety of therapeutic options for opportunistic infec-
Risk factors
H I.V. drug users who share needles or syringes
H Unprotected sexual intercourse
H Placental transmission
H History of sexually transmitted disease
H Homosexual lifestyle
H Contact with infected blood
Incidence
H Average time between exposure to the virus and diag-
nosis of AIDS: 8 to 10 years, but can be shorter and

longer
H May produce no symptoms for years
H Flulike symptoms
Complications
H Repeated opportunistic infections
H Neoplasms
H Premalignant diseases
H Organ-specific syndrome
10
tions (the leading cause of morbidity and mortality in

patients infected with HIV)
H Disease-specific therapy for a variety of neoplastic
and premalignant diseases and organ-specific syndromes
H Symptom management (fatigue and anemia)
H Regular exercise, as tolerated, with adequate rest
periods
Medications
H Immunomodulatory agents
H Anti-infectives, as appropriate
H Antineoplastics
H Highly active antiretroviral therapy (HAART)
Primary therapy
H Protease inhibitors, such as ritonavir, amprenavir,
and nelfinavir
H Nucleoside reverse transcriptase inhibitors, such as
zidovudine and lamivudine
H Nonnucleoside reverse transcriptase inhibitors, such
as delavirdine and nevirapine
Acquired immunodeficiency syndrome and human immunodeficiency virus
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Preventing HIV transmission

H Use precautions in all situations that risk exposure to
blood, body fluids, and secretions. Diligently practicing
standard precautions can prevent the inadvertent
transmission of human immunodeficiency virus (HIV),
hepatitis B, and other infectious diseases that are
transmitted by similar routes.
H Teach the patient, his family, sexual partners, and friends
about disease transmission and prevention of extending
the disease to others.
H Tell the patient not to donate blood, blood products,
organs, tissue, or sperm.
H If the patient uses I.V. drugs, caution him not to share
needles.
Key outcomes
The patient will:
H achieve management of symptoms of illness
H demonstrate use of protective measures, including
conservation of energy, maintenance of wellbalanced diet, and getting adequate rest
H follow safer sex practices
H use available support systems to help with coping
H express feelings about changes in sexual identity and
social response to disease
H develop no complications of illness
H comply with the treatment regimen.
H Inform the patient that high-risk sexual practices for HIV

transmission are those that exchange body fluids, such
as vaginal or anal intercourse without a condom.
H Discuss safer sexual practices, such as hugging, petting,
mutual masturbation, and protected sexual intercourse.
Abstinence is the most effective method to prevent
transmission.
H Advise the female patient of childbearing age to avoid
pregnancy. Explain that an infant may become infected
before birth, during delivery, or during breast-feeding.
Patient teaching
Be sure to cover:
H medication regimens
H importance of informing potential sexual partners,
caregivers, and health care workers of HIV infection
(see Preventing HIV transmission)
H signs of impending infection and the importance of
seeking immediate medical attention
H symptoms of AIDS dementia and its stages and
progression.
Discharge planning
H Refer the patient to a local support group.
H Refer the patient to hospice care, as indicated.
H Help the patient cope with an altered body image, the
emotional burden of serious illness, and the threat of

death.
H Avoid glycerin swabs for mucous membranes. Use
normal saline or bicarbonate mouthwash for daily
oral rinsing.
H Ensure adequate fluid intake during episodes of
diarrhea.
H Provide meticulous skin care, especially in the debilitated patient.
H Encourage the patient to maintain as much physical
activity as he can tolerate. Make sure his schedule
includes time for exercise and rest.
Monitoring
H Fever, noting any pattern
H Skin integrity
H Signs of illness, such as cough, sore throat, and
diarrhea
H Swollen, tender lymph nodes
H Laboratory values
H Calorie intake
H Progression of lesions in Kaposis sarcoma
H Opportunistic infections or signs of disease
progression
H Compliance with medication regimen
Acquired immunodeficiency syndrome and human immunodeficiency virus
11
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Acute poststreptococcal
glomerulonephritis
Assessment
History
H Untreated respiratory streptococcal infection 1 to
Overview
Description
H Renal disease in which the glomeruli become
inflamed
3 weeks before
H Decreased urination
H Smoky or coffee-colored urine
H Fatigue
H Dyspnea and orthopnea
H Usually associated with a postinfectious state, com-
Physical findings
monly a streptococcal infection of the respiratory

tract or, less commonly, a skin infection such as
impetigo
H Up to 95% recovery in children and 70% in adults
H Possible chronic renal failure within months in elderly patients
H Relatively common
H Also called acute glomerulonephritis
H Oliguria
H Mild to moderate periorbital edema
H Mild to severe hypertension
H Bibasilar crackles (with heart failure)
Pathophysiology
H Antigen-antibody complexes are produced in re-
sponse to group A beta-hemolytic streptococcus

infection.
H Entrapment and collection of antigen-antibody complexes occurs in the glomerular capillary membranes.
H Inflammatory damage results, impeding glomerular
function.
H Immune complement may further damage the glomerular membrane.
H Damaged and inflamed glomeruli lose the ability to
be selectively permeable.
H Red blood cells (RBCs) and proteins then filter
through as the glomerular filtration rate decreases.
H Uremic poisoning may result.
Causes
H Untreated group A beta-hemolytic streptococcus in-
fection, especially of the respiratory tract
Risk factors
H Streptococcal infection
H Impetigo
Incidence
H Occurs most commonly in boys ages 3 to 7; can oc-
cur at any age
Test results
Laboratory
H Electrolyte imbalances are evident.
H Blood urea nitrogen (BUN) and creatinine levels are
elevated.
H Serum protein levels are decreased.
H The presence of RBCs, white blood cells, mixed cell
casts, and protein in the urine indicates renal failure.
H Fibrin-degradation products and C3 protein levels
are high.
Special populations
Proteinuria in an elderly patient usually isnt as
pronounced.
H Antistreptolysin-O titers (in 80% of patients), strep-
tozyme, and anti-DNase B titers are elevated; serum

complement levels, which verify recent streptococcal
infection, are low.
H Group A beta-hemolytic streptococci is revealed by
throat culture.
Imaging
H Kidney-ureter-bladder radiography reveals bilateral
kidney enlargement.
Diagnostic procedures
H Renal biopsy or assessment of renal tissue confirms
diagnosis.
Treatment
General
H Correction of electrolyte imbalances (possible dialy-
H Oliguria
H Fluid overload
H Periorbital edema
H Fluid restriction
H High-calorie, low-protein, low-sodium, low-
Complications
H Bed rest
H Progressive deterioration of renal function
sis)
potassium diet
Medications
H Antibiotics if appropriate
H Loop diuretics, such as metolazone and furosemide
12
Acute poststreptococcal glomerulonephritis
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Key outcomes
The patient will:
H avoid or minimize complications
H maintain fluid balance
H maintain urine specific gravity within the designated
limits
H report increased comfort
H identify risk factors that exacerbate the condition and
modify lifestyle accordingly.
H Encourage verbalization.
H Provide support.
Monitoring
H Vital signs
H Electrolyte values and serum creatinine and BUN
levels
H Urine creatinine clearance test results
H Intake and output
H Daily weight
Patient teaching
Be sure to cover:
H importance of follow-up examinations to monitor
renal function
adverse effects.
Discharge planning
H Refer the patient to appropriate resources for infor-
mation and support.
Acute poststreptococcal glomerulonephritis
13
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Acute pyelonephritis
Overview
Description
H Inflammation of the kidney occurring mainly in the
interstitial tissue and renal pelvis and occasionally in

the renal tubules
H Affecting one or both kidneys
H Good prognosis; extensive permanent damage rarely
occurs
H Also called acute infective tubulointerstitial
nephritis
Pathophysiology
H Infection spreads from the bladder to the ureters to
the kidneys, commonly through vesicoureteral reflux.

H Vesicoureteral reflux may result from congenital
weakness at the junction of the ureter and bladder.

H Bacteria refluxed to intrarenal tissues may create
colonies of infection within 24 to 48 hours.

H Female anatomy allows for higher incidence of
infection.
Causes
H Bacterial infection of the kidneys
Risk factors
H Renal procedures that involve instrumentation such
as cystoscopy
H Hematogenic infection such as septicemia
H Sexually active women
H Pregnant women
H Neurogenic bladder
H Obstructive disease
H Renal diseases
Incidence
Assessment
History
H Pain over one or both kidneys
H Urinary urgency and frequency
H Burning during urination
H Dysuria, nocturia, hematuria
H Anorexia, vomiting, diarrhea
H Fatigue
H Symptoms that develop rapidly over a few hours or a
few days
Physical findings
H Pain on flank palpation
H Cloudy urine
H Ammonia-like or fishy odor to urine
H Fever of 102 F (38.9 C) or higher
H Shaking chills
Test results
Laboratory
H Urinalysis and culture and sensitivity testing reveal
pyuria, significant bacteriuria, low specific gravity
and osmolality, slightly alkaline urine pH, or proteinuria, glycosuria, and ketonuria (less frequent).
H White blood cell count, neutrophil count, and erythrocyte sedimentation rate are elevated.
Imaging
H Kidney-ureter-bladder radiography reveals calculi,
tumors, or cysts in the kidneys or urinary tract.
H Excretory urography shows asymmetrical kidneys,
possibly indicating a high frequency of infection.
Treatment
General
H Identification and correction of predisposing factors
to infection, such as obstruction or calculi
H More common in females than in males

H Community-acquired cases in 15 per 100,000
H Short courses of therapy for uncomplicated infec-
annually
H Hospital-acquired cases in 7 per 10,000 annually
H Increased fluid intake
H Antibiotics, as appropriate
H Urinary analgesics such as phenazopyridine
H Pain over one or both kidneys

H Dysuria
H Nocturia
tions
Medications
Complications
Key outcomes
H Renal calculi
H Renal failure
H Renal abscess
H Multisystem infection
H Septic shock
H Chronic pyelonephritis
The patient will:

limits
H identify risk factors that exacerbate decreased tissue
perfusion and modify lifestyle appropriately
H report increased comfort.
14
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Monitoring
H Vital signs
H Intake and output
H Characteristics of urine
H Pattern of urination
H Daily weight
H Renal function studies
Patient teaching
Be sure to cover:
H avoidance of bacterial contamination by following hygienic toileting practices (wiping the perineum from
front to back after bowel movements for women)
H proper technique for collecting a clean-catch urine
specimen
adverse effects
H routine checkup with a history of urinary tract
infections
H signs and symptoms of recurrent infection.
15
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Life-threatening disorder
Incidence
H Patients with three concurrent causes: 85% probabil-
ity of developing ARDS
Acute respiratory
distress syndrome
Overview
Complications
Description
H Severe form of alveolar injury or acute lung injury
H A form of pulmonary edema; may be difficult to
H Shortness of breath
H Dry cough with thick, frothy sputum
H Bloody, sticky secretions
H Metabolic acidosis
H Respiratory acidosis
H Cardiac arrest
H Multiple organ dysfunction syndrome
recognize
H Hallmark sign: hypoxemia despite increased supple-
mental oxygen
H A four-stage syndrome; can rapidly progress to intractable and fatal hypoxemia
H Little or no permanent lung damage in patients who
recover
H May coexist with disseminated intravascular coagulation (DIC)
H Also known as ARDS, adult respiratory distress syndrome and shock, stiff, white, wet, or Da Nang
lung
Pathophysiology
H Increased permeability of the alveolocapillary mem-
branes allows fluid to accumulate in the lung interstitium, alveolar spaces, and small airways, causing the
lung to stiffen.
H Ventilation is impaired, reducing oxygenation of pulmonary capillary blood.
H Elevated capillary pressure increases interstitial and
alveolar edema.
H Alveolar closing pressure then exceeds pulmonary
pressures.
H Closure and collapse of the alveoli occurs.
Causes
H Indirect or direct lung trauma (most common)
H Anaphylaxis
H Aspiration of gastric contents
H Diffuse pneumonia (especially viral)
H Drug overdose
H Idiosyncratic drug reaction
H Inhalation of noxious gases
H Near-drowning
H Oxygen toxicity
H Coronary artery bypass grafting
H Hemodialysis
H Leukemia
H Acute miliary tuberculosis
H Pancreatitis
H Thrombotic thrombocytopenic purpura
H Uremia
H Venous air embolism
16
Acute respiratory distress syndrome
Assessment
History
H Causative factor (one or more)
H Dyspnea, especially on exertion
Physical findings
Stage I
H Shortness of breath, especially on exertion
H Normal to increased respiratory and pulse rates
H Diminished breath sounds
Stage II
H Respiratory distress
H Use of accessory muscles for respiration
H Pallor, anxiety, and restlessness
H Dry cough with thick, frothy sputum
H Bloody, sticky secretions
H Cool, clammy skin
H Tachycardia and tachypnea
H Elevated blood pressure
H Basilar crackles
Stage III
H Respiratory rate greater than 30 breaths/minute
H Tachycardia with arrhythmias
H Labile blood pressure
H Productive cough
H Pale, cyanotic skin
H Crackles and rhonchi possible
Stage IV
H Acute respiratory failure with severe hypoxia
H Deteriorating mental status (may become comatose)
H Pale, cyanotic skin
H Lack of spontaneous respirations
H Bradycardia with arrhythmias
H Hypotension
H Metabolic and respiratory acidosis
Test results
Laboratory
H Arterial blood gas (ABG) analysis initially shows a
reduced partial pressure of arterial oxygen (PaO2)
(less than 60 mm Hg) and a decreased partial pressure of arterial carbon dioxide (PaCO2) (less than
35 mm Hg).
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H ABG analysis later shows increased PaCO2 (more than
45 mm Hg) and decreased bicarbonate levels (less

than 22 mEq/L) and decreased PaO2 despite oxygen
therapy.
H Gram stain and sputum culture and sensitivity show
infectious organism.
H Blood cultures reveal infectious organisms.
H Toxicology tests show drug ingestion in overdose.
H Serum amylase levels are increased in pancreatitis.
Imaging
H Chest X-rays may show early bilateral infiltrates; in
later stages, a ground-glass appearance and, eventually, whiteouts of both lung fields.
H Pulmonary artery catheterization may show a pulmonary artery wedge pressure of 12 to 18 mm Hg.
Treatment
General
H Treatment of the underlying cause
H Correction of electrolyte and acid-base imbalances
For mechanical ventilation

H Target low tidal volumes; use of increased respiratory
rates
H Target plateau pressures less than or equal to
40 cm H2O
H Positive end-expiratory pressure (PEEP) as necessary
H Fluid restriction
H Tube feedings or parenteral nutrition
H Bed rest
Medications
H Humidified oxygen
H Bronchodilators, such as albuterol and theophylline
H Diuretics, such as furosemide and torsemide
H Maintain a patent airway.
H Perform tracheal suctioning, as necessary.
H Ensure adequate humidification.
H Reposition the patient often.
H Consider prone positioning for alveolar recruitment.
H Administer tube feedings or parenteral nutrition, as
ordered.
H Allow periods of uninterrupted sleep.
H Perform passive range-of-motion exercises.
H Provide meticulous skin care.
H Reposition the endotracheal (ET) tube per facility
policy.
H Provide emotional support.
H Provide alternative communication means.
Monitoring
H Vital signs and pulse oximetry
H Hemodynamics
H Intake and output
H Respiratory status (breath sounds, ABG results)
H Mechanical ventilator settings
H Sputum characteristics
H Level of consciousness
H Daily weight
H Laboratory studies
H Complications, such as cardiac arrhythmias, DIC, GI
bleeding, infection, malnutrition, or pneumothorax

H Nutritional status
ALERT
Because PEEP may lower cardiac output, check for
hypotension, tachycardia, and decreased urine
output. To maintain PEEP, suction only as needed.
For mechanical ventilation

H Sedatives
H Opioids
H Neuromuscular blockers
H Short course of high-dose corticosteroids if fatty
emboli or chemical injury
H Sodium bicarbonate if severe metabolic acidosis
H Fluids and vasopressors if hypotensive
H Antimicrobials, as appropriate, for nonviral infection
If the patient requires mechanical

ventilation
H Ventilator settings
H Cuff pressure
H Complications of mechanical ventilation
H ET tube position and patency
H Signs and symptoms of stress ulcer
Surgery
Patient teaching
H Possible tracheostomy
Key outcomes
The patient will:
H maintain adequate ventilation
H maintain a patent airway
H use effective coping strategies
H maintain skin integrity
H report feelings of increased comfort.
Be sure to cover:
H complications, such as GI bleeding, infection, and
malnutrition
H recovery time.
Discharge planning
H Refer the patient to a pulmonary rehabilitation
program, if indicated.
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Acute respiratory
failure
Overview
Description
H Inadequate ventilation resulting from the inability of
the lungs to adequately maintain arterial oxygenation

or eliminate carbon dioxide
Pathophysiology
H If respiratory failure is primarily hypercapnic, its the
result of inadequate alveolar ventilation.
H Metabolic alkalosis
H Respiratory and cardiac arrest
Assessment
History
Precipitating events
H Infection
H Accumulated pulmonary secretions secondary to
cough suppression
H Trauma
H MI
H Heart failure
H Pulmonary emboli
H Exposure to irritants (smoke or fumes)
H Myxedema
H If respiratory failure is primarily hypoxemic, its the
Physical findings
result of inadequate exchange of oxygen between the

alveoli and capillaries.
H Many people have a combined hypercapnic and
hypoxemic respiratory failure.
H Cyanosis of the oral mucosa, lips, and nail beds

H Yawning and use of accessory muscles
H Pursed-lip breathing
H Nasal flaring
H Ashen skin
H Rapid breathing
H Cold, clammy skin
H Asymmetrical chest movement
H Decreased tactile fremitus over an obstructed
Causes
H Any condition that increases the work of breathing
and decreases the respiratory drive of patients with

chronic obstructive pulmonary disease
H Respiratory tract infection
H Bronchospasm
H Accumulated secretions secondary to cough suppression
H Ventilatory failure
H Gas exchange failure
H Central nervous system depression
H Myocardial infarction (MI)
H Heart failure
H Pulmonary emboli
H Airway irritants
H Endocrine or metabolic disorders
H Thoracic abnormalities
Incidence
H Occurs in patients with hypercapnia and hypoxemia
H Occurs in patients who have an acute deterioration in
arterial blood gas (ABG) values
H Rapid breathing
H Restlessness
H Anxiety
H Depression
H Lethargy
H Agitation
H Confusion
Complications
H Tissue hypoxia
H Chronic respiratory acidosis
18
Acute respiratory failure
bronchi or pleural effusion

H Increased tactile fremitus over consolidated lung
tissue
H Hyperresonance
H Diminished or absent breath sounds
H Wheezes (in asthma)
H Rhonchi (in bronchitis)
H Crackles (in pulmonary edema)
Test results
Laboratory
H ABG analysis reveals hypercapnia and hypoxemia.
H Serum white blood cell count is increased in bacterial infections.
H Serum hemoglobin level and hematocrit show decreased oxygen-carrying capacity.
H Serum electrolyte results reveal hypokalemia and
hypochloremia.
H Blood cultures, Gram stain, and sputum cultures
show the pathogen. (See Identifying respiratory
failure.)
Imaging
H Chest X-rays may show underlying pulmonary diseases or conditions, such as emphysema, atelectasis,
lesions, pneumothorax, infiltrates, and effusions.
H Electrocardiography may show arrhythmias, cor pulmonale, and myocardial ischemia.
H Pulse oximetry may show decreased arterial oxygen
saturation.
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H Pulmonary artery catheterization may show pulmo-
nary or cardiovascular causes of acute respiratory

failure.
Treatment
General
H Mechanical ventilation with an endotracheal (ET) or
a tracheostomy tube
Identifying respiratory failure

Use these measurements to identify respiratory failure:
H vital capacity less than 15 cc/kg
H tidal volume less than 3 cc/kg
H negative inspiratory force less than 25 cm H2O
H respiratory rate more than twice the normal rate
H diminished partial pressure of arterial oxygen despite
increased fraction of inspired oxygen
H elevated partial pressure of arterial carbon dioxide with
pH lower than 7.25.
H High-frequency ventilation, if the patient doesnt
respond to conventional mechanical ventilation

H Fluid restriction with heart failure
H Activity as tolerated
Medications
H Cautious oxygen therapy to increase partial pressure
of arterial oxygen
H Antacids
H Histamine-receptor antagonists, such as cimetidine
and ranitidine
H Bronchodilators, such as albuterol and theophylline
H Corticosteroids
H Positive inotropics, such as digoxin and milrinone
H Vasopressors, such as dopamine and dobutamine
Surgery
Key outcomes
The patient will:
H use a support system to assist with coping
H modify lifestyle to minimize the risk of decreased
tissue perfusion.
H Orient the patient frequently.
H Administer oxygen, as ordered.
H Encourage pursed-lip breathing.
H Encourage the use of an incentive spirometer.
H Reposition the patient every 1 to 2 hours.
H Help clear the patients secretions with postural
drainage and chest physiotherapy.

H Assist with or perform oral hygiene.
H Position the patient for comfort and optimal gas
exchange.
H Maintain normothermia.
H Schedule care to provide frequent rest periods.

ventilation
H Obtain blood samples for ABG analysis, as ordered.
H Suction the trachea after hyperoxygenation, as
needed.
H Provide humidification.
H Secure the ET tube per facility policy.
H Prevent infection.
H Prevent tracheal erosion.
H Maintain skin integrity.
H Provide sedation, as necessary.
Monitoring
H Intake and output
H Daily weight
H Cardiac rate and rhythm
H Respiratory status (breath sounds and ABG results)
H Chest X-ray results
H Complications
H Sputum quality, consistency, and color
H Signs and symptoms of infection

ventilation
H Ventilator settings
H Cuff pressures
H Complications of mechanical ventilation
H ET tube position and patency
H Signs and symptoms of stress ulcers
Patient teaching
Be sure to cover:
H smoking cessation, if appropriate
H communication techniques, if intubated
H signs and symptoms of respiratory infection.
Discharge planning
H Refer the patient to a smoking-cessation program, if
applicable.
Acute respiratory failure
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Acute tubular necrosis
Physical findings
Overview
H Evidence of bleeding abnormalities, such as petechi-
H Acute tubular necrosis usually in advanced stage
when diagnosis made
Description
H Injury to the nephrons tubular segment resulting
from ischemic or nephrotoxic injury and causing

renal failure and uremic syndrome
H Also known as acute tubulointerstitial nephritis
Pathophysiology
H In ischemic injury, circulatory collapse, severe hy-
potension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, and
reactions to transfusions may cause disruption of
blood flow to the kidneys.
H Nephrotoxic injury may follow ingestion of certain
chemical agents, such as contrast medium or antibiotics, or result from a hypersensitive reaction of the
kidneys.
Causes
H Diseased tubular epithelium
H Obstructed urine flow
H Ischemic injury to glomerular epithelial cells or vas-
cular endothelium
Incidence
H Accounts for about 75% of acute renal failure cases
H Most common cause of acute renal failure in critical-
ly ill patients
H Decreased urine output
H Hyperkalemia
H Uremic syndrome with oliguria or, rarely, anuria
Complications
H Heart failure
H Uremic pericarditis
H Pulmonary edema
H Uremic lung
H Anemia
H Anorexia, intractable vomiting
H Poor wound healing due to debilitation
ALERT
Fever and chills may signal the onset of an infection, the leading cause of death in acute tubular
necrosis.
Assessment
History
H Ischemic or nephrotoxic injury
H Low urine output (less than 400 ml/24 hours)
H Fever and chills
20
ae and ecchymosis
H Dry, pruritic skin
H Dry mucous membranes
H Uremic breath
H Cardiac arrhythmia, if hyperkalemic
H Muscle weakness
Test results
Laboratory
H Urinary sediment contains red blood cells (RBCs)
and casts.
H Urine specific gravity is low (1.010).
H Urine osmolality is low (less than 400 mOsm/kg).
H Urine sodium level is high(40 to 60 mEq/L).
H Potassium, blood urea nitrogen, and serum creatinine levels are elevated.
H Complete blood count shows decreased RBC count,
hemoglobin level, and hematocrit.
H Metabolic acidosis is evident from blood gas and
electrolyte study results.
H Electrocardiography may show arrhythmias and, with
hyperkalemia, a widening QRS complex, disappearing P waves, and tall, peaked T waves.
Treatment
General
Acute phase
H Vigorous supportive measures until normal kidney
function resumes
Long-term management
H Daily replacement of projected and calculated fluid
loss (including insensible loss)
H Peritoneal dialysis or hemodialysis if the patient is
catabolic or if hyperkalemia and fluid volume overload arent controlled by other measures
H Fluid restriction
H Low-sodium, low-potassium diet
H Rest periods when fatigued
Medications
H Diuretics
H Transfusion of packed RBCs
H Epoetin alfa
H Emergency I.V. administration of 50% glucose, regu-
lar insulin, and sodium bicarbonate (with hyperkalemia)

H Sodium polystyrene sulfonate with sorbitol by mouth
or enema (with hyperkalemia)
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Key outcomes
The patient will:
H maintain hemodynamic stability
limits
H have improved kidney function.
H Give prescribed drugs and blood products.
H Restrict foods containing high sodium and potassium
levels.
H Use aseptic technique, particularly when handling
catheters.
H Provide good skin care.
Monitoring
H Intake and output
H Vital signs
H Complications
Patient teaching
Be sure to cover:
H signs of infection and when to report them to the
physician
H dietary restrictions
H how to set goals that are realistic for the patients
prognosis.
Discharge planning
H Refer the patient to appropriate supportive services
or social service.
21
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Adrenal hypofunction
Overview
Description
H Primary adrenal hypofunction or insufficiency (Addi-
sons disease) originating within the adrenal gland

and characterized by the decreased secretion of mineralocorticoids, glucocorticoids, and androgens
H Secondary adrenal hypofunction due to a disorder
outside the gland such as impaired pituitary secretion of corticotropin; characterized by decreased glucocorticoid secretion
H Adrenal crisis (addisonian crisis), a critical deficiency of mineralocorticoids and glucocorticoids generally following acute stress, sepsis, trauma, surgery, or
the omission of steroid therapy in patients who have
chronic adrenal insufficiency; adrenal crisis, a medical emergency that needs immediate, vigorous treatment
Pathophysiology
H Dysfunction of the adrenal gland results from the
partial or complete destruction of the adrenal cortex.

H It manifests as a clinical syndrome in which the
symptoms are associated with deficient production of

the adrenocortical hormones cortisol, aldosterone,
and androgen.
H High levels of corticotropin and corticotropinreleasing hormone are produced.
H Addisons disease involves all zones of the cortex,
causing deficiencies of the adrenocortical secretions,
glucocorticoids, androgens, and mineralocorticoids.
H Cortisol deficiency causes decreased liver gluconeogenesis (the formation of glucose from molecules
that arent carbohydrates); resulting low blood glucose levels can become dangerously low in patients
who take insulin routinely.
H An aldosterone deficiency causes increased renal
sodium loss and enhances potassium reabsorption.
H Hypotension then develops due to sodium excretion.
H Angiotensin II production increases due to the low
plasma volume and decreased arteriolar pressure.
H Androgen deficiency may decrease hair growth in
axillary and pubic areas (less noticeable in men)
as well as on the extremities of women.
Causes
Primary hypofunction
H Autoimmune process in which circulating antibodies
react specifically against the adrenal tissue
H Tuberculosis (once the chief cause, now responsible
for less than 20% of adult cases)
H Bilateral adrenalectomy
H Hemorrhage into the adrenal gland
H Neoplasms
H Infections (histoplasmosis, cytomegalovirus)
22
H Family history of autoimmune disease (may predis-
pose the patient to Addisons disease and other

endocrinopathies)
Secondary hypofunction
H Hypopituitarism
H Abrupt withdrawal of long-term corticosteroid
therapy
H Removal of a corticotropin-secreting tumor
Adrenal crisis
H Exhausted body stores of glucocorticoids in a patient
with adrenal hypofunction after trauma, surgery, or
other physiologic stress
Incidence
H Relatively uncommon
H Can occur at any age and in both sexes
Autoimmune Addisons disease
H Most common in white females (genetic predisposition likely)
H More common in patients with a familial predisposition to autoimmune endocrine diseases
Special populations
Most people with Addisons disease are diagnosed
in their 20s to 40s.
H Conspicuous bronze color of the skin
H Darkening of scars, areas of vitiligo (absence of pigmentation), and increased pigmentation of the mucous membranes, especially the buccal mucosa
H Decreased tolerance for even minor stress
H Fasting hypoglycemia
H Craving for salty food
Secondary hypofunction
H Similar to primary hypofunction, but without hyperpigmentation
Addisonian crisis
H Profound weakness and fatigue
H Nausea, vomiting, and dehydration
H Hypotension
H High fever followed by hypothermia (occasionally)
Complications
H Hyperpyrexia
H Psychotic reactions
H Deficient or excessive steroid treatment
H Shock
H Profound hypoglycemia
H Ultimate vascular collapse, renal shutdown, coma,
and death (if untreated)
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Assessment
History
Key outcomes
H Synthetic steroid use, adrenal surgery, or recent
The patient will:

H maintain an adequate fluid balance
H remain free from signs and symptoms of infection
H develop adequate coping skills.
infection
H Muscle weakness
H Fatigue
H Weight loss
H Craving for salty food
H Decreased tolerance for stress
H GI disturbances
H Dehydration
H Amenorrhea (in females)
H Impotence (in males)
Physical findings
H Poor coordination
H Decreased axillary and pubic hair (in females)
H Bronze coloration of the skin, darkening of scars
H Areas of vitiligo
H Increased pigmentation of mucous membranes
H Weak, irregular pulse
H Hypotension
Test results
Laboratory
H Rapid corticotropin stimulation test: low corticotropin level indicates a secondary disorder; elevated
level indicates a primary disorder.
H Plasma cortisol level is decreased (less than 10
mcg/dl in the morning; less in the evening).
H Serum sodium and fasting blood glucose levels are
decreased.
H Serum potassium, calcium, and blood urea nitrogen
levels are increased.
H Hematocrit is elevated and lymphocyte and eosinophil counts are increased.
Imaging
H Chest X-ray shows small heart.
H Computed tomography scan of the abdomen shows
adrenal calcification (if the cause is infectious).
Treatment
General
H I.V. fluids
H Periods of rest
H Small, frequent, high-protein meals
Medications
H Lifelong corticosteroid replacement, usually with
cortisone or hydrocortisone
H Oral fludrocortisone
H Hydrocortisone
H I.V. saline and glucose solutions (for adrenal crisis)
H Until onset of mineralocorticoid effect, encourage
fluids to replace excessive fluid loss.

H Arrange for a diet that maintains sodium and potassi-
um balances; if the patient is anorexic, suggest six

small meals per day to increase caloric intake.
H Observe for cushingoid signs such as fluid retention
around the eyes and face.
H Check for petechiae.
H If the patient receives glucocorticoids alone, observe
for orthostatic hypotension or electrolyte abnormalities.
Monitoring
H Vital signs
H Signs of shock (decreased level of consciousness and
urine output)
H Hyperkalemia before treatment; hypokalemia after
treatment
H Cardiac rhythm
H Blood glucose levels
H Daily weight
H Intake and output
Patient teaching
Be sure to cover:
H lifelong steroid therapy requirement
H symptoms of steroid overdose (swelling, weight gain)
and steroid underdose (lethargy, weakness)
H risk for developing diabetes
H dosage may need to be increased during times of
stress or illness (when the patient has a cold, for
example)
H infection, injury, or profuse sweating in hot weather
may precipitate adrenal crisis
H importance of carrying a medical identification card
that states the patient is on steroid therapy (name of
the drug and its dosage should be included on the
card)
H how to give a hydrocortisone injection and to keep
an emergency kit containing hydrocortisone in a prepared syringe available for use in times of stress
H stress-management techniques.
Discharge planning
H Refer the patient to the National Adrenal Diseases
Foundation for support and information.
23
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Adrenogenital
syndrome
Overview
Description
H A group of disorders resulting from hyperplasia of
the adrenal cortex

H May be inherited (congenital adrenal hyperplasia
[CAH]) or acquired, usually as a result of an adrenal

tumor (adrenal virilism)
H May cause fatal adrenal crisis in neonates (salt-losing
CAH)
Pathophysiology
H Deficiencies occur in the enzymes needed for adre-
nocortical secretion of cortisol and, possibly, aldosterone.

H Compensatory secretion of corticotropin produces
varying degrees of adrenal hyperplasia.
Simple virilizing CAH
H Deficiency of the enzyme 21-hydroxylase results in
underproduction of cortisol.
H This cortisol deficiency stimulates increased secretion of corticotropin, producing large amounts of
cortisol precursors and androgens that dont require
21-hydroxylase for synthesis.
Salt-losing CAH
H 21-hydroxylase is almost completely absent.
H Corticotropin secretion increases, causing excessive
production of cortisol precursors, including saltwasting compounds.
H Plasma cortisol and aldosterone levels both dependent on 21-hydroxylase fall precipitously and,
in combination with the excessive production of saltwasting compounds, precipitate acute adrenal crisis.
H Corticotropin hypersecretion stimulates adrenal androgens and produces masculinization.
Causes
H Transmitted as an autosomal recessive trait
Incidence
H Acquired adrenal virilism: rare and affects twice as
many females as males
Special populations
CAH is the most prevalent adrenal disorder in infants and children; simple virilizing CAH and saltlosing CAH are the most common forms.
H Ambiguous genitalia but normal genital tract and gonads (Female neonates may present with labioscrotal
24
Adrenogenital syndrome
fusion and an enlarged clitoris with a urethral opening at its base.)

Salt-losing CAH
FEMALES
H More complete virilization than the simple form
H Results in development of male external genitalia
without testes
MALES
H No external genital abnormalities
H Difficult immediate neonatal diagnosis; commonly
delayed until the infant develops severe systemic

symptoms
Complications
H Hypertension
H Hyperkalemic infertility
H Adrenal tumor
H Adrenal crisis
H Altered growth, external genitalia, and sexual
maturity
Salt-losing CAH
H Cardiovascular collapse
H Cardiac arrest
Assessment
History
H Failure to begin menstruation
H Frequent erections at an early age
Salt-losing CAH
H Apathy, failure to eat, and diarrhea (in infants)
H Symptoms of adrenal crisis in the first week of life
(vomiting, dehydration from hyponatremia, hyperkalemia)
Physical findings
H In CAH, pseudohermaphroditism in females or pre-
cocious puberty in both sexes

Salt-losing CAH
H Signs of progressive virilization at an early age: early
appearance of pubic and axillary hair, deep voice,
acne, facial hair
H Small testes
H Possible greater height than other children of the
same age
Test results
Laboratory
H Plasma 17-ketosteroid (17-KS) levels , which can be
suppressed by administering oral dexamethasone,
are elevated.
H Urine levels of hormone metabolites, particularly
pregnanetriol, are elevated.
H Plasma 17-hydroxyprogesterone level is elevated.
H Urine levels of 17-hydroxycorticosteroids are normal
or decreased.
H Plasma aldosterone and cortisol levels are decreased.
H Serum DHEA sulfate levels are high.
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Special populations
Adrenal hypofunction or adrenal crisis in the first
week of life suggests salt-losing CAH. Hyperkalemia, hyponatremia, and hypochloremia with excessive urinary 17-KS and pregnanetriol and decreased urinary aldosterone levels confirm it.
H Gonadal biopsy and chromosomal studies confirm
hermaphrodism.
Other
H Sex chromatin and karyotype studies determine the
genetic sex of patients with ambiguous external genitalia.
H X-ray evaluates accelerated bone aging.
Treatment
General
H No activity restriction
Medications
H Daily administration of cortisone or hydrocortisone
Salt-losing CAH with patient in adrenal crisis
H Immediate I.V. sodium chloride and glucose infusion
H Desoxycorticosterone I.M. and hydrocortisone I.V.
H Maintenance includes mineralocorticoid (desoxycorticosterone, fludrocortisone, or both) and glucocorticoid (cortisone or hydrocortisone) replacement
Monitoring
H Body weight
H Blood pressure
H Serum electrolyte levels
H Edema, weakness, and hypertension for the patient
receiving desoxycorticosterone or fludrocortisone
Patient teaching
Be sure to cover:
H possible adverse effects (cushingoid symptoms) of
long-term therapy (lifelong maintenance therapy with
hydrocortisone, cortisone, or the mineralocorticoid
fludrocortisone is essential)
H importance of not withdrawing therapeutic drugs
suddenly because potentially fatal adrenal hypofunction will result
H need to report stress and infection, which require increased steroid dosages
H importance of carrying a medical identification card
that states the patient is on steroid therapy (name of
the drug and its dosage should be included on the
card)
H risk of developing diabetes due to long-term
cortisone therapy.
Discharge planning
H Refer the patient for psychological counseling to help
accept this disorder.
Surgery
H Reconstructive surgery based on the determined sex
and external genitalia
Key outcomes
The patient will:
H maintain adequate fluid balance
H have normal laboratory test results
H express understanding of the disorder and treatment
modality, as will his family.
H Maintain I.V. access, infuse fluids, and give steroids,
as ordered.
H Watch for cyanosis, hypotension, tachycardia, tachyp-
nea, and signs of shock.

H Minimize external stressors.
H If a child is receiving maintenance therapy with
steroid injections, rotate I.M. injection sites to

prevent atrophy; tell the parents to do the same.
Adrenogenital syndrome
25
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Age-related macular
degeneration
Causes
Overview
H Smoking
H Age
H Race
H High blood pressure
H Vascular disease
H High intake of saturated fat and cholesterol
H Farsightedness
H Exposure to sunlight
Description
H Deterioration of the macular portion of the retina,
which is responsible for detailed vision

H May be atrophic, also called involutional or dry
H May be exudative, also called hemorrhagic or wet
H No cure for atrophic form
H Commonly affects both eyes
H Also known as AMD
Pathophysiology
H Pathologic changes occur primarily in the retinal pig-
ment epithelium, Bruchs membrane, and choriocapillaries in the macular region that result from the
hardening and obstruction of retinal arteries.
H Formation of new blood vessels in the macular area
obscures central vision.
H Vision loss occurs as the retinal pigment epithelium
detaches and becomes atrophic.
H Exudative macular degeneration develops as new
blood vessels in the choroid project through abnormalities in Bruchs membrane, invading the potential
space underneath the retinal pigment epithelium.
H The vessels leak, and fluid in the retinal pigment epithelium increases, resulting in blurry vision.
H Unknown
H Genetic in origin
Risk factors
Incidence
H Affects as many as 15 million Americans
H Leading cause of vision loss in people older than age
60 in the United States

H Irreversible central vision loss in at least 10% of
elderly people
H Atrophic form in about 85% of patients
H More common in whites, but affects all races
H Decreased central vision, for near and distance (see
How AMD affects central vision)

H Progressive worsening
H Blind spots
Complications
H Blindness
H Nystagmus
How AMD affects central vision

Central vision occurs in the macula and involves the ability
to perceive sharp, detailed images. At the center of the macula is the fovea containing the highest concentration of
rods and cones and the most light-sensitive portion of
the macula.
Light entering the cornea and lens are focused on the
fovea. If any part of the macula deteriorates, the eye must
Lens
Visual
axis
Cornea
Iris
Macula
Fovea
Optic nerve
26
Age-related macular degeneration
rely on the less-sensitive, outer portion of the retina, which

is responsible for peripheral vision.
With age-related macular degeneration (AMD), grayness,
haziness, or a blind spot may appear in the area of central
vision. Words may be blurred on a page; straight lines may
appear to have kinks in them; colors may seem dimmer.
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Assessment
History
H Blank spot seen in the center of a page (scotoma)
while reading
Monitoring
H Visual acuity
H Environment (for safety purposes)
Patient teaching
H Central vision that blurs intermittently and has graduH Straight lines appearing distorted
H Letters appearing fragmented
Be sure to cover:
H ways to modify the home environment for safety
H effects on peripheral vision.
Physical findings
Discharge planning
H Tiny yellowish spots (drusen) beneath retina
H Refer the patient to the American Foundation for
Test results
the Blind or Associated Services for the Blind, as

indicated.
ally worsened
H Indirect ophthalmoscopy may show changes in the
macular region of the fundus.
H Fluorescein angiography may show leaking vessels in
subretinal neovascular net.
H Amsler grid test may detect visual distortion.
Treatment
General
H Laser treatment, if leaking blood vessels have devel-
oped away from the fovea

H Diet high in vitamins A, C, and E; beta-carotene; and
zinc
H Activity restrictions based on visual acuity
Medications
H Copper and zinc supplements
H Lutein, vitamins C and E, and beta-carotene
Surgery
H In exudative form, argon laser photocoagulation
(may slow the progression of severe visual loss)
Key outcomes
The patient will:
H express feelings and concerns over diminishing eyesight
H sustain no harm or injury
H verbalize understanding of the condition and treatment
H maintain optimal visual function or adapt as necessary.
H Help the patient obtain optical aids such as magni-
fiers.
H Offer the patient emotional support.
H Encourage expression of fears and concerns.
Age-related macular degeneration
27
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Alcoholism
Overview
Description
H Chronic disorder of uncontrolled intake of alcoholic
beverages
H Interferes with physical and mental health, social and
familial relationships, and occupational responsibilities
Pathophysiology
H Alcohol is soluble in water and lipids and permeates
all body tissues.

H Liver metabolizes 90% of alcohol absorbed and is the
most severely affected organ; hepatic steatosis followed by hepatic fibrosis is evident days after heavy
drinking.
H Laennecs cirrhosis may develop after inflammatory
response (alcoholic hepatitis) or in absence of inflammation, as a consequence of direct activation of
lipocytes (Ito cells).
H Lactic acidosis and excess uric acid is promoted; gluconeogenesis, B-oxidation of fatty acids, and the
Krebs cycle are opposed; and hypoglycemia and hyperlipidemia develop.
H Toxicity of cells occurs through reduction of mitochondrial oxygenation utilization, depletion of deoxyribonucleic acid, and other actions.
Causes
H Biological factors
H Psychological factors
H Sociocultural factors
Risk factors
H Male gender
H Low socioeconomic status
H Family history
H Depression
H Anxiety
H History of other substance abuse disorders
Incidence
H Affects all social and economic groups
H 10% of the population accounts for 50% of all alco-
hol consumed
H About 13% of all adults older than age 18 have suf-
fered from alcohol abuse or dependence

H Males are two to five times more likely to abuse alco-
hol than females

H Occurs at all stages of the life cycle, beginning as
early as elementary school age
H Prevalent in 20% of adult hospital inpatients
Special populations
Prevalence of drinking is highest between ages 21
and 34, but current statistics show that up to 19%
28
Alcoholism
of 12- to 17-year-olds have serious drinking problems. Research also suggests that alcoholism affects
2% to 10% of adults older than age 60.
H Hide or deny addiction
H May temporarily manage to maintain a functional
lifestyle
Complications
H Cardiomyopathy
H Pneumonia
H Cirrhosis
H Esophageal varices
H Pancreatitis
H Alcoholic dementia
H Wernickes encephalopathy
H Seizure disorder
H Depression
H Multiple substance abuse
H Hypoglycemia
H Leg and foot ulcers
H Suicide and homicide
H Death
Assessment
History
H Need for daily or episodic alcohol use for adequate
function
H Inability to discontinue or reduce alcohol intake
H Episodes of anesthesia or amnesia during intoxica-
tion
H Episodes of violence during intoxication
H Interference with social and familial relationships
and occupational responsibilities

H Malaise, dyspepsia, mood swings or depression, and
an increased incidence of infection

H Secretive behavior
Physical findings
H Poor personal hygiene
H Unusually high tolerance for sedatives and opioids
H Signs of nutritional deficiency
H Signs of injury
H Withdrawal signs and symptoms
H Major motor seizures
DSM-IV-TR criteria
A diagnosis is confirmed when the patient meets at least
three of these signs and symptoms:
H more alcohol ingested than intended
H persistent desire or efforts to diminish alcohol use
H excessive time spent obtaining alcohol
H frequent intoxication or withdrawal symptoms
H impairment of social, occupational, or recreational
activities
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H continued alcohol consumption despite knowledge
of a social, psychological, or physical problem thats

caused or exacerbated by alcohol use
H marked tolerance
H characteristic withdrawal symptoms
H alcohol used to relieve or avoid withdrawal symptoms
H persistent symptoms for at least 1 month or recurrence over a longer time.
Test results
Laboratory
H Blood alcohol tests show levels of at least 0.10%
weight/volume (200 mg/dl).
H Serum electrolyte levels are abnormal.
H Serum ammonia levels are increased.
H Serum amylase levels are increased.
H Urine toxicology may show abuses of other drugs.
H Liver function study results are abnormal.
Other
H CAGE screening test: two affirmative responses make
patient 7 times more likely to be alcohol dependent.
Key outcomes
The patient (or family) will:
H report feeling safe in hospital environment
H join gradually in self-care and the decision-making
process
H engage in appropriate social interaction with others
H demonstrate a decrease in negative self-evaluation
verbally and behaviorally
H identify support systems to assist them and participate in mobilizing these systems.
H Institute seizure precautions.
H Orient the patient to reality.
H Maintain a calm environment, minimizing noise and
shadows.
H Avoid restraints, unless necessary for protection.
H Use a nonthreatening approach.
H Alcohol disorders identification test (AUDIT): score
Monitoring
greater than 8 indicates alcohol dependency.

H Michigan alcohol screening test (MAST): score
greater than 5 indicates alcohol dependency.
H Mental status
H Vital signs
H Safety measures
H Nutritional and hydration status
H Intake and output
Treatment
General
Immediate
H Support for respiration
H Prevention of aspiration of vomitus
H Replacement of fluids
H Administration of I.V. glucose
H Correction of hypothermia or acidosis
H Treatment of trauma, infection, or GI bleeding
Long-term
H Total abstinence
H Detoxification, rehabilitation, and aftercare program
H Supportive counseling
H Individual, group, or family psychotherapy
H Ongoing support groups
H Safety precautions, including preventing aspiration
of vomitus
H Seizure precautions
Patient teaching
Be sure to cover:
H alcohol abstinence
H plan for relapse
adverse effects
H effects of disorder on significant others.
Discharge planning
H Refer the patient to a rehabilitation program.
H Refer the patient to social services.
H Refer the patient to support services.
H Refer the patient to personal and family counseling.
Medications
H Anticonvulsants
H Antiemetics
H Antidiarrheals
H Tranquilizers, particularly benzodiazepines
H Naltrexone
H Antipsychotics
H Daily oral disulfiram
H Vitamin supplements
Alcoholism
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Allergic purpura
Overview
Description
H An acute or chronic vascular inflammation affecting
the skin, joints, and GI and genitourinary (GU)

tracts, in association with allergy symptoms
H Purpura associated with other conditions such as
erythema nodosum
H A nonthrombocytopenic purpura
H Known as Henoch-Schnlein syndrome or anaphylactoid purpura when it primarily affects the GI tract
and is accompanied by joint pain
Pathophysiology
H An autoimmune reaction triggered by a bacterial in-
fection is directed against vascular walls.

H Inflammation of the veins and capillaries disrupts the
vascular wall, resulting in loss of red blood cells and

bleeding and leakage into the skin and mucous
membranes.
Causes
H Bacterial infection (particularly streptococcal infec-
tion)
H Allergic reactions to some drugs and vaccines, insect
bites, and foods (such as wheat, eggs, milk, and

chocolate)
Henoch-Schnlein syndrome
H Transient or severe colic
H Tenesmus (spasmodic contraction of the anal
sphincter)
H GI bleeding
H Rheumatoid pains and periarticular effusions, usually
affecting the legs and feet
Complications
H Renal disease (renal failure and acute glomeru-
lonephritis)
H Hypertension
Assessment
History
H Bacterial infection or exposure to allergen
H Moderate and irregular fever
H Headache
H Anorexia
H Pruritus and paresthesia in areas of lesions
Physical findings
H Characteristic lesions that usually appear in symmet-
rical patterns on the arms, legs, and buttocks

H In children, urticarial skin lesions that expand and
become hemorrhagic
H Possibly scattered petechiae on the legs, buttocks,
and perineum
H Localized edema of the hands, feet, or scalp
Incidence
Test results
H Affects more males than females

H Most prevalent in children ages 3 to 7
Laboratory
H Results of tests for blood in the urine and stool may
be positive.
H Increased blood urea nitrogen and creatinine levels
may indicate renal involvement.
H Skin lesions that are purple, macular, ecchymotic,
and of varying size and are caused by vascular leakage into the skin and mucous membranes (see Identifying purpuric lesions)
Identifying purpuric lesions

Lesions of allergic purpura, such as those pictured on the
foot and leg below, characteristically vary in size.
ALERT
No laboratory test clearly identifies allergic purpura (although white blood cell count and erythrocyte
sedimentation rate are elevated).
Imaging
H Small-bowel X-rays may reveal areas of transient
edema.
Treatment
General
H Symptomatic
Medications
H Steroids
H Analgesics
30
Allergic purpura
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Key outcomes
The patient will:
H express feelings of comfort and relief of pain
H exhibit improved or healed lesions
H identify precipitating factors with appropriate skin
care regimen.
H Encourage maintenance of an elimination diet to
help identify specific allergenic foods.

H Provide analgesics, as needed.
H Provide passive range-of-motion exercises, if appro-
priate.
H Provide emotional support and reassurance, espe-
cially if the patient is temporarily disfigured by florid

skin lesions.
Monitoring
H Condition and number of skin lesions
H Level of pain
H GI and GU complications
Patient teaching
Be sure to cover:
H need for the patient to immediately report recurrence of symptoms (most common about 6 weeks
after initial symptoms)
H importance of returning for follow-up urinalysis as
scheduled.
Allergic purpura
31
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Allergic rhinitis
Overview
Description
H An immune response of the upper airways triggered
by inhaled airborne allergens

H Seasonal allergic rhinitis: an immunoglobulin (Ig) E-
mediated type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible person
H Perennial rhinitis: inhaled allergens provoke antigen
responses that produce signs and symptoms
year-round
Pathophysiology
H The bodys immune system overresponds to common
Perennial allergic rhinitis

H Chronic and extensive nasal obstruction or stuffiness
Physical findings
Seasonal allergic rhinitis
H Pale, cyanotic, edematous nasal mucosa
H Red and edematous eyelids and conjunctivae
H Excessive lacrimation
H Nasal polyps
H Dark circles under the eyes (allergic shiners)
Test results
Laboratory
H Sputum and nasal secretions show a high number of
eosinophils.
H IgE levels are normal or elevated, possibly linked to
seasonal overproduction of interleukin-4 and -5
(involved in the allergic inflammatory process).
allergens in the nose.

H Antibodies attach to mast cells, which release several
chemicals, including histamine, which cause dilation

of blood vessels, skin redness, and swollen membranes in the nose.
Causes
H Tree pollens (in spring)
H Grass and weed pollens (in summer)
H Weed pollens (in fall)
H Mold spores (occasionally, in summer and fall)
H House dust and dust mites
H Molds
H Animal dander
H Tobacco smoke
H Processed materials or industrial chemicals
Incidence
H Affects more than 20 million Americans
H Can affect anyone at any age
H Most prevalent in young children and adolescents
H Swollen nasal membranes
Complications
Treatment
General
H Elimination of environmental antigens, if possible
H Increased fluid intake to loosen secretions
H Restriction of activities in areas of allergen exposure
Medications
H Antihistamines, such as cetirizine, diphenhydramine,
and loratadine
H Intranasal corticosteroids, such as budesonide and
triamcinolone
H Leukotriene receptor antagonists such as mon-
telukast
H Nasal decongestants, such as oxymetazoline and
pseudoephedrine
Long-term management
H Immunotherapy or desensitization with injections of
allergen extracts administered before or during the
allergy season or perennially
Key outcomes
H Secondary sinus and middle ear infections

H Nasal polyps

H maintain current health status
H verbalize feelings and concerns
H express feelings of increased comfort.
Assessment
History
H Paroxysmal sneezing, profuse watery rhinorrhea
H Nasal obstruction or congestion
H Pruritus of the nose and eyes
H Headache or sinus pain
H Itchy throat, malaise, and fever
32
Allergic rhinitis
H Implement measures to relieve signs and symptoms
and increase the patients comfort.

H Encourage increased fluid intake to loosen secre-
tions.
H Elevate the head of the bed and provide humidifica-
tion to ease breathing.
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ALERT
Before giving a desensitization injection, assess the
patients symptoms. After giving the injection, observe him for 30 minutes to detect adverse reactions, including anaphylaxis and severe localized
erythema. Make sure epinephrine and emergency
resuscitation equipment are available.
Monitoring
H Compliance with the prescribed drug regimen
H Changes in control of signs and symptoms
H Indications of drug misuse
Patient teaching
Be sure to cover:
H importance of calling the physician if the patient experiences a delayed reaction to the desensitizing injections
H reduction of environmental exposure to airborne allergens
H skin protectant applications
H possible lifestyle changes, such as relocation to a
pollen-free area either seasonally or year-round, in
severe and resistant allergic rhinitis
adverse effects.
Allergic rhinitis
33
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Alopecia
Overview
Description
H More commonly known as hair loss, typically occurs
on the scalp; less common and conspicuous elsewhere on the body

H Can be irreversible because scarring alopecia usually
destroys hair follicle
H Nonscarring form (noncicatricial alopecia): hair
generally regrows
H Most common form of nonscarring alopecia known
as male-pattern alopecia or androcentric alopecia
H Telogen effluvium: a diffuse alopecia in which numerous hair follicles simultaneously change from the
growing anagen phase to the resting telogen phase of
the hair growth cycle
H Alopecia areata (idiopathic form): a generally reversible and self-limiting disorder most prevalent in
young and middle-aged adults of both sexes
H Time of onset, degree of baldness, speed with which
it spreads, and pattern of hair loss dependent on genetic predisposition
H Poor prognosis for regrowth with hair loss that persists for more than 1 year
Pathophysiology
H In male-pattern alopecia, a genetically predisposed
response to androgens causes transformation of the

androgen-sensitive follicles into vellus follicles; normal hair is shed and replaced by fine, light, short
hair.
H In female-pattern alopecia, theres usually an elevation in serum adrenal androgen dehydroepiandrosterone sulfate.
Causes
Nonscarring alopecia
H Genetic predisposition
H Androgen response
H Aging
H Radiation
H Chemotherapy
H Drugs (see Cancer drugs that cause alopecia)
H Bacterial and fungal infections
H Psoriasis
H Seborrhea
H Endocrine disorders
H Excess vitamin A
Scarring alopecia
H Physical or chemical trauma
H Radiation
H Chemotherapy
H Chronic tension on a hair shaft
H Destructive skin tumors
H Granulomas
H Lupus erythematosus
H Scleroderma
34
Alopecia
H Follicular lichen planus

H Severe bacterial or viral infections
Incidence
H Affects males more than females
H Occurs most commonly in males older than age 50
in male-pattern alopecia
H Rises with increasing age in male-pattern alopecia
H Occurs to some degree in 37% of postmenopausal
women
H Hair loss
Complications
H Impaired self-image
Assessment
History
Male-pattern alopecia
H Presence of predisposing factors
H Family history of hair loss
H Gradual onset of hair loss
H Typically describes hairline as receding and his
crown becoming bald
Female-pattern alopecia
H Typically describes a widening of her part and increasing visibility of her front scalp or crown
Telogen effluvium
H Loss of about 400 hairs per day, which is four to five
times greater than the normal daily hair loss
Alopecia areata
H Sudden loss of hair
Physical findings
H Small patches of visible scalp or entire scalp visible
(alopecia totalis); may involve the entire body

(alopecia universalis)
H Generally, normal scalp appearance
H Exclamation point hairs (loose hairs with dark,
rough, brushlike tips on narrow, less pigmented
shafts) at the periphery of new patches
H Regrowth initially as fine, white, downy hair; replaced by normal hair
Test results
Laboratory
H Direct microscopic examination shows structural
abnormalities or signs of infection.
TELOGEN EFFLUVIUM
H Pluck or pull test reveals positive results if more than
four hairs come out.

H Woods lamp examination shows presence of fungal
infection.
H Trichogram shows abnormal ratio of anagen to
telogen hairs.
H Scalp biopsy shows hair phase and the extent of
structural damage.
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Cancer drugs that cause alopecia

Certain cancer drugs can cause hair loss ranging from sporadic thinning to complete baldness. Some drugs damage hair follicles and cause hair roots to atrophy.
Mild alopecia
H bleomycin
H carmustine
H fluorouracil
H hydroxyurea
H melphalan
Moderate alopecia
Severe alopecia
H busulfan
H etoposide
H floxuridine
H methotrexate
H mitomycin
Treatment
General
H Identification and treatment of underlying cause
H Cosmetic interventions, such as hairpieces, weaving,
or bonding
H cyclophosphamide
H daunorubicin
H doxorubicin
H vinblastine
H vincristine
H For the patient undergoing radiation therapy or
chemotherapy with drugs that cause alopecia, suggest selecting a hair replacement before treatment.
H Encourage the patient to express his feelings. Help
him develop interests that contribute to a positive
self-image.
H Occlusive dressing that promotes normal hair growth
Monitoring
by protecting the site of hair loss (in trichotillomania)

H Cold cap application and scalp tourniquet that reduce the blood supply to the scalp and thereby preserve more hair structure
H Complications
Medications
H Topical application of minoxidil
H Oral finasteride
ALERT
Finasteride is contraindicated in women of childbearing age.
H Corticosteroids
H Photochemotherapy with methoxsalen and ultraviolet
Patient teaching
Be sure to cover:
H familial link in male-pattern alopecia
H well-balanced diet with adequate protein
H avoidance of excess vitamin A
H myths concerning commercial preparations
H signs and symptoms of skin infection
H possibility that hair may grow back in a different color or type, such as curly or straight.
light
H Dermatomucosal agents
H Antibiotics
H Antifungal agents
Surgery
H Surgical redistribution of hair follicles by auto-
grafting
H Hair transplantation and tunnel grafting
Key outcomes
The patient will:
H express concerns about his condition or treatment
H avoid complications
H verbalize feelings about changed body image.
H Reassure the patient with female-pattern alopecia
that hair thinning doesnt lead to total baldness. Suggest that she wear a wig or hairpiece.
Alopecia
35
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Alzheimers disease
H Pneumonia and other infections

H Malnutrition and dehydration
Overview
Assessment
Description
History
H Degenerative disorder of the cerebral cortex (espe-
H History obtained from a family member or caregiver

H Insidious onset
H Initial changes almost imperceptible
H Forgetfulness and subtle memory loss
H Recent memory loss
H Difficulty learning and remembering new information
H General deterioration in personal hygiene
H Inability to concentrate
H Tendency to perform repetitive actions and experi-
cially the frontal lobe), which accounts for more

than 50% of all cases of dementia
H Poor prognosis
H No cure or definitive treatment
Pathophysiology
H Alzheimers disease is a genetic abnormality on chro-
mosome 21.
H Brain damage is caused by a genetic substance (amy-
loid).
H There are three distinguishing features of brain tissue: neuro-fibrillary tangles, neuritic plaques, and
granulovascular degeneration.
Causes
H Unknown
Risk factors
Neurochemical
H Deficiencies of the neurotransmitters
Environmental
H Aluminum and manganese
H Trauma
H Genetic abnormality on chromosome 21
H Slow-growing central nervous system viruses
Incidence
H Severe form in patients older than age 65
H May affect 5 million Americans
H Affects 13% or 1 in 8 people older than age 65 and
nearly 50% of those older than age 85
ence restlessness
H Negative personality changes (irritability, depression,
paranoia, hostility)
H Nocturnal awakening
H Disorientation
H Suspicious and fearful of imaginary people and situa-
tions
H Misperceives own environment
H Misidentifies objects and people
H Complains of stolen or misplaced objects
H Emotions may be described as labile
H Mood swings, sudden angry outbursts, and sleep dis-
turbances
Physical findings
H Impaired sense of smell (usually an early symptom)
H Impaired stereognosis
H Gait disorders
H Tremors
H Positive snout reflex
H Organic brain disease in adults
H Urinary or fecal incontinence
H Seizures
Test results
H Gradual loss of recent and remote memory

H Loss of sense of smell
H Flattening of affect and personality
H Difficulty with learning new information
H Deterioration in personal hygiene
H Increasing difficulty with abstraction and judgment
H Impaired communication
H Loss of coordination
H Inability to write or speak
H Nocturnal awakenings
H Signs of anxiety
H Loss of eye contact and fearful look
H Acute confusion, agitation, obsessive-compulsive
H Diagnosed by exclusion; tests are performed to rule
behavior
Complications
H Injury from violent behavior, wandering, or unsuper-
vised activity
36
Alzheimers disease
out other diseases.

H Positive diagnosis is made on autopsy.
Imaging
H Position-emission tomography reveals metabolic
activity of the cerebral cortex.
H Computed tomography scan shows excessive and
progressive brain atrophy.
H Magnetic resonance imaging rules out intracranial
lesions.
H Cerebral blood flow studies reveal abnormalities in
blood flow to the brain.
H Cerebrospinal fluid analysis shows chronic neurologic infection.
H EEG evaluates the brains electrical activity and may
show slowing of the brain waves in late stages of the
disease.
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Other
H Neuropsychologic tests may show impaired cognitive
ability and reasoning.
Treatment
General
H Behavioral interventions (patient-centered or care-
Monitoring
H Fluid intake and nutrition status
Patient teaching
Medications
Be sure to cover:
H the disease process
H exercise regimen
H importance of cutting food and providing finger
foods, if indicated
H use of plates with rim guards, built-up utensils, and
cups with lids
H independence.
H Psychostimulators
H Antidepressants, such as paroxetine, sertraline, and
Discharge planning
giver training) focused on managing cognitive and

behavioral changes
H Well-balanced diet (may need to be monitored)
H Safe activities as tolerated (may need to be
monitored)
fluoxetine
H Anxiolytics, such as alprazolam and diazepam
H Antipsychotics, such as haloperidol, risperidone, and
quetiapine
H Anticonvulsants, such as valproic acid, gabapentin,
and lamotrigine
H Anti-inflammatories (experimental)
H Anticholinesterase agents, such as donepezil, rivastigmine, and galantamine
H Vitamin E (experimental)
H N-methyl-D-aspartate receptor antagonists such as
memantine
H Refer the patient to the Alzheimers Association.

H Refer the patient to social services for additional sup-
port.
Key outcomes
The patient will:
H perform activities of daily living
H maintain daily calorie requirements
H perform self-care needs
H use support systems and develop adequate coping
behaviors.
H Provide an effective communication system.
H Use soft tones and a slow, calm manner when speak-
ing to the patient.

H Allow the patient sufficient time to answer questions.
H Protect the patient from injury.
H Provide rest periods.
H Provide an exercise program.
H Encourage independence.
H Offer frequent toileting.
H Assist with hygiene and dressing.
H Provide familiar objects to help with orientation and
behavior control.
Alzheimers disease
37
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Amebiasis
Overview
Description
H An acute or chronic protozoal infection caused by
Entamoeba histolytica
H Produces varying degrees of illness, from no symp-
toms to mild diarrhea to fulminant dysentery

H Extraintestinal type: may induce hepatic abscess and
infections of the lungs, pleural cavity, pericardium,

peritoneum and, rarely, the brain
H Also known as amebic dysentery
Pathophysiology
H E. histolytica exists in two forms, as a cyst (which
can survive outside the body) and a trophozoite

(which cant survive outside the body).
H The ingested cysts pass through the intestine, where
digestive secretions break them down and liberate
the motile trophozoites within.
H The trophozoites multiply and either invade and ulcerate the mucosa of the large intestine or simply
feed on intestinal bacteria.
H As the trophozoites are carried slowly toward the
rectum, theyre encysted and then excreted in feces.
Causes
H Ingestion of feces-contaminated food or water
Incidence
H Occurs worldwide: most common in the tropics, sub-
tropics, and other areas with poor sanitation and

health practices
H In the United States: overall incidence between 1%
and 3% but may be higher among homosexuals and
institutionalized people, in whom fecal-oral contamination is more common and in immigrants from developing countries
H The clinical effects of amebiasis varying with the
severity of the infestation

Acute amebic dysentery
H Sudden high temperature of 104 to 105 F (40 to
40.6 C)
H Profuse, bloody, mucoid diarrhea with tenesmus
Chronic amebic dysentery
H Intermittent diarrhea that lasts for 1 to 4 weeks and
recurs several times per year
Amebic granuloma
H Blood and mucus in the stool
H Partial or complete bowel obstruction
Complications
H Subacute appendicitis
H Perforation of the intestinal wall with spread to the
liver, lungs, pleural cavity, peritoneum, and brain.
38
Amebiasis
Assessment
History
H Fever, chills
H Abdominal cramping
H Profuse, bloody, mucoid diarrhea
H Multiple (4 to 18) foul-smelling mucus- and bloodtinged stools daily
H Mild fever
H Vague abdominal cramps
H Possible weight loss
Physical findings
H Diffuse abdominal tenderness
H Tenderness over the cecum and ascending colon
H Hepatomegaly (occasionally)
Test results
Laboratory
H Stool or aspirates from abscesses, ulcers, or tissue
show E. histolytica.
H Indirect hemagglutination test with current or previous infection is positive.
H Complement fixation is positive (usually only during
active disease).
Imaging
H Barium studies rule out nonamebic causes of diarrhea, such as polyps and cancer.
H Sigmoidoscopy detects rectosigmoid ulceration.
Treatment
General
H Small, frequent meals
H Frequent rest periods
H Avoidance of enemas
Medications
H Metronidazole
H Emetine hydrochloride
H Iodoquinol (diiodohydroxyquin)
H Chloroquine
H Tetracycline (in combination with emetine hydro-
chloride, metronidazole, or paromomycin)
Surgery
H Exploratory surgery hazardous; can lead to peritoni-
tis, perforation, and pericecal abscess
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Key outcomes
The patient will:
H maintain or improve weight
H return to a normal elimination pattern
H express feelings of increased comfort and relief from
pain.
H Encourage adequate fluid intake.
H Apply perirectal protective cream to prevent excoria-
tion and skin breakdown.
Monitoring
H Vital signs, especially temperature
H Fluid and electrolyte balance
H Daily weight
H Frequency, amount, and character of stools
H Skin integrity
Patient teaching
Be sure to cover:
H need for avoiding alcohol ingestion when taking
metronidazole, which can cause nausea, vomiting,
and headache
H importance of returning for follow-up appointments
H advising family and sexual partners to seek medical
attention for amebiasis
H how to handle infectious material and perform
proper hand washing
H safer sex practices
H boiling untreated or contaminated water when traveling to endemic areas.
Amebiasis
39
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Amenorrhea
Overview
Description
H The abnormal absence or suppression of menstrua-
tion
H Primary amenorrhea: the absence of menarche in an
adolescent (age 16 and older)

H Secondary amenorrhea: the failure of menstruation
for at least 3 months after the normal onset of
menarche
Pathophysiology
Primary amenorrhea
H The hypothalamic-pituitary-ovarian axis is dysfunctional.
H Anatomic defects of the central nervous system cause
the ovary not to receive the hormonal signals that
normally initiate the development of secondary sex
characteristics and the beginning of menstruation.
Secondary amenorrhea
H The endometrium is sufficiently scarred and no functional endometrium exists.
Causes
H Pregnancy
H Hormonal abnormalities
H Lack of ovarian response to gonadotropins
H Constant presence of progesterone or other en-
docrine abnormalities
H Absence of a uterus
H Endometrial damage
H Ovarian, adrenal, or pituitary tumors
H Emotional disorders
H Malnutrition and intense exercise
Incidence
H Primary amenorrhea: 0.3% of women
H Secondary amenorrhea: 5% of women
H Absence of menstruation
H Vasomotor flushes, vaginal atrophy, hirsutism (ab-
normal hairiness), and acne (secondary amenorrhea)
Complications
H Infertility
H Endometrial adenocarcinoma
H Estrogen deficiency syndrome
H Osteoporosis
Assessment
History
H Failure to menstruate in females age 16 and older
40
Amenorrhea
H Absence of menstruation for 3 months in a previously
established menstrual pattern

H Change in menstrual pattern
H Dependent on cause: may include headaches, hot
flashes, nausea, weight gain or loss, emotional upset,

trauma, extreme exercise, prolonged use of hormonal contraceptives
Physical findings
H Based on cause of amenorrhea: may include hir-
sutism, acne, abdominal mass, signs of malnutrition
Test results
Laboratory
H Pregnancy test is positive (when pregnancy is the
cause).
H Pituitary gonadotropin levels are either elevated or
low.
H Thyroid levels are abnormal.
H Serum progesterone levels are abnormal.
H Serum androgen levels are abnormal.
H Urine 17-ketosteroid levels are elevated with excessive androgen secretions.
H Plasma follicle-stimulating hormone (FSH) level is
greater than 50 International Units/L, depending on
the laboratory; this suggests primary ovarian failure.
H FSH level is either normal or low; this suggests possible hypothalamic or pituitary abnormality, depending
on the clinical situation.
Imaging
H X-rays identify ovarian, adrenal, and pituitary tumors.
H Microscopic examination shows ferning of cervical
mucus (an estrogen effect).
H Vaginal cytologic examination and endometrial biopsy evaluate hormone levels.
Other
H Pelvic examination reveals anatomic abnormalities.
Treatment
General
H Based on cause
H Moderate exercise routine
Medications
H Progestational agents (to stimulate menstruation)
H Calcium supplement (if cause is hypoestrogenism)
H Clomiphene citrate (may induce ovulation in women
with amenorrhea caused by gonadotropin deficiency,

polycystic ovary syndrome, or excessive weight loss
or gain)
H FSH and human menopausal gonadotropins for
women with pituitary disease
Surgery
H Removal of tumor or obstruction
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Key outcomes
The patient will:
H maintain adequate nutrition
H express understanding of disorder
H communicate feelings about the situation.
H Provide reassurance and emotional support.
Monitoring
H Signs and symptoms
H Intake and output
H Laboratory test results
Patient teaching
Be sure to cover:
H how to keep an accurate record of menstrual cycles
to aid early detection of recurrent amenorrhea.
Discharge planning
H Refer the patient for psychological counseling, if
appropriate.
Amenorrhea
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Amyotrophic lateral
sclerosis
Overview
Description
H Most common motor neuron disease of muscular
atrophy
H Chronic, progressive, and debilitating disease thats
invariably fatal
H Also known as Lou Gehrig disease
Pathophysiology
H An excitatory neurotransmitter accumulates to toxic
levels.
H Motor units no longer innervate.
H Progressive degeneration of axons cause loss of
myelin.
H Progressive degeneration of upper and lower motor
neurons occurs.
H Progressive degeneration of motor nuclei in the cere-
bral cortex and corticospinal tracts occurs.
Causes
H 10% of patients inherit as an autosomal dominant
trait
H Virus that creates metabolic disturbances in motor
neurons
H Immune complexes such as those formed in autoim-
mune disorders
Precipitating factors that cause acute
deterioration
H Severe stress such as myocardial infarction
H Traumatic injury
H Viral infections
H Physical exhaustion
Incidence
H Three times more common in males than in females
H Affects people ages 40 to 70
H Muscle weakness
H Atrophy
H Fasciculations
Complications
H Respiratory tract infections
H Complications of physical immobility
Assessment
History
H Mental function intact
H Family history of amyotrophic lateral sclerosis (ALS)
H Asymmetrical weakness first noticed in one limb
42
Amyotrophic lateral sclerosis
H Easy fatigue and easy cramping in the affected mus-
cles
Physical findings
H Location of the affected motor neurons
H Severity of the disease
H Fasciculations in the affected muscles
H Progressive weakness in muscles of the arms, legs,
and trunk
H Brisk and overactive stretch reflexes
H Difficulty talking, chewing, swallowing, and breathing
H Shortness of breath and occasional drooling
Test results
Laboratory
H Cerebrospinal fluid analysis shows increased protein
levels.
Imaging
H Computed tomography scan rules out other disorders.
H Muscle biopsy discloses atrophic fibers.
Other
H EEG rules out other disorders.
H Electromyography shows the electrical abnormalities
of involved muscles.
H Nerve conduction studies appear normal.
Treatment
General
H Rehabilitative measures
H May need tube feedings
Medications
H Muscle relaxants or antispasmodics such as dantro-
lene and baclofen

H I.V. or intrathecal administration of thyrotropin-
releasing hormone
H Riluzole to slow progression
Key outcomes
The patient will:
H maintain a patent airway and adequate ventilation
H maintain joint mobility and range of motion (ROM)
H maintain daily calorie requirements
H seek support systems and exhibit adequate coping
behaviors
H remain free from infection.
H Provide emotional and psychological support.
H Promote independence.
H Turn and reposition the patient frequently.
H Provide airway and respiratory management.
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Modifying the home for a patient with ALS

To help the patient with amyotrophic lateral sclerosis (ALS)
live safely at home, follow these guidelines:
H Explain basic safety precautions, such as keeping stairs
and pathways free from clutter; using nonskid mats in
the bathroom and in place of loose throw rugs; keeping
stairs well lit; installing handrails in stairwells and the
shower, tub, and toilet areas; and removing electrical and
telephone cords from traffic areas.
H Discuss the need for rearranging the furniture, moving
items in or out of the patients care area, and obtaining a
hospital bed, a commode, or oxygen equipment.
H Recommend devices to ease the patients and caregivers

work, such as extra pillows or a wedge pillow to help the
patient sit up, a draw sheet to help him move up in bed,
a lap tray for eating, or a bell for calling the caregiver.
H Help the patient adjust to changes in the environment.
Encourage independence.
H Advise the patient to keep a suction machine handy to
reduce the fear of choking due to secretion accumulation
and dysphagia. Teach him how to suction himself when
necessary.
H Promote nutrition.
H Maintain aspiration precautions.
Monitoring
H Muscle weakness
H Respiratory status
H Speech
H Swallowing ability
H Skin integrity
H Complications
Patient teaching
Be sure to cover:
H swallowing therapy regimen
H medications and adverse effects
H skin care
H ROM exercises
H deep-breathing and coughing exercises
H safety in the home. (See Modifying the home for a
patient with ALS.)
Discharge planning
H Refer the patient to a local ALS support group.
H Refer the patient to hospice, as appropriate.
Amyotrophic lateral sclerosis
43
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Anaphylaxis
Overview
Description
H A lump in the patients throat caused by angioedema

H Dyspnea and complaints of chest tightness
Physical findings
H Hives
H Hoarseness or stridor, wheezing
H Severe abdominal cramps, nausea, diarrhea
H Urinary urgency and incontinence
H Dizziness, drowsiness, headache, restlessness, and
seizures
H Dramatic, acute atopic reaction to an allergen

H Marked by sudden onset of rapidly progressive ur-
H Hypotension, shock; sometimes, angina and cardiac
ticaria and respiratory distress

H More severe the sooner signs and symptoms appear
after exposure to the antigen
H Vascular collapse, leading to systemic shock and,
possibly, death from severe reaction
H Angioedema
Pathophysiology
H After initial exposure to an antigen, the immune sys-
tem produces specific immunoglobulin (Ig) antibodies in the lymph nodes. Helper T cells enhance the
process.
H The antibodies (IgE) then bind to membrane receptors located on mast cells and basophils.
H After the body re-encounters the antigen, the IgE antibodies, or cross-linked IgE receptors, recognize the
antigen as foreign; this activates the release of power
chemical mediators.
H IgG or IgM enters into the reaction and activates the
release of complement factors.
Causes
H Systemic exposure to sensitizing drugs, foods, insect
venom, or other specific antigens
Incidence
H Most common anaphylaxis-causing antigen is peni-
cillin, which induces a reaction in 1 to 4 of every

10,000 patients treated
H Apprehension and anxiety
H Dyspnea
H Hoarseness
H Angioedema
Complications
H Respiratory obstruction
H Systemic vascular collapse
H Death
Assessment
History
H Immediately after exposure, complaints of a feeling
of impending doom or fright and exhibiting apprehension, restlessness, cyanosis, cool and clammy
skin, erythema, edema, tachypnea, weakness, sweating, sneezing, dyspnea, nasal pruritus, and urticaria
44
Anaphylaxis
arrhythmias
Test results
H No tests are required to identify anaphylaxis. The pa-
tients history and signs and symptoms establish the

diagnosis.
Laboratory
H Skin testing may help identify a specific allergen.
Treatment
General
H Patent airway (establish and maintain)
H Cardiopulmonary resuscitation, if cardiac arrest oc-
curs
H Nothing by mouth, until stable
H Bed rest, until stable
Medications
H Immediate injection of epinephrine 1:1,000 aque-
ous solution, 0.1 to 0.5 ml subcutaneously or I.V.

H Corticosteroids
H Diphenhydramine I.V.
H Volume expander infusions, as needed
H Vasopressors, such as norepinephrine and dopamine
H Aminophylline I.V.
H Antihistamines
Key outcomes
The patient will:
H express feelings of increased comfort and decreased
pain
H maintain normal cardiac output and normal heart
rate
H identify causative allergen.
H Provide supplemental oxygen and prepare to assist
with insertion of an endotracheal tube, if necessary.

H Insert a peripheral I.V. line
H Administer medications as prescribed.
H Continually reassure the patient, and explain all tests
and treatments.
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H If the patient undergoes skin or scratch testing, mon-
itor for signs of a serious allergic reaction. Keep

emergency resuscitation equipment readily available.
ALERT
If a patient must receive a drug to which hes allergic, prevent a severe reaction by making sure he
receives careful desensitization with gradually increasing doses of the antigen or with advance administration of corticosteroids. Closely monitor the
patient during testing and have resuscitation
equipment and epinephrine readily available.
Monitoring
H Vital signs
H Adverse reactions from radiographic contrast media
H Serious allergic response after skin or scratch testing
H Neurologic status
H Complications
H Degree of edema
Patient teaching
Be sure to cover:
H risk for delayed symptoms and importance of reporting them immediately
H avoidance of exposure to known allergens
H importance of carrying and becoming familiar with
an anaphylaxis kit and learning to use it before the
need arises
H need for medical identification jewelry to identify allergy.
Anaphylaxis
45
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Anemia, aplastic
Overview
H Bibasilar crackles, tachycardia, and a gallop murmur

H Fever, oral and rectal ulcers, and sore throat
H Nausea
H Decreased hair and skin quality
H Petechial rash
Description
Test results
H Potentially fatal marrow failure syndrome resulting
Laboratory
H RBC count is 1 million/mm3 or less, usually with normochromic and normocytic cells; absolute reticulocyte count is very low.
H Serum iron levels are elevated (unless bleeding
occurs), but total iron-binding capacity is normal or
slightly reduced.
H Serum platelet and white blood cell counts are decreased.
H Bone marrow biopsies performed at several sites
may yield a dry tap or show severely hypocellular or
aplastic marrow, with a varying amount of fat, fibrous
tissue, or gelatinous replacement; absence of tagged
iron and megakaryocytes; and depression of erythroid elements.
from injury to or destruction of stem cells in bone

marrow or the bone marrow matrix
H Causes pancytopenia (anemia, leukopenia, thrombocytopenia) and bone marrow hypoplasia
Pathophysiology
H Aplastic anemia usually develops when damaged or
destroyed stem cells inhibit red blood cell (RBC)

production.
H Less commonly, this disease develops when damaged
bone marrow microvasculature creates an unfavorable environment for cell growth and maturation.
Causes
H Result of adverse drug reaction
H Immunologic factors; severe disease, especially hep-
atitis; viral infection, especially in children; and preleukemic and neoplastic infiltration of bone marrow
H Congenital hypoplastic anemia, also known as
Diamond-Blackfan anemia, which develops
between ages 2 and 3 months and Fanconis
syndrome, between birth and age 10
H May be idiopathic
Treatment
General
H Elimination of identifiable cause
H Vigorous supportive measures, such as packed
H Pallor and ecchymoses
RBCs, platelets, and experimental histocompatibility

antigen-matched leukocyte transfusions
H Respiratory support with oxygen
H Prevention of infection ranging from frequent hand
washing to filtered airflow
H Neutropenic precautions, if appropriate
Complications
Medications
H Hemorrhage
H Infection
H Heart failure
H Antibiotics
H Marrow-stimulating agents, such as erythropoietin,
Incidence
H More common in children and young adults
Assessment
History
H Fatigue
H Weakness
H Weight loss
H Dizziness
H Syncope
H Bruising
H Nosebleeds
Physical findings
H Pallor, ecchymosis, petechiae, or retinal hemorrhage
H Alterations in level of consciousness, weakness, fa-
tigue
46
Anemia, aplastic
and colony-stimulating factors, such as filgrastim and

sargramostim
H Immunosuppressants
Corticosteroids such as methylprednisolone
Antithymocyte globulin
Cyclosporine
Surgery
H Bone marrow transplantation (for severe aplasia and
patients who need constant RBC transfusions)
Key outcomes
The patient will:
H state the need to increase activity level gradually
H maintain vital signs within prescribed limits during
activity
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H maintain normal cardiac output

H exhibit adequate ventilation
pain.
H Help the patient to prevent or manage hemorrhage,
infection, adverse effects of drug therapy, and blood

transfusion reaction.
H If the patients platelet count is low (less than
20,000/mm3), prevent hemorrhage by avoiding I.M.
injections, and suggesting the use of an electric razor
and a soft toothbrush. Apply pressure to venipuncture sites until bleeding stops.
H Follow neutropenic precautions.
H Make sure throat, urine, nasal, stool, and blood cultures are done regularly and correctly to check for
infection.
H Schedule frequent rest periods.
H Administer oxygen therapy.
H Ensure a comfortable environmental temperature.
H If blood transfusions are necessary, administer according to facility policy and assess for transfusion
reactions.
Monitoring
H Blood studies in patients receiving anemia-inducing
drugs
H Early detection of bleeding
Patient teaching
Be sure to cover:
H avoidance of contact with potential sources of infection, such as crowds, soil, and standing water that
can harbor organisms
H the disorder and its treatment
H prescribed drugs and possible adverse reactions and
when to report them
H normal lifestyle with appropriate restrictions until remission occurs (for the patient who doesnt require
hospitalization).
Discharge planning
H Refer the patient to the Aplastic Anemia Foundation
of America for additional information, assistance,

and support.
Anemia, aplastic
47
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Anemia, folic acid

(folate) deficiency
H Palpitations
H Weakness and light-headedness
H Numbness or tingling in hands and feet
Overview
H Generalized pallor and jaundice

H Weight loss
H Wasted or malnourished appearance
H Possible reddened lips with fissures (cheilosis)
H Red, swollen, smooth, shiny, and tender tongue
Description
H A common, slowly progressive megaloblastic anemia
H Caused by a deficiency of the vitamin folate
Pathophysiology
H When folic acid stores in the body are low or diet is
deficient in folic acid, the bone marrow produces

large red blood cells or megaloblasts resulting in
anemia.
Causes
H Alcohol abuse
H Poor diet
H Impaired absorption from small intestine
H Bacteria competing for available folic acid
H Excessive cooking of foods, which destroys the avail-
able nutrient
H Limited storage capacity in infants
H Prolonged drug therapy with such drugs as anticon-
vulsants, estrogens, and methotrexate

H Increased folic acid requirements during pregnancy,
rapid growth periods in infancy, childhood and adolescence, and in patients with neoplastic diseases or
some skin diseases such as exfoliative dermatitis
Physical findings
(glossitis)
H Reduced sense of taste
H Tachycardia
Test results
Laboratory
H Folic acid deficiency anemia and pernicious anemia
can be distinguished by the Schilling test and a therapeutic trial of vitamin B12 injections.
H Blood studies show macrocythemia, decreased reticulocyte count, increased mean corpuscular volume,
abnormal platelets, and serum folate levels less than
4 mg/ml.
Treatment
General
H Elimination of contributing causes
H Well-balanced diet high in folic acid (see Foods high
in folic acid)
H Frequent rest periods during activity, as needed
Incidence
Medications
H Most prevalent in infants, adolescents, pregnant and
H Folic acid supplements

H Vitamin supplementation (should begin at least 3
lactating women, alcoholics, elderly people, and people with malignant or intestinal diseases
H Progressive fatigue
H Systemic signs of anemia
Complications
H Pregnant women deficient in folic acid have an in-
creased risk for giving birth to a neonate with a neural tube defect.
Assessment
History
H Severe, progressive fatigue, the hallmark of
folic acid deficiency

H Diarrhea
H Nausea
H Anorexia
H Headaches
H Forgetfulness
H Irritability
H Chest pain
48
Anemia, folic acid (folate) deficiency
months before conception in women trying to become pregnant)

H Blood transfusions in severe cases
Key outcomes
The patient will:
H state the need to increase activity level gradually
activity
H remain hemodynamically stable
H have normal bowel movements
H experience no further weight loss.
H Plan activities, rest periods, and necessary diagnostic
tests to conserve energy.

H Advise the patient to report signs and symptoms of
decreased perfusion to vital organs (dyspnea, chest

pain, dizziness).
H If the patient has glossitis, emphasize the importance
of good oral hygiene.
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Foods high in folic acid

The body needs folic acid to develop healthy red blood cells
and synthesize deoxyribonucleic acid. Although body stores
are comparatively small (about 70 mg), this vitamin is plentiful in most well-balanced diets. But because folic acid is
water-soluble and heat-labile, its easily destroyed by cooking. Also, about 20% of folic acid intake is excreted unabsorbed. Daily folic acid intake less than 50 mcg/day usually
induces folic acid deficiency within 4 months. Heres a list of
foods high in folic acid.
Food
mcg/100 g
Asparagus spears
Beef liver
Broccoli spears
Collards (cooked)
Mushrooms
Oatmeal
Peanut butter
Red beans
Wheat germ
109
294
54
102
24
33
57
180
305
H Ask the dietitian to give the patient nonirritating
foods because a sore mouth and tongue make eating

painful. If these symptoms make talking difficult,
supply a pad and pencil or some other aid to facilitate communication.
H To ensure accurate Schilling test results, make sure
that all urine excreted over a 24-hour period is collected and that the specimens remain uncontaminated by bacteria.
H Provide a well-balanced diet, including foods high in
folate, such as dark green leafy vegetables, organ
meats, eggs, milk, oranges, bananas, dry beans, and
whole-grain breads.
Monitoring
H Vital signs
Patient teaching
Be sure to cover:
H importance of a well-balanced diet high in folic acid
H use of commercially prepared formulas for mothers
who arent breast-feeding
H daily folic acid requirements and the need to keep
taking the supplements even when he begins to feel
better
H importance of guarding against infections and reporting signs of infection promptly.
Anemia, folic acid (folate) deficiency
49
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Anemia, iron deficiency
Overview
Complications
Description
H Decreased total iron body content diminishing ery-
thropoiesis
H Produces smaller (microcytic) cells with less color
H Fatigue
H Infection
H Pneumonia
H Overreplacement of oral or I.M. iron supplements,
which can affect the liver, heart, pituitary glands, and

joints
on staining (hypochromia)
Special populations
Pathophysiology
H Body stores of iron, including plasma iron, decrease.
H Transferrin, which binds with and transports iron,
also decreases.
In a child, iron deficiency anemia can cause pica,

which may lead to eating lead-based paint resulting in lead poisoning.
H Insufficient body stores of iron lead to a depleted red
blood cell mass and to a decreased hemoglobin concentration.

H Anemic state results in decreased oxygen-carrying
capacity of the blood. (See Iron absorption and
storage.)
Causes
H Inadequate dietary intake of iron
H Iron malabsorption
H Blood loss secondary to drug-induced GI bleeding or
Assessment
History
H Can persist for years without signs and symptoms
H Fatigue
H Headache, shortness of breath (especially on exer-
tion)
due to heavy menses, hemorrhage from trauma, GI

ulcers, malignant tumors, and varices
H Pregnancy
H Intravascular hemolysis-induced hemoglobinuria or
paroxysmal nocturnal hemoglobinuria
H Mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filter
H Can be related to lead poisoning in children
H Increased frequency of infections

H Pica, an uncontrollable urge to eat strange things,
Incidence
Physical findings
H Common worldwide
H Affects 10% to 30% of the adult population of the
H Red, swollen, smooth, shiny, and tender tongue
United States
H Most prevalent among premenopausal women, infants, children, adolescents, alcoholics, and elderly
people
H Corners of the mouth may be eroded, tender, and
Iron absorption and storage

Found in abundance throughout the body, iron is needed
for erythropoiesis. Two-thirds of total-body iron is found
in hemoglobin; the other third, mostly in the reticuloendothelial system (liver, spleen, and bone marrow), with
small amounts in muscle, serum, and body cells.
Adequate iron in the diet and recirculation of iron released from disintegrating red blood cells maintain iron
supplies. The duodenum and upper part of the small intestine absorb dietary iron. Such absorption depends on gastric acid content, the amount of reducing substances
(ascorbic acid, for example) present in the alimentary
canal, and amount of iron intake. If iron intake is deficient,
the body gradually depletes its iron stores, causing decreased hemoglobin levels and, eventually, signs and
symptoms of iron deficiency anemia.
50
such as clay, starch, ice and, in children, lead

H Menorrhagia
H Dysphagia
H Vasomotor disturbances
H Numbness and tingling of the extremities
H Neuralgic pain
(glossitis)
swollen (angular stomatitis)
H Spoon-shaped, brittle nails
H Tachycardia
Test results
Laboratory
H Serum hemoglobin levels are decreased (males, less
than 12 g/dl; females, less than 10 g/dl) or, in severe
anemia, decreased mean corpuscular hemoglobin
level.
H Serum hematocrit is decreased (males, less than
47 ml/dl; females, less than 42 ml/dl).
H Serum iron levels are decreased with high binding
capacity.
H Serum ferritin levels are decreased.
H Serum red blood cell (RBC) count is decreased with
microcytic and hypochromic cells (in early stages,
RBC count may be normal, except in infants and children).
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H Bone marrow studies reveal depleted or absent iron
stores (done by staining) as well as normoblastic
hyperplasia.
H GI studies, such as guaiac stool tests, barium swallow
and enema, endoscopy, and sigmoidoscopy, rule out
or confirm the diagnosis of bleeding causing the iron
deficiency.
Recognizing iron overdose

Excessive iron replacement may produce signs and symptoms, such as diarrhea, fever, severe stomach pain, nausea, and vomiting.
When these signs and symptoms occur, notify the
physician and give prescribed treatment, which may include chelation therapy, vigorous I.V. fluid replacement,
gastric lavage, whole-bowel irrigation, and supplemental
oxygen.
Treatment
General
Monitoring
H Determination of underlying cause

H Nutritious, nonirritating foods
H Planned rest periods during activity
H Vital signs
H Compliance with prescribed iron supplement therapy
H Iron replacement overdose (see Recognizing iron
Medications
H Oral preparation of iron or a combination of iron
and ascorbic acid

H I.M. iron in rare cases
H Total-dose I.V. infusions of supplemental iron for
pregnant and elderly patients with severe disease
Key outcomes
The patient will:
H maintain weight without further loss
activity
H express feelings of increased energy
pain.
H Note the patients signs or symptoms of decreased
overdose)
Patient teaching
Be sure to cover:
H dangers of lead poisoning, especially if the patient
reports pica
H importance of continuing therapy, even after the patient begins to feel better
H absorption interference with milk or antacid of iron
supplementation
H increased absorption with vitamin C
H avoidance of staining teeth by drinking liquid supplemental iron through a straw
H when to report adverse effects of iron therapy
H basics of a nutritionally balanced diet
H importance of avoiding infection and when to report
signs of infection
H need for regular checkups
H compliance with prescribed treatment.
perfusion to vital organs.

H Provide oxygen therapy, as necessary.
H Assess the familys dietary habits for iron intake, not-
ing the influence of childhood eating patterns, cultural food preferences, and family income on adequate
nutrition.
H Ask the dietitian to give the patient nonirritating
foods.
H Give prescribed analgesics for headache and other
discomfort.
H Evaluate the patients drug history. Certain drugs,
such as pancreatic enzymes and vitamin E, can interfere with iron metabolism and absorption; aspirin,
steroids, and other drugs can cause GI bleeding.
H Provide frequent rest periods.
H If the patient receives iron I.V., monitor the infusion
rate carefully and observe for an allergic reaction.
H Use the Z-track injection method when administering
iron I.M. to prevent skin discoloration, scarring, and
irritating iron deposits in the skin.
H Provide good nutrition and meticulous care of I.V.
sites.
51
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Anemia, pernicious
Overview
Description
H Deficiency of vitamin B12 causing serious neurologic,
psychological, gastric, and intestinal abnormalities
H Characterized by decreased gastric production of hy-
drochloric acid and deficiency of intrinsic factor, essential for vitamin B12 absorption
H Also known as Addisons anemia
Pathophysiology
H An inherited autoimmune response may cause gastric
mucosal atrophy and resultant decreased hydrochloric acid and intrinsic factor production, a substance
normally secreted by the parietal cells of the gastric
mucosa.
H Intrinsic factor deficiency impairs vitamin B12 absorption.
H Vitamin B12 deficiency inhibits the growth of all
cells, particularly red blood cells (RBCs), leading to
insufficient and deformed RBCs with poor oxygencarrying capacity.
Causes
H Secondary pernicious anemia results from partial
removal of the stomach

H Chronic gastric inflammation
Incidence
Assessment
History
H Characteristic triad of symptoms: weakness; a beefy
red, sore tongue; and numbness and tingling in the

extremities
H GI disturbance: nausea, vomiting, anorexia, weight
loss, flatulence, diarrhea, and constipation
H Peripheral numbness and paresthesia
H Light-headedness
H Headache
H Diplopia and blurred vision
H Loss of taste
H Tinnitus
Physical findings
H Smooth, beefy red, painful tongue
H Slightly jaundiced sclera and pale to bright yellow
skin
H Tachycardia
H Systolic murmur
H Enlarged liver and spleen
H Weakness in the extremities
H Disturbed position sense
H Lack of coordination
H Impaired fine finger movement
H Loss of bowel and bladder control
H Impotence (in males)
H Irritable, depressed, delirious, and ataxic
H Memory loss
H Positive Babinskis and Rombergs signs
H Optic muscle atrophy
H In the United States, most common in New England
Test results
and the Great Lakes region because of ethnic concentration

H Common in Northern Europeans of fair complexion
H Rare in children, Blacks, and Asians
H Onset typically between ages 50 and 60; incidence
increases with advancing age
Laboratory
H Hemoglobin level is decreased.
H RBC count is decreased.
H Mean corpuscular volume is increased (less than
120 mm3); mean corpuscular hemoglobin concentration is also increased.
H White blood cell and platelet counts may be decreased, and the platelets are large and malformed.
H Serum vitamin B12 tests may show levels less than
0.1 mcg/ml.
H Serum lactate dehydrogenase levels are elevated.
H Bone marrow studies reveal erythroid hyperplasia
with increased numbers of megaloblasts but few normally developing RBCs.
H Gastric analysis shows an absence of free hydrochloric acid after histamine or pentagastrin injection.
H The Schilling test may reveal a urinary excretion of
less than 3% in the first 24 hours in patients with
pernicious anemia; may reveal normal excretion of
vitamin B12 when repeated with intrinsic factor
added.
H Weakness
H Beefy red, sore tongue
Complications
H Heart failure with severe anemia
H Myocardial ischemia
H Paralysis
H Psychotic behavior
H Loss of sphincter control of bowel and bladder
H Peptic ulcer disease
52
Anemia, pernicious
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Treatment
General
H Based on underlying cause
H Well-balanced diet, including foods high in vitamin
B12
Dietary sources of vitamin B12

The following foods are good sources of vitamin B12:
H Meat, especially organ meats
H Poultry, fresh fish, and seafood
H Eggs
H Dairy products
H Fortified cereals and flours
H Sodium and fluid restriction for heart failure

H If anemia causes extreme fatigue, bed rest until
hemoglobin level increases
Medications
H Early I.M. vitamin B12 replacement
H Maintenance levels (monthly) of vitamin B12 doses,
after the patients condition improves
H observance of and when to report confusion and irri-
tability
H prevention of pernicious anemia, by taking vitamin
B12 supplements, in patients who have had extensive

gastric resections or who follow strict vegetarian
diets.
Key outcomes
The patient will:
H state his understanding of the need to increase activity level gradually
H modify lifestyle to minimize risk for decreased tissue
perfusion
H maintain normal hemoglobin level and hematocrit
H maintain normal coagulation profile.
H If the patient has severe anemia, plan activities, rest
periods, and necessary diagnostic tests to conserve

his energy.
H To ensure accurate Schilling test results, make sure
that all urine excreted over a 24-hour period is collected.
H Provide a well-balanced diet, including foods high in
vitamin B12. (See Dietary sources of vitamin B12.)
H Institute safety precautions to prevent falls.
Monitoring
H Vital signs
H Mental and neurologic status
Patient teaching
Be sure to cover:
H protection against infections and when to report
signs of infection
H when to report signs and symptoms of decreased
perfusion to vital organs and symptoms of neuropathy
H avoidance of irritating foods
H avoidance of exposure to extreme heat or cold on the
extremities
H continuation of vitamin B12 replacement even after
symptoms subside
H proper injection techniques
Anemia, pernicious
53
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Anemia, sickle cell

Overview
Description
H Congenital hemolytic disease that results from a de-
fective hemoglobin (Hb) molecule, HbS, that causes

red blood cells (RBCs) to become sickle-shaped
H Impaired circulation caused by sickle cells resulting
in chronic ill health (fatigue, dyspnea on exertion,
swollen joints), periodic crises, long-term complications, and premature death
H No cure
Pathophysiology
H The abnormal HbS found in the patients RBCs be-
comes insoluble whenever hypoxia occurs.

H The RBCs become rigid, rough, and elongated, form-
ing a crescent or sickle shape.

H Sickling can produce hemolysis (cell destruction).
H The altered cells accumulate in capillaries and small-
er blood vessels, making the blood more viscous.

H Normal circulation is impaired, causing pain, tissue
infarctions, and swelling.
Causes
H Homozygous inheritance of the HbS-producing gene
(defective Hb gene from each parent)
Incidence
H Most common in tropical Africans and in people of
African descent
H Abnormal gene about 1 in 10 blacks (if two such
carriers have offspring, each child has a 1-in-4

chance of developing the disease)
H Found in one in every 500 blacks in the United States
H Also occurs in Puerto Rico, Turkey, India, the Middle
East, and the Mediterranean area
H Chronic fatigue
H Intense pain due to vascular occlusion in a sickling
episode
H Frequent bacterial infections due to involvement of
spleen
Complications
H Chronic obstructive pulmonary disease
H Heart failure
H Retinopathy
H Nephropathy
54
Anemia, sickle cell
Assessment
History
H Signs and symptoms usually dont develop until after
age 6 months
H Chronic fatigue
H Unexplained dyspnea or dyspnea on exertion
H Joint swelling
H Aching bones
H Chest pain
H Ischemic leg ulcers
H Increased susceptibility to infection
H Pulmonary infarctions and cardiomegaly
Physical findings
H Jaundice or pallor
H May appear small in stature for age
H Delayed growth and puberty
H Spiderlike body build (narrow shoulders and hips,
long extremities, curved spine, and barrel chest) in

adult
H Tachycardia
H Hepatomegaly and, in children, splenomegaly
H Systolic and diastolic murmurs
H Sleepiness with difficulty awakening
H Hematuria
H Pale lips, tongue, palms, and nail beds
H Body temperature greater than 104 F (40 C) or a
temperature of 100 F (37.8 C) that persists for 2
or more days
In painful crisis
H Most common crisis and the hallmark of the disease,
usually appears periodically after age 5, characterized by severe abdominal, thoracic, muscle, or bone
pain and, possibly, increased jaundice, dark urine,
and a low-grade fever
In aplastic crisis
H Pallor, lethargy, sleepiness, dyspnea, possible coma,
markedly decreased bone marrow activity, and RBC
hemolysis
In acute sequestration crisis
H Occurs in infants between ages 8 months and 2
years, causes lethargy and pallor and, if untreated,
progresses to hypovolemic shock and death
In hemolytic crisis
H Liver congestion and hepatomegaly
Test results
Laboratory
H Stained blood smear shows sickle cells and Hb electrophoresis shows HbS. (Electrophoresis should be
done on umbilical cord blood samples at birth to
provide sickle cell disease screening for all neonates
at risk.)
H RBC counts and erythrocyte sedimentation rate are
decreased; white blood cell and platelet counts are
elevated; and serum iron levels are increased.
H RBC survival is decreased and reticulocytosis is present; Hb levels are normal or low.
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Imaging
H A lateral chest X-ray detects the characteristic Lincoln log deformity. (This spinal abnormality develops in many adults and some adolescents with sickle
cell anemia, leaving the vertebrae resembling logs
that form the corner of a cabin.)
H Ophthalmoscopic examination reveals corkscrew or
comma-shaped vessels in the conjunctivae.
Treatment
General
H Avoidance of extreme temperatures
H Avoidance of stress
H Adequate amounts of folic acidrich foods
H Adequate fluid intake
H Bed rest during crises
Medications
H Vaccines, such as polyvalent pneumococcal vaccine
and Haemophilus influenzae B vaccine

H Anti-infectives, as appropriate
H Analgesics
H Iron supplements
H Transfusion of packed RBCs, if Hb level decreases
suddenly or if condition deteriorates rapidly
H Sedation and administration of analgesics, blood
transfusion, oxygen therapy, and large amounts of
oral or I.V. fluids, in an acute sequestration crisis
Key outcomes
The patient will:
H demonstrate age-appropriate skills and behaviors to
the extent possible
H maintain collateral circulation
H maintain balanced fluid volume where input will
equal output
pain
H maintain normal peripheral pulses
H maintain normal skin color and temperature.
H Encourage the patient to talk about his fears and
concerns.
H If a male patient develops sudden, painful priapism,
reassure him that such episodes are common and
have no permanent harmful effects.
H Make sure that the patient receives adequate
amounts of folic acidrich foods such as green,
leafy vegetables.
H Apply warm compresses, warmed thermal blankets,
and warming pads or mattresses to painful areas of

the patients body, unless he has neuropathy.
H Administer analgesics and antipyretics, as needed.
H When cultures demonstrate the presence of infection,
administer prescribed antibiotics.
H Administer prescribed prophylactic antibiotics.
H Use strict sterile technique when performing treatments.
H Encourage bed rest with the head of the bed elevated
to decrease tissue oxygen demand.
H Administer oxygen, as needed.
H Administer blood transfusions.
H If the patient requires general anesthesia for surgery,
help ensure that he receives adequate ventilation to
prevent hypoxic crisis.
Monitoring
H Vital signs
H Intake and output
H Complete blood count and other laboratory study
results
Patient teaching
Be sure to cover:
H avoidance of tight clothing that restricts circulation
H conditions that provoke hypoxia, such as strenuous
exercise, vasoconstricting medications, cold temperatures, unpressurized aircraft, and high altitude
H importance of normal childhood immunizations,
meticulous wound care, good oral hygiene, regular
dental checkups, and a balanced diet as safeguards
against infection
H need for prompt treatment of infection
H need to increase fluid intake to prevent dehydration,
which can cause increased blood viscosity
H symptoms of vaso-occlusive crisis
H need for hospitalization in a vaso-occlusive crisis in
which I.V. fluids, parenteral analgesics, oxygen therapy, and blood transfusions may be necessary
H need to inform all health care providers that the patient has this disease before undergoing any treatment, especially major surgery
H pregnancy and the disease
H balanced diet, including folic acid supplements during pregnancy.
Discharge planning
H Refer parents of children with sickle cell anemia for
genetic counseling to answer their questions about

the risk to future offspring.
H Refer other family members for genetic counseling to
determine if theyre heterozygote carriers.
H If necessary, refer the patient for psychological counseling to help him cope.
H Refer women with sickle cell anemia for birth control counseling.
Anemia, sickle cell
55
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Anemia, sideroblastic
Overview
Description
Physical findings
H Pale skin and oral mucous membranes
H Slight jaundice
H Petechiae or bruises
H Enlarged lymph nodes
H Hepatosplenomegaly
H A group of heterogenous disorders with a common
Test results
defect that causes failure to use iron in hemoglobin

synthesis despite the availability of adequate iron
stores
H Can be acquired or hereditary; the acquired form, in
turn, can be primary or secondary
Laboratory
H Red blood cell (RBC) indices that are revealed by
microscopic examination of blood show erythrocytes
to be hypochromic or normochromic and slightly
macrocytic; RBC precursors may be megaloblastic,
with anisocytosis (abnormal variation in RBC size)
and poikilocytosis (abnormal variation in RBC
shape).
H Vitamin B12 and folic acid levels are normal unless
combined anemias are present.
H Serum reticulocyte count is low because young cells
die in the marrow.
H Ringed sideroblasts on microscopic examination of
bone marrow aspirate stained with Prussian blue dye
confirms the diagnosis. (See Ringed sideroblast.)
Pathophysiology
H Normoblasts fail to use iron to synthesize hemoglo-
bin.
H Iron is deposited in the mitochondria of normo-
blasts, rather than in the hemoglobin molecules.

H Iron toxicity can cause organ damage.
Causes
H Hereditary; may be due to a rare genetic defect on
the X chromosome
H Acquired form may be secondary to ingestion of or
exposure to toxins, such as alcohol and lead, or to

drugs such as isoniazid and chloramphenicol
H Complication of neoplastic and inflammatory diseases, such as lymphoma, rheumatoid arthritis, lupus
erythematosus, multiple myeloma, tuberculosis, and
severe infections
H Primary acquired form cause unknown
Incidence
H Most prevalent in young males
H Appears to be transmitted by X-linked inheritance; fe-
males are carriers and usually show no signs of this

disorder
H Primary acquired form most common in elderly people but occasionally found in young people
H Anorexia and fatigue
Complications
Treatment
General
H Underlying cause determines the course of treatment
(for example, in acquired secondary form, the causative drug or toxin is removed)
H Nutritious diet
H Chelation therapy to decrease iron overload from
repeated transfusions
Medications
In hereditary sideroblastic anemia
H High doses of pyridoxine
In primary acquired anemia
H Transfusion or high doses of androgens
In chronic iron overload
H Deferoxamine
H Severe cardiac, hepatic, splenic, and pancreatic
disease
H Acute myelogenous leukemia
Key outcomes
Assessment
History
H Anorexia
H Fatigue
H Weakness
H Dizziness
H Dyspnea
56
The patient will:

H not develop infection
H show improvement or healing in his lesions or
wounds
pain.
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H Provide frequent rest periods. Plan activities and di-
agnostic tests so the patient can rest in between.

H Institute safety measures to prevent falls.
H Provide comfort measures; have the patient perform
Ringed sideroblast
Electron microscopy shows large iron deposits in the mitochondria that surround the nucleus, forming the characteristic ringed sideroblast.
relaxation techniques to facilitate coping.

H Administer blood transfusions. Notify the physician if
signs of a transfusion reaction occur.

H If the patient has jaundice or pruritus, provide metic-
ulous skin care.

H Ask about possible exposure to lead in the home
(especially for children) or on the job.
Monitoring
H Vital signs
H Complications
H Signs and symptoms of neuropathy
H Signs and symptoms of decreased perfusion
Patient teaching
Be sure to cover:
H prescribed treatment and possible complications
H importance of continuing prescribed therapy, even
after the patient begins to feel better
H precautions for parents about house paint and not allowing children to eat paint chips because of the possibility of lead
H recognition of and when to report adrenergic adverse effects, if androgens are used as part of the
treatment
H recognition of and when to report signs and symptoms of heart failure
H need for proper hygiene and other measures to
guard against infections and when to report signs
and symptoms of infection.
Discharge planning
H Identify patients who abuse alcohol and refer them
for appropriate therapy.
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Aneurysm,
abdominal aortic
H Lower back pain unaffected by movement

H Gastric or abdominal fullness
H Sudden onset of severe abdominal pain or lumbar
pain with radiation to flank and groin

H May note a pulsating mass in the periumbilical area:
Overview
Description
H Abnormal dilation in the arterial wall of the aorta,
commonly between the renal arteries and iliac

branches
H Can be fusiform (spindle-shaped), saccular (pouchlike), or dissecting
Pathophysiology
H Focal weakness in the tunica media layer of the aorta
due to degenerative changes allows the tunica intima

and tunica adventitia layers to stretch outward.
H Blood pressure within the aorta progressively weakens vessel walls and enlarges the aneurysm.
Causes
H Arteriosclerosis or atherosclerosis (95%)
H Trauma
H Syphilis; other infections
Risk factors
H Hypertension
H Smoking
H Hypercholesterolemia
H Obesity
Incidence
H Seven times more common in hypertensive males
than in females
H Most common in whites ages 50 to 80
H Located in the infrarenal aorta (98%)
H Most develop at bifurcations in the vessels
Complications
H Hemorrhage
H Shock
H Dissection
dont palpate
Ruptured aneurysm
H Into the peritoneal cavity, severe, persistent abdominal and back pain
H Into the duodenum, GI bleeding with massive hematemesis and melena
H Mottled skin; poor distal perfusion
H Absent peripheral pulses distally
H Decreased level of consciousness
H Diaphoresis
H Hypotension
H Tachycardia
H Oliguria
H Distended abdomen
H Ecchymosis or hematoma in the abdominal, flank, or
groin area
H Paraplegia if aneurysm rupture reduces blood flow to
the spine
H Systolic bruit over the aorta
H Tenderness over affected area
Test results
Imaging
H Abdominal ultrasonography or echocardiography
determines the size, shape, and location of the
aneurysm.
H Anteroposterior and lateral abdominal X-rays detect
aortic calcification, which outlines the mass, at least
75% of the time.
H Computed tomography scan can visualize the aneurysms effect on nearby organs.
H Aortography shows the condition of vessels proximal
and distal to the aneurysm and the extent of the
aeurysm; aneurysm diameter may be underestimated
because it shows only the flow channel and not the
surrounding clot.
Treatment
General
H Delayed surgery if aneurysm is small and produces
Assessment
History
H Asymptomatic until the aneurysm enlarges and com-
presses surrounding tissue

H Syncope when aneurysm ruptures
H Asymptomatic when clot forms and bleeding stops or
abdominal pain when bleeding continues into the

peritoneum
Physical findings
Intact aneurysm
H Gnawing, generalized, steady abdominal pain
58
Aneurysm, abdominal aortic
no symptoms
H Careful control of hypertension
H Fluid and blood replacement
H Weight reduction, if appropriate
H Low-fat diet
Medications
H Beta-adrenergic blockers such as metoprolol
H Antihypertensives
H Analgesics
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Endovascular grafting for repair of AAA

Endovascular grafting is a minimally invasive procedure for the patient who
requires repair of an abdominal aortic aneurysm (AAA). Endovascular
grafting reinforces the walls of the aorta to prevent rupture and expansion
of the size of the aneurysm.
The procedure is performed with fluoroscopic guidance, whereby a delivery catheter with an attached compressed graft is inserted through a
small incision into the femoral or iliac artery over a guidewire. The delivery
catheter is advanced into the aorta, where its positioned across the
aneurysm. A balloon on the catheter expands the graft and affixes it to the
vessel wall. The procedure usually takes 2 to 3 hours to perform. Patients
are instructed to walk the first day after surgery and are discharged from
the hospital in 1 to 3 days.
Surgery
H Endovascular grafting or resection of large aneu-
rysms or those that produce symptoms (see Endovascular grafting for repair of AAA)
H Bypass procedures for poor perfusion distal to
aneurysm
H Repair of ruptured aneurysm with a graft replacement
Key outcomes
The patient will:
H maintain adequate cardiac output
H maintain palpable pulses distal to the aneurysm site
H maintain adequate urine output (output equivalent to
intake)
pain.
In a nonacute situation
H Allow the patient to express his fears and concerns
and identify effective coping strategies.
H Offer the patient and his family psychological support.
In an acute situation
H Insert an I.V. line with at least a 14G needle to facilitate blood replacement.
H Obtain blood samples for laboratory tests as ordered.
ALERT
Be alert for signs of rupture, which may be immediately fatal. If rupture does occur, surgery needs to
be immediate. Medical antishock trousers may be
used while transporting the patient to surgery.
After surgery
H Assess peripheral pulses for graft failure or occlusion.
H Watch for signs of bleeding retroperitoneally from
the graft site.

H Maintain blood pressure in prescribed range with
fluids and medications.
ALERT
Assess the patient for severe back pain, which can
indicate that the graft is tearing.
H Have the patient cough, or suction the endotracheal
tube, as needed.
H Provide frequent turning, and assist with ambulation
as soon as the patient is able.
Monitoring
H Cardiac rhythm and hemodynamics
H Vital signs, intake and output hourly, neurologic sta-
tus, and pulse oximetry

H Respirations and breath sounds at least every hour
H Arterial blood gas values as ordered
H Daily weight
H Fluid status
H Nasogastric intubation for patency, amount, and type
of drainage
H Abdominal dressings
H Wound site for infection
Patient teaching
Be sure to cover:
H surgical procedure and expected postoperative care
H importance of taking all medications as prescribed
and carrying a list of medications at all times, in case
of an emergency
H physical activity restrictions until medically cleared
by the physician
H need for regular examination and ultrasound checks
to monitor progression of the aneurysm, if surgery
wasnt performed.
Aneurysm, abdominal aortic
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Aneurysm,
femoral and popliteal
Overview
Description
H Progressive atherosclerotic changes occurring in the
walls (medial layer) of the femoral and popliteal

arteries resulting in a dilation or outpouching (see
Arteries of the leg)
H May be fusiform (spindle-shaped) or saccular
(pouchlike)
H Usually progressive, eventually ending in thrombosis,
embolization, and gangrene
Pathophysiology
H Atherosclerotic plaque formation or loss of elastin
and collagen in the vessel wall causes localized outpouching or dilation of a weakened arterial wall.
Causes
H Atherosclerosis
H Congenital weakness in the arterial wall (rare)
H Trauma (blunt or penetrating)
H Bacterial infection
H Peripheral vascular reconstructive surgery (which
causes suture line or false aneurysms, whereby a

blood clot forms a second lumen)
Incidence
H Most common in males older than age 50
H Pain
H Edema and venous distention
H Symptoms of severe ischemia in the leg or foot
Complications
H Gangrene
Assessment
History
H Pain in affected extremity
Physical findings
H Loss of pulse and color, coldness in the affected leg
or foot
H Distal petechial hemorrhages (from aneurysmal emboli)
H Pulsating mass above or below the inguinal ligament
H Firm, nonpulsating mass above or below the inguinal
ligament when thrombosis has occurred
Test results
H Arteriography or ultrasonography reveals aneurysm.
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Aneurysm, femoral and popliteal
Treatment
General
H Nothing by mouth before surgery
H Limited movement of the affected extremity
Medications
H Analgesics
H Antibiotics (before surgery), as appropriate
H Anticoagulants, such as warfarin and heparin
Surgery
H Surgical bypass and reconstruction of the artery, usu-
ally with an autogenous saphenous vein graft replacement

H Leg amputation if arterial occlusion causes severe
ischemia and gangrene
Key outcomes
The patient will:
H maintain pulses and adequate circulation to damaged
aneurysm site
pain
H carry out activities of daily living without excess fatigue or exhaustion.
Before corrective surgery
H Evaluate the patients circulatory status, noting the location and quality of peripheral pulses in the affected
arm or leg.
H Administer a prophylactic antibiotic or anticoagulant,
as needed.
H Discuss expected postoperative procedures with the
patient, and review the surgical procedure.
After arterial surgery
H Correlate condition of extremity with preoperative
circulatory assessment. Mark the sites on the patients skin where pulses are palpable, to facilitate repeated checks.
H Help the patient walk soon after surgery, to prevent
venostasis and thrombus formation.
Monitoring
H Neurovascular condition of affected extremity (pulse,
temperature, sensation, color)

H Vital signs
H Pain control
Patient teaching
Be sure to cover:
H importance of immediately informing the physician
of any recurrence of symptoms
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Arteries of the leg

Front view
Back view
Abdominal
aorta
Common
iliac artery
Internal
iliac artery
External
iliac artery
Deep femoral
artery
Deep femoral
artery
Superficial
femoral artery
Superficial
femoral artery
Popliteal artery
Popliteal artery
Anterior tibial
artery
Anterior
tibial artery
Posterior tibial
artery
Dorsalis pedis
Medial plantar
artery
Lateral plantar
artery
H how to apply antiembolism stockings (Warn the pa-
tient against wearing constrictive clothing.)

H measures to prevent bleeding (if an anticoagulant is
prescribed) such as using an electric razor
H importance of reporting signs of bleeding immediately (bleeding gums, easy bruising, or black, tarry
stools)
H importance of follow-up blood studies to monitor an-
ticoagulant therapy.
Aneurysm, femoral and popliteal
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Aneurysm, intracranial
Overview
Description
Assessment
History
H Headache
H Intermittent nausea
H Seizure
H Photophobia
H Blurred vision
H Weakness in the wall of a cerebral artery that causes
Physical findings
localized dilation
H Most common form is the berry aneurysm, a saclike
outpouching in a cerebral artery
H Usually occurs at an arterial junction in the Circle of
Willis, the circular anastomosis forming the major
cerebral arteries at the base of the brain
H Commonly ruptures and causes subarachnoid hemorrhage
Typically, the severity of a ruptured intracranial

aneurysm is graded according to the patients signs and
symptoms. (See Determining severity of an intracranial aneurysm rupture.)
H Nuchal rigidity
H Back and leg pain
H Fever
H Restlessness
H Irritability
H Hemiparesis
H Hemisensory defects
H Dysphagia
H Visual defects (diplopia, ptosis, dilated pupil, and inability to rotate the eye caused by compression on
the oculomotor nerve if aneurysm is near the internal
carotid artery)
Pathophysiology
H Blood flow exerts pressure against a congenitally
weak arterial wall, stretching it like an overblown

balloon and making it likely to rupture.
H Such a rupture is followed by a subarachnoid hemorrhage, in which blood spills into the space normally
occupied by cerebrospinal fluid.
H Blood spills into brain tissue, where a clot can cause
potentially fatal increased intracranial pressure and
brain tissue damage.
Causes
H Congenital defect
H Degenerative process
H Combination of congenital defect and degenerative
process
H Trauma
Incidence
H Slightly higher in females than in males, especially
those in their late 40s or early- to mid-50s
Test results
Imaging
H Computed tomography scan reveals subarachnoid or
ventricular bleeding with blood in subarachnoid
space and displaced midline structures.
H Magnetic resonance imaging shows a cerebral blood
flow void.
H Skull X-rays may reveal calcified wall of the aneurysm
and areas of bone erosion.
H Cerebral angiography reveals altered cerebral blood
flow, vessel lumen dilation, and differences in arterial
filling.
H May occur at any age in either sex
Treatment
H Headache
H Nuchal rigidity
H Stiff back and legs
General
With rupture
H Sudden severe headache
H Altered level of consciousness (LOC)
H Avoidance of coffee, other stimulants, and aspirin
Complications
H Neurologic deficits
H Recurrent bleeding
H Vasospasm
H Death
H Bed rest in a quiet, darkened room with minimal
stimulation
Medications
H Analgesics
H Antihypertensive agents
H Sedatives
H Calcium channel blockers, such as nicardipine and
diltiazem for vasodilation

H Corticosteroids
H Anticonvulsants
H Aminocaproic acid to control bleeding
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Determining severity of an intracranial aneurysm rupture

The severity of symptoms varies from patient to patient, depending on the site and amount of bleeding. Five grades
characterize a ruptured cerebral aneurysm:
H Grade I: minimal bleeding The patient is alert with no
neurologic deficit; he may have a slight headache and
nuchal rigidity.
H Grade II: mild bleeding The patient is alert, with a mild
to severe headache and nuchal rigidity; he may have
third-nerve palsy.
Surgery
H Grade III: moderate bleeding The patient is confused

or drowsy, with nuchal rigidity and, possibly, a mild focal
deficit.
H Grade IV: severe bleeding The patient is stuporous,
with nuchal rigidity and, possibly, mild to severe
hemiparesis.
H Grade V: moribund (usually fatal) If the rupture is
nonfatal, the patient is in a deep coma or decerebrate.
Patient teaching
H Surgical repair by clipping, ligation, or wrapping
(before or after rupture)
Key outcomes
The patient will:
H maintain or improve LOC
H maintain hemodynamic stability.
Be sure to cover:
H how to recognize signs of rebleeding.
Discharge planning
H Refer the patient to a visiting nurse or a rehabilita-
tion center when necessary.
H Establish and maintain a patent airway.
H Position the patient to promote pulmonary drainage
and prevent upper airway obstruction.

H Impose aneurysm precautions (bed rest in a quiet,
darkened room, keeping the head of the bed flat or

less than 30 degrees, as ordered; limited visitation;
avoidance of strenuous physical activity and straining
with bowel movements; and restricted fluid intake).
H Assist with active range-of-motion (ROM) exercises;
if the patient is paralyzed, perform regular passive
ROM exercises.
H If the patient has facial weakness, assess the gag reflex and assist him during meals, placing food in the
unaffected side of his mouth. If he cant swallow, insert a nasogastric tube, as ordered, and administer
tube feedings.
H If the patient cant speak, establish a simple means of
communication or use cards or a notepad. Encourage his family to speak to him in a normal tone, even
if he doesnt seem to respond.
H Provide emotional support, and include the patients
family in his care as much as possible. Encourage
family members to adopt a realistic attitude, but
dont discourage hope.
Monitoring
H Vital signs
H Neurologic status
H Arterial blood gas levels
H Intake and output
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Aneurysm, thoracic
aortic
Overview
Description
H Dyspnea
H Cyanosis
H Leg weakness
H Transient paralysis
H Abrupt onset of intermittent neurologic deficits
H Abrupt loss of radial and femoral pulses and right
and left carotid pulses

H Increasing area of flatness over the heart, suggesting
Incidence
cardiac tamponade and hemopericardium

In dissecting ascending aneurysm
H Pain with a boring, tearing, or ripping sensation in
the thorax or the right anterior chest; may extend to
the neck, shoulders, lower back, and abdomen
H Pain most intense at onset
H Murmur of aortic insufficiency, a diastolic murmur
H Pericardial friction rub (if hemopericardium present)
H Blood pressure may be normal or significantly elevated, with a large difference in systolic blood pressure
between the right and left arms
In dissecting descending aneurysm
H Sharp, tearing pain located between the shoulder
blades that usually radiates to the chest
H Carotid and radial pulses present and equal
bilaterally
H Systolic blood pressure equal
H May detect bilateral crackles and rhonchi if pulmonary edema present
In dissecting transverse aneurysm
H Sharp, boring, and tearing pain that radiates to the
shoulders
H Hoarseness
H Dyspnea
H Throat pain
H Dysphagia
H Dry cough
H Ascending thoracic aorta most common site

H Occurs predominantly in males younger than age 60
Test results
H Abnormal widening of the ascending, transverse, or
descending part of the thoracic aorta

H May be saccular (outpouching), fusiform (spindle-
shaped), or dissecting
Pathophysiology
H Thoracic aortic aneurysm is caused by a circumfer-
ential or transverse tear of the aortic wall intima,

usually within the medial layer.
H This occurs in about 60% of patients; its usually an
emergency with poor prognosis.
Causes
H Atherosclerosis
H Blunt chest trauma
H Bacterial infections, usually at an atherosclerotic
plaque
H Coarctation of the aorta
H Syphilis infection
H Rheumatic vasculitis
H Marfan syndrome
Risk factors
H Cigarette smoking
H Hypertension
who have coexisting hypertension

H Descending thoracic aortic aneurysms most common
in younger patients who have had chest trauma
H Asymptomatic until dissection
Complications
H Cardiac tamponade
H Dissection
Assessment
History
H Without signs and symptoms until aneurysm expands
and begins to dissect

H Sudden pain and possibly syncope
Physical findings
H Pallor
H Diaphoresis
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Aneurysm, thoracic aortic
Laboratory
H Hemoglobin levels are normal or decreased due to
blood loss caused by a leaking aneurysm.
Imaging
H Posteroanterior and oblique chest X-rays show
widening of the aorta and mediastinum.
H Aortography shows lumen of the aneurysm and its
size and location.
H Magnetic resonance imaging and computed tomography scan help confirm and locate the presence of
aortic dissection.
H Electrocardiography helps rule out the presence of
myocardial infarction.
H Echocardiography may help identify dissecting
aneurysm of the aortic root.
H Transesophageal echocardiography can be used to
measure the aneurysm in the ascending and descending aorta.
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Treatment
General
H I.V. fluids and whole blood transfusions, if needed
H Low-fat diet
H No activity restrictions unless surgery
Medications
H Antihypertensives
H Analgesics
Surgery
H Surgical resection with a Dacron or Teflon graft
replacement
Key outcomes
The patient will:
H maintain adequate cardiac output and hemodynamic
stability
pain
H show no signs or symptoms of infection
H maintain adequate fluid volume.
ALERT
After surgical repair, monitor for signs that resemble those of the initial dissecting aneurysm, suggesting a tear at the graft site.
Patient teaching
Be sure to cover:
H the diagnosis
H procedure and expected postoperative care, if
surgery is scheduled
H compliance with antihypertensive therapy, including
the need for such drugs and the expected adverse
effects
H monitoring of blood pressure
H when to call the physician if the patient has any sharp
pain in the chest or back of the neck.
Discharge planning
indicated.
H In a nonemergency situation, allow the patient to ex-
press his fears and concerns and identify and use effective coping strategies.
H Offer the patient and his family psychological support.
H Give prescribed analgesics to relieve pain.
After repair of thoracic aneurysm
H Maintain blood pressure in prescribed range with
fluids and medications.
H Give prescribed analgesics.
H After stabilization of vital signs, encourage and assist
the patient in turning, coughing, and deep breathing.
H Help the patient walk as soon as hes able.
H Assist the patient with range-of-motion exercises.
Monitoring
H Vital signs and hemodynamics
H Chest tube drainage
H Heart and lung sounds
H Laboratory results
H Distal pulses
H Level of consciousness and pain
H Signs of infection
H I.V. therapy and intake and output
Aneurysm, thoracic aortic
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Aneurysm, ventricular
Overview
Description
H An outpouching, almost always of the left ventricle,
that produces ventricular wall dysfunction

H May develop within days to weeks after myocardial
infarction (MI) or may be delayed for years
Pathophysiology
H When MI destroys a large muscular section of the left
ventricle, necrosis reduces the ventricular wall to a

thin sheath of fibrous tissue.
H Under intracardiac pressure, the thin sheath stretches and forms a separate noncontractile sac (aneurysm).
H Abnormal muscle wall movement accompanies ventricular aneurysm.
H During systolic ejection, the abnormal muscle wall
movements cause the remaining normally functioning myocardial fibers to increase the force of contraction to maintain stroke volume and cardiac
output.
H At the same time, a portion of the stroke volume is
lost to passive distention of the noncontractile sac.
Causes
H MI
Incidence
H Occurs in about 20% of patients after MI
H Occurs after MI
Complications
H Ventricular arrhythmias
H Cerebral embolization
H Heart failure
H Double, diffuse, or displaced apical impulse

H Gallop rhythm
H Crackles and rhonchi
Test results
Imaging
H Two-dimensional echocardiography demonstrates
abnormal motion in the left ventricular wall.
H Left ventriculography reveals left ventricular enlargement, with an area of akinesia or dyskinesia (during
cineangiography) and diminished cardiac function.
H Chest X-rays may disclose an abnormal bulge distorting the hearts contour if the aneurysm is large;
X-rays may be normal if the aneurysm is small.
H Noninvasive nuclear cardiology scan may indicate the
site of infarction and suggest the area of aneurysm.
H Electrocardiography may show persistent ST-T wave
elevations.
Treatment
General
H Depends on the size of the aneurysm and the pres-
ence of complications
H May require only routine medical examination to fol-
low the patients condition

H May require aggressive measures, such as cardiover-
sion, defibrillation, and endotracheal intubation

H Low-fat diet
H No activity restrictions, unless surgery
Medications
H Antiarrhythmics, such as lidocaine and procainamide
H Cardiac glycosides such as digoxin
H Fluid and electrolyte replacement
H Analgesics
H Antihypertensives, as appropriate
H Nitrates
H Anticoagulants, such as heparin and warfarin
Assessment
Surgery
History
H Embolectomy
H Aneurysmectomy with myocardial revascularization
H Previous MI
H Dyspnea
H Fatigue
Physical findings
Key outcomes
H Edema
H Visible or palpable systolic precordial bulge
H Distended jugular veins, if heart failure is present
H Irregular peripheral pulse rhythm
H Arrhythmias such as premature ventricular contrac-
The patient will:

H express feelings of increased energy and decreased
fatigue
H express feelings of decreased anxiety.
tions
H Pulsus alternans
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H Prepare for surgery, if indicated.
ALERT
Be alert for sudden changes in sensorium that may
indicate cerebral embolization and for any signs
that suggest renal failure or MI.
H Provide psychological support for the patient and his
family.
Monitoring
Heart failure
H Vital signs and heart sounds
H Cardiac rhythm, especially for ventricular arrhythmias
H Intake and output; and fluid and electrolyte balance
H Blood urea nitrogen and serum creatinine levels
After surgery
H Pulmonary artery catheter pressures
H Type and amount of chest tube drainage
Patient teaching
Be sure to cover:
H expected postoperative care, if the patient is scheduled to undergo resection
H monitoring pulse irregularity and rate changes.
Discharge planning
H Refer family or caregiver to a community-based car-
diopulmonary resuscitation training program.

H Refer the patient to a weight-reduction program, if
indicated.
indicated.
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Ankylosing spondylitis
Overview
Description
H Rheumatoid disease primarily affecting sacroiliac,
apophyseal, and costocervical joints and adjacent ligamentous or tendinous attachments to bone
H Usually occurs as a primary disorder; may occur secondary to Reiters syndrome, psoriatic arthritis, or
inflammatory bowel disease
H Also called rheumatoid spondylitis or MarieStrmpell disease
Pathophysiology
H Disease begins in the sacroiliac; gradually progresses
to the lumbar, thoracic, and cervical spine.

H Bone and cartilage deterioration leads to fibrous
tissue formation and eventual fusion of the spine

or peripheral joints.
Causes
H Unknown
H Familial tendency
H Initial inflammation may result from immune system
activation by bacterial infection
Incidence
H Affects males two to three times more commonly
than females
H Well-recognized in males but commonly overlooked
or missed in females
H More peripheral joint involvement in females
H Symptoms can unpredictably remit, exacerbate, or
arrest at any stage
Complications
H Atlantoaxial subluxation of cervical vertebrae
H Deposits of amyloid material in the kidneys, which
may lead to renal impairment or failure
Detecting ankylosing spondylitis

in women
Ankylosing spondylitis seldom occurs in women, which is
why if a womans symptoms include pelvic pain diagnosticians typically overlook ankylosing spondylitis and suspect pelvic imflammatory disease. However, its important
to assess a female patient with apparent pelvic disease
carefully especially if culture results identify no apparent cause of her discomfort. Otherwise, misdiagnosis can
lead to unwarranted invasive tests and treatments and
cause the patient needless anxiety related to contracting a
sexually transmitted disease. Asking the patient if theres a
family history of ankylosing spondylitis and the performance of a thorough health and social history is advisable.
68
Assessment
History
H Intermittent lower back pain most severe in the
morning or after inactivity and relieved by exercise

H Mild fatigue, fever, anorexia, and weight loss
H May describe pain in shoulders, hips, knees, and an-
kles
H Pain over the symphysis pubis, which may lead to its
being mistaken for pelvic inflammatory disease (see

Detecting ankylosing spondylitis in women)
Physical findings
H Stiffness or limited motion of the lumbar spine
H Pain and limited chest expansion
H Kyphosis
H Iritis
H Warmth, swelling, or tenderness of affected joints
H Sausage shape to small joints such as toes
H Aortic murmur caused by insufficiency
H Cardiomegaly
H Upper lobe pulmonary fibrosis, which mimics tuber-
culosis, that may reduce vital capacity to 70% or less

of predicted volume
Test results
H Diagnosis of primary ankylosing spondylitis requires
meeting established criteria. (See Diagnosing primary ankylosing spondylitis.)

Laboratory
H HLA antigen typing test shows serum findings that include HLA-B27 in about 95% of patients with primary
ankylosing spondylitis and up to 80% of patients with
secondary disease.
H Serum rheumatoid factor tests show the absence of
rheumatoid factor, which helps rule out rheumatoid
arthritis, which has similar symptoms.
H Serum alkaline phosphate and creatine kinase tests
show slightly elevated erythrocyte sedimentation rate,
serum alkaline phosphate levels, and creatine kinase
levels in active disease.
H Serum immunoglobulin (Ig) profile shows elevated
serum IgA levels.
Imaging
H X-ray studies define characteristic changes, such as
bilateral sacroiliac involvement (the hallmark of the
disease); blurring of the joints bony margins in early
disease; patchy sclerosis with superficial bony erosions; eventual squaring of vertebral bodies; and
bamboo spine with complete ankylosis.
Treatment
General
H Good posture; stretching and deep-breathing
exercises
H Braces and lightweight supports, if appropriate
H Heat, warm showers, baths, and ice
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H Nerve stimulation
H Nutritious diet
H Encourage activity as tolerated
Medications
H Nonsteroidal anti-inflammatory drugs such as
ibuprofen
H Sulfasaline
H Methotrexate
H Corticosteroids
H Tumor-necrosis-factor alpha inhibitors
Surgery
H Hip replacement surgery with severe hip involvement
H Spinal wedge osteotomy with severe spinal involve-
ment
Diagnosing primary ankylosing

spondylitis
For a reliable diagnosis, the patient must meet:
H criterion 7 and any one of criteria 1 through 5, or
H any five of criteria 1 through 6 if he doesnt have
criterion 7.
Seven criteria
1. Axial skeleton stiffness for at least 3 months thats
relieved by exercise
2. Lumbar pain that persists at rest
3. Thoracic cage pain of at least 3 months duration that
persists at rest
4. Past or current iritis
5. Decreased lumbar range of motion
6. Decreased chest expansion (age-related)
7. Bilateral, symmetrical sacroiliitis demonstrated by
radiographic studies
Key outcomes
The patient will:
pain
H recognize limitations imposed by illness and express
feelings about these limitations
H identify factors that increase the risk for injury.
H Keep in mind the patients limited range of motion
(ROM) when planning self-care tasks and activities.

H Offer support and reassurance.
H Apply heat locally and massage, as indicated.
H Have the patient perform active ROM exercises.
H Pace periods of exercise and rest to help the patient
achieve comfortable energy levels and lung oxygenation.
H If treatment includes surgery, ensure proper body
alignment and positioning.
H Involve other caregivers, such as a social worker, visiting nurse, and dietitian.
H avoidance of prolonged walking, standing, sitting, or
driving
H regular stretching and deep-breathing exercises;
swimming on a regular basis, if possible

H measurement of patients height every 3 to 4 months
to detect kyphosis
H nutrition and weight maintenance.
Discharge planning
H Refer the patient to physical therapy, as needed.
H Refer the patient to the Spondylitis Association of
America or the Arthritis Foundation for additional

support and information.
Monitoring
H Mobility and comfort level
H Heart sounds
Patient teaching
Be sure to cover:
H avoidance of physical activity that places stress on the
back such as lifting heavy objects
H importance of standing upright; sitting upright in a
high, straight-back chair; and avoiding leaning over a
desk
H importance of sleeping in a prone position on a hard
mattress and avoiding using pillows under the neck
or knees
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Anorexia nervosa
H Limits or restricts food intake; eats small portions
Overview
Complications
Description
H Psychological disorder of self-imposed starvation re-
sulting from a distorted body image and an intense

and irrational fear of gaining weight
H Actual loss of appetite, which is rare
H May occur simultaneously with bulimia nervosa
Pathophysiology
H Decreased calorie intake depletes body fat and pro-
tein stores.
H Estrogen deficiency occurs (in females) due to lack
of lipid substrate for synthesis, causing amenorrhea.

H Testosterone levels fluctuate (in males), and de-
creased erectile function and sperm count occurs.

H Ketoacidosis occurs from increased use of fat as en-
(see Criteria for hospitalizing a patient with

anorexia nervosa)
H Suicide
H Electrolyte imbalances
H Malnutrition
H Dehydration
H Esophageal erosion, ulcers, tears, and bleeding
H Tooth and gum erosion and dental caries
H Decreased left ventricular muscle mass and chamber
size
H Decreased cardiac output
H Hypotension
H Electrocardiogram (ECG) changes
H Heart failure
H Amenorrhea
H Anemia
H Death
ergy fuel.
Causes
Assessment

H Social attitudes that equate slimness with beauty
H Subconscious effort to exert personal control over
History
H Low self-esteem
H Compulsive personality
H High achievement goals
H 15% or greater weight loss for no organic reason

H Morbid fear of being fat
H Compulsion to be thin
H Angry disposition
H Tendency to minimize weight loss
H Ritualistic
H Amenorrhea
H Infertility
H Loss of libido
H Fatigue
H Sleep alterations
H Intolerance to cold
H Constipation or diarrhea
Incidence
Physical findings
H 5% to 10% of the population; more than 90% of
H Hypotension
H Bradycardia
H Emaciated appearance
H Skeletal muscle atrophy
H Loss of fatty tissue
H Atrophy of breast tissue
H Blotchy or sallow skin
H Lanugo on the face and body
H Dryness or loss of scalp hair
H Calluses of the knuckles
H Abrasions and scars on the dorsum of the hand
H Dental caries
H Oral or pharyngeal abrasions
H Painless salivary gland enlargement
H Bowel distention
H Slowed reflexes
life or to protect oneself from dealing with issues

surrounding sexuality
H Elaborate food preparation and eating rituals
H Achievement pressure
H Dependence and independence issues
H Stress caused by multiple responsibilities
H History of sexual abuse
Risk factors
those affected are females
Special populations
Anorexia nervosa occurs primarily in adolescents
and young adults but may also affect older females
and, occasionally, males.
H Preoccupation with body size
H Tendency to describe self as fat
H Dissatisfaction with a particular aspect of physical
appearance
H Compulsive exercising
H Self-induced vomiting
H Laxative or diuretic abuse
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DSM-IV-TR criteria
These criteria must be documented:
H Refusal to maintain or achieve normal weight for age
and height
H Intense fear of gaining weight or becoming fat, even
though underweight
H Disturbance in perception of body weight, size, or
shape
H Absence of at least three consecutive menstrual cycles when otherwise expected to occur (in females)
Test results
Laboratory
H Hemoglobin level, platelet count, and white blood
cell count are decreased.
H Bleeding time is prolonged.
H Erythrocyte sedimentation rate is decreased.
H Serum creatinine, blood urea nitrogen, uric acid,
cholesterol, total protein, albumin, sodium, potassium, chloride, calcium, and fasting blood glucose
levels are decreased.
H Alanine aminotransferase and aspartate aminotransferase levels are elevated in severe starvation states.
H Serum amylase levels are elevated.
H In females, serum luteinizing hormone and folliclestimulating hormone levels are decreased.
H Triiodothyronine levels are decreased.
H Urinalysis shows dilute urine.
H ECG may show nonspecific ST interval, T-wave
changes, and prolonged PR interval; ventricular
arrhythmias may also be present.
Treatment
General
H Behavior modification
H Curtailed activity for cardiac arrhythmias
H Group, family, or individual psychotherapy
H Balanced diet with a normal eating pattern
H Parenteral nutrition, if necessary
H Gradual increase in physical activity when weight
gain and stabilization occur
Criteria for hospitalizing a patient

with anorexia nervosa
A patient with anorexia nervosa can be successfully treated on an outpatient basis. However, if the patient displays
any of the signs listed here, hospitalization is mandatory:
H rapid weight loss equal to 15% or more of normal body
mass
H persistent bradycardia (50 beats/minute or less)
H hypotension with a systolic reading less than or equal
to 90 mm Hg
H hypothermia (core body temperature less than or equal
to 97 F (36.1 C)
H presence of medical complications, suicidal ideation
H persistent sabotage or disruption of outpatient
treatment resolute denial of condition and the need
for treatment.
H Support the patients efforts to achieve target weight.
H Negotiate an adequate food intake with the patient.
H Supervise the patient one-on-one during meals and
for 1 hour afterward.
Monitoring
H Vital signs
H Intake and output
H Electrolyte and complete blood count levels
H Weight on a regular schedule
H Activity for compulsive exercise
ALERT
Monitor the patient for 1 hour after meals to ensure no self-induced vomiting.
Patient teaching
Be sure to cover:
H nutrition
H importance of keeping a food journal
H avoidance of discussions about food between the
patient and her family.
Medications
Discharge planning
H Vitamin and mineral supplements

H Electrolyte replacement
H Serotonin reuptake inhibitors, such as citalopram,
fluoxetine, and sertraline, after weight gain is established
Key outcomes
The patient will:
H acknowledge change in body image
H express positive feelings about self
H achieve and maintain expected body weight
H achieve expected state of wellness.
Anorexia nervosa
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Anthrax
Incidence
H Occurs worldwide
H Most common in developing countries
H Most common in domestic herbivores, including
sheep, cattle, horses, and goats, and wild herbivores

H Estimates of 20,000 to 100,000 cases per year (Ap-
Overview
Description
proximately 95% of human anthrax are the cutaneous form; about 5% are the inhalation form; GI anthrax is rare.)
H An acute bacterial infection occurring most com-
monly in herbivorous animals; the natural resistance

of humans to anthrax greater than that of these
animals
H Also known as a potential agent for use in bioterrorism and biological warfare; classified as a Category A
biological disease
H Three forms of anthrax in humans, depending on the
mode of transmission: cutaneous, inhalation (woolsorters disease), and GI
H Cutaneous anthrax: the most common form
H Without treatment, mortality rate from cutaneous anthrax, 20%; mortality rate less than 1% with treatment
H Even with treatment, inhalation anthrax usually fatal
H With treatment, death in 25% to 60% of cases of GI
anthrax
H No screening test for anthrax
H History of exposure to B. anthracis spores

H Clinical manifestation will depend on the form of
Pathophysiology
H Bacillus anthracis is an encapsulated, aerobic,
chain-forming, gram-positive rod that forms oval

spores; spores are hardy and can survive for years
under adverse conditions.
H B. anthracis, an extracellular pathogen, evades
phagocytosis, invades the bloodstream, and multiplies rapidly.
H In cutaneous anthrax, spores enter the body through
abraded or broken skin or by biting flies; the spores
germinate within hours, the vegetative cells multiply,
and anthrax toxin is produced.
H In inhalation anthrax, spores are deposited directly
into the alveoli and phagocytized by macrophages;
some are carried to and germinate in mediastinal
nodes. This may result in overwhelming bacteremia,
hemorrhagic mediastinitis, and secondary pneumonia.
H In GI anthrax, primary infection can occur in the intestine by organisms that survive passage through the
stomach; acute inflammation of the intestinal tract
results.
Causes
H Bacterial infection with B. anthracis
Risk factors
H Laboratory and industrial workers at risk for occupa-
tional exposure
72
Anthrax
anthrax
Complications
H Septicemia
H Hemorrhagic mediastinitis
H Pneumonia
H Respiratory failure
H Hemorrhagic thoracic lymphadenitis
H Meningitis
H Death
Assessment
History
Cutaneous anthrax
H Painless ulcer
H Mild or no constitutional symptoms
Inhalation anthrax
H Initial prodromal flulike symptoms:
Malaise; dry cough
Mild fever; chills
Headache; myalgia
Severe respiratory distress
Chest pain
GI anthrax
H Nausea; vomiting
H Decreased appetite
H Fever
H Abdominal pain
H Vomiting blood
H Severe bloody diarrhea
Physical findings
Cutaneous anthrax
H Initially, a small, papular, pruritic lesion that resembles an insect bite
H Lesion that develops into a vesicle in 1 to 2 days
H Lesion that finally becomes a small, painless ulcer
with a necrotic center, surrounded by nonpitting
edema
H Smaller secondary vesicles that may surround some
lesions
H Lesions that are generally located on exposed areas
of the skin
H Painful, regional, nonspecific lymphadenitis
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Inhalational anthrax
H Increasing fever
H Dyspnea, stridor
H Hypoxia; cyanosis
H Hypotension; shock
GI anthrax
H Fever
H Rapidly developing ascites
Test results
Laboratory
H Gram stain, direct fluorescent antibody staining, and
culture show presence of B. anthracis.
H Blood cultures show presence of B. anthracis.
H Cerebrospinal fluid analysis reveals presence of
B. anthracis.
H Complete blood count shows polymorphonuclear
leukocytosis in severe disease.
H Serum antibody tests reveal the presence of the
specific antibody to B. anthracis.
Imaging
H Chest X-ray show symmetrical mediastinal widening
in hemorrhagic mediastinitis.
Treatment
General
H Encourage verbalization of fears and concerns.

H Provide adequate hydration.
H Provide a well-balanced diet.
H Assist the patient in the development of effective cop-
ing mechanisms.
H Provide adequate rest periods.
Monitoring
H Vital signs
H Intake and output
H Neurologic status
H Cardiovascular status
H Skin lesions
H GI status
H Complications
H Progression of infection
Patient teaching
Be sure to cover:
H anthrax prevention.
H Treatment initiated as soon as exposure to anthrax is
suspected (essential to preventing anthrax infection;

may also help prevent death)
H No dietary restrictions
H Physical activity as tolerated
Medications
H Antibiotics, such as ciprofloxacin, doxycycline, and
amoxicillin
H Oxygen, as needed
Surgery
H May be necessary for complications such as hemor-
rhagic mediastinitis
Key outcomes
The patient will:
H maintain adequate nutrition and hydration
H verbalize feelings of fear and anxiety
H demonstrate effective coping mechanisms
H maintain tissue perfusion and cellular oxygenation
H maintain effective ventilation.
H Maintain patent airway and adequate ventilation.
H Report any case of anthrax in either livestock or hu-
mans to the local board of health.

H Maintain standard precautions.
Anthrax
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Aortic insufficiency
Overview
Description
H A heart condition in which blood flows back into the
left ventricle, causing excess fluid volume

H Also called aortic regurgitation
Pathophysiology
H Blood flows back into the left ventricle during dias-
tole, causing increased left ventricular diastolic pressure.

H This results in volume overload, dilation and, eventually, hypertrophy of the left ventricle.
H Excess fluid volume also eventually results in increased left atrial pressure and increased pulmonary
vascular pressure.
Causes
H Rheumatic fever
H Primary disease of the aortic valve leaflets, the wall
or the aortic root, or both

H Hypertension
H Infective endocarditis
H Trauma
H Idiopathic valve calcification
H Aortic dissection
H Aortic aneurysm
H Connective tissue diseases
Incidence
H Occurs most commonly in males
H When associated with mitral valve disease: more
common in females
H Typically asymptomatic until the fourth or fifth
decade of life
H Orthopnea
H Paroxysmal nocturnal dyspnea
H Exertional dyspnea
Complications
H Left-sided heart failure
H Pulmonary edema
Assessment
History
H Exertional dyspnea, orthopnea, paroxysmal noctur-
nal dyspnea
H Sensation of a forceful heartbeat, especially in supine
position
H Angina, especially nocturnal
H Fatigue
74
H Palpitations, head pounding

H Symptoms of heart failure, in late stages
Physical findings
H Corrigans pulse
H Pulsus bisferiens
H Pulsating nail beds and Quinckes sign
H Wide pulse pressure
H Diffuse, hyperdynamic apical impulse, displaced lat-
erally and inferiorly

H Systolic thrill at base or suprasternal notch
H S3 gallop with increased left ventricular end-diastolic
pressure
H High frequency, blowing early-peaking, diastolic de-
crescendo murmur best heard with the patient sitting

leaning forward and in deep fixed expiration (see
Identifying the murmur of aortic insufficiency)
H Austin Flint murmur
H Head bobbing with each heartbeat
H Tachycardia, peripheral vasoconstriction, and pulmonary edema if severe aortic insufficiency
Test results
Imaging
H Chest X-rays may show left ventricular enlargement
and pulmonary vein congestion.
H Echocardiography may show left ventricular enlargement, increased motion of the septum and posterior
wall, thickening of valve cusps, prolapse of the valve,
flail leaflet, vegetations, or dilation of the aortic root.
H Electrocardiography shows sinus tachycardia, left
axis deviation, left ventricular hypertrophy, and left
atrial hypertrophy in severe disease.
H Cardiac catheterization shows presence and degree
of aortic insufficiency, left ventricular dilation and
function, and coexisting coronary artery disease.
Treatment
General
H Periodic noninvasive monitoring of aortic insufficien-
cy and left ventricular function with echocardiogram

H Medical control of hypertension
H Low-sodium diet
H Planned periodic rest periods to avoid fatigue
Medications
H Vasodilators such as nitrates
H Antihypertensives
H Antiarrhythmics, such as amiodarone and
propafenone
H Infective endocarditis prophylaxis, as appropriate
H Anticoagulants such as warfarin
H Antiplatelets, such as clopidogrel and ticlopidine
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ALERT
Avoid using beta-adrenergic blockers due to their
negative inotropic effects.
Identifying the murmur of aortic

insufficiency
A high-pitched, blowing decrescendo murmur that radiates from the aortic valve area to the left sternal border
characterizes aortic insufficiency.
Surgery
H Valve replacement
SYSTOLE
S1
DIASTOLE
S2
SYSTOLE
S1
S2
Key outcomes
The patient will:
H carry out activities of daily living without excess fatigue or decreased energy
H maintain cardiac output, demonstrate hemodynamic
stability, and not develop arrhythmias
H maintain adequate ventilation.
H If the patient needs bed rest, stress its importance;
provide a bedside commode.

H Alternate periods of activity and rest.
H Allow the patient to express his concerns about the
effects of activity restrictions on his responsibilities

and routines.
H Keep the patients legs elevated while he sits in a
chair.
H Place the patient in an upright position, if necessary,
and administer oxygen.
H Keep the patient on a low-sodium diet. Consult a dietitian.
H Following surgery, watch for hypotension, arrhythmias, and thrombus formation.
Monitoring
Patient teaching
Be sure to cover:
H periodic rest periods in the patients daily routine
H leg elevation whenever the patient sits
H signs and symptoms of heart failure
H importance of consistent follow-up care
H monitoring of pulse rate and rhythm
H blood pressure control.
Discharge planning
H Refer the patient to an outpatient cardiac rehabilita-
tion program, if indicated.

indicated.
indicated.
H Signs and symptoms of heart failure

H Pulmonary edema
H Adverse reactions to drug therapy
H Complications
After surgery
H Vital signs and cardiac rhythm
H Heart sounds
H Neurologic status
H Intake and output; daily weight
H Blood chemistry studies, prothrombin time, and
International Normalized Ratio values
H Pulmonary artery catheter pressures
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Aortic stenosis
Overview
Description
H Narrowing of the aortic valve that affects blood flow
in the heart
H Classified as either acquired or rheumatic
Pathophysiology
H Stenosis of the aortic valve results in impedance to
forward blood flow.

H The left ventricle requires greater pressure to open
the aortic valve.

H Added workload increases myocardial oxygen demands.
H Diminished cardiac output reduces coronary artery
blood flow.
H Left ventricular hypertrophy and failure result.
Causes
H Idiopathic fibrosis and calcification
H Congenital aortic bicuspid valve
H Rheumatic fever
H Atherosclerosis
Risk factors
H Diabetes mellitus
Incidence
H Possibly asymptomatic until ages 50 to 70, even
though stenosis present since childhood

H About 80% of patients: male
H Long latent period
H Classic triad of angina pectoris, syncope, and
dyspnea
Complications
H Right-sided heart failure
H Cardiac arrhythmias, especially atrial fibrillation
H Sudden death
H Left ventricular hypertrophy
Physical findings
H Small, sustained arterial pulses that rise slowly
H Distinct lag between carotid artery pulse and apical
pulse
H Orthopnea
H Prominent jugular vein a waves
H Peripheral edema
H Diminished carotid pulses with delayed upstroke
H Apex of the heart may be displaced inferiorly and lat-
erally
H Suprasternal thrill
Special populations
An early systolic ejection murmur may be present
in children and adolescents who have noncalcified
valves. The murmur is low-pitched, rough, and
rasping and is loudest at the base in the second intercostal space.
H Split S2 develops as stenosis becomes more severe
H Prominent S4
H Harsh, rasping, mid- to late-peaking systolic murmur
thats best heard at the base and commonly radiates

to carotids and apex (see Identifying the murmur
of aortic stenosis)
Test results
Imaging
H Chest X-ray shows valvular calcification, left ventricular enlargement, pulmonary vein congestion and, in
later stages, left atrial, pulmonary artery, right atrial,
and right ventricular enlargement.
H Echocardiography shows decreased valve area, increased gradient, and increased left ventricular wall
thickness.
H Cardiac catheterization shows increased pressure
gradient across the aortic valve, increased left ventricular pressures, and presence of coronary artery
disease.
H Electrocardiography may show left ventricular hypertrophy, atrial fibrillation, or other arrhythmia.
Treatment
General
H Periodic noninvasive evaluation of the severity of
valve narrowing
Assessment
History
H May be asymptomatic
H Dyspnea on exertion
H Angina
H Exertional syncope
H Fatigue
H Palpitations
76
Aortic stenosis
H Lifelong treatment and management of congenital
aortic stenosis
H Low-sodium, low-fat, low-cholesterol diet
H Planned rest periods
Medications
H Antibiotic infective endocarditis prophylaxis
H Anticoagulants, such as warfarin
H Antiplatelets such as clopidogrel and ticlopidine
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ALERT
The use of diuretics and vasodilators may lead to
hypotension and inadequate stroke volume.
Surgery
H In adults, valve replacement after they become symp-
Identifying the murmur of aortic stenosis

A low-pitched, harsh crescendo-decrescendo murmur that
radiates from the aortic valve area to the carotid artery
characterizes aortic stenosis.
SYSTOLE
S1
DIASTOLE
S2
SYSTOLE
S1
S2
tomatic with hemodynamic evidence of severe obstruction

H Percutaneous balloon aortic valvuloplasty
H In children without calcified valves, simple commissurotomy under direct visualization
H Ross procedure in patients younger than age 5
Key outcomes
The patient will:
H perform activities of daily living without excess fatigue or exhaustion
H maintain cardiac output
H demonstrate hemodynamic stability
H maintain balanced fluid status
H maintain joint mobility and range of motion
H develop and demonstrate adequate coping skills.
H Maintain a low-sodium diet. Consult with a dietitian.
H If the patient requires bed rest, stress its importance.
Provide a bedside commode.

H Allow the patient to voice concerns about the effects
of activity restrictions.
H Keep the patients legs elevated while he sits in a
chair.
H Place the patient in an upright position, and administer oxygen, as needed.
H Allow the patient to express his fears and concerns.
Patient teaching
Be sure to cover:
H periodic rest in the patients daily routine
H leg elevation whenever the patient sits
H dietary and fluid restrictions
H infective endocarditis prophylaxis
H pulse rate and rhythm
H monitoring for atrial fibrillation and other arrhythmias.
Discharge planning
indicated.
indicated.
Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of progressive aortic stenosis
H Daily weight
H Arrhythmias
H Prothrombin time and International Normalized
Ratio
If the patient has surgery
H Signs and symptoms of thrombus formation
H Hemodynamics
H Arterial blood gas results
H Blood chemistry results
Aortic stenosis
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Appendicitis
Overview
Description
H Inflammation of the vermiform appendix
H Most common major abdominal surgical disease
H Fatal if left untreated; gangrene and perforation de-
velop within 36 hours
Pathophysiology
H Mucosal ulceration triggers inflammation, which
temporarily obstructs the appendix.

H Obstruction causes mucus outflow, increasing pres-
sure in the distended appendix; the appendix then

contracts.
H Bacteria multiply and inflammation and pressure increase, restricting blood flow and causing thrombus
and abdominal pain.
Causes
H Foreign body
H Neoplasm
H Mucosal ulceration
H Fecal mass
H Stricture
H Barium ingestion
H Viral infection
Risk factors
H Anorexia
H Nausea, vomiting
Physical findings
H Low-grade fever, tachycardia
H Adjusts posture to decrease pain
H Guarding
H Normoactive bowel sounds, with possible constipa-
tion or diarrhea
H Rebound tenderness and spasm of the abdominal
muscles
H Rovsings sign (pain in right lower quadrant that oc-
curs with palpation of left lower quadrant)

H Psoas sign (abdominal pain that occurs when the pa-
tient flexes his hip with pressure applied to his knee)

H Obturator sign (abdominal pain that occurs when the
hip is rotated)
H Absent abdominal tenderness or flank tenderness
with retrocele or pelvic appendix
Test results
Laboratory
H White blood cell count is moderately elevated, with
an increased numbers of immature cells.
Imaging
H Abdominal or transvaginal ultrasound shows appendiceal inflammation.
H Barium enema reveals nonfilling appendix.
H Abdominal computed tomography scan demonstrates
suspected perforation or abscess.
H Adolescent male
Treatment
Incidence
General
H Can occur at any age; however, the majority of cases
H Delaying surgery until antibiotic therapy has been ini-
occur between ages 11 and 20

H Affects both sexes; however, between puberty and age
25, more prevalent in men
H Nothing by mouth until after surgery, then gradual re-
H Early postoperative ambulation

H Incentive spirometry
H Abdominal pain
H Anorexia
H Vomiting
Medications
Complications
H Wound infection
H Intra-abdominal infection
H Fecal fistula
H Intestinal obstruction
H Incisional hernia
H Peritonitis (most common)
H Death
Assessment
History
H Abdominal pain thats initially generalized, then lo-
calizes in the right lower abdomen (McBurneys

point)
78
Appendicitis
tiated, if an abscess suspected

turn to regular diet
H I.V. fluids
H Analgesics
H Antibiotics preoperatively and if peritonitis develops
Surgery
H Appendectomy
Key outcomes
The patient will:
H exhibit no signs of infection
H maintain calorie requirement
H maintain normal fluid volume.
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H Maintain nothing-by-mouth status until surgery is
performed.
H Administer I.V. fluids
H Avoid administering analgesics until the diagnosis is
confirmed.
H Avoid administering cathartics or enemas that may
rupture the appendix.

H Place the patient in Fowlers position to decrease
pain.
ALERT
Never apply heat to the right lower abdomen; this
can cause the appendix to rupture.
Monitoring
After surgery
H Vital signs
H Intake and output
H Pain control
H Bowel sounds, passing of flatus, or bowel movements
H Wound healing
Patient teaching
Be sure to cover:
H preoperative teaching
H possible complications
H appropriate wound care
adverse reactions
H postoperative activity limitations.
Appendicitis
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Arterial occlusive
disease
Overview
Description
H An obstruction or narrowing of the lumen of the aor-
ta and its major branches

H May affect arteries, including the carotid, vertebral,
innominate, subclavian, femoral, iliac, renal, mesenteric, and celiac

H Prognosis dependent on location of the occlusion
and development of collateral circulation that counteracts reduced blood flow
Pathophysiology
H Narrowing of vessel leads to interrupted blood flow,
usually to the legs and feet.

H During times of increased activity or exercise, blood
flow to surrounding muscles cant meet the metabolic demand.

H This results in pain in affected areas.
Causes
H Atherosclerosis
H Immune arteritis
H Embolism
H Thrombosis
H Thromboangiitis obliterans
H Raynauds disease
H Fibromuscular disease
H Atheromatous debris (plaques)
H Indwelling arterial catheter
H Direct blunt or penetrating trauma
Risk factors
H Smoking
H Hypertension
H Dyslipidemia
H Diabetes mellitus
H Advanced age
Incidence
H More common in males than in females
H Usually occurs in people older than age 50
H Higher incidence in patients with diabetes
H Arteries in the legs more commonly affected
H Intermittent claudication
H Decreased temperature in arms and legs
H Numbness or paresthesia
Complications
H Severe ischemia
H Skin ulceration
H Gangrene
H Limb loss
80
Arterial occlusive disease
Assessment
History
H One or more risk factors
H Family history of vascular disease
H Rest pain
H Poor healing wounds or ulcers
H Impotence
H Dizziness or near syncope
H Transient ischemic attack symptoms
Physical findings
H Trophic changes of involved arm or leg
H Diminished or absent pulses in arm or leg
H Presence of ischemic ulcers
H Pallor with elevation of arm or leg
H Dependent rubor
H Arterial bruit
H Hypertension
H Pain
H Pulselessness distal to the occlusion
H Paralysis and paresthesia occurring in the affected
arm or leg
H Cool extremities
Test results
Imaging
H Arteriography shows type, location, and degree of
obstruction, and the establishment of collateral circulation.
H Ultrasonography and plethysmography show decreased blood flow distal to the occlusion.
H Doppler ultrasonography shows a relatively
low-pitched sound and a monophasic waveform.
H EEG and computed tomography scan may show the
presence of brain lesions.
Other
H Segmental limb pressures and pulse volume measurements show the location and extent of the occlusion.
H Ophthalmodynamometry shows the degree of obstruction in the internal carotid artery.
H Electrocardiography may show presence of cardiovascular disease.
Treatment
General
H Smoking cessation
H Hypertension, diabetes, and dyslipidemia control
H Foot and leg care
H Weight control
H Low-fat, low-cholesterol, high-fiber diet
H Regular walking program
Medications
H Antiplatelets, such as clopidogrel and ticlopidine
H Lipid-lowering agents
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H Hypoglycemics
H Antihypertensives
H Thrombolytics, such as alteplase and streptokinase
H Anticoagulants, such as warfarin and heparin
H Niacin or vitamin B complex
Surgery
H Embolectomy
H Endarterectomy
H Atherectomy
H Laser angioplasty
H Endovascular stent placement
H Percutaneous transluminal angioplasty
H Laser surgery
H Patch grafting
H Bypass graft
H Lumbar sympathectomy
H Amputation
H Bowel resection
Key outcomes
The patient will:
H report increased comfort and decreased pain
H maintain palpable pulses and collateral circulation
H develop no signs or symptoms of infection.
For chronic arterial occlusive disease
H Use preventive measures, such as minimal pressure
mattresses, heel protectors, a foot cradle, or a footboard.
H Avoid using restrictive clothing such as antiembolism
stockings.
H Allow the patient to express fears and concerns.
For preoperative care during an acute episode
H Assess the patients circulatory status.
H Give prescribed heparin or thrombolytics.
H Wrap the patients affected foot in soft cotton batting,
and reposition it frequently to prevent pressure on
any one area.
H Strictly avoid elevating or applying heat to the affected leg.
For postoperative care
H Watch the patient closely for signs of hemorrhage.
H In mesenteric artery occlusion, connect a nasogastric
tube to low intermittent suction.
H Assist with early ambulation, but dont allow the patient to sit for an extended period.
H If amputation has occurred, check the stump carefully for drainage, and note and record its color and
amount and the time.
H Elevate the stump as ordered.
Monitoring
H Signs and symptoms of fluid or electrolyte imbalance
or renal failure
H Signs and symptoms of stroke
H Vital signs
H Intake and output
H Distal pulses
H Neurologic status
H Bowel sounds
Ratio
Patient teaching
Be sure to cover:
H regular exercise program
H foot care
H signs and symptoms of graft occlusion
H signs and symptoms of arterial insufficiency and
occlusion
H avoidance of wearing constrictive clothing, crossing
legs, or wearing garters
H risk factor modification
H avoidance of temperature extremes.
Discharge planning
H Refer the patient to a physical and occupational ther-
apist, as indicated.
H Refer the patient to a podiatrist for foot care, as
needed.
H Refer the patient to an endocrinologist for glucose
control, as indicated.
H Refer the patient to a smoking-cessation program,
as indicated.
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Arteriovenous
malformations
H Symptoms of intracranial (intracerebral, subarach-
noid, or subdural) hemorrhage, including sudden

severe headache, seizures, confusion, lethargy, and
meningeal irritation
H Hydrocephalus
Overview
Complications
Description
H Aneurysm development and subsequent rupture

H Hemorrhage (intracerebral, subarachnoid, or sub-
H Tangled masses of thin-walled, dilated blood vessels
between arteries and veins that dont connect by capillaries

H Common in the brain, primarily in the posterior portion of the cerebral hemispheres
H Adequate perfusion of brain tissue prevented due to
abnormal channels between arterial and venous system mixing oxygenated and unoxygenated blood
H Range in size from a few millimeters to large malformations extending from the cerebral cortex to the
ventricles
H Commonly more than one arteriovenous malformation (AVM) present
Pathophysiology
dural, depending on the location of the AVM)

H Hydrocephalus
Assessment
History
H Chronic headache
H Seizures
H Change in mental status
Physical findings
H Systolic carotid bruit
H Typical structural characteristics of the blood vessels
Test results
arent present.
H Vessels of an AVM are very thin. (One or more arteries feed into the AVM, causing it to appear dilated
and torturous.)
H Typically, high-pressured arterial flow moves into the
venous system through the connecting channels to
increase venous pressure, engorging and dilating the
venous structures.
H If the AVM is large enough, the shunting can deprive
the surrounding tissue of adequate blood flow.
H Thin-walled vessels may ooze small amounts of blood
or actually rupture, causing hemorrhage into the
brain or subarachnoid space.
H Cerebral arteriogram confirms the presence of AVMs
and evaluates blood flow.
H Doppler ultrasonography of cerebrovascular system
indicates abnormal, turbulent blood flow.
Treatment
General
H Support measures, including aneurysm precautions
to prevent possible rupture
Causes
H Nothing by mouth, if scheduled for surgery

H Limited activity
H Quiet atmosphere
H Congenital (hereditary)
H Penetrating injuries such as trauma
Medications
Incidence
H Males and females equally affected
H AVMs possibly familial
H Most AVMs present at birth; however, typically asymp-
tomatic until ages 10 to 20
H Chronic mild headache and confusion
H Seizures
H Systolic bruit over carotid artery, mastoid process, or
orbit
H Focal neurologic deficits (depending on the location
of the AVM) resulting from compression and diminished perfusion
82
Arteriovenous malformations
H I.V. fluid
H Analgesics
H Sedatives
H Stool softener
Surgery
H Block dissection, laser, or ligation to repair the com-
municating channels and remove the feeding vessels

H Embolization or radiation therapy, if surgery isnt
possible, to close the communicating channels and

feeder vessels and thus reduce the blood flow to the
AVM
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Key outcomes
The patient will:
H maintain stable neurologic status
H express an understanding of the disorder and treatment.
H Control hypertension and seizure activity.
H Maintain a quiet atmosphere and provide relaxation
techniques.
H If the AVM has ruptured, work to control elevated in-
tracranial pressure and intracranial hemorrhage.
Monitoring
H Vital signs
H Neurologic status
Patient teaching
Be sure to cover:
H importance of reporting signs of intracranial bleeding immediately (sudden severe headache, vision
changes, decreased movement in extremities, change
in level of consciousness).
Discharge planning
H Refer the patient to social service for support ser-
vices if neurologic deficits have occurred due to a

ruptured AVM.
Arteriovenous malformations
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Asbestosis
Overview
Description
H Lung disease characterized by diffuse interstitial pul-
monary fibrosis resulting from prolonged exposure

to airborne asbestos particles
H May develop many years (about 15 to 20) after regular exposure to asbestos ceases
H Pleural plaques and mesotheliomas of the pleura and
the peritoneum formed by exposure
H A form of pneumoconiosis
H Also known as mesothelioma
Pathophysiology
H Inhaled asbestos fibers travel down the airway and
penetrate respiratory bronchioles and alveolar walls.

H Mucus production and goblet cells are stimulated to
protect the airway and aid in expectoration.

H Fibers become encased in a brown, iron-rich, pro-
teinlike sheath, called asbestosis bodies.

H Chronic irritation by the fibers continues, causing
edema of the airways.

H Fibrosis develops in response to the chronic irrita-
tion.
Causes
H Prolonged inhalation of asbestos fibers from indus-
tries, such as mining and milling, construction, fireproofing, and textile

H Production of paints, plastics, and brake and clutch
linings
H Exposure to fibrous dust shaken off workers clothing
H Exposure to fibrous dust or waste piles from nearby
asbestos plants
Incidence
Assessment
History
H Exposure to asbestos fibers
H Exertional or rest dyspnea
H Cough
H Chest pain
H Recurrent respiratory tract infections
Physical findings
H Tachypnea
H Clubbing of the fingers
H Characteristic dry crackles in the lung bases
Test results
Laboratory
H Arterial blood gas (ABG) analysis shows decreased
partial pressures of arterial oxygen and carbon dioxide.
Imaging
H Chest X-rays may show fine, irregular, and linear diffuse infiltrates; a honeycomb or ground-glass appearance to lungs; and pleural thickening and pleural calcification, bilateral obliteration of costophrenic
angles, and an enlarged heart with shaggy border.
Other
H Pulmonary function tests may show decreased vital
capacity, forced vital capacity (FVC), and total lung
capacity; decreased or normal forced expiratory volume in 1 second (FEV1) a normal ratio of FEV1 to
FVC; and reduced diffusing capacity for carbon
monoxide.
Treatment
General
H Controlled coughing and postural drainage with
chest percussion and vibration
H Commonly occurring between ages 40 and 75

H Affects males more commonly than females
H At least 3 qt (3 L) of fluids daily

H High-calorie, high-protein, low-sodium diet
Medications
H Exposure to asbestos fibers

H Exertional or rest dyspnea
H Dry cough
H Chest pain
H Inhaled mucolytics such as acetylcysteine

H Supplemental oxygen
Complications
Surgery
H Pulmonary fibrosis
H Pulmonary hypertension
H Cor pulmonale
H Lung transplantation, in severe cases
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Asbestosis
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Key outcomes
The patient will:
H maintain adequate caloric intake
H express understanding of the illness
H identify measures to prevent or reduce fatigue.
H Give prescribed drugs and provide oxygen therapy.
H Provide supportive care.
H Provide chest physiotherapy.
H Provide high-calorie, high-protein, low-sodium foods
in small, frequent meals.

H Encourage oral fluid intake.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Respiratory status (breath sounds, ABG results)
H Sputum production
H Mentation
H Complications
Patient teaching
Be sure to cover:
H transtracheal catheter care, if applicable
H prevention of infection
H influenza and pneumococcus immunizations
H home oxygen therapy, if required
H importance of follow-up care
H chest physiotherapy
H high-calorie, high-protein, low-sodium diet
H adequate oral fluid intake
H energy conservation techniques.
Discharge planning
indicated.
Asbestosis
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Ascariasis
Overview
Description
H Intestinal infection caused by the parasitic worm As-
caris lumbricoides, a large roundworm resembling

an earthworm
H Never passes directly from person to person
H Also known as roundworm infection
Pathophysiology
H After ingestion, A. lumbricoides ova hatch and re-
lease larvae, which penetrate the intestinal wall and

reach the lungs through the bloodstream.
H After about 10 days in pulmonary capillaries and
alveoli, the larvae migrate to the bronchioles,
bronchi, trachea, and epiglottis.
H From the epiglottis, the larvae are swallowed and
return to the intestine to mature into worms.
Causes
H Ingestion of food, drink, or soil contaminated with
A. lumbricoides ova
Incidence
H Occurs worldwide but most common in tropical ar-
eas with poor sanitation and in Asia, where farmers

use human stool as fertilizer
H In the United States, more prevalent in the South,
particularly among younger children
H Stomach discomfort
H Vomiting
Test results
Laboratory
H Microscopic studies show ova in the stool, or adult
worm is observed in emesis.
H Complete blood count: shows eosinophilia
Imaging
H Abdominal X-rays show whirlpool pattern of intraluminal worms. (Intestinal obstruction may be noted.)
H Chest X-rays show characteristic bronchovascular
markings infiltrates, patchy areas of pneumonitis,
and widening of hilar shadows (if migrated to lungs).
Treatment
General
H Nasogastric (NG) suctioning (with intestinal obstruc-
tion)
H Nothing by mouth until stable
H Rest as needed
Medications
H I.V. fluids
H Mebendazole and albendazole
H Anthelmintic therapy (pyrantel or piperazine) (avoid
use if intestinal obstruction is present)
ALERT
Piperazine is contraindicated in patients with
seizure disorder and may cause stomach upset,
dizziness, and urticaria. Pyrantel produces red
stool and vomitus and may cause stomach upset,
headache, dizziness, and rash. Albendazole and
mebendazole may cause abdominal pain and diarrhea.
Complications
Surgery
H Pneumonitis
H Intestinal surgery to relieve obstruction, if necessary
Assessment
History
H Stomach discomfort or pain
H Nausea and vomiting
H Recent travel to endemic area
H Restlessness
H Disturbed sleep
Physical findings
H Dehydration
H Crackles, wheezing, and tachypnea (if migrated to
the lungs)
86
Ascariasis
Key outcomes
The patient will:
H regain normal intestinal function
H express understanding of proper sanitation of food
and hands.
H Isolation is unnecessary; proper disposal of stool and
soiled linen, using standard precautions, should be

adequate.
H If the patient is receiving NG suctioning, provide
good mouth care.
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Monitoring
H Vital signs
H Intake and output
H Appearance of stools (for worms)
Patient teaching
Be sure to cover:
H proper hand washing, especially before eating and
after defecating
H bathing and changing underwear and bed linens
daily
H adverse effects of medications prescribed for the
patient.
Discharge planning
H Refer the patient to social services if living conditions
are questionable regarding cleanliness.
Ascariasis
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Aspergillosis
H Organ transplants
H TB or another cavitary lung disease (in asper-
gilloma)
Incidence
H Aspergillus: found worldwide, commonly in ferment-
Overview
Description
H An opportunistic, sometimes life-threatening infec-
tion, growth, or allergic response caused by fungi of

the genus Aspergillus, usually A. fumigatus, A.
flavus, or A. niger, occurring in:
Aspergilloma: produces a fungus ball in the lungs
(called a mycetoma)
Allergic aspergillosis: a hypersensitive asthmatic
reaction to Aspergillus antigens
Aspergillosis endophthalmitis: an infection of the
anterior and posterior chambers of the eye that
can lead to blindness
Invasive aspergillosis: an acute infection that produces septicemia, thrombosis, and infarction of
virtually any organ, especially the heart, lungs,
brain, and kidneys
H Variable prognosis according to each form (aspergilloma possibly causing fatal hemoptysis)
Pathophysiology
H Conidia (asexual spores) travel into the alveoli via in-
halation or, in aspergillosis endophthalmitis, through

a wound or other tissue injury.
H Pulmonary macrophages may be able to kill the conidia.
H The alternative complement pathway is activated, resulting in recruitment of neutrophils and monocytes.
H The disease may be accompanied by hyphal invasion
of the blood vessels in the involved tissues.
H In aspergilloma, colonization of the bronchial tree
with Aspergillus produces plugs and atelectasis and
forms a tangled ball of hyphae (fungal filaments),
fibrin, and exudate in a cavity left by a previous illness such as tuberculosis (TB).
Causes
H Contact with Aspergillus, commonly found growing
on dry leaves, stored grain, compost piles, or decaying vegetation
Risk factors
H Excessive or prolonged use of antibiotics, glucocorti-
coids, or other immunosuppressants

H Radiation therapy
H Acquired immunodeficiency syndrome
H Hodgkins disease
H Leukemia
H Azotemia
H Alcoholism
H Sarcoidosis
H Bronchitis and bronchiectasis
88
Aspergillosis
ing compost piles and damp hay
Aspergilloma
H May produce no symptoms
H Mimics TB, causing a productive cough and purulent
or blood-tinged sputum, dyspnea, empyema, and
lung abscesses
Allergic aspergillosis
H Wheezing
H Dyspnea
H Cough with some sputum production
H Pleural pain
H Fever
Aspergillosis endophthalmitis
H Usually appears 2 to 3 weeks after an eye injury or
surgery
H Clouded vision
H Eye pain
H Reddened conjunctivae
Invasive aspergillosis
H Thrombosis
H Infarctions
H Sepsis
Complications
H Infection of the ear (otomycosis), cornea (mycotic
keratitis), or prosthetic heart valve (endocarditis)

H Pneumonia (especially in those receiving an im-
munosuppressant such as an antineoplastic drug or

high-dose steroid therapy)
H Sinusitis
H Brain abscesses
H Life-threatening hemoptysis
H Septicemia
Assessment
History
Aspergilloma and allergic aspergillosis
H Immunosuppression
H Dyspnea
H Cough with sputum production
H Eye pain
H Vision changes
H Recent eye injury or surgery
H History based on infected organ
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Physical findings
Aspergilloma and allergic aspergillosis

H Adventitious breath sounds
H Cough with sputum production
H Reddened conjunctivae
H Blurred vision
H Findings based on infected organ
H Perform chest physiotherapy every 2 hours.

H Encourage coughing and deep breathing every hour.
Test results
Laboratory
ASPERGILLOMA
H Serum is positive for anti-Aspergillus antibodies.
ALLERGIC ASPERGILLOSIS
H Sputum culture reveals hyphae that grow Aspergillus
Monitoring
H Vital signs
H Sputum production, amount, color, and character
Patient teaching
Be sure to cover:
H adverse effects of medications.
and eosinophils.
H Serum is positive for immunoglobulin (Ig) E and IgG
anti-Aspergillus antibodies.
ASPERGILLOSIS ENDOPHTHALMITIS
H Eye culture or exudate shows Aspergillus.
INVASIVE ASPERGILLOSIS
H Bronchoscopy and open lung biopsy are performed
to obtain a tissue sample that confirms diagnosis.

Imaging
ASPERGILLOMA
H Chest X-ray shows a round to oval mass with a radi-
olucent crescent over the upper portion of the mass

(Monods sign).
Treatment
General
H Supportive therapy
Medications
Allergic aspergillosis
H Desensitization
H Steroids
H Amphotericin B
H Antifungal therapy
Surgery
Aspergilloma
H Local excision of the lesion
H Lobectomy
Key outcomes
The patient will:
H express understanding of the disorder and treatment.
Aspergillosis
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Asphyxia
Overview
Description
H Altered respiratory rate

H Little or no air movement
H Intercostal rib retractions
H Pale skin
H Cyanosis in mucous membranes, lips, and nail beds
H Erythema and petechiae on the upper chest (trauma)
H Cherry-red mucous membranes (carbon monoxide
poisoning)
H Decreased or absent breath sounds
H A condition of insufficient oxygen and accumulating
Test results
carbon dioxide in the blood and tissues

H Leads to cardiopulmonary arrest; fatal without
prompt treatment
Laboratory
H Decreased partial pressure of arterial oxygen (less
than 60 mm Hg) and increased partial pressure of
arterial carbon dioxide (more than 50 mm Hg) are
indicated by arterial blood gas (ABG) analysis.
H Toxicology tests show drugs, chemicals, or abnormal
hemoglobin level.
Imaging
H Chest X-rays may detect a foreign body, pulmonary
edema, or atelectasis.
H Pulmonary function tests may indicate respiratory
muscle weakness.
H Bronchoscopy can locate foreign body.
Pathophysiology
H An interference with respiration causes insufficient
oxygen intake and hypoxemia.

H Carbon dioxide accumulates due to the lack of gas
exchange in the lungs.

H This leads to inadequate tissue perfusion and cell
death.
Causes
H Opioid abuse
H Respiratory muscle paralysis
H Airway obstruction
H Aspiration
H Pulmonary edema
H Near drowning
H Tumor
H Strangulation
H Trauma to airway
H Carbon monoxide poisoning
H Smoke inhalation
Incidence
H Can occur at any age
Treatment
General
H Establish airway and ventilation
H Treat the underlying cause
H Nothing by mouth until able to protect airway
H Activity based on outcome of interventions
Medications
H Oxygen
H Narcan (if caused by opioid abuse)
Surgery
H Tumor removal
H Altered respirations
H Changes in level of consciousness
H Cardiac arrest
Complications
Key outcomes
H Neurologic damage
H Death
The patient will:

H maintain acceptable cardiac output
H demonstrate knowledge of safety measures to prevent
suffocation.
Assessment
History
H Cause of the asphyxia possibly apparent
H Causes of signs and symptoms varying
Physical findings
H Anxiousness or agitation
H Confusion
H Dyspnea
H Prominent neck muscles
H Wheezing and stridor
90
Asphyxia
H Perform abdominal thrust, if obstruction is present.
H Maintain patent airway.
H Begin cardiopulmonary resuscitation, if necessary.
H Insert a nasogastric tube or an Ewald tube for lavage
(for opioid abuse).

H Reassure the patient and his family.
H Ensure I.V. access.
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Monitoring
H ABG levels, pulse oximetry
H Cardiac status
H Vital signs
H Neurologic status
Patient teaching
Be sure to cover:
H cause of asphyxia (with patient and family members,
discuss measures to prevent recurrence, if appropriate)
H safety measures if the victim is a child.
Discharge planning
H Refer the patient to the proper authorities, if criminal
intent was involved.

H Refer the patient to resource and support services, if
appropriate.
Asphyxia
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Asthma
H Psychological stress
H Cold air
H Exercise
Incidence
H Can occur at any age; about 50% of all patients with
Overview
Description
H A chronic reactive airway disorder involving episod-
ic, reversible airway obstruction resulting from bronchospasms, increased mucus secretions, and mucosal edema
H Signs and symptoms that range from mild wheezing
and dyspnea to life-threatening respiratory failure
H Signs and symptoms of bronchial airway obstruction
that may persist between acute episodes
Pathophysiology
H Tracheal and bronchial linings overreact to various
stimuli, causing episodic smooth-muscle spasms that

severely constrict the airways.
H Mucosal edema and thickened secretions further
block the airways.
H Immunoglobulin (Ig) E antibodies, attached to
histamine-containing mast cells and receptors on cell
membranes, initiate intrinsic asthma attacks.
H When exposed to an antigen such as pollen, the IgE
antibody combines with the antigen. On subsequent
exposure to the antigen, mast cells degranulate and
release mediators.
H The mediators cause the bronchoconstriction and
edema of an asthma attack.
H During an asthma attack, expiratory airflow decreases, trapping gas in the airways causing alveolar hyperinflation.
H Atelectasis may develop in some lung regions.
H The increased airway resistance initiates labored
breathing.
Causes
H Sensitivity to specific external allergens or from in-
ternal, nonallergenic factors

Extrinsic causes
H Pollen
H Animal dander
H House dust or mold
H Kapok or feather pillows
H Food additives containing sulfites and any other sensitizing substance
Intrinsic causes
H Emotional stress
H Genetic factors
Bronchoconstriction
H Hereditary predisposition
H Sensitivity to allergens or irritants such as pollutants
H Viral infections
H Drugs, such as aspirin, beta-adrenergic blockers,
and nonsteroidal anti-inflammatory drugs
H Tartrazine
92
Asthma
asthma are younger than age 10; affects twice as

many boys as girls
H In about one-third of patients, onset between ages 10
and 30
H In about one-third of patients, two or more patients
in same immediate family
H Coexistence of intrinsic and extrinsic causes in many
patients
H Wheezing
H Shortness of breath, feelings of suffocation
H Tightness in chest
H Extrinsic asthma in children; commonly accompa-
nied by other manifestations of atopy
Complications
H Status asthmaticus
H Death
Assessment
History
H Often preceded by severe respiratory tract infections,
especially in adults
H Irritants, emotional stress, fatigue, endocrine
changes, temperature and humidity variations, and

exposure to noxious fumes possibly aggravating intrinsic asthma attacks
H An asthma attack possibly beginning dramatically,
with simultaneous onset of severe, multiple symptoms, or insidiously, with gradually increasing respiratory distress
H Exposure to a particular allergen then followed by a
sudden onset of dyspnea and wheezing and by tightness in the chest also accompanied by a cough that
produces thick, clear, or yellow sputum
Physical findings
H Visibly dyspneic
H Ability to speak only a few words before pausing for
breath
H Use of accessory respiratory muscles
H Diaphoresis
H Increased anteroposterior thoracic diameter
H Hyperresonance
H Tachycardia; tachypnea; mild systolic hypertension
H Inspiratory and expiratory wheezes
H Prolonged expiratory phase of respiration
H Cyanosis, confusion, and lethargy indicating the onset
of life-threatening status asthmaticus and respiratory

failure
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Test results
Laboratory
H Arterial blood gas (ABG) analysis reveals hypoxemia.
H Serum IgE levels are increased due to an allergic reaction.
H Complete blood count with differential shows increased eosinophil count.
Imaging
H Chest X-rays may show hyperinflation with areas of
focal atelectasis.
H Pulmonary function tests (PFTs) may show decreased
peak flows and forced expiratory volume in 1 second, low-normal or decreased vital capacity, and increased total lung and residual capacities.
H Skin testing may identify specific allergens.
H Bronchial challenge testing shows the clinical significance of allergens identified by skin testing.
Other
H Pulse oximetry measurements may show decreased
oxygen saturation.

H report feelings of comfort
H maintain skin integrity.
H Place the patient in high Fowlers position.
H Encourage pursed-lip and diaphragmatic breathing.
H Administer prescribed humidified oxygen.
H Adjust oxygen according to the patients vital signs
and ABG values.

H Assist with intubation and mechanical ventilation, if
appropriate.
H Perform postural drainage and chest percussion, if
tolerated.
H Suction an intubated patient, as needed.
H Treat the patients dehydration with I.V. or oral fluids
as tolerated.
H Anticipate bronchoscopy or bronchial lavage.
H Keep the room temperature comfortable.
H Advise the patient to use an air conditioner or a fan
in hot, humid weather.
Treatment
General
H Identification and avoidance of precipitating factors
H Desensitization to specific antigens
H Establishment and maintenance of patent airway
H Fluid replacement
Medications
H Bronchodilators, such as albuterol, pirbuterol, sal-
Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of theophylline toxicity
H Breath sounds
H ABG results
H PFT results
H Pulse oximetry
H Complications of corticosteroids
H Level of anxiety
meterol, and theophylline

H Corticosteroids
H Histamine antagonists, such as cetirizine and diphen-
hydramine
H Leukotriene antagonists, such as montelukast, zafirlukast, and zileuton
H Anti-inflammatories, such as cromolyn and nedocromil
H Low-flow oxygen
ALERT
The patient with increasingly severe asthma that
doesnt respond to drug therapy is usually admitted
for treatment with corticosteroids, epinephrine,
and sympathomimetic aerosol sprays. He may require endotracheal intubation and mechanical
ventilation.
Patient teaching
Be sure to cover:
H avoidance of known allergens and irritants
H metered-dose inhaler or dry powder inhaler use
H pursed-lip and diaphragmatic breathing
H use of peak flow meter
H effective coughing techniques
H maintaining adequate hydration.
Discharge planning
H Refer the patient to a local asthma support group.
Key outcomes
The patient will:
Asthma
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Atelectasis
Overview
Description
H Incomplete expansion of alveolar clusters or lung
segments leading to partial or complete lung collapse

H May be chronic or acute
H Good prognosis with prompt removal of any airway
obstruction, relief of hypoxia, and re-expansion of

the collapsed lung
Pathophysiology
H Due to incomplete expansion, certain regions of the
lung are removed from gas exchange.

H Unoxygenated blood passes unchanged through these
regions and produces hypoxia.

H Alveolar surfactant causes increased surface tension,
permitting complete alveolar deflation.
Causes
H Bronchial occlusion
H Bronchiectasis
H Cystic fibrosis
H Bed rest in a supine position
H General anesthesia
H Pleural effusion
H Pulmonary embolism
H Sarcoidosis
H Bronchogenic carcinoma
H Inflammatory lung disease
H Idiopathic respiratory distress syndrome of the
neonate
H Oxygen toxicity
H Pulmonary edema
H External compression
Incidence
Assessment
History
H Recent abdominal or other major surgery
H Prolonged immobility
H Mechanical ventilation
H CNS depression
H Smoking
H COPD
H Rib fractures, tight chest dressings
Physical findings
H Decreased chest wall movement
H Cyanosis
H Diaphoresis
H Substernal or intercostal retractions
H Anxiety
H Decreased fremitus
H Mediastinal shift to the affected side
H Dullness or flatness over lung fields
H End-inspiration crackles
H Decreased (or absent) breath sounds
H Tachycardia
Test results
Laboratory
H Arterial blood gas analysis shows hypoxia.
Imaging
H Chest X-rays show characteristic horizontal lines in
the lower lung zones and characteristic dense shadows.
H Bronchoscopy may show an obstructing neoplasm,
foreign body, or pneumonia.
H Pulse oximetry shows decreased oxygen saturation.
Treatment
H Common in patients after upper abdominal or tho-
General
racic surgery
H More common in patients with prolonged immobility,
on mechanical ventilation, or with central nervous
system (CNS) depression
H Increased predisposition in patients who smoke and
those with chronic obstructive pulmonary disease
(COPD)
H Incentive spirometry
H Chest percussion
H Postural drainage
H Frequent coughing and deep-breathing exercises
H Bronchoscopy if above measures fail
H Humidity
H Intermittent positive-pressure breathing therapy
H Radiation possibly required for obstructing neoplasm
H Diet based on patients condition as tolerated
H Increased fluids
H Activity as tolerated; discourage bed rest
H Chest pain
H Anxiety
Complications
H Hypoxemia
H Acute respiratory failure
H Pneumonia
Medications
H Bronchodilators, such as albuterol, pirbuterol, and
salmeterol
H Analgesics after surgery
Surgery
H May be required if obstructing neoplasm present
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Atelectasis
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Key outcomes
The patient will:
H report feelings of increased comfort
H use support systems to assist with anxiety and fear.
H Give prescribed drugs and provide oxygen therapy.
H Encourage coughing and deep breathing.
H Encourage and assist with ambulation as soon as
possible.
H Help the patient use an incentive spirometer.
H Humidify inspired air.
H Loosen secretions with postural drainage and chest
percussion.
H Provide suctioning, as needed.
H Offer the patient reassurance and emotional support.
Monitoring
H Vital signs
H Intake and output
H Pulse oximetry
H Respiratory status (breath sounds, arterial blood gas
results)
Patient teaching
Be sure to cover:
H use of incentive spirometer
H postural drainage and percussion
H coughing and deep-breathing exercises
H importance of splinting incisions
H energy-conservation techniques
H stress-reduction strategies
H importance of mobilization.
Discharge planning
indicated.
indicated.
Atelectasis
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Atopic dermatitis
Overview
Description
H A chronic skin disorder characterized by superficial
skin inflammation and intense itching
Pathophysiology
H The allergic mechanism of hypersensitivity results in
a release of inflammatory mediators through sensitized antibodies of the immunoglobulin (Ig) E class.
H Histamine and other cytokines induce acute inflammation.
H Abnormally dry skin and a decreased threshold for
itching set up the itch-scratch-itch cycle, which
eventually causes lesions (excoriations, lichenification).
Causes
Incidence
H May appear at any age but typically begins during in-
fancy or early childhood (may then subside spontaneously, followed by exacerbations in late childhood,
adolescence, or early adulthood)
H Affects less than 1% of the population
H Erythematous, weeping lesions, usually located in ar-
eas of flexion and extension, such as the neck, antecubital fossa, popliteal folds, and behind the ears
In children with atopic dermatitis
H Pink pigmentation and swelling of the upper eyelid
and a double fold under the lower lid (Morgans line
or Dennies sign)
Complications
H Scarring
H Severe viral infections
H Bacterial and fungal skin infections
H Ocular disorders
H Allergic contact dermatitis
H The exact etiology of atopic dermatitis unknown;
however, genetic predisposition likely

H Possible contributing factors:
Food allergy
Infection
Chemical irritants
Extremes of temperature and humidity
Psychological stress or strong emotions
Special populations
About 10% of juvenile cases of atopic dermatitis
are caused by allergic reactions to certain foods,
especially eggs, peanuts, milk, and wheat.
Assessment
History
H Atopy, such as asthma, hay fever, or urticaria (or
similar family history)(see Factors contributing to

atopy)
H Exposure to allergen
H Pruritus
Physical findings
H Erythematous, weeping lesions (see Signs of atopic
dermatitis)
H Pink pigmentation and swelling of the upper eyelid
and a double fold under the lower lid
Factors contributing to atopy

H Changes associated with industrialization, such as
exposure to new chemicals like diesel fumes, have
proven to increase the antigenicity of common pollens.
H Increased exposure to antigens, such as dust mites (in
wall-to-wall carpets), especially at an early age,
contributes to a predisposition to developing allergies.
H Dietary changes, such as increased fat intake and an
earlier weaning from human breast milk, may be
contributing factors.
H Vaccination may cause a shift in T-cell function away
from the normal helper T cell (Th1) response to the
Th2 allergic response by limiting early bacterial and
viral infections.
H Lack of exposure to intestinal parasites may contribute
to a similar shift in T-cell functioning.
H Frequent use of antibiotics, especially in early
childhood, may decrease normal intestinal flora and
further contribute to the shift.
Test results
Laboratory
H Complete blood count shows eosinophilia.
H Serum IgE levels are elevated.
Other
H Skin testing shows specific allergen.
Treatment
General
H Meticulous skin care
H Environmental control of offending allergens
H Nonirritating topical lubricants
Medications
H Corticosteroids
H Antipruritics such as hydroxyzine
H Antihistamines, such as diphenhydramine and fexofe-
nadine
H Antibiotics if secondary infection develops
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Atopic dermatitis
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Key outcomes
The patient will:
H express relief from itching and pain
H demonstrate improved skin condition
H remain free from infection.
H Offer support to help the patient and his family cope
with this chronic disorder.

H Dissuade the patient from scratching during urticaria
Signs of atopic dermatitis

This illustration shows the typical lesions involved in
atopic dermatitis.
Edema, crusting,
and scaling
Erythematous
areas on dry
skin
to help prevent infection.

H Apply prescribed topical medications.
Monitoring
H Compliance with drug therapy
H Treatment of lesions
Patient teaching
Be sure to cover:
H when and how to apply topical corticosteroids
H importance of regular personal hygiene using only
water with little soap
H signs and symptoms of secondary infection
H avoidance of laundry additives, such as fragrances
and dyes
H avoidance of allergens.
Atopic dermatitis
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Complications
Atrial fibrillation
H Transient ischemic attack

H Stroke
H Heart failure
H Thromboembolism
Overview
Description
H Rhythm disturbance of the atria
H Characterized by an irregularly irregular cardiac rate
and rhythm (see Recognizing atrial fibrillation)
Pathophysiology
H Rapid discharges from numerous ectopic foci in the
atria occur.
H This leads to erratic and uncoordinated atrial
rhythm.
Assessment
History
H Palpitations
H Fatigue
H Dyspnea
H Chest pain
H Syncope
Physical findings
Causes
H Hypertension
H Heart failure
H Cardiomyopathy
H Hypersympathetic state associated with acute alcohol
ingestion
H Pericarditis
H Hyperthyroidism
H Valvular disease
H Cardiothoracic surgery
H Atrial fibrosis
Incidence
H Seen more commonly in patients older than age 70
H Males affected more than females
H Cardiac rhythm: irregularly irregular
H Irregular pulse
H Possible tachycardia
H Hypotension
H Signs of heart failure
Test results
Laboratory
H Cardiac enzymes show myocardial damage (with MI).
H Thyroid function studies reveal hyperthyroidism.
H Complete blood count checks for anemia, if the patient has a history of recent blood loss.
Imaging
H Chest X-ray may determine if pulmonary edema is
present.
H Echocardiogram or transesophageal echocardiography may help identify valvular disease, left ventricular
dysfunction, or atrial clots.
H Electrocardiography may indicate irregular rhythm.
H Holter monitor may diagnose paroxysmal atrial fibrillation.
Recognizing atrial fibrillation

The following rhythm strip shows atrial fibrillation.
H Rhythm: Irregular
H Rate: Atrial indiscernible;
ventricular 130 beats/minute
98
Atrial fibrillation
H P wave: Absent; replaced by fine

fibrillatory waves
H PR interval: Indiscernible
H QRS complex: 0.08 second
H T wave: Indiscernible
H QT interval: Unmeasurable
H Other: None
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Treatment
General
Discharge planning
H Refer the patient to programs such as Coumadin
Clinic to monitor anticoagulant therapy.
H Possible electrical cardioversion

H Atrial fibrillation suppression pacemaker
H Ablation
H Surgical maze procedure
H Low-fat, low-sodium diet
H Fluid restriction, if indicated
H Planned rest periods, as needed
Medications
H Calcium channel blockers, such as cardizem and am-
lodipine
H Beta-adrenergic blockers, such as metoprolol and
atenolol
H Antiarrhythmics, such as amiodarone, propafenone,
and sotalol
Key outcomes
The patient will:
H report ways to reduce activity intolerance
H identify effective coping mechanisms to manage
anxiety
H discuss the causes of fatigue
H verbalize understanding of medication regimen.
H Encourage the patient and his family to talk about
feelings and concerns.

H Plan rest periods.
Monitoring
H Vital signs at rest and after physical activity
H Signs and symptoms of embolism
H Intake and output
H Daily weight
H Abnormal bleeding
Ratio
Patient teaching
Be sure to cover:
H instructions on how to monitor pulse
H anticoagulation precautions
H abnormal bleeding
H signs and symptoms of embolic events.
Atrial fibrillation
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Atrial septal defect

Overview
Description
H An acyanotic congenital heart defect featuring an
opening between the left and right atria that allows

blood to flow from left to right, resulting in ineffective pumping of the heart, thus increasing the risk of
heart failure
H Three types:
Ostium secundum defect, the most common type:
occurs in the region of the fossa ovalis and, occasionally, extends inferiorly, close to the vena cava
Sinus venosus defect: occurs in the superiorposterior portion of the atrial septum, sometimes
extending into the vena cava, and almost always
associated with abnormal drainage of pulmonary
veins into the right atrium
Ostium primum defect: occurs in the inferior portion of the septum primum and usually associated
with atrioventricular valve abnormalities (cleft mitral valve) and conduction defects
Pathophysiology
H Blood shunts from the left atrium to the right atrium
because the left atrial pressure is normally slightly

higher than the right atrial pressure.
H This pressure difference forces large amounts of
blood through a defect.
H This shunt results in right heart volume overload,
affecting the right atrium, right ventricle, and pulmonary arteries.
H Eventually, the right atrium enlarges, and the right
ventricle dilates to accommodate the increased blood
volume.
H If pulmonary artery hypertension develops, increased
pulmonary vascular resistance and right ventricular
hypertrophy follow.
H Irreversible pulmonary artery hypertension causes
reversal of the shunt direction in some adults, which
results in unoxygenated blood entering the systemic
circulation, causing cyanosis.
Causes
H No known cause
H Ostium primum defects commonly occurring in
patients with Down syndrome
H Fatigue after exertion
H Early to midsystolic murmur at the second or third
left intercostal space

H Low-pitched diastolic murmur at the left lower ster-
nal border; more pronounced on inspiration

H Fixed, widely split S2
H Systolic click or late systolic murmur at the apex
H Clubbing and cyanosis, if a right-to-left shunt
develops
ALERT
An infant may be cyanotic because he has a cardiac or pulmonary disorder. Cyanosis that worsens
with crying most likely has a cardiac cause because
crying increases pulmonary resistance to blood
flow, resulting in an increased right-to-left shunt.
Cyanosis that improves with crying most likely has
a pulmonary cause because deep breathing improves tidal volume.
Complications
H Physical underdevelopment
H Respiratory infections
H Heart failure
H Atrial arrhythmias
H Mitral valve prolapse
Assessment
History
H Increasing fatigue
H Chest pain
H Dyspnea
H Coughing
H Dizziness or syncope
Physical findings
H Early to midsystolic murmur at the second or third
left intercostal space

H Low-pitched diastolic murmur at the left lower ster-
nal border, more pronounced on inspiration

H Fixed, widely split S2
H Systolic click or late systolic murmur at the apex
H Peripheral edema
H Cyanosis
H Distended jugular veins
Incidence
Test results
H Accounts for about 10% of congenital heart defects

H Appears almost twice as often in females than in
Imaging
H Chest X-ray shows an enlarged right atrium and right
ventricle, a prominent pulmonary artery, and increased pulmonary vascular markings.
H Electrocardiography results may be normal, but
commonly show right axis deviation, a prolonged
PR interval, varying degrees of right bundle-branch
males, with a strong familial tendency

H Usually benign defect during infancy and childhood
(Delayed development of symptoms and complications makes it one of the most common congenital
heart defects diagnosed in adults.)
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block, right ventricular hypertrophy, atrial fibrillation

(particularly in severe cases in patients older than
age 30) and, in ostium primum defect, left axis deviation.
H Echocardiography measures right ventricular enlargement, may locate the defect, and shows volume
overload in the right side of the heart. It may reveal
right ventricular and pulmonary artery dilation.
H Two-dimensional echocardiography with color
Doppler flow, contrast echocardiography, or both has
supplanted cardiac catheterization as the confirming
test for atrial septal defects (ASDs). Cardiac catheterization is used if inconsistencies exist in the clinical
data or if significant pulmonary hypertension is suspected.
Patient teaching
Be sure to cover:
H pretest and posttest procedures to the child and his
parents (If possible, use drawings or other visual
aids to explain it to the child.)
H postoperative procedures, tubes, dressings, and
monitoring equipment
H antibiotic prophylaxis to prevent infective endocarditis.
Treatment
General
H Low-fat, low-cholesterol diet
Medications
H Analgesics
Surgery
H Minimally invasive heart surgery may be required for
the patient with an uncomplicated ASD with evidence

of significant left-to-right shunting.
H A large defect may need immediate surgical closure
with sutures or a patch graft.
H Cardiac catheterization closure the insertion of an
umbrella-like patch or septal occluder through a
cardiac catheter may be performed.
Key outcomes
The patient will:
H maintain an optimal cardiac output
H experience no cardiac arrhythmias.
H Encourage the child to engage in any activity he can
tolerate.
Monitoring
H Vital signs
H Central venous and intra-arterial pressures
H Intake and output
H Cardiac rhythm
H Oxygenation
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Attention deficit
hyperactivity disorder
Overview
Description
H A behavioral problem characterized by difficulty with
inattention, impulsivity, hyperactivity, and boredom

H Also called ADHD and ADD
Pathophysiology
H Alleles of dopamine genes may alter dopamine, sero-
tonin, and adrenalin transmission in the neural networks.

H During fetal development, bouts of hypoxia and hypotension could selectively damage neurons located
in some of the critical regions of the anatomical networks.
Causes
H Underlying cause unknown
H Limited evidence of a genetic component
H May result from altered neurotransmitter levels in the
brain
Risk factors
H Family history
H History of learning disability
H Mood or conduct disorder
Incidence
H Present at birth, but diagnosis before age 4 or 5 is
difficult; some patients undiagnosed until adulthood

H Occurs in 3% to 5% of school-age children
H Affects males three times more than females
H Impulsive behavior
H Inattentiveness
H Disorganization in school
H Tendency to jump quickly from one partly completed
project, thought, or task to another

H Difficulty meeting deadlines and keeping track of
school or work tools and materials
Complications
H Emotional and social complications
H Poor nutrition
Assessment
History
H Characterized as a fidgeter and a daydreamer
H Appears inattentive and lazy
H Performs sporadically at school or work
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Attention deficit hyperactivity disorder
Physical findings
Symptoms of inattention
H Makes careless mistakes
H Struggles to sustain attention
H Fails to finish activities
H Difficulty with organization
H Avoids tasks that require sustained mental effort
H Distracted or forgetful
Symptoms of hyperactivity
H Fidgets
H Cant sit still for sustained period
H Difficulty playing quietly
H Talks excessively
Symptoms of impulsivity
H Interrupts
H Cant wait patiently
DSM-IV-TR criteria
These criteria confirm a diagnosis:
H six symptoms or more from the inattention or hyperactivity-impulsivity categories
H symptoms present for at least 6 months
H symptoms evident before age 7
H impairment present in two or more settings
H symptoms arent accounted for by another mental
disorder.
Test results
H Complete psychological, medical, and neurologic
evaluations rule out other problems; specific tests include continuous performance test, behavior rating
scales, and learning disability.
Treatment
General
H Education regarding the nature and effect of the dis-
order
H Behavior modification
H External structure
H Supportive psychotherapy
H Elimination of sugar, dyes, and additives from diet
H Monitor activity (for safety purposes)
Medications
H Stimulants, such as methylphenidate, dextroampheta-
mine, and pemoline

H Tricyclic antidepressants, such as desipramine and
imipramine
H Mood stabilizers such as bupropion
H Beta-adrenergic blockers such as propranolol
H Selective norepinephrine reuptake inhibitors such as
atomoxetine
H Alpha2-agonists such as clonidine
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Key outcomes
H demonstrate effective social interaction skills in oneon-one and group settings
H report improvement in family and social interactions
H demonstrate effective coping behavior.
H Set realistic expectations and limits to avoid frustrat-
ing the patient.

H Maintain a calm and consistent manner.
H Keep all instructions short and simple make one-
step requests.
H Provide praise, rewards, and positive feedback when-
ever possible.
H Provide diversional activities suited to a short atten-
tion span.
Monitoring
H Activity level
H Adverse drug reactions
H Complications
H Activity (for safety purposes)
Patient teaching
Be sure to cover:
H behavior therapy
H reinforcement of good behavior
H realistic expectations
H nutrition.
Discharge planning
H Refer the patient to family therapy.
Attention deficit hyperactivity disorder
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Autistic disorder
Overview
Description
H A severe, pervasive developmental disorder
H Degree of impairment varies
H Usually apparent before age 3
H Poor prognosis
H Sometimes called Kanners autism
Pathophysiology
H Defects in the central nervous system (CNS) may
arise from prenatal complications.
Causes
H Defects in CNS from prenatal complications such as
rubella
H Nutritional deficiency
H Disease caused or triggered by immunizations
Risk factors
H High-risk pregnancy
Incidence
H Affects an estimated 1 in 1,000 children
H Three to four times more likely in males than in
females, usually the firstborn male
H Unresponsive to social contact
H Gross deficit in intelligence and language develop-
H Pronoun reversal
H Bizarre or self-destructive behavior
H Extreme compulsion for sameness
H Abnormal reaction to sensory stimuli
H Cognitive impairment
H Eating, drinking, and sleeping problems
H Mood disorders
DSM-IV-TR criteria
At least 6 of these 12 characteristics must be present,
including at least 2 items from the first section, 1 from
the second, and 1 from the third.
H Qualitative impairment in social interaction:
Impaired nonverbal behavior
Absence of peer relationships
Failure to seek or share enjoyment, interests, or
achievements
Lack of social or emotional reciprocity
H Qualitative impairment in communication:
Delay or lack of language development
Inability to initiate or sustain conversation
Idiosyncratic or repetitive language
Lack of appropriate imaginative play
H Restricted repetitive and stereotyped patterns of behavior, interests, and activities:
Abnormal preoccupation with a restricted pattern
of interest
Inflexible routines or rituals
Repetitive motor mannerisms
Preoccupation with parts of objects
H The diagnostic criteria also include delays or abnormal functioning in at least one of these areas before
age 3:
Social interaction and language skills
Symbolic or imaginative play
ment
H Ritualistic and compulsive behavior
H Restricted capacity for developmentally appropriate
activities and interests

H Bizarre response to the environment
Complications
H Epileptic seizures
H Depression
During stress
H Catatonic phenomena
H Undifferentiated psychotic state
Treatment
General
H Structured treatment plan
H Behavioral techniques
H Pleasurable sensory and motor stimulation
H Monitor activities (for safety purposes)
Medications
H Serotonin receptor reuptake inhibitors, such as flu-
voxamine and sertratine
Assessment
History
H Becomes rigid or flaccid when held
H Cries when touched
H Shows little or no interest in human contact
Physical findings
H Delayed smiling response
H Severe language impairment
H Lack of socialization and imaginative play
H Echolalia
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Autistic disorder
H Antidepressants, such as doxepin, imipramine, and
clomipramine
H Antipsychotics, such as haloperidol, thioridazine, and
risperidone
H Stimulants, such as dextroamphetamine and
methylphenidate
H Alpha2-agonists such as clonidine
H Bet-adrenergic blockers such as propranolol
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Key outcomes
H identify and contact available resources, as needed
H openly share feelings about the present situation
H as much as possible, demonstrate age-appropriate
skills and behaviors
H practice safety measures and take safety precautions
in the home
H interact with family or friends.
H Institute safety measures when appropriate.
H Provide positive reinforcement.
H Encourage development of self-esteem.
H Encourage self-care.
H Prepare the child for change by telling him about it.
H Help family members develop strong one-on-one
relationships with the patient.
Monitoring
H Complications
H Patterns of behavior
H Social interaction
H Communication skills
H Activity
Patient teaching
Be sure to cover:
H physical care for the childs needs
H importance of identifying signs of excessive stress
and coping skills.
Discharge planning
H Refer the parents to resource and support services.
Autistic disorder
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Avian influenza
Overview
Description
H Extremely virulent virus occurring naturally in birds
H Rapidly mutating and has been transmitted from
birds to mammals, including humans

H Risk of pandemic as the virus evolves and more hu-
man cases occur each year

H International concern because virus spreads by mi-
gratory birds
Pathophysiology
H The virus invades the epithelium of the respiratory
tract, causing inflammation.
H Eye infections
H Cytokine storm
Hypotension
Tachycardia
Dyspnea
Fever
Uncontrollable hemmorrhage
Signs of multisystem organ failure from ischemia
or insufficient tissue perfusion
Test results
Laboratory
H Oropharyngeal, nasal, nasopharyngeal, or lower respiratory tract specimen culture shows causative organism.
H Serology for influenza H5N1-specific antibody shows
causative organism.
H The immune system releases inflammatory mediators
(cytokines, oxygen free radicals and coagulation factors).

H Cytokine storm, an inappropriate and exaggerated
immune response, is caused by rapidly proliferating
and active T-cells.
H If the immune response isnt limited, the lungs are
permanently damaged.
H Patients develop acute respiratory distress syndrome,
sepsis, and multisystem organ failure.
Treatment
Causes
captopril, enalapril and lisinopril and angiotensin II

receptor blockers, such as candesartan, valsartan
and irbesartan to treat cytokine storm
H Corticosteroids
H Vaccine produced and approved for distribution by
public-health officials if needed (Further vaccine research is underway.)
H Influenza A, H5N1 virus strain
Incidence
H Few hundred cases per year world-wide
H No recent cases in the United States
H Affects all age-groups and both sexes
H Primarily in those with exposure to infected poultry
H Greater than 50% mortality
H Influenza-like symptoms
Complications
H Acute respiratory distress
H Viral pneumonia
H Multisystem organ failure
Assessment
History
H Close contact with infected poultry or contaminated
surfaces
H Rarely, close contact with infected human
Physical findings
H Influenza-like symptoms
106
Fever
Cough
Sore throat
Muscle aches
Avian influenza
General
H Supportive measures
Medications
H Antibiotics as appropriate
H Anti-viral medications (effectiveness under study)
H Angiotensin-converting enzyme inhibitors, such as
Key outcomes
The patient will:
H develop no complications
regimen
H Observe standard and respiratory precautions to pre-
vent transmission of the disease.

H Provide supportive care and emotional support.
Monitoring
H Vital signs
H Complications
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Patient teaching
Be sure to cover:
H measures to prevent the spread of disease
H medication administration, dosage, and possible adverse effects
H importance of continuing the prescribed antibiotic
until the entire prescription is finished
H disposal of secretions and the use of proper handwashing technique
H fact that seasonal influenza vaccine doesnt protect
against avian flu
Discharge planning
H Refer the patient to an infectious disease specialist, if
necessary.
Avian influenza
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Basal cell carcinoma

Overview
Description
H Nonmelanoma skin cancer

H Slow-growing, destructive cancerous skin tumor
H Two major types: noduloulcerative and superficial
H Most common malignant tumor that affects whites
(see Identifying basal cell carcinoma)
Pathophysiology
H Although the pathogenesis is uncertain, some experts
hypothesize that it originates when undifferentiated

basal cells become carcinomatous instead of differentiating into sweat glands, sebum, and hair.
Causes
H Prolonged sun exposure (90% of tumors occur on
sun-exposed areas of the body)
Risk factors
H Arsenic ingestion
H Radiation exposure
H Burns
H Immunosuppression
H Vaccinations (rare)
H History of previous nonmelanoma skin cancer
Incidence
H Usually occurs in people older than age 40
H Most prevalent in blond, fair-skinned males
H Lesion found on face, head, neck, and back
H Five warning signs
An open sore
Identifying basal cell carcinoma

This illustration shows an enlarged nasal nodule in basal
cell carcinoma. Note its depressed center and firm, elevated border.
A reddish patch
A shiny bump
A pink growth
A scarlike area
Complications
H Disfiguring lesions of the eyes, nose, and cheeks
Assessment
History
H Odd-looking skin lesion
H Prolonged exposure to the sun
H Nonhealing sore of varying duration
Physical findings
H Lesions characterized as small, smooth, pinkish, and
translucent papules (early-stage noduloulcerative)

H Telangiectatic vessels across surface and lesions may
be pigmented
H Lesions enlarge with depressed centers and firm and
elevated borders (also called rodent ulcers)

H Multiple oval or irregularly shaped, lightly pigmented
plaques on chest or back

H Head and neck possibly showing waxy, sclerotic, yel-
low to white plaques without distinct borders
Test results
H Incisional or excisional biopsy and histologic study
may help determine the tumor type and histologic
subtype.
Other
H All types of basal cell carcinomas are diagnosed by
clinical appearance.
Treatment
General
H Depends on the size, location, and depth of the le-
sion
H Irradiation, if the tumor location requires it; pre-
ferred for elderly or debilitated patients who might

not tolerate surgery
H Cryotherapy (liquid nitrogen that freezes the cells
and kills them)
H Well-balanced diet; no restrictions
H Avoidance of sun exposure
Medications
H Chemotherapy such as topical fluorouracil
H Immune response modifier such as topical
imiquimod
Surgery
H Curettage and electrodesiccation
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H Microscopically controlled surgical excision, known
as Mohs surgery, that carefully removes recurrent

lesions until a tumor-free plane is achieved (after
removal of large lesions, skin grafting may be required)
H Simple excision
H Chemosurgery
Key outcomes
The patient will:
H exhibit healing lesions or wounds
H demonstrate effective coping mechanisms.
H Encourage verbalization and provide support.
H Provide appropriate wound care.
Monitoring
H Complications of treatment
H Wound healing
H Skin surveillance for additional lesions
Patient teaching
Be sure to cover:
H importance of avoiding excessive sun exposure,
wearing protective clothing, and using a strong sunscreen or sunshade to protect the skin.
Discharge planning
H Refer the patient to resource and support services, as
needed.
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Bells palsy
Overview
H Local traumatic injury

H Autoimmune disease
H Lyme disease
H Tumor
H Bacterial infections such as meningitis
Description
Incidence
H Condition in which the impulses from the seventh
H Affects all age-groups

H Most common between ages 20 and 60
H Affects males and females equally
cranial nerve are blocked, causing muscle weakness

or paralysis
H Rapid onset
H Subsides spontaneously in 80% to 90% of patients
H Complete recovery in 1 to 8 weeks
H Delayed recovery in elderly people
H Partial recovery: contractures may develop on the
paralyzed side of the face
H May recur on same or opposite side of the face
Pathophysiology
H Unilateral facial weakness
H Aching at jaw angle
H Drooping mouth
H Distorted and loss of taste
H Impaired ability to fully close eye on affected side
H Tinnitus
H An inflammatory reaction occurs around the seventh
Complications
cranial nerve (motor innervation of the facial muscles).

H Inflammation is usually at the internal auditory
meatus.
H Unilateral facial weakness or paralysis results.
H Corneal ulceration and blindness

H Impaired nutrition secondary to paralysis of the low-
Causes
Assessment
H Unknown
H Ischemia
H Viral disease, such as herpes simplex or herpes
History
zoster
Facial paralysis in Bells palsy

Unilateral facial paralysis characterizes Bells palsy. The
paralysis produces a distorted appearance and an inability
to wrinkle the forehead, close the eyelid, smile, show the
teeth, or puff out the cheek on the affected side.
er face
H Long-term psychosocial problems
H Pain on the affected side around the angle of the jaw
or behind the ear for a few hours or days before onset of weakness
H Difficulty chewing on the affected side
H Difficulty speaking clearly
Physical findings
H Mouth droops on the affected side (see Facial paral-
ysis in Bells palsy)

H Smooth forehead
H Distorted taste perception
H Inability to raise eyebrow, smile, show teeth, or puff
out cheek
H Impaired ability to close eye on the weak side
H Eye rolls upward (Bells phenomenon) when at-
tempting to close the eye

H Excessive tearing
Test results
H Diagnosis is based on clinical presentation.
Imaging
H Magnetic resonance imaging rules out tumor.
Treatment
General
H Eliminating the source of damage to the nerve immeSMILING
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Bells palsy
diately
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H Oral hygiene maintenance

H Eye protection such as sunglasses
H Hearing protection
H Moist heat
H Diet, as tolerated
H Activity, as tolerated
Medications
H Oral corticosteroids, such as prednisone and
hydrocortisone
H Analgesic such as ibuprofen
H Antiviral such as acyclovir
Surgery
H Exploration of the facial nerve (possibly)
H Facial reanimation, such as direct facial nerve repair
or facial nerve grafting
Key outcomes
The patient will:
H experience increased comfort and relief from pain
H consume an adequate amount of calories daily
H express understanding of the condition and treatment regimen
H exhibit improvement in facial muscle movement.
H Provide psychological support.
H Apply moist heat to the affected side of the face.
H Massage the patients face with a gentle upward
motion.
H Provide a facial sling.
H If the patient had surgery, provide preoperative and
postoperative care.
H Administer medication, as ordered.
Monitoring
H Neurologic function
H Signs and symptoms of peptic ulceration, pancreati-
tis, or other GI adverse effects of prednisone and

hydrocortisone
H Facial muscle movement
Patient teaching
Be sure to cover:
H the disorder
H medication and adverse effects
H protection of affected eye
H exercises of the facial muscles
H nutritional management program.
Bells palsy
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Benign prostatic
hyperplasia
Overview
Description
H Enlargement of prostate gland enough to compress
urethra, causing overt urinary obstruction
H Urinary hesitancy and frequency

H Difficulty initiating urination
H Nocturia, hematuria
H Dribbling, incontinence
H Urine retention
Physical findings
H Visible midline mass above the symphysis pubis from
distended bladder
H Enlarged prostate on digital rectal examination
H May be treated surgically or symptomatically, de-
Test results
pending on the size of prostate, age and health of

patient, and extent of obstruction
H Referred to as BPH
Laboratory
H Elevated blood urea nitrogen and serum creatinine
levels suggest impaired renal function.
H Bacterial count that exceeds 100,000/mm3 reveals
hematuria, pyuria, and UTI.
Imaging
H Excretory urography may indicate urinary tract obstruction, hydronephrosis, calculi or tumors, and
bladder filling and emptying defects.
H Cystourethroscopy determines the best surgical intervention and shows prostate enlargement, bladder
wall changes, calculi, and raised bladder.
Other
H International Prostate Symptom Score classifies
disorders severity.
Pathophysiology
H Changes occur in periurethral glandular tissue.
H Prostate enlarges and may extend into the bladder.
H Compression or distortion of prostatic urethra
obstructs urine outflow.

H BPH may cause diverticulum through the muscula-
ture leading to urinary retention.
Causes
H Unknown
H Possible link with hormonal activity
Risk factors
H Age
H Intact testes
Treatment
Incidence
General
Special populations
BPH occurs in 80% of all males older than age 40,
and in 95% of all males older than age 80.
H Changes in voiding patterns and urine stream
Complications
H Urinary stasis, urinary tract infection (UTI), or renal
calculi
H Bladder wall trabeculation
H Detrusor muscle hypertrophy
H Bladder diverticula and saccules
H Urethral stenosis
H Hydronephrosis
H Paradoxical (overflow) incontinence
H Acute or chronic renal failure
H Acute postobstructive diuresis
Assessment
History
H Decreased urine stream caliber and force
H Interrupted urinary stream
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Benign prostatic hyperplasia
H Prostatic massage
H Short-term fluid restriction (prevents bladder disten-
tion)
H Avoidance of lifting, performing strenuous exercises,
and taking long automobile rides for at least 1 month

after surgery
H No sexual intercourse for several weeks after surgery
Medications
H Antibiotics, such as cefepime and levofloxacin, if
infection present
H Alpha-1-adrenergic blockers, such as doxazosin and
terazosin
H 5-Alpha-reductase inhibitors such as dutasteride and
finasteride
Surgery
H For relief of acute urine retention, hydronephrosis,
severe hematuria, and recurrent UTI or for palliative

relief of intolerable symptoms
H Suprapubic (transvesical) prostatectomy
H Perineal prostatectomy
H Retropubic (extravesical) prostatectomy
H Transurethral resection of the prostate
H Balloon dilatation, ultrasound needle ablation, and
use of stents
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Key outcomes
The patient will:
H express understanding of disorder and treatment
H demonstrate skill in managing urinary elimination
H express feelings about potential or actual changes in
sexual activity.
H Avoid giving sedatives, alcohol, antidepressants, or
anticholinergics (which can worsen the obstruction).

H Provide I.V. therapy, as ordered.
H Administer continuous bladder irrigation, as pre-
scribed.
H Keep the head of the bed elevated at least 30 degrees
to prevent pneumonia.
H Encourage coughing, deep breathing, and incentive
spirometer use.
Monitoring
H Vital signs
H Intake and output
H Daily weight
ALERT
Watch for signs of postobstructive diuresis, characterized by polyuria exceeding 2 L in 8 hours and
excessive electrolyte losses. Although usually selflimiting, it can result in vascular collapse and
death if not promptly treated.
After prostatic surgery

H Pain control
H Catheter function and drainage
H Continuous bladder irrigation function
Patient teaching
Be sure to cover:
H signs of UTI that should be reported
H when to seek medical care (fever, unable to void, or
passing bloody urine).
Benign prostatic hyperplasia
113
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Bipolar disorder
Overview
Description
H An affective disorder marked by severe pathologic
mood swings from hyperactivity and euphoria to

sadness and depression
H In cyclothymia, a variant of bipolar disorder: numerous episodes of hypomania and depressive symptoms
too mild to meet the criteria for major depression or
bipolar disorder (see Cyclothymic disorder)
H Manic episodes that emerge over a period of days to
weeks, but onset possible within hours
H Untreated episodes that can last weeks or as long as
8 to 12 months, with some having an unremitting
course
H Found in 15% of patients, mostly female, rapid cycling, in which four or more episodes of either depression or mania occur in 1 year
H Difficulties in work performance and psychosocial
functioning in about half of all patients with this disorder
Pathophysiology
H Bipolar disorder may be an effect of neurotransmit-
ter imbalance.
H Mood swings may involve membrane changes in
sodium- and potassium-activated adenosine triphosphatase involving disordered intracellular signals.
Manic phase
H Accelerated speech
H Frequent changes of topic
H Flight of ideas
Depressive phase
H Loss of self-esteem
H Overwhelming inertia
H Social withdrawal
H Feelings of hopelessness
H Apathy or self-reproach
H Suicidal thoughts
Bipolar II disorder
H Meets all the diagnostic criteria for a manic episode
H May experience recurrent depressions, separated by
periods of mild activation and increased energy
Complications
H Emotional and social consequences
H Sexually transmitted disease
H Exhaustion
H Nutritional deficits
H Sleep disturbances
H Suicide
Assessment
History
H Sleeping and eating disturbances
H Exhibits expansive, grandiose, sometimes irritable
mood alternating with symptoms of depression
Causes
Physical findings
H Exact cause unclear

H Autosomal dominant inheritance found in genetic
Mania
H Increased psychomotor activity
H Excessive social extroversion
H Impulsive actions
H Impaired judgment
H Delusions
H Paranoid thinking
H Limited attention span
H Inflated sense of self-esteem
H Rapid responses to external stimuli
Depression
H Slow speech and response
H No obvious disorientation or intellectual impairment
H Psychomotor retardation
H Lethargy
H Low muscle tone
H Weight loss
H Slowed gait
studies
H Some evidence that links to an X chromosome
disorder
H May be triggered by death, separation, or divorce
H Imbalances in the biochemistry that controls food
(biochemical) imbalances
Risk factors
H Family history
H Substance abuse
Incidence
H Affects over 5 million people in the United States
H Equally common in females and males
H Females: likely to have more depressive episodes
H Males: likely to have more manic episodes
H Higher among relatives of affected patients than in
the general population
Special populations
Age of onset is usually between ages 20 and 35, but
35% of patients experience onset between ages 35
and 60.
114
Bipolar disorder
DSM-IV-TR criteria
Diagnosis is confirmed when the patient meets the criteria established for a manic or hypomanic episode:
H experiences a distinct period of abnormally and persistently elevated, expansive, or irritable mood
H during the mood disturbance, at least three of these
symptoms must persist (four, if the mood is only irritable) and be present to a significant degree:
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inflated self-esteem or grandiosity

decreased need for sleep
excessive talking
flight of ideas
easily distracted
psychomotor agitation
excessive involvement in dangerous activities
symptoms dont meet criteria for a mixed episode
impairment in occupational function, usual social
activities, or relations with others severe enough
to require hospitalization to prevent harm to self
or others
substance use or other causative medical conditions not present.
Treatment
General
H Group and individual therapy
H Monitoring of activity when in manic phase
Medications
H Anticonvulsants, such as carbamazepine and valproic
acid
H Antimanic such as lithium
H Antipsychotics, such as aripiprazole, olanzapine,
quetiapine, risperidone, and ziprasidone

H Antidepressant such as fluoxetine
Key outcomes
The patient will:
H identify effective coping techniques
H recognize symptoms and comply with medication
regimen
H express feelings related to self-esteem
processes.
For the manic patient
H Encourage activities that require gross motor movements.
H Assist with personal hygiene; encourage responsibility for personal care.
H Protect from overstimulation.
H Set realistic goals and limits for the patients behavior.
H Provide diversional activities suited to a short attention span.
H Reorient to reality.
H Avoid power struggles.
For the depressed patient
H Avoid overwhelming expectations.
H Allow increased time for activities and responses.
H Provide a structured routine.
H Promote interaction with others.
Cyclothymic disorder
A chronic mood disturbance of at least 2 years duration,
cyclothymic disorder involves numerous episodes of hypomania or depressive symptoms that arent of sufficient
severity or duration to qualify as a major depressive
episode.
In the hypomanic phase, the patient may experience insomnia; hyperactivity; inflated self-esteem; increased productivity and creativity; overinvolvement in pleasurable
activities, including an increased sexual drive; physical
restlessness; and rapid speech. Depressive symptoms
may include insomnia, feelings of inadequacy, decreased
productivity, social withdrawal, loss of libido, loss of interest in pleasurable activities, lethargy, depressed speech,
and crying.
A number of medical disorders (for example, endocrinopathies, such as Cushings disease, stroke, brain tumors, head trauma, and drug overdose) can produce a
similar pattern of mood alteration. These organic causes
must be ruled out before making a diagnosis of cyclothymic disorder.
H Encourage verbalization; provide support.

H Institute safety measures.
H Encourage physical activity.
Monitoring
H Patterns of behavior
H Complications
Patient teaching
Be sure to cover:
H importance of continuing the prescribed medication
regimen.
Discharge planning
H Refer the patient for psychological counseling.
Bipolar disorder
115
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Bladder cancer
Overview
Description
H Malignant tumor that develops on the bladder wall
Assessment
History
H Gross, painless, intermittent hematuria, usually with
clots
H Suprapubic pain after voiding suggesting invasive
lesions
surface or grows within the wall and quickly invades

underlying muscles
H Less common bladder tumors: adenocarcinomas,
epidermoid carcinomas, squamous cell carcinomas,
sarcomas, tumors in bladder diverticula, and carcinoma in situ
H Most common cancer of the urinary tract
H Bladder irritability, urinary frequency, nocturia, and
Pathophysiology
Test results
H About 90% of bladder cancers are transitional cell
Laboratory
H Complete blood count helps detect anemia.
H Urinalysis detects blood and malignant cells in the
urine.
Imaging
H Excretory urography can identify a large, early-stage
tumor or an infiltrating tumor; delineate functional
problems in the upper urinary tract; assess hydronephrosis; and detect rigid deformity of the bladder
wall.
H Retrograde cystography evaluates bladder structure
and integrity; it also helps confirm a bladder cancer
diagnosis.
H Bone scan can detect metastasis.
H Computed tomography scan defines the thickness of
the involved bladder wall and discloses enlarged
retroperitoneal lymph nodes.
H Ultrasonography reveals metastasis in tissues beyond
the bladder and can distinguish a bladder cyst from a
bladder tumor.
H Cystoscopy and biopsy confirm bladder cancer diagnosis; if the test results show cancer cells, further
studies will determine the cancer stage and treatment.
Other
H Bimanual examination may be performed during a
cystoscopy if the patient has received an anesthetic;
this helps to determine whether the bladder is fixed
to the pelvic wall.
carcinomas, arising from the transitional epithelium

of mucous membranes. (They may result from malignant transformation of benign papillomas.)
Causes
H Associated with chronic bladder irritation and infec-
tion in people with renal calculi, indwelling urinary

catheters, chemical cystitis caused by cyclophosphamide, or pelvic irradiation
Risk factors
H Certain environmental carcinogens, such as
2-naphthylamine, tobacco, nitrates, and coffee

H Occupational exposure to carcinogens
Incidence
H Bladder tumors most prevalent in people older than
age 50
H Occurs more commonly in densely populated indus-
trial areas
H Asymptomatic in early stages for 25% of patients
H First sign: gross, painless, intermittent hematuria,
with or without clots

H Suprapubic pain after voiding most commonly
associated with invasive lesions
dribbling
H Flank pain possibly indicating an obstructed ureter
Physical findings
H Gross hematuria
H Flank tenderness if ureteral obstruction present
H Bladder irritability
H Urinary frequency
H Nocturia
H Dribbling
Treatment
Complications
H Cancers stage, patients lifestyle, other health prob-
H Bone metastasis
H Problems resulting from tumor invasion of contigu-
ous viscera
116
Bladder cancer
General
lems, and mental outlook influencing selection of
therapy
H Initially postoperatively, avoidance of heavy lifting
and contact sports
H After recovery, no activity restrictions
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Medications
Discharge planning
H Intravesical chemotherapy, such as thiotepa and
H Refer the patient to resource and support services.

H Before discharge, arrange for follow-up home nurs-
mitomycin
H Attenuated live bacille Calmette-Gurin vaccine
H Chemotherapy, such as cisplatin and doxorubicin
Surgery
ing care.
H Refer the patient to an enterostomal therapist and for
services provided by the therapist.
H Transurethral resection (cystoscopic approach) and
fulguration (electrically)
H Segmental bladder resection
H Radical cystectomy
H Ureterostomy, nephrostomy, continent vesicostomy
(Kock pouch), ileal bladder, and ureterosigmoidostomy
Key outcomes
The patient will:
pain
H exhibit adequate coping mechanisms
sexual activity.
H Provide support and encourage verbalization.
H Provide preoperative teaching; discuss procedure
and postoperative course.

spirometer use.
H Provide skin care.
H Provide stoma care.
Monitoring
H Vital signs
H Wound site
H Postoperative complications, such as pneumonia,
deep vein thrombosis, and infection

H Intake and output
H Pain control
Patient teaching
Be sure to cover:
H stoma care
H skin care and evaluation
H avoidance of heavy lifting and contact sports (postoperatively with a urinary stoma)
H encouragement of participation in usual athletic and
physical activities.
Bladder cancer
117
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Blastomycosis
Overview
Description
H Fungal infection that usually affects the lungs and
produces bronchopneumonia
H May develop into extrapulmonary disease
H Also called Gilchrists disease
Pathophysiology
H Blastomycosis is generally contracted by inhalation of
aerosolized conidial forms of the fungus from its natural soil habitat.
H The conidia then transforms to the yeast phase at
body temperature (thermal dimorphism).
H Inflammatory response is evoked by multiplication
of organism.
H Dissemination is possible through the blood and
lymphatics to other organs.
Causes
H Inhalation of the yeastlike fungus Blastomyces
dermatitidis
Incidence
H Generally found in North America, where B. der-
matitidis normally inhabits the soil

H Endemic to the southeastern United States
H More common in males than females
H Onset most common between ages 30 and 50, but
can occur at any age
H Signs and symptoms of a viral upper respiratory tract
infection
H Small, painless, nonpruritic, and nondistinctive macules or papules on exposed body parts
Complications
H Osteomyelitis
H Central nervous system, skin, and genital disorders
H Addisons disease (adrenal insufficiency)
H Pericarditis
H Arthritis
Physical findings
H Thick sputum (may contain blood)
H Bronchial breath sounds; dullness on chest percus-
sion
H Decreased breath sounds
H Tachypnea
H Decreased pulse oximetry
H Raised and reddened lesions
H Chest pain
H Dyspnea
Extrapulmonary findings
H Skin lesions
H Osteolytic lesions
H Joint swelling
Test results
Laboratory
H Culture from skin lesions, pus, sputum, or pulmonary secretions shows presence of B. dermatitidis.
H White blood cell count and erythrocyte sedimentation
rate are increased.
H Serum globulin levels are slightly increased, and mild
normochromic anemia occurs.
H Alkaline phosphatase level is increased (with bone
lesions).
Imaging
H Chest X-ray may show pulmonary infiltrates.
H Biopsy of tissue from the skin or lungs or of bronchial washings, sputum, or pus shows infecting
organism.
Other
H Immunodiffusion testing detects antibodies for the A
and B antigens of blastomycosis.
Treatment
General
H Respiratory treatments
H Rest periods, as needed
Medications
H Antifungals, such as amphotericin B, itraconazole,
and ketoconazole
H Antipyretic such as acetaminophen
Assessment
History
Key outcomes
H Fever, chills
H Dry, hacking, productive cough
H Weight loss
H Night sweats
H Pleuritic chest pain
H Malaise
H Myalgia
The patient will:

H maintain adequate oxygenation
H improve skin integrity
H report increased comfort and decreased pain.
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Blastomycosis
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H Provide a cool room; if the patient is feverish, admin-
ister a tepid sponge bath.

H Elevate painful joints and apply heat.
H Provide appropriate skin care.
Monitoring
H Vital signs
H Pulse oximetry
H Laboratory tests
H Sputum production for hemoptysis
H Level of consciousness and pupil response
H Hematuria
H Lesion healing
Patient teaching
Be sure to cover:
H proper administration of medications
H skin care.
Discharge planning
H Stress appropriate follow-up care.
Blastomycosis
119
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Blepharitis
Overview
Description
H Common inflammation of eyelash follicles and
meibomian glands of the upper or lower eyelids

H May affect both eyes
H May affect upper and lower eyelids
H Ulcerative type: may coexist with seborrheic bleph-
aritis
Pathophysiology
H Inflammatory responses of the eyelids to bacteria or
seborrheic dermatitis occurs.
Causes
Seborrheic blepharitis
H Generally results from seborrhea of the scalp, eyebrows, and ears
Ulcerative blepharitis
H Generally results from a Staphylococcus aureus infection
H Pediculosis
Incidence
H More common in elderly people
H Most common ocular disease
H Eye drainage
H Burning, itching, and swelling of eyes
H Tends to recur
H May become chronic
Complications
H Ocular involvement
H Keratitis
H Excess tearing or dry eye
Assessment
History
H Eyelids itch or burn
H Feeling of foreign body
H Crusty eyelids, which stick together when awakening
H Loss of eyelashes
Physical findings
H Continual blinking
H Red-rimmed appearance to the eyelid margins
H Swelling of eyelids
Seborrheic blepharitis
H Scales along eyelids, especially upon awakening
H Dandruff on scalp and eyebrows
120
Blepharitis
Ulcerative blepharitis
H Flaky scales on eyelashes, especially in morning
H Missing eyelashes
H Ulcerations on eyelid margins
Test results
Laboratory
H Culture of the ulcerated eyelid margin reveals
S. aureus in ulcerative blepharitis.
Treatment
General
H Early treatment to prevent recurrence or complica-
tions
H Daily cleansing (using diluted baby-shampoo on a
cotton-tipped applicator or washcloth) to remove

scales from eyelid margins
H Warm eye compresses
H Removal of nits with forceps for blepharitis caused
by pediculosis
H Avoidance of eye makeup
H Avoidance of contact lens use until resolved
Medications
H Antibiotic eye ointment such as gentamicin
H Ophthalmic physostigmine or other insecticidal
ointment for blepharitis caused by pediculosis
Key outcomes
The patient will:
H verbalize feelings and concerns
H identify available health resources
H demonstrate appropriate coping skills
H maintain current visual acuity.
H Provide eyelid care at least twice daily.
H Apply warm compresses, four times daily.
H Apply ointments, as ordered. (See Applying an
ophthalmic ointment.)
H Maintain infection-control techniques.
Monitoring
H Adverse reactions to medication
H Complications
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Applying an ophthalmic ointment

Follow these directions to apply an ophthalmic ointment
cleanly and quickly:
H Tilt the patients head back, and ask him to look toward
the ceiling.
H Gently pull the lower eyelid down, and squeeze a small
ribbon of ointment along the edge of the conjunctival
sac from the inner to the outer canthus.
H Take care to avoid touching the eye with the tip of the
ointment tube.
H Repeat this procedure for the other eye, if ordered.
Patient teaching
Be sure to cover:
H daily eyelid care
H removal of scales from eyelids
H application of warm compresses
H medications and possible adverse effects
H infection control
H potential complications
H importance of keeping follow-up appointments.
Blepharitis
121
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Blood transfusion
reaction
Risk factors
H Multiple transfusions
H Rare blood type
Incidence
H Mild reactions in 1% to 2% of transfusions
Overview
Description
H A hemolytic reaction following the transfusion of mis-
matched blood
H Mild to severe fever within the first 15 minutes of
transfusion or within 2 hours after its completion

H Chills
H Urticaria
H Accompanies or follows I.V. administration of blood
Complications
components
H Mediated by immune or nonimmune factors
H From mild to severe
H Bronchospasm
H Acute tubular necrosis leading to acute renal failure
H Anaphylactic shock
H Vascular collapse
Pathophysiology
H Recipients antibodies, immunoglobulin (Ig) G or
IgM, attach to donor red blood cells (RBCs), leading

to widespread clumping and destruction of recipients RBCs.
H Transfusion with Rh-incompatible blood triggers a
less serious reaction, known as Rh isoimmunization, within several days to 2 weeks. (See Understanding the Rh system.)
H A febrile nonhemolytic reaction the most common
type of reaction develops when cytotoxic or agglutinating antibodies in the recipients plasma attack
antigens on transfused lymphocytes, granulocytes, or
plasma cells.
Causes
H Transfusion with incompatible blood
Assessment
History
H Transfusion of blood product
H Chills, nausea, vomiting, chest tightness, or chest and
back pain
Physical findings
H Fever, tachycardia, and hypotension
H Dyspnea, anxiety, and restlessness
H Urticaria and angioedema
H Wheezing
H In a surgical patient, blood oozing from mucous
membranes or the incision site

H In a hemolytic reaction: fever, an unexpected de-
Understanding the Rh system

The Rh system contains more than 30 antibodies and
antigens. Of the worlds population, about 85% are Rh
positive, which means that their red blood cells carry the
D or Rh antigen. The rest of the population are Rh negative and dont have this antigen.
Effects of sensitization
When an Rh-negative person receives Rh-positive blood
for the first time, he becomes sensitized to the D antigen
but shows no immediate reaction to it. If he receives Rhpositive blood a second time, he experiences a massive
hemolytic reaction.
For example, an Rh-negative mother who delivers an
Rh-positive baby is sensitized by the babys Rh-positive
blood. During her next Rh-positive pregnancy, her sensitized blood will cause a hemolytic reaction in the fetal circulation.
Preventing sensitization
To prevent the formation of antibodies against Rh-positive
blood, an Rh-negative mother should receive Rho(D) immune globulin (human) (RhoGAM) I.M. within 72 hours
after delivering an Rh-positive baby.
122
Blood transfusion reaction
crease in serum hemoglobin level, frank blood in

urine, and jaundice
Test results
Laboratory
H Serum hemoglobin levels are decreased.
H Serum bilirubin levels and indirect bilirubin levels
are elevated.
H Urinalysis reveals hemoglobinuria.
H Indirect Coombs test or serum antibody screen is
positive for serum anti-A or anti-B antibodies.
H Prothrombin time is increased and fibrinogen level is
decreased.
H Blood urea nitrogen and serum creatinine levels are
increased.
Treatment
General
H Immediate halt of transfusion
H Dialysis (may be necessary if acute tubular necrosis
occurs)
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H Bed rest
Medications
H Osmotic or loop diuretics, such as mannitol and
furosemide
H I.V. normal saline solution
H I.V. vasopressors, such as dopamine and phenyl-
ephrine
Patient teaching
Be sure to cover:
H signs and symptoms of transfusion reaction (before
transfusion begins)
H importance of notifying health care providers of
history of reaction
H wearing or carrying rare blood type identification.
H Adrenergic such as epinephrine

H Antihistamine such as diphenhydramine
H Corticosteroid such as dexamethasone
Key outcomes
The patient will:
H show no signs of active bleeding
H express understanding of disorder.
H Stop the blood transfusion.
H Maintain a patent I.V. line with normal saline
solution.
H Report early signs of complications.
H Cover the patient with blankets to ease chills.
H Administer supplemental oxygen, as needed.
H Document the transfusion reaction on the patients
chart, noting the duration of the transfusion and the

amount of blood absorbed.
H Follow your facilitys blood transfusion policy and
procedure.
ALERT
Double-check the patients name, identification
number, blood type, and Rh status before administering blood. If you find any discrepancy, dont administer the blood. Notify the blood bank immediately and return the unopened unit.
Monitoring
H Vital signs
H Intake and output
H Signs of shock
H Cardiac status
H Pulse oximetry
Blood transfusion reaction
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Bone tumors, primary

malignant
Assessment
Overview
History
Description
H Rare type of bone cancer (less than 1% of all malig-
nant tumors)
H Also known as osteoblastoma or
H Hemorrhage
H Local recurrence
H Pathologic fractures
osteosarcoma
H Localized, dull bone pain

H Weight loss
H Impaired mobility
H Pathologic fracture
Pathophysiology
Physical findings
H Proliferation of cancerous cells clump together to
H Palpable mass
H Cachectic appearance
H Abnormal gait
H Swelling and redness at the site
form a tumor, which is able to spread beyond the

original site.
H Osseous bone tumors arise from the bony structure
itself and include osteogenic sarcoma (most common), parosteal osteogenic sarcoma, chondrosarcoma (chondroblastic), and malignant giant cell tumor.
H Nonosseous bone tumors arise from hematopoietic,
vascular, and neural tissues and include Ewings sarcoma, fibrosarcoma (fibroblastic), and chordoma.
Causes
H No immediately apparent cause in most cases
H Genetic abnormalities (retinoblastoma, Rothmund-
Thomson syndrome)
H Exposure to carcinogens
H Heredity, trauma, and excessive radiation therapy,
Test results
Laboratory
H Serum alkaline phosphatase levels are elevated (with
sarcoma).
Imaging
H Bone X-rays and radioisotope bone and computed
tomography (CT) scans show tumor size.
H Bone scans and CT scans of the lungs reveal metastatic disease.
H Incision or aspiration biopsy confirms primary
malignancy.
according to theories
Incidence
Treatment
H Account for less than 0.2% of all cancers

H Higher incidence in children and adolescents, al-
General
though some types occurring in patients between

ages 35 and 60 (see Types of primary malignant
bone tumors)
Special populations
Osteogenic and Ewings sarcomas are the most
common bone tumors in children.
H Localized, dull bone pain
H Usually more intense at night
H Presence of a mass or tumor
Special populations
Limb pain, refusal to walk, and limited range of
motion (ROM) are common findings in children
with bone tumors.
Complications
H Infection
124
Bone tumors, primary malignant
H High-protein, high-calorie diet

H Physical therapy
H Radiation therapy
Medications
H Chemotherapy, such as gemcitabine and docetaxel
H Analgesics, such as morphine, oxycodone, hydro-
codone, and fentanyl
Surgery
H Excision of the tumor
H Radical surgery, such as hemipelvectomy or inter-
scapulothoracic or limb amputation
Key outcomes
The patient will:
H maintain weight within an acceptable range
H maintain joint mobility and ROM
H express feelings of comfort and decreased pain
H express feelings and fears.
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Types of primary malignant bone tumors

Type
Clinical features
Treatment
Chondrosarcoma
Develops from cartilage

Painless; grows slowly; locally recurrent and invasive
Occurs most commonly in pelvis, proximal femur, ribs, and
shoulder girdle
Usually in males ages 30 to 50
Hemipelvectomy, surgical resection (ribs)

Radiation (palliative)
Chemotherapy
Malignant
giant cell tumor
Arises from benign giant cell tumor

Found most commonly in long bones, especially in the knee
area
Usually in females ages 18 to 50
Curettage
Total excision
Radiation for recurrent disease
Osteogenic
sarcoma
Osteoid tumor present in specimen

Tumor arises from bone-forming osteoblast and bonedigesting osteoclast
Occurs most commonly in femur, but also tibia and humerus; occasionally, in fibula, ileum, vertebra, or mandible
Surgery (tumor resection, high

thigh amputation, hemipelvectomy, interscapulothoracic
surgery)
Chemotherapy
Parosteal
osteogenic
sarcoma
Develops on surface of bone instead of interior

Progresses slowly
Occurs most commonly in distal femur, but also in tibia,
humerus, and ulna
Usually in females ages 30 to 40
Surgery (tumor resection, possible amputation, interscapulothoracic surgery, hemipelvectomy)

Chemotherapy
Combination of the above
OSSEOUS ORIGIN
NONOSSEOUS ORIGIN
Chordoma
Derived from embryonic remnants of notochord

Progresses slowly
Usually found at end of spinal column and in sphenooccipital, sacrococcygeal, and vertebral areas
Characterized by constipation and visual disturbances
Surgical resection (commonly

resulting in neural defects)
Radiation (palliative, or when
surgery not applicable, as in
occipital area)
Ewings sarcoma
Originates in bone marrow and invades shafts of long and

flat bones
Usually affects lower extremities, most commonly femur,
innominate bones, ribs, tibia, humerus, vertebra, and fibula;
may metastasize to lungs
Pain increasingly severe and persistent
Prognosis poor
High-voltage radiation (tumor is

radiosensitive)
Chemotherapy to slow growth
Amputation only if theres no evidence of metastasis
Fibrosarcoma
Relatively rare
Originates in fibrous tissue of bone
Invades long or flat bones (femur, tibia, mandible) but also
involves periosteum and overlying muscle
Amputation
Radiation
Chemotherapy
Bone grafts (with low-grade fibrosarcoma)
H Encourage communication, and help the patient set
realistic goals.
H Administer prescribed I.V. infusions and drugs.
H Postoperative care, including coughing, deep breath-
ing, incentive spirometer use, and turning.

H Keep the head of the bed elevated at least 30 degrees.
H Elevate the foot of the bed or place the affected
stump on a pillow for the first 24 hours. (Be careful not to leave the stump elevated for more than
48 hours because this may lead to contractures.)
Monitoring
H Vital signs
H Circulation to the affected extremity
H Wound dressings
Patient teaching
Be sure to cover:
H use of assistive devices
H wound care
H reporting new pain or masses
H the need for antibiotic prophylaxis when undergoing
dental procedures (with bone grafts or prosthetic
implants).
Discharge planning
H Refer the patient to the American Cancer Society for
information and support.
Bone tumors, primary malignant
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H Symptoms 18 to 30 hours after ingestion of con-
Botulism
taminated food; may be delay of up to 10 days before

symptoms appear
H Range in severity and can mimic other illnesses,
especially neurologic disorders
Overview
Complications
Description
H Life-threatening paralytic illness
H Results from an exotoxin produced by the gram-
positive, anaerobic bacillus Clostridium botulinum

H Occurs as botulism food poisoning, wound botulism,
and infant botulism (see Infant botulism)
H Paralytic ileus
H Death
Assessment
H Mortality about 25%, with death most commonly
History
caused by respiratory failure during the first week of

illness
H Critical and potentially fatal illness signaled by onset
within 24 hours
H Consumption of home-canned food 18 to 30 hours
before onset of symptoms
H Clostridium botulinum bacteria
H Vertigo
H Sore throat
H Weakness
H Diplopia
H Blurred vision
H Dysarthria
H Dysphagia
H Dyspnea
H Heroin use
Risk factors
Physical findings
H Eating improperly preserved foods

H Use of injectable street drugs
H Ptosis
H Dilated, nonreactive pupils
H Appearance of dry, red, and crusted oral mucous
Pathophysiology
H Endotoxin acts at the neuromuscular junction of
skeletal muscle, preventing acetylcholine release and

blocking neural transmission, eventually resulting in
paralysis.
Causes
Incidence
H Occurs worldwide
H Average yearly occurrence of about 110 cases in the
United States
H Affects adults more than children
membranes
H Abdominal distention with absent bowel sounds
H Descending weakness or paralysis of muscles in the
extremities or trunk
H Deep tendon reflexes may be intact, diminished, or
absent
Infant botulism
Infant botulism, which usually afflicts neonates and infants between 3 and 20 weeks old, is commonly caused
by ingesting the spores of botulinum bacteria, which then
grow in the intestines and release toxin. This disorder can
produce floppy infant syndrome, characterized by constipation, a feeble cry, a depressed gag reflex, and an inability to suck. The infant also exhibits a flaccid facial expression, ptosis, and ophthalmoplegia the result of cranial
nerve deficits.
As the disease progresses, the infant develops generalized weakness, hypotonia, areflexia, and sometimes a
striking loss of head control. Almost 50% of affected infants develop respiratory arrest.
Intensive supportive care allows most infants to recover
completely. Antitoxin therapy isnt recommended because
of the risk of anaphylaxis.
H Unexplained orthostatic hypotension

H Urine retention
H Photophobia
H Slurred speech
Test results
Laboratory
H Mouse bioassay detects toxin thats found in the patients serum, stool, or gastric contents.
H Electromyography shows diminished muscle action
potential after a single supramaximal nerve stimulus.
Treatment
General
H Early tracheotomy and ventilatory assistance in respi-
ratory failure
H Nasogastric (NG) suctioning
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H Total parenteral nutrition

H Bed rest
Medications
H I.V. or I.M. botulinum antitoxin
Surgery
H Debridement of wounds to remove source of toxin-
producing bacteria
Key outcomes
The patient will:
H maintain stable neurologic status.
H Administer I.V. fluids, as ordered.
H Administer oxygen as needed.
H Perform NG suctioning as needed.
ALERT
Immediately report all cases of botulism to the
local board of health.
Monitoring
H Neurologic status
H Cardiac and respiratory function
H Cough and gag reflexes
H Intake and output
H Arterial blood gas analysis
H Pulse oximetry
Patient teaching
Be sure to cover:
H proper techniques in processing and preserving
foods
H never tasting food from a bulging can or one with a
peculiar odor
H sterilizing utensils by boiling what came in contact
with suspected contaminated food
H not feeding honey to infants (can be fatal if contaminated).
Discharge planning
H If botulism exposure appears to be related to adverse
socioeconomic conditions, refer the patient to the

appropriate community agency.
Botulism
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Brain tumor
Overview
Description
H Abnormal growth among cells within the intracranial
space
H May affect brain tissue, meninges, pituitary gland,
and blood vessels
H In adults, most common tumor types: gliomas and
meningiomas (usually benign), which usually occur
above the covering of the cerebellum, and supratentorial tumors
H In children, most common tumor types: astrocytomas, medulloblastomas, ependymomas, and brain
stem gliomas
Pathophysiology
H Tumor is classified based on histology or grade of
cell malignancy.
H Central nervous system changes occur due to cancer
cells invading and destroying tissues and by secondary effect mainly compression of the brain, cranial nerves, and cerebral vessels; cerebral edema;
and increased intracranial pressure (ICP).
Causes
H Unknown
Risk factors
H Preexisting cancer
Incidence
H Slightly more common in males than in females
H Gliomas, meningiomas, and schwannomas: overall
incidence of 4.5 per 100,000

H Can occur at any age, but most in children before age
1 or between ages 2 and 12

H In adults, incidence highest between ages 40 and 60
H Increased ICP
H Headache
H Decreased motor strength and coordination
H Seizures
H Altered vital signs
H Papilledema
Complications
H Radiation encephalopathy
Special populations
Brain tumors are the most common cause of cancer death in children.
Life-threatening complications from

increased ICP
H Coma
H Respiratory or cardiac arrest
H Brain herniation
Assessment
History
H Insidious onset
H Headache
Physical findings
H May vary according to size and location of tumor
Signs and symptoms of increased ICP

H Weakness, paralysis
H Aphasia, dysphagia
H Ataxia, incoordination
H Seizure
H Decreased level of consciousness
Test results
Imaging
H Skull X-rays confirm presence of tumor.
H Brain scan confirms presence of tumor.
H Computed tomography scan confirms presence of
tumor.
H Magnetic resonance imaging confirms presence of
tumor.
H Cerebral angiography confirms presence of tumor.
H Positron-emission tomography confirms presence of
tumor.
H Tissue biopsy confirms type of tumor.
Other
H Lumbar puncture shows increased cerebrospinal
fluid (CSF) pressure, which reflects ICP, increased
protein levels, decreased glucose levels and, occasionally, tumor cells in CSF.
Treatment
General
H Specific treatments varying with the tumors histolog-
ic type, radiosensitivity, and location

H No dietary restrictions unless swallowing impaired
H Possibly altered physical ability based on neurologic
status
Medications
H Chemotherapy, such as carmustine, cisplatin, and
lomustine
H Steroid such as dexamethasone
H Histamine-receptor antagonists, such as cimetidine,
famotidine, and ranitidine

H Anticonvulsants, such as phenytoin and fosphenytoin
H Analgesic such as codeine
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Surgery
For glioma
H Resection by craniotomy
H Radiation therapy and chemotherapy follow resection
For low-grade cystic cerebellar astrocytoma
H Surgical resection
For astrocytoma
H Repeated surgeries, radiation therapy, and shunting
of fluid from obstructed CSF pathways
For oligodendroglioma and ependymoma
H Surgical resection and radiation therapy
For medulloblastoma
H Surgical resection
H Possibly, intrathecal infusion of methotrexate or
another antineoplastic drug
For meningioma
H Surgical resection, including dura mater and bone
For schwannoma
H Microsurgical technique
Patient teaching
Be sure to cover:
H the disease process, diagnosis, and treatment
H signs of infection or bleeding that may result from
chemotherapy
H adverse effects of chemotherapy and other treatments
and actions that may alleviate them
H early signs of tumor recurrence.
Discharge planning
H Consult with occupational and physical therapy staff
for postdischarge care plan.

Key outcomes
The patient will:
feelings about them
H continue to function in usual roles as much as
possible
H enlist support from available sources
H Take steps to protect the patients safety.
H After supratentorial craniotomy, elevate the head of
the bed about 30 degrees.

H After infratentorial craniotomy, keep the patient flat
for 48 hours.
H As appropriate, instruct the patient to avoid Valsalvas
maneuver and isometric muscle contractions when

moving or sitting up in bed.
H Provide postoperative care.
H Encourage incentive spirometer use.
H Consult with occupational, speech, and physical
therapists.
Monitoring
H Neurologic status
H Vital signs
H Wound site
H Postoperative complications
H Pulse oximetry
H Pain level, location, and effectiveness of treatment
Brain tumor
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Breast cancer
Overview
Description
H Malignant proliferation of epithelial cells lining the
ducts or lobules of the breast

H Early detection and treatment influencing the prognosis considerably
ALERT
The most reliable detection method of breast cancer is regular breast self-examination, followed by
an immediate professional evaluation of any abnormality. (Theoretically, slow-growing breast cancer may take up to 8 years to become palpable at
1 cm.)
H With adjunctive therapy, 10-year (or longer) 70% to
75% survival in females with negative nodes, compared to 20% to 25% survival in females with positive
nodes
Pathophysiology
H Breast cancer spreads by way of the lymphatic system
H Estrogen therapy
H Antihypertensive therapy
H Alcohol and tobacco use
H Preexisting fibrocystic disease
Incidence
H A female living in the United States to age 80 a
1-in-8 chance of developing invasive breast cancer

sometime during her life
H The second-leading cause of cancer death in females
after lung cancer
H Most common after age 50; but may develop anytime
after puberty
H Seldom occurs in males
Special populations
Breast cancer is the leading cause of cancer deaths
among females ages 35 to 54.
H Lump or mass in the breast (see Breast tumor
sources and sites)

H Breast pain
H Change in symmetry or size of breast
H Change in skin, such as thickening, scaly skin around
the nipple, dimpling, edema, or ulceration
and the bloodstream through the right side of the

heart to the lungs and to the other breast, chest wall,
liver, bone, and brain.
Classification
H Adenocarcinoma (ductal) arises from the epithelium.
H Intraductal cancer develops within the ducts (includes Pagets disease).
H Infiltrating cancer occurs in the breasts parenchymal
tissue.
H Inflammatory cancer (rare) grows rapidly and causes overlying skin to become edematous, inflamed,
and indurated.
H Lobular carcinoma in situ involves the lobes of glandular tissue.
H Medullary or circumscribed cancer is an enlarged tumor with a rapid growth rate.
H Nipple discharge
Causes
H Clear, milky, or bloody discharge from the nipple,
H Unknown
Risk factors
H Family history of breast cancer, particularly first-
degree relatives, including mother, sister, maternal

grandmother, and maternal aunt
H Positive tests for genetic mutations (BRCA1)
H A female older than age 45 and premenopausal
H Long menstrual cycles
H Early onset of menses, late menopause
H Nulliparous or first pregnancy after age 30
H High-fat diet
H Endometrial or ovarian cancer
H History of unilateral breast cancer
H Radiation exposure
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Breast cancer
Complications
H Distant metastasis
H Infection
H Central nervous system effects
H Respiratory effects
Assessment
History
H Detection of a painless lump or mass in the breast
H Change in breast tissue
H History of risk factors
Physical findings
nipple retraction, scaly skin around the nipple, and
skin changes, such as dimpling or inflammation
H Arm edema
H Hard lump, mass, or thickening of breast tissue
H Lymphadenopathy
Test results
Laboratory
H Hormonal receptor assay determines whether the
tumor is estrogen- or progesterone-dependent; also
guides decisions to use therapy that blocks the action
of the estrogen hormone that supports tumor growth.
H In Vitro Diagnostic Multivariate Index Assay predicts
the odds that an early-stage breast cancer will metastasize in 5 to 10 years.
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Imaging
H Mammography can reveal a tumor thats too small to
palpate.
H Ultrasonography can distinguish between a
fluid-filled cyst and solid mass.
H Chest X-rays can pinpoint metastasis in the chest.
H Scans of the bone, brain, liver, and other organs can
detect distant metastasis.
H Fine-needle aspiration and excisional biopsy provide
cells for histologic examination that may confirm the
diagnosis.
Breast tumor sources and sites

About 90% of all breast tumors arise from the epithelial
cells lining the ducts. About half of all breast cancers develop in the breasts upper outer quadrant the section
containing the most glandular tissue.
The second most common cancer site is the nipple,
where all the breast ducts converge.
The next most common site is the upper inner quadrant,
followed by the lower outer quadrant and, finally, the lower inner quadrant.
Treatment
General
50%
H The choice of treatment usually depends on: stage
15%
and type of disease, age, menopausal status, and any

disfiguring effects of surgery
H Therapy may include: any combination of surgery,
radiation, chemotherapy, and hormone therapy
H Arm motion and exercises possibly needed after
surgery
H Primary radiation therapy
H Preoperative breast irradiation
18%
11%
6%
Medications
H Chemotherapy, such as a combination of drugs, in-
cluding anastrozole, capecitabine, cyclophosphamide, docetaxel, epirubicin, ememestane, fluorouracil, methotrexate, doxorubicin, vincristine,
paclitaxel, prednisone, and trastuzumab
H Regimen of cyclophosphamide, methotrexate, and
fluorouracil (used in premenopausal and postmenopausal females)
H Antiestrogen therapy such as tamoxifen
H Hormonal therapy, including estrogen, progesterone,
androgen, or antiandrogen aminoglutethimide
therapy
Surgery
H Lumpectomy
H Partial, total, or modified radical mastectomy
Key outcomes
The patient will:
feelings about these limitations
H report feelings of comfort
H express increased sense of well-being
H use situational supports to reduce fear.

H Provide postoperative care, such as turning, cough-
ing, deep breathing, and incentive spirometer use.

H Encourage early ambulation.
Monitoring
H Wound site
H Vital signs
H Intake and output
H White blood cell count
H Pain control
H Psychological status
Patient teaching
Be sure to cover:
H all procedures and treatments
H activities or exercises that promote healing
H breast self-examination
H risks and signs and symptoms of recurrence
H avoidance of venipuncture or blood pressure monitoring on the affected arm.
H Provide information about the disease process, diag-
Discharge planning
nostic tests, and treatment.

H Refer the patient to local and national support
groups.
Breast cancer
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Bronchiectasis
H Dramatically decreased incidence over the past 20
Overview
years due to the availability of antibiotics to treat

acute respiratory infections
H Highest among Inuit populations in the northern
hemisphere and the Maoris of New Zealand
Description
H Lung disease characterized by abnormal dilation of
H Chronic cough productive for copious, foul-smelling,
the bronchi and destruction of the bronchial walls

H Results from conditions associated with repeated
damage to bronchial walls and with abnormal mucociliary clearance, causing a breakdown of supporting tissue adjacent to the airways
H Can occur throughout the tracheobronchial tree, or
may be confined to one segment or lobe
H Usually bilateral and involves the basilar segments of
the lower lobes
H Occurs in three forms: cylindrical (fusiform), varicose, and saccular (cystic)
Pathophysiology
H Hyperplastic squamous epithelium, denuded of cilia,
replaces ulcerated columnar epithelia.
mucopurulent secretions
H Dyspnea
H Weight loss
H Malaise
Complications
H Chronic malnutrition
H Amyloidosis
H Right-sided heart failure
H Cor pulmonale
Assessment
H Abscess formation occurs, involving all layers of the
History
bronchial walls, which produces inflammatory cells

and fibrous tissues, resulting in dilation and narrowing of the airways.
H Sputum stagnates in the dilated bronchi and leads to
secondary infection, characterized by inflammation
and leukocytic accumulations.
H Additional debris collects in the bronchi and occludes them.
H Building pressure from the retained secretions induces mucosal injury.
H Extensive vascular proliferation of bronchial circulation occurs and produces frequent hemoptysis.
H Frequent bouts of pneumonia

H Coughing up of blood or blood-tinged sputum
H Chronic cough that produces copious, foul-smelling,
Causes
H Cystic fibrosis
H Mucoviscidosis
H Immune disorders
H Recurrent bacterial respiratory tract infections
H Complications of measles, pneumonia, pertussis, or
influenza
H Obstruction with recurrent infection
H Inhalation of corrosive gas
H Repeated aspiration of gastric juices
H Congenital anomalies (rare) such as bronchomalacia
H Various rare disorders such as immotile cilia syn-
drome
Risk factors
H Occupational exposure to damaging inhalants
H Risky behaviors that lead to immunodeficiency disor-
ders, such as human immunodeficiency virus and acquired immunodeficiency syndrome
Incidence
H Affects people of both sexes and of all ages
132
Bronchiectasis
mucopurulent secretions
H Dyspnea
H Weight loss
H Malaise
Physical findings
H Sputum that may show a cloudy top layer, a central
layer of clear saliva, and a heavy, thick, purulent bottom layer upon settling
H Clubbed fingers and toes
H Cyanotic nail beds
H Dullness over affected lung fields, if pneumonia or
atelectasis present
H Crackles during inspiration over affected area
H Occasional wheezes
Test results
Laboratory
H Sputum culture and Gram stain show predominant
pathogens.
H Complete blood count reveals anemia and leukocytosis.
Imaging
H Computed tomography scan shows bronchiectasis.
H Bronchography shows location and extent of disease.
H Chest X-rays show peribronchial thickening, atelectatic areas, and scattered cystic changes.
H Bronchoscopy may show the source of secretions or
the bleeding site in hemoptysis.
H Pulmonary function studies show decreased vital
capacity, expiratory flow, and hypoxemia.
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Other
H A sweat electrolyte test may show cystic fibrosis as
the underlying cause.
Treatment
General
H Postural drainage and chest percussion
H Bronchoscopy to remove secretions
H Well-balanced, high-calorie diet
H Adequate hydration
Medications
H Antibiotics, such as cefdinir, cefpodoxime, and
levofloxacin
H Bronchodilators, such as albuterol and aformoterol
H Oxygen
H Mucolytic such as acetylcysteine
Surgery
For poor pulmonary function
H Segmental resection
H Bronchial artery embolization
H Lobectomy

H Complications
H Chest tube drainage after surgery
H Pain control
Patient teaching
Be sure to cover:
H proper disposal of secretions
H infection control techniques
H frequent rest periods
H preoperative and postoperative instructions, if
surgery is required
H postural drainage and percussion
H coughing and deep-breathing techniques
H avoidance of air pollutants and people with known
upper respiratory tract infections
H immunizations
H balanced, high-protein diet
H avoidance of milk products
H adequate hydration.
Discharge planning
indicated.
Key outcomes
The patient will:
H utilize energy conservation techniques
H Perform preoperative and postoperative teaching.
H Perform chest physiotherapy.
H Provide a warm, quiet, comfortable environment.
H Alternate rest and activity periods.
H Provide well-balanced, high-calorie meals.
H Offer small, frequent meals.
H Provide frequent mouth care.
H Encourage incentive spirometer use, coughing, and
deep breathing.
Monitoring
H Vital signs
H Intake and output
H Cardiac status
H Sputum production
H Pulse oximetry
Bronchiectasis
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Bronchitis, chronic
Overview
Description
H An inflammation of the lining of the bronchial tubes
H Form of chronic obstructive pulmonary disease
H Characterized by excessive production of tracheo-
bronchial mucus with a cough for at least 3 months

each year for 2 consecutive years
H Severity linked to the amount of cigarette smoke or
other pollutants inhaled and inhalation duration
H Respiratory tract infections that typically exacerbate
the cough and related symptoms
H Development of significant airway obstruction seen in
few patients with chronic bronchitis
Pathophysiology
H Hypertrophy and hyperplasia of the bronchial mu-
cous glands, increased goblet cells, ciliary damage,

squamous metaplasia of the columnar epithelium,
and chronic leukocytic and lymphocytic infiltration
of bronchial walls results.
H Additional effects include widespread inflammation,
airway narrowing, and mucus within the airways
all producing resistance in the small airways and, in
turn, a severe ventilation-perfusion imbalance. (See
What happens in chronic bronchitis.)
Causes
H Cigarette smoking
H Possible genetic predisposition
H Environmental pollution
H Organic or inorganic dusts and noxious gas exposure
Incidence
H About 20% of males affected
H More than 8.8 million people in the United States di-
agnosed annually
H More prevalent in females than in males
H Children of parents who smoke: higher risk for con-
tracting chronic bronchitis than children of parents

who dont smoke
H Long-time smoker
H Frequent upper respiratory tract infections
H Productive cough
Complications
H Cor pulmonale
H Right ventricular hypertrophy
H Acute respiratory failure
Assessment
History
H Longtime smoker
H Frequent upper respiratory tract infections
H Productive cough
H Cough, initially prevalent in winter, but gradually
becoming year-round
H Increasingly severe coughing episodes
H Worsening dyspnea
Physical findings
H Cough producing copious gray, white, or yellow
sputum
H Cyanosis
H Accessory respiratory muscle use
H Tachypnea
H Substantial weight gain
H Pedal edema
H Jugular vein distention
H Wheezing
H Prolonged expiratory phase
H Rhonchi
Test results
Laboratory
H Arterial blood gas analysis shows decreased partial
pressure of oxygen and normal or increased partial
pressure of carbon dioxide.
H Sputum culture reveals microorganisms and neutrophils.
Imaging
H Chest X-ray may show hyperinflation and increased
bronchovascular markings.
H Pulmonary function tests show increased residual
volume, decreased vital capacity and forced expiratory flow, and normal static compliance and diffusing
capacity.
H Electrocardiography may show atrial arrhythmias;
peaked P waves in leads II, III, and aVF; and right
ventricular hypertrophy.
Treatment
General
H Smoking cessation
H Avoidance of air pollutants
H Chest physiotherapy
H Ultrasonic or mechanical nebulizer treatments
H High-calorie, protein-rich diet
H Activity, as tolerated with frequent rest periods
Medications
H Oxygen
H Antibiotics, such as cefdinir, cefpodoxime, and
levofloxacin
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Bronchitis, chronic
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What happens in chronic bronchitis

In chronic bronchitis, irritants inhaled
for a prolonged period inflame the tracheobronchial tree. The inflammation
leads to increased mucus production
and a narrowed or blocked airway.
As inflammation continues, the
mucus-producing goblet cells undergo
hypertrophy, as do the ciliated epithelial cells that line the respiratory tract.
Hypersecretion from the goblet cells
blocks the free movement of the cilia,
which normally sweep dust, irritants,
and mucus from the airways.
As a result, the airway stays
blocked, and mucus and debris accumulate in the respiratory tract.
CROSS SECTION OF THE NORMAL

BRONCHIAL TREE
Cilia
Cilia
Goblet cell
H Bronchodilators, such as aformoterol, salmeterol,
and tiotropium
H Corticosteroids, such as fluticasone, hydrocortisone,
methylprednisolone, and prednisone
H Diuretics such as furosemide
Surgery
NARROWED BRONCHIAL TUBE IN

CHRONIC BRONCHITIS
Epithelial cell
Goblet cell
Epithelial cell
H Daily weight
H Edema
Patient teaching
H Tracheostomy in advanced disease
Key outcomes
The patient will:
H identify measures to prevent or reduce fatigue
H maintain a patent airway.
H Encourage expression of fears and concerns.
H Include the patient and his family in care decisions.
H Provide a high-calorie, protein-rich diet.
H Encourage energy-conservation techniques.
H Ensure adequate oral fluid intake.
H Encourage daily activity.
H Provide diversional activities, as appropriate.
Be sure to cover:
H infection control practices
H influenza and pneumococcus immunizations
H home oxygen therapy, if required
H postural drainage and chest percussion
H inhaler use
H high-calorie, protein-rich meals
H adequate hydration
H avoidance of inhaled irritants
H prevention of bronchospasm
H respiratory hygiene and cough etiquette.
Discharge planning
indicated.
H Refer the patient to the American Lung Association
for information and support.

H Refer the patient to support services for respiratory
care equipment and supplies.
spirometer use.
Monitoring
H Vital signs
H Intake and output
H Sputum production
H Respiratory status, including breath sounds and
pulse oximetry
Bronchitis, chronic
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Brucellosis
Overview
Description
H An acute febrile illness transmitted to humans from
animals
H Also known as undulant fever, Malta fever, or
Bangs disease
Pathophysiology
H Brucellosis is transmitted through the consumption
of unpasteurized dairy products or uncooked or undercooked contaminated meat, and through contact
with infected animals or their secretions or excretions.
Causes
H The nonmotile, nonspore-forming, gram-negative
coccobacilli of the genus Brucella, notably B. suis

(found in swine), B. melitensis (in goats), B. abortus (in cattle), and B. canis (in dogs)
Risk factors
H Occupational exposure to animals
Incidence
H Most common among farmers, stock handlers,
butchers, and veterinarians

H Six times more common in males than in females
H Less common in children
H People with chlorhydria particularly susceptible be-
cause hydrochloric acid in gastric juices kills Brucella bacteria

H Most prevalent in the Middle East, Africa, Russia, India, South America, and Europe; uncommon in the
United States
Acute phase
H Fever
H Chills
H Profuse sweating
H Fatigue
H Headache
H Backache
H Weight loss
H Abscess and granuloma formulation in subcutaneous
tissues, lymph nodes, liver, and spleen
Chronic phase
H Recurrent depression
H Fatigue
H Headache
H Sweating
H Sexual impotence
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Brucellosis
Complications
H Abscesses in the testes, ovaries, kidneys, and brain
(meningitis and encephalitis)

H Osteomyelitis
H Orchitis
H Subacute bacterial endocarditis
H Pleural effusions
H Pneumothorax
H Eczematous rashes, petechiae, purpura
Assessment
History
H Direct exposure to animals
H Ingestion of unpasteurized dairy products
H Recent travel to an endemic area
H Fatigue
H Headache
H Intermittent fever
H Profuse sweating
H Anxiety
H General aching
Physical findings
H Excessive perspiration
H Chills
H Weakness
H Lymphadenopathy
H Tenderness in the right upper quadrant
Test results
Laboratory
H Agglutinin titers are 1:160 or higher.
H Definitive diagnosis is provided by three to six
cultures of blood and bone marrow and biopsies
of infected tissue (for example, the spleen).
H Erythrocyte sedimentation rate is increased.
H White blood cell count is either normal or reduced.
Treatment
General
H Bed rest during the acute phase
H High-calorie, high-protein diet
H Secretion precautions until lesions stop draining
Medications
H Antibiotic such as tetracycline
H Corticosteroids, such as hydrocortisone, methylpred-
nisolone, and prednisone
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Key outcomes
The patient will:
H be free from signs and symptoms of infection
H attain relief from immediate symptoms
H experience feelings of comfort or absence of pain
H regain or maintain skin integrity.
H Keep suppurative granulomas and abscesses dry.
H Maintain contact precautions: double-bag and prop-
erly dispose of all secretions and soiled dressings.

H Reassure the patient that this infection is curable.
Monitoring
H Vital signs
H Complications
H Depression and disturbed sleep pattern
H Lesion healing
H Neurologic status
Patient teaching
Be sure to cover:
H continuing medication for the prescribed duration
H preventing recurrence by cooking meat thoroughly
and avoiding unpasteurized milk
H advice to meat packers and other people at risk for
occupational exposure to wear rubber gloves and
goggles.
Brucellosis
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Buergers disease
Overview
H Digital ischemia
H Trophic nail changes
H Absent or diminished radial, ulnar, or tibial pulses
H Ischemic ulcers on the toes, feet, or fingers
H Superficial thrombophlebitis
Description
Test results
H An inflammatory, nonatheromatous occlusive condi-
Imaging
H Doppler ultrasonography shows diminished circulation in the peripheral vessels.
H Arteriography locates lesions and rules out atherosclerosis.
H Plethysmography helps detect decreased circulation
in the peripheral vessels.
Other
H Allens test results are abnormal. (See Performing
Allens test.)
tion that impairs circulation to the legs, feet and, occasionally, hands
H Sometimes called thromboangiitis obliterans
Pathophysiology
H Polymorphonuclear leukocytes infiltrate the walls of
small and medium-sized arteries and veins.

H Thrombus develops in the vascular lumen, eventually
occluding and obliterating portions of the small vessels, resulting in decreased blood flow to the feet and
legs.
H This diminished blood flow may produce ulceration
and, eventually, gangrene.
Treatment
Causes
General
H Unknown
H Linked to smoking (suggesting a hypersensitivity
H Smoking cessation
H Nothing by mouth, if surgery is needed
H Exercise program that uses gravity to fill and drain
reaction to nicotine)
Incidence
H Most patients ages 20 to 45
H Affects natives of India, Japan, and Korea and Ashke-
nazic Jews
the blood vessels
Medications
H Antibiotics, such as cefuroxime, gentamicin, and
tobramycin, for secondary infection

H Analgesics, such as morphine, hydromorphone, and
ketarolac
H Intermittent claudication of the instep, aggravated by
Surgery
exercise and relieved by rest

H Initially, coldness, cyanosis, and numbness in feet
during exposure to low temperature; later, redness,
heat, and tingling
H Impaired peripheral pulses and migratory superficial
thrombophlebitis
H In severe disease, a lumbar sympathectomy to in-
Complications
H Ulceration
H Muscle atrophy
H Gangrene
Assessment
History
H Exposure to secondhand smoke
H Use of nicotine patch
H Use of chewing tobacco
H Smoking
H Painful, intermittent claudication of the instep, aggra-
vated by exercise and relieved by rest
Physical findings
H Feet that are cold, numb, and cyanotic when exposed
to low temperatures
138
Buergers disease
crease blood supply to the skin

H Amputation for nonhealing ulcers, intractable pain,
or gangrene
Key outcomes
The patient will:
pain
H maintain tissue integrity
H carry out previous roles without the limitations of the
disease process
H develop adequate coping mechanisms.
H Position the patient for comfort with the head of the
bed elevated at least 30 degrees.

H Provide a padded footboard or bed cradle to prevent
pressure from bed linens.

H Protect the feet with soft padding.
H Administer medications, as ordered.
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Performing Allens test

Dont obtain an arterial blood gas specimen from the radial artery until you assess collateral arterial blood supply using the
Allens test.
Direct the patient to close his hand
while you occlude his radial and ulnar
arteries for 10 to 30 seconds, watching for the hand to blanch.
Tell the patient to open his hand.
Release pressure on the ulnar artery.

Color should return to the patients
hand in 15 seconds. If the color
doesnt return, select another site
for an arterial puncture.
Monitoring
H Skin integrity
H Peripheral circulation
H Infection
H Pain control
Patient teaching
Be sure to cover:
H avoiding precipitating factors, such as emotional
stress, exposure to extreme temperatures, and
trauma
H proper foot care, especially the importance of wearing well-fitting shoes and cotton or wool socks.
Discharge planning
H Refer the patient to a self-help group to help him
stop smoking.
needed.
H If the patient has undergone amputation, refer him
to physical therapists, occupational therapists, and

social service agencies, as needed.
Buergers disease
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Bulimia nervosa
Overview
Description
H Behavioral disorder characterized by eating binges
followed by feelings of guilt, humiliation, and

self-deprecation
H Self-induced vomiting, the use of laxatives or diuretics, or strict dieting or fasting to overcome the effects
of the binges
H Seldom incapacitating
Pathophysiology
H Decreased caloric intake depletes body fat and pro-
H Distinguished for participation in competitive activi-
ties
Complications
H Dental caries
H Erosion of tooth enamel
H Parotitis
H Gum infections
H Dehydration
H Arrhythmias
H Cardiac failure
H Sudden death
H Esophageal tears
H Gastric ruptures
H Mucosal damage to intestine
H Suicide
tein stores.
H Estrogen deficiency occurs in women due to lack of
lipid substrate for synthesis, causing amenorrhea.

H Testosterone levels fluctuate in men, causing de-
creased erectile function and sperm count.

H Ketoacidosis occurs from increased use of fat as en-
ergy fuel.
Causes
Risk factors
H Family disturbance or conflict
H Sexual abuse
H Maladaptive learned behavior
H Struggle for control or self-identity
H Cultural overemphasis on physical appearance
H Parental obesity
H Female gender
H Adolescent or young adult
Incidence
H Affects nine females for every one male
H Between 1% and 3% of adolescent and young fe-
males meeting the diagnostic criteria; 5% to 15%

having some symptoms of the disorder
Assessment
History
H Episodic binge eating
H Continues eating until abdominal pain, sleep, or the
presence of another person interrupts it

H Preferred food usually sweet, soft, and high in calo-
ries and carbohydrate content

H Exaggerated sense of guilt
H Depression
H Childhood trauma
H Parental obesity
H Unsatisfactory sexual relationships
Physical findings
H Thin or slightly overweight
H Use of diuretics, laxatives, vomiting, and exercise
H Abdominal and epigastric pain
H Amenorrhea
H Painless swelling of the salivary glands
H Unusual swelling of cheeks or jaw area
H Hoarseness
H Throat irritation or lacerations
H Calluses of the knuckles or abrasions and scars on
the dorsum of the hand
Special populations
Bulimia has been found to begin in adolescence or
early adulthood.
H Strongly associated with depression
H Can occur simultaneously with anorexia nervosa
H More prone to psychoactive substance abuse
H Hyperactivity
H Peculiar eating habits or rituals
H Frequent weighing
H Perceived by others as a perfect student, mother,
or career woman
140
Bulimia nervosa
DSM-IV-TR criteria
Diagnosis of bulimia nervosa can be confirmed when
these criteria are met, on average, twice per week for
3 months:
H recurrent episodes of binge eating
H repeated inappropriate behaviors to prevent weight
gain.
Test results
Laboratory
H Serum electrolyte studies show elevated bicarbonate,
decreased potassium, and decreased sodium levels.
Other
H The Beck Depression Inventory may identify coexisting depression.
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Treatment
General
H Inpatient or outpatient psychotherapy
H Self-help groups
H Drug rehabilitation
H Balanced diet
H Monitoring of eating pattern
H Monitoring of activity
Medications
H Antidepressant such as fluoxetine
Key outcomes
The patient will:
H acknowledge change in body image
H participate in decision-making about her case
H achieve expected state of wellness.
H Supervise mealtime and for a specified period after
meals, usually up to 1 hour.

H Set a time limit for each meal.
H Provide a pleasant, relaxed environment for eating.
H Use behavior modification techniques.
H Establish a food contract, specifying the amount and
type of food to be eaten at each meal.

Monitoring
H Suicide potential
H Elimination patterns
H Eating patterns
H Complications
H Activity
Patient teaching
Be sure to cover:
H importance of keeping a food journal
H risks of laxative, emetic, and diuretic abuse
H assertiveness training
adverse effects.
Discharge planning
H Refer the patient to support services or specialized
inpatient care.
Bulimia nervosa
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Burns
Overview
Description
H Heat or chemical injury to tissue
H May be permanently disfiguring and incapacitating
H May be partial thickness or full thickness
Pathophysiology
Superficial, partial-thickness burns
H These burns cause localized injury to the epidermis
that isnt life-threatening.
Deep, partial-thickness burns
H These burns cause destruction of the epidermis and
some dermis resulting in thin-walled and fluid-filled
blisters.
H Nerve endings are exposed to air as blisters break.
H Pain develops when blisters are exposed to air.
H Barrier function of the skin is lost.
Full-thickness burns
H These burns affect every body system and organ and
extend into the subcutaneous tissue layer damaging
muscle, bone, and interstitial tissues.
H Interstitial fluids result in edema and an immediate
immunologic response occurs.
H These burns carry a threat of wound sepsis.
H Depending on the level of nerve damage, the patient
may have no pain.
Causes
H Residential fires
H Motor vehicle accidents
H Improper use or handling of matches
H Improperly stored gasoline
H Space heater or electrical malfunctions
H Improper handling of firecrackers
H Scalding accidents
H Child or elder abuse
H Contact, ingestion, inhalation, or injection of acids,
alkali, or vesicants
H Contact with faulty electrical wiring
H Contact with high-voltage power lines
H Chewing electric cords
H Friction or abrasion
H Sun exposure
Incidence
H Affects more than 2 million people each year
H 70,000 hospitalizations
H 20,000 specialized burn unit admissions
Superficial, partial-thickness burns
H Localized pain
H Erythema
H Blanching
H Chills
H Headache
142
Burns
Deep, partial-thickness burns

H Thin-walled, fluid-filled blisters
H Mild to moderate pain
H White, waxy appearance of damaged area
Full-thickness burns
H Pale, white, brown, or black leathery tissue
H Visible thrombosed vessels
H No blister formation
H Painless
Electrical burns
H Silver-colored, raised area at contact site
H Smoke inhalation and pulmonary damage
H Singed nasal hair
Mucosal burns
H Sores in mouth or nose
H Voice changes
H Coughing, wheezing
H Darkened sputum
Complications
H Respiratory complications
H Sepsis
H Hypovolemic shock
H Anemia
H Malnutrition
H Multiple organ dysfunction syndrome
Assessment
History
H Cause of the burn revealed
H Preexisting medical conditions
Physical findings
H Depth and size of the burn assessed
H Severity of the burn estimated
H Major more than 10% of the patients body sur-
face area (BSA); more than 20% of a childs BSA

H Moderate 3% to 10% of a patients BSA; 10% to
20% of a childs BSA

H Minor less than 3% of a patients BSA; less than
10% of a childs BSA

H Respiratory distress and cyanosis
H Edema
H Alteration in pulse rate, strength, and regularity
H Stridor, wheezing, crackles, and rhonchi
H S3 or S4
H Hypotension
Test results
Laboratory
H Arterial blood gas levels show hypoxia.
H Complete blood count shows decreased hemoglobin
level and hematocrit, if blood loss has occurred.
H Electrolyte levels are abnormal due to fluid losses
and shifts.
H Blood urea nitrogen levels are increased with fluid
losses.
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H Glucose level is decreased in children due to limited
glycogen storage.
H Urinalysis shows myoglobinuria and hemoglobinuria.
H Carboxyhemoglobin level is increased.
H Electrocardiography may show myocardial ischemia,
injury, or arrhythmias, especially in electrical burns.
H Fiber-optic bronchoscopy may show airway edema.
Treatment
General
H Burn source cessation
H Airway secured
H Hypoxia prevention
H Giving I.V. fluids through a large-bore I.V. line
Adult: maintain urine output of 30 to 50 ml/hour.

Child less than 66 lb (30 kg): maintain urine output of 1 ml/kg/hour.
H Nasogastric tube and urinary catheter insertion
H Wound care
H Nothing by mouth until severity of burn established,
then high-protein, high-calorie diet
H Increased hydration with high-calorie, high-protein
drinks, not free water
H Total parenteral nutrition if unable to take food by
mouth
H Activity limitation based on extent and location of
burn
H Physical therapy
Medications
H Booster of tetanus toxoid
H Analgesic such as morphine
H Antibiotics, such as gentamicin, tobramycin, and
H Remove constricting items.

spirometer use.
H Perform appropriate wound care.
H Weigh the patient daily.
H Perform range-of-motion exercises.
Monitoring
F
T
f
F
E
H Wound healing
H Vital signs
H Respiratory status, including pulse oximetry
H Intake and output
H Hydration and nutritional status
H Pain control
H Cardiac status
S
E
Patient teaching
Be sure to cover:
H the injury, diagnosis, and treatment
adverse effects
H developing a dietary plan
H signs and symptoms of complications.
Discharge planning
H Refer the patient to rehabilitation, if appropriate.
H Refer the patient to psychological counseling, if
needed.
vancomycin
H Antianxiety agent such as lorazepam
Surgery
H Loose tissue and blister debridement
H Escharotomy
H Skin grafting
Key outcomes
The patient will:
H attain the highest degree of mobility
H maintain fluid balance within the acceptable range
H demonstrate effective coping techniques.
H Apply immediate, aggressive burn treatment.
H Use strict sterile technique.
H Remove clothing thats still smoldering; soak first
with normal saline solution if its stuck to patients

skin.
Burns
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Campylobacteriosis
H More common in the summer months
Overview
H Mild or severe diarrhea

H Abdominal cramps
H Malaise
Description
H In humans and animals, intestinal infection caused
Complications
by the Campylobacter organism, a spiral-shaped

bacteria
H Signs and symptoms developing 2 to 5 days after exposure to Campylobacter
H May spread to the bloodstream in persons with compromised immune systems, causing a life-threatening
infection
H Bacteremia
H Severe dehydration and electrolyte disturbances
H Guillain-Barr syndrome
H Reiters syndrome
Pathophysiology
History
H The organism invades and destroys the epithelial
H Exposure to contaminated food or water

H Acute onset of diarrhea
H Recent close contact with a person who has diarrhea
cells of the jejunum, ileum, and colon.

H This produces an increase in motility and secretions
that results in diarrhea.
Causes
H Ingestion of contaminated food or water or unpas-
teurized milk
H Occasionally from infected pets or wild animals
H Contact with an infected persons stool
Risk factors
H Occupational exposure to cattle, sheep, and other
Assessment
Physical findings
H Cramping abdominal pain
H Fever
H Traces of blood in the stool
Test results
Laboratory
H Stool culture identifies Campylobacter.
farm animals
H Laboratory worker
H Homosexual men
Treatment
Incidence
General
H Most common bacterial cause of diarrheal illness in
H Contact precautions (see Contact precautions)

H Correction of fluid and electrolyte imbalances
the United States
Contact precautions
In addition to standard precautions, follow these precautions:
H Place the patient in a private room. If a private room
isnt available, consult with infection control personnel.
As an alternative, he may be placed in a room with a
patient who has an active infection with the same microorganism.
H Wear gloves whenever you enter the patients room. Always change them after contact with infected material.
Remove them before leaving the room. Wash your
hands immediately with an antimicrobial soap, or rub
them with a waterless antiseptic. Then avoid touching
contaminated surfaces.
H Wear a gown when entering the patients room if you
think your clothing will have extensive contact with him
or anything in his room or if he has diarrhea or is incontinent. Remove the gown before leaving the room.
H Limit the patients movement from the room, and
check with infection control personnel whenever he
must leave it.
Medications
H Oral antibiotics, such as doxycycline, minocycline,
and tetracycline
Key outcomes
The patient will:
H regain or maintain normal fluid and electrolyte balance
H have an elimination pattern that returns to normal.
H Follow contact precautions for those with active diar-
rhea.
H Isolate a patient who cant practice good hygiene.
H Replace lost fluids and electrolytes through diet or
I.V. fluids.
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Campylobacteriosis
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Monitoring
H Intake and output
H Vital signs
H Signs of dehydration
H Electrolytes
H Amount and characteristics of stool
H Abdominal status
Patient teaching
Be sure to cover:
H proper hand-washing technique
H proper food-handling practices
H complications and when to notify the physician
H preventive measures.
Campylobacteriosis
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Candidiasis
Overview
Description
H Mild, superficial fungal infection
H Can lead to severe disseminated infections and
fungemia in immunocompromised patient, transplant

recipient, burn patient, low-birth-weight neonate, or
patient on hyperalimentation
H Prognosis variable, depending on patients resistance
H Also known as candidosis and moniliasis
Pathophysiology
H Change in the patients resistance to infection, his im-
munocompromised state, and antibiotic use permit

the sudden proliferation of Candida albicans.
Causes
H Total parenteral nutrition

H Surgery
H Use of antibiotic agents
Incidence
H Affects 14% of immunocompromised patients
H Causative fungi infecting the nails (paronychia), skin
(diaper rash), or mucous membranes, especially the

oropharynx (thrush), vagina (vaginitis), esophagus,
and GI tract (see Identifying thrush)
H Systemic infection predominating among drug
abusers and diabetic and immunosuppressed
patients
Complications
H Dissemination with organ failure of the kidneys,
brain, GI tract, eyes, lungs, and heart
H In most cases, infection with C. albicans or C. tropi-
calis
Risk factors
H Maternal vaginitis present during vaginal delivery
H Preexisting diabetes mellitus, cancer, or immunosup-
pressant illness
H Immunosuppressant drug use
H Radiation
H Aging
H Irritation from dentures
H I.V. or urinary catheterization
H Drug abuse
Identifying thrush
Candidiasis of the oropharyngeal mucosa (thrush) causes
cream-colored or bluish white pseudomembranous patches on the tongue, mouth, or pharynx (as shown). Fungal
invasion may extend to circumoral tissues.
Assessment
History
H Underlying illness
H Recent course of antibiotic or antineoplastic therapy
H Drug abuse
H Hyperalimentation
Physical findings
H Scaly, erythematous, papular rash, possibly covered
with exudate and erupting in breast folds, between

fingers, and at the axillae, groin, and umbilicus
H Red, swollen, darkened nailbeds; occasionally, purulent discharge; possibly nail separation from the
nailbed
H Scales in the mouth and throat
H White or yellow vaginal discharge, with local excoriation; white or gray raised patches on vaginal walls,
with local inflammation
H Cream-colored or bluish white lacelike patches of
exudate on the tongue, mouth, or pharynx revealing
bloody engorgement when scraped
H Hemoptysis, cough; coarse breath sounds in the
infected lung fields
H Flank pain, dysuria, hematuria, cloudy urine with
casts
H Headache, nuchal rigidity, seizures, focal neurologic
deficits
H Blurred vision, orbital or periorbital pain, eye exudate, floating scotomata, and lesions with a white,
cotton-ball appearance seen during ophthalmoscopy
H Chest pain and arrhythmias
H Septic shock
Test results
Laboratory
H Fungal serological panel shows the presence of the
candidal organism.
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Candidiasis
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Treatment
General
H Treatment of predisposing condition
H No dietary restrictions unless oral infection
H With oral infection, spicy food only as tolerated
Medications
H Antifungals, such as amphotericin B, anidulafungin,
clotrimazole, and nystatin
Surgery
H Abscess drainage; surgically or percutaneously
Key outcomes
The patient will:
H express increased comfort
H avoid or have minimal complications
H express understanding of disorder and treatment.
H Follow standard precautions.
H Provide a nonirritating mouthwash to loosen tena-
cious secretions and a soft toothbrush to avoid irritation.

H Observe high-risk patients daily for patchy areas, irritation, sore throat, oral and gingival bleeding, and
other signs of superinfection.
H Assess the patient for underlying systemic causes.
Monitoring
H Vital signs
H Intake and output
H Blood urea nitrogen, serum creatinine, and urine
blood and protein levels

H Potassium levels
Patient teaching
Be sure to cover:
H good oral hygiene practices
H (for a woman in her third trimester of pregnancy)
the need for examination for vaginitis to protect her
neonate from thrush infection at birth.
Candidiasis
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Cardiac tamponade
Overview
Description
H Rapid increase in intrapericardial pressure caused
by fluid accumulation in the pericardial sac

H Impaired diastolic filling of the heart
Pathophysiology
H Progressive accumulation of fluid in the pericardial
sac causes compression of the heart chambers.

H Compression of the heart chambers obstructs blood
flow into the ventricles and reduces the amount of

blood pumped out with each contraction.
H With each contraction, more fluid accumulates,
decreasing cardiac output. (See Understanding
cardiac tamponade.)
Causes
H May be idiopathic
H Effusion in cancer, bacterial infections, tuberculosis
and, rarely, acute rheumatic fever

H Trauma
H Hemorrhage from nontraumatic cause
H Viral, postirradiation, or idiopathic pericarditis
H Acute myocardial infarction
H Chronic renal failure
H Drug reaction
H Connective tissue disorders
H Cardiac catheterization
H Cardiac surgery
Incidence
H Occurs with 2% of penetrating chest traumas
H Systemic hypotension
H Muffled heart sounds
Physical findings
H Vary with volume of fluid and speed of fluid accumu-
lation
H Diaphoresis
H Anxiety and restlessness
H Pallor or cyanosis
H Edema
H Rapid, weak pulses
H Hepatomegaly
H Decreased arterial blood pressure
H Increased central venous pressure
H Pulsus paradoxus
H Narrow pulse pressure
H Muffled heart sounds
Test results
Imaging
H Chest X-rays show slightly widened mediastinum and
enlargement of the cardiac silhouette.
H Electrocardiography may show low voltage complexes in the precordial leads.
H Hemodynamic monitoring shows equalization of
mean right atrial, right ventricular diastolic, pulmonary artery wedge, and left ventricular diastolic pressures.
H Echocardiography may show an echo-free space, indicating fluid accumulation in the pericardial sac.
Treatment
General
H Pericardiocentesis, if necessary
H Bed rest with the head of the bed elevated at least 30
degrees
Medications
H Intravascular volume expansion
H Inotropic agents, such as digoxin, milrinon, and
inamrinone
H Oxygen
Surgery
H Cardiogenic shock
H Death
H Pericardial window
H Subxiphoid pericardiotomy
H Complete pericardectomy
H Thoracotomy
Assessment
History
Key outcomes
H Presence of one or more causes

H Dyspnea
H Chest pain
The patient will:

H not develop arrhythmias
Complications
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Understanding cardiac tamponade

The pericardial sac, which surrounds
and protects the heart, is composed of
several layers. The fibrous pericardium
is the tough outermost membrane; the
inner membrane, called the serous
membrane, consists of the visceral and
parietal layers. The visceral layer clings
to the heart and is also known as the
epicardial layer of the heart. The parietal layer lies between the visceral layer
and the fibrous pericardium. The pericardial space between the visceral
and parietal layers contains 10 to
30 ml of pericardial fluid. This fluid
lubricates the layers and minimizes
friction when the heart contracts.
NORMAL HEART AND PERICARDIUM
Aorta
Superior vena cava
Parietal pericardium
Visceral pericardium
Fibrous pericardium
Pericardial space
Attachment of fibrous
pericardium to diaphragm
Diaphragm
In cardiac tamponade, blood or fluid

fills the pericardial space, compressing
the heart chambers, increasing intracardiac pressure, and obstructing venous
return. As blood flow into the ventricles
falls, so does cardiac output. Without
prompt treatment, low cardiac output
can be fatal.
CARDIAC TAMPONADE
Aorta
Superior vena cava
Fibrous pericardium
Parietal pericardium
Visceral pericardium
Pericardial space filled
with excess fluid
Compressed heart
Diaphragm
H Provide reassurance.
H Assist with pericardiocentesis, if necessary.
H Infuse I.V. solutions, as ordered.
H Administer oxygen therapy, as needed.
H Maintain the chest drainage system, if used.
Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of increasing tamponade
H Cardiovascular status, including cardiac rhythm
H Hemodynamics
H Complications
H Pulse oximetry
Patient teaching
Be sure to cover:
H preoperative and postoperative care
H emergency procedures.
Cardiac tamponade
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Cardiomyopathy, dilated
Overview
Description
H Disease of the heart muscle fibers
H Also called congestive cardiomyopathy
Pathophysiology
H Extensively damaged myocardial muscle fibers re-
duce contractility of left ventricle.

H The hearts pumping ability is reduced.
H As systolic function declines, cardiac output falls.
H The sympathetic nervous system is stimulated to increase heart rate and contractility.
H When compensatory mechanisms can no longer
maintain cardiac output, the heart begins to fail.
(See Understanding dilated cardiomyopathy.)
H Dry cough at night

H Fatigue
H Weight gain
Complications
H Intractable heart failure
H Arrhythmias
H Emboli
Assessment
History
H Possible history of a disorder that can cause cardio-
myopathy
H Gradual onset of shortness of breath, orthopnea,
dyspnea on exertion, paroxysmal nocturnal dyspnea,

fatigue, dry cough at night, palpitations, and vague
chest pain
Causes
Physical findings
H Viral or bacterial infections

H Hypertension
H Peripartum syndrome related to toxemia
H Ischemic heart disease
H Valvular disease
H Drug hypersensitivity
H Chemotherapy
H Cardiotoxic effects of drugs or alcohol
H Peripheral edema
H Ascites
H Peripheral cyanosis
H Tachycardia even at rest and pulsus alternans in late
Incidence
H Most commonly affects middle-aged males but can
occur in any age-group and females
Understanding dilated cardiomyopathy
stages
H Hepatomegaly and splenomegaly
H Narrow pulse pressure
H Irregular rhythms, diffuse apical impulses, pansys-
tolic murmur
H S3 and S4 gallop rhythms
H Pulmonary crackles
ALERT
Dilated cardiomyopathy may need to be differentiated from other types of cardiomyopathy. (See Assessment findings in cardiomyopathies.)
Test results
H Greatly increased chamber size

H Thinning of left ventricular muscle
H Increased atrial chamber size
H Increased myocardial mass
H Normal ventricular inflow resistance
H Decreased contractility
150
Imaging
H Chest X-rays demonstrate moderate to marked cardiomegaly and possible pulmonary edema.
H Echocardiography may reveal ventricular thrombi,
global hypokinesis, and the degrees of left ventricular
dilation and systolic dysfunction.
H Gallium scans may identify patients with dilated cardiomyopathy and myocarditis.
H Cardiac catheterization evaluates heart structure and
function.
H Transvenous endomyocardial biopsy may be useful in
determining underlying disorder in some patients.
H Electrocardiography evaluates ischemic heart disease
and identifies arrhythmias and intraventricular conduction defects.
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Assessment findings in cardiomyopathies

Type
Assessment findings
Dilated cardiomyopathy
Generalized weakness, fatigue

Chest pain, palpitations
Syncope
Tachycardia
Narrow pulse pressure
Pulmonary congestion, pleural effusions
Jugular vein distention, peripheral edema
Paroxysmal nocturnal dyspnea, orthopnea, dyspnea on exertion
Hypertrophic cardiomyopathy
Angina, palpitations
Syncope
Orthopnea, dyspnea on exertion
Pulmonary congestion
Loud systolic murmur
Life-threatening arrhythmias
Sudden cardiac arrest
Restrictive cardiomyopathy
Generalized weakness, fatigue

Bradycardia
Dyspnea
Jugular vein distention, peripheral edema
Liver congestion, abdominal ascites
Treatment
General
H No ingestion of alcohol if cardiomyopathy caused by
alcoholism
H Low-sodium diet supplemented by vitamin therapy
H Rest periods
H develop no complications of excess fluid volume

H recognize and accept limitations of chronic illness
fatigue.
H Administer prescribed medications.
H Alternate periods of rest with required activities of
daily living.
Special populations
A woman of childbearing age with dilated cardiomyopathy should avoid pregnancy.
Medications
H Cardiac glycoside such as digoxin
H Diuretic such as furosemide
benazepril and captopril

H Oxygen
H Anticoagulant such as warfarin
H Vasodilator such as isosorbide
H Antiarrhythmic such as esmolol
H Beta-adrenergic blocker such as metoprolol
Surgery
H Heart transplantation
H Possible cardiomyoplasty
Key outcomes
The patient will:
stability
H Consult with dietitian to provide a low-sodium diet.

H Check serum potassium levels for hypokalemia, es-
pecially if therapy includes a cardiac glycoside.

H Offer support and let the patient express his feelings.
H Allow patient and family to express fears and con-
cerns; help them identify effective coping strategies.
Monitoring
H Cardiac rhythm
H Intake and output
H Daily weights
Patient teaching
Be sure to cover:
H sodium and fluid restrictions
H signs and symptoms of worsening heart failure.
Discharge planning
H Refer family members to community cardiopul-
monary resuscitation classes.
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Cardiomyopathy,
hypertrophic
Overview
Description
H Dyspnea
H Fatigue
Complications
H Heart failure
H Ventricular arrhythmias
H Primary disease of cardiac muscle characterized by
left ventricular hypertrophy

H Also known as idiopathic hypertrophic subaortic
stenosis, hypertrophic obstructive cardiomyopathy, and muscular aortic stenosis
Pathophysiology
H The hypertrophied ventricle becomes stiff, noncom-
pliant, and unable to relax during ventricular filling.

H Ventricular filling time is reduced as compensation
to tachycardia.
H Reduced ventricular filling leads to low cardiac output. (See Understanding hypertrophic cardiomyopathy.)
Causes
Assessment
History
H Generally, no visible clinical features until disease
well advanced
H Atrial fibrillation
H Possible family history of hypertrophic cardiomyop-
athy
H Orthopnea
H Anginal pain
H Fatigue
H Syncope, even at rest
H Transmission by autosomal dominant trait (about
Physical findings
one-half of all cases)

H Associated with hypertension
H Rapidly rising carotid arterial pulse possible

H Pulsus bisferiens
H Double or triple apical impulse, possibly displaced
Incidence
H Affects 5 to 8 people per 100,000 in the United States
H More common in blacks
laterally
H Bibasilar crackles if heart failure present
H Harsh systolic murmur heard after S1 at the apex
near the left sternal border
H Possible S4
Understanding hypertrophic
cardiomyopathy
ALERT
Hypertrophic cardiomyopathy may need to be differentiated from other types of cardiomyopathy.
(See Assessment findings in cardiomyopathies, page
151.)
Test results
H Normal right and decreased left chamber size

H Thickened interventricular septum (hypertrophic
obstructive cardiomyopathy)
H Atrial chamber size increased on left
H Increased myocardial mass
H Increased ventricular inflow resistance
H Increased or decreased contractility
152
Cardiomyopathy, hypertrophic
Imaging
H Chest X-rays may show a mild to moderate increase
in heart size.
H Thallium scan usually reveals myocardial perfusion
defects.
H Angiography reveals a dilated, diffusely hypokinetic
left ventricle.
H Echocardiography shows left ventricular hypertrophy
and a thick, asymmetrical intraventricular septum in
obstructive hypertrophic cardiomyopathy, whereas
hypertrophy affects various ventricular areas in
nonobstructive hypertrophic cardiomyopathy.
H Cardiac catheterization reveals elevated left ventricular end-diastolic pressure and, possibly, mitral insufficiency.
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H Electrocardiography usually shows left ventricular
hypertrophy, ST-segment and T-wave abnormalities,

Q waves in leads II, III, aVF, and in V4 to V6 (because
of hypertrophy, not infarction), left anterior hemiblock, left axis deviation, and ventricular and atrial
arrhythmias.
Treatment
General
H Cardioversion for atrial fibrillation
H Fluid restrictions
H Avoidance of alcohol
H Activity limitations individualized
H Bed rest, if necessary
Medications
H Beta-adrenergic blocker such as propranolol
H Calcium channel blocker such as diltiazam
H Antiarrhythmic such as amiodarone (if atrioventricu-
lar block isnt present)
ALERT
If beta-adrenergic blockers will be discontinued,
dont stop the drug abruptly; doing so may cause
rebound effects, resulting in myocardial infarction
or sudden death.
H Offer support and let the patient express his feelings.
H Allow the patient and his family to express their fears
and concerns and identify effective coping strategies.
Monitoring
H Vital signs
H Cardiac rhythm
H Hemodynamics
H Intake and output
H Respiratory status (amiodarone may cause lung
toxicity)
H Emotional status
Patient teaching
H Antibiotic prophylaxis such as amoxicillin
ALERT
Angiotensin-converting enzyme inhibitors, nitrates, other beta-adrenergic blockers, and digoxin
are contraindicated in hypertrophic cardiomyopathy.
Surgery
H Ventricular myotomy alone or combined with mitral
valve replacement
Key outcomes
Be sure to cover:
H that propranolol can cause depression and the need
to notify the physician if symptoms occur
H instructions to take medication as ordered
H the need to notify any physician caring for the patient
that he shouldnt be given nitroglycerin, digoxin, or
diuretics because they can worsen the obstruction
H the need for antibiotic prophylaxis before dental
work or surgery to prevent infective endocarditis
H warnings against strenuous activity, which may precipitate syncope or sudden death
H the need to avoid Valsalvas maneuver or sudden
position changes.
Discharge planning
H Refer family members to community cardiopulmo-
nary resuscitation classes.
The patient will:

stability
H develop no complications of excess fluid volume
H carry out activities of daily living (ADLs) without excess fatigue or decreased energy
H develop adequate coping mechanisms.
H Alternate periods of rest with required ADLs and
treatments.
H Provide personal care, as needed, to prevent fatigue.
H Provide active or passive range-of-motion exercises.
H Obtain daily weight.
Cardiomyopathy, hypertrophic
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Cardiomyopathy,
restrictive
Overview
H Fatigue
H Dyspnea
H Orthopnea
H Chest pain
H Edema
H Systolic murmurs
Description
Complications
H Disease of the heart muscle fibers resulting in re-
H Heart failure
H Arrhythmias
H Systemic or pulmonary embolization
H Sudden death
strictive filling and reduced diastolic volume of one

or both ventricles
H Irreversible if severe
Pathophysiology
H Stiffness of the ventricle is caused by left ventricular
hypertrophy and endocardial fibrosis and thickening,

thus reducing the ventricles ability to relax and fill
during diastole.
H Failure of the rigid myocardium to contract completely during systole causes decreased cardiac output. (See Understanding restrictive cardiomyopathy.)
Causes
H Idiopathic or associated with other disease (for ex-
ample, amyloidosis or endomyocardial fibrosis)

H Heart transplant
H Mediastinal radiation
H Carcinoid heart disease
Incidence
H Rare; accounts for 5% of all cases of primary heart
disease
H Occurs equally in males and females
Understanding restrictive
cardiomyopathy
Assessment
History
H Fatigue
H Viral infection
H Dyspnea
H Chest pain
Physical findings
H Peripheral edema
H Liver engorgement
H Peripheral cyanosis
H Pallor
H S3 or S4 gallop rhythms (due to heart failure)
H Systolic murmurs
ALERT
Restricted cardiomyopathy may need to be differentiated from other types of cardiomyopathy. (See
Assessment findings in cardiomyopathies, page 151.)
Test results
Laboratory
H Complete blood count reveals eosinophilia.
Imaging
H Chest X-ray may reveal cardiomegaly.
H Echocardiography may reveal left ventricular muscle
mass, normal or reduced left ventricular cavity size,
and decreased systolic function.
H Electrocardiography may reveal low-voltage hypertrophy, arterioventricular conduction defects, and arrhythmias.
H Cardiac catheterization shows reduced systolic function and increased left ventricular end-diastolic pressures.
H Decreased ventricular chamber size

H Increased atrial chamber size
H Normal myocardial mass
H Increased ventricular inflow resistance
H Decreased contractility
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Cardiomyopathy, restrictive
Treatment
General
H Treatment of underlying cause
H Low-sodium diet
H Initially, bed rest, then activity, as tolerated
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Medications
H Angiotensin-converting enzyme inhibitor such as
captopril
H Anticoagulant such as warfarin
H Corticosteroid such as prednisone
Surgery
H Permanent pacemaker
Key outcomes
The patient will:
stability
H express understanding of the disorder
H recognize and accept limitations of chronic illness
H seek support and establish coping mechanisms.
H Provide appropriate diversionary activities for the pa-
tient restricted to prolonged bed rest.
Monitoring
H Cardiac rhythm
H Vital signs
H Intake and output
H Hemodynamics
H Daily weight
Patient teaching
Be sure to cover:
H signs of digoxin toxicity
H importance of recording daily weight and reporting
weight gain of 2 lb (0.9 kg) or more
H dietary restrictions.
Discharge planning
H Refer for psychosocial counseling, as necessary, for
assistance in coping with restricted lifestyle.
Cardiomyopathy, restrictive
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Carpal tunnel syndrome
Pathophysiology
H Space-occupying lesion or direct pressure within the
carpal canal increases pressure on the median nerve,

resulting in compression.
H Compression of the median nerve interrupts normal
function. (See The carpal tunnel.)
Overview
Description
H Compression of the median nerve in the wrist
H Most common nerve entrapment syndrome
H May pose a serious occupational health problem
Causes
H Repetitive wrist motions involving excessive flexion
or extension
The carpal tunnel

The carpal tunnel is clearly visible in this palmar view and
cross section of a right hand. Note the median nerve, flexor tendons of fingers, and blood vessels passing through
the tunnel on their way from the forearm to the hand.
Flexor
tendons
of fingers
Radial nerve
Median nerve
CARPAL
TUNNEL
Ulnar nerve
H Dislocation
H Acute sprain that may damage the median nerve
H Tumors
H Gout
H Amyloidosis
H Edema-producing conditions
Risk factors
H Diabetes
H Pregnancy
H Alcoholism
H Hypothyroidism
H Renal failure
Incidence
H Most common in females ages 30 to 60
H Occurs in people who move their wrists continually
H Weakness, pain, burning, numbness, tingling in the
hand
H Thumb, forefinger, middle finger, and half of fourth
finger affected by paresthesia

H Inability to clench fist
H Atrophic nails
H Dry and shiny skin
Complications
H Tendon inflammation
H Compression
H Neural ischemia
H Permanent nerve damage with loss of movement and
sensation
Assessment
History
H Occupation or hobby requiring strenuous or repeti-
tive use of the hands

H Condition that causes swelling in carpal tunnel struc-
tures
H Weakness, pain, burning, numbness, or tingling that
occurs in one or both hands

Flexor tendons
of fingers
Transverse
carpal ligament
H Paresthesia that worsens at night and in the morning

H Pain that spreads to the forearm and, in severe cases,
as far as the shoulder

H Pain can be relieved by:
shaking hands vigorously

dangling the arms at sides
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Physical findings
H Inability to make a fist
H Fingernails may be atrophied, with surrounding dry,
shiny skin
Test results
Imaging
H Electromyography shows a median nerve motor conduction delay of more than 5 milliseconds.
H Digital electrical stimulation shows median nerve
compression by measuring the length and intensity of
stimulation from the fingers to the median nerve in
the wrist.
Other
H Compression test result supports the diagnosis.
H the prescribed medication regimen

H adverse reactions to drugs
H avoidance of NSAIDs in pregnancy.
Discharge planning
H Refer the patient for occupational counseling if a job
change is necessary.
Treatment
General
H Conservative initially:
Splinting the wrist for 1 to 2 weeks

Possible occupational changes
Correction of any underlying disorder
Medications
H Nonsteroidal anti-inflammatory drug (NSAID) such
as ibuprofen
H Vitamin supplement such as vitamin B complex
Surgery
H Decompression of the nerve
H Neurolysis
Key outcomes
The patient will:
H express feelings of increased comfort and pain relief
H maintain muscle strength
H perform activities of daily living.
H Promote self-care.
Monitoring
H Response to analgesia
H After surgery, vital signs
H Color, sensation, and motion of the affected hand
Patient teaching
Be sure to cover:
H splint application
H hand exercises in warm water
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Cataract
Overview
Description
H Opacity of the lens or lens capsule of the eye
H Common cause of gradual vision loss
H Commonly affects both eyes
H Traumatic cataracts usually unilateral
Pathophysiology
H The clouded lens blocks light shining through the
cornea.
H Images cast onto the retina are blurred.
H A hazy image is interpreted by the brain.
Causes
H Classified according to cause
Senile cataracts
H Chemical changes in lens proteins in elderly patients
Congenital cataracts
H Inborn errors of metabolism
H Maternal rubella infection during the first trimester
H Congenital anomaly
H Genetic causes (usually autosomal dominant)
H Recessive cataracts may be sex-linked
Traumatic cataracts
H Foreign bodies causing aqueous or vitreous humor
to enter lens capsule
Complicated cataracts
H Uveitis
H Glaucoma
H Retinitis pigmentosa
H Retinal detachment
H Diabetes
H Hypoparathyroidism
H Atopic dermatitis
H Ionizing radiation or infrared rays
Toxic cataracts
H Drug or chemical toxicity:
ergot
dinitrophenol
naphthalene
phenothiazines
Incidence
H Most prevalent in people older than age 70
H Painless, gradual vision loss
H Glare
H Milky white pupil
Complications
H Hyphema
H Pupillary block glaucoma
H Infection
Assessment
History
H Painless, gradual vision loss
H Blinding glare from headlights with night driving
H Poor reading vision
H Annoying glare
H Poor vision in bright sunlight
H Better vision in dim light than in bright light (central
opacity)
Physical findings
H Milky white pupil on inspection with a penlight
H Grayish white area behind the pupil (advanced
cataract)
H Red reflex lost (mature cataract)
Test results
H Indirect ophthalmoscopy reveals a dark area in the
normally homogeneous red reflex.
H Slit-lamp examination confirms lens opacity.
H Visual acuity test establishes the degree of vision loss.
Treatment
General
H Before surgery, eyeglasses and contact lenses that
may help to improve vision

H Sunglasses in bright light and lamps that provide re-
flected lighting rather than direct lighting, decreasing

glare and aiding vision
H Restricted activity according to vision loss
Medications
For cataract removal
H Nonsteroidal anti-inflammatory drugs, such as
ketorolac and bromfenac
Surgery
H Lens extraction and implantation of intraocular lens
(see Comparing methods of cataract removal)

H Extracapsular cataract extraction
H Intracapsular cataract extraction
H Phacoemulsification
H Complete vision loss
Key outcomes
Possible complications of surgery

H Loss of vitreous
H Wound dehiscence
The patient will:

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Cataract
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Comparing methods of cataract removal

Cataracts can be removed by intracapsular or extracapsular techniques.
Intracapsular cataract extraction
Lens
Cryoprobe
In this technique, the surgeon makes a partial incision at

the superior limbus arc. He then removes the lens using
specially designed forceps or a cryoprobe, which freezes
and adheres to the lens to facilitate its removal.
Cornea
Extracapsular cataract extraction

In this technique, the surgeon may use irrigation and aspiration or phacoemulsification. In the former approach, the surgeon makes an incision at the limbus, opens the anterior lens capsule with a cystotome, and exerts pressure from below
to express the lens. He then irrigates and suctions the remaining lens cortex.
In phacoemulsification, he uses an ultrasonic probe to break the lens into minute particles, which are aspirated by the
probe.
PHACOEMULSIFICATION
IRRIGATION AND ASPIRATION

Cortical and nuclear cataract
material aspirated through
needle
Nucleus and cortex fragmented

and aspirated by probe
Cystotome
Lens
Ultrasonic probe
Lens
H voice feelings and concerns

H regain visual function.
H Perform routine postoperative care.
H Assist with early ambulation.
H Apply an eye shield or eye patch postoperatively, as
ordered.
Monitoring
H Vital signs
H Visual acuity
H Complications of surgery
Patient teaching
Be sure to cover:
H the need to avoid activities that increase intraocular
pressure, such as straining with coughing, bowel
movements, or lifting
H the need to abstain from sexual intercourse until the
patient receives physicians approval
H proper instillation of ophthalmic ointment or drops.
ALERT
If the patient has increased eye discharge, sharp
eye pain thats unrelieved by analgesics, or deterioration in vision, instruct him to notify his physician immediately.
Cataract
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Celiac disease
Overview
Description
H A multisystem intestinal intramucosal enzyme defect
H Characterized by poor food absorption and inability
to digest gluten, a protein found in wheat and wheat

products, rye, barley and, possibly, oats
H Also known as idiopathic steatorrhea, nontropical
sprue, gluten enteropathy, celiac sprue
Pathophysiology
H A toxic reaction in response to the ingestion of gluten
causes damage to the small intestines mucosal surface.

H Villi in the small intestine atrophy.
H Activity and amount of enzymes in the surface of the
epithelium decrease.
H Interference with nutrient absorption results.
Causes
H Exact mechanism unknown
H Environmental factors
H Genetic predisposition (associated with a group of
genes on chromosome 6)
H May be autoimmune in nature
H Strongly associated with two human leukocyte antigen haplotypes, DR3 and DQw2
H Can appear at any time in a persons life
H Triggers include surgery, infection, severe emotional
stress, and childbirth
Risk factors
H Family history
Incidence
H Affects 1 in every 133 persons in United States
H Affects twice as many females as males
H Primarily affects whites and those of European ances-
try
H Commonly associated with type 1 diabetes mellitus,
lactose intolerance, thyroid disease, Down syndrome,

liver disease, and autoimmune disorders, such as
rheumatoid arthritis and systemic lupus erythematosus
H Varying significantly from person to person
H Some people asymptomatic
Complications
Prognosis usually good with treatment compliance
Without treatment:
H Anemia
H Central and peripheral nervous system disorders
H Intestinal lymphomas
H Neurologic changes
H Osteoporosis or osteopenia
160
Celiac disease
H Pancreatic insufficiency
H Skin disorders (dermatitis herpetiformis)
H Unexplained infertility or miscarriage
H Vitamin K deficiency with risk of hemorrhage
H Vitamin and mineral deficiencies
Assessment
History
H GI symptoms, including chronic diarrhea or consti-
pation (or both) and recurrent attacks of steatorrhea

(pale, foul-smelling, or fatty stool)
H Abdominal pain
H Anorexia or increased appetite without weight gain
H Fatigue
H Bone or joint pain (especially in lower back, rib
cage, and pelvis)
H Muscle cramps
H Mood changes and irritability
H Tingling or numbness in the legs
H Seizures
H Amenorrhea
H Itchy skin rash
Physical findings
H Abdominal distention
H Muscle wasting
H Compression fractures
H Unexplained short stature
H Peripheral neuropathy
H Dry skin, eczema, psoriasis, dermatitis herpetiformis,
or acne rosacea
H Generalized fine, sparse, prematurely gray hair
H Brittle nails
H Localized hyperpigmentation on the face, lips, and
mucosa
H Pale sores inside the mouth, called aphthous ulcers
H Tooth discoloration or loss of enamel
Special populations
Infants, toddlers, and children are commonly
found to have delayed growth, failure to thrive,
rickets, vomiting, a bloated abdomen, and behavioral changes.
Test results
Laboratory
H Alkaline phosphatase level is elevated possibly due to
bone loss.
H Cholesterol, albumen, and serum carotene levels are
decreased and may reflect malabsorption and malnutrition.
H Unexplained decrease in hemoglobin level and
hematocrit is noted; white blood cell and platelet
counts are reduced.
H Liver enzyme levels are mildly elevated.
H Prothrombin time is decreased.
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H Antibody blood testscombined are sensitive and
specific indicator.
Patient teaching
H Total serum immunoglobulin A (IgA), IgA anti-
endomysium antibodies (AEA), anti-tissue transglutaminase (tTGA), and antigliadin (IgA and IgG) levels
are elevated.
H Small-bowel biopsy specimens obtained by esophagogastroduodenoscopy show histologic changes that
confirm the diagnosis.
Treatment
General
Be sure to cover:
H the reasons for not beginning a gluten-free diet before a diagnosis is made
H foods that are allowed on a gluten-free diet
H food product labels and how to identify ingredients
that may contain hidden gluten
H that gluten may be used as a binder in some medications and vitamins as well as stamp and envelope adhesives
H importance of contacting a dietitian
H testing of family members.
H Life-long gluten-free dietfull return to normal in
months or may never occur

H Eliminate all wheat, barley, rye, and oat products as
well as foods made from these grains, such as breads

and baked goods
Medications
H Corticosteroids for short-term use
H Supportive treatment with vitamin B12, iron, folic
acid, and vitamin K
Key outcomes
The patient will:
H express understanding of the disease and treatment
regimen
H consume an adequate number of calories daily
H develop a normal bowel elimination pattern
H demonstrate adaptive coping behaviors.
H Assess the patients acceptance and understanding of
the disease and treatment regimen.

H Observe the patients nutritional status and progress
by daily calorie counts and weight checks.

H Assess the patients pain and administer pain medica-
tion as ordered.
H Provide fluid replacement as ordered, and observe
for signs and symptoms of dehydration and electrolyte imbalance.

H Encourage the patient to use support systems to assist with coping.
Monitoring
H Signs and symptoms of complications
H Compliance with dietary restrictions
H Frequency and characteristics of stools
Celiac disease
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Cellulitis
Overview
Description
H Acute infection of the dermis and subcutaneous tis-
Complications
H Sepsis
H Deep vein thrombosis (DVT)
H Progression of cellulitis
H Local abscesses
H Thrombophlebitis
H Lymphangitis
H Amputation
sue causing inflammation of the cells

H May follow damage to the skin, such as a bite or
wound
H Prognosis usually good with timely treatment
H With other comorbidities, such as diabetes, in-
creased risk of developing or spreading cellulitis
Pathophysiology
H A break in skin integrity almost always precedes in-
fection.
H As the offending organism invades the compromised
area, it overwhelms the defensive cells, including the

neutrophils, eosinophils, basophils, and mast cells,
that normally contain and localize the inflammation.
H As cellulitis progresses, the organism invades tissue
around the initial wound site.
Causes
H Bacterial infections, usually by Staphylococcus au-
reus and group A beta-hemolytic streptococci

H Fungal infections
H Extension of a skin wound or ulcer
H Furuncles or carbuncles
Risk factors
H Venous and lymphatic compromise
H Edema
H Diabetes mellitus
H Underlying skin lesion
H Prior trauma
Special populations
Cellulitis of the lower extremity is more likely to
develop into thrombophlebitis in an elderly patient.
Incidence
H Occurs most commonly in the lower extremities
Special populations
Perianal cellulitis occurs more commonly in children, especially boys.
Assessment
History
H Presence of one or more risk factors
H Tenderness
H Pain at the site and possibly surrounding area
H Erythema and warmth
H Edema
H Possible fever, chills, malaise
Physical findings
H Erythema with indistinct margins
H Fever
H Warmth and tenderness of the skin
H Regional lymph node enlargement and tenderness
H Red streaking visible in skin proximal to area of cel-
lulitis
Test results
Laboratory
H White blood cell count shows mild leukocytosis.
H Erythrocyte sedimentation rate shows mild elevation.
H Culture and Gram stain may show the causative
organism.
Treatment
General
H Immobilization and elevation of the affected
extremity
H Moist heat
H Bed rest, with the head of bed elevated at least
30 degrees, possibly necessary in severe infection
Medications
H Antibiotics, such as cefuroxime and cephalexin
H Topical antifungal such as mupirocin
H Analgesics, such as ibuprofen and acetaminophen
Surgery
H Tracheostomy possibly needed for severe cellulitis of
head and neck
H Tenderness
H Pain
H Erythema
H Warmth
H Edema
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Cellulitis
H Possible abscess drainage

H Amputation (with gas-forming cellulitis [gangrene])
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Key outcomes
The patient will:
H avoid injury
H verbalize feelings and concerns.
H Elevate affected extremity.
H Apply moist heat, as ordered.
H Encourage a well-balanced diet.
H Encourage verbalization of feelings and concerns.
H Institute safety precautions.
H Institute contact precautions if a draining wound is
present.
Monitoring
H Vital signs
H Pain control
H Edema
H Complications
H Cellulitis progression
Patient teaching
Be sure to cover:
H use of warm compresses
H prevention of injury and trauma
H infection control
H signs and symptoms of DVT.
Discharge planning
H Refer the patient for management of diabetes melli-
tus, as indicated.
Cellulitis
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Cerebral contusion
Overview
Description
H Ecchymosis of brain tissue resulting from injury to
the head
Pathophysiology
H Trauma to the head causes tearing or twisting of the
structures and blood vessels of the brain.

H Scattered hemorrhages form over the surface.
H Functional disruption occurs and may be prolonged.
Causes
Test results
Imaging
H Computed tomography scan shows contusion.
Treatment
General
H Establishment of a patent airway
H Administration of oxygen as needed
H Administration of I.V. fluids
H Minimization of environmental stimuli
H Activity based on neurologic status
H Initially, bed rest with the head of bed elevated at
least 30 degrees
H Avoidance of contact sports
H Acceleration-deceleration or coup-contrecoup
Medications
injuries
H Head trauma
H Analgesics, such as codeine and acetaminophen
Risk factors
H Craniotomy
Surgery
H Unsteady gait
H Participation in contact sports
H Receiving anticoagulant therapy
Incidence
Key outcomes
H Occurs at any age
The patient will:

H use support systems to assist with coping
H maintain a stable neurologic state
H express feelings of comfort and pain relief
H Change in level of consciousness
H Hypertension
H Dizziness
H Headache
H Pupil changes
H Hemiparesis
H Memory loss or forgetfulness
H Seizure
H Perform neurologic examinations.
H Give prescribed drugs (no aspirin).
H Protect from injury.
Complications
Monitoring
H Intracranial hemorrhage
H Hematoma
H Tentorial herniation
H Increased intracranial pressure (see What happens
H Vital signs
H Neurologic and respiratory status
H Check for cerebrospinal fluid (CSF) leakage
H Pain control
with increased ICP)
Assessment
History
H Head injury or motor vehicle accident
H Loss of consciousness
Physical findings
H Unconscious patient: pale and motionless; altered
vital signs
H Conscious patient: drowsy or easily disturbed
H Scalp wound
H Possible involuntary evacuation of bowel and bladder
H Hemiparesis
164
Cerebral contusion
Patient teaching
Be sure to cover:
H the need to avoid coughing, sneezing, or blowing the
nose until after recovery
H observation for CSF drainage
H how to detect and report mental status changes
H signs and symptoms of infection.
Discharge planning
H Refer the patient to a neurologist for follow-up, as
indicated.
H Refer the patient for rehabilitation, as needed.
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What happens with increased ICP

Intracranial pressure (ICP) is the pressure exerted within the intact skull by the intracranial volume, which is comprised of
about 10% blood, 10% cerebrospinal fluid (CSF), and 80% brain tissue. The rigid skull allows very little space for expansion
of these substances. When ICP increases to pathologic levels, brain damage can result.
The brain compensates for increases in ICP by regulating the volumes of the three substances in the following ways:
H limiting blood flow to the head
H displacing CSF into the spinal canal
H increasing absorption or decreasing production of CSF withdrawing water from brain tissue into the blood and excreting it through the kidneys.
When compensatory mechanisms become overworked, small changes in volume lead to large changes in pressure.
Brain insult
Trauma (contusion, laceration, intracranial hemorrhage)
Cerebral edema (following surgery, stroke, infection, hypoxia)
Hydrocephalus
Space-occupying lesion (tumor, abscess)
Slight increase in ICP
Attempt at normal regulation of ICP by decreased blood flow to head
Slight decrease in cerebral perfusion pressure (CPP)
Loss of autoregulatory mechanism of constriction or dilation

of cerebral blood vessels if increased ICP persists
Passive dilation
Increased cerebral blood flow; venous congestion
Further increase in ICP
Cellular hypoxia
Uncal or central herniation
Further decrease in CPP
BRAIN DEATH
Cerebral contusion
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Cerebral palsy
H Poisoning
H Any condition resulting in cerebral thrombus or em-
bolus
Overview
Description
H Most common crippling neuromuscular disease in
children
H Comprises several neuromuscular disorders
H Results from prenatal, perinatal, or postnatal central
nervous system (CNS) damage

H Three types (sometimes occur in mixed forms):
spastic (affecting about 70% of children with cerebral palsy)
athetoid (affecting about 20%)
ataxic (affecting about 10%)
H Motor impairment may be minimal or severely disabling
H Associated defects:
seizures
speech disorders
mental retardation
H Prognosis varies
Pathophysiology
H A lesion or an abnormality occurs in the early stages
of brain development.
H Structural and functional defects occur, impairing
Incidence
H Highest in premature neonates and in those who are
small for gestational age

H Slightly more common in boys than in girls
H More common in whites
H Excessive lethargy or irritability
H High-pitched cry
H Poor head control
H Weak sucking reflex
H Delayed motor development
H Abnormal head circumference
H Abnormal postures
H Abnormal reflexes
H Abnormal muscle tone and performance
Complications
H Seizure disorders
H Speech, vision, and hearing problems
H Language and perceptual deficits
H Mental retardation (in up to 40% of patients)
H Dental problems
H Respiratory difficulties
H Poor swallowing and gag reflexes
motor or cognitive function.

H Defects may not be distinguishable until months after
birth.
Assessment
Causes
History
H Conditions that result in cerebral anoxia, hemor-
H Maternal or patient history revealing possible cause
rhage, or other CNS damage

Prenatal causes
H Rh factor incompatibility
H ABO blood type incompatibility
H Maternal infection (especially rubella in the first
trimester)
H Maternal diabetes
H Irradiation
H Anoxia
H Toxemia
H Malnutrition
H Abnormal placental attachment
H Isoimmunization
Parturition causes
H Trauma during delivery
H Depressed maternal vital signs from general or spinal
anesthesia
H Asphyxia from the cord wrapping around the neck
H Prematurity
H Prolonged or unusually rapid labor
H Multiple births (neonates born last in a multiple
birth have an especially high rate of cerebral palsy)
Postnatal causes
H Infections, such as meningitis and encephalitis
H Head trauma
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Cerebral palsy
(see When to suspect cerebral palsy)
Physical findings
H Child with retarded growth and development
H Difficulty chewing and swallowing
Spastic cerebral palsy

H Underdevelopment of affected limbs
H Characteristic scissors gait
H Walks on toes
H Crosses one foot in front of the other
H Hyperactive deep tendon reflexes
H Increased stretch reflexes
H Rapid alternating muscle contraction and relaxation
H Muscle weakness
H Impaired fine and gross motor skills
H Contractures in response to manipulation of muscles
Athetoid cerebral palsy
H Involuntary movements
H Grimacing
H Wormlike writhing
H Dystonia
H Sharp jerks that impair voluntary movement
H Involuntary facial movements (speech difficult)
H Drooling
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Ataxic cerebral palsy

H Lack of leg movement during infancy
H Wide gait when child begins to walk
H Disturbed balance
H Incoordination (especially of the arms)
H Hypoactive reflexes
H Nystagmus
H Muscle weakness
H Tremors
Test results
Imaging
H Computed tomography scan and magnetic resonance
imaging of the brain may show structural abnormalities of the brain such as cerebral atrophy.
H EEG may show the source of seizure activity.
When to suspect cerebral palsy

Early detection of cerebral palsy is essential for effective
treatment and requires careful clinical observation during
infancy and precise neurologic assessment. Suspect cerebral palsy whenever a neonate:
H has difficulty sucking or keeping the nipple or food in
his mouth
H seldom moves voluntarily or has arm or leg tremors
with voluntary movement
H crosses his legs when lifted from behind rather than
pulling them up or bicycling like a normal neonate
H has legs that are hard to separate, making diaper
changing difficult
H persistently uses only one hand or, as he gets older,
uses his hands well but not his legs.
Treatment
H Provide a safe physical environment.

General
Monitoring
H Braces or splints
H Special appliances, such as adapted eating utensils
H Pain control
H Seizure activity
H Speech
H Visual and auditory acuity
H Swallowing function
H Neurologic status
H Skin integrity
H Motor development
H Muscle strength
and low toilet seat with arms

H Range-of-motion (ROM) exercises
H Prescribed exercises to maintain muscle tone
Medications
H Anticonvulsant such as phenytoin
H Muscle relaxant such as dantrolene
H Antianxiety agent such as lorazepam
Surgery
H Orthopedic surgery
H Neurosurgery
Patient teaching
Be sure to cover:
H the prescribed medication regimen
H adverse drug reactions
H daily skin inspection and massage
H the need to place food far back in patients mouth to
facilitate swallowing
H the need to chew food thoroughly
H drinking through a straw
H sucking lollipops to develop muscle control
H proper nutrition
H opportunities for learning, such as summer camps or
Special Olympics
H correct use of assistive devices.
Key outcomes
The patient will:
H consume calorie requirements daily
H develop adequate coping mechanisms
H develop effective communication skills.
H Speak slowly and distinctly.
H Give all care in an unhurried manner.
H Allow participation in care decisions.
H Provide a diet with adequate calories. Stroking the
throat may aid swallowing.

H Provide frequent mouth and dental care.
H Perform prescribed exercises to maintain muscle
tone.
H Care for associated hearing and vision disturbances,
as necessary.
H Postoperatively, give analgesics, as ordered.
Discharge planning
H Refer family members to community support groups
such as the local chapter of the United Cerebral Palsy

Association.
Cerebral palsy
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Cervical cancer
Incidence
H Typically occurs between ages 30 and 45; rarely,
before age 20
Overview
Description
H Proliferation of cancer cells in the cervix
H Third most common cancer of the female reproduc-
tive system
H Classified as either preinvasive (curable in 75% to
90% of patients with early detection and proper
treatment) or invasive
Pathophysiology
Preinvasive cancer
H Preinvasive cancer ranges from minimal cervical dysplasia, in which the lower third of the epithelium
contains abnormal cells, to carcinoma in situ, in
which the full thickness of the epithelium contains
abnormally proliferating cells.
Invasive cancer
H Cancer cells penetrate the basement membrane and
can spread directly to contiguous pelvic structures or
disseminate to distant sites by way of lymphatic
routes.
H Most (95%) cases are squamous cell carcinoma; 5%
of cases are adenocarcinomas.
H Abnormal vaginal bleeding
Complications
H Renal failure
H Vaginal stenosis
H Ureterovaginal or vesicovaginal fistula
H Proctitis
H Cystitis
H Bowel obstruction
Assessment
History
H One or more risk factors present
Preinvasive cancer
H No symptoms or other clinical changes
Invasive cancer
H Abnormal vaginal bleeding or discharge
H Gradually increasing flank pain
Physical findings
H Unknown
H Vaginal discharge
H Postcoital bleeding
H Irregular bleeding
Risk factors
Test results
H Frequent intercourse at a young age (younger than
Imaging
H Lymphangiography can show metastasis.
H Cystography can show metastasis.
H Organ and bone scans can show metastasis.
H Papanicolaou (Pap) test shows abnormal cells, and
colposcopy shows the source of the abnormal cells
seen on the Pap test. (See Testing for cervical cancer.)
H Cone or punch biopsy is performed if endocervical
curettage is positive.
H Vira Pap test permits examination of the specimens
deoxyribonucleic acid structure to detect HPV.
Causes
age 16)
H Multiple sexual partners
H Multiple pregnancies
H Human papillomavirus (HPV) infection
H Bacterial or viral venereal infections
H Exposure to diethylstilbestrol in utero
H Human immunodeficiency virus
H Smoking (see Preventing cervical cancer)
Prevention
Preventing cervical cancer

Cervical cancer can be prevented by following these
guidelines:
H Delay sexual intercourse.
H Limit the number of sexual partners.
H Avoid sexual activity with people who have had many
other sexual partners.
H Use barrier protection.
H Dont smoke.
H Receive the human papilloma virus vaccine.
168
Cervical cancer
Treatment
General
H Accurate clinical staging used to determine type of
treatment
H Well-balanced diet, as tolerated
Medications
H Chemotherapy, such as bleomycin, cisplatin, ifos-
famide, and topotecan
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Testing for cervical cancer

To analyze cervical cells, the ThinPrep may be collected in
the same manner as a Papanicolaou (Pap) test using a cytobrush and plastic spatula. The specimens are deposited in
a bottle provided with a fixative and sent to the laboratory.
A filter is then inserted into the bottle and excess mucus,
blood, and inflammatory cells are filtered out by centrifuge.
Remaining cells are then placed on a slide in a uniform, thin
layer and read as a Pap test. This causes fewer slides to be
classified as unreadable, significantly reducing the incidence
of false negatives and the need for repeat tests.
When the ThinPrep test is used, screening can also be
easily done for the human papillomavirus (HPV), of which
certain strains have been identified as the primary cause of
cervical cancer. The Digene hc2 HPV deoxyribonucleic acid
(DNA) test has been approved by the Food and Drug Administration to determine if those identified as high risk for developing cervical cancer have been exposed to HPV. The
Surgery
Preinvasive lesions
H Total excisional biopsy
H Cryosurgery
H Laser destruction
H Conization, followed by frequent Pap test follow-ups
H Hysterectomy (rare)
Invasive squamous cell carcinoma
H Radical hysterectomy and radiation therapy (internal,
external, or both)
H Pelvic exenteration (rare; may be performed for recurrent cervical cancer)
specimen is collected as a Pap smear but is dispersed with

ThinPrep solution. Separate aliquots are used for each test,
from brushings of the endocervix. The brush is then inserted
into the specialized tube and snapped off at the shaft, capping securely. The target solution in the tube disrupts the
virus and releases target DNA, which combines with specific
ribonucleic acid (RNA) probes creating RNA:DNA hybrids.
The hybrids are captured, bound, and able to be magnified
and measured using a luminometer.
If a patient is positive for HPV, it means she had been infected with the virus. Depending on the type of HPV found
through DNA testing, those harboring high-risk HPV strains
have a high risk of developing cervical cancer. These patients should have a colposcopy in which the cervix is
viewed under microscope and a biopsy taken from the tissue
sample.
Patient teaching
Be sure to cover:
H the disease process, diagnosis, and treatment
H how treatment wont radically alter the patients
lifestyle or prohibit sexual intimacy
adverse effects.
Discharge planning
Key outcomes
The patient will:
H express increased comfort and decreased pain
H express feelings and perceptions about changes in
sexual activity
H experience no signs or symptoms of infection
H use support systems and develop coping strategies.
Monitoring
H Vital signs
H Complications
H Pain control
H Vaginal discharge
H Renal status
Cervical cancer
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Chalazion
H Infection
H Vision disturbance
Overview
Assessment
Description
History
H Painless, slowly growing nodule on the eyelid

H Common disorder of the sebaceous gland in the
H Nodule on eyelid
H Rosacea or blepharitis
eyelid
H May become large enough to press on the eyeball,
Physical findings
producing astigmatism
H May be chronic
H Palpable small lump in the eyelid

H Red, elevated area on the conjunctival surface (see
Pathophysiology
Recognizing chalazion)
H Granulomatous inflammation in the upper or lower
Test results
eyelid is the result of an obstruction of the meibomian (sebaceous) gland duct.

H Edema is usually contained on the conjunctival portion of the eyelid.
Other
H Visual examination and palpation of the eyelid
reveals chalazion.
H Biopsy rules out meibomian cancer.
Causes
H Rosacea
H Chronic blepharitis
H Seborrhea
H Meibomian cancer
Treatment
General
H Warm compresses to the affected eyelid
Incidence
Medications
H Higher incidence in fair-skinned males than in other
H Antibiotic such as sulfacetamide

groups, possibly because of that groups higher incidence of rosacea and blepharitis
H More common in adults ages 30 to 50
Surgery
H Incision and curettage of the chalazion under local
anesthetic (possibly)
H Painless, hard lump that usually points toward the
conjunctival side of the eyelid
Complications
H Cosmetic deformity
H Bleeding after surgery
Recognizing chalazion
A chalazion is a nontender granulomatous inflammation of
a meibomian gland on the upper or lower eyelid.
Key outcomes
The patient will:
H report improvement of condition of eyelid
H maintain positive outlook regarding body image
H remain free from signs of bleeding or infection.
H Apply warm compress after surgery.
H Apply eye patch to the affected eye for 24 hours. (See
Applying an eye patch.)

H Instill eyedrops, as ordered.
Monitoring
H Bleeding (after surgery)
Patient teaching
Be sure to cover:
H proper instillation of eyedrops
H reporting recurrence.
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Chalazion
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Applying an eye patch

You may apply an eye patch for various reasons: to protect the eye after injury or surgery, to prevent accidental damage to
an anesthetized eye, to promote healing, to absorb secretions, to protect the eye from drying when the patient is comatose
or unable to close the eye as in Bells palsy, or to prevent the patient from touching or rubbing his eye.
A thicker patch, called a pressure patch, may be used to help corneal abrasions heal, compress postoperative edema, or
control hemorrhage from traumatic injury. Application requires an ophthalmologists prescription and supervision.
To apply a patch, choose a gauze pad of appropriate size
for the patients face, place it gently over the closed eye (as
shown), and secure it with two or three strips of tape. Extend the tape from midforehead across the eye to below
the earlobe.
A pressure patch, which is markedly thicker than a singlethickness gauze patch, exerts extra tension against the
closed eye. After placing the initial gauze pad, build it up
with additional gauze pieces. Tape it firmly so that the
patch exerts even pressure against the closed eye (as
shown).
For increased protection of an injured eye, place a plastic

or metal shield (as shown) on top of the gauze pads and
apply tape over the shield.
Occasionally, you may use a head dressing to secure a
pressure patch. The dressing applies additional pressure
or, in burn patients, holds the patch in place without tape.
ALERT
Tell the patient to start applying warm compresses
at the first sign of lid irritation to increase the
blood supply and keep the lumen open.
Discharge planning
H Encourage follow-up care, as ordered.
Chalazion
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Chancroid

H Occurs at any age but is most common among young,
sexually active people
Overview
Description
H Multiple papules that ulcerate

H Lesions possibly healing spontaneously and usually
H Sexually transmitted disease

H Characterized by painful genital ulcers and inguinal
adenitis
H Common cause of genital ulcers in patients in devel-
oping countries
Pathophysiology
H Organisms are carried from the site of entry through
the lymphatics to regional lymph nodes, resulting in

node swelling.
H The initial lesion is a papule that ulcerates within
24 hours. (See Chancroidal lesion.)
H Untreated infections disseminate to other organs,
causing systemic inflammation and specific organ
dysfunction.
Causes
H Haemophilus ducreyi, a short, nonmotile, gram-
negative bacillus
Risk factors
H Unprotected sex
H Multiple sex partners
H Uncircumcised males
Incidence
H Increasing in the United States
Chancroidal lesion
Chancroid produces a soft, painful chancre, similar to that
of syphilis. Without treatment, it may progress to inguinal
adenitis and formation of buboes (enlarged, inflamed
lymph nodes).
responding well to treatment when no secondary

infections present
Complications
H Phimosis and urethral fistulas in males
H Secondary infection
H Abscess formation
H Inguinal adenitis and formation of buboes
Assessment
History
H May report unprotected sexual contact with an infect-
ed person or with unknown or multiple partners

H Pain from ulcers and lymphadenopathy
H Headaches and malaise
Physical findings
H Genital area initially with single or multiple papules
surrounded by redness that rapidly become pustular

and then ulcerate
H Ulcers nonindurated with ragged edges, a base of
granulation tissue, and bleed easily; range from 1 to
2 mm in diameter
H Lesions on the tongue, lip, or breast
H Suppuration with bubo formation in the untreated
patient; rupture of abscess may follow
H Tender, fluctuant inguinal nodes
Test results
Laboratory
H Cultures from the lesion show H. ducreyi.
Treatment
General
H Aspiration of fluid-filled nodes
H Good personal hygiene
H Abstinence from sexual activity (until genital lesions
are healed)
H Evaluation of patient for syphilis, herpes simplex
virus, and human immunodeficiency virus (HIV)
Medications
H Antibiotics, such as azithromycin, doxycycline,
erythromycin, minocylcine, and tetracycline
Surgery
H Surgical drainage for large abscess
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Chancroid
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Key outcomes
The patient will:
H communicate feelings about changes in body image
H regain skin integrity with decrease in size of chancroids
H state infection risk factors
H voice feelings about changes in sexual activity.
H Wash the affected area with soap and water, followed
by a bactericidal agent.
H Dry the affected area thoroughly.
H Report all cases of chancroid to the local board of
health.
Monitoring
H Adverse effects of medications
H Compliance with treatment regimen
H Complications
Patient teaching
Be sure to cover:
H need to avoid applying creams, lotions, or oils on or
near genitalia or on other lesion sites
H abstaining from sexual contact until follow-up shows
that healing is complete
H proper washing techniques of the genitalia
H HIV infection and recommend testing
H following safer sex practices.
Discharge planning
H Refer the patient and affected sexual partners for
treatment.
Chancroid
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Chlamydial infections
Overview
Description
H Infection that results in urethritis in males, cervicitis
in females, and lymphogranuloma venereum in both

sexes
H Trachoma inclusion conjunctivitis: seldom occurs in
United States, but is leading cause of blindness in developing countries
H Most common sexually transmitted disease (STD) in
the United States
H Urethral and rectal strictures

H Perihepatitis
H Cervical cancer
H Trachoma
H Urethritis and epididymitis (in males)
H Sterility
H Stillbirth, neonatal death, premature labor (with in-
fected pregnant females)
Assessment
History
H Unprotected sexual contact with an infected person
H Previous STD
Pathophysiology
Physical findings
H Chlamydial infections are transmitted by direct con-
H Two-thirds of patients asymptomatic
tact (such as sexual).

H Infection produces local inflammation.
H Endometritis and salpingitis occur as the organism
ascends the genitourinary tract.
Female
H Pelvic or abdominal pain
H Dyspareunia
H Cervical erosion
H Mucopurulent discharge
H Dysuria
H Urinary frequency
Male
H Dysuria
H Urinary frequency
H Pruritus
H Urethral discharge (copious and purulent)
H Meatal erythema
H Severe scrotal pain
Lymphogranuloma venereum
H Painless vesicle or nonindurated ulcer, 2 to 3 mm in
diameter, on the glans or shaft of the penis; on the
labia, vagina, or cervix; or in the rectum
H Enlarged inguinal lymph nodes
H Regional nodes appearing as series of bilateral
buboes
H Untreated buboes possibly rupturing and forming
sinus tracts that discharge thick, yellow, granular
secretion
Causes
H Transmission of Chlamydia trachomatis, by sexual
contact (oral, anal, or vaginal)

H Neonate infection caused by transport through the
infected mothers birth canal
Risk factors
H Multiple sex partners or new sex partner
H Unprotected sex
H Coinfection with another STD
Incidence
H About 4 million cases annually
H Affects primarily the Native American population of
the southwest United States

H Occurs more commonly among minorities and lower
socioeconomic groups and people living in urban

areas
Special populations
Chlamydial infections have a 10% incidence
among sexually active adolescent girls.
H Primarily occurring after vaginal or rectal inter-
course or oral-genital contact with an infected person

H Late appearance of signs and symptoms during the
course of the disease
H No symptoms in 75% of females, 50% of males
H Sexual transmission of organism that occurs unknowingly
Complications
H Infertility
H Pelvic inflammatory disease
174
Test results
Laboratory
H Swab culture of the infection site shows C. trachomatis. (See Chlamydia trachomatis.)
H Culture of aspirated blood, pus, or cerebrospinal
fluid establishes epididymitis, prostatitis, and
lymphogranuloma venereum.
H Serologic studies reveal previous exposure.
H Enzyme-linked immunosorbent assay shows C. trachomatis antibody.
Treatment
General
H Symptomatic treatment (sex partners also treated)
H Abstinence from sexual activity until infection re-
solved
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Medications
H Antibiotics, such as azithromycin, doxycycline,
erythromycin, levofloxacin, and tetracycline
Chlamydia trachomatis
In chlamydial infections, microscopic examination reveals
Chlamydia trachomatis, a unicellular parasite with a rigid
cell wall.
Key outcomes
The patient will:
H voice feelings about changes in sexuality
H express concern about self-concept, self-esteem, and
body image
H exhibit improved or healed lesions or wounds
H express relief from pain.
H Check the neonate of an infected mother for signs of
infection.
H Report cases of chlamydial infection to the local
board of health.
Monitoring
H Adverse effects of medication
H Complications
Patient teaching
Be sure to cover:
H the disorder, signs and symptoms, and treatment
H abstinence from intercourse or use of condoms
H importance of getting tested for the human immunodeficiency virus
H dealing with long-term risks and complications from
infection
H transmission of infection
H prevention of STDs by following safer sex practices
H follow-up care
H complications.
Discharge planning
H Advise rescreenings at 3 to 4 months and annual
screenings for sexually active teens and females ages

20 to 25.
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Cholelithiasis,
cholecystitis,
and related disorders
Overview
Description
Cholelithiasis
H Leading biliary tract disease
H Formation of calculi (gallstones) in the gallbladder
Cholecystitis
H Related disorder that arises from formation of gallstones
H Acute or chronic inflammation of gallbladder
H Usually caused by a gallstone lodged in the cystic
duct
H Acute form most common during middle age
H Chronic form most common among elderly persons
Choledocholithiasis
H Related disorder arising from formation of gallstones
H Partial or complete biliary obstruction due to gallstones lodged in the common bile duct
Cholangitis
H Related disorder that arises from formation of gallstones
H Infected bile duct
H Commonly linked to choledocholithiasis
H Rapid response of nonsuppurative type to antibiotic
treatment
H Poor prognosis of suppurative type unless surgery to
correct obstruction and drain infected bile performed promptly
Gallstone ileus
H Related disorder that arises from obstruction of the
small bowel by a gallstone
H Most common in elderly persons
Pathophysiology
H Calculi formation in the biliary system causes ob-
struction.
immobility, chronic dieting, adhesions, prolonged

anesthesia, and opioid abuse)
Risk factors
H High-calorie, high-cholesterol diet
H Obesity
H Elevated estrogen levels due to hormonal contracep-
tive use, postmenopausal hormone-replacement

therapy, or pregnancy
H Diabetes mellitus, ileal disease, hemolytic disorders,
hepatic disease (cirrhosis), or pancreatitis
H Rapid weight loss
Incidence
H Six times more common in females ages 20 to 50
H Males and females equal after age 50; increases with
each succeeding decade
H Epigastric or right upper quadrant abdominal pain
H Nausea, vomiting
H Low-grade fever
Complications
Cholelithiasis
H Cholangitis
H Cholecystitis
H Choledocholithiasis
H Gallstone ileus
Cholecystitis
H Gallbladder complications, such as empyema,
hydrops or mucocele, and gangrene
H Chronic cholecystitis and cholangitis
Choledocholithiasis
H Cholangitis
H Obstructive jaundice
H Pancreatitis
H Secondary biliary cirrhosis
Cholangitis
H Septic shock
H Death
Gallstone ileus
H Bowel obstruction
H Obstruction of hepatic duct leads to intrahepatic re-
tention of bile; increased release of bilirubin into the

bloodstream occurs.
H Obstruction of cystic duct leads to inflammation of
the gallbladder; increased gallbladder contraction
and peristalsis occurs.
H Obstruction of bile causes impairment of digestion
and absorption of lipids.
Causes
H Calculi formation; type of disorder that develops de-
pendent on where in the gallbladder or biliary tract

the calculi collect
H Acute cholecystitis also a result of conditions that alter gallbladders ability to fill or empty (trauma, reduced blood supply to the gallbladder, prolonged
176
Assessment
History
H Gallbladder disease possibly producing no symptoms
(even when X-rays reveal gallstones)

Acute cholecystitis
H Sudden onset of severe steady or aching pain in the
midepigastric region or the right upper abdominal
quadrant
H Pain radiating to the back, between the shoulder
blades or over the right shoulder blade, or just to the
shoulder area
H Attack occurring after eating a fatty meal or a large
meal after fasting for an extended time
H Attack occurring in the middle of the night
Cholelithiasis, cholecystitis, and related disorders
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H Nausea, vomiting, and chills

H Low-grade fever
H History of milder GI symptoms that preceded the
acute attack; indigestion, vague abdominal discomfort, belching, and flatulence after eating meals or
snacks rich in fats
H Bile salts
H Analgesics
H Antispasmodics
H Anticholinergics
H Antiemetics
H Antibiotics
Physical findings
Surgery
H Severe pain
H Pallor
H Diaphoresis
H Low-grade fever (high in cholangitis)
H Exhaustion
H Jaundice (chronic)
H Dark-colored urine and clay-colored stools
H Tachycardia
H Tenderness over the gallbladder, which increases on
H Cholecystectomy (laparoscopic or abdominal), cho-
inspiration (Murphys sign)
lecystectomy with operative cholangiography, choledochostomy, or exploration of the common bile duct
Other
H Endoscopic retrograde cholangiopancreatography to
visualize and remove calculi

H Lithotripsy
H Palpable, painless, sausagelike mass (calculus-filled
gallbladder without ductal obstruction)

H Hypoactive bowel sounds
Key outcomes
Test results
Laboratory
H Blood studies may reveal elevated levels of serum alkaline phosphatase, lactate dehydrogenase, aspartate
aminotransferase, icteric index, and total bilirubin;
white blood cell count is slightly elevated during
cholecystitis attack.
Imaging
H Plain abdominal X-rays show gallstones if they contain enough calcium to be radiopaque. X-rays are
also helpful in identifying porcelain gallbladder, limy
bile, and gallstone ileus.
H Ultrasonography of the gallbladder confirms
cholelithiasis in most patients and distinguishes between obstructive and nonobstructive jaundice; calculi as small as 2 mm can be detected.
H Oral cholecystography confirms the presence of gallstones, although this test is gradually being replaced
by ultrasonography.
H Technetium-labeled iminodiacetic acid scan of the
gallbladder indicates cystic duct obstruction and
acute or chronic cholecystitis if the gallbladder cant
be seen.
H Percutaneous transhepatic cholangiography, imaging
performed under fluoroscopic guidance, supports
the diagnosis of obstructive jaundice and is used to
visualize calculi in the ducts.
Treatment
General
H Low-fat diet
H Nothing by mouth if surgery required
Medications
The patient will:

H show no signs of infection
H have laboratory values that return to within normal
parameters
H avoid complications.
H Position the patient for comfort and reposition at
least every 2 hours.

spirometer use.
H Encourage early ambulation postoperatively.
H Maintain nothing-by-mouth status.
Monitoring
H Vital signs
H Intake and output
H Pain control
H Abdominal status
After surgery
H T tube patency and drainage
H Cardiac status
Patient teaching
Be sure to cover:
H the disease, diagnosis, and treatment
H how to breathe deeply, cough, expectorate, and perform leg exercises that are necessary after surgery
H dietary modifications
adverse effects
H wound care.
H Gallstone dissolution therapy
Cholelithiasis, cholecystitis, and related disorders
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Cholera
Overview
Description
H Acute enterotoxin-mediated GI infection
H Transmitted through food and water contaminated
with fecal material from carriers or people with active infections

H Food poisoning caused by Vibrio parahaemolyticus,
a similar bacterium (see Vibrio parahaemolyticus
food poisoning)
H Also known as Asiatic cholera or epidemic cholera
Pathophysiology
H Humans are the only hosts and victims of V. choler-
ae, a motile, aerobic organism.

H The incubation period is several hours to 5 days.
H Enterotoxins cause profuse watery diarrhea and vom-
iting without nausea.

H Massive fluid and electrolyte loss occurs and, if not
corrected, leads to metabolic acidosis, uremia, and

possibly coma and death.
H Infection doesnt confer permanent immunity.
Causes
H Gram-negative bacillus V. cholerae
Risk factors
H Deficiency or absence of hydrochloric acid
Incidence
H Most common in Africa, Southern and Southeast
Asia, and the Middle East, although outbreaks have

occurred in Japan, Australia, and Europe
H Occurs during the warmer months; most prevalent
among lower socioeconomic groups
H Common among children ages 1 to 5 in India, but
equally distributed among all age-groups in other
endemic areas
H Acute, painless, profuse, watery diarrhea
H Effortless vomiting (without preceding nausea)
Complications
H Dehydration
H Hypovolemic shock
H Uremia
H Coma and death
Assessment
History
H Profuse, watery diarrhea
H Vomiting
H Intense thirst
H Weakness
H Muscle cramps (especially in the extremities)
Physical findings
H Stools containing white flecks of mucus (rice-water
stools)
Vibrio parahaemolyticus food poisoning

Vibrio parahaemolyticus is a common cause of gastroenteritis in Japan. Outbreaks also occur on American cruise
ships and in the eastern and southeastern coastal areas of
the United States, especially during the summer.
V. parahaemolyticus, which thrives in a salty environment, is transmitted through the ingestion of uncooked or
undercooked contaminated shellfish, particularly crab and
shrimp. After an incubation period of 2 to 48 hours,
V. parahaemolyticus causes watery diarrhea, moderately
severe cramps, nausea, vomiting, headache, weakness,
chills, and fever. Food poisoning is usually self-limiting
and subsides spontaneously within 2 days. Occasionally,
however, its more severe and may even be fatal in debilitated or elderly persons.
Diagnosis requires bacteriologic examination of vomitus, blood, stool smears, or fecal specimens collected by
rectal swab. Diagnosis must rule out not only other causes of food poisoning but also other acute GI disorders.
Treatment is supportive, consisting primarily of bed rest
and oral fluid replacement. I.V. replacement therapy is seldom necessary, but oral tetracycline may be prescribed.
Thorough cooking of seafood prevents this infection.
178
Cholera
H Loss of skin turgor, wrinkled skin, sunken eyes

H Pinched facial expression
H Cyanosis
H Tachycardia
H Tachypnea
H Thready or absent peripheral pulses
H Hypotension
H Fever
H Inaudible, hypoactive bowel sounds
Test results
Laboratory
H A culture of V. cholerae from feces or vomitus indicates cholera.
H Microscopic examination of fresh feces shows rapidly moving bacilli (like shooting stars).
H Agglutination reveals reactions to group- and typespecific antisera.
Other
H In endemic areas or during epidemics, typical clinical features strongly suggest cholera.
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Treatment
General
H Standard precautions
H Supportive care
Medications
H Rapid I.V. infusion of large amounts (50 to 100 ml/
minute) of isotonic saline solution, alternating with

sodium bicarbonate or sodium lactate
H Antibiotic such as tetracycline
Key outcomes
The patient will:
H regain and maintain adequate fluid and electrolyte
balance
H have normal elimination patterns
H have stable vital signs
H produce adequate urine volume.
H Maintain standard precautions.
H Carefully observe jugular veins.
Monitoring
H Vital signs
H Intake and output
H Laboratory values
H I.V. infusion
H Jugular veins
H GI status
Patient teaching
Be sure to cover:
H administration of cholera vaccine to travelers in
endemic areas
H need for increased fluid intake.
Discharge planning
H Explain the use of oral tetracycline to family mem-
bers.
H If the physician orders a cholera vaccine, tell the
patient that hell need a booster 3 to 6 months later

for continuing protection.
Cholera
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Chronic fatigue and

immune dysfunction
syndrome
Overview
Incidence
H Affects people of all ages, occupations, and income
levels
H More common in females than in males or children,
especially females younger than age 45

H Sporadic incidence and epidemic clusters
H Estimated to affect about 200 out of every 100,000
persons in the United States
Special populations
Description
H Characterized by prolonged overwhelming fatigue
H Also called chronic fatigue syndrome, chronic
Epstein-Barr virus, myalgic encephalomyelitis,

and Yuppie flu
Chronic fatigue and immune dysfunction syndrome is most prevalent among professionals in
their 20s and 30s.
Pathophysiology
H Infectious agents or environmental factors trigger
H Suggests viral illness in some cases

H Characterized by incapacitating fatigue
H Waxing and waning symptoms
H Severely debilitating; can last for months or years
H Depression and anxiety after the syndromes onset
H Fever
H Pharyngitis
H Lymphadenopathy
an abnormal immune response and hormonal alterations.
Causes
H Possibly cytomegalovirus, herpes simplex virus types
1 and 2, human herpesvirus 6, Inoue-Melnick virus,

human adenovirus 2, enteroviruses, measles virus, or
a retrovirus that resembles human T-cell lymphotropic virus type II
H May result from overactive immune system
Risk factors
H Hormonal balance
H Neuropsychiatric factors
H Gender
H Previous illness
H Stressful environment
Diagnosing chronic fatigue syndrome

Chronic fatigue and immune dysfunction syndrome is defined by:
H New or relapsing fatigue that isnt the result of ongoing
exertion or alleviated by rest and reduces occupational,
educational, social, or personal activities or efforts.
H Four or more of the following symptoms, occurring for
6 months or more:
self-reported impairment in short-term memory or
concentration
sore throat
tender cervical or axillary nodes
muscle pain
multiple joint pain without redness or swelling
headaches of a new pattern or severity
nonrefreshing sleep
postexertional malaise lasting 24 hours or longer.
180
Complications
H Social and occupational impairment
Assessment
History
H Characteristic complaints of prolonged, overwhelm-
ing fatigue (see Diagnosing chronic fatigue syndrome)
Physical findings
H Myalgia
H Cognitive dysfunction
Test results
Laboratory
H Lymphocyte differential reveals reduced natural killer
cell cytotoxicity, abnormal CD4+:CD8+ T-cell ratios,
and mild lymphocytosis.
H Immunoglobulin profile shows decreased immunoglobulin subclasses.
H Immune complex profile reveals circulating immune
complexes.
H Antimicrosomal antibody testing reveals increased
levels of antimicrosomal antibodies.
Chronic fatigue and immune dysfunction syndrome
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Treatment
General
H Focus on supportive care
H Psychiatric evaluation
H Behavioral therapy
H Well-balanced diet high in vitamins and minerals
H Physical therapy
H Frequent rest periods, as needed
H Avoidance of strenuous activities
Medications
H Nonsteroidal anti-inflammatory drug such as ibu-
profen
H Antidepressants, such as sertraline and paroxetine
H Antihistamines, such as loratidine and fexofenidine
Key outcomes
The patient will:
H verbally report having an increased energy level
H express feelings about diminished capacity to
perform usual roles
H recognize limitations imposed by illness
H make decisions regarding the course of treatment
and management of the illness
H voice feelings related to self-esteem.
H Begin a graded exercise program.
Monitoring
H Complications
Patient teaching
Be sure to cover:
H the need to decrease activities when fatigue is
greatest
H the need to avoid bed rest, which has no proven
therapeutic value
adverse effects
H appropriate activity planning.
Discharge planning
Chronic fatigue and immune dysfunction syndrome
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Cirrhosis
Overview
Description
H Chronic hepatic disease
H Several types
Pathophysiology
H Diffuse destruction and fibrotic regeneration of
hepatic cells occurs.

H Necrotic tissue yields to fibrosis.
H Liver structure and normal vasculature are altered.
H Blood and lymph flow are impaired.
H Hepatic insufficiency occurs.
Causes
Lannecs or micronodular cirrhosis
(alcoholic or portal cirrhosis)
H Chronic alcoholism
H Malnutrition
Postnecrotic or macronodular cirrhosis
H Complication of viral hepatitis
H Possible after exposure to such liver toxins as
arsenic, carbon tetrachloride, and phosphorus
Biliary cirrhosis
H Prolonged biliary tract obstruction or inflammation
Idiopathic cirrhosis (cryptogenic)
H No known cause
H Sarcoidosis
H Chronic inflammatory bowel disease
Risk factors
H Alcoholism
H Toxins
H Biliary obstruction
H Hepatitis
H Metabolic disorders
Incidence
H Tenth most common cause of death in the United
States
H Most common among those ages 45 to 75
H Occurs in twice as many males as females
H Abdominal pain
H Pruritus
H Jaundice
H Ascites
H Indigestion
H Anemia
Complications
H Portal hypertension
H Bleeding esophageal varices
H Hepatic encephalopathy
H Hepatorenal syndrome
H Death
182
Cirrhosis
Assessment
History
H Malnutrition
H Viral hepatitis
H Exposure to liver toxins such as arsenic and certain
medications
H Prolonged biliary tract obstruction or inflammation
Early stage
H Vague signs and symptoms
H Abdominal pain
H Diarrhea, constipation
H Fatigue
H Nausea, vomiting
H Muscle cramps
Later stage
H Chronic dyspepsia
H Constipation
H Pruritus
H Weight loss
H Bleeding tendency, such as frequent nosebleeds, easy
bruising, and bleeding gums
Physical findings
H Telangiectasis on the cheeks
H Spider angiomas on the face, neck, arms, and trunk
H Gynecomastia
H Umbilical hernia
H Distended abdominal blood vessels
H Ascites
H Testicular atrophy
H Menstrual irregularities
H Palmar erythema
H Clubbed fingers
H Thigh and leg edema
H Ecchymosis
H Jaundice
H Palpable, large, firm liver with a sharp edge (early
finding)
H Enlarged spleen
H Asterixis
H Slurred speech, paranoia, hallucinations
Test results
Laboratory
H Liver enzyme levels, such as alanine aminotransferase, aspartate aminotransferase, total serum bilirubin, and indirect bilirubin are elevated.
H Total serum albumin and protein levels are decreased.
H Prothrombin time is prolonged.
H Hemoglobin, hematocrit, and serum electrolyte levels
are decreased.
H Vitamins A, C, and K are deficient.
H Urine levels of bilirubin and urobilinogen are increased; fecal urobilinogen levels are decreased.
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Imaging
H Abdominal X-rays show an enlarged liver and spleen
and cysts or gas in the biliary tract or liver; liver calcification; and massive ascites.
H Computed tomography and liver scans determine
liver size, identify liver masses, and visualize hepatic
blood flow and obstruction.
H Radioisotope liver scans show liver size, blood flow,
or obstruction.
H Liver biopsy is the definitive test for cirrhosis, revealing hepatic tissue destruction and fibrosis.
H Esophagogastroduodenoscopy reveals bleeding
esophageal varices, stomach irritation or ulceration,
and duodenal bleeding and irritation.
Treatment

H Maintain patient safety.
Monitoring
H Vital signs
H Laboratory values
H GI status
H Hemodynamic status
H Abdominal girth
H Weight
H Bleeding tendencies
H Skin integrity
H Changes in mentation, behavior
H Neurologic status
General
Patient teaching
H Removal or alleviation of underlying cause

H I.V. fluids
H Blood transfusion
H Restricted sodium consumption
H Restricted fluid intake
H No alcohol intake
H High-calorie diet
H Paracentesis
H Esophageal balloon tamponade
H Sclerotherapy
Be sure to cover:
H over-the-counter medications that may increase
bleeding tendencies
H the need to avoid infections and abstain from alcohol
H the need to avoid sedatives and acetaminophen (hepatotoxic)
H high-calorie diet and small, frequent meals.
Medications
H Refer the patient to Alcoholics Anonymous, if appro-
H Vitamin supplementation such as thiamine

H Posterior pituitary hormone such as vasopressin
H Potassium-sparing diuretic such as spirolactone
H Ammonia detoxicant such as lactoluse
H Antiemetic such as metoclopramide
H Antidiarrheal such as octreotide
Discharge planning
priate.
needed.
Surgery
H May be required to divert ascites into venous circula-
tion; if so, peritoneovenous shunt used

H Portal-systemic shunts
H Transjugular intrahepatic portosystemic shunt
Key outcomes
The patient will:
H maintain caloric intake, as required
H maintain normal fluid volume
H incur no injuries
H exhibit no bleeding.
H Give prescribed I.V. fluids and blood products.
Cirrhosis
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Cleft lip and cleft palate

Overview
Description
H Imperfect fusion of front and sides of the face and
the palatine shelves during pregnancy

H May occur separately or in combination
H Can occur unilaterally, bilaterally or, rarely, in the
midline
H May affect just the lip or extend into the upper jaw or
nasal cavity (see Types of cleft deformities)
Pathophysiology
H Chromosomal abnormality, exposure to teratogens,
genetic abnormality, or environmental factors cause

the lip or palate to fuse imperfectly during the second month of pregnancy.
H A complete cleft includes the soft palate, the bones of
the maxilla, and the alveolus on one or both sides of
the premaxilla.
H A double cleft runs from the soft palate forward to either side of the nose, separating the maxilla and premaxilla into freely moving segments. The tongue and
other muscles can displace the segments, enlarging
the cleft.
ALERT
Isolated cleft palate occurs more commonly with
congenital defects other than isolated cleft lip. The
constellation of U-shaped cleft palate, mandibular
hypoplasia, and glossoptosis known as Robin sequence can occur as an isolated defect or one feature of many different syndromes.These infants
should have comprehensive genetic evaluation. Because of their mandibular hypoplasia and glossoptosis, the airway in infants with Robin sequence
must be carefully evaluated and managed.
H Obvious cleft lip or cleft palate
H Feeding difficulties from incomplete fusion of the
palate
Complications
H Malnutrition
H Hearing impairment
H Permanent speech impediment
Assessment
History
H Family history of cleft defects
H Maternal exposure to teratogens during pregnancy
H Clinical presentation obvious at birth
Physical findings
H Cleft that runs from the soft palate forward to either
side of the nose
Test results
Imaging
H Prenatal targeted ultrasound reveals abnormality.
Treatment
General
H Orthodontic prosthesis to improve sucking
H Use of a contoured speech bulb attached to the pos-
terior of a denture to occlude the nasopharynx when

a wide horseshoe defect makes surgery impossible
(to help the child develop intelligible speech)
H Use of a large, soft nipple with large holes, such as a
lambs nipple, to improve feeding patterns and promote adequate nutrition
Medications
ALERT
Causes
H Chromosomal or Mendelian syndrome (cleft defects
caused by more than 300 syndromes)

H Exposure to teratogens during fetal development
H Combined genetic and environmental factors
Incidence
H Twice as common in males than in females
H More common in children with a family history of
cleft defects
H Cleft lip with or without cleft palate occurs in about 1
in 1,000 births among Whites; incidence higher in

Asians (1.7 in 1,000) and Native Americans (more
than 3.6 in 1,000), but lower in Blacks (1 in 2,500)
184
Daily use of folic acid before conception decreases

the risk for isolated (not associated with another
genetic or congenital malformation) cleft lip or
palate by up to 25%. Women of childbearing age
should be encouraged to take a daily multivitamin
containing folic acid until menopause or until
theyre no longer fertile.
Surgery
H Surgical correction of cleft lip in the first few days of
life and again at 12 to 18 months, after the infant

gains weight and is infection-free
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Key outcomes
The patient will:
H exhibit normal growth and development patterns
within the confines of the disorder
H not aspirate feedings.
The family will:
H express an understanding of the condition and
treatment
H seek appropriate resources to assist with coping.
Types of cleft deformities

These illustrations show variations of cleft lip and cleft
palate.
NOTCH IN THE VERMILLION BORDER
(JUNCTION OF THE LIP AND SURROUNDING SKIN)
H Encourage the mother of an infant with cleft lip to
breast-feed if the cleft doesnt prevent effective

sucking.
H Suction, as necessary.
H Help the parents deal with their feelings about the
childs deformity.
UNILATERAL CLEFT LIP AND PALATE
ALERT
Never place a child with Robin sequence on his
back because his tongue could fall back and obstruct his airway. Place the infant on his side for
sleeping. Most other infants with a cleft palate can
sleep on their backs without difficulty.
Monitoring
BILATERAL CLEFT LIP AND PALATE
H Weight gain
H Intake and output
Patient teaching
Be sure to cover:
H treatment plan
H how to best feed the infant
H burping the infant frequently
H gently cleaning the palatal cleft with a cotton-tipped
applicator dipped in half-strength hydrogen peroxide
or water after each feeding.
CLEFT PALATE
Discharge planning
H Refer the patient to speech therapy to correct speech
patterns.
H Refer the parents to a social worker who can guide
them to community resources, if needed, and to a

genetic counselor to determine the recurrence risk.
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Clostridium difficile
infection
Overview
Description
H A gram-positive anaerobic bacterium commonly
resulting in antibiotic-associated diarrhea
H Hemorrhage
H Pseudomembranous colitis
Assessment
History
H Recent antibiotic therapy
H Abdominal pain
H Cramping
H Symptoms ranging from asymptomatic carrier states
Physical findings
to severe pseudomembranous colitis caused by

exotoxins (Toxin A is an enterotoxin and toxin B
is a cytotoxin.)
H Within 14 to 30 days of treatment, recurrence with
the same organism possible in 10% to 20% of
patients
H Soft, unformed, or watery diarrhea (more than three
Pathophysiology
H Antibiotics may trigger toxin production.
H Toxin A mediates alteration in fluid secretion, en-
hances inflammation, and causes leakage of albumin

from the postcapillary venules.
H Toxin B causes damage and exfoliation to the superficial epithelial cells and inhibits adenosine diphosphate ribosylation of Rho proteins.
H Both toxins cause electrophysiologic alterations of
colonic tissue.
Causes
H Antibiotics that disrupt the bowel flora
H Enemas and intestinal stimulants
H Transmission from infected person
H Some antifungal and antiviral agents
Risk factors
stools in a 24-hour period) that may be foul smelling

or grossly bloody
H Fever
Test results
Laboratory
H Cell cytotoxin test shows toxins A and B.
H Enzyme immunoassay identifies C. difficile; its
slightly less sensitive than cell cytotoxin test but
has a turnaround time of only a few hours.
H Stool culture identifies C. difficile.
Treatment
General
H Withdrawal of causative antibiotic
H Avoidance of antimotility agents
H Good skin care
H Increased fluid intake, if appropriate
H Rest periods, if fatigued
H Contaminated equipment and surfaces

H Antibiotics
H Abdominal surgery
H Antineoplastic agents that have an antibiotic activity
H Immunocompromised state
Medications
Incidence
Key outcomes
H More common in people in nursing homes and day-
care facilities
H One of the most common nosocomial infections
(contracted by about 20% of hospitalized patients
taking antibiotics)
The patient will:

H maintain normal electrolyte levels
H maintain adequate fluid volume
H Watery, foul-smelling diarrhea

H Institute contact precautions for those with active
Complications
H Electrolyte abnormalities
H Hypovolemic shock
H Toxic megacolon
H Colonic perforation
H Peritonitis
H Sepsis
186
Clostridium difficile infection
H Antibiotics, such as vancomycin and metronidazole
diarrhea.
H Wash your hands with an antiseptic soap after direct
contact with the patient or his immediate environment.

H Make sure reusable equipment is disinfected with a
bleach-based solution before its used on another
patient.
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Monitoring
H Vital signs
H Intake and output
H Complications
H Serum electrolytes
H Amount and characteristics of stools
H Skin integrity
H GI status
Patient teaching
Be sure to cover:
H proper disinfection of contaminated clothing or
household items
H adequate fluid intake
H signs and symptoms of dehydration
H perirectal skin care.
Clostridium difficile infection
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Clubfoot
H Heredity
H Idiopathic
H Suspected muscle abnormalities, leading to varia-
tions in length and tendon insertions
Overview
Incidence
Description
H Foot deformity caused by a deformed talus and short-
ened Achilles tendon, giving the foot a characteristic

clublike appearance
H In talipes equinovarus: foot points downward (equinus) and turns inward (varus), and front of foot
curls toward the heel (forefoot adduction)
H Also known as talipes: most common congenital disorder of lower extremities
H 1 per 1,000 live births

H Usually occurs bilaterally
H Twice as common in boys as in girls
H May be linked to other birth defects, such as
myelomeningocele, spina bifida, and arthrogryposis
H Inward deformity of the foot (see Recognizing club-
foot)
Pathophysiology
Complications
H Unknown, but contributing factors may include:
H Abnormal gait
H Stress changes on lateral side of the foot
H Residual deformity
defective cartilage with ligamentous laxity

muscle imbalance
abnormal intrauterine position
central nervous system anomaly
persistence of a normal fetal relationship.
Assessment
Causes
History
H Combination of genetic and environmental factors in
H Family history
H Muscular atrophy or dystrophy
utero
Recognizing clubfoot
Clubfoot (talipes) may have
various names, depending
on the orientation of the deformity, as shown in the illustrations at right.
188
Clubfoot
TALIPES EQUINUS
TALIPES CALCANEUS
TALIPES CAVUS
TALIPES VARUS
TALIPES EQUINOVARUS
TALIPES CALCANEOVARUS
TALIPES VALGUS
TALIPES CALCANEOVALGUS
TALIPES EQUINOVALGUS
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Physical findings
H Deformed talus with a shortened Achilles tendon, the
H Proper foot alignment

H Pain control
calcaneus somewhat shortened and flattened

H Shortened, underdeveloped calf muscles, with soft
tissue contractures at the site of the deformity
Patient teaching
H Foot tight in its deformed position and resistant of
manual efforts to push it back into normal position
Test results
Imaging
H X-rays show superimposition of the talus and the
calcaneus and a ladderlike appearance of the
metatarsals.
Treatment
Be sure to cover:
H the need for prompt treatment
H signs of circulatory impairment
H proper skin care
H use of exercise, night splints, and orthopedic shoes
to maintain alignment.
Discharge planning
H Refer the patient to rehabilitation resources, as
needed.
General
H Correction of the deformity
H Activity according to ability
H Maintaining the correction until the foot regains nor-
mal muscle balance

H Close observation to prevent the deformity from re-
curring
Sequential correction
H For forefoot adduction: uncurling the front of the
foot away from the heel (forefoot abduction)
H For varus deformity: turning the foot so the sole faces
outward (eversion)
H For equinus: casting the foot with the toes pointing
up (dorsiflexion)
Medications
H Analgesics
Surgery
H Subcutaneous tenotomy of the Achilles tendon and
posterior capsulotomy of the ankle joint (may need

to be done with the equinus stage of correction)
H In severe cases, bone surgery, such as wedge resections, osteotomy, or astragalectomy possibly appropriate (After surgery, a cast is applied to preserve
the correction.)
Key outcomes
The patient will:
H show no evidence of complications.
H After casting, elevate the childs feet with pillows.
H Perform proper skin and cast care.
Monitoring
H Neurovascular status of affected extremity after cast-
ing or surgery
Clubfoot
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Coarctation of the aorta

Overview
Description
H A narrowing of the aorta, usually just below the left
subclavian artery, near the site where the ligamentum

arteriosum (the remnant of the ductus arteriosus, a
fetal blood vessel) joins the pulmonary artery to the
aorta
H May occur with aortic valve stenosis (usually of a bicuspid aortic valve) and with severe cases of hypoplasia of the aortic arch, patent ductus arteriosus
(PDA), and ventricular septal defect
H Ineffective pumping of the heart and increased risk
due to heart failure caused by the obstruction of
blood flow
Pathophysiology
H Coarctation of the aorta may develop as a result of
spasm and constriction of the smooth muscle in the

ductus arteriosus as it closes.
H This contractile tissue extends into the aortic wall,
causing narrowing.
H The obstructive process causes hypertension in the
aortic branches above the constriction (arteries that
supply the arms, neck, and head) and diminished
pressure in the vessel below the constriction.
H Restricted blood flow through the narrowed aorta increases the pressure load on the left ventricle and
causes dilation of the proximal aorta and ventricular
hypertrophy.
H As oxygenated blood leaves the left ventricle, a portion travels through the arteries that branch off the
aorta proximal to the coarctation.
H If PDA is present, the rest of the blood travels
through the coarctation, mixes with deoxygenated
blood from the PDA, and travels to the legs.
H If PDA is closed, the legs and lower portion of the
body must rely solely on the blood that gets through
the coarctation.
Causes
H Unknown
H Turners syndrome
Incidence
H Accounts for about 7% of all congenital heart defects
in children
H Twice as common in males as in females
H In females, commonly linked to Turners syndrome, a
chromosomal disorder that causes ovarian dysgenesis
H Resting systolic hypertension in the upper body
H Absent or diminished femoral pulses
190

Complications
H Heart failure
H Severe hypertension
H Cerebral aneurysms and hemorrhage
H Rupture of the aorta
H Aortic aneurysm
H Hypoperfusion of lower extremities
Assessment
History
H Tachypnea
H Dyspnea
H Failure to thrive
H Headache
H Vertigo
H Epistaxis
H Claudication
Physical findings
H Pallor
H Hypertension
H Crackles
H Edema
H Tachycardia
H Cardiomegaly
H Hepatomegaly
H Hypertension
H Pink upper arms and cyanotic legs
H Absent or diminished femoral pulses
H Arm blood pressure greater than leg blood pressure
H Chest and arms more developed than legs
Test results
Imaging
H Chest X-rays may show left ventricular hypertrophy,
heart failure, a wide ascending and descending aorta,
and notching of the ribs undersurfaces due to erosion by collateral circulation. (See Recognizing
coarctation of the aorta.)
H Echocardiography may show increased left ventricular muscle thickness, coexisting aortic valve abnormalities, and the coarctation site.
H Electrocardiography may reveal left ventricular hypertrophy.
H Cardiac catheterization evaluates collateral circulation and measures pressure in the right and left ventricles and in the ascending and descending aortas
(on both sides of the obstruction).
H Aortography locates the site and extent of coarctation.
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Treatment
General
H Low-sodium diet
H Limited activity
Recognizing coarctation of the aorta

Collateral circulation develops to bypass the occluded aortic lumen, and can be seen on X-ray as notching of the
ribs. By adolescence, palpable, visible pulsations may be
evident.
Coarctation
Medications
H Oxygen
H Sedative such as chloral hydrate
H Prostaglandin infusion to keep the ductus open
H Antibiotic prophylaxis such as amoxicillin
H Antihypertensive such as enalaprilat
Surgery
H A flap of the left subclavian artery may be used to
reconstruct the aorta.

H Balloon angioplasty or resection with end-to-end
anastomosis or use of a tubular graft may also be

performed.
Key outcomes
The patient will:
H carry out activities of daily living without weakness or
fatigue
H remain free from signs and symptoms of infection.
H Offer emotional support.
H Regulate environmental temperature.
Monitoring
H Hemodynamics
H Vital signs
H Intake and output
H Blood glucose levels
H Postoperative pain
Patient teaching
Be sure to cover:
H exercise restrictions
H endocarditis prophylaxis.
Discharge planning
H Stress the need for follow-up care, as ordered.
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Coccidioidomycosis
Overview
Description
H Fungal infection occurring primarily as a respiratory
tract infection, although generalized dissemination

may occur
H Also known as valley fever or San Joaquin Valley
fever
Pathophysiology
Assessment
History
H Living or traveling to an endemic area
H Fever
H Dry cough
H Sore throat
H Chills
H Malaise
H Headache
H Joint pain
H After spores are inhaled, cell activation and cytokine
Physical findings
formation stimulate inflammatory cells and facilitate

killing of the organism.
H Immunosuppression may delay resolution of the infection.
H Fever
H Itchy macular rash
H Hemoptysis
H Local swelling and redness in involved sites (with
Causes
H Bronchial breath sounds
H Inhaled spores of Coccidioides immitis found in
the soil or dust from dressings or plaster casts of infected persons
Risk factors
H Occupational exposure to dust, such as with farmers
and construction workers

H Impaired immune system
Incidence
H Disseminated illness more common in dark-skinned
males, pregnant females, and patients taking an immunosuppressant

H Endemic to the southwestern United States, especially
between the San Joaquin Valley in California and
southwestern Texas; also found in Mexico, Guatemala, Honduras, Venezuela, Colombia, Argentina,
and Paraguay
H Generally affects Filipino Americans, Mexican Americans, Native Americans, and Blacks because of population distribution and an occupational link (common in migrant farm laborers)
Primary coccidioidomycosis
H Acute or subacute respiratory signs and symptoms
H Fever that persists for weeks
Disseminated coccidioidomycosis
H Fever
H Abscesses throughout the body, especially in skeletal,
central nervous system, splenic, hepatic, renal, and
subcutaneous tissues
Complications
H Meningitis
H Bronchiectasis
H Osteomyelitis
H Liver failure
192
Coccidioidomycosis
musculoskeletal involvement)
Test results
Laboratory
H Serum precipitins (immunoglobulins) are positive.
H C. immitis spores is detected through immunodiffusion testing of sputum, pus from lesions, and tissue
biopsy.
H Antibodies are present in pleural and joint fluid and
a rising serum or body fluid antibody titer indicates
dissemination.
H White blood cell count is increased.
H Eosinophil count is increased.
Imaging
H Chest X-ray shows bilateral diffuse infiltrates.
Other
H Coccidioidin skin test result is abnormal.
Treatment
General
H Bed rest
H Symptomatic measures
Medications
H I.V. fluids
H Antifungal such as amphotericin B
H Analgesics, such as acetaminophen and morphine
H Oxygen
Surgery
H Excision or drainage of lesions
H Lobectomy for severe pulmonary lesions
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Key outcomes
The patient will:
H be free from pain
H cough effectively.
H Administer oxygen as prescribed.
spirometer use.
H Encourage bed rest, with head of the bed elevated
30 degrees.
H Provide measures to relieve pain and increase
comfort.
Monitoring
H Pain control
H Intake and output
H Vital signs
H Sputum color, consistency, and amount
Patient teaching
Be sure to cover:
H wound care.
Coccidioidomycosis
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Colorectal cancer
Overview
Description
H Malignant tumors of colon or rectum almost always
adenocarcinomas (about one-half are sessile lesions

of rectosigmoid area; all others, polypoid lesions)
H Slow progression
H Five-year survival rate 50%; potentially curable in
75% of patients if early diagnosis allows resection
before nodal involvement
H Second most common visceral neoplasm in United
States and Europe
Pathophysiology
H Most lesions of the large bowel are moderately differ-
entiated adenocarcinomas.
H Tumors tend to grow slowly and produce no symp-
toms for long periods.

H Tumors in the sigmoid and descending colon under-
go circumferential growth and constrict the intestinal

lumen.
H Tumors in the ascending colon are usually large at
diagnosis and are palpable on physical examination.
Assessment
History
H Right colon tumors: no signs and symptoms in early
stages because stool is liquid in that part of colon

H Transverse colon tumors: may cause cramps, gas,
partial or complete obstruction

H Descending colon tumors and rectal tumors: may
cause pencil-shaped stools if the tumor partially

obstructs the intestine
H Black, tarry stools
H Abdominal aching, pressure, or dull cramps
H Weakness
H Diarrhea, anorexia, obstipation, weight loss, and
vomiting
H Rectal bleeding
H Intermittent abdominal fullness
H Rectal pressure
H Urgent need to defecate on arising
Physical findings
H Abdominal distention or visible masses
H Enlarged abdominal veins
H Enlarged inguinal and supraclavicular nodes
H Abnormal bowel sounds
H Abdominal masses (right-side tumors that usually
H Unknown
feel bulky; tumors of transverse portion more easily

detected)
H Generalized abdominal tenderness
Risk factors
Test results
H Excessive intake of saturated animal fat

H Digestive tract diseases
H Older than age 40
H History of ulcerative colitis
H Familial polyposis
H Family history of colon cancer
H High-protein, low-fiber diet
Laboratory
H Fecal occult blood test may show blood in stools, a
warning sign of rectal cancer.
H Carcinoembryonic antigen allows patient monitoring
before and after treatment to detect metastasis or
recurrence.
Imaging
H Excretory urography verifies bilateral renal function
and allows inspection for displacement of the kidneys, ureters, or bladder by a tumor pressing against
these structures.
H Barium enema studies use a dual contrast of barium
and air and reveal the location of lesions that arent
detectable manually or visually. Barium examination
shouldnt precede colonoscopy or excretory urography because barium sulfate interferes with these
tests.
H Computed tomography scan allows better visualization if a barium enema yields inconclusive results or
if metastasis to the pelvic lymph nodes is suspected.
H Proctoscopy or sigmoidoscopy permits visualization
of the lower GI tract. It can detect up to 66% of colorectal cancers.
H Colonoscopy permits visual inspection and photography of the colon up to the ileocecal valve and provides access for polypectomies and biopsies of suspected lesions.
Causes
Incidence
H Equally distributed among males and females
H Greater in areas of higher economic development
H Changes in bowel habits
H Symptoms of direct extension to bladder, prostate,
ureters, vagina, or sacrum

H Symptoms of local obstruction
Complications
H Abdominal distention and intestinal obstruction as
tumor growth encroaches on abdominal organs

H Anemia
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Colorectal cancer
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Other
H Digital rectal examination can be used to detect almost 15% of colorectal cancers; specifically, it can
be used to detect suspicious rectal and perianal lesions.
Treatment
General
H Radiation preoperatively and postoperatively to
induce tumor regression

H High-fiber diet
H After surgery, avoidance of heavy lifting and contact
sports
Medications
H Antibiotics such as metronidazole postoperatively
H Chemotherapy, such as bevacizumab, capecitabine,
cetuximab, fluorouracil, irinotecan, oxaliplatin, and

panitumunab
H Analgesic such as morphine
Surgery
H Resection or right hemicolectomy for advanced dis-
ease; may include resection of the terminal segment

of the ileum, cecum, ascending colon, and right half
of the transverse colon with corresponding mesentery for tumor of cecum and ascending colon
H Right colectomy that includes the transverse colon
and mesentery corresponding to midcolic vessels, or
segmental resection of the transverse colon and associated midcolic vessels for proximal and middle
transverse colon tumor
H Resection usually limited to the sigmoid colon and
mesentery for sigmoid tumor
H Anterior or low anterior resection for upper rectal
tumor
H Abdominoperineal resection and permanent sigmoid
colostomy required for lower rectal tumor
Monitoring
H Stools
H Diet
Postoperative
H Vital signs
H Intake and output
H Electrolyte levels
H Wound and stoma site
H GI status
H Pain control
Patient teaching
Be sure to cover:
H the disease process, treatment, and postoperative
course
H stoma care
H avoidance of heavy lifting
H the need for keeping follow-up appointments
H risk factors and signs of recurrence.
Discharge planning
Key outcomes
The patient will:
H maintain intact mucous membranes
H report feeling less pain
H express increased sense of well-being
H use support systems and employ coping strategies.
H Encourage early ambulation postoperatively.
spirometer use.
H Provide stoma care.
Colorectal cancer
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Common cold
Overview
Description
H Acute, usually afebrile viral infection that causes in-
flammation of the upper respiratory tract

H Transmission through airborne respiratory droplets
or through contact with contaminated objects, including hands

H Accounts for 30% to 50% of time lost from work by
adults and 60% to 80% of time lost from school by
children, more than any other illness
H Communicable for 2 to 3 days after onset of symptoms
H Usually benign and self-limiting
Pathophysiology
H Rhinoviruses may infect cells by attaching to specific
receptors.
H Infiltration with neutrophils, lymphocytes, plasma
cells, and eosinophils occurs.
H Mucus-secreting glands become hyperactive and
nasal turbinates become engorged. (See What happens in the common cold.)
Causes
Complications
H Secondary bacterial infection causing sinusitis, otitis
media, pharyngitis, or lower respiratory tract infection
Assessment
History
H Exposure to persons with the common cold
H Sore throat
H Fatigue
H Malaise
H Myalgia
H Fever
Physical findings
H Copious nasal discharge that commonly irritates the
nose
H Increased erythema of nasal and pharyngeal mucous
membranes
H Nasal quality to voice
H Excoriated skin around nose
Test results
H There isnt an explicit diagnostic test.
Laboratory
H White blood cell count and differential are within
normal limits.
H Viral infection of the upper respiratory tract passages
and consequent mucous membrane inflammation responsible for 90% of cases

H More than 200 viruses, including rhinoviruses, coronaviruses, myxoviruses, adenoviruses, coxsackieviruses, and echoviruses
H Mycoplasma
Risk factors
H Exposure to an infected person or contact with con-
taminated objects
H Compromised immune system
Incidence
H Most common infectious disease
H More prevalent in children, adolescent boys, and
adult females
H In temperate climates, occurring more commonly in
the colder months
H In the tropics, occurring more commonly during the
rainy season
H Initial complaints of nasal congestion, headache, and
burning, watery eyes, chills, myalgia, arthralgia,

malaise, lethargy, sore throat, and a hacking, nonproductive or nocturnal cough
H Most patients afebrile, although fever possibly occurring, especially in children
196
Common cold
Treatment
General
H Use of humidified inspired air
H Prevention of chilling
Medications
H Throat lozenges
H Antitussive such as dextromethorphan
H In infants, saline nose drops and mucus aspiration
with a bulb syringe
Key outcomes
The patient will:
H express feeling of increased comfort
H cope effectively with illness
H reestablish normal temperature
H have respiratory secretions that remain clear and
odorless
H maintain adequate air exchange.
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What happens in the common cold
Virus-infected droplets enter the body and

attack the cells lining the throat and nose.
The virus particles then multiply rapidly.
Body cell
The immune system responds by sending lymphocytes to the infected mucosa,

causing blood vessels in the nasal
mucosa to swell. This swelling causes
secretion of excess fluid the classic
cold symptom of a runny nose.
Infected
nasal lining
Virus
particles
Blood vessel
Lymphocyte
Phagocytes engulf and destroy dead virus

particles and damaged cells. Soon the cold
symptoms disappear.
Antibodies
Phagocyte
Some lymphocytes
immobilize the virus
particles with virusspecific proteins
(antibodies); others
kill infected cells with
a chemical substance.
Chemicals
Damaged
virus particles
H Provide a lubricant for nostrils to decrease irritation.
H Relieve throat irritation with sugarless hard candy or
cough drops.
H A warm bath or heating pad can reduce aches and
pains.
H Suggest a hot or cold steam vaporizer to relieve nasal
congestion.
Monitoring
Lymphocyte
Patient teaching
Be sure to cover:
H advice against overuse of nose drops or sprays
H how to avoid spreading colds
H proper hand-washing technique.
Discharge planning
H Refer the patient for medical care if a high fever per-
sists, level of consciousness changes, or significant

respiratory symptoms develop.
H Body temperature
H Complications
Common cold
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Complex regional pain

syndrome
Overview
Description
H A chronic pain disorder resulting from abnormal
healing after minor or major injury to a bone,

muscle, or nerve
H Also known as reflex sympathetic dystrophy
(RSD/CRPS1) or causalgia (CRPS2)
Pathophysiology
H Abnormal functioning of the sympathetic nervous sys-
tem causes development of symptoms commonly disproportionate to the injurys severity.

H Interference with normal signals for sensations, temperature, and blood flow may be caused by impaired
communication between the damaged nerves of the
sympathetic nervous system and the brain.
Causes
H Muscle wasting (see Stages of complex regional
pain syndrome)
Test results
Imaging
H Bone X-rays rule out other conditions.
Treatment
General
H Physical therapy
Medications
H Anti-inflammatory such as ibuprofen
H Antidepressant such as venlafaxine
H Analgesics, such as diclofenac and oxycodone
Surgery
H Nerve or regional blocks
Key outcomes
Precipitating factors
H Trauma
H Neurologic disorder
H Herpes zoster infection
H Myocardial infarction
H Musculoskeletal disorder (shoulder rotator cuff
injury)
H Malignancy
The patient will:

H express increased comfort
H use support systems and develop coping techniques
H demonstrate effective relaxation techniques.
Incidence
H Can occur at any age but is less common in children
H Reported more commonly in women
H Apply antiembolism stockings.
H Apply heat or cold therapy.
Monitoring
H Pain control
H Effects of medications
H Blood glucose level
H Severe, constant pain
Complications
H Impaired mobility
H Depression
Assessment
History
H Injury
H Severe pain that worsens after activity
Physical findings
H Altered blood flow, feeling either warm or cool to the
touch, with discoloration, sweating, or swelling to the

affected extremity
H Skin, hair, and nail changes
H Impaired mobility and weakness
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Complex regional pain syndrome
Patient teaching
Be sure to cover:
H the disease and treatment
H relaxation techniques
adverse effects.
Discharge planning
H Refer the patient for home therapy.
H Refer the patient to a pain care specialist.
H Refer the patient for psychological counseling and
support groups, as indicated.
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Stages of complex regional pain syndrome

Complex regional pain syndrome is divided into three stages. The stages arent always distinct and not all of the signs may
be present.
Stage
Duration
Pain, swelling,
and immobility
Skin
Hair and
nails
Osteoporosis
Symptoms
begin within
hours, days,
or weeks of
the injury; this
stage lasts
several weeks
Gradual or abrupt
onset of severe
aching, throbbing,
and burning pain at
site of injury
Pain may be accompanied by sensitivity
to touch, swelling,
muscle spasm, stiffness, and limited
mobility
Warm, red,
dry skin at
onset;
changes to
bluish and
becomes cold
and sweaty
Accelerated
hair and nail
growth
Early
osteoporosis
symptoms
Continuous burning,
aching, or throbbing
pain thats more severe than stage I
Swelling spreads
and changes from
soft to brawny and
firm
Loss of range of
motion, muscle
wasting
Cool, pale,
bluish,
sweaty
Altered hair
growth;
cracked,
grooved, or
ridged nails
More apparent
osteoporosis
Pain spreads proximally and may be intractable, but sometimes lessens and
stabilizes
More distinct dystrophic changes and
irreversible tissue
damage
Muscle atrophy and
contractures
Thin, shiny
Increasingly
brittle and
ridged nails
Marked diffuse
osteoporosis
I (Acute)
II (Subacute or dystrophic)
Lasts 3 to
6 months
III (Chronic or atrophic)
Lasts more
than 6 months
Complex regional pain syndrome
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Concussion
Overview
Description
H Blow to the head forceful enough to jostle the brain
and make it strike the skull

H Acceleration-deceleration injury
H Causes temporary (less than 48 hours) neural dys-
function
Assessment
History
H Trauma to head
H Short-term loss of consciousness
H Vomiting
H Antegrade and retrograde amnesia
H Change in level of consciousness (LOC)
H Dizziness
H Nausea
H Severe headache
Pathophysiology
Physical findings
H Concussion causes diffuse soft tissue damage.

H Inflammation occurs.
H Structural damage is usually minimal.
H Tenderness or hematomas on skull palpation
Causes
H Trauma to the head
Incidence
H More than 2 million instances of concussion per year
in the United States

H May occur in up to 20% of football players
H Most commonly affects those ages 15 to 24
H Short-term loss of consciousness
H Dizziness
H Retrograde amnesia
H Erratic behavior
H Headache
H Blurred vision
Complications
H Seizures
H Persistent vomiting
H Intracranial hemorrhage (rare)
What to look for after a concussion

Before the patients discharge, follow these teaching
guidelines: Instruct the caregiver to awaken the patient
every 2 hours through the night and to ask his name and
whether he can identify the caregiver.
Advise the caregiver to return the patient to the facility
immediately if he is difficult to arouse, is disoriented,
has seizures, or experiences a persistent or worsening
headache, forceful or constant vomiting, blurred vision,
changes in personality, abnormal eye movements, a staggering gait, or twitching. If the patient is a child, explain to
the parents that some children have no apparent ill effects
immediately after a concussion but may grow lethargic or
somnolent a few hours later. Teach the patient the signs of
postconcussion syndrome headache, vertigo, anxiety,
personality changes, memory loss, and fatigue. Explain
that these signs may persist for several weeks.
200
Concussion
Test results
Imaging
imaging help rule out fractures and more serious
injuries.
Treatment
General
H Observation for changes in mental status
H Clear liquids if vomiting occurs
H Bed rest initially with head of the bed elevated at
least 30 degrees
H Avoidance of contact sports until fully recovered
Medications
H Nonopioid analgesic such as acetaminophen
Key outcomes
The patient will:
H state appropriate interactions for pain relief
H identify factors that increase the potential for injury
H recover or be rehabilitated from physical injuries to
the extent possible.
H Give prescribed drugs, and avoid opioids that may
decrease LOC.
H Reorient the patient to time and place, if necessary.
Monitoring
H Vital signs
H Neurologic status
H Pain control
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Patient teaching
Be sure to cover:
H nonopioid analgesics for a headache and avoidance
of products containing aspirin
H change in LOC or projectile vomiting, which requires
a return to the hospital
H signs and symptoms of increased intracranial pressure.
Discharge planning
H Arrange for continued observation at home. (See
What to look for after a concussion.)
Concussion
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Conjunctivitis
H Transmission by contaminated towels, washcloths, or
ones own hand

H Systemic diseases, such as erythema multiforme and
thyroid disease
Overview
H Candidal infection
Description
Incidence
H Inflammation of palpebral or bulbar conjunctiva

H Characterized by hyperemia of the conjunctiva
H Usually spreads rapidly from one eye to the other
H Usually benign and self-limiting
H Seldom affects vision
H If chronic, may signal degenerative changes or dam-
H Most common eye disorder in the Western hemi-
age from repeated acute attacks

H Acute bacterial conjunctivitis (pink eye) usually lasting about 2 weeks
H Other viral conjunctival infections lasting 2 to
3 weeks; chronic and may produce severe disability
Pathophysiology
H Conjunctivitis is an inflammatory response of the
conjunctiva that usually begins in one eye and may

rapidly spread to the other eye.
H Vernal conjunctivitis is linked to a severe form of immunoglobulin E-mediated mast cell hypersensitivity
reaction.
sphere
H Responsible for about 30% of all eye complaints
H Reddened conjunctiva
H Edema of eyelid
H Pain in the eye
H Increased lacrimation
H Burning in eyes
Complications
H Tic
H Corneal infiltrates
H Corneal ulcers
H Eye loss
Assessment
Causes
History
H Allergens
H Bacteria
H Viruses
H Chemical irritations
H Eye pain
H Photophobia
H Burning, itching, and sensation of a foreign body in
the eye
H Sore throat and fever, in children
Physical findings
Recognizing conjunctival papillae
If you see papillae in the conjunctiva of the upper eyelid,
your patient may have vernal (allergic) conjunctivitis.
These cobblestone bumps are the telltale sign. They result
from swollen lymph tissue within the conjunctival membrane.
H Conjunctival hyperemia
H Discharge
H Tearing
H Crust of sticky, mucopurulent discharge (in bacterial
conjunctivitis)
H Profuse, purulent discharge (in gonococcal conjunc-
tivitis)
H Copious tearing and minimal discharge (in viral con-
junctivitis)
H Conjunctival papillae (in vernal conjunctivitis) (see
Recognizing conjunctival papillae)

H Ipsilateral preauricular lymph node enlargement (in
viral conjunctivitis)
Test results
Laboratory
H Culture and sensitivity tests may identify the bacterial
pathogen.
H Stained smears of conjunctival scrapings may show
mostly monocytes with viral conjunctivitis; polymorphonuclear cells (neutrophils) are predominate with
bacterial conjunctivitis; and eosinophils are predominate with allergic conjunctivitis.
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Conjunctivitis
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Treatment
General
H Warm compresses
H Depends on cause
Medications
H Antibiotics, such a ciprofloxacin, erythromycin, and
mixofloxacin
H Histamine-1 receptor antagonist such as azelastine
H Oral antihistamine such as loratidine
Key outcomes
The patient will:
H Apply warm compresses.
H Apply therapeutic ointment or eyedrops, as ordered.
H Avoid irrigating the eye to prevent the spread of in-
fection.
H Notify public health officials if culture results identify
Neisseria gonorrhoeae.
H Obtain culture specimens before antibiotic therapy.
Monitoring
H Adverse reactions
H Visual acuity
Patient teaching
Be sure to cover:
H instillation of eyedrops and ointments
H completing the prescribed antibiotics
H methods for preventing disease transmission
H importance of avoiding chemical irritants
H avoiding eye makeup and contact lens use until the
infection has cleared.
ALERT
Caution the patient to avoid rubbing the infected
eye so that he can prevent the spread of infection
to the other eye or to other people.
Conjunctivitis
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Corneal abrasion
Overview
Description
Test results
H Fluorescein staining of the injured area of the cornea
appears green when illuminated.
H Slit-lamp examination discloses the depth of the
abrasion.
H Scratch on the epithelial surface of the cornea

H Prognosis usually good with appropriate treatment
Treatment
Pathophysiology
General
H Epithelial layers of cornea are lost due to trauma.

H Superficial abrasions dont involve Bowmans mem-
H Eye irrigation (see Performing eye irrigation)

H Removal of foreign body
H Warm compresses
H Eye patch for 24 hours
H Eye protection with potentially dangerous activities
brane.
H Deep abrasions penetrate Bowmans membrane.
Causes
H Eye trauma
H Foreign bodies embedded under eyelid
H Contact lenses
H Chemicals
H Fingernails
H Hair brushes
H Tree branches
H Dust
Incidence
Medications
H Antibiotic eyedrops or ointment, such as ciproflox-
acin, erythromycin, gentamicin, and tobramycin

Surgery
H Surgical repair of corneal lacerations by an ophthal-
mologist
Key outcomes
H Difficulty opening the eye

H Eye pain
H Erythema
H Feeling of foreign body in eye
H Increased lacrimation
The patient will:

H regain visual function
H verbalize feelings and concerns.
Complications
H Corneal erosion
H Corneal ulceration
H Permanent vision loss
H Use a flashlight to inspect the cornea.

H Check visual acuity before treatment begins.
H If a foreign body is present, irrigate the eye with
Assessment
History
H Eye trauma
H Prolonged contact lens wear
H Sensation of foreign body in eye
H Sensitivity to light
H Decreased visual acuity
H Eye pain
Physical findings
H Redness in eye
H Increased tearing
H Possibly a foreign object embedded under the eyelid,
uncovered by eyelid eversion

H Disruption of corneal surface
204
Corneal abrasion
normal saline solution.

H Give prescribed antibiotics and cycloplegics.
H Instill prescribed topical anesthetics.
ALERT
Never give the patient topical anesthetic drops for
self-administration. Abuse of this medication can
delay healing, especially if the patient rubs the
numb eye and further injures it.
Monitoring
H Visual acuity
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Performing eye irrigation

SQUEEZE BOTTLE
I.V. TUBE
MORGAN LENS
For moderate-volume irrigation to

remove eye secretions, for example
apply sterile ophthalmic irrigant to the
eye directly from the squeeze bottle
container. Direct the stream at the inner canthus and position the patient so
that the stream washes across the
cornea and exits at the outer canthus.
For copious irrigation to treat chemical burns, for example set up an

I.V. bag and tubing without a needle.
Use the procedure described for moderate irrigation to flush the eye for at
least 15 minutes. Alkali burns may require irrigation for several hours.
Connected to irrigation tubing, a Morgan lens permits continuous lavage

and delivers medication to the eye.
Use an adapter to connect the lens to
the I.V. tubing and the solution container. Begin the irrigation at the prescribed flow rate. To insert the device,
ask the patient to look down as you insert the lens under the upper eyelid.
Then have her look up as you retract
and release the lower eyelid over the
lens.
ALERT
Pulse oximeter probes should be applied to the
middle, ring, or preferably little finger, but never
the index finger, in order to minimize the likelihood of corneal abrasion, especially as patients
emerge from anesthesia.
Patient teaching
Be sure to cover:
H healing process
H proper instillation of antibiotic eyedrops or ointment
H effects of untreated corneal infection
H need to wear safety glasses in the workplace, if
appropriate
H contact lens care and instructions for wear.
Corneal abrasion
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Coronary artery disease

Overview
Description
H Heart disease that results from narrowing of coro-
nary arteries over time due to atherosclerosis

H Primary effect: loss of oxygen and nutrients to myo-
cardial tissue because of diminished coronary blood

flow
Pathophysiology
H Increased blood levels of low-density lipoprotein
(LDL) irritate or damage the inner layer of coronary

vessels.
H LDL enters the vessel after damaging the protective
barrier, accumulates, and forms a fatty streak.
H Smooth muscle cells move to the inner layer to engulf the fatty substance, produce fibrous tissue, and
stimulate calcium deposition.
H Cycle continues, resulting in transformation of the
fatty streak into fibrous plaque and, eventually, a
coronary artery disease (CAD) lesion evolves.
H Oxygen deprivation forces the myocardium to shift
from aerobic to anaerobic metabolism, leading to
accumulation of lactic acid and reduction of cellular pH.
H The combination of hypoxia, reduced energy availability, and acidosis rapidly impairs left ventricular
function.
H The strength of contractions in the affected myocardial region is reduced as the fibers shorten inadequately, resulting in less force and velocity.
H Wall motion is abnormal in the ischemic area, resulting in less blood being ejected from the heart with
each contraction.
Causes
H Atherosclerosis
H Dissecting aneurysm
H Infectious vasculitis
H Syphilis
H Congenital defects
H Coronary artery spasm
Risk factors
H Family history
H High cholesterol level
H Smoking
H Diabetes
H Hormonal contraceptives
H Obesity
H Sedentary lifestyle
H Stress
H Increased homocystine levels
Incidence
H Occurs after age 40
206
H Males eight times more susceptible than premeno-
pausal females
H Risk increased by positive family history
H White males more susceptible than nonwhite males;
nonwhite females more susceptible than white females

H Occurs in about 11 million Americans
H Angina
Complications
H Arrhythmias
H Heart failure
Assessment
History
H Angina that may radiate to the left arm, neck, jaw, or
shoulder blade
H Commonly occurring after physical exertion but pos-
sibly following emotional excitement, exposure to

cold, or ingestion of a large meal
H May develop during sleep; symptoms wake the
patient
H Nausea
H Vomiting
H Fainting
H Sweating
H Stable angina (predictable and relieved by rest or nitrates)
H Unstable angina (increases in frequency and duration and is more easily induced and generally indicates extensive or worsening disease and, untreated,
may progress to MI)
H Crescendo angina (an effort-induced pain occurring
with increasing frequency and decreasing provocation)
H Prinzmetals or variant angina pectoris (severe noneffort-produced pain occurs at rest without provocation due to spasm)
Physical findings
H Cool extremities
H Xanthoma
H Arteriovenous nicking of the eye
H Obesity
H Hypertension
H Positive Levines sign (holding fist to chest)
H Decreased or absent peripheral pulses
Test results
Imaging
H Myocardial perfusion imaging with radionucleotide
during treadmill exercise shows ischemic areas of
the myocardium, visualized as cold spots.
H Pharmacologic myocardial perfusion imaging in arteries with stenosis shows decrease in blood flow
proportional to the percentage of occlusion.
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H Coronary angiography reveals the location and de-
gree of coronary artery stenosis or obstruction, collateral circulation, and the condition of the artery
beyond the narrowing.
H Stress echocardiography may show abnormal wall
motion.
H Multiple-gated acquisition scanning demonstrates
cardiac wall motion and reflects injury to cardiac
tissue.
H Electrocardiography may be normal between anginal
episodes. During angina, it may show ischemic
changes.
H Exercise stress testing may be performed to detect
ST-segment changes during exercise, indicating
ischemia, and to determine a safe exercise prescription.
Treatment
General
Preventing coronary artery disease

Because coronary artery disease is so widespread, prevention is important. Dietary restrictions aimed at reducing the intake of calories (in obesity) and of salt, fats, and
cholesterol minimize the risk, especially when supplemented with regular exercise. Abstention from smoking
and reduction of stress are also essential.
Other preventive actions include control of hypertension
(with diuretics or sympathetic beta-adrenergic blockers),
control of elevated serum cholesterol or triglyceride levels
(with antilipemics such as HMG-CoA reductase inhibitors,
including atorvastatin, pravastatin, or simvastatin), and
measures to minimize platelet aggregation and the danger
of blood clots (with aspirin, for example).
H Ask the patient to grade the severity of his pain on a
scale of 0 to 10.
H Keep nitroglycerin available for immediate use. In-
and maintaining ideal body weight (see Preventing

coronary artery disease)
H Activity restrictions possible
H Regular exercise
struct the patient to call immediately whenever he

feels pain and before taking nitroglycerin.
H Observe for signs and symptoms that may signify
worsening of condition.
H Maintain bed rest immediately postoperatively with
the head of the bed elevated at least 30 degrees.
spirometer use postoperatively.
H Encourage early ambulation after surgery.
Medications
Monitoring
H Antianginals, such as ranolazine and nitroglycerin

H Beta-adrenergic blocker such as metoprolol
H Calcium channel blocker such as diltiazem
H Antiplatelets, such as ticlopidine and aspirin
H Antilipemic such as simvastatin
H Antihypertensive such as lisinopril
H Vital signs
H Intake and output
H Effectiveness of pain medication during anginal
Surgery
H Chest tube drainage, after surgery
H Cardiac rate and rhythm
H Stress reduction techniques essential, especially if
known stressors precipitate pain

H Lifestyle modifications, such as smoking cessation
H Coronary artery bypass graft

H Keyhole or minimally invasive surgery
H Angioplasty
H Endovascular stent placement
H Laser angioplasty
H Atherectomy
Key outcomes
The patient will:
H plan menus appropriate to prescribed diet
H demonstrate understanding of the disease process
body image
pain.
episodes
H Abnormal bleeding and distal pulses following inter-
vention procedures
Patient teaching
Be sure to cover:
H risk factors for CAD
H avoidance of activities that precipitate pain
H effective coping mechanisms to deal with stress
H the need to follow the prescribed drug regimen
H low-sodium and low-calorie diet
H the importance of regular, moderate exercise.
Discharge planning
H Refer the patient to a weight-loss program, if needed.
needed.
H Refer the patient to a cardiac rehabilitation program,
if indicated.
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Cor pulmonale
H In response to hypoxia, the bone marrow produces
more red blood cells, causing polycythemia.

H The bloods viscosity increases, further aggravating
pulmonary hypertension. This increases the right

ventricles workload, causing heart failure. (See Cor
pulmonale: An overview.)
Overview
Description
H Hypertrophy and dilation of the right ventricle sec-
Causes
ondary to disease affecting the structure or function

of the lungs or their vasculature
H Can occur at the end stage of various chronic disorders of the lungs, pulmonary vessels, chest wall, or
respiratory control center
H Also called right-sided heart failure
H Disorders affecting the pulmonary parenchyma

H Bronchial asthma
H Primary pulmonary hypertension
H Vasculitis
H Pulmonary emboli
H External vascular obstruction resulting from a tumor
Pathophysiology
H An occluded vessel impairs the hearts ability to gen-
erate enough pressure.

H Increased blood flow creates pulmonary hyperten-
sion.
H Pulmonary hypertension increases the hearts work-
load.
H To compensate, the right ventricle hypertrophies to
force blood through the lungs.
or aneurysm
H Kyphoscoliosis
H Pectus excavatum (funnel chest)
H Muscular dystrophy
H Poliomyelitis
H Obesity
H High altitude
Incidence
H Accounts for 6% to 7% of all types of adult heart
disease in the United States
Cor pulmonale: An overview

Although pulmonary restrictive disorders (such as fibrosis
or obesity), obstructive disorders (such as bronchitis), or
primary vascular disorders (such as recurrent pulmonary
emboli) may cause cor pulmonale, these disorders share
this common pathway.
H Dyspnea
H Tachypnea
Complications
Pulmonary disorder
Anatomic alterations in the pulmonary blood vessels and

functional alterations in the lung
H Right- and left-sided heart failure

H Hepatomegaly
H Edema
H Ascites
H Pleural effusions
H Thromboembolism due to polycythemia
Assessment
Increased pulmonary vascular resistance
Pulmonary hypertension
History
H Dyspnea
H Chronic productive cough
H Fatigue
H Weakness
Physical findings
Right ventricular hypertrophy (cor pulmonale)
HEART FAILURE
208
Cor pulmonale
H Wheezing respirations
H Tachypnea
H Dependent edema
H Enlarged, tender liver
H Hepatojugular reflux
H Tachycardia
H Pansystolic murmur at the lower left sternal border
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Test results
Monitoring
Laboratory
H Arterial blood gas analysis detects decreased
partial pressure of arterial oxygen (usually less
than 70 mm Hg and rarely more than 90 mm Hg).
H Hematocrit is typically over 50%.
H Serum hepatic tests may show an elevated level of
aspartate aminotransferase levels.
Imaging
H Echocardiography demonstrates right ventricular
enlargement.
H Angiography shows right ventricular enlargement.
H Chest X-rays reveal large central pulmonary arteries
and right ventricular enlargement.
H Magnetic resonance imaging measures the right ventricular mass, wall thickness, and ejection fraction.
H Cardiac catheterization measures pulmonary vascular
pressures.
H Electrocardiography shows arrhythmias, such as premature atrial and ventricular contractions and atrial
fibrillation during severe hypoxia, and also right
bundle-branch block, right axis deviation, prominent
P waves, and an inverted T wave in right precordial
leads.
H Pulmonary function studies reflect underlying pulmonary disease.
Other
H Pulmonary artery catheterization shows increased
right ventricular and pulmonary artery pressures.
H Vital signs
H Oxygenation
H Intake and output
H Laboratory values
Patient teaching
Be sure to cover:
H medication administration and possible adverse effects.
Discharge planning
H Refer the patient for home services, as indicated.
Treatment
General
H Low-sodium diet
H Limited activity or bed rest
H Phlebotomy, if necessary
Medications
H Antibiotics, such as amoxicillin and ampicillin
H Oxygen
Key outcomes
The patient will:
H use support services and develop coping mechanisms.
H Administer oxygen as prescribed.
Cor pulmonale
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Creutzfeldt-Jakob
disease
H Sporadic form of unknown etiology

H Iatrogenic or acquired form due to inadvertent expo-
sure to CJD-contaminated equipment or material as

a result of brain surgery, corneal grafts, or use of human pituitary-derived growth hormones or gonadotropin
Incidence
Overview
Description
H Rapidly progressive infectious disease attacking the
central nervous system (CNS)

H Manifested by progressive dementia, tremors, and
muscle wasting
H About one case in 1 million people worldwide
annually
H Most cases sporadic, accounting for about 85% of all
cases
H About 5% to 15% of cases familial, with an autoso-
mal dominant pattern of inheritance

H Usually patients older than age 55; median age of
death in the United States: 68
H Always fatal
H Not transmitted by normal casual contact (although
H Affects males and females of diverse ethnic back-
iatrogenic transmission can occur)

H Has a 15- to 20-month incubation period
H Typical duration: 6 months
H New variant of Creutzfeldt-Jakob disease emerged in
Europe in 1996 (see Understanding new-variant
Creutzfeldt-Jakob disease)
H No cure and cant slow progression
H Also known as CJD
H Most cases in Libya, North Africa, and Slovakia
Pathophysiology
grounds
H Rapidly progressive dementia
H Prominent myoclonus
Complications
H Severe, progressive dementia
H CNS abnormalities
H Death
H CJD is caused by the abnormal accumulation or me-
tabolism of prion proteins.

H These modified proteins are resistant to proteolytic
digestion and aggregate in the brain to produce rodlike particles.

H The accumulation of these modified cellular proteins
results in neuronal degeneration and spongiform
changes in brain tissue.
Causes
H Familial or genetically inherited form
Understanding new-variant
Creutzfeldt-Jakob disease
Like conventional Creutzfeldt-Jakob disease (CJD), variant
CJD (vCJD) is a rare, fatal neurodegenerative disease.
Most cases have been reported in the United Kingdom,
and its most likely caused by exposure to bovine spongiform encephalopathy (BSE), a fatal brain disease in cattle
also known as mad cow disease. Ingestion of beef products from cattle with BSE is the most probable route of
exposure.
vCJD affects patients at a much younger age than CJD,
and the duration of the illness is much longer (14 months
versus 6 months).
Regulations have been established in Europe to control
outbreaks of BSE in cattle and to prevent contaminated
meat from entering the food supply. vCJD and its relationship with BSE are still being explored by the Centers for
Disease Control and Prevention and the World Health Organization.
210
Assessment
History
H Mood changes
H Emotional lability
H Poor concentration
H Lethargy
H Impaired judgment
H Memory loss
H Involuntary muscle movements
H Vision disturbances or other types of hallucinations
H Gait disturbances
Physical findings
H Dementia
H Myoclonus
H Spasticity
H Agitation
H Tremor
H Clumsiness
H Ataxia
H Hypokinesis and rigidity
H Hyperreflexia
Test results
Laboratory
H Cerebral spinal fluid (CSF) immunoassay may show
abnormal protein species.
H CSF analysis may show mildly elevated protein level.
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Imaging
imaging of the brain may show evidence of generalized cortical atrophy.
H EEG may show burst suppression changes in brainwave activity.
H Brain biopsy may show spongiform changes.
Other
H Autopsy of brain tissue allows definitive diagnosis.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and supportive treatment
H prevention of disease transmission
H effective coping strategies
H safety precautions.
Discharge planning
H Refer the patient and his family to CJD support
Treatment
groups.
H Refer the patient for hospice care, as appropriate.
General
H Palliative care to make the patient comfortable and to
ease symptoms
Medications
H Antiparkinsonian such as amantadine
Surgery
H Possible brain biopsy for diagnosis
Key outcomes
The patient will:
H verbalize feelings of anxiety and fear
H demonstrate effective coping techniques
H remain free from injury
H maintain social interaction to the extent possible
H utilize support systems.
H Assist the patient and his family through the grieving
process.
H Encourage verbalization of concerns and fears.
H Encourage involvement of the patient and his family
in care decisions.
Monitoring
H Vital signs
H Intake and output
H Neurologic status
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Crohns disease
H Perforation
H Nutritional deficiencies caused by malabsorption and
maldigestion
Overview
Description
Assessment
H Inflammatory bowel disease possibly affecting any
History
part of the GI tract but commonly involving the terminal ileum

H Fifty percent of cases involving colon and small bowel; 33% involving terminal ileum; 10% to 20% involving only colon
H Extends through all layers of the intestinal wall; possibly involving regional lymph nodes and mesentery
H Gradual onset of signs and symptoms, marked by pe-
Pathophysiology
H Crohns disease involves slow, progressive inflamma-
tion of the bowel.
riods of remission and exacerbation

H Fatigue and weakness
H Fever, flatulence, nausea
H Steady, colicky, or cramping abdominal pain usually
occurring in the right lower quadrant

H Diarrhea possibly worsening after emotional upset
or ingestion of poorly tolerated foods, such as milk,

fatty foods, and spices
H Weight loss
H Lymphatic obstruction is caused by enlarged lymph
Physical findings
nodes.
H Edema, mucosal ulceration, fissures, and abscesses
occur.
H Elevated patches of closely packed lymph follicles
(Peyers patches) develop in the small intestinal lining.
H Fibrosis occurs, thickening the bowel wall and causing stenosis.
H Inflamed bowel loops adhere to other diseased or
normal loops.
H The diseased bowel becomes thicker, shorter, and
narrower.
H Possible soft or semiliquid stool, usually without
Causes
H Lymphatic obstruction and infection among con-
tributing factors
Risk factors
H History of allergies
H Immune disorders
H Genetic predisposition 10% to 20% of patients
with the disease have one or more affected relatives;

sometimes occurs in monozygotic twins
Incidence
H More common in Jewish people
H Onset usually before age 30
H Diarrhea
H Abdominal pain
H Weight loss
gross blood
H Right lower quadrant tenderness or distention
H Possible abdominal mass, indicating adherent loops
of bowel
H Hyperactive bowel sounds
H Bloody diarrhea
H Perianal and rectal abscesses
Test results
Laboratory
H Occult blood is seen in stools.
H Hemoglobin level and hematocrit are decreased.
rate are increased.
H Serum potassium, calcium, and magnesium levels
are decreased.
H Hypoproteinemia is present due to intestinal protein
loss.
H Vitamin B12 and folate levels are decreased.
Imaging
H Small-bowel X-rays may show irregular mucosa, ulceration, and stiffening.
H Barium enema reveals the string sign (segments of
stricture separated by normal bowel) and may also
show fissures and narrowing of the lumen.
H Sigmoidoscopy and colonoscopy show patchy areas
of inflammation and may also reveal the characteristic coarse irregularity (cobblestone appearance) of
the mucosal surface.
H Biopsy reveals granulomas in up to half of all specimens.
Complications
Treatment
H Anal fistula
H Perineal abscess
H Fistulas of the bladder or vagina or to the skin in an
General
old scar area

212
Crohns disease
H Stress reduction
H Avoidance of foods that worsen diarrhea
H Adequate caloric, protein, and vitamin intake
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H Parenteral nutrition, if necessary

H Reduced physical activity
Medications
H Corticosteroid such as budesonide
H Immunosuppressants, such as adalimumab and
infliximab
H Sulfonamide such as sulfasalazine
H Antibacterials and antiprotozoals, such as metronida-
zole and nitazoxanide

H Antidiarrheal such as octreotide
H Opioid such as morphine
H Vitamin supplements, such as vitamin B12 and folate
H Antispasmodic such as alosetron
H Iron supplement such as ferrous sulfate
Surgery
H Indicated for acute intestinal obstruction
H Colectomy with ileostomy
Patient teaching
Be sure to cover:
H information about the disease, symptoms, and complications
H ordered diagnostic tests and pretest guidelines
H the importance of adequate rest
H how the patient can identify and reduce sources of
stress
H prescribed dietary changes
H prescribed medications, administration, and possible
adverse effects.
Discharge planning
appropriate.
H Refer the patient to enterostomal therapist, if indi-
cated.
Key outcomes
The patient will:
H regain normal bowel movements
H verbalize understanding of the disease process and
treatment regimen
H exhibit adequate coping mechanisms and seek
appropriate sources of support.
H Provide emotional support to the patient and his
family.
H Provide meticulous skin care after each bowel
movement.
H Schedule patient care to include rest periods
throughout the day.

H Assist with dietary modification.
H Give prescribed iron supplements and blood
transfusions.
Monitoring
H GI status
H Vital signs
H Intake and output, including amount of stool
H Daily weight
H Serum electrolyte, glucose, and Hb levels and stools
for occult blood

H Signs of infection or obstruction
H Bleeding, especially with steroid use
H Pain control
H Skin integrity
Crohns disease
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Croup
Overview
Description
H Viral infection causing severe inflammation and ob-
struction of the upper airway

H Childhood disease manifested by acute laryngotracheobronchitis (most commonly), laryngitis, acute
spasmodic laryngitis, and febrile rhinitis
H Incubation period about 3 to 6 days; contagious
while febrile
H Recovery usually complete
Pathophysiology
H Viral invasion of the laryngeal mucosa leads to in-
flammation, hyperemia, edema, epithelial necrosis,

and shedding.
H This leads to irritation and cough, reactive paralysis
and continuous stridor, or collapsible supraglottic or
inspiratory stridor and respiratory distress.
H A thin, fibrinous membrane covers the mucosa of the
epiglottis, larynx, and trachea. (See How croup affects the upper airways.)
Causes
H Parainfluenza viruses
H Adenoviruses
H Respiratory syncytial virus
H Influenza viruses
H Measles viruses
H Bacteria (pertussis and diphtheria)
Incidence
Special populations
Occurs mainly in children ages 3 months to 5
years.
H Affects boys more commonly than girls
H Usually occurs in late autumn and early winter
Special populations
Acute spasmodic laryngitis affects children
between ages 1 and 3, particularly those with
allergies.
H Sharp, barklike, or brassy cough progressing to
stridor
H Hoarse or muffled vocal sounds
Complications
214
Croup
H Dehydration
H Ear infection
H Pneumonia
H Hypoxia
H Hypercapnia
Assessment
History
H Recent upper respiratory infection
Laryngotracheobronchitis
H Fever and breathing problems usually occurring at
night
H Difficulty exhaling
Laryngitis in children
H Mild sore throat
H Cough
H Marked hoarseness (rare)
H No respiratory distress
Laryngitis in infants
Acute spasmodic laryngitis
H Mild to moderate hoarseness
H Nasal discharge
H Characteristic cough and noisy inspiration
H Anxiety
H Increased dyspnea
H Transient cyanosis
Physical findings
H Rhinorrhea
H Use of accessory muscles
H Nasal flaring
H Barklike cough
H Hoarse, muffled vocal sounds
H Inspiratory stridor
Laryngotracheobronchitis
H Edema of bronchi and bronchioles
H Expiratory rhonchi
H Scattered crackles
Laryngitis
H Suprasternal and intercostal retractions
H Inspiratory stridor
H Dyspnea, tachypnea
H Severe dyspnea and exhaustion in later stages
Acute spasmodic laryngitis
H Labored breathing with retractions
H Clammy skin
H Rapid pulse rate
Test results
Laboratory
H Throat cultures show bacteria and sensitivity to
antibiotics.
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Imaging
H Neck X-ray may show upper airway narrowing and
edema in subglottic folds; helps to differentiate croup
from bacterial epiglotidititis.
H Computed tomography scan helps differentiate between croup, epiglotidititis, and noninfection.
H Laryngoscopy may reveal inflammation and obstruction in epiglottal and laryngeal areas.
How croup affects the upper airways

In croup, inflammatory swelling and spasms constrict the
larynx, thereby reducing airflow. This cross-sectional
drawing (from chin to chest) shows the upper airway
changes caused by croup. Inflammatory changes almost
completely obstruct the larynx (which includes the epiglottis) and significantly narrow the trachea.
Treatment
General
H Home or hospitalized care
H Humidification during sleep
H Intubation if other means of preventing respiratory
failure unsuccessful
H Parenteral fluids, if required
H Rest periods
Medications
H Oxygen therapy, as needed
H Antibiotics, such as cefuroxime and cefprozil, if
Inflamed
laryngeal area
Inflamed
subglottic tissue
Narrowed
trachea
cause is bacterial
H Adrenergic, aerosolized racemic epinephrine for
moderately severe croup

H Corticosteroids for acute laryngotracheobronchitis
Surgery
H Tracheostomy (rare)
Key outcomes
The patient will:
H maintain normal temperature
H verbalize understanding of the disorder.
H Adminster oxygen, as prescribed.
H Administer I.V. fluids, as prescribed.
H Provide quiet diversional activities.
H Engage parents in the care of the infant or child.
H Position an infant in an infant seat or prop him up
H Use sponge baths and hypothermia blanket, as or-
dered, for temperatures above 102 F (38.9 C).
Monitoring
H Vital signs
H Intake and output
H Signs and symptoms of dehydration
Patient teaching
Be sure to cover:
H humidification
H hydration
H signs and symptoms of ear infection
H signs and symptoms of pneumonia.
with a pillow.
H Position an older child in Fowlers position.
H Avoid milk-based fluids if the patient has thick mucus
or swallowing difficulties.
H Isolate patients for respiratory syncytial virus and
parainfluenza infections.
Croup
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Cryptococcosis
Overview
Description
H Fungal infection that usually begins as asymptomatic
pulmonary infection in patient who presents with

meningoencephalitis
H Also known as torulosis and European blastomycosis
Pathophysiology
H Small granulomas and cysts in the cerebral cortex
and, later, in deep cerebral tissues produce a minimal inflammatory response.

H In chronic cases, dense basilar arachnoiditis occurs.
H Lung lesions with intense granulomatous inflammation occur.
Causes
H Airborne fungus Cryptococcus neoformans found in
dust particles contaminated by pigeon stool

H Transmission by inhalation of cryptococci
Incidence
H Prevalent in immunocompromised patients and those
taking immunosuppressant drugs

H Increasing, especially in patients with acquired im-
munodeficiency syndrome
H Disseminates to extrapulmonary sites, including the
central nervous system (CNS), skin, bones, prostate

gland, liver, and kidneys
H Without treatment, leads to CNS infection and death
H Mortality dramatically reduced with treatment; neurologic deficits, such as paralysis and hydrocephalus,
not necessarily reduced with treatment
Complications
H Optic atrophy
H Ataxia
H Hydrocephalus
H Deafness
H Paralysis
H Organic mental syndrome
H Personality changes
H Coma
H Death
Assessment
History
H Human immunodeficiency virus infection or another
immunosuppressive disorder
H Usually asymptomatic but patient may complain of
dull chest pain and cough producing slight amount

of white, blood-streaked sputum
216
Cryptococcosis
Physical findings
H Progressively severe frontal and temporal headache
H Diplopia, blurred vision, and papilledema
H Tinnitus, dizziness, ataxia, and aphasia
H Vomiting
H Memory changes, inappropriate behavior, irritability,
and psychosis
H Facial weakness
H Hyperactive reflexes and seizures in the late stage
H Pain in the long bones, skull, spine, and joints
H Red facial papules and other skin abscesses, with or
without ulceration
H Rarely, pleural friction rub or crackles
H Photophobia
Test results
Imaging
H Chest X-ray or computed tomography scan of the
chest reveals lesions in pulmonary cryptococcosis.
Laboratory
H Analysis or cultures of the sputum, urine, prostatic
secretions, or bone marrow aspirate show C. neoformans.
H Tissue or neural biopsy shows myriad cryptococci.
H India ink preparation of cerebrospinal fluid (CSF)
diagnosing CNS infection when C. neoformans is
detected.
H Blood cultures are positive only in severe infection.
H Antigen titer in serum and CSF is elevated in disseminated infection.
H Protein levels and white blood cell count are elevated
in CNS infection.
H CSF glucose levels are moderately decreased in about
50% of patients.
Other
H Lumbar puncture shows increased CSF pressure.
Treatment
General
H Early treatment for cryptococcal disease
Medications
H Combination of antifungal antibiotics amphotericin B
and flucytosine, or amphotericin B alone
Key outcomes
The patient will:
H be free from pain
H be free from injury
H maintain patent airway
H increase activity, as tolerated.
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H Before therapy, obtain electrolyte and creatinine
levels.
H Observe for adverse effects such as diarrhea.
H Evaluate the need for long-term venous access for
administering amphotericin B.
H Provide psychological support to help the patient
cope with long-term treatment.

H If vision loss occurs, provide a safe environment.
Monitoring
H Vital signs
H Neurologic checks
H Headache, vomiting, and nuchal rigidity
H Intake and output
H Blood urea nitrogen, creatinine levels, and complete
blood count results

H Urinalysis results
H Magnesium and potassium levels and liver function
test results
H Blood levels of flucytosine
Patient teaching
Be sure to cover:
H medication therapy, including dosage, desired drug
actions, adverse effects, and need for long-term treatment.
Discharge planning
H Urge the patient to return for follow-up care and
evaluation every few months for 1 year.

H Refer the patient for resource and support services,
as needed.
Cryptococcosis
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Cryptorchidism
H True undescended testes remain along the path of
Overview
Causes
normal descent, while ectopic testes deviate from

that path.
Description
H Congenital disorder in which one or both testes fail
to descend into the scrotum, remaining in the abdomen or inguinal canal or at the external ring
H May be bilateral, but more commonly affects the
right testis (see Varieties of cryptorchidism)
H Hormonal factors
H Testosterone deficiency
H Structural factors
Incidence
H Occurs in 30% of premature male neonates, but in
only 3% of those born at term
Pathophysiology
H In about 80% of affected infants: testes descend
H In the male fetus, testosterone normally stimulates
the formation of the gubernaculum. A fibromuscular

band connects the testes to the scrotal floor.
H This band probably helps pull the testes into the
scrotum by shortening as the fetus grows.
H Thus, cryptorchidism may result from inadequate
testosterone levels or a defect in the testes or the gubernaculum.
H Because the testis is maintained at a higher temperature, spermatogenesis is impaired, leading to reduced fertility.
spontaneously during first year; in the rest: testes

may descend later
H Testis on the affected side not palpable in the scro-
tum; underdeveloped scrotum (unilateral cryptorchidism)

H Scrotum enlarged on the unaffected side
H Infertility
Varieties of cryptorchidism
Descent interrupted beyond
external inguinal ring
Descended but not to

bottom of scrotum
218
Cryptorchidism
Partially descended
Testis retained in
abdomen
Normal
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Complications
H Sterility
H Increased risk for testicular cancer
H Increased vulnerability of the testes to trauma
Assessment
Physical findings
H Nonpalpable testes
H Underdeveloped scrotum
Test results
Laboratory
H Buccal smear (cells from oral mucosa) determines
genetic sex (a male sex chromatin pattern).
H Serum gonadotropin confirms the presence of testes
by showing presence of circulating hormone.
Treatment
Medications
H Human chorionic gonadotropin
Surgery
H Orchiopexy
Key outcomes
The patient will:
H express or demonstrate feelings of increased comfort
H be free from complications.
H Encourage the parents of the child with undescended
testes to express their concern about his condition.

H Tell the parents that a rubber band may be taped to
the patients thigh for about 1 week after surgery to

keep the testis in place. Explain that his scrotum may
swell but shouldnt be painful.
Monitoring
After surgery
H Vital signs
H Intake and output
H Operative site
H Pain control
Patient teaching
Be sure to cover:
H the disorder, treatment, and effect on reproduction
H surgery or medications prescribed.
Cryptorchidism
219
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Cushings syndrome
H Menstrual disturbances
H Sexual dysfunction
H Psychiatric problems, ranging from mood swings to
Overview
frank psychosis
Description
Assessment
H Clinical manifestations of glucocorticoid excess, par-
ticularly cortisol
H May also reflect excess secretion of mineralocorti-
coids and androgens

H Classified as primary, secondary, or iatrogenic, depending on etiology
H Prognosis dependent on early diagnosis, identification of underlying cause, and effective treatment
Pathophysiology
H A loss of normal feedback inhibition by cortisol
occurs.
H Elevated levels of cortisol dont suppress hypothala-
mic and anterior pituitary secretion of corticotropinreleasing hormone and adrenocorticotropic hormone (ACTH).
H The result is excessive levels of circulating cortisol.
Causes
H Pituitary microadenoma
H Excess production of corticotropin
H Corticotropin-producing tumor in another organ
H Chronic use of synthetic glucocorticoids or corti-
cotropin
H Cortisol-secreting adrenal tumor
Special populations
In neonates, the usual cause of Cushings syndrome
is adrenal carcinoma.
Incidence
H Can affect a person at any age
H Adiposity of the face, neck, and trunk
H Purple striae on the skin
H Truncal weight gain
H Glucose intolerance
Complications
H Osteoporosis and pathologic fractures
H Peptic ulcer
H Dyslipidemia
H Impaired glucose tolerance
H Diabetes mellitus
H Frequent infections
H Slow wound healing
H Suppressed inflammatory response
H Hypertension
H Ischemic heart disease; heart failure
220
Cushings syndrome
History
H Use of synthetic steroids
H Fatigue
H Muscle weakness
H Polyuria
H Thirst
H Frequent infections
H Water retention
H Amenorrhea
H Decreased libido
H Irritability; emotional instability
H Symptoms resembling those of hyperglycemia
H Impotence
H Headache
Physical findings
H Thin hair
H Moon-shaped face
H Hirsutism
H A buffalo-humplike back
H Thin extremities
H Muscle wasting and weakness
H Petechiae, ecchymoses, and purplish striae
H Delayed wound healing
H Swollen ankles
H Hypertension
H Central obesity
H Acne
Test results
Laboratory
H Salivary free cortisol level is elevated.
H ACTH is decreased in adrenal disease and excess
pituitary or ectopic secretion of ACTH is increased.
H Blood chemistry may show hypernatremia, hypokalemia, hypocalcemia, and elevated blood glucose
level.
H Urinary free cortisol level is elevated.
H Serum cortisol level is elevated in the morning.
H Glycosuria occurs.
Imaging
H Ultrasonography, computed tomography scan, and
magnetic resonance imaging may show the location
of a pituitary or adrenal tumor.
H A low-dose dexamethasone suppression test shows
failure of plasma cortisol levels to be suppressed.
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Treatment
General
H Management to restore hormone balance and re-
verse Cushings syndrome, including radiation, drug

therapy, or surgery
H High-protein, high-potassium, low-calorie, lowsodium diet
Medications
H Antihypertensive such as atenolol
H Glucocorticoid such as dexamethasone
H Potassium supplements
H Antihormone agents, such as ketoconazole, amino-
glutethimide, and mitotane

H Pituitary hormone such as pitressin
ALERT
Glucocorticoid administration on the morning of
surgery can help prevent acute adrenal insufficiency during surgery. Cortisol therapy is essential during and after surgery to help the patient tolerate
the physiologic stress caused by removal of the
pituitary or adrenal glands.
Surgery
H Possible hypophysectomy or pituitary irradiation
H Bilateral adrenalectomy
H Excision of nonendocrine, corticotropin-producing
tumor, followed by drug therapy
Key outcomes
The patient will:
H remain free from infection
H perform activities of daily living as tolerated within
the confines of the disorder
With transsphenoidal approach to

hypophysectomy
H Maintain nasal packing.
H Avoid activities that increase intracranial pressure
(ICP).
Monitoring
H Vital signs
H Intake and output
H Daily weights
H Serum electrolyte results
After bilateral adrenalectomy and

hypophysectomy
H Neurologic status
H Severe nausea, vomiting, and diarrhea
H GI status
H Adrenal hypofunction
H Increased ICP
H Hypopituitarism
H Transient diabetes insipidus
H Hemorrhage and shock
After transsphenoidal approach to
hypophysectomy
H Cerebrospinal fluid leak
Patient teaching
Be sure to cover:
H lifelong steroid replacement
H signs and symptoms of adrenal crisis
H medical identification bracelet
H stress reduction strategies.
Discharge planning
H Refer the patient to a mental health professional for
additional counseling, if necessary.
H Consult a dietitian.
H Use protective measures to reduce the risk of
infection.
H Use meticulous hand-washing technique.
H Schedule adequate rest periods.
H Help to develop effective coping strategies.
Cushings syndrome
221
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Cystic fibrosis
Overview
Description
H Chronic, progressive, inherited, incurable disease af-
fecting exocrine (mucus-secreting) glands

H Transmitted as an autosomal recessive trait
H Genetic mutation that involves chloride transport
across epithelial membranes (more than 100 specific mutations of the gene identified)
H Characterized by major aberrations in sweat gland,
respiratory, and GI functions
H Accounts for almost all cases of pancreatic enzyme
deficiency in children
H Signs and symptoms apparent soon after birth or not
for several years
H Death typically from pneumonia, emphysema, or
atelectasis
Pathophysiology
H The viscosity of bronchial, pancreatic, and other mu-
cous gland secretions increases, obstructing glandular ducts.

H The accumulation of thick, tenacious secretions in
the bronchioles and alveoli causes respiratory
changes, eventually leading to severe atelectasis and
emphysema.
H The disease also causes characteristic GI effects in
the intestines, pancreas, and liver.
H Obstruction of the pancreatic ducts results in a deficiency of trypsin, amylase, and lipase. This prevents
the conversion and absorption of fat and protein in
the intestinal tract and interferes with the digestion of
food and absorption of fat-soluble vitamins.
H In the pancreas, fibrotic tissue, multiple cysts, thick
mucus, and fat replace the acini, producing signs of
pancreatic insufficiency.
Causes
H Dyspnea
H Poor weight gain
Complications
H Bronchiectasis
H Pneumonia
H Atelectasis
H Dehydration
H Distal intestinal obstructive syndrome
H Malnutrition
H Gastroesophageal reflux
H Cor pulmonale
H Hepatic disease
H Diabetes
H Arthritis
H Biliary disease
H Clotting problems
H Retarded bone growth
H Delayed sexual development
H Azoospermia in males
H Secondary amenorrhea in females
H Cardiac arrhythmias
H Potentially fatal shock
H Death
Assessment
History
H Recurring bronchitis and pneumonia
H Nasal polyps and sinusitis
H Wheezing
H Dry, nonproductive cough
H Abdominal distention, vomiting, constipation
H Frequent, bulky, foul-smelling, and pale stool with a
high fat content

H Poor weight gain
H Poor growth
H Ravenous appetite
H Hematemesis
H Autosomal recessive mutation of gene on chromo-
some 7
H Causes of symptoms: increased viscosity of bronchial,
pancreatic, and other mucous gland secretions and

consequent destruction of glandular ducts
Incidence
H Most common fatal genetic disease of white children
H Twenty-five percent chance of transmission with each
pregnancy: both parents carriers of the recessive

gene
H Highest in people of northern European ancestry
H Less common in Blacks, Native Americans, and people of Asian ancestry
H Equally common in both sexes
H Wheezy respirations
H Dry, nonproductive, paroxysmal cough
222
Cystic fibrosis
Special populations
Neonates may exhibit meconium ileus and develop
symptoms of intestinal obstruction, such as abdominal distention, vomiting, constipation, dehydration, and electrolyte imbalance.
Physical findings
H Wheezy respirations
H Dry, nonproductive, paroxysmal cough
H Dyspnea
H Tachypnea
H Bibasilar crackles and hyperresonance
H Barrel chest
H Cyanosis, and clubbing of the fingers and toes
H Distended abdomen
H Thin extremities
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H Sallow skin with poor turgor

H Delayed sexual development
H Neonatal jaundice
H Hepatomegaly
H Rectal prolapse
H Failure to thrive
Test results
Laboratory
H Sweat test reveals sodium and chloride values.
H Stool specimen analysis shows absence of trypsin.
H Deoxyribonucleic acid testing shows presence of the
delta F 508 deletion.
H Liver enzyme tests may show hepatic insufficiency.
H Sputum culture may show such organisms as
Pseudomonas and Staphylococcus.
H Serum albumin level is decreased.
H Serum electrolytes may show hypochloremia and
hyponatremia.
H Arterial blood gas shows hypoxemia.
Imaging
H Chest X-rays may show early signs of lung obstruction.
H High-resolution chest computed tomography scan
shows bronchial wall thickening, cystic lesions, and
bronchiectasis.
H Pulmonary function tests show decreased vital capacity, elevated residual volume, and decreased forced
expiratory volume in 1 second.
Treatment
General
H Based on organ systems involved
H Chest physiotherapy, nebulization, and breathing ex-
ercises several times per day

H Postural drainage
H Gene therapy (experimental)
H Salt supplements
H High-fat, high-protein, high-calorie diet
H Activity, as tolerated, encouraged
Medications
H Pulmonary enzyme, such as dornase alfa, given by
aerosol nebulizer
H Antibiotic, as appropriate
H Oxygen therapy, as needed
H Oral pancreatic enzymes such as pancreatin
H Bronchodilator such as albuterol
H Vitamin A, D, E, and K supplements
H Annual influenza vaccination
Surgery
H Heart-lung transplantation
H Feeding tube placement for nutritional support
Key outcomes
The patient will:
H consume adequate calories daily
H use a support system to assist with coping
H express an understanding of the illness.
H Administer pancreatic enzymes with meals and
snacks.
H Perform chest physiotherapy and postural drainage.
H Administer oxygen therapy, as needed.
H Provide a well-balanced, high-calorie, high-protein
diet; include adequate fats.

H Provide vitamin A, D, E, and K supplements, if indi-
cated.
H Ensure adequate oral fluid intake.
H Provide exercise and activity periods.
H Encourage breathing exercises.
H Provide the young child with play periods.
H Enlist the help of the physical therapy department
and play therapists, if available.

H Include family members in all phases of the childs
care.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Hydration and nutrition
H Pulse oximetry
H GI status
Patient teaching
Be sure to cover:
H aerosol therapy
H complications.
Discharge planning
H Refer family members for genetic counseling, as
appropriate.
H Refer the patient and his family to a local support
group such as the Cystic Fibrosis Foundation.
Cystic fibrosis
223
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Cytomegalovirus
infection
Overview
Description
H Infection with a member of the herpesvirus group
H Also called generalized salivary gland disease and
cytomegalic inclusion disease
Neonatal complications
H Stillbirth
H Neonatal retinitis
H Microcephaly
H Mental retardation
H Seizures
H Hearing loss
H Thrombocytopenia
H Hemolytic anemia
Assessment
Pathophysiology
History
H Cytomegalovirus (CMV) is found in the saliva, urine,
H Immunosuppressive condition
semen, breast milk, feces, blood, and vaginal and

cervical secretions of infected people. It can be detected in body fluids for weeks or months after infection.
H CMV usually remains latent, but reactivation occurs
when T-lymphocyte-mediated immunity is compromised, as in organ transplantation, lymphoid neoplasms, and certain acquired immunodeficiencies.
H CMV spreads through the body in lymphocytes or
mononuclear cells to the lungs, liver, GI tract, eyes,
and central nervous system (CNS), typically producing inflammatory reactions.
Causes
H Results from a deoxyribonucleic acid virus belonging
to the herpes family

H Transmitted by human contact; once infected, CMV
carried for life

H Transmission through direct contact with secretions
and excretions, through blood transfusions, transplacentally, and through transplanted organs
Risk factors
H Poor hygiene
H Immunosuppression
H Child care workers
Incidence
H Occurs worldwide
H Occurs in approximately 30% to 50% of acquired
immunodeficiency syndrome patients

H One of the most opportunistic pathogens in patients
infected with human immunodeficiency virus
H Mild fatigue, myalgia, and headache or no clinical
symptoms
Complications
H Pneumonia
H Hepatitis
H Ulceration of the GI tract and esophagus
H Retinitis
H Encephalopathy
224
Cytomegalovirus infection
Physical findings
H Fever common
H Lethargy
H In immunocompetent patient with CMV mononucleo-
sis, 3 or more weeks of irregular high fever may be

only finding
H Tachypnea
H Dyspnea
H Cyanosis
H Cough
H Jaundice
H Spider angiomas
H Hepatomegaly
H Splenomegaly
H In infants, CNS damage (mental retardation, hearing
loss, seizures), jaundice, petechial rash, respiratory
distress
Test results
Laboratory
H Isolating the virus or demonstrating increasing serologic titers by complement fixation studies, hemagglutination inhibition antibody tests and, in congenital infections, indirect immunofluorescent tests for
CMV immunoglobulin M antibody allows diagnosis.
Imaging
H Chest X-ray reveals bilateral, diffuse, white infiltrates.
H Computed tomography scan or magnetic resonance
imaging shows CNS involvement.
H Endoscopy shows GI involvement.
H Fundoscopy may show retinitis.
Treatment
General
H Rest, as needed
Medications
H Antivirals, such as cidofovir and ganciclovir
H Immune serum such as cytomegalovirus immune
globulin
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Key outcomes
The patient will:
H maintain normal temperature
H demonstrate skill in conserving energy while carrying
out daily activities to tolerance level
H verbally report having an increased energy level
H articulate factors that intensify pain and modify behavior accordingly
H maintain respiratory rate within 5 breaths of baseline
H express feeling of comfort while maintaining air
exchange.
H Institute standard precautions.
H If vision impairment occurs, provide a safe environ-
ment and encourage optimal independence.
Monitoring
H Intake and output
H Ventilation and oxygenation if the respiratory system
involved
H Vital signs
Patient teaching
Be sure to cover:
H need for parents to wear gloves when in contact with
secretions or changing diapers and to dispose of diapers or soiled articles properly and wash hands thoroughly
H need for female health care workers trying to get
pregnant to have CMV titers drawn to identify their
risk of contracting the infection
H need for an immunosuppressed or pregnant patient
to avoid contact with any person who has confirmed
or suspected CMV infection
H need for an immunosuppressed patient whos CMVseronegative to carry this information with him so he
wont be given CMV-positive blood.
Discharge planning
H Provide emotional support and counseling to the
parents of a child with severe CMV infection. Help

them find support systems, and coordinate referrals
to other health care professionals.
H For information and support, refer the patient and
his family to a local chapter of the National Center for
Infectious Diseases.
Cytomegalovirus infection
225
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Dacryocystitis
Overview
Description
H Infection of the lacrimal sac resulting from obstruc-
tion of the nasolacrimal duct
H Acute, chronic, or congenital
Pathophysiology
H The lacrimal excretory system is a mucous mem-
brane-lined tract thats contiguous with conjuctival

and nasal mucosa.
H Conjuctival and nasal mucosa are normally colonized
with bacteria.
H Inability to drain tears due to a blocked lacrimal
drainage system results in infection. (See A close
look at tears.)
Causes
Acute form
H Staphylococcus aureus
H Beta-hemolytic streptococci
Chronic form
H Streptococcus pneumonia
H Fungus, such as Actinomyces or Candida albicans
H Chronic mucosal degeneration
H Secondary tumors from sinuses, nose, and eye orbits
Risk factors
H Congenital blockage of nasolacrimal duct
Incidence
H More common in adults older than age 40
H More common on the left side than the right side
H Rare in blacks
H Affects females more commonly than males
Acute form
H Sudden onset of pain
H Redness in the medial canthal region
Chronic form
H Incidious onset of watery eyes
Complications
H Hemorrhage
H Infection
H Cerebrospinal fluid leakage
Assessment
History
H Eye pain
H Fever
A close look at tears

Tears begin in the lacrimal gland and drain through the nasolacrimal duct into the nose.
Lacrimal gland
Punctum
Lacrimal canals
Lacrimal sac
Nasolacrimal duct
226
Dacryocystitis
Iris
Pupil
Sclera
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Physical findings
H Severe erythematous swelling around nasal aspect of
lower eyelid
H Tenderness of eyelid
H Tearing
H Conjunctival injection
H Palpable mass inferior to the medial canthal tendon
H Orbital cellulitis
Patient teaching
Be sure to cover:
H applying warm compresses and eyedrops
H reporting signs of worsening infection.
Test results
Laboratory
H Culture of discharge shows causative organism.
H Complete blood count shows elevated white blood
cell count.
Imaging
H X-ray after injection of radiopaque medium locates
atresia.
H Dacryocystography and dacryoscintigraphy identify
anatomical abnormalities of the nasolacrimal
drainage system.
Treatment
General
H Warm compresses
Medications
H Antibiotic eyedrops such as polymyxin/trimethoprim
H Antibiotics, such as gentamicin, amoxicillin, and
clavulanate potassium
Surgery
H Incision and drainage
H Dacryocystorhinostomy (chronic cases)
Key outcomes
The patient will:
H remain free from signs of infection.
H Administer prescribed antibiotics.
H Apply compresses.
Monitoring
H Temperature
H Pain
H Visual acuity
Dacryocystitis
227
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Dermatitis
Overview
Description
H Skin condition characterized by inflammation
H Can be acute or chronic
H Occurs in several forms, including contact, seborrhe-
ic, nummular, exfoliative, and stasis dermatitis (see

Types of dermatitis, pages 230 and 231)
H Typically associated with other atopic diseases
Pathophysiology
H The allergic mechanism of hypersensitivity results in
a release of inflammatory mediators through sensitized antibodies of immunoglobulin (Ig) E.

H Histamine and other cytokines induce an inflammatory response resulting in edema, skin breakdown,
and pruritus.
Causes
H Possible underlying metabolic or biochemical causes
H Possible genetic link to elevated serum IgE levels
H Possible defective T-cell function
H Precipitating factors:
Infections
Allergens
Temperature extremes
Humidity
Sweating
Stress
Incidence
H Common in infants and toddlers between ages 6
H Exposure to an allergen or irritant

H Intense itching
Physical findings
H Depend on type of dermatitis
H Erythematous patches in excessively dry areas
Special populations
In children, look for lesions on the forehead,
cheeks, and extensor surfaces of the arms and legs.
H Lesions usually at flexion points in adults
H During a flare-up: edema, scaling, and vesiculation;
pus-filled vesicles
H In chronic disease: multiple areas of dry, scaly skin,
with white dermatographism, blanching, and lichenification
Test results
H Results depend on type of dermatitis.
Laboratory
H Serum analysis shows elevated IgE levels.
H Tissue cultures may rule out bacterial, viral, or fungal superinfections.
H Allergy testing may disclose allergic rhinitis or
asthma.
H Patch testing and distribution of lesions are used to
pinpoint the provoking allergen.
Other
H Firm stroking of the patients skin with a blunt instrument causes a white not reddened hive to appear on the skin of 70% of patients with atopic dermatitis.
H Food elimination diet may help to identify at least one
allergen.
months and 2 years

H Common in those with strong family histories of
atopic disease
Treatment
General
H Pruritus
H Skin lesions
H Dependent on type of dermatitis

H Elimination of allergens
H Avoidance of precipitating factors
H Ultraviolet B light therapy to increase the thickness of
Complications
H Permanent skin damage
H Lichenification
H Altered pigmentation
H Scarring
H Bacterial, fungal, and viral infections
H Kaposis varicelliform eruption
Assessment
History
H Depends on type of dermatitis
H Family history of atopic dermatitis
228
Dermatitis
the stratum corneum

H Avoidance of food allergens
H Avoidance of overheating
Medications
H Antihistamines, such as diphenhydramine
H Corticosteroids, such as betamethasone and hydro-
cortisone
H Antibiotics such as gentamicin
H Antifungals such as ketoconazole
H Antivirals such as acyclovir
H Antipruritics such as hydroxyzine hydrochloride
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Surgery
H Vein stripping, sclerotherapy, or skin grafts in stasis
dermatitis
Key outcomes
The patient will:
H demonstrate understanding of skin care regimen
H verbalize feelings about altered body image.
Nursing interventions are guided by the type of dermatitis.
H Assist with daily skin care, and avoid using perfumed
soaps.
H Apply intermittent occlusive dressings to lichenified
skin.
H Apply cool, moist compresses.
H Offer emotional support and reassurance.
H Administer medications as prescribed.
H Prevent rubbing and scratching of the affected area.
Monitoring
H Adverse reactions
H Complications
Patient teaching
Be sure to cover:
H skin care
H prescribed medications and possible adverse effects
H signs and symptoms of corticosteroid overdose and
notifying the practitioner immediately if they occur
H control of pruritus
H meticulous hand washing and good personal hygiene
H use of plain, tepid water (96 F [35.6 C]) and nonperfumed soaps
H application of occlusive dressings when skin is
lichenified
H application of wet-to-dry dressings
H identification and avoidance of aggravating factors
H avoidance of temperature extremes.
Discharge planning
H Refer the patient to the American Academy of Derma-
tology.
Dermatitis
229
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Types of dermatitis
Type
Causes
Assessment
findings
Diagnosis
Treatment
and intervention
Thick, lichenified, single or multiple lesions

on any part of the
body (commonly on
the hands)
Inflammation and
scaling
Recurrence after long
remissions
No characteristic pattern or
course; diagnosis based on
detailed history
and physical
findings
Elimination of known allergens and decreased exposure

to irritants, wearing protective
clothing such as gloves, and
washing immediately after
contact with irritants or allergens
Antibiotics for secondary infection
Avoidance of excessive washing and drying of hands and
of accumulation of soaps and
detergents under rings
Use of emollients with topical
steroids
Mild irritants and allergens: erythema and

small vesicles that
ooze, scale, and itch
Strong irritants: blisters and ulcerations
Classic allergic response: clearly defined lesions, with
straight lines following points of contact
Severe allergic reaction: marked edema
of affected areas
Patient history
Patch testing
to identify allergens
Shape and distribution of lesions
Same as for chronic dermatitis

Topical anti-inflammatories
(such as steroids), systemic
steroids for edema and bullae,
antihistamines, and local applications of Burows solution
(for blisters)
Other nursing interventions
similar to those for atopic dermatitis
Generalized dermatitis, with acute loss of

stratum corneum, and
erythema and scaling
Sensation of tight skin
Hair loss
Possibly fever, sensitivity to cold, shivering, gynecomastia,
and lymphadenopathy
Identification
of the underlying cause
Hospitalization, with protective isolation and hygienic

measures to prevent secondary bacterial infection
Open wet dressings, with colloidal baths
Bland lotions over topical
steroids
Maintenance of constant environmental temperature to prevent chilling or overheating
Careful monitoring of renal
and cardiac status
Systemic antibiotics and
steroids
Other nursing interventions
similar to those for atopic dermatitis
CHRONIC DERMATITIS
Characterized by
inflammatory
eruptions of the
hands and feet
Usually unknown but may

result from progressive contact
dermatitis
Secondary factors: trauma,
infections, redistribution of
normal flora,
photosensitivity,
and food sensitivity, which
may perpetuate
this condition
CONTACT DERMATITIS
Commonly,
sharply demarcated skin inflammation and irritation
due to contact
with concentrated
substances to
which the skin is
sensitive, such as
perfumes or
chemicals
Mild irritants:
chronic exposure to detergents or solvents
Strong irritants:
damage on contact with acids
or alkalis
Allergens: sensitization after
repeated exposure
EXFOLIATIVE DERMATITIS
Severe, chronic
skin inflammation
characterized by
redness and widespread erythema
and scaling
Progression of
preexisting skin
lesions to exfoliative stage, as
in contact dermatitis, drug reaction, lymphoma, or
leukemia
LOCALIZED NEURODERMATITIS (LICHEN SIMPLEX CHRONICUS, ESSENTIAL PRURITUS)
Superficial skin
inflammation
characterized by
itching and papular eruptions that
appear on thickened, hyperpigmented skin
230
Dermatitis
Chronic
scratching or
rubbing of a
primary lesion
or insect bite,
or other skin
irritation
Intense, sometimes
continual scratching
Thick, possibly dry,
scaly lesions, with
sharp borders and
raised papules
Usually affects easily
reached areas, such
as ankles, lower legs,
anogenital area, back
of neck, and ears
Physical findings
Scratching must stop; then

erosions will disappear in
2 weeks
Fixed dressing or Unnas boot
to cover affected area
Topical steroids (occlusive
dressings or intralesional injections)
Antihistamines and open wet
dressings
Emollients
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Types of dermatitis (continued)

Type
Causes
Assessment
findings
Diagnosis
Treatment
and intervention
Round, nummular
(coin-shaped) lesions,
usually on arms and
legs, with distinct borders of crusts and
scales
Possibly oozing and
severe itching
Summertime remissions common, with
wintertime recurrence
Physical findings and patient history;

history of
atopic dermatitis in middleaged or older
patient
Exclusion of
fungal infections, atopic or
contact dermatitis, and
psoriasis
Elimination of known irritants

Measures to relieve dry skin:
increased humidification, limited frequency of baths and
use of bland soap and bath
oils, and application of emollients
Wet dressings in acute phase
Topical steroids (occlusive
dressings or intralesional injections) for persistent lesions
Tar preparations and antihistamines for itching and antibiotics for infection
Other interventions similar to
those for atopic dermatitis
Eruptions in areas
with many sebaceous
glands (usually scalp,
face, and trunk) and
in skin folds
Itching, redness, and
inflammation of affected areas; lesions
that may appear
greasy; possibly
fissures
Indistinct, occasionally yellowish scaly
patches from excess
stratum corneum
(dandruff may be mild
seborrheic dermatitis)
Patient history
and physical
findings, especially distribution of lesions
in sebaceous
gland areas
Exclusion of
psoriasis
Removal of scales by frequent

washing and shampooing
with selenium sulfide suspension, zinc pyrithione, tar and
salicylic acid shampoo or ketoconazole shampoo
Application of topical steroids
and antifungal agents to nonhairy areas
For infants, baby shampoo
Varicosities and
edema common, but
obvious vascular insufficiency not always
present
Usually affects the
lower leg, just above
internal malleolus, or
sites of trauma or irritation
Early signs: dusky red
deposits of hemosiderin in skin, with
itching and dimpling
of subcutaneous tissue; later signs:
edema, redness, and
scaling of large area
of legs
Possibly fissures,
crusts, and ulcers
Positive history of venous

insufficiency
and physical
findings such
as varicosities
Measures to prevent venous

stasis: avoidance of prolonged
sitting or standing, use of
support stockings, and weight
reduction for obese patients
Corrective surgery for underlying cause
After ulcer develops, rest periods with legs elevated; open
wet dressings; Unnas boot
(provides continuous pressure to areas); and antibiotics
for secondary infection after
wound culture
NUMMULAR DERMATITIS
Chronic form of
dermatitis characterized by coinshaped, vesicular,
crusted scales
and, possibly, pruritic lesions
Possibly precipitated by stress;

or dryness, irritants, or
scratching
SEBORRHEIC DERMATITIS
An acute or subacute disease that

affects the scalp,
face and, occasionally, other areas and is characterized by lesions
covered with yellow or brownish
gray scales
Unknown;
stress and neurologic conditions may be
predisposing
factors
STASIS DERMATITIS
Condition usually
caused by impaired circulation
and characterized
by eczema of the
legs with edema,
hyperpigmentation, and persistent inflammation
Secondary to
peripheral vascular diseases
affecting legs,
such as recurrent thrombophlebitis and resultant chronic
venous insufficiency
Dermatitis
231
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Developmental
dysplasia of the hip
H Can be unilateral or bilateral

H Occurs in three forms of varying severity (see De-
Overview
H Excessive or abnormal movement of the joint during
Description
H An abnormality of the hip joint present at birth
H Most common disorder affecting the hip joints in
children younger than age 3
Degrees of hip dysplasia

Normally, the head of the femur fits snugly into the
acetabulum, allowing the hip to move properly. In
developmental hip dysplasia, flattening of the acetabulum
prevents the head of the femur from rotating adequately.
The childs hip may be unstable, subluxated (partially
dislocated), or completely dislocated, with the femoral
head lying totally outside the acetabulum. The degree of
dysplasia and the childs age are considered in
determining the treatment choice.
grees of hip dysplasia)
Pathophysiology
a traumatic birth may cause dislocation.
H Displacement of bones within the joint may damage
joint structures, including articulating surfaces,

blood vessels, tendons, ligaments, and nerves.
H Disruption of blood flow to the joint may lead to ischemic necrosis.
Causes
H Unknown
Risk factors
H Breech delivery
H Elevated maternal relaxin (hormone secreted by the
corpus luteum during pregnancy that causes relaxation of pubic symphysis and cervical dilation)
H Large neonates and twins
Incidence
H About 85% of cases: female
NORMAL HIP
H Level of knees uneven
H Limited abduction on the dislocated side
H Buttock fold on the affected side higher with the
Acetabulum
Head of the femur
child lying prone (see Ortolanis and Trendelenburgs signs)
Complications
H Degenerative hip changes
H Abnormal acetabular development
H Lordosis (abnormally increased concave curvature of
the lumbar and cervical spine)

SUBLUXATED HIP
H Joint malformation
H Sciatic nerve injury (paralysis)
H Avascular necrosis of femoral head
H Soft tissue damage
H Permanent disability
Assessment
History
DISLOCATED HIP
H Traumatic birth
H Large birth size
H Twin
Physical findings
H Extra fold on the thigh of the affected side
H Limited abduction on the dislocated side
H Level of knees uneven
H Swaying from side to side (duck waddle) because
of uncorrected bilateral dysplasia

H Limp due to uncorrected unilateral dysplasia
232
Developmental dysplasia of the hip
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Test results
Imaging
H X-rays show the location of the femur head and a
shallow acetabulum.
H Computed tomography scan shows the location and
extent of the deformity.
H Sonography and magnetic resonance imaging assess
reduction.
Other
H Physical examination helps to confirm the diagnosis.
Treatment
Treatment of developmental dysplasia of the hip varies
with the patients age.
Younger than age 3 months:
H Gentle manipulation to reduce the dislocation, followed by splint-brace or Pavlik harness
H Splint-brace or Pavlik harness worn continuously for
2 to 3 months, then a night splint for another month
Older than age 3 months:
H Bilateral skin traction (in infants) or skeletal traction
(in children who have started walking)
H Bryants traction or divarication traction (both extremities placed in traction, even if only one is affected, to help maintain immobilization) for children
younger than 3 years and weighing less than 35 lb
(15.9 kg) for 2 to 3 weeks
H Immobilization in a spica cast for about 3 months for
children ages 6 to 12 months
Special populations
Treatment begun after age 5 rarely restores satisfactory hip function.
General
Surgery
H Gentle closed reduction under general anesthesia to
further abduct the hips, followed by a spica cast for 3

months (if traction fails)
H In children older than age 18 months, open reduction and pelvic or femoral osteotomy to correct bony
deformity, followed by immobilization in a spica cast
for 6 to 8 weeks
H In children ages 2 to 5 years, skeletal traction and
subcutaneous adductor tenotomy (surgical cutting of
the tendon)
Ortolanis and Trendelenburgs signs

A positive Ortolanis or Trendelenburgs sign confirms
developmental dysplasia of the hip.
Ortolanis sign
H Place the infant on his back, with hip flexed and in

abduction. Adduct the hip while pressing the femur
downward.
H Next, abduct the hip while moving the femur upward. A
click or a jerk (produced by the femoral head moving
over the acetabular rim) indicates subluxation in an
infant younger than 1 month. The sign indicates
subluxation or complete dislocation in an older infant.
Trendelenburgs sign
H When the child rests his weight on the side of the

dislocation and lifts his other knee, the pelvis drops on
the normal side because abductor muscles in the
affected hip are weak.
H However, when the child stands with his weight on the
normal side and lifts the other knee, the pelvis remains
horizontal.
H achieve the highest level of mobility possible within
the confines of the disease.
H Provide reassurance to the parents.
H Turn the child every 2 hours.
H Provide appropriate cast care.
Monitoring
H Parental care of cast or equipment
H Skin integrity
H Color, sensation, and motion of the infants legs and
feet
H Comfort
Patient teaching
Be sure to cover:
H how to correctly splint or brace the hips, as ordered
H good hygiene
H signs and symptoms of cast compression (cyanosis,
cool extremities, or pain).
Discharge planning
H Stress the need for frequent checkups.
H Refer the child and parents to a child life specialist to
ensure continued developmental progress.
Key outcomes
The patient will:
Developmental dysplasia of the hip
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Diabetes insipidus
Overview
Description
H Disorder in which secretion of antidiuretic hormone
is inadequate, causing an inability to concentrate

urine
H Two types: primary and secondary
H May occur transiently during pregnancy, usually after
the fifth or sixth month of gestation
H Impaired or absent thirst mechanism increasing risk
of complications
H If uncomplicated, prognosis good
H If complicated by underlying disorder, such as cancer, prognosis variable
H Also referred to as DI
Pathophysiology
H Vasopressin (antidiuretic hormone) is synthesized in
the hypothalamus and stored by the posterior pituitary gland.

H Once released into the general circulation, vasopressin acts on the distal and collecting tubules of
the kidneys.
H Vasopressin increases the water permeability of the
tubules and causes water reabsorption.
H The absence of vasopressin allows filtered water to
be excreted in the urine instead of being reabsorbed.
Causes
H Failure of vasopressin secretion in response to nor-
mal physiologic stimuli

H Failure of the kidneys to respond to vasopressin,
called nephrogenic DI
H Familial
H Idiopathic
H Congenital malformation of the central nervous system (CNS)
H Infection
H Trauma
H Tumors
H Neurosurgery, skull fracture, or head trauma
H Granulomatous disease
H Vascular lesions
H Psychogenic
H Pregnancy (gestational DI)
H Damage to hypothalamus or pituitary gland
H Certain medications such as lithium
Incidence
H Primary DI in 50% of patients
H Polyuria with low specific gravity and osmolality
H Nocturia
H Dehydration
234
Diabetes insipidus
H Polydipsia
H Weight loss
H Fatigue
Complications
H Hypovolemia
H Hyperosmolality
H Circulatory collapse
H CNS changes
H Bladder distention
H Hydroureter
H Hydronephrosis
Assessment
History
H Abrupt onset of extreme polyuria
H Extreme thirst
H Extraordinarily large oral fluid intake
H Weight loss
H Dizziness; weakness; fatigue
H Constipation
H Nocturia
Special populations
In children, reports of enuresis, sleep disturbances,
irritability, anorexia, thirst, and decreased weight
gain and linear growth are common.
Physical findings
H Fever
H Dyspnea
H Pale, voluminous urine
H Poor skin turgor
H Tachycardia
H Decreased muscle strength
H Hypotension
Test results
Laboratory
H Urinalysis shows colorless urine with specific gravity
1.005 or less and osmolality less than 200 mOsm/kg.
H 24-hour urine sample shows decreased specific gravity and increased volume.
H Serum chemistries show elevated sodium, blood urea
nitrogen (BUN), and creatinine levels.
H Serum osmolality is increased.
H Serum vasopressin level is decreased.
H Dehydration test or water deprivation test shows an
increase in urine osmolality after vasopressin administration exceeding 9%.
H Magnetic resonance imaging may show a pituitary tumor or brain tumor.
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H Computed tomography scan may reveal head trauma,
pituitary tumor, or brain tumor.
Treatment
General
H Identification and treatment of underlying cause
H Control of fluid balance; administration of I.V. fluids
to match urine output

H Dehydration prevention
H Free access to oral fluids
H With nephrogenic DI, low-sodium diet
Medications
H Posterior pituitary hormones, such as vasopressin
and desmopressin
H Thiazide diuretics, such as hydrochlorothiazide, in
nephrogenic DI
H I.V. fluids:
If serum sodium > 150 mEq/L: 5% dextrose in

water
If serum sodium < 150 mEq/L: normal saline solution
H Signs and symptoms of hypovolemic shock

H Changes in mental or neurologic status
H Cardiac rhythm
Patient teaching
Be sure to cover:
H when to notify the practitioner
H signs and symptoms of dehydration
H daily weight
H intake and output
H use of a hydrometer to measure urine specific gravity
H need for medical identification jewelry
H need for ongoing medical care.
Discharge planning
additional counseling, as indicated.
Surgery
H Not indicated, unless required to treat underlying
cause such as a tumor
Key outcomes
The patient will:
H demonstrate balanced fluid volume
H display adaptive coping behaviors
H demonstrate normal laboratory values.
H Administer I.V. fluid to match urine output.
H Provide meticulous skin and mouth care.
ALERT
Use caution when administering vasopressin to a
patient with coronary artery disease because it can
cause coronary artery constriction.
H Offer encouragement while providing a realistic as-
sessment of the situation.

Monitoring
H Intake and output
H Vital signs
H Daily weight
H Urine specific gravity
H Serum electrolytes and BUN
Diabetes insipidus
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Diabetes mellitus
Overview
Description
H Chronic disease of absolute or relative insulin defi-
ciency or resistance
H Characterized by disturbances in carbohydrate, pro-
tein, and fat metabolism
Complications
H Ketoacidosis
H Hyperosmolar hyperglycemic nonketotic syndrome
H Cardiovascular disease
H Peripheral vascular disease
H Retinopathy, blindness
H Nephropathy
H Diabetic dermopathy
H Impaired resistance to infection
H Cognitive depression
H Hypoglycemia
H Two primary forms:
Type 1, characterized by absolute insufficiency

Type 2, characterized by insulin resistance with
varying degrees of insulin secretory defects
Pathophysiology
H The effects of diabetes mellitus (DM) result from in-
sulin deficiency or resistance to endogenous insulin.
Special populations
Neonates of diabetic mothers have a two to three
times greater incidence of congenital malformations and fetal distress, unless the mothers blood
glucose levels are well-controlled before conception
and during pregnancy.
H Insulin allows glucose transport into the cells for use
as energy or storage as glycogen.

H Insulin also stimulates protein synthesis and free fatty
acid storage in the adipose tissues.

H Insulin deficiency compromises the body tissues ac-
cess to essential nutrients for fuel and storage.
Causes
H Genetic factors
H Autoimmune disease (type 1)
Risk factors
H Viral infections (type 1)
H Obesity (type 2)
H Physiologic or emotional stress
H Sedentary lifestyle (type 2)
H Pregnancy
H Medication, such as thiazide diuretics, adrenal corti-
costeroids, and hormonal contraceptives
Incidence
H Type 1 usually occurs before age 30, although it
may occur at any age

H More common in males
H Type 2 usually occurs in obese adults after age 30,
although it may be seen in obese North American

youths of African-American, Native American, or Hispanic descent
H Affects about 8% of the population of the United
States
H About one-third of patients undiagnosed
H Increases with age (type 2)
H Polyuria
H Polydipsia
H Polyphagia
H Weight loss
H Fatigue
236
Diabetes mellitus
Assessment
History
H Polyuria, nocturia
H Dehydration
H Polydipsia
H Poor skin turgor
H Weight loss and hunger
H Weakness; fatigue
H Vision changes
H Frequent skin and urinary tract infections
H Dry, itchy skin
H Sexual problems
H Numbness or pain in the hands or feet
H Postprandial feeling of nausea or fullness
H Nocturnal diarrhea
Type 1
H Rapidly developing symptoms
Type 2
H Vague, long-standing symptoms that develop
gradually
H Family history of DM
H Pregnancy
H Severe viral infection
H Other endocrine diseases
H Recent stress or trauma
H Use of drugs that increase blood glucose levels
Physical findings
H Retinopathy or cataract formation
H Skin changes, especially on the legs and feet
H Muscle wasting and loss of subcutaneous fat (type 1)
H Obesity, particularly in the abdominal area (type 2)
H Poor skin turgor
H Decreased peripheral pulses
H Cool skin temperature
H Diminished deep tendon reflexes
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H Orthostatic hypotension
H Characteristic fruity breath odor in ketoacidosis
H Possible hypovolemia and shock in ketoacidosis and
hyperosmolar hyperglycemic state
Test results
Laboratory
H Fasting plasma glucose level is greater than or equal
to 126 mg/dl on at least two occasions.
H Random blood glucose level is greater than or equal
to 200 mg/dl.
H Two-hour postprandial blood glucose level is greater
than or equal to 200 mg/dl.
H Glycosylated hemoglobin (Hb A1C) level is increased.
H Urinalysis may show acetone or glucose.
H Ophthalmologic examination may show diabetic
retinopathy.
Treatment
General
H Exercise and diet control
H Tight glycemic control for prevention of complica-
tions
H Provide meticulous skin care, especially to the feet
and legs.
H Treat all injuries, cuts, and blisters immediately.
H Avoid constricting hose, slippers, or bed linens.
H Help to develop effective coping strategies.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Serum glucose
H Urine acetone
H Renal status
H Signs and symptoms of:
Hypoglycemia
Hyperglycemia
Hyperosmolar coma
Urinary tract and vaginal infections
Diabetic neuropathy
Patient teaching
H Modest caloric restriction for weight loss or mainte-
Be sure to cover:
H prescribed meal plan
H prescribed exercise program
H signs and symptoms of:
urinary tract and vaginal infection
hypoglycemia
hyperglycemia
diabetic neuropathy
H self-monitoring of blood glucose
H complications of hyperglycemia
H foot care
H annual regular ophthalmologic examinations
H safety precautions
H management of diabetes during illness.
Key outcomes
Discharge planning
The patient will:

H maintain optimal body weight
H verbalize understanding of the disorder and treatment
H demonstrate adaptive coping behaviors.
H Refer the patient to a dietitian.

H Refer the patient to a podiatrist, if indicated.
H Refer the patient to an ophthalmologist.
H Refer the adult patient who is planning a family for
nance
H American Diabetes Association recommendations to
reach target glucose, Hb A1c lipid, and blood pressure levels

H Regular aerobic exercise
Medications
H Exogenous insulin (type 1 or possibly type 2)
H Oral antidiabetics (type 2), such as arcabose, exe-
natide, glimeperide, glipizide, glyburide, metformin,

pioglitazone, and sitagliptin
Surgery
H Pancreas transplantation
preconception counseling.
H Refer the patient to the Juvenile Diabetes Research
Foundation, the American Association of Diabetes

Educators, and the American Diabetes Association to
obtain additional information.
H Administer prescribed drugs.

H Give rapidly absorbed carbohydrates for hypo-
glycemia or, if the patient is unconscious, glucagon

or I.V. dextrose, as ordered.
H Administer I.V. fluids and insulin replacement for hyperglycemic crisis, as ordered.
Diabetes mellitus
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Diphtheria
Overview
Description
H Acute, highly contagious, toxin-mediated infection
that usually infects the respiratory tract primarily

the tonsils, nasopharynx, and larynx
H GI and urinary tracts, conjunctivae, and ears rarely
involved
Pathophysiology
H The organism proliferates at the site of implantation.
H Endotoxins are produced, absorbed by the blood,
and transported to the heart and central nervous system.
Causes
H Corynebacterium diphtheriae, a gram-positive rod
H Transmission usually through intimate contact, air-
borne respiratory droplets, or a break in the skin
Risk factors
H Crowded living conditions
H Poor hygiene
H In cutaneous diphtheria, yellow spots or skin lesions
(resembles impetigo)
Complications
H Thrombocytopenia
H Myocarditis
H Neurologic involvement (primarily affecting motor
fibers but possibly also sensory neurons)

H Renal involvement
H Pulmonary involvement (bronchopneumonia)
Assessment
History
H Fever
H Sore throat
H Rasping cough
H Malaise
H Vomiting
H Dysphagia
Physical findings
H Hoarseness or stridor
H Thick, patchy, grayish green membrane over the mu-
Incidence
cous membranes of the pharynx, larynx, tonsils, soft

palate, and nose
H Swelling of the palate
H Yellow spots or lesions (cutaneous)
H More prevalent during the colder months

H Rare in many parts of the world, including the United
Test results
States
H Cutaneous diphtheria on the increase since 1972, especially in the Pacific Northwest and the Southwest
H More prevalent in children younger than age 15
Laboratory
H Throat culture or culture of other suspect lesions
grows C. diphtheriae.
H Arterial blood gas results may reveal hypoxemia.
H Thick, patchy, grayish green membrane over the mu-
cous membranes of the pharynx, larynx, tonsils, soft

palate, and nose
H Symptoms similar to croup
H Bleeding when membrane dislodged
Droplet precautions
Droplet precautions prevent the spread of infectious diseases transmitted by contact with nasal or oral secretions
(droplets arising from coughing or sneezing) from the infected patient with the mucous membranes of the susceptible host.
Effective droplet precautions require a single room
(not necessarily a negative-pressure room), and the door
doesnt need to be closed. Persons having direct contact
with, or who will be within 3 feet of, the patient should
wear a surgical mask covering the nose and mouth.
When handling infants or young children who require
droplet precautions, you may also need to wear gloves
and a gown to prevent soiling of clothing with nasal and
oral secretions.
238
Diphtheria
Treatment
General
H Symptomatic
H Droplet precautions (see Droplet precautions)
H Endotracheal intubation and mechanical ventilation,
as necessary
Medications
H Diphtheria antitoxin
H Antibiotics, such as penicillin and erythromycin
H Oxygen therapy
Surgery
H Tracheotomy (if airway obstruction occurs)
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Key outcomes
The patient will:
H maintain patent airway
H have adequate ventilation
H Enforce droplet precautions.
H Obtain cultures, as ordered.
H Report all cases to local public health authorities.
Monitoring
H Vital signs
H Pulse oximetry
H Signs of shock
H Cardiac rhythm and cardiovascular status
H Intake and output
Patient teaching
Be sure to cover:
H proper disposal of nasopharyngeal secretions
H maintaining isolation precautions until two consecutive negative nasopharyngeal cultures at least 1
week after drug therapy stops.
Discharge planning
H Stress the need for childhood immunizations to all
parents.
Diphtheria
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Dislocations and
subluxations
Overview
Description
H Dislocation displacement of joint bones so that ar-
ticulating surfaces totally lose contact (see Common

dislocation)
H Subluxation partial displacement of articulating
surfaces
H May accompany fractures of joints
Pathophysiology
H Trauma causes displacement of the joint.
H Joint structures (blood vessels, ligaments, tendons,
and nerves) are damaged.
Common dislocation
The elbow is a common site of dislocation.
NORMAL ELBOW JOINT
H Injuries may result in deposition of fracture frag-
ments between joint surfaces, damaging surrounding

structures.
H Joint function is impaired.
Causes
H Congenital
H Trauma
H Pagets disease of surrounding joint tissues
Risk factors
Incidence
H Shoulder dislocations more than half of disloca-
tions seen in emergency departments

H Hip dislocations from trauma, more common in
those younger than age 35; from falls, more common

in those older than age 65
H Visible deformity of affected extremity
H Shortening of affected extremity
H Local pain
H Swelling
H Limitation of function
H Numbness of affected extremity
Complications
H Damage to surrounding muscle, ligaments, nerves,
and blood vessels

H Avascular necrosis
H Bone necrosis
Assessment
History
H Trauma or fall
H Extreme pain at injury site
Physical findings
ELBOW JOINT WITH
LATERAL DISLOCATION
H Joint surface fractures

H Deformity around the joint
H Change in the length of the involved extremity
H Impaired joint mobility
H Point tenderness
Test results
Imaging
H X-rays confirm the diagnosis and reveal any associated fractures.
Treatment
General
H Ice application
H Immediate reduction and immobilization
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Dislocations and subluxations
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H Nothing by mouth if surgery scheduled

H Activity limitations based on injury
H Active range-of-motion (ROM) exercises for adjacent
joints not immobilized
Medications
H Sedative, such as lorazepam
H Analgesics, such as ibuprofen and oxycodone
H Muscle relaxants, such as carisoprodol and cy-
H medication administration, dosage, and possible ad-
verse effects.
Discharge planning
H Refer the patient to a rehabilitation program, if ap-
propriate.
H Refer the patient for home health care, if appropri-
ate.
clobenzaprine
Surgery
H Open reduction
H Skeletal traction
H Ligament repair
Key outcomes
The patient will:
H identify factors that intensify pain
H identify factors that increase the risk for injury
H maintain muscle strength and tone
H maintain joint ROM.
H Provide proper positioning of the affected area.
H Apply ice, as ordered.
H Encourage ROM exercises, as ordered, for adjacent
nonmobilized joints.
ALERT
Immediately report signs and symptoms of severe
vascular compromise, such as pallor, pain, loss of
pulse, paralysis, and paresthesia; the patient needs
an immediate orthopedic examination and emergency reduction.
Monitoring
H Respiratory status when I.V. sedatives used
H Neurovascular status of involved extremity
H Integrity of skin
Patient teaching
Be sure to cover:
H the need to report numbness, pain, cyanosis, and
coldness of the extremity below the cast or splint
H how to evaluate skin integrity
H how to assess neurovascular status
H the use of assistive devices
H the importance of follow-up visits
Dislocations and subluxations
241
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Disseminated
intravascular
coagulation
Overview
Description
H Abnormal bleeding
H Hemorrhage
Complications
H Cardiac tamponade
H Hemothorax
H Renal failure
H Hepatic damage
H Stroke
H Ischemic bowel
H Death (mortality is greater than 50%)
H Intracerebral bleed
H Syndrome of activated coagulation characterized by
bleeding or thrombosis
H Complicates diseases and conditions that accelerate
clotting, causing occlusion of small blood vessels, organ necrosis, depletion of circulating clotting factors
and platelets, and activation of the fibrinolytic system
H Also known as DIC, consumption coagulopathy,
and defibrination syndrome
Pathophysiology
H Typical accelerated clotting results in generalized ac-
tivation of prothrombin and a consequent excess of

thrombin.
H Excess thrombin converts fibrinogen to fibrin, producing fibrin clots in the microcirculation.
H This process consumes exorbitant amounts of coagulation factors (especially platelets, factor V, prothrombin, fibrinogen, and factor VIII), causing
thrombocytopenia, deficiencies in factors V and VIII,
hypoprothrombinemia, and hypofibrinogenemia.
H Circulating thrombin activates the fibrinolytic system,
which lyses fibrin clots into fibrinogen degradation
products (FDPs).
H The hemorrhage that occurs may be due largely to
the anticoagulant activity of FDPs and depletion of
plasma coagulation factors.
Causes
H Infection, sepsis
H Obstetric complications
H Neoplastic disease
H Disorders that produce necrosis, such as extensive
burns and trauma

H Other disorders, such as heatstroke, shock, incom-
patible blood transfusion, drug reactions, cardiac arrest, surgery necessitating cardiopulmonary bypass,
acute respiratory distress syndrome, diabetic ketoacidosis, pulmonary embolism, and sickle cell anemia
H Snakebite
Incidence
H Dependent on the cause
242
Disseminated intravascular coagulation
Assessment
History
H Abnormal bleeding without a history of a serious
hemorrhagic disorder; bleeding possibly occurring

at all bodily orifices
H Possible presence of one of the causes of DIC
H Possible signs of bleeding into the skin, such as
cutaneous oozing, petechiae, ecchymoses, and
hematomas
H Possible bleeding from surgical or invasive procedure sites, such as incisions or venipuncture sites
H Possible nausea and vomiting; severe muscle, back,
and abdominal pain; chest pain; hemoptysis; epistaxis; seizures; and oliguria
H Possible GI bleeding, hematuria
Physical findings
H Petechiae
H Acrocyanosis
H Dyspnea, tachypnea
H Mental status changes, including confusion
Test results
Laboratory
H Serum platelet count is less than 150,000/mm3.
H Serum fibrinogen level is less than 170 mg/dl.
H Prothrombin time is more than 19 seconds.
H Partial thromboplastin time is more than 40 seconds.
H FDPs are increased (commonly greater than 45
mcg/ml, or positive at less than 1:100 dilution).
H Result of D-dimer test (specific fibrinogen test for
DIC) is positive at less than 1:8 dilution.
H Thrombin time is prolonged.
H Blood clotting factors V, VIII, X, XII, and protein C
are diminished.
H Complete blood count shows decreased hemoglobin
level (less than 10 g/dl).
H Blood urea nitrogen level is greater than 25 mg/dl,
and serum creatinine level is greater than 1.3 mg/dl.
H Antithrombin III level is decreased.
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Treatment
H Limit venipunctures whenever possible.

H Watch for transfusion reactions and signs of fluid
General
H Measure the amount of blood lost, weigh dressings
H Treatment of underlying condition

H Possibly supportive care alone if the patient not ac-
H Weigh the patient daily, particularly in renal involve-
tively bleeding
H Fluid replacement
H Oxygen therapy
H Endotracheal intubation and mechanical ventilation,
as necessary
Medications
If the patient is actively bleeding
H Administration of blood, fresh frozen plasma,
platelets, or packed red blood cells
H Cryoprecipitate
H Antithrombin III and gabexate
H Anticoagulant such as heparin
H Analgesics such as morphine
Key outcomes
The patient will:
H maintain balanced intake and output
pain
H have laboratory values return to normal
H use available support systems to assist in coping with
fears.
overload.
and linen, and record drainage.
ment.
H Elevate the head of the bed at least 30 degrees.
H Provide nutritional support.
H Maintain bed rest with range-of-motion exercises.
Monitoring
H Vital signs
H Results of serial blood studies
H Signs of shock
H Intake and output, especially when administering
blood products
Patient teaching
Be sure to cover (for the patient and his family):
H an explanation of the disorder
H the signs and symptoms of the problem, diagnostic
procedures required, and treatment that the patient
will receive.
ALERT
Focus on early recognition of signs of abnormal
bleeding, prompt treatment of the underlying disorders, and prevention of further bleeding.
H Give prescribed analgesics as necessary.
H Reposition the patient every 2 hours, and provide
meticulous skin care.

H Give prescribed oxygen therapy.
ALERT
To prevent clots from dislodging and causing fresh
bleeding, dont vigorously rub the affected areas
when bathing.
H Protect the patient from injury.
H If bleeding occurs, use pressure and topical hemo-
static agents to control bleeding.
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Diverticular disease
Complications
Overview
H Rectal hemorrhage
H Portal pyemia
H Fistula
H Sepsis
H Ruptured diverticula that cause abdominal abscesses
or peritonitis
Description
H Bulging pouches (diverticula) in GI wall pushing the
mucosal lining through surrounding muscle

H Sigmoid colon most common site, but possibly devel-
oping anywhere, from proximal end of the pharynx

to the anus
H Other typical sites:
The duodenum, near the pancreatic border or the
ampulla of Vater
The jejunum
H Diverticular disease of the ileum (Meckels diverticulum) most common congenital anomaly of the GI
tract
H Two clinical forms:
Diverticulosis: diverticula present but dont cause
symptoms
Diverticulitis: diverticula inflamed and may cause
complications
Pathophysiology
H Pressure in the intestinal lumen is exerted on weak
areas, such as points where blood vessels enter the

intestine, causing a break in the muscular continuity
of the GI wall, creating a diverticulum.
H Diverticulitis occurs when retained undigested food
mixed with bacteria accumulates in the diverticulum,
forming a hard mass (fecalith). This substance cuts
off the blood supply to the diverticulums thin walls,
increasing its susceptibility to attack by colonic bacteria.
H Inflammation follows bacterial infection, causing abdominal pain.
Causes
H Diminished colonic motility and increased intralumi-
nal pressure
H Defects in colon wall strength
Risk factors
H Age
H Low-fiber diet
Incidence
H Most common in adults ages 45 and older
H Affects 30% of adults older than age 60
H Left lower quadrant abdominal pain
H Generalized abdominal pain
H Diarrhea or constipation
H Palpable mass
H Nausea, vomiting
244
Assessment
History
Diverticulosis
H May be symptom-free
H Occasional intermittent pain in the left lower abdominal quadrant, which may be relieved by defecation
or the passage of flatus
H Alternating bouts of constipation and diarrhea
Diverticulitis
H History of diverticulosis
H Low fiber consumption
H Recent consumption of foods containing seeds or
kernels or indigestible roughage, such as celery and
corn
H Complaints of moderate dull or steady pain in the left
lower abdominal quadrant, aggravated by straining,
lifting, or coughing
H Mild nausea, gas, diarrhea, or intermittent bouts of
constipation, sometimes accompanied by rectal
bleeding
Physical findings
Diverticulitis
H Distressed appearance
H Left lower quadrant abdominal tenderness
H Low-grade fever
H Palpable mass
Acute diverticulitis
H Muscle spasms
H Signs of peritoneal irritation
H Guarding and rebound tenderness
Test results
Laboratory
H Complete blood count reveals leukocytosis.
H Erythrocyte sedimentation rate is elevated (in diverticulitis).
H Stool test is positive for occult blood (in 25% of patients with diverticulitis).
Imaging
H Barium studies reveal barium-filled diverticula or
outlines, but barium doesnt fill diverticula blocked
by impacted stools. This procedure isnt performed
for acute diverticulitis due to potential rupture.
H Radiography may reveal colonic spasm if irritable
bowel syndrome accompanies diverticular disease.
H Abdominal X-rays rule out perforation.
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H Colonoscopy or flexible sigmoidoscopy shows diverticula or inflamed mucosa. It isnt usually performed
in the acute phase.
H Biopsy results may rule out cancer.
H Computed tomography scan of the abdomen evaluates the presence of abscess.
Treatment
General
H For asymptomatic diverticulosis, no treatment
H Bed rest
For symptomatic diverticulosis

H Liquid or low-residue diet (if experiencing pain)
H Increased water consumption, if appropriate
H High-residue diet
For severe diverticulitis
H Nothing by mouth
H Nasogastric (NG) decompression
Medications
For diverticulosis
H Stool softeners such as docusate sodium
H Bulk medication such as calcium polycarbophil
For diverticulitis
H Antibiotics, such as metronidazole and ceftazidime
H I.V. therapy for severe diverticulitis
Surgery
H Colon resection
H May require temporary colostomy to drain abscesses
or to rest the colon for 6 to 8 weeks

H Needed for rupture or to correct cases refractory to
medical treatment
Key outcomes
H Maintain bed rest for acute diverticulitis.

H Maintain the prescribed diet.
H If surgery is scheduled, provide routine preoperative
care.
After colon resection
H Provide meticulous wound care.
H Encourage coughing and deep breathing and incentive spirometer use to prevent atelectasis.
H Administer I.V. fluids and prescribed drugs.
H Provide colostomy care, if appropriate.
H Apply sequential compression device.
Monitoring
H GI status
H Vital signs
H Pain control
H Stools for color, consistency, and frequency
H NG drainage, if appropriate
After colon resection

H Signs of infection and postoperative bleeding
H Intake and output
Patient teaching
Be sure to cover:
H bowel and dietary habits (in uncomplicated diverticulosis)
H preoperative teaching (for a patient needing surgery)
H postoperative teaching (for a patient who must care
for his colostomy)
H the desired actions and possible adverse effects of
prescribed medications.
Discharge planning
H Refer the patient to an enterostomal therapist, if ap-
propriate.
H Refer the patient to a dietitian, if needed.
The patient will:

H have bowel movements that return to normal
H verbalize understanding of the disease process and
treatment regimen.
ALERT
Remember that diverticulitis produces more serious signs and symptoms as well as complications,
and requires more interventions than diverticulosis.
H If the patient is anxious, provide psychological sup-
port.
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Down syndrome
Overview
Description
H A chromosomal aberration that results in mental and
physical abnormalities
H Average IQ between 30 and 50 (some higher)
H Also known as mongolism and trisomy 21 syn-
drome
Pathophysiology
H Down syndrome is an aberration in which chromo-
some 21 has three copies instead of the normal two

because of faulty meiosis (nondisjunction) of the
ovum or, sometimes, the sperm.
H Theres unbalanced translocation, in which the long
arm of chromosome 21 breaks and attaches to another chromosome.
H The result is a karyotype of 47 chromosomes instead
of the normal 46.
Causes
H Trisomy 21
H Mosaicism and trisomy 21
H Robertsonian translation and partial trisomy 21
Risk factors
H Maternal age, especially older than age 35
Incidence
H Occurs in 1 per 800 to 1,000 live births
H Increases with maternal age, especially after age 35
H Abnormal facial features
H Heart defects
H Other congenital defects
Complications
H Death
H Congenital heart defects
H Premature senile dementia
H Leukemia
H Acute and chronic infections
H Diabetes mellitus
H Thyroid disorders
H Brushfields spots on the iris

H Small skull
H Flat bridge across the nose
H Flattened face
H Small external ears
H Short neck with excess skin
H Dry, sensitive skin with decreased elasticity
H Umbilical hernia
H Short stature
H Short extremities with broad, flat, and squarish
hands and feet

H Dysplastic middle phalanx of the fifth finger
H Wide space between the first and second toes
H Abnormal fingerprints and footprints
H Impaired reflex development
H Absent Moros reflex and hyperextensible joints
H Impaired posture, coordination, and balance
H Clubfoot
H Imperforate anus
H Cleft lip and palate
H Pelvic bone abnormalities
Test results
Laboratory
H Karyotype analysis or chromosome mapping shows
the chromosomal abnormality and confirms the diagnosis of Down syndrome.
H Prenatal serum alpha-fetoprotein reveals reduced
levels of alpha-fetoprotein.
Imaging
H Prenatal ultrasonography can suggest Down syndrome if a duodenal obstruction or an atrioventricular canal defect is present.
H Amniocentesis allows prenatal diagnosis.
Other
H Developmental screening tests show severity and
progress of retardation.
Treatment
General
H Early intervention
H Special education programs
H Special athletic programs
H Maximal environmental simulation for infants
H Safety precautions for children and adults in a con-
trolled environment
Medications
H Antibiotics, depending on the infective organism, for
Assessment
History
H Neonate lethargic and a poor feeder
Physical findings
H Slanting, almond-shaped eyes
H Small, open mouth, protruding tongue
H Single transverse palmar crease
246
Down syndrome
recurrent infections
H Thyroid hormone replacement with levothyroxine for
hypothyroidism
Surgery
H Open-heart surgery to correct cardiac defects, such
as ventricular or atrial septal defects

H Plastic surgery to correct congenital abnormalities,
such as protruding tongue, cleft lip, and cleft palate
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Key outcomes
The patient will:
the extent possible
H perform health maintenance activities according to
level of ability
H participate in developmental stimulation programs to
increase skill levels.
H Establish a trusting relationship with the childs par-
ents.
H Encourage the parents to hold and nurture their
child.
Monitoring
H Complications
H Growth and development
H Thyroid function test results
Patient teaching
Be sure to cover:
H the need for adequate exercise and maximal environmental stimulation
H realistic goals for the parents and child
H information about a balanced diet
H the importance of remembering the emotional needs
of other children in the family.
Discharge planning
H Refer the parents to infant stimulation classes.
H Refer the parents and older siblings for genetic and
psychological counseling, as appropriate.

H Refer the patient and his parents to support services.
Down syndrome
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Dysmenorrhea
Overview
Description
H Obesity
H Smoking
Incidence
H Affects more than 45% of females of reproductive age
H Usually peaks in the early 20s, then slowly decreases
H Painful menstruation unassociated with pelvic dis-
ease
H Most common gynecologic complaint
H A primary disorder that begins 6 to 12 months after
the onset of ovulation
H A secondary disorder that typically begins between
ages 20 and 30, but possible any time after menarche
H Sharp, intermittent, cramping, lower abdominal pain,
Pathophysiology
H Pain may result from increased prostaglandin secre-
tion in menstrual blood, which intensifies normal

uterine contractions.
H Prostaglandins intensify myometrial smooth muscle
contraction and uterine blood vessel constriction,
thereby worsening the uterine hypoxia normally associated with menstruation.
H Intense muscle contractions and hypoxia cause the
intense pain of dysmenorrhea.
Causes
Primary
H Increased prostaglandin secretion caused by sloughing endometrial cells
Secondary
H Endometriosis
H Cervical stenosis
H Uterine leiomyomas (benign fibroid tumors)
H Pelvic inflammatory disease
H Pelvic tumors (see Causes of pelvic pain)
Risk factors
Primary
H Early-onset menarche
H Null parity
Causes of pelvic pain

The characteristic pelvic pain of dysmenorrhea must be
distinguished from the acute pain caused by many other
disorders, such as:
H GI disorders: appendicitis, acute diverticulitis, acute or
chronic cholecystitis, chronic cholelithiasis, acute pancreatitis, peptic ulcer perforation, intestinal obstruction
H urinary tract disorders: cystitis, renal calculi
H reproductive disorders: acute salpingitis, chronic inflammation, degenerative fibroid, ovarian cyst torsion
H pregnancy disorders: impending abortion (pain and
bleeding early in pregnancy), ectopic pregnancy, abruptio placentae, uterine rupture, leiomyoma degeneration,
toxemia
H emotional conflicts: psychogenic (functional) pain.
Other conditions that may mimic dysmenorrhea include
ovulation and normal uterine contractions experienced in
pregnancy.
usually radiating to the back, thighs, groin, and vulva

H Pain typically starting with or immediately before
menstrual flow and peaking within 24 hours
Complications
H Dehydration
Assessment
History
H Pelvic disease
H Urinary frequency
H Nausea
H Vomiting
H Diarrhea
H Headache
H Backache
H Chills
H Depression
H Irritability
Physical findings
H Painful breasts
Test results
Imaging
H Laparoscopy, hysteroscopy, and pelvic ultrasound
help diagnose underlying disorders (in secondary
dysmenorrhea).
Other
H Pelvic examination and a detailed patient history help
identify the cause.
Treatment
General
H Heat applied locally to the lower abdomen
Medications
H Analgesics, such as acetaminophen, diclofenac, and
ketoprofen
H Prostaglandin inhibitors, such as aspirin and ibupro-
fen
Surgery
H Surgical treatment of underlying disorders, such as
endometriosis or uterine leiomyomas (secondary)
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Dysmenorrhea
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Key outcomes
The patient will:
H remain free from pain
H Administer prescribed analgesics.
Monitoring
H Depression
H Hydration
H Pain control
H Menstrual cycle
Patient teaching
Be sure to cover:
H explanation of normal female anatomy and physiology as well as the nature of dysmenorrhea
H information on pregnancy and contraception
H keeping a detailed record of her menstrual cycle and
symptoms
H seeking medical care if symptoms persist.
Discharge planning
appropriate.
Dysmenorrhea
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Ebola virus infection
Risk factors
H Travel to endemic areas of Africa
H Exposure to animals, humans, or contaminated nee-
dles
Incidence
Overview
H Not endemic to the United States

H Affects males and females of all ages
Description
H An unclassified ribonucleic acid virus that results in
H Flulike symptoms
H Severe diarrhea
H Vomiting
H Internal and external hemorrhage
H Macular papular rash
bleeding
H Four known strains: Ebola Zaire (EBO-Z), Ebola Sudan (EBO-S), Ebola Tai (EBO-C), and Ebola Reston
(affects only monkeys)
H Poor prognosis
Pathophysiology
H The virus is transmitted by direct contact with infect-
ed blood, body secretions, or infected tissues.

H It can be transmitted by nosocomial and community-
acquired modes.
H Viral replication causes focal tissue necrosis, most
Complications
H Liver and kidney dysfunction
H Dehydration
H Hemorrhage
H Abortion
H Myocarditis
H Pulmonary edema
severely in the liver.

H Microvasculature damage causes increased vascular
permeability and bleeding.

H Ebola virus remains contagious even after the patient
has died.
Causes
H EBO-Z, EBO-S, or EBO-C virus strains
Prevention
Preventing the spread of Ebola virus

The Centers for Disease Control and Prevention recommends the following guidelines to help prevent the spread
of this deadly disease:
H Keep the patient in isolation throughout the course of
the disease.
H If possible, place the patient in a negative-pressure
room at the beginning of hospitalization to avoid the
need for transfer as the disease progresses.
H Restrict nonessential staff members from entering the
patients room.
H Make sure that anyone who enters the patients room
wears gloves and a gown to prevent contact with any
surface in the room that may have been soiled.
H Use barrier precautions to prevent skin and mucous
membrane exposure to blood or other body fluids, secretions, or excretions when caring for the patient.
H If you must come within 3 (1 m) of the patient, also
wear a face shield or a surgical mask and goggles or
eyeglasses with side shields.
H Dont reuse gloves or gowns unless they have been
completely disinfected.
H Make sure any patient who dies of the disease is
promptly buried or cremated. Precautions to avoid
contact with the patients body fluids and secretions
should continue even after the patients death.
250
Assessment
History
H Contact with an infected person
H Headache
H Malaise
H Myalgia
H Fever
H Cough
H Sore throat
H Nausea
H Vomiting
Physical findings
H Conjunctival injection
H Bruising
H Maculopapular eruptions
H Melena
H Hematemesis
H Bleeding gums
Test results
Laboratory
H Blood studies show specific antigens or antibodies
and may show the isolated virus.
H Blood studies show neutrophil leukocytosis, hypofibrinogenemia, thrombocytopenia, and microangiopathic hemolytic anemia.
H Blood studies show elevated blood urea nitrogen and
creatinine levels.
H Blood studies show elevated aspartate aminotransferase and alanine aminotransferase levels.
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Treatment
General
H Supportive care
H Strict isolation (see Preventing the spread of Ebola
virus)
H Diet as tolerated or total parental nutrition
H Bed rest or limited activity
Medications
H I.V. fluids
H Blood transfusions
Key outcomes
The patient will:
H understand the implications of his illness.
H Enforce strict isolation.
H Administer prescribed I.V. solutions and blood prod-
ucts.
H Provide safety precautions.
H Provide nutritional support.
Monitoring
H Vital signs
H Signs of bleeding
H Intake and output
H GI status
Patient teaching
Be sure to cover:
H signs of bleeding
H isolation precautions.
Discharge planning
H Refer the patient for home care, if appropriate.
H Stress to the patient the need for continued follow-up
care.
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Ectopic pregnancy
Overview
Description
H Implantation of a fertilized ovum outside the uterine
cavity, most commonly in the fallopian tube (see Implantation sites of ectopic pregnancy)
H Prognosis good with prompt diagnosis, appropriate
surgical intervention, and control of bleeding
H Very few fetuses carried to term; rarely, with abdominal implantation, fetus survives to term
H About one in three chance of giving birth to live
neonate in subsequent pregnancy
H Previous surgery, such as tubal ligation or resection

H Transmigration of the ovum
H Congenital defects in reproductive tract
H Ectopic endometrial implants in the tubal mucosa
H Sexually transmitted tubal infection
H Intrauterine device
H Smoking
Incidence
H In whites, about 1 of 200 pregnancies
H In nonwhites, about 1 of 120 pregnancies
Pathophysiology
H Minimal vaginal bleeding
H Amenorrhea
H The transport of a blastocyst to the uterus is delayed.

H The blastocyst implants at another available vascular-
Complications
ized site, usually the fallopian tube lining.

H Normal signs of pregnancy are initially present.
H Uterine enlargement occurs in about 25% of cases.
H Human chorionic gonadotropin (HCG) hormonal
levels are lower than in uterine pregnancies.
H If not interrupted, internal hemorrhage occurs with
rupture of the fallopian tube.
H Rupture of fallopian tube

H Hemorrhage
H Shock
H Peritonitis
H Infertility
H Death
Causes
H Abnormal reproductive organ anatomy
H Delay in reproductive events such as movement of
zygote to uterus
H Unknown
Assessment
History
H Amenorrhea
H Abnormal menses (after fallopian tube implantation)
H Slight vaginal bleeding
H Unilateral pelvic pain over the mass
H If fallopian tube ruptures, sharp lower abdominal
Risk factors
H Endosalpingitis
H Diverticula
H Tumors pressing against the tube
pain, possibly radiating to the shoulders and neck
Implantation sites of ectopic pregnancy

In about 95% of patients with ectopic pregnancy, the
ovum implants in part of the fallopian tube: the fimbria,
ampulla, or isthmus. Other possible abnormal sites of implantation include the interstitium, ovarian ligament,
ovary, abdominal viscera, and internal cervical os.
ALERT
Ectopic pregnancy sometimes produces symptoms
of normal pregnancy or no symptoms other than
mild abdominal pain (especially in abdominal
pregnancy), making diagnosis difficult.
Physical findings
Ampulla
Fimbria
Isthmus
H Possible extreme pain when cervix is moved and ad-
nexa palpated
Interstitium
H Boggy and tender uterus

H Adnexa possibly enlarged
Test results
Ovary
Ovarian ligament
252
Ectopic pregnancy
Internal cervical os
Laboratory
H Serum HCG level is abnormally low; when repeated
in 48 hours, it remains lower than levels found in a
normal intrauterine pregnancy.
Imaging
H Real-time ultrasonography shows intrauterine pregnancy or ovarian cyst.
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H Laparoscopy may reveal pregnancy outside the
uterus.
Treatment
H Signs of impending shock

Patient teaching
Medications
Be sure to cover:
H postoperative care
H prevention of recurrent ectopic pregnancy
H prompt treatment of pelvic infections
H risk factors for ectopic pregnancy, including surgery
involving the fallopian tubes and pelvic inflammatory
disease.
H Transfusion with packed red blood cells

H Broad-spectrum I.V. antibiotics, according to isolated
Discharge planning
General
H Initially, in the event of pelvic-organ rupture, man-
agement of shock
H Diet determined by clinical status
H Activity determined by clinical status
organism
H Supplemental iron
additional counseling, if necessary.
Surgery
H Laparotomy and salpingectomy; possibly after lap-
aroscopy to remove affected fallopian tube and control bleeding

H Microsurgical repair of the fallopian tube for patients
who wish to have children
H Oophorectomy for ovarian pregnancy
H Hysterectomy for interstitial pregnancy
H Laparotomy to remove the fetus for abdominal pregnancy
Key outcomes
The patient will:
H express feelings about the current situation
H use available support systems to aid in coping.
H Prepare the patient with excessive blood loss for
emergency surgery.
H Administer prescribed blood transfusions.
H Administer Rho(D) immune globulin (RhoGAM), as
ordered, if the patient is Rh-negative.

H Determine the date and description of her last men-
strual period.
H Provide a quiet, relaxing environment.
H Encourage the patient to express her feelings of fear,
loss, and grief.

H Help the patient to develop effective coping strate-
gies.
Monitoring
H Vital signs
H Vaginal bleeding
H Pain control
H Intake and output
H Signs of hypovolemia
Ectopic pregnancy
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Electric shock
Overview
Description
H Electric current passing through body
H Physical damage depending on intensity of current,
resistance of the tissues it passes through, type of

current, and frequency and duration of current flow
H Classified as lightning, low voltage (less than 600 V),
and high voltage (greater than 600 V)
H Burns the most common injury
Pathophysiology
H Electrical energy results in altered cell membrane
resting potential, causing depolarization in muscles

and nerves.
H Electric shock alters normal electrical activity of the
heart and brain.
H Electric shock resulting from a high-frequency current generates more heat in tissues than a lowfrequency current, resulting in burns and local tissue
coagulation and necrosis.
H Muscle tetany is elicited.
H Tissue destruction and coagulative necrosis occur.
Causes
H Accidental contact with an exposed part of an electri-
cal appliance or wiring

H Lightning
H Flash of electric arcs from high-voltage power lines
or machines
Incidence
Assessment
History
H Exposure to electricity or lightning
H Muscle pain
H Fatigue
H Headache
H Nervous irritability
Physical findings
H Determined by voltage exposure
H Burns
H Local tissue coagulation
H Entrance and exit injuries
H Cyanosis
H Apnea
H Markedly decreased blood pressure
H Cold skin
H Unconsciousness
H Numbness or tingling or sensorimotor deficits
Test results
Laboratory
H Laboratory test results evaluate internal damage and
guide treatment:
Arterial blood gas analysis may show hypoxemia
and acid-base imbalance.
Urine may test positive for myoglobin.
Blood urea nitrogen and creatinine levels may be
elevated.
Imaging
H If chest injury or shortness of breath occurred, chest
X-rays evaluate internal damage and guide treatment.
H Electrocardiography evaluates internal damage and
guides treatment.
H Causes more than 1,000 deaths annually

H More common in males ages 20 to 40
Treatment
General
H Cutaneous burn
H Variable deep tissue damage
H Separation of victim from current source

H Stabilization of cervical spine
H Emergency measures to maintain airway, breathing,
Complications
H Sepsis
H Neurologic dysfunction
H Cardiac dysfunction
H Psychiatric dysfunction
H Renal failure
H Electrolyte abnormalities
H Peripheral nerve injuries
H Vascular disruption
H Thrombi
H Death
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Electric shock
and circulation
H Treatment of acid-base imbalance
H Vigorous fluid replacement
H No dietary restrictions if swallowing ability intact
H Activity based on outcome of interventions
Medications
H Tetanus prophylaxis with tetanus toxoid
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Key outcomes
The patient will:
H maintain stable cardiac rhythm
H maintain cardiac output
H regain skin integrity
H have wounds and incisions that appear clean, pink,
and free from purulent drainage.
H Separate the victim from the current source.
H Provide emergency treatment to maintain airway,
breathing, and circulation.

H Give rapid I.V. fluid infusion.
H Obtain a 12-lead electrocardiogram.
H Provide wound care.
Monitoring
H Vital signs
H Cardiac rhythm (continuously) and cardiovascular
status
H Intake and output (hourly)
H Neurologic status
H Sensorimotor deficits
H Peripheral neurovascular status
Patient teaching
Be sure to cover:
H information about the injury, diagnosis, and treatment
H how to avoid electrical hazards at home and at work
H electrical safety regarding children.
Electric shock
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Emphysema
Overview
Description
H Progressive, chronic lung disease characterized by
permanent enlargement of air spaces distal to the

terminal bronchioles and by exertional dyspnea
H One of several diseases usually labeled collectively as
chronic obstructive pulmonary disease or chronic
obstructive lung disease
Pathophysiology
H Recurrent inflammation associated with the release
of proteolytic enzymes from lung cells causes abnormal, irreversible enlargement of the air spaces distal
to the terminal bronchioles.
H This enlargement leads to the destruction of alveolar
walls, which results in a breakdown of elasticity. (See
What happens in emphysema.)
Causes
H Cigarette smoking
H Air pollutants
Risk factors
H Genetic deficiency of alpha1-antitrypsin
Incidence
H Most common cause of death from respiratory dis-
ease in the United States

H More prevalent in males than in females
H About 2 million U.S. residents affected
H Affects 1 in 3,000 neonates
H Chronic cough
H Anorexia and weight loss
H Malaise
Complications
Physical findings
H Barrel chest
H Pursed-lip breathing
H Use of accessory muscles
H Cyanosis
H Clubbed fingers and toes
H Tachypnea
H Decreased tactile fremitus
H Decreased chest expansion
H Hyperresonance
H Crackles
H Inspiratory wheeze
H Prolonged expiratory phase with grunting respira-
tions
H Distant heart sounds
Test results
Laboratory
H Arterial blood gas analysis shows decreased partial
pressure of oxygen; partial pressure of carbon dioxide remains normal until late in the disease.
H Red blood cell count shows an increased hemoglobin level late in the disease.
Imaging
H Chest X-ray may show:
a flattened diaphragm
reduced vascular markings at the lung periphery
overaeration of the lungs
a vertical heart
enlarged anteroposterior chest diameter
large retrosternal air space.
H Pulmonary function tests typically show:
increased residual volume and total lung capacity
reduced diffusing capacity
increased inspiratory flow.
H Electrocardiography may show tall, symmetrical P
waves in leads II, III, and aVF; a vertical QRS axis;
and signs of right ventricular hypertrophy late in the
disease.
Treatment

H Cor pulmonale
H Peptic ulcer disease
H Spontaneous pneumothorax
H Pneumomediastinum
General
Assessment
Medications
History
H Smoking
H Chronic cough
H Malaise
256
Emphysema
H Chest physiotherapy
H Possible transtracheal catheterization and home oxy-
gen therapy
H Bronchodilators such as formoterol

H Anticholinergics such as tiotropium
H Mucolytics such as acetylcysteine
H Corticosteroids such as fluticasone
H Antibiotics according to the isolated organism
H Oxygen
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H Immunizations, such as influenza virus vaccine and
pneumococcal vaccine
Surgery
H Chest tube insertion for pneumothorax
H Lung volume reduction surgery
Key outcomes
The patient will:
H demonstrate energy conservation techniques
H demonstrate effective coping strategies.
What happens in emphysema

In normal, healthy breathing, air moves in and out of the
lungs to meet metabolic needs. A change in airway size
compromises the lungs ability to circulate sufficient air.
In a patient with emphysema, recurrent pulmonary inflammation damages and eventually destroys the alveolar
walls, creating large air spaces. This breakdown leaves the
alveoli unable to recoil normally after expanding and results in bronchiolar collapse on expiration. This traps air
within the lungs.
Associated pulmonary capillary destruction usually allows a patient with severe emphysema to match ventilation to perfusion and thus avoid cyanosis.
NORMAL ALVEOLI
Bronchiole
H Help the patient adjust to lifestyle changes necessitat-
ed by a chronic illness.
H Encourage the patient to express his fears and con-
cerns.
H Provide a high-calorie, protein-rich diet.
H Give small, frequent meals.
H Encourage daily activity and diversional activities.
Alveoli
ABNORMAL ALVEOLI
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Complications
H Activity tolerance
Patient teaching
Be sure to cover:
H avoidance of smoking and areas where smoking is
permitted
H avoidance of crowds and people with known infections
H home oxygen therapy, if indicated
H transtracheal catheter care, if needed
H the proper use of handheld inhalers
H high-calorie, protein-rich diet
H adequate oral fluid intake
H avoidance of respiratory irritants
H signs and symptoms of pneumothorax.
ALERT
Urge the patient to notify the practitioner if he experiences a sudden onset of worsening dyspnea or
sharp pleuritic chest pain exacerbated by chest
movement, breathing, or coughing.
Discharge planning
indicated.
H Refer the patient for influenza and pneumococcal
pneumonia immunizations, as needed.

H Refer the family of patients with familial emphysema
for alpha1-antitrypsin deficiency screening.
Emphysema
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Encephalitis
Overview
Description
H Severe inflammation of the brain
Pathophysiology
H Intense lymphocytic infiltration of brain tissues and
the leptomeninges results in:

cerebral edema
degeneration of the brains ganglion cells
diffuse nerve cell destruction (gray matter more
than white).
Causes
H Mosquito- or tick-borne arboviruses specific to rural
areas
H Sore throat and upper respiratory tract symptoms

H Sudden onset of altered level of consciousness
H Seizures
Physical findings
H Confusion, disorientation, or hallucinations
H Tremors
H Cranial nerve palsies
H Exaggerated deep tendon reflexes and absent superfi-
cial reflexes
H Paresis or paralysis of the arms and legs
H Stiff neck when the head is bent forward
H Fever
H Cerebral hemispheres
H Aphasia
H Involuntary movements
H Ataxia
H Sensory defects
H Enteroviruses in urban areas (coxsackievirus, po-
Test results
liovirus, and echovirus)

H Herpesvirus
H Mumps virus
H Adenoviruses
H Demyelinating diseases after measles, varicella,
rubella, or vaccination
H Human immunodeficiency virus
Laboratory
H Blood analysis identifies the virus.
H Serologic studies in herpes encephalitis show rising
titers of complement-fixing antibodies.
Imaging
H Magnetic resonance imaging locates the lesion.
H Computed tomography scan shows cerebral edema.
H Cerebrospinal fluid (CSF) analysis identifies the
virus.
H Lumbar puncture discloses CSF pressure.
H EEG shows slowing of waveforms.
Incidence
H About 1,500 cases annually in the United States
H More common in elderly people and infants
H Dysuria; pyuria
H Fever
H Myalgia
H Photophobia
H Stiff neck; headache
H Localized seizures
H Acute confusion or amnesic state
Complications
H Bronchial pneumonia
H Urinary retention and urinary tract infection
H Pressure ulcers
H Coma
H Epilepsy
H Parkinsonism
H Mental deterioration
Assessment
History
H Headache
H Muscle stiffness and malaise
258
Encephalitis
Treatment
General
H Airway maintenance
H Oxygen administration
H Adequate fluid and electrolyte intake
H Diet as tolerated
Medications
H Osmotic diuretics such as mannitol
H Corticosteroids such as dexamethasone
H Anticonvulsants such as phenytoin
H Antipyretics such as acetaminophen
H Antibiotics according to isolated organism
H Antivirals such as vidarabine
H Oxygen
H Stool softeners such as docusate sodium
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Key outcomes
The patient will:
H exhibit fluid balance within normal limits
H exhibit temperature within normal limits
H consume adequate calorie requirements daily
H verbalize feelings of increased comfort and relief
from pain.
H Ensure adequate fluid intake.
H Position and turn the patient often.
H Assist with range-of-motion exercises.
H Maintain adequate nutrition.
H Administer laxatives or stool softeners.
H Administer mouth care.
H Maintain a quiet environment.
H Start seizure precautions, if necessary.
H Reorient the patient often, if necessary.
H Keep the head of the bed elevated, as ordered.
Monitoring
H Vital signs
H Neurologic status
H Intake and output
H Intracranial pressure (severe cases)
Patient teaching
Be sure to cover:
H transient behavior changes
H the medication regimen
H adverse effects of medication
H follow-up care.
Discharge planning
H Refer the patient to an outpatient rehabilitation pro-
gram, as indicated.
Encephalitis
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Endocarditis
Overview
Description
H Inflammation or infection of the endocardium, heart
valves, or cardiac prosthesis

H Classified as infective (bacterial or fungal) or noninfective
Pathophysiology
H Fibrin, neutrophils, lymphocytes, and platelets clus-
ter on valve tissue and engulf bacteria, fungi, or

necrotic tissue. (See Degenerative changes in endocarditis.)
H This produces vegetation, which may cover the valve
surfaces, causing deformities and destruction of
valvular tissue, and may extend to the chordae
tendineae, causing them to rupture, leading to valvular insufficiency.
H Vegetative growth on the heart valves, endocardial
lining of a heart chamber, or the endothelium of a
blood vessel may embolize to the spleen, kidneys,
central nervous system, and lungs.
Causes
H Bacterial or fungal infection
H Advanced stages of cancer
H Immune system disorders
Risk factors
H Cardiac valvular disease
H I.V. drug use
H Rheumatic heart disease
H Prosthetic heart valves
H Congenital heart disease
H Degenerative heart disease
H Calcific aortic stenosis (in elderly patients)
H Asymmetrical septal hypertrophy
H Marfan syndrome
H Syphilitic aortic valve
H Long-term hemodialysis
H Systemic lupus erythematosus
Incidence
H No underlying heart disease in up to 40% of patients
Native valve endocarditis

H Most patients older than age 50
H Uncommon in children
H Rheumatic valvular disease in about 25% of cases
H Mitral valve most commonly involved valve
H Drug abusers with endocarditis (frequently young
males)
260
Endocarditis
H Heart murmur
Complications
H Valve stenosis or regurgitation
H Myocardial erosion
H Embolic debris lodged in the small vasculature of the
visceral tissue causing multiple organ infarcts

H Stroke
H Heart failure
H Acute renal failure
Assessment
History
H Predisposing condition
H Complaint of nonspecific symptoms, such as weak-
ness, fatigue, weight loss, anorexia, arthralgia, night

sweats, and intermittent fever, that may recur for
weeks
Physical findings
H Petechiae on the skin (especially common on the up-
per anterior trunk) and on the buccal, pharyngeal,

or conjunctival mucosa
H Splinter hemorrhages under the nails
H Clubbing of the fingers in long-standing disease
H Heart murmur in all patients except those with early
acute endocarditis and I.V. drug users with tricuspid
valve infection
H Murmur that changes suddenly or new murmur that
develops with a fever (classic physical sign)
H Oslers nodes
H Roths spots
H Janeway lesions
H Splenomegaly in long-standing disease
H Dyspnea, tachycardia, and bibasilar crackles possible
with left-sided heart failure
H Splenic infarction causing pain in the upper left
quadrant, radiating to the left shoulder, and abdominal rigidity
H Renal infarction causing hematuria, pyuria, flank
pain, and decreased urine output
H Cerebral infarction causing hemiparesis, aphasia,
and other neurologic deficits
H Pulmonary infarction causing cough, pleuritic pain,
pleural friction rub, dyspnea, and hemoptysis
H Peripheral vascular occlusion causing numbness and
tingling in arm, leg, finger, or toe or signs of impending peripheral gangrene
Test results
Laboratory
H Three or more blood cultures over 24 to 48 hours
identify the causative organism in up to 90% of patients.
H White blood cell count with differential are normal
or elevated.
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H Complete blood count shows normocytic, normo-
chromic anemia in subacute infective endocarditis.

H Erythrocyte sedimentation rate and serum creatinine
levels are elevated.
H Serum rheumatoid factor is positive in about half of
patients after the disease is present for 6 weeks.
H Urinalysis shows proteinuria and microscopic hematuria.
Imaging
H Echocardiography may identify valvular damage in up
to 80% of patients with native valve disease.
H Electrocardiography may show atrial fibrillation and
other arrhythmias that accompany valvular disease.
Degenerative changes in endocarditis

This illustration shows typical vegetations on the endocardium produced by fibrin and platelet deposits on infection sites.
Treatment
General
H Prompt therapy that continues for several weeks
H Selection of anti-infective drug based on type of in-
fecting organism and sensitivity studies

H If blood cultures negative (10% to 20% of subacute
cases), possible I.V. antibiotic therapy (usually for 4

to 6 weeks) against probable infecting organism
H Sufficient fluid intake
H Bed rest
Medications
H Antiplatelets or antipyretics such as aspirin
H Antibiotics, according to isolated organism
Surgery
H With severe valvular damage, especially aortic insuffi-
ciency or infection of a cardiac prosthesis, possible

corrective surgery if refractory heart failure develops
or if an infected prosthetic valve must be replaced
Monitoring
H Vital signs
H Cardiac rhythm and cardiovascular status
H Neurologic status
H Intake and output
H Renal status
H Arterial blood gas analysis, as needed
ALERT
Watch for signs of embolization, a common occurrence during the first 3 months of treatment. Tell
the patient to watch for and report these signs.
Patient teaching
Key outcomes
Be sure to cover:
H anti-infectives the patient needs to continue taking
H the need to watch closely for fever, anorexia, and
other signs of relapse about 2 weeks after treatment
stops
H the need for prophylactic antibiotics before dental
work and some surgical procedures
H proper dental hygiene and avoiding flossing the teeth
H how to recognize symptoms of endocarditis and to
notify the practitioner immediately if such symptoms
occur.
The patient will:

fatigue
H maintain hemodynamic stability with adequate cardiac output
H exhibit no arrhythmias
H express feelings about diminished capacity to perform usual roles.
H Stress the importance of bed rest.
H Provide a bedside commode.
H Allow the patient to express his concerns.
H Obtain a history of allergies.
H Administer antibiotics, as prescribed.
H Administer oxygen.
Discharge planning
H Encourage follow-up care with a cardiologist.
Endocarditis
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Endometriosis
Overview
Description
H Poorly understood gynecologic condition character-
ized by pain that occurs with menstruation

H Endometrial tissue appears outside uterine cavity
lining
H Ectopic tissue generally confined to the pelvic
area, but can appear anywhere in the body
Pathophysiology
H Endometrial cells respond to estrogen and proges-
terone with proliferation and secretion.

H During menstruation, ectopic tissue bleeds and caus-
es inflammation of the surrounding tissues.

H Inflammation leads to fibrosis.
H Fibrosis leads to adhesions that produce pain and in-
fertility.
Assessment
History
H Cyclic pelvic pain that peaks 5 to 7 days before
menses and lasts 2 to 3 days

H Infertility
H Acquired dysmenorrhea
H Pain in lower abdomen, vagina, posterior pelvis and
back; often radiates down legs

H Additional symptoms depending on site of involve-
ment:
Hypermenorrhea (oviducts and ovaries)
Deep-thrust dyspareunia (ovaries and cul-de-sac)
Suprapubic pain, dysuria, and hematuria (bladder)
Dyschezia, rectal bleeding with menses, and pain
in the coccyx or sacrum (rectovaginal septum and
colon)
Nausea and vomiting that worsen before menses
(small bowel and appendix)
Abdominal cramps (small bowel and appendix)
Causes
Physical findings
H Direct cause unknown

H Familial susceptibility
H Direct implantation
H Transportation (retrograde menstruation)
H Formation in situ
H Induction of labor
H Immune system defects
H Lymphatic spread theory
H Inflammatory influence
H Environmental contaminants
H Multiple tender nodules on uterosacral ligaments or
Incidence
H Usually occurs between ages 20 and 40; uncommon
before age 20
H More common in females who postpone childbear-
ing
H More common in white females
H Early menarche
H Menstrual flow lasting longer than 7 days
H Cycles lasting longer than 27 days
H Family history of endometriosis
H Multiparity
H Cyclic pelvic pain
H Severe dysmenorrhea
Complications
H Infertility
H Spontaneous abortion
H Anemia secondary to excessive bleeding
H Emotional problems secondary to infertility
H Pelvic adhesions
H Severe dysmenorrhea
H Ovarian cyst
H Ovarian cancer
rectovaginal septum
H Enlarged nodules (tender during menses)
H Ovarian enlargement with endometrial cysts on the
ovaries
H Thickened, nodular adnexa
Test results
H A scoring and staging system created by the American
Fertility Society quantifies endometrial implants according to size, character, and location:
Stage I indicates minimal disease (1 to 5 points).
Stage II indicates mild disease (6 to 15 points).
Stage III indicates moderate disease (16 to 40
points).
Stage IV indicates severe disease (more than 40
points).
H Laparoscopy confirms the diagnosis and identifies
the disease stage.
H Ultrasonography helps confirm the diagnosis.
Treatment
General
H Determined by stage of disease, patients age, and de-
sire to have children

H Pregnancy, if possible (provides temporary relief)
Medications
H Progestins such as medroxyprogesterone
H Hormonal contraceptives such as norethindrone
H Gonadotropin-releasing hormone, such as goserelin
and leuprolide
H Analgesics such as ibuprofen
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Endometriosis
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Surgery
H Laparoscopy to lyse adhesions, remove small im-
plants, and cauterize implants; for laser vaporization

of implants; usually followed by hormonal therapy to
suppress return of endometrial implants
H Total abdominal hysterectomy with bilateral
salpingo-oophorectomy in stages III and IV
Key outcomes
The patient will:
H develop adequate coping behaviors.
H Encourage the patient to express her feelings about
the disorder.
H Encourage using open communication before and
during intercourse.
Monitoring
H Effect of treatment
H Complications
H Coping ability
H Pain control
Patient teaching
Be sure to cover:
H associated complications
H avoiding minor gynecologic procedures immediately
before and during menstruation
H not postponing childbearing due to potential for infertility
H annual pelvic examination and Papanicolaou test.
Discharge planning
H Refer the patient and her partner to a mental health
professional for additional counseling, if necessary.

H Refer the patient to a support group such as the En-
dometriosis Association.
Endometriosis
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Enterobacteriaceae
infections
Overview
Description
Assessment
History
H Recent travel to another country
H Ingestion of contaminated food or water
H Recent close contact with a person who has diarrhea
H Abrupt onset of watery diarrhea
H Variety of infections caused by a family of mostly aer-
Physical findings
obic, gram-negative bacilli

H Cause local and systemic infections, including invasive diarrhea resembling shigellosis and noninvasive,
toxin-mediated diarrhea resembling cholera
H Escherichia coli: the cause of most nosocomial infections
H Cramping abdominal pain with hyperactive bowel
Pathophysiology
H When infected, incubation takes 12 to 72 hours.
H Noninvasive diarrhea results from two toxins pro-
duced by enterotoxigenic or enteropathogenic strains

of E. coli.
H Toxins interact with intestinal juices and promote excessive loss of chloride and water.
H The invasive form directly attacks the intestinal mucosa without producing enterotoxins, causing local
irritation, inflammation, and diarrhea. This form
produces sporadic and outbreak-associated bloody
diarrhea due to hemorrhagic colitis, which can be
life-threatening at age extremes.
Causes
sounds
H Blood and pus in infected stools
H Vomiting and anorexia
H Low-grade fever
H Signs of dehydration, especially in children
H Signs and symptoms of hyponatremia, hypokalemia,
hypomagnesemia, and hypocalcemia from electrolyte

losses
H Rapid, thready pulse
H Initially in infants, loose, watery stools that change
from yellow to green and contain little mucus or
blood
H Listlessness and irritability in infants
Test results
Laboratory
H Cultures growth of E. coli in a normally sterile location, including the bloodstream, cerebrospinal fluid, biliary tract, pleural fluid, or peritoneal cavity
suggest E. coli infection at that site.
H Some strains of E. coli that are part of normal GI flo-
ra but cause infection in immunocompromised patients

H Infection usually from nonindigenous strains
H Transmission directly from an infected person
H Ingestion of contaminated food or water or contact
with contaminated utensils
H Enterotoxigenic E. coli (major cause of diarrhea
among those who travel from industrialized to developing regions)
H Most common food source: ground beef
Treatment
Incidence
H May be major cause of diarrheal illness in children
in United States
H Incidence highest among travelers returning from
abroad, especially Mexico (noninvasive form),

Southeast Asia (noninvasive form), and South America (invasive form)
General
H Contact enteric precautions
H Initially, nothing by mouth
H Increased fluid intake (if appropriate)
H Avoidance of foods that cause diarrhea
H Small frequent meals until bowel function returns to
normal
Medications
H I.V. antibiotics such as cotrimoxazole
Key outcomes
H Diarrhea (cardinal symptom)
The patient will:

H regain or maintain normal fluid and electrolyte balance
H have an elimination pattern that returns to normal
H show no further evidence of weight loss
H maintain normal cardiac output.
Complications
H Bacteremia
H Severe dehydration and life-threatening electrolyte
disturbances
H Acidosis
H Shock
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Enterobacteriaceae infections
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H Institute contact enteric precautions and use proper
hand-washing technique.
H Replace fluids and electrolytes, as needed.
H Clean the perianal area after each episode of diar-
rhea and apply skin protectant, as needed.

H During epidemics, screen all facility personnel and
visitors for diarrhea, and prevent people with the disorder from having direct patient contact.
Monitoring
H Intake and output
H Stool volume measurement and presence of blood
and pus
H Signs and symptoms of gram-negative septic shock
H Vital signs
H GI status
Patient teaching
Be sure to cover:
H the need to avoid unbottled water, ice, unpeeled fruit,
and uncooked vegetables in other countries
H signs of dehydration and seeking prompt medical attention if these occur (if the patient will be cared for
at home).
Enterobacteriaceae infections
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Epididymitis
Overview
Description
H Infection of the epididymis (cordlike excretory duct
of the testis)
H One of most common infections of the male repro-
ductive tract
Pathophysiology
H Organisms enter the epididymis by the vas deferens
or lymphatics.
H Inflammation occurs.
H Other organs, such as the testes and prostate, may be
Incidence
H Usually affects males ages 19 to 40 or older than 60
H Affects 1 in 1,000 males anually
H Rare before puberty
H Dull, aching groin pain
H Fever
Complications
H Orchitis (see Understanding orchitis)
H Sterility
H Abscess
H Atrophy
H Pyocele
H Infarction
H Sepsis
affected.
Causes
H Pyogenic organisms, such as staphylococci, Es-
cherichia coli, streptococci, chlamydia, Neisseria

gonorrhoeae, and Treponema pallidum
H Tuberculosis
H Sarcoidosis
H Brucellosis
H Leprosy
H Trauma
H Certain drugs such as amiodarone
H Obstruction
Risk factors
H Urinary tract infection
H Unprotected sex
H Prostatitis
H Trauma
Assessment
History
H Chills
H Fever
H Unilateral, dull, aching pain
H Pain radiating to spermatic cord, lower abdomen,
and flank
H Scrotal pain
H Dysuria, frequency, urgency, and urine retention
H Mild scrotal cellulitis
H Scrotal edema
Physical findings
H Erythema
H High fever
H Characteristic waddle (attempt to protect groin and
scrotum while walking)
Understanding orchitis
Orchitis, an infection of the testes, is a serious complication of epididymitis. It may also result from mumps,
which can lead to sterility or, less commonly, another systemic infection.
Signs and symptoms

Typical effects of orchitis include unilateral or bilateral tenderness and redness, sudden onset of pain, and swelling
of the scrotum and testes. Nausea and vomiting also occur. Sudden cessation of pain indicates testicular ischemia, which can cause permanent damage to one or
both testes. Hydrocele may also be present.
Treatment
Appropriate treatment consists of immediate antibiotic
therapy in bacterial infection or, in mumps orchitis, injection of 20 ml of lidocaine near the spermatic cord of the
affected testis, which may relieve swelling and pain. Severe orchitis may require surgery to incise and drain the
hydrocele and to improve testicular circulation. Other
treatments are similar to those for epididymitis.
To prevent mumps orchitis, suggest that prepubertal
males receive the mumps vaccine (or gamma globulin injection after contracting mumps).
266
Epididymitis
H Urethral discharge
H Prehn sign: elevation of hemiscrotum relieves pain
H Scrotal abscess
Test results
Laboratory
H Urinalysis shows an increased white blood cell
(WBC) count, indicating infection.
H Urine culture and sensitivity tests may show the
causative organism.
H Serum WBC count is greater than 10,000/l, indicating infection.
Imaging
H Ultrasonography shows an enlarged epididymis
(larger than 17 mm) and can rule out testicular torsion.
Treatment
General
H Scrotal elevation
H Ice bag to groin
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H Increased oral fluids

H Bed rest until condition improves
H Use of an athletic supporter until recovered
Medications
H Broad-spectrum antibiotics such as cefazolin
H Analgesics such as ibuprofen
H Antipyretics such as acetaminophen
Surgery
H Scrotal exploration for complications of acute epi-
didymitis
H Epididymectomy under local anesthesia, if disease is
refractory to antibiotic therapy
Key outcomes
The patient will:
H express concern about self-concept and body image
sexual activity.
H Apply ice packs for comfort.
Monitoring
H Signs of abscess formation
H Vital signs
H Pain control
H Intake and output
Patient teaching
Be sure to cover:
H the use of a scrotal support while sitting, standing, or
walking
H safer sex practices.
Epididymitis
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Epidural hematoma
Overview
Assessment
History
H Injury to head
H Headache
H Nausea, vomiting
Description
Physical findings
H Acceleration-deceleration or coup-contrecoup in-
H Head wound
H Neurologic signs based on the extent of bleeding
juries that disrupt normal nerve functions in bruised

area and cause intracranial bleeding
Pathophysiology
H Injury is directly beneath the site of impact when the
brain rebounds against the skull from the force of a

blow (a beating with a blunt instrument, for example), when the force of the blow drives the brain
against the opposite side of the skull, or when the
head is hurled forward and stopped abruptly (as in
an automobile accident when a drivers head strikes
the windshield).
H Brain continues moving and slaps against the skull
(acceleration), then rebounds (deceleration). Brain
may strike bony prominences inside the skull (especially the sphenoidal ridges), causing intracranial
hemorrhage or hematoma that may result in tentorial
herniation.
Causes
H Trauma
H Anticoagulation
H Thrombolysis
H Lumbar puncture
H Epidural anesthesia
H Coagulopathy or bleeding diathesis
H Hepatic disease with portal hypertension
H Vascular malformation
H Disk herniation
H Paget disease of bone
H Valsalvas maneuver
H Hypertension
H Intracerebral lesion
Incidence
H Rare in people younger than age 2 and older than
age 60
H Four times more common in males than in females
dilated pupils, weakness, sensory deficits, alterations

in reflexes, alterations in bladder or anal sphincter
tone
H Bradycardia and hypertension (with increased ICP)
Test results
Laboratory
H Coagulation studies show clotting abnormalities (if
cause is anticoagulation).
Imaging
imaging identifies abnormal masses or structural
shifts within the cranium.
Treatment
General
H Supportive: airway, breathing, circulation
H Wound care
H Head of the bed elevated 30 degrees with intracere-
bral injury
H Diet based on extent of injury
H Nothing by mouth if surgery is necessary
H Bed rest initially, then activity, as tolerated
Medications
H Vitamin K, fresh frozen plasma, platelets, or clotting
products (if coagulation studies are abnormal)

H Analgesics such as codeine
H Osmotic diuretics such as mannitol
H Prophylactic antibiotics
Surgery
H Placement of burr holes

H Evacuation of the hematoma
H Craniotomy
H Brief loss of consciousness

H Headache
H Deteriorating mental status
Complications
Key outcomes
H Increased intracranial pressure (ICP)

H Seizures
H Respiratory depression and failure
The patient will:

H be hemodynamically stable
H recover or be rehabilitated from physical injuries to
the greatest extent possible
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H express a feeling of increased comfort and pain
relief.
Monitoring
H Vital signs
H Neurologic status
H Wound healing
H Seizure activity
H Cardiovascular status, including cardiac rhythm
Patient teaching
Be sure to cover:
H reporting changes in neurologic status
H avoiding aspirin as a pain treatment
H observing for cerebrospinal fluid drainage and signs
of infection.
Discharge planning
H Refer the patient to physical, occupational, and
speech therapy, as appropriate.

H Refer the patient to social service for extended ser-
vices, as appropriate.
Epidural hematoma
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Epiglottiditis
Overview
Description
H Acute inflammation of the epiglottis and surrounding
area
H Life-threatening emergency that rapidly causes edema and induration
H If untreated, results in complete airway obstruction
H Mortality 8% to 12%, typically in children
Pathophysiology
H Apprehension
H Irritability
Complications
H Death
H Sepsis
H Vocal cord paralysis
Assessment
History
H Recent upper respiratory tract infection
H Sore throat
H Dysphagia
H Sudden onset of high fever
H An infection of the epiglottis and surrounding area
Physical findings
leads to intense inflammation of the supraglottic region.

H Swelling of the epiglottis, aryepiglottic folds, arytenoid cartilage, and ventricular bands leads to acute
airway obstruction.
H Stridor
H Red and inflamed throat
H Fever
H Drooling
H Pale or cyanotic skin
H Restlessness and irritability
H Nasal flaring
H Tendency to sit in tripod position with mouth open
Causes
H Viral infection, usually Haemophilus influenzae
type B
and tongue protruding
H Pneumococci or group A streptococci
Incidence
H Higher incidence in Blacks and Hispanics
H Most common in children ages 2 to 6 years
H Occurs in any season
H Sore throat
H Dysphagia
Airway crisis
Epiglottiditis can progress to complete airway obstruction
within minutes. To prepare for this medical emergency,
keep these tips in mind:
H Watch for the inability to speak; weak, ineffective
cough; high-pitched sounds or no sounds while inhaling; increased difficulty breathing; and possible
cyanosis. These are warning signs of total airway obstruction and the need for an emergency tracheotomy.
H Keep the following equipment available at the patients
bedside in case of sudden, complete airway obstruction: a tracheotomy tray, endotracheal tubes, a handheld resuscitation bag, oxygen equipment, and a laryngoscope with blades of various sizes.
H Remember that using a tongue blade or throat culture
swab can initiate sudden, complete airway obstruction.
H Before examining the patients throat, request trained
personnel, such as an anesthesiologist, to stand by if
emergency airway insertion is needed.
270
Epiglottiditis
H Thick and muffled voice sounds

H Subcostal, suprasternal, and intercostal retractions
Test results
Laboratory
H Arterial blood gas (ABG) analysis may show hypoxia.
H Blood studies reveal elevated white blood cell count.
Imaging
H Lateral neck X-rays show an enlarged epiglottis and
distended hypopharynx.
H Direct laryngoscopy shows swollen, beefy-red
epiglottis.
Other
H Pulse oximetry may show decreased oxygen saturation.
Treatment
General
H Emergency hospitalization
H Humidification of airway
H Parenteral fluids
H Endotracheal intubation and mechanical ventilation
Medications
H Parenteral antibiotics according to infective organism
H Corticosteroids such as hydrocortisone
H Oxygen therapy
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Surgery
H Possible tracheotomy
Key outcomes
The patient will:
H maintain a patent airway (see Airway crisis)
H use alternate means of communication.
H Place the patient in a sitting position.
H Place the patient in a cool-mist tent.
H Encourage the parents to remain with their child.
H Offer reassurance and support.
H Ensure adequate fluid intake.
H Minimize external stimuli.
Monitoring
H Swallowing
H Vital signs
H Intake and output
H ABG results
H Pulse oximetry
H Signs and symptoms of secondary infection
Patient teaching
Be sure to cover:
H when to call the practitioner
H humidification
H signs and symptoms of respiratory distress
H signs and symptoms of dehydration.
Discharge planning
H Refer the patient for H. influenzae b conjugate vac-
cine, preferably at age 2 months, if indicated.
Epiglottiditis
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Epilepsy
H Also known as seizure disorder
H Headache
H Mood changes
H Lethargy
H Myoclonic jerking
H Description of an aura
H Pungent smell
H GI distress
H Rising or sinking feeling in the stomach
H Dreamy feeling
H Unusual taste in the mouth
H Vision disturbance
H Incontinence
Pathophysiology
Physical findings
H Seizures are paroxysmal events involving abnormal
H Findings possibly normal while patient isnt having a
Overview
Description
H Neurologic condition characterized by recurrent
seizures
H Good seizure control in about 80% of patients with
strict adherence to prescribed treatment
electrical discharges of neurons in the brain and cell

membrane potential.
H On stimulation, the neuron fires, the discharge
spreads to surrounding cells, and stimulation continues to one side or both sides of the brain, resulting
in seizure activity.
Causes
H Idiopathic in half of cases
Nonidiopathic epilepsy
H Birth trauma
H Anoxia
H Perinatal infection
H Genetic abnormalities (tuberous sclerosis and
phenylketonuria)
H Perinatal injuries
H Metabolic abnormalities (hypoglycemia, pyridoxine
deficiency, hypoparathyroidism)
H Brain tumors or other space-occupying lesions
H Meningitis, encephalitis, or brain abscess
H Traumatic injury
H Ingestion of toxins, such as mercury, lead, or carbon
monoxide
H Stroke
H Apparent familial incidence in some seizure disorders
seizure and when the cause is idiopathic

H Findings related to underlying cause of the seizure
Test results
Laboratory
H Serum glucose and calcium study results rule out
other diagnoses.
Imaging
imaging may indicate abnormalities in internal structures.
H Skull radiography may show certain neoplasms within the brain substance or skull fractures.
H Brain scan may show malignant lesions when X-ray
findings are normal or questionable.
H Cerebral angiography may show cerebrovascular abnormalities, such as aneurysm or tumor.
Other
H EEG shows paroxysmal abnormalities. (A negative
EEG doesnt rule out epilepsy because paroxysmal
abnormalities occur intermittently.)
Treatment
General
Incidence
H Airway protection during seizure

H Vagus nerve stimulation by pacemaker (see Vagus
H Patients usually younger than age 20

H Affects both sexes
H First seizure usually during childhood or after age 50
H A detailed presurgical evaluation to characterize
nerve stimulation)
Complications
seizure type, frequency, site of onset, psychological

functioning, and degree of disability to select candidates for surgery in medically intractable patients
H Safety measures
H Anoxia
H Traumatic injury
Medications
H Recurring seizures
Assessment
History
H Seizure occurrence unpredictable and unrelated to
activities
H Precipitating factors or events possibly reported
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Epilepsy

H Benzodiazepines such as lorazepam
Surgery
H Removal of a demonstrated focal lesion
H Correction of the underlying problem
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Vagus nerve stimulation

The vagus nerve stimulator is a Food and Drug Administrationapproved method to treat medically refractory
epilepsy. The stimulator device is about the size of a pacemaker and is surgically placed in a pocket under the skin
in the upper chest. Leadwires from the stimulator are tunneled under the skin to a neck incision where the vagus
nerve has been exposed. The electrode coils are then
placed around the nerve. The treating practitioner has a
computer, which can be used to alter the stimulation
parameters, thereby optimizing the treatment of seizures.
The device stimulates the vagus nerve for 30 seconds
every 5 minutes to prevent seizure occurrence. A magnet
over the area can activate the device to give extra, ondemand stimulation if the patient feels a seizure coming
on. Adverse effects are voice change, throat discomfort,
shortness of breath, and coughing and are usually experienced only when the device is on.
Discharge planning
H Refer the patient to the Epilepsy Foundation of Amer-
ica.
H Refer the patient to his states motor vehicle depart-
ment for information about a drivers license.
Key outcomes
The patient will:
H communicate understanding of the condition and
treatment regimen
H use support systems and develop adequate coping
H maintain usual participation in social situations and
activities.
H Prepare the patient for surgery, if indicated.
H Administer prescribed anticonvulsants.
Monitoring
H Neurologic status
H Response to anticonvulsants
H Vital signs
H Seizure activity
H Associated injuries
Patient teaching
Be sure to cover:
H maintaining a normal lifestyle
H compliance with the prescribed drug schedule
H adverse drug effects
H care during a seizure
H the importance of regular meals and checking with
the practitioner before dieting
H the importance of carrying a medical identification
card or wearing medical identification jewelry.
Epilepsy
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Erectile dysfunction
Overview
Description
H Inability to attain or maintain penile erection long
enough to complete intercourse

H Classified as primary or secondary:
Assessment
History
H Long-standing inability to achieve erection
H Sudden loss of erectile function
H Gradual decline in sexual function
H Medical disorders, drug therapy, or psychological
trauma
H Achievement of erection through masturbation but
Primary impotence: never achieving sufficient

erection
Secondary impotence: patient has achieved erection and completed intercourse in the past
H Also called impotence
Physical findings
Pathophysiology
DSM-IV-TR criteria
H A lack of autonomic signal or impairment of perfu-
H Diagnosis confirmed when patient meets criteria:
sion may interfere with arteriolar dilation due to inappropriate adrenergic stimulation.
H Premature collapse of the sacs of the corpus cavernosum occurs.
H Pelvic steal syndrome can cause loss of erection before ejaculation due to increased blood flow to pelvic
muscles.
Causes
not with a partner

H Anxious appearance
H Signs of depression
Persistent or recurrent partial or complete failure

to attain or maintain erection until completion of
sexual activity
Marked distress or interpersonal difficulty as a result of erectile dysfunction
Erectile dysfunction not better accounted for by
another Axis I disorder and not caused by a drug
or medical condition
H 80% of cases believed to have an organic cause, such
Test results
as vascular insufficiency and veno-occlusive dysfunction

H 20% of cases believed to be psychogenic in origin
Laboratory
H Hormone levels may be decreased.
Imaging
H Ultrasonography evaluates vascular function.
H Angiography evaluates vaso-occlusive disease.
Other
H Direct injection of prostaglandin E1 (alprostadil)
into the corpora evaluates the quality of erection.
H Nocturnal penile tumescence testing helps distinguish psychogenic impotence from organic impotence.
Risk factors
H Medication
H Pelvic injury or surgery
H Alcohol use
H Increasing age
H Smoking
H Obesity
H Hypertension
H Diabetes mellitus
H Scleroderma
H Renal failure
H Cancer treatment
H Stroke
H Multiple sclerosis
H Alzheimers disease
H Depression
Incidence
H Affects males of all age-groups, but incidence in-
creases with age
H Depression
H Inability to obtain or maintain an erection
Complications
H Serious disruption of marital or other sexual rela-
tionships
274
Treatment
General
H Sex therapy for psychogenic impotence
H Treatment of cause for organic impotence
H Psychological counseling
H External vacuum device
Medications
H Intracavernosal injection therapy
H Medicated Urethral System for Erections
intraurethral suppository
H Hormone replacement such as testosterone
H Phosphodiesterase type-5 inhibitors, such as silde-
nafil and vardenafil
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Surgery
H Surgically inserted inflatable or semirigid penile
prosthesis
Key outcomes
The patient will:
H acknowledge a problem in sexual function
H discuss feelings and perceptions about changes in
sexual performance
H develop and maintain a positive attitude toward sexuality and sexual performance.
H As needed, refer the patient to a physician, nurse,
psychologist, social worker, or counselor trained in

sex therapy.
After penile prosthesis surgery
H Apply ice packs to the penis for 24 hours.
H Empty the drainage device when its full.
H If the patient has an inflatable prosthesis, provide instructions for use.
Monitoring
H Complications
H Postoperative bleeding
H Postoperative infection
Patient teaching
Be sure to cover:
H the anatomy and physiology of the reproductive system and the human sexual response cycle
H the need to avoid intercourse until the incision heals,
usually 6 weeks after penile implant surgery
H signs of infection.
Discharge planning
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Erythroblastosis fetalis
Overview
Description
H Hemolytic disease of the fetus and neonate
H Stems from an incompatibility of fetal and maternal
blood
H Also known as hemolytic disease of the newborn
Pathophysiology
ABO incompatibility
H Each blood group has specific antigens on red blood
cells (RBCs) and specific antibodies in the serum.
H The maternal immune system forms antibodies
against fetal cells when blood groups differ.
What happens in Rh isoimmunization

Rh-negative woman before pregnancy
H This can cause hemolytic disease even if fetal ery-
throcytes dont escape into the maternal circulation

during pregnancy.
Rh incompatibility
H During her first pregnancy, an Rh-negative female becomes sensitized (during delivery or abortion) by exposure to Rh-positive fetal blood antigens inherited
from the father.
H A female may also become sensitized from receiving
blood transfusions with alien Rh antigens; from inadequate doses of Rh0(D) (RhoGAM); or from failure
to receive Rh0(D) after significant fetal-maternal
leakage during abruptio placentae (premature detachment of the placenta).
H A subsequent pregnancy with an Rh-positive fetus
provokes maternal production of agglutinating antibodies, which cross the placental barrier, attach to
Rh-positive cells in the fetus, and cause hemolysis
and anemia.
H To compensate, the fetal blood-forming organs step
up the production of RBCs, and erythroblasts (immature RBCs) appear in the fetal circulation.
H Extensive hemolysis releases more unconjugated
bilirubin than the liver can conjugate and excrete,
causing hyperbilirubinemia and hemolytic anemia.
Causes
H ABO incompatibility
H Rh isoimmunization (see What happens in Rh
isoimmunization)
Incidence
H Rh negativity 15% of Whites, 5% to7% of Blacks,
Pregnancy with Rh-positive fetus
rare in Asians
H About 4,000 cases per year
H ABO incompatibility frequently occurs during first
pregnancy; present in about 12% of pregnancies

Placental separation
Maternal sensitization to Rh-positive blood
H Jaundice
H Anemia
H Hydrops fetalis
Complications
Next pregnancy with Rh-positive fetus
Maternal anti-Rh antibodies enter fetal circulation
H Fetal death in utero

H Severe anemia
H Heart failure
H Kernicterus
Assessment
History
Anti-Rh antibody to fetal Rh-positive red blood cells (RBCs)
H Mother Rh-positive; father Rh-negative

H Antigen-antibody response developed during previ-
ous pregnancy
Hemolysis of fetal RBCs
H Blood transfusion
H Maternal history (for erythroblastotic stillbirths,
abortions, previously affected children, previous antiRh titers)
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Physical findings
H Pallor
H Edema
H Petechiae
H Bile-stained umbilical cord
H Yellow- or meconium-stained amniotic fluid
H Mild to moderate hepatosplenomegaly
H Heart murmur
H Jaundice
Test results
Laboratory
H Paternal blood is typed for ABO and Rh.
H Amniotic fluid analysis shows increased bilirubin and
anti-Rh titers.
H Direct Coombs test of umbilical cord blood measures RBC (Rh-positive) antibodies in the neonate
(positive only when the mother is Rh negative and
the fetus is Rh positive).
H Cord hemoglobin level in neonate is less than 10 g,
indicating severe disease.
H Many nucleated peripheral RBCs are present.
Imaging
H Radiologic studies show edema and, in hydrops fetalis, the halo sign (edematous, elevated, subcutaneous
fat layers) and the Buddha position (fetuss legs are
crossed).
H maintain fluid balance within normal limits

H maintain normal temperature.
H Encourage expression of fears by parents concerning
possible complications of treatment.

H Promote normal parental bonding.
H Administer Rho(D) I.M., as ordered.
Monitoring
H Vital signs
H Cardiac rhythm and rate
H Temperature
H Transfusion complications
H Intake and output
Patient teaching
Be sure to cover:
H medications, drug routes, and administration
H preventive measures for reoccurrence.
Discharge planning
H Encourage follow-up appointments.
Treatment
General
H Phototherapy (exposure to ultraviolet light to reduce
bilirubin levels)
H Intubation of neonate
H Removal of excess fluid
H Maintenance of body temperature
Medications
H Intrauterine-intraperitoneal transfusion (if amniotic
fluid analysis suggests the fetus is severely affected

and not mature enough to deliver)
H Exchange transfusion
H Albumin infusion
H Gamma globulin containing anti-Rh antibody
(Rho[D])
Surgery
H Planned delivery (usually 2 to 4 weeks before term
date, depending on maternal history, serologic test

results, and amniocentesis)
Key outcomes
The patient will:
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Esophageal cancer
Overview
Description
H Esophageal tumors usually fungating and infiltrating
and nearly always fatal

H Common sites of metastasis are liver and lungs
H Includes two types of malignant tumors: squamous
cell carcinoma and adenocarcinoma
H Grim prognosis (5-year survival rates occur in less
than 5% of cases; most patients die within 6 months
of diagnosis)
Pathophysiology
H Most esophageal cancers are poorly differentiated
squamous cell carcinomas, with 50% occurring in

the lower portion of the esophagus, 40% in the middle portion, and 10% in the upper or cervical esophagus.
H Adenocarcinomas occur less frequently and are contained to the lower third of the esophagus.
H The tumor partially constricts the lumen of the
esophagus.
H Regional metastasis occurs early by way of submucosal lymphatics, often fatally invading adjacent vital
intrathoracic organs. (If the patient survives primary
extension, the liver and lungs are the usual sites of
distant metastases; unusual metastasis sites include
the bone, kidneys, and adrenal glands.)
Causes
H Unknown
Risk factors
H Human papillomavirus
H Chronic irritation from heavy smoking
H Excessive use of alcohol
H Stasis-induced inflammation, as in achalasia or stric-
ture
H Previous head and neck tumors
H Nutritional deficiency, such as in untreated sprue and
Complications
H Direct invasion of adjoining structures
H Inability to control secretions
H Obstruction of the esophagus
H Loss of lower esophageal sphincter control (may re-
sult in aspiration pneumonia)
Assessment
History
H Feeling of fullness, pressure, indigestion, or subster-
nal burning
H Dysphagia and weight loss; the degree of dysphagia
varies, depending on the extent of disease

H Hoarseness
H Pain on swallowing or pain that radiates to the back
H Anorexia, vomiting, and regurgitation of food
Physical findings
H Chronic cough (possibly from aspiration)
H Cachexia and dehydration
Test results
Laboratory
H Complete blood count reveals anemia.
H Bleeding time may be prolonged.
Imaging
H X-rays of the esophagus, with barium swallow and
motility studies, are used to delineate structural and
filling defects and reduced peristalsis.
H Computed tomography scan may help to diagnose
and monitor esophageal lesions.
H Esophagogastroduodenoscopy shows tumor and permits biopsy.
H Esophagoscopy, punch and brush biopsies, and exfoliative cytologic tests confirm esophageal tumors.
H Bronchoscopy (usually performed after an esophagoscopy) may reveal tumor growth in the tracheobronchial tree.
H Endoscopic ultrasonography of the esophagus combines endoscopy and ultrasound technology to measure the depth of penetration of the tumor.
Plummer-Vinson syndrome
H Exposure to nitrosamines
Incidence
H Occurs worldwide, but most common in Japan, Rus-
sia, China, the Middle East, and the Transkei region

of South Africa
H Dysphagia
H Weight loss
H Esophageal obstruction
H Acute pain
H Hoarseness, coughing
H Cachexia
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Esophageal cancer
Treatment
General
H Surgery and other treatments to relieve disease ef-
fects
H Palliative therapy used to keep esophagus open:
Dilatation of the esophagus

Laser therapy
Radiation therapy
Installation of prosthetic tubes (such as Celestins
tube)
H Liquid to soft diet, as tolerated
H High-calorie supplements
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Medications
H Chemotherapy such as fluorouracil
Surgery
H Radical surgery to excise tumor and resect esopha-
gus or stomach and esophagus

H Gastrostomy or jejunostomy
Other
H Endoscopic laser treatment and bipolar electrocoag-
ulation
Key outcomes
The patient will:
H maintain weight
H maintain fluid volumes within the normal range
H not aspirate
pain.
H Position the patient with the head of the bed elevated
at least 30 degrees to prevent aspiration.

H Provide tube feedings, as ordered.
H Encourage incentive spirometer use.
Monitoring
H Vital signs
H Intake and output
H Pain control
Patient teaching
Be sure to cover:
H the disease process, treatment, and postoperative
course
H dietary needs
H the need for rest between activities.
Discharge planning
H Arrange for home care follow-up after discharge.
H Refer the patient to the American Cancer Society.
Esophageal cancer
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Exophthalmos
Overview
Description
Assessment
History
H Vision changes
H Eye trauma
H Unilateral or bilateral bulging or protrusion of the
Physical findings
eyeballs or their apparent forward displacement

(with lid retraction)
H Also called proptosis
H Eye protrusion (see Detecting unilateral exophthal-
Pathophysiology
H Increase in volume within the fixed bony orbital con-
fines displaces the globular orbit anteriorly.
Causes
H Ophthalmic Graves disease
H Trauma
H Hemorrhage
H Varicosities
H Thrombosis
H Edema
H Infection
H Orbital cellulitis
H Panophthalmitis
H Tumors and neoplastic diseases
H Vasculitis
Incidence
H Occurs more often in females than in males
H Can occur at any age, but more common between
ages 30 and 50
H Bulging eyeball (see Recognizing exophthalmos)
H Diplopia
Complications
H Vision changes
mos)
H Visible rim of the sclera
H Infrequent blinking
H Limited ocular movement
H Ocular tenderness
Test results
Laboratory
H Culture of discharge determines the infecting organism.
H Sensitivity testing indicates appropriate antibiotic
therapy.
Imaging
H Computed tomography scan detects swollen extraocular muscles or lesions within the orbit.
H Exophthalmometer readings confirm diagnosis by
showing the degree of anterior projection and asymmetry between the eyes. (Normal bar readings range
from 12 to 20 mm.)
Treatment
General
H Cold and warm compresses (trauma)
Medications
H Antibiotics such as cefazolin to treat infection
H Antithyroid therapy such as propylthyrouracil for
Graves disease
H Corticosteroids such as dexamethasone to treat optic
neuropathy
H Eye lubricants
Surgery
Recognizing exophthalmos
This photo shows the characteristic forward protrusion of
the eyes from the orbit associated with exophthalmos.
H Orbital decompression (removal of the superior and
lateral orbital walls) if vision threatened, followed by

lid (blepharoplasty) and muscle surgery
H Surgical exploration of the orbit and excision of the
tumor
Key outcomes
The patient will:
H maintain functional eyesight
H understand cause and treatment of exopthalmus
H experience normal eye movement.
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Exophthalmos
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Detecting unilateral exophthalmos

If one of the patients eyes seems more prominent than
the other, examine both eyes from above the patients
head. Look down across his face, gently draw his lids up,
and compare the relationship of the corneas to the lower
lids. Abnormal protrusion of one eye suggests unilateral
exophthalmos.
Dont perform this test if you suspect eye trauma.
H Apply cold and warm compresses, as ordered, for
fracture or other trauma.

H Protect the exposed cornea with lubricants to prevent
corneal drying.
Monitoring
H Response to therapy
H Visual acuity
Patient teaching
Be sure to cover:
H eye care
H proper administration of eyedrops.
Discharge planning
H Encourage follow-up care.
Exophthalmos
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Failure to thrive
Overview
H Young or single mother without social supports

H Parents who are overly focused on career
H Caregivers with inadequate adaptive and social skills
H Depression (in parent or in adult patient with failure
to thrive)
Description
Incidence
H Failure to maintain weight (and sometimes height)
H Exact figures unknown

H 1% to 5% of children younger than age 2 years who
above the fifth percentile

H Deviation from established growth curve
H Three types
Organic
Nonorganic
Mixed
H Occurs in infants, children, adolescents, and adults
Pathophysiology
are admitted to hospitals

H An estimated 10% of children in primary care set-
tings
H Higher in children from families with medical and
psychosocial problems, those of low socioeconomic

status, and undeveloped countries
H Nonorganic form slightly higher in females
H Organic
Calorie intake is less than required for nutritional

needs due to the presence of a physiologic disorder.
H Nonorganic
A complex dynamic exists between the caregiver
and the patient, including a decreased emotional
attachment.
Sufficient food is available, but the patient may be
fed an unusual or overly restricted diet.
H Mixed
This is a combination of organic and nonorganic
explanations.
H Absence of weight gain or weight loss

H Altered body posture
H Thin appearance
H Muscle wasting
Causes
Assessment
H Organic
Complications
H Disease susceptibility
H Growth retardation
H Developmental delays
H Impaired bonding
H Altered family relationships
Acute or chronic illness

Defects in major organ systems
Malabsorption syndrome
Endocrine deficiencies
Congenital heart defects
Fetal alcohol syndrome
Cystic fibrosis
Feeding difficulties
Long-term gastroenteritis
Premature birth
Dementia (in adults)
H Nonorganic
Psychological problem between patient and primary caregiver
Failure to bond
Dysfunctional parenting behaviors
Economic problems
Poor eating habits
Neglect or abuse
Parental ignorance about appropriate child care
H Mixed
Combination of organic and nonorganic causes
History
Risk factors
Physical findings
H Untreated medical conditions

H Low-birth-weight or premature infant
H Domestic violence
H Poverty
H Short stature
H Weight below fifth percentile
H Small head circumference
H Decreased skin-fold thickness
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Failure to thrive
H Prenatal
Use of drugs, alcohol, cigarettes

Diseases
H Labor and delivery
H Family medical and social history, including genetic
disorders
H Early neonatal
Birth weight
Initial weight loss
Birth defects
H Feeding
Nursing patterns of breast-fed infant; frequency
and time spent nursing
Maternal diet
Formula; type, amount, and frequency
Current eating patterns
H Psychosocial family problems
H Age at which the problem was first observed
H Previous growth information
H Medications
H Caregivers knowledge of appropriate care
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H Delayed motor function

H Developmental delays
H Neuromuscular weakness
H Gaze avoidance
H Minimal smiling
H Signs and symptoms of underlying disease
H Caregiver-patient interactions
Test results
Laboratory
H Complete blood count shows anemia.
H Stool analysis shows abnormal absorption or blood
indicating possible underlying disorder.
H Erythrocyte sedimentation rate is elevated, indicating
possible underlying disorder.
H Decreased electrolyte levels show poor nutritional intake.
H Blood lead level indicates lead poisoning.
H Thyroid test results indicate a hyperthyroid state.
H Elevated liver function study results point to an underlying disorder.
H Sweat-chloride test is done to rule out cystic fibrosis.
H Elevated glucose or glycosylated hemoglobin level indicates diabetes.
H Elevated blood urea nitrogen and creatinine levels indicate a kidney disorder.
X-rays
H GI studies may detect an organic cause.
H Bone X-rays establish bone age.
Other
H Short-term hospitalization determines whether disorder is nonorganic (child will gain weight).
H Developmental testing shows delays.
H Plot the childs growth and weight, as ordered.
H Assess for signs and symptoms of organic disease.
H Provide supportive environment.
H Encourage positive parenting.
Monitoring
H Caregiver compliance with patients nutritional needs
H Weight
Patient teaching
Be sure to cover:
H importance of maintaining the feeding schedule
H normal growth and development
H where and how to obtain help during crisis situations
H the proper care of infants and children.
Discharge planning
H Refer the patient to social worker and nutrition spe-
cialist, as appropriate.
H Refer the patient to community agencies, education
programs, stress management training, and support

groups, as indicated.
Treatment
General
H Underlying medical condition
H Liquid nutritional supplements
H High-calorie balanced diet
Medications
H Vitamins
Key outcomes
The patient will:
H receive appropriate medical care
H display age-appropriate nutrient intake
H demonstrate normal growth and development.
The caregiver will:
H verbalize understanding of the need for adequate nutrition
H demonstrate appropriate feeding techniques
H participate in developing a plan to promote parenting
skills, as appropriate
H seek psychological care and social assistance, as
needed.
Failure to thrive
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Fibrocystic breast
disease
Complications
H Benign condition usually not leading to breast cancer
H Makes it more challenging to do breast self-examina-
tions
H May make mammography more difficult to interpret;
Overview
early cancerous lesions possibly being overlooked
Description
Assessment
H Common, benign breast condition

H Changes in breast tissue related to hormonal cycles
H Typically resolves after menopause
History
Pathophysiology
H Hormonal variations during the menstrual cycle are
normal.
H Estrogen and progesterone cause breast tissue cells
to grow and multiply.

H Prolactin, growth factor, insulin, and thyroid hor-
mone also affect breast tissue.

H They stimulate growth of breast glandular tissue and
increase the activity of blood vessels, cell metabolism, and supporting tissue.
H Secretions produced by glandular cells may not be
completely reabsorbed, causing fibrosis.
H Secretions become trapped in glandular cells, forming cysts.
Causes
H Fluctuations in hormone levels during menstrual
cycle
H Changes typically right before menstruation
H Dietary factors, including consumption of caffeine,
excessive saturated fats, and salts
H Estradiol excess (can occur from taking oral contraceptives or other synthetic forms of estrogen)
H Diabetes or thyroid dysfunction
Risk factors
H Premenstrual breast tenderness and swelling that im-
proves after menstrual period

H Dull, heavy pain and tenderness
H Feeling of fullness in breasts
H Nipple sensation changes; possibly itching
Physical findings
H Dense, irregular, and bumpy cobblestone consis-
tency in breast tissue

H Usually found in outer upper quadrants and under-
side of the breast

H Can occur as an isolated lump, in clusters, or wide-
spread
H Free movement of lumps in breast tissue
H Lumps usually smooth, round, fluid-filled, and slight-
ly elastic; varying in texture and size

H Possibly severe breast tenderness and pain
H Non-bloody nipple discharge; varying from clear and
watery to sticky
Test results
Imaging
H Mammography, ultrasonography, or magnetic resonance imaging rule out malignancy.
H Needle aspiration and biopsy confirm benign condition.
H Hormone replacement therapy

H Nullipara
H Irregular menstrual cycles
H Family history of fibrocystic breast disease or breast
Treatment
cancer
H Dietary factors
H Dietary changes such as:
Incidence
H Present in about 30% of females in United States
H Most common between the ages of 30 and 50
H Estimated to affect over 60% of all females
H Rare in postmenopausal females
H Tends to be symmetrical but can occur in only one
breast
H Lumps that move freely in the breast tissue and vary
in texture and size

H Breast tenderness and pain ranging from mild to se-
vere
284
Fibrocystic breast disease
General
Reducing or eliminating caffeine consumption
(controversial); includes chocolate, sodas, coffee,
and tea
Reducing sugar and salt intake
Limiting consumption of saturated fats
Avoiding commercially raised meats containing
hormones
Eating a high-fiber diet, including many plantbased foods, fruits and vegetables, beans and peas,
raw seeds and nuts, and whole grains
Increasing seafood consumption, such as salmon,
trout, and mackerel (high in omega-3 fatty acids
and iodine)
H Increased vitamin and mineral intake
Vitamin A to reduce the pain symptoms and the
size of the breast lesions
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Vitamin E to reduce pain and tenderness as well as

size of cysts
Magnesium supplement to help relieve cyclic
breast pain
Evening primrose oil, a source of the essential fatty acid, linoleic acid, and its chemical derivative,
gamma linolenic acid, to relieve symptoms and
possibly aid in correction of hormonal irregularities
H Application of heat to relieve pain
H Use of bra with good support to restrict motion
H Avoidance of estrogen supplementation
Medications
H Diuretics, such as furosemide, hydrochlorothiazide,
and triamterene
H Drugs that alter hormone levels, such as bromocrip-
tine, tamoxifen, and danazol

H Acetaminophen or nonsteroidal anti-inflammatory
drugs, such as ibuprofen and naproxen
Surgery
H Removal of lumps in the most severe cases
Key outcomes
The patient will:
H express feelings of comfort and reduced pain
H verbalize understanding of the disease and its treatment
H demonstrate correct procedure for performing
breast self-examination
H acknowledge need to contact practitioner if changes
occur in breasts.
H Provide pain medication, as ordered.
H Assist with breast examination.
Monitoring
H Pain signs and symptoms
H Changes in breast lumps
Patient teaching
Be sure to cover:
H the disease and its treatment
H the correct method of breast self-examination
H when to contact the practitioner.
Fibrocystic breast disease
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Fibromyalgia syndrome
H Sleep disturbances with frequent arousal and frag-
Overview
mented sleep or frequent waking throughout night

(patient unaware of arousals)
H Possible report of irritable bowel syndrome, tension
headaches, puffy hands, and paresthesia
Description
Physical findings
H A diffuse chronic pain syndrome

H Referred to as FMS
H Previously called fibrositis
H Tender points are elicited by applying a moderate
Pathophysiology
Test results
H Several theories describe FMS:
H Diagnostic testing in FMS not associated with an un-
Blood flow to the muscle is decreased (due to

poor muscle aerobic conditioning, rather than
other physiologic abnormalities).
Blood flow in the thalamus and caudate nucleus is
decreased, leading to a lowered pain threshold.
Endocrine dysfunction such as abnormal
pituitary-adrenal axis responses or abnormal
levels of the neurotransmitter serotonin in brain
centers affects pain and sleep.
The functioning of other pain-processing pathways
is abnormal.
Causes
H Unknown
H May be primary disorder or associated with underly-
ing disease
H Possible association with infection
H May be multifactorial and influenced by stress, physical conditioning, abnormal-quality sleep, neuroendocrine factors, psychiatric factors and, possibly,
hormonal factors (due to predominance in females)
Incidence
H Observed in up to 15% of patients seen in general
rheumatology practice and 5% of general medicine

clinic patients
H May occur at almost any age; peak incidence among
those ages 20 to 60
H Widespread pain and fatigue
Complications
H Pain
H Depression
H Sleep deprivation
Assessment
History
amount of pressure to a specific location. (See Tender points of fibromyalgia.)
derlying disease is generally negative for significant

abnormalities.
Treatment
General
H Massage therapy
H Ultrasound treatments
H Regular, low-impact aerobic exercise program such
as water aerobics
H Preexercise and postexercise stretching to minimize
injury
Medications
H Serotonin reuptake inhibitors such as paroxetine
H Tricyclic antidepressants, such as amitriptyline and
nortriptyline
H Nonsteroidal anti-inflammatory drugs such as
ibuprofen
H Magnesium supplements
H Lidocaine injections
Key outcomes
The patient will:
pain
H attain the highest degree of mobility possible within
the confines of the disease
H express feelings about limitations
H express an increased sense of well-being.
H Encourage the patient to perform regular stretching
exercises safely and effectively.

H Provide reassurance that FMS can be treated.
H Diffuse, dull, aching pain across neck and shoulders
Monitoring
and in lower back and proximal limbs

H Pain typically worse in morning, sometimes with stiffness; can be exacerbated by stress, lack of sleep,
weather changes, and inactivity
H Sensory disturbances
H Pain control
H Fatigue
H Depression
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Tender points of fibromyalgia

The patient with fibromyalgia syndrome may complain of specific areas of tenderness, which are shown in the
illustrations below.
Occiput:
Suboccipital muscle
insertions
Trapezius:
Midpoint of the upper
border
Supraspinatus:
Above the scapular spine
near the medial border
Gluteal:
Upper outer quadrants
of buttocks
Greater trochanter:
Posterior to the
trochanteric prominence
Low cervical:
Anterior aspects of the intertransverse spaces at C5 to C7
Second rib:
Second costochondral
junctions
Lateral epicondyle:
2 cm distal to the
epicondyles
Knee:
Medial fat pad proximal
to the joint line
Patient teaching
Be sure to cover:
H the importance of exercise in maintaining muscle
conditioning, improving energy and, possibly, improving sleep quality
H the importance of taking the tricyclic antidepressant
dose 1 to 2 hours before bedtime, which can improve sleep benefits while reducing the morningafter effect
H the avoidance of decongestants and caffeine before
bedtime
H the need for a low-fat diet, high in complex carbohydrates, to decrease symptoms.
Discharge planning
H Refer the patient to appropriate counseling, as
needed.
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Folliculitis,
furunculosis, and
carbunculosis
Carbunculosis
H Abscess of adjacent furuncles
H Develops more slowly
Pathophysiology
H The infecting organism invades the hair follicle.
H An inflammatory reaction within the hair follicle re-
sults. (See Hair follicles and bacterial infection.)
Overview
Causes
Description
H Bacterial infection, typically coagulase-positive
Folliculitis
H Superficial bacterial infection of hair follicles that
usually heals without scarring
H Characterized by the formation of pustules
H Typically a localized eruption
H Predilection for perifollicular (hairy) areas and flexural surfaces
H May occur in the beard region (sycosis barbae)
H May occur in the scalp or on extremities (follicular
impetigo)
H May lead to the development of furuncles (furunculosis) or carbuncles
H Prognosis depending on severity, patients physical
condition, and ability to resist infection
Furunculosis
H Deeper infections characterized by deeper, more tender, and erythematous nodules or boils
H Worsened by irritation, friction, or perspiration
Hair follicles and bacterial infection

The degree of hair follicle involvement in bacterial skin infection ranges from superficial folliculitis (erythema and a
pustule in a single follicle) to deep folliculitis (extensive
follicle involvement), to furunculosis (red, tender nodules
that surround follicles with a single draining point) and, finally, to carbunculosis (deep abscesses that involve several follicles with multiple draining points).
Superficial folliculitis
Deep folliculitis
Staphylococcus aureus
H Contamination from an infected wound elsewhere on
the body
Risk factors
H Debilitation
H Immunosuppression
H Diabetes mellitus
H Occlusive agents or chemicals such as cosmetics
H Tight-fitting clothing
H Improper shaving technique
H Occlusive therapy, using steroids
H Obesity
H Chronic colonization of S. aureus in nares or per-
ineum
Incidence
Folliculitis
H Common infection
H Affects all ages
Furunculosis
H Uncommon in children unless immunocompromised
H Increased frequency after puberty
H More common in adolescents and young adults
Carbunculosis
H Not uncommon for several family members to be affected at the same time
H More common in patients with diabetes and in patients who are immunocompromised
Furunculosis
Carbunculosis
H Pustules
H Pain
H Erythema
Complications
H Cellulitis
H Septicemia
H Hematogenous seeding to heart valves, joints, and
other organs
H Residual scarring
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Assessment
History
H Presence of risk factors
H Pain and erythema for several days or longer
H Malaise
Physical findings
Folliculitis
H Localized pustules, usually on the scalp or extremities
H Pustules possibly also in beard area or on eyelids
(styes)
Furunculosis
H Hard, painful, or fluctuant nodules usually on neck,
face, axillae, or buttocks
H If nodules enlarge and rupture, pus and necrotic material on the skin surface
H Erythema that may persist for days or weeks after
nodule rupture
Carbunculosis
H Fever
H Extremely painful, deep abscesses
H Abscesses drain through multiple openings onto the
skin surface
H Pain, tenderness, and edema around pustule sites
H Hard or fluctuant nodules under skin surface
H Localized lymphadenopathy
Test results
Laboratory
H Wound culture and sensitivity results show the infecting organism.
H Complete blood count may reveal leukocytosis.

H demonstrate understanding of proper skin care regi-
men.
H Perform wound care.
H Properly dispose of contaminated dressings.
H Apply warm, moist compresses.
H Assist with general hygiene and comfort measures, as
needed.
H Administer prescribed pain medications and antibi-
otics.
Monitoring
H Level of comfort
H Complications
Patient teaching
Be sure to cover:
H meticulous hand-washing technique
H good personal hygiene
H how to prevent the spread of the infection
H lesion care
H the prescribed medication and possible adverse effects.
Discharge planning
H Refer patients with recurrent furunculosis for a phys-
ical examination to assess for underlying diseases.
Treatment
General
H Thorough cleaning of infected area with soap and
water
H Avoidance of occlusive agents
H Application of warm, moist compresses
Medications
H Topical or systemic antibiotics, according to the iso-
lated organism
Surgery
H Possible incision and drainage in patients with furun-
culosis or carbunculosis
Key outcomes
The patient will:
Folliculitis, furunculosis, and carbunculosis
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Fragile X syndrome
Overview
Description
H Most common inherited cause of mental retardation;
average IQ about 30 to 70
H Signs and symptoms of the syndrome apparent in
about 85% of males and 50% of females who inherit

the fragile X mental retardation-1 (FMR1) gene
H Distinct physical features, behavioral difficulties, and
cognitive impairment often found in postpubescent
males with syndrome
H More subtle symptoms usually found in females with
syndrome
Pathophysiology
H This X-linked condition doesnt follow a simple
X-linked inheritance pattern.

H Full mutation typically causes abnormal methylation
(methyl groups attach to components of the gene) of

FMR1.
H Methylation inhibits gene transcription and, thus,
protein production.
H The reduced or absent protein production leads to
the clinical features of fragile X syndrome.
Assessment
History
H Hyperactivity, speech difficulties, language delay, and
autistic-like behaviors
H Excessive shyness or social anxiety
Physical findings
H A prominent jaw and forehead
H Head circumference exceeding the 90th percentile
H Long, narrow face with long or large ears that may be
posteriorly rotated
H Hyperextension of the fingers
H Severe pectus excavatum
H Unusually large testes after puberty
Test results
Laboratory
H Positive genetic test, preferably deoxyribonucleic
acid analysis of blood or buccal samples, detects the
size of the cytosine-guanine-guanine repeat and the
methylation status of FMR1.
Imaging
H Echocardiography reveals a floppy mitral valve.
Treatment
Causes
General
H Genetic defect of the X-chromosome

H Well-defined mutation at a specific location on the
H Early intervention during preschool years

H Special education tailored to the childs needs
FMR1 gene
Incidence
Medications
H Estimated to occur in about 1 in 1,500 males and
1 in 2,500 females
H Occurs in almost all races and ethnic populations

H Antidepressants such as clomipramine
H Sedatives such as diazepam
Surgery
Males
H Physical manifestations
H Hyperactivity, speech difficulties, language delay, and
autistic-like behaviors
Females
H Some degree of cognitive impairment, most commonly learning disabilities (math difficulties, language deficits, and attentional problems)
H Autistic-like features (rare)
H Excessive shyness or social anxiety
H Mitral valve repair
Complications
H Behavioral or learning difficulties

H Cognitive impairment
H Connective tissue abnormalities

Key outcomes
The patient will:
H function at the highest level possible
H be free from signs and symptoms of infection
H demonstrate effective learning related to potential.
family.
H Encourage appropriate activities for the patients
ability.
H Encourage the family to follow a routine schedule.
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Fragile X syndrome
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Monitoring
H Language development
H Seizures
H Hyperactivity
Patient teaching
Be sure to cover:
Discharge planning
H Refer the patient and family for genetic counseling.
H Refer the family to a support group.
H Advocate for special education services and individu-
alized speech, language, and occupational therapy

services during the patients schooling.
Fragile X syndrome
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Frostbite
Overview
Description
H Damage to skin and other tissues caused by freezing
H Caused by sustained exposure to cold temperatures
or to certain chemicals without proper protection

H Signs or symptoms persisting longer than 30 minutes
after start of rewarming

H Classified by degree of injury as first-, second-,
third-, or fourth-degree
H Frost nip: less severe cold exposure with complete
resolution within 30 minutes of starting to rewarm
Pathophysiology
H Loss of body heat causes a fall in tissue temperature.
H Tissue hypoxia and acidosis occurs as blood vessels
narrow in response to cold.

H Tissues begin to freeze; ice crystals form and force
water out of cells, causing cell death.

H Blood no longer flows through the capillaries, and
H First-degree frostbite characterized by white or blue
skin, edema, waxy appearance, spongy texture of the

tissue, and sensory deficits
H Second-degree frostbite characterized by white,
blotchy, or blue skin; edema; and formation of vesicles filled with clear or milky fluid (form within 24
hours of injury)
H Third-degree frostbite characterized by presence of
blood-filled vesicles, which progress to a black eschar
H Fourth-degree frostbite characterized by fullthickness damage affecting muscles, tendons, and
bone, with resultant tissue loss
Complications
H Wound-related sepsis
H Gangrene
H Compartment syndrome
H Loss of affected part; amputation
H Increased sensitivity to cold
H Pain with use of the affected area
H Altered sensation in the affected area, possibly lasting
throughout life
clots form in the arterioles and venules from increased blood viscosity.
H Inflammatory mediators are released, causing further
damage.
H Extent of permanent injury depends on duration of
frozen tissue.
H Tetanus
H Osteoporosis
H Muscle atrophy
H Phantom pain of amputated extremities
H Death, when associated with hypothermia or sepsis
Causes
Assessment
H Exposure to cold temperatures, without proper pro-
tection
H Time for this to occur affected by air temperature,
wind speed, and moisture (in the air as well as wet

clothing and skin)
H Chemical exposure, such as to dry ice or highly compressed gases
Risk factors
H Outdoor winter activities
H Workers in cold environments
H Homelessness
H Alcohol consumption and smoking
H Fatigue
H Inadequate, tight, or wet clothing
H Previous cold injury
H Young children and older adults
H Diseases, including diabetes, atherosclerosis, and
thyroid disease
H Infections
H Medications such as beta-adrenergic blockers
Incidence
H Hands or feet affected in 90% of injuries
H Ears, nose, chin, cheeks, or penis affected in remain-
ing 10% of injuries

H Males affected more often than females
292
Frostbite
History
H Prolonged exposure to cold or exposure without ad-
equate protection
H Numbness in affected part
H Feeling of clumsiness and confusion
H Possible shivering
H Pain, burning, or throbbing on rewarming
Physical findings
H Skin
Color: White, blotchy, or blue; purple in large affected area

Waxy appearance
Stiff to touch
H Spongy feeling to underlying tissue
H Edema
H Vesicles filled with clear or milky fluid or blood
H Joint stiffness and pain
H Sweating
Test results
Laboratory
H Complete blood count may show hemoconcentration.
Imaging
H X-rays determine bone involvement.
H Angiography determines extent of blood vessel damage.
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H Thermography measures blood flow.

H Technetium-99 pertechnetate scintigraphy deter-
mines extent of deep-tissue injury and assesses the

response of damaged tissue to therapy.
Treatment
General
H Replacement of wet or tight clothing with dry, loose
clothing
H Protection of injured area
H Rewarming affected part for 20 to 40 minutes in wa-
ter at 100 to 108 F (37.8 to 42.2 C) to halt ice

crystal formation and dilate blood vessels
H Hydration with warm fluids
H Physical therapy
H Acupuncture and homeopathic and botanical therapies
H Hyperbaric therapy
Medications
H Tetanus toxoid immunization and appropriate antibi-
otics, if needed, with open injuries

ibuprofen and naproxen, for inflammation and pain

H Opioids, such as morphine, meperidine, and
propoxyphene, for severe pain
H Vasodilators, such as nifedipine, to increase perfusion
H Aloe vera cream to debride blisters and prevent further trauma
H Anticlotting agent, tissue plasminogen activator, to reduce the risk of amputation (experimental)
H Assist with rewarming and other treatments, as or-
dered.
H Maintain aseptic technique when changing dressings.
H Provide pain medication, as ordered.
Monitoring
H Wound condition
H Pain level
H Capillary refill time
H Sensation
H Peripheral pulses
H Hydration status
Patient teaching
Be sure to cover:
H possible long-term effects
H need for smoking or alcohol cessation, if indicated
H increased susceptibility to cold
H how to prevent future cold injuries. (See Preventing
frostbite.)
Discharge planning
H Refer the patient to a social service agency, if indi-
cated.
Surgery
H Debridement or fasciotomy, if indicated
H Amputation, as needed (necessity usually unknown
for at least 1 month)
Key outcomes
The patient will:
H express understanding of the injury and how to prevent future occurrences
H experience no further injury from frostbite
H express feelings of increased comfort and reduced
pain
H show progressive wound healing
H maintain optimal perfusion to affected areas
H demonstrate effective coping.
H Provide a bed cradle to keep covers off lower ex-
tremities, if indicated.
Prevention
Preventing frostbite
H Anticipate poor weather, and dress appropriately.
H Be aware that wet and windy conditions worsen the
chill factor and increase the risk of cold injury.
H Limit exposure time.
H Wear layers of loose-fitting clothing. Mittens provide
more warmth than gloves.
H Wear head, face, and ear coverings at all times.
H Wear two pairs of socks. An outer layer of wool socks
worn over synthetic socks that wick moisture away
from the skin provides the best insulation.
H Wear waterproof shoes or boots.
H Avoid smoking cigarettes and drinking alcohol, which
impair circulation.
H Remove metal jewelry, which conducts cold.
Frostbite
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Gas gangrene
H Most common in extremities and abdominal wounds;
less common in uterus
Overview
H Sudden, severe pain at wound site
Description
Complications
H Rare condition caused by local infection with anaero-
H Renal failure
H Hypotension and shock
H Hemolytic anemia
H Tissue death requiring amputation of the affected
bic, spore-forming, gram-positive, rod-shaped bacillus Clostridium perfringens or another clostridial

species
H Occurs in devitalized tissues and results from compromised arterial circulation
body part
Assessment
Pathophysiology
H Incubation is 1 to 4 days but can vary from 3 hours
to 6 weeks or longer.
H C. perfringens invades soft tissues, producing
thrombosis of regional blood vessels, tissue necrosis,

and localized edema. (See Effects of Clostridium
perfringens.)
H Necrosis releases carbon dioxide and hydrogen subcutaneously, producing interstitial gas bubbles.
History
H Recent surgery (within 72 hours)
H Traumatic injury
H Septic abortion
H Delivery
Physical findings
H Normothermia, followed by a moderate increase,
Causes
usually not above 101 F (38.3 C)
H C. perfringens
H Transmission when the organism enters the body
during trauma or surgery
H Toxemia (hypotension, tachycardia, tachypnea)

H Localized swelling and discoloration (often dusky
brown or reddish)
H Bullae and tissue necrosis
H Dark red or black necrotic muscle
H Foul-smelling, watery, or frothy discharge
H Subcutaneous emphysema (hallmark of gas gan-
Risk factors
H Diabetes mellitus
Incidence
grene)
H Rare, although more than 30% of deep wounds in-
fected with clostridia
H In later stages, altered level of consciousness that
may deteriorate to delirium and coma
H Most common in deep wounds, especially when tis-
sue necrosis further reduces oxygen supply
Effects of Clostridium perfringens

As C. perfringens grows in a closed wound, it destroys
cell walls and causes hemolysis, local tissue death, and
increasing edema.
C. perfringens
and necrotic
muscle in
closed wound
Test results
Laboratory
H Anaerobic cultures of wound drainage disclose
C. perfringens.
H Gram stain of wound drainage shows large,
gram-positive, rod-shaped bacteria.
H Blood studies show leukocytosis and, later,
hemolysis.
Imaging
H X-rays reveal gas in tissues.
Treatment
Increased
edema
General
Destruction
of cell walls
Edema
H Hyperbaric oxygen therapy

H Nothing by mouth if surgery is planned
H Bed rest until recovery begins
Medications
Local
tissue
death
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Gas gangrene
Hemolysis
H I.V. antibiotics such as vancomycin

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Surgery
H Immediate wide surgical excision of all affected tis-
sues and necrotic muscle in myositis

H Amputation of the affected part
Key outcomes
The patient will:
H have skin that remains warm, dry, and intact
pain.
H Provide adequate fluid replacement.
H Maintain the airway and ventilation.
H Provide appropriate skin care and meticulous wound
care; place the patient on an air mattress or an

air-fluidized bed.
Monitoring
H Vital signs
H Intake and output
H Pulmonary and cardiac status
H Wound site
H Pain control
Patient teaching
Be sure to cover:
H the need to report severe pain at the wound site immediately
H the need to report foul odor or drainage from the
wound site.
Discharge planning
H After recovery, refer the patient for physical rehabili-
tation, as necessary.
H After extensive surgery, such as amputation, refer the
patient for psychological support, as necessary.
Gas gangrene
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Gastric cancer
H Vague feeling of fullness, heaviness, and moderate
abdominal distention after meals
Overview
H Weight loss, nausea, vomiting

H Weakness and fatigue
H Dysphagia
Description
Physical findings
H Cancer of the GI tract classified according to gross
H Palpable mass
H Palpable lymph nodes, especially the supraclavicular
appearance (polypoid, ulcerating, ulcerating and infiltrating, or diffuse)

H Prognosis depending on stage of disease at time of
diagnosis (5-year survival rate about 15%)
Pathophysiology
and axillary nodes

H Other assessment findings that depend on extent of
disease and location of metastasis
H The most commonly affected areas of the stomach
Test results
are the pylorus and antrum.

H The remaining areas affected in order of descending
frequency are the lesser curvature of the stomach,
the cardia, the body of the stomach, and the greater
curvature of the stomach.
H Rapid metastasis occurs to the regional lymph nodes,
omentum, liver, and lungs.
Laboratory
H Complete blood count may show iron deficiency anemia.
H Liver function studies may be elevated with metastatic
spread of tumor to liver.
H Carcinoembryonic antigen radioimmunoassay may
be elevated.
Imaging
H Barium X-rays of the GI tract with fluoroscopy show
changes that suggest gastric cancer, including a tumor or filling defect in the outline of the stomach,
loss of flexibility and distensibility, and abnormal gastric mucosa with or without ulceration.
H Gastroscopy with fiber-optic endoscope helps rule
out other diffuse gastric mucosal abnormalities by allowing direct visualization.
H Gastroscopic biopsy permits evaluation of gastric
mucosal lesions.
Other
H Gastric acid stimulation test discloses whether the
stomach secretes acid properly.
Causes
H Unknown
Risk factors
H Gastritis with gastric atrophy
H Type A blood (10% increased risk)
H Family history of gastric cancer
H Smoked foods, pickled vegetables, and salted fish
and meat
H High alcohol consumption
H Smoking
H Helicobacter pylori infection
Incidence
H Common worldwide in all races
H Incidence greater in males older than age 40
H Mortality high in Japan, Iceland, Chile, and Austria
H Incidence decreased 50% over the past 25 years;
death rate now one-third that of 30 years ago
H Feeling of fullness
H Back, epigastric, or retrosternal pain
Complications
H Malnutrition
H GI obstruction
H Iron deficiency anemia
H Metastasis
Assessment
History
H Back, epigastric, or retrosternal pain not relieved
with nonprescription medications
296
Gastric cancer
Treatment
General
H Radiation therapy combined with chemotherapy (not
indicated preoperatively because it may damage viscera and impede healing)

H Diet based on the extent of the disorder and clinical
condition
H Parenteral feeding with an inability to consume adequate calories
Medications
H Chemotherapy, such as fluorouracil and doxorubicin
H Antiemetics, such as aprepitant and dolasetron
H Opioid analgesics such as morphine
H Antibiotics such as tetracycline
Surgery
H Excision of lesion with appropriate margins (in more
than one-third of patients)

H Gastroduodenostomy
H Gastrojejunostomy
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H Partial gastric resection

H Total gastrectomy (If metastasis has occurred, omen-
tum and spleen may have to be removed.)
Key outcomes
The patient will:
H maintain weight
H report feeling less tension and pain
spirometer use.
H Provide a high-protein, high-calorie diet with dietary
supplements.
H Provide parenteral nutrition, as appropriate.
H After surgery, provide supportive care.
Monitoring
H Pain control
H Vital signs
H Nasogastric tube function and drainage
H Wound site
H Effects of medication
H Intake and output
Patient teaching
Be sure to cover:
H the dietary plan
H effective pulmonary toileting
H avoidance of crowds and people with known infection
H medication administration, dosage, and possible adverse effects.
Discharge planning
H Refer the patient and his family to support services.
H Refer the patient for home services, as necessary.
H Refer the patient for physical or occupational thera-
py, as necessary.
Gastric cancer
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Gastritis
Overview
Description
H Inflammation of the gastric mucosa
H May be acute or chronic
H Most common stomach disorder (acute)
Pathophysiology
Acute gastritis
H The protective mucosal layer is altered.
H Acid secretion produces mucosal reddening, edema,
and superficial surface erosion.
Chronic gastritis
H Progressive thinning and degeneration of gastric mucosa occur.
Causes
Acute gastritis
H Chronic ingestion of irritating foods and alcohol
H Drugs, such as aspirin and other nonsteroidal
anti-inflammatory drugs (in large doses), cytotoxic
agents, caffeine, corticosteroids, antimetabolites,
phenylbutazone, and indomethacin
H Ingested poisons, especially dichloro-diphenyltrichloroethane (DDT), ammonia, mercury, carbon
tetrachloride, or corrosive substances
H Endotoxins released from infecting bacteria, such as
staphylococci, Escherichia coli, and salmonella
H Complication of acute illness
Chronic gastritis
H Recurring exposure to irritating substances, such as
drugs, alcohol, cigarette smoke, and environmental
agents
H Pernicious anemia, renal disease, or diabetes mellitus
H Helicobacter pylori infection (common cause of
nonerosive gastritis)
Risk factors
H Age older than 60
H Exposure to toxic substances
H Hemodynamic disorder
Incidence
H May occur at any age; increased incidence of H. py-
lori in people older than age 60

H Occurs equally in both sexes
H Acute gastritis in 8 of 1,000 people; chronic gastritis
in 2 of 10,000 people
H Abdominal pain
H Indigestion
Complications
H Hemorrhage
H Obstruction
298
Gastritis
H Perforation
H Peritonitis
H Gastric cancer
Assessment
History
H Exposure to one or more causative agents
H Rapid onset of symptoms (acute gastritis)
H Epigastric discomfort
H Indigestion
H Cramping
H Anorexia
H Nausea, hematemesis, and vomiting
H Coffee-ground emesis or melena (if GI bleeding is
present)
Physical findings
H Possible normal appearance
H Grimacing
H Restlessness
H Pallor
H Tachycardia
H Hypotension
H Abdominal distention, tenderness, and guarding
H Normoactive to hyperactive bowel sounds
Test results
Laboratory
H Occult blood is found in vomitus or stools (or both)
if the patient has gastric bleeding.
H Hemoglobin (Hb) level and hematocrit are decreased.
H Urea breath test shows H. pylori.
H Upper GI endoscopy reveals gastritis when its performed within 24 hours of bleeding.
H Biopsy reveals inflammatory process.
Treatment
General
H Elimination of cause
H For massive bleeding:
Blood transfusion
Iced saline lavage
Angiography with vasopressin
H Nothing by mouth if bleeding occurs
H Elimination of irritating foods
H Activity, as tolerated (encourage mobilization)
Medications
H Histamine antagonists, such as famotidine, ranitidine,
and cimetidine
H Proton pump inhibitors such as pantoprazole
H Prostaglandins such as misoprostol
H Vitamin B12
H Antibiotic therapy, according to infective agent
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Surgery
H When conservative treatment fails
H Vagotomy, pyloroplasty
H Partial or total gastrectomy (rarely)
Key outcomes
The patient will:
H maintain weight
H express concerns about current condition
H verbalize understanding of the disorder and treatment regimen.
H Provide physical and emotional support.
H Administer prescribed drugs and I.V. fluids.
H Assist the patient with diet modification.
H If surgery is necessary, prepare the patient preopera-
tively and provide appropriate postoperative care.

H Consult a dietitian, as necessary.
Monitoring
H Vital signs
H Fluid intake and output
H Electrolyte and Hb levels
H Returning symptoms as food is reintroduced
H Response to medication
H Pain control
H GI status
Patient teaching
Be sure to cover:
H lifestyle and diet modifications
H preoperative teaching if surgery is necessary
H stress-reduction techniques
Discharge planning
indicated.
H Refer the patient to an alcohol treatment program, if
indicated.
Gastritis
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Gastroenteritis
H Viruses, such as adenoviruses, echoviruses, and cox-
sackieviruses
H Ingestion of toxins, such as poisonous plants and
Overview
Description
H Self-limiting inflammation of the stomach and small
intestine
H Intestinal flu, travelers diarrhea, viral enteritis, and
food poisoning
Pathophysiology
toadstools
H Drug reactions from antibiotics
H Food allergens
H Enzyme deficiencies
Risk factors
H Consumption of improperly prepared food or conta-
minated water
H Travel or residence in areas of poor sanitation
H The bowel reacts to the various causes of gastroen-
Incidence
teritis with increased luminal fluid that cant be absorbed.

H This results in abdominal pain, vomiting, severe diarrhea (primarily), and secondary depletion of intracellular fluid.
H Dehydration and electrolyte loss occur.
H Occurs at any age

H Major cause of morbidity and mortality in underde-
Causes
H Can be life-threatening in elderly and debilitated pa-
veloped nations
H Ranks second to common cold as cause of lost work
time in the United States

H Fifth most common cause of death among young
children
H Bacteria, such as Staphylococcus aureus, Salmonel-
la, Shigella, Clostridium botulinum, Clostridium

perfringens, and Escherichia coli
H Amoebas, especially Entamoeba histolytica
H Parasites, such as Ascaris, Enterobius, and
Trichinella spiralis
Prevention
Preventing travelers diarrhea

If the patient travels, especially to developing nations, discuss precautions that he can take to reduce his chances
of getting travelers diarrhea. Explain that travelers diarrhea is caused by inadequate sanitation and occurs after
bacteria-contaminated food or water is ingested. These
organisms attach to the lining of the small intestine,
where they release a toxin that causes diarrhea and
cramps. To minimize this risk, advise him to:
H drink water (or brush his teeth with water) only if its
chlorinated or bottled (Chlorination protects the water
supply from bacterial contaminants such as Escherichia coli.)
H avoid beverages in glasses that may have been washed
in contaminated water
H refuse ice cubes that may have been made from contaminated water
H drink only beverages made with boiled water, such as
coffee and tea, or those in bottles or cans
H sanitize impure water by adding 2% tincture of iodine
(5 drops/L of clear water, 10 drops/L of cloudy water)
or by adding liquid laundry bleach (about 2 drops/L of
clear water; 4 drops/L of cloudy water)
H avoid uncooked vegetables, unpeeled fresh fruits, salads, unpasteurized milk, and other dairy products
H beware of foods offered by street vendors.
If travelers diarrhea occurs despite precautions, bismuth subsalicylate, diphenoxylate with atropine, or loperamide can be used to relieve symptoms.
tients
H Diarrhea
Complications
H Severe dehydration
H Electrolyte imbalance
Assessment
History
H Acute onset of diarrhea
H Abdominal pain and discomfort
H Nausea, vomiting
H Malaise and fatigue
H Exposure to contaminated food
H Recent travel (see Preventing travelers diarrhea)
Physical findings
H Slight abdominal distention
H Poor skin turgor (with dehydration)
H Decreased blood pressure
Test results
Laboratory
H Gram stain, stool culture (by direct rectal swab), or
blood culture shows the causative bacteria.
Treatment
General
H Supportive treatment for nausea, vomiting, and diar-
rhea
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Gastroenteritis
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H Antidiarrheals generally not given; they can prolong
the infection
H Rehydration
H Initially, clear liquids as tolerated
H Electrolyte solutions
H Avoidance of milk products
H Activity, as tolerated (encourage mobilization)
Medications
H Antiemetics such as prochlorperazine
H Antibiotics, according to the infective organism
H I.V. fluids
Key outcomes
The patient will:
H maintain weight without further loss
H maintain normal vital signs.
H Allow uninterrupted rest periods.
H Replace lost fluids and electrolytes through diet or
I.V. fluids.
Monitoring
H Intake and output
H Vital signs
H Electrolytes
H GI status
Patient teaching
Be sure to cover:
H preventive measures
H how to perform warm sitz baths three times per day
to relieve anal irritation.
Gastroenteritis
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Gastroesophageal reflux
disease
Overview
Description
Assessment
History
H Minimal or no symptoms in one-third of patients
H Heartburn that typically occurs 112 to 2 hours after
eating
H Heartburn that worsens with vigorous exercise,
into the esophagus and past the lower esophageal

sphincter (LES), without associated belching or vomiting
H Reflux of gastric acid, causing acute epigastric pain,
usually after a meal
H Popularly called heartburn
H Also called GERD
bending, lying down, wearing tight clothing, coughing, constipation, and obesity
H Reported relief by using antacids or sitting upright
H Regurgitation without associated nausea or belching
H Feeling of fluid accumulation in the throat with a
sour or bitter taste
H Chronic pain radiating to the neck, jaws, and arms
that may mimic angina pectoris
H Nocturnal hypersalivation and wheezing
Pathophysiology
Physical findings
H Reflux occurs when LES pressure is deficient or pres-
H Odynophagia (sharp substernal pain on swallowing),
H Backflow of gastric or duodenal contents, or both,
sure in the stomach exceeds LES pressure. The LES

relaxes, and gastric contents regurgitate into the
esophagus.
H The degree of mucosal injury is based on the amount
and concentration of refluxed gastric acid, proteolytic enzymes, and bile acids.
Causes
H Pyloric surgery (alteration or removal of the py-
lorus), which allows reflux of bile or pancreatic juice

H Hiatal hernia with incompetent sphincter
H Condition or position that increases intra-abdominal
pressure
Risk factors
H Any agent that lowers LES pressure: acidic and fatty
food, alcohol, cigarettes, anticholinergics (atropine,

belladonna, propantheline) or other drugs (morphine, diazepam, calcium channel blockers, meperidine)
H Nasogastric (NG) intubation for longer than 4 days
possibly followed by a dull substernal ache

H Bright red or dark brown blood in vomitus
H Laryngitis and morning hoarseness
H Chronic cough
Test results
Imaging
H Barium swallow with fluoroscopy shows evidence of
recurrent reflux.
H Esophageal acidity test reveals degree of gastroesophageal reflux.
H Gastroesophageal scintillation testing shows reflux.
H Esophageal manometry reveals abnormal LES pressure and sphincter incompetence.
H Acid perfusion (Bernstein) test confirms esophagitis.
H Esophagoscopy and biopsy confirm pathologic
changes in the mucosa.
Treatment
Incidence
General
H Affects about 7 million U.S. residents

H Affects all ethnic groups and socioeconomic classes
H Most common in people ages 45 to 64
H Modification of lifestyle
H Positional therapy
H Removal of cause
H Avoidance of dietary causes
H Avoidance of eating 2 hours before sleep (see Fac-
H Epigastric pain, usually after a meal or when lying
down
Complications
H Reflux esophagitis
H Esophageal stricture
H Esophageal ulcer
H Barretts esophagus (metaplasia and possible in-
creased risk of neoplasm)

H Anemia from esophageal bleeding
H Reflux aspiration leading to chronic pulmonary disease
302
Gastroesophageal reflux disease
tors affecting LES pressure)

H Parenteral nutrition or tube feedings
H No activity restrictions for medical treatment
H Lifting restrictions for surgical treatment
Medications
H Histamine-2 receptor antagonists, such as cimeta-
dine, ranitidine, and famotidine

H Proton pump inhibitors, such as esomeprazole, lan-
soprazole, pantoprazole, and rabeprazole
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Factors affecting LES pressure

Various dietary and lifestyle elements can increase or decrease lower esophageal sphincter (LES) pressure. Take
these into account as you plan the patients treatment program.
What increases LES pressure

H Protein
H Carbohydrates
H Nonfat milk
H Low-dose ethanol
What decreases LES pressure

H Fat
H Whole milk
H Orange juice
H Tomatoes
H Antiflatulent (simethicone)
H Chocolate
H High-dose ethanol
H Cigarette smoking
H Lying on right or left side
H Sitting
Patient teaching
Be sure to cover:
H causes of gastroesophageal reflux
H prescribed antireflux regimen of medication, diet,
and positional therapy
H developing a dietary plan
H the need to identify situations or activities that increase intra-abdominal pressure
H the need to refrain from using substances that reduce
sphincter control
H signs and symptoms to watch for and report.
Discharge planning
H Refer the patient to a dietitian, as appropriate.
Surgery
H Hiatal hernia repair
H Vagotomy or pyloroplasty
H Esophagectomy
Key outcomes
The patient will:
H state and demonstrate understanding of the disorder
and its treatment
H show no signs of aspiration
H have minimal or no complications.
H Offer emotional and psychological support.
H Assist with diet modification.
H Use semi-Fowlers position for the patient with an NG
tube.
Monitoring
After surgery
H Pain control
H Intake and output
H Vital signs
H GI status
Gastroesophageal reflux disease
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Generalized anxiety
disorder
Overview
Description
H Anger
H Difficulty concentrating, eating, and sleeping
Physical findings
H Trembling
H Tachycardia
H Sweating
H Feeling of apprehension sometimes described as an
DSM-IV-TR criteria
exaggerated feeling of impending doom, dread, or

uneasiness
H Reaction to an internal threat
H Uncontrollable, unreasonable worry that persists for
at least 6 months and narrows perceptions or interferes with normal functioning
A diagnosis is confirmed when the patients symptoms

match the following criteria:
H Excessive anxiety and worry about a number of
events or activities occur more days than not for at
least 6 months.
H The person finds it difficult to control the worry.
H The anxiety and worry are associated with at least
three of the following six symptoms:
restlessness or feeling keyed up or on edge
being easily fatigued
difficulty concentrating or mind going blank
irritability
muscle tension
sleep disturbances (difficulty falling or staying
asleep, or restless, unsatisfying sleep).
H The focus of the anxiety and worry isnt confined to
features of an axis disorder.
H The anxiety, worry, or physical symptoms cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.
H The disturbance isnt due to the direct physiologic effects of a substance or a general medical condition
and doesnt occur exclusively during a mood disorder, a psychotic disorder, or a pervasive, developmental disorder.
Pathophysiology
H Aberration in benzodiazepine receptor regulation oc-
curs.
Causes
H Unknown
H Roles played by biologic and physiologic factors
Risk factors
H Stressful life situations
H Learned maladaptive behaviors
Incidence
H Can begin at any age but typically begins between
ages 20 and 40
H Twice as common in females as in males
Mild anxiety
H Psychological symptoms
H Unusually self-aware and alert to surroundings
Moderate anxiety
H Selective inattention, but can concentrate on a single
task
Severe anxiety
H Inability to concentrate on more than scattered details of a task
H Panic state with acute anxiety causing complete loss
of concentration, typically with unintelligible speech
Complications
Test results
Laboratory
H Tests, such as cardiac enzymes, troponin level, and
thyroid studies, rule out organic causes of symptoms.
H Electrocardiography excludes myocardial ischemia.
Other
H Psychiatric evaluation helps confirm the diagnosis.
Treatment
H Impaired social or occupational functioning

H Substance abuse
General
Assessment
Medications
History
H Benzodiazepines, such as diazepam and lorazepam

H Tricyclic antidepressants such as doxepin
H Serotonin receptor reuptake inhibitors, such as ser-
H Muscle aches and spasms

H Headaches
H Inability to relax
H Apprehension
H Fear
304
Generalized anxiety disorder
H Psychotherapy
H Relaxation techniques
traline, paroxetine, and escitalopram
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Key outcomes
The patient will:
H develop effective coping strategies
H identify anxiety triggers
H experience reduced anxiety.
H Reduce environmental stimuli.
H Help identify triggers to anxiety.
Monitoring
Patient teaching
Be sure to cover:
H prescribed drugs
H effective coping strategies.
Discharge planning
Generalized anxiety disorder
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Genital herpes
Overview
H Fever
H Malaise
H Dysuria
H Fluid-filled vesicles that develop into shallow, painful
ulcers with yellow, oozing centers
Description
H Acute inflammatory disease of the genitalia
H Usually self-limiting but able to cause painful local or
systemic disease (see Understanding the genital

herpes cycle)
Pathophysiology
H Virus invades and replicates in neurons and epider-
mal and dermal cells.

H Virions travel to sensory dorsal root ganglion.
H Replication in the sensory ganglia leads to recurrent
Complications
H Herpetic keratitis, which may lead to blindness
H Herpetic encephalitis
Assessment
History
Causes
H Intimate contact with an infected person

H Fever
H Malaise
H Dysuria
H Leukorrhea (females)
H Herpes simplex virus (HSV), type 1 or type 2

H Typically transmitted through sexual intercourse,
Physical findings
clinical outbreaks.
orogenital sexual activity, kissing, hand-to-body contact, and vaginal delivery
Risk factors
H Unprotected sexual activity
Incidence
H One in five adults in the United States serologically
H Shallow, reddened, painful ulcers with yellow, oozing
centers usually on the cervix (the primary infection

site) and possibly on the labia, perianal skin, vulva,
or vagina and on the glans penis, foreskin, or penis
H Extragenital lesions, possibly on the mouth or anus
H Marked edema
H Tender inguinal lymph nodes
HSV-positive
Test results
Understanding the genital herpes cycle
Laboratory
H Vesicular fluid reveals HSV.
H Antigen testing identifies specific antigens.
After a patient is infected with genital herpes, a latency period follows. The virus takes up permanent residence in
the nerve cells surrounding the lesions, and intermittent
viral shedding may take place.
Repeated outbreaks may develop at any time, again followed by a latent stage during which the lesions heal
completely. Outbreaks may recur as often as three to eight
times yearly.
Although the cycle continues indefinitely, some people
remain symptom-free for years.
INITIAL INFECTION
Highly infectious period marked by fever, aches, adenopathy, pain,
and ulcerated skin and mucous membranes
LATENCY
Intermittently infectious period marked by viral dormancy or viral
shedding and no disease symptoms
RECURRENT INFECTION
Highly infectious period similar to initial infection with milder
symptoms that resolve faster
306
Genital herpes
Treatment
General
H Adequate rest periods
Medications
H Antivirals, such as acyclovir, famciclovir, and valacy-
clovir
Key outcomes
The patient will:
H express an understanding of the disorder and its
treatment
H practice safe sex
H demonstrate improved skin integrity.
H Encourage expression of feelings and concerns.
H Keep lesions dry.
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Monitoring
H Skin integrity
H Wound healing
Patient teaching
Be sure to cover:
H avoiding sexual intercourse during the active stage of
this disease (while lesions are present)
H using condoms during all sexual encounters
H urging sexual partners to seek medical examination
H having a Papanicolaou test every 6 months (females).
Discharge planning
H Refer the patient to the Herpes Resource Center for
support.
Genital herpes
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Genital warts
H Genital tract dysplasia

H Cervical and vulvar cancer in females, penile cancer
in males, and some rectal carcinomas in both sexes
Overview
Description
Assessment
H Papillomas that consist of fibrous tissue overgrowth
History
from the dermis and thickened epithelial coverings

H Also known as venereal warts and condylomata
acuminata
H Unprotected sexual contact with a partner with a
Pathophysiology
H Warts on moist genital surfaces (subpreputial sac,
H Infection is transmitted by sexual contact and incu-
known infection, a new partner, or many partners
Physical findings
bates for 1 to 6 months (2 months, average) before

warts erupt.
H Infection of the basal cells occurs, with proliferation
of all epidermal layers, producing acanthosis, parakeratosis, and hyperkeratosis.
urethral meatus, penile shaft, scrotum, vulva, vaginal

and cervical walls) and around the anus and inside
the rectum
H Tiny red or pink swellings that may grow as large as
10 cm and that may be pedunculated
H Infected lesions that become malodorous
Causes
Test results
H Infection with one of more than 60 strains of human
Laboratory
H Dark-field microscopy of wart-cell scrapings shows
marked epidermal cell vascularization.
H Application of 5% acetic acid (white vinegar) turns
warts white if theyre papillomas.
papillomavirus (HPV)
Risk factors
Incidence
H One of the most common sexually transmitted dis-
eases (STDs) in the United States
H Appearance of small, pink to red, moist warts with ir-
regular surfaces (see Recognizing genital warts)
Treatment
General
H Good hygiene practices
H Contact precautions
H Usually located around the external genitalia and
Medications
possibly inside the urethra or vagina or on the cervix

H No symptoms in most patients
H Topical interferon alfa 2-b

H Vaccine preparations such as HPV recombinant vac-
Complications
H Immune response modifier such as imiquimod
H During pregnancy, genital warts in the vaginal and
cervical walls that grow large enough to impede vaginal delivery
Recognizing genital warts

Genital warts are marked by clusters of flesh-colored papillary growths that may be barely visible or several inches
in diameter.
cine
Surgery
H Cryosurgery
H Electrodesiccation
H Surgical excision
H Laser ablation
H Circumcision to prevent recurrence
Key outcomes
The patient will:
H remain free from all signs and symptoms of infection
H acknowledge the change in body image
H voice feelings about potential or actual changes in
sexuality
pain.
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H Provide a nonthreatening, nonjudgmental atmos-
phere that encourages verbalization, and provide

support.
H Institute contact precautions to avoid transmission.
Monitoring
H Signs and symptoms of infection (postoperative)
H Concomitant STDs or infections
H Papanicolaou (Pap) test results
Patient teaching
Be sure to cover:
H the need for sexual abstinence or condom use during
intercourse until healing is complete
H evaluation of the patients sexual partners
H the importance of testing for human immunodeficiency virus infection and other STDs
H the emphasis that genital warts can recur and that the
virus can mutate, causing infection with warts of a
different strain
H recommendation that female patients have a Pap test
every 6 months.
Genital warts
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H Roughly 5% incidence of preeclampsia progressing
to eclampsia
Gestational
hypertension
Overview
Complications
Description
H Abruptio placentae
H HELLP syndrome: hemolysis, elevated liver enzyme
H Hypertension
H Sudden weight gain
H Irritability
H Emotional tension
H High blood pressure, most commonly occurring after
levels, low platelet count
the 20th week of gestation in a nulliparous woman

H Carries a high risk for fetal mortality because of the
increased incidence of premature delivery
H Among the most common causes of maternal death
in developed countries (especially when complications occur)
H Nonconvulsive form (also called preeclampsia) occurring after the 20th week of gestation; may be mild
or severe
H Convulsive form (also called eclampsia) occurring
between the 24th week of gestation and the end of
the first postpartum week
H Coagulopathy
H Stillbirth
H Seizures
H Coma
H Premature labor
H Renal failure
H Maternal hepatic damage
Pathophysiology
H Generalized arteriolar vasoconstriction is thought to
cause decreased blood flow through the placenta and

maternal organs.
H This leads to intrauterine growth retardation or restriction, placental infarcts, and abruptio placentae.
Causes
H Unknown
H Contributing factors:
Geographic, ethnic, racial, nutritional, immunologic, and familial factors

Preexisting vascular disease
Maternal age
Autolysis of placental infarcts
Autointoxication
Uremia
Maternal sensitization to total proteins
Pyelonephritis
Diabetes
Special populations
Adolescents and primiparas older than age 35 are
at higher risk for preeclampsia.
Risk factors
H First-time pregnancy
H Multiple fetuses
H History of vascular disease
Incidence
H Occurs in about 7% of pregnancies; more common
in females from lower socioeconomic groups
310
Gestational hypertension
Assessment
History
H Sudden weight gain
H Irritability
H Emotional tension
H Severe frontal headache
H Blurred vision
H Epigastric pain or heartburn
Physical findings
H Preeclampsia: blood pressure of 160/110 mm Hg or
higher
H Eclampsia: systolic blood pressure of 180 or
200 mm Hg or higher
H Generalized edema, especially of the face
H Pitting edema of the legs and feet
H Hyperreflexia
H Oliguria
H Vascular spasm, papilledema, retinal edema or de-
tachment, and arteriovenous nicking or hemorrhage

(seen on ophthalmoscopy)
H Seizures
Test results
Laboratory
H In preeclampsia: proteinuria is more than
300 mg/24 hours [1+].
H In severe eclampsia: proteinuria is 5 g/24 hours
[5+] or more.
H In HELLP syndrome: hemolysis, elevated liver enzymes and decreased platelet count are evident.
Imaging
H Ultrasonography aids evaluation of fetal well-being.
H Stress and nonstress tests and biophysical profiles
help evaluate fetal well-being.
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Treatment
General
H Measures to halt progression of the disorder and en-
sure fetal survival

H Prompt labor induction, especially if the patient is
near term (advocated by some clinicians)

H Adequate nutrition
H Low-sodium diet, if indicated
H Limited caffeine
H Complete bed rest
H Left lateral lying position
Medications
H Antihypertensives
H Magnesium sulfate
H Oxytocin
H Oxygen
Surgery
Emergency interventions for gestational

hypertension
When caring for a patient with gestational hypertension,
be prepared to perform the following interventions:
H Observe for signs of fetal distress by closely monitoring results of stress and nonstress tests.
H Keep emergency resuscitative equipment and anticonvulsants at hand in case of seizures and cardiac or respiratory arrest.
H Carefully monitor magnesium sulfate administration.
Signs of drug toxicity include absence of patellar reflexes, flushing, muscle flaccidity, decreased urinary
output, significant blood pressure drop (> 15 mm Hg),
and a respiratory rate below 12 per minute. Keep calcium gluconate at the bedside to counteract the toxic
effects of magnesium sulfate.
H Prepare for emergency cesarean delivery, if indicated.
Alert the anesthesiologist and pediatrician.
H To protect the patient from injury, maintain seizure precautions. Dont leave an unstable patient unattended.
Maintain a patent airway, and have supplemental oxygen readily available.
H Possible cesarean delivery
Patient teaching
Key outcomes
Be sure to cover:
H signs and symptoms of preeclampsia and eclampsia
H importance of bed rest in the left lateral position, as
ordered
H adequate nutrition and a low-sodium diet
H good prenatal care
H control of preexisting hypertension
H early recognition and prompt treatment of
preeclampsia
H likelihood that the neonate will be small for gestational age, with the probability that hell do better
than other premature neonates of the same weight.
The patient will:

H maintain normal vital signs
H remain oriented to the environment.
H Elevate edematous arms or legs.
H Eliminate constricting hose, slippers, and bed linens.
H Assist with or insert an indwelling urinary catheter, if
necessary.
H Provide a quiet, darkened room.
H Enforce absolute bed rest.
H Encourage the patient to express feelings.
Discharge planning
H Refer the patient for professional counseling, as indi-
cated.
(See Emergency interventions for gestational

hypertension.)
Monitoring
H Vital signs
H Fetal heart rate
H Vision
H Edema
H Daily weight
H Intake and output
H Deep tendon reflexes
H Headache unrelieved by medication
H Complications
Gestational hypertension
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Giardiasis
Overview
Description
H Infection of the small bowel by Giardia lamblia, a
symmetrical flagellate protozoan

H Reinfection possible because infection doesnt confer
H Drinking of suspect water

H Institutionalization
Physical findings
H Possibly, no intestinal symptoms in mild infection
H Abdominal cramps, bloating
H Belching, flatus
H Nausea, vomiting
H Explosive pale, loose, greasy, malodorous, frequent
stools (occurring 2 to 10 times daily)
immunity
H Also called G. enteritis and lambliasis
H Fatigue, weight loss

H Hyperactive bowel sounds in the right upper and left
Pathophysiology
H General upper and right lower quadrant discomfort
H Cysts enter the small bowel and release trophozoites,
which attach to the bowels epithelial surface.

H Attachment causes superficial mucosal invasion and
destruction, inflammation, and irritation.
H Trophozoites become encysted again, travel down the
colon, and are excreted. (Unformed stool may contain trophozoites as well as cysts.)
Causes
lower quadrants just before bowel movements

and guarding
Test results
Laboratory
H Examination of a fresh stool specimen shows cysts or
examination of duodenal aspirate or biopsy shows
trophozoites.
H Ingestion of G. lamblia cysts in stool-contaminated
Treatment
water
H Fecal-oral transfer of cysts from an infected person
General
Incidence
H Occurs worldwide but most common in developing
countries and other areas where sanitation and hygiene are poor (G. lamblia has been found in municipal water sources, nursing homes, and day-care
centers.)
H Children generally more likely to develop giardiasis
than adults
H In the United States, most common in travelers recently returned from endemic areas, campers who
drink water from contaminated streams, male homosexuals, patients with congenital immunoglobulin A
deficiency, and children in day-care centers
H Diarrhea
H Abdominal pain
H Bloating
H Belching
H Flatus
Complications
H Malabsorption
H Dehydration
H Lactose intolerance
H Possible death, in hypogammaglobulinemia
H Examination for possible testing and treatment for
people living with an infected person or those having

had sexual contact with an infected person
H Parenteral fluid replacement to prevent dehydration
Medications
H Antiprotozoals, such as nitazoxanide and tinidazole
Key outcomes
The patient will:
H avoid skin breakdown or infection
H have an elimination pattern that returns to normal
pain.
H Institute enteric contact precautions, and quickly dis-
pose of all fecal material.

H Place a child or an incontinent adult in a private
room.
H Keep the perianal area clean, especially after each
bowel movement.
Assessment
H Administer I.V. fluid therapy, as needed.

H Provide nutritionally adequate foods.
H Report to public health authorities.
History
Monitoring
H Recent travel to an area with poor sanitation

H Sexual practices that involve oral-anal contact
H Frequency and characteristics of bowel movements

H Nutritional intake (to prevent malnutrition)
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H Adverse drug effects

H Skin integrity
H Intake and output
Patient teaching
Be sure to cover:
H prescribed medications, including precautions and
adverse effects
H need for the patient whos taking metronidazole or
furazolidone to avoid alcohol while taking the drug
and for 3 days after completing treatment
H need for the family and others in contact with the patient to have their stools tested for G. lamblia cysts
H need for good personal hygiene, especially proper
hand washing as well as correct handling of infectious material by the patient and his family
H importance of safer sex practices
H need for campers to purify all stream and lake water
before drinking it
H need for travelers to endemic areas to avoid drinking
tap or suspect water and to avoid eating uncooked
and unpeeled fruits or vegetables.
Discharge planning
H Encourage the patient to return for follow-up ap-
pointments because relapses can occur.
Giardiasis
313
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Glaucoma
Overview
Description
H Eye disorder characterized by high intraocular pres-
sure (IOP) and optic nerve damage

H Two forms:
Open-angle (also known as chronic, simple, or

wide-angle) glaucoma, which begins insidiously
and progresses slowly
Angle-closure (also known as acute or narrowangle) glaucoma, which occurs suddenly and can
cause permanent vision loss in 48 to 72 hours
Pathophysiology
Risk factors
Open-angle glaucoma
H Family history
H Myopia
H Ethnic origin
Angle-closure glaucoma
H Family history
H Cataracts
H Hyperopia
Incidence
H A leading cause of blindness; accounts for about 12%
of newly diagnosed blindness in the United States

H Affects about 2% of Americans older than age 40
H Highest incidence among males and Black and Asian
populations
H Open-angle glaucoma commonly familial
Open-angle glaucoma
H Degenerative changes in the trabecular meshwork
block the flow of aqueous humor from the eye, increasing IOP and resulting in optic nerve damage.
H Obstruction to the outflow of aqueous humor is
caused by an anatomically narrow angle between the
iris and the cornea.
H IOP increases suddenly.
Causes
Assessment
Open-angle glaucoma
H Degenerative changes
H Anatomically narrow angle between the iris and the
cornea
H Attacks triggered by trauma, pupillary dilation, stress,
or ocular changes that push the iris forward
Optic disk changes

Ophthalmoscopy and slit-lamp examination show cupping
of the optic disk, which is characteristic of glaucoma.

H Nausea and vomiting (from increased IOP)
H Eye pain
Complications
H Varying degrees of vision loss
H Total blindness
History
Open-angle glaucoma
H Possibly no symptoms
H Dull, morning headache
H Mild aching in the eyes
H Loss of peripheral vision
H Halos around lights
H Reduced visual acuity (especially at night) not corrected by glasses
H Pain and pressure over the eye
H Blurred vision
H Halos around lights
Physical findings
H Unilateral eye inflammation
H Cloudy cornea
H Moderately dilated pupil, nonreactive to light
H With gentle fingertip pressure to the closed eyelids,
one eye feels harder than the other (in angle-closure

glaucoma)
Test results
H Tonometry measurement shows increased IOP.
H Slit-lamp examination shows effects of glaucoma on
the anterior eye structures. (See Optic disk
changes.)
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Glaucoma
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H Gonioscopy shows angle of the eyes anterior cham-
Monitoring
ber.
H Ophthalmoscopy aids visualization of the fundus.
H Perimetry or visual field tests show extent of peripheral vision loss.
H Fundus photography shows optic disk changes.
H Vital signs
H Visual acuity
Treatment
ALERT
Angle-closure glaucoma typically has a rapid onset
and is an emergency.
General
H Reduction of IOP by decreasing aqueous humor pro-
duction with medications

H Bed rest (with acute angle-closure glaucoma)
Patient teaching
Be sure to cover:
H need for meticulous compliance with prescribed
drug therapy
H all procedures and treatments, especially surgery
H the fact that lost vision cant be restored but treatment can usually prevent further loss
H modification of the patients environment for safety
H signs and symptoms that require immediate medical
attention, such as sudden vision change or eye pain
H the importance of glaucoma screening for early detection and prevention.
Medications
H Beta-adrenergic blockers, such as levobunolol and
timolol
H Prostaglandin analogues such as bimatoprost
H Selective alpha2 agonists such as brimonidine
ALERT
Occasionally, systemic absorption of a betaadrenergic blocker from eyedrops can be sufficient
to cause bradycardia, hypotension, heart block,
bronchospasm, impotence, or depression.
Surgery
H For patients unresponsive to drug therapy:
Argon laser trabeculoplasty

Trabeculectomy
H Laser iridectomy
H Surgical peripheral iridectomy
H In end-stage glaucoma, tube shunt or valve
Key outcomes
The patient will:
H express feelings and concerns
H maintain present vision.
H After surgery, protect the affected eye.
H Encourage ambulation immediately after surgery.
H Encourage the patient to express his concerns relat-
ed to the chronic condition.
Glaucoma
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Glomerulonephritis
Overview
Special populations
Goodpastures syndrome, a type of RPGN, is rare,
but occurs most commonly in males ages 20 to 30.
Description
H Bilateral inflammation of the glomeruli, typically fol-
H Decreased urination or oliguria

H Dyspnea and orthopnea
H Periorbital edema
H Mild to severe hypertension
lowing a streptococcal infection

H Also called poststreptococcal acute glomerulonephritis or PSAGN
Pathophysiology
H Epithelial or podocyte layer of the glomerular mem-
brane is disturbed, resulting in a loss of negative

charge.
H Acute poststreptococcal glomerulonephritis results
from the entrapment and collection of antigenantibody complexes in the glomerular capillary
membranes, after infection with group A betahemolytic streptococcus.
H Antigens stimulate the formation of antibodies.
H Circulating antigen-antibody complexes become
lodged in the glomerular capillaries.
H Complexes initiate complement activation and the release of immunologic substances that lyse cells and
increase membrane permeability.
H Antibody damage to basement membranes causes
crescent formation.
H Antibody or antigen-antibody complexes in the
glomerular capillary wall activate biochemical mediators of inflammation complement, leukocytes,
and fibrin.
H Activated complement attracts neutrophils and
monocytes, which release lysosomal enzymes that
damage the glomerular cell walls and cause a proliferation of the extracellular matrix, affecting glomerular blood flow.
H Membrane permeability increases and causes a loss
of negative charge across the glomerular membrane
as well as enhanced protein filtration.
H Membrane damage leads to platelet aggregation, and
platelet degranulation releases substances that increase glomerular permeability.
Causes
H Impetigo
H Immunoglobulin A nephropathy (Bergers disease)
H Lipoid nephrosis
Incidence
H Acute glomerulonephritis most common in boys ages
3 to 7 but can occur at any age

H Rapidly progressive glomerulonephritis (RPGN) most
common between ages 50 and 60
316
Glomerulonephritis
ALERT
The presenting features of glomerulonephritis in
children may be encephalopathy with seizures and
local neurologic deficits. An elderly patient with
glomerulonephritis may report vague, nonspecific
symptoms, such as nausea, malaise, and arthralgia.
Complications
H Pulmonary edema
H Heart failure
H Sepsis
H Renal failure
H Severe hypertension
H Cardiac hypertrophy
Assessment
History
H Recent streptococcal infection of the respiratory tract
H Household member with PSAGN
Physical findings
H Dyspnea
H Periorbital edema
H Increased blood pressure
H Pallor
Test results
Laboratory
H Throat culture shows group A beta-hemolytic streptococcus.
H Electrolyte, blood urea nitrogen, and creatinine levels are elevated.
H Serum protein level is decreased.
H Hemoglobin level is decreased in chronic glomerulonephritis.
H Antistreptolysin-O titers are elevated.
H Streptozyme and anti-DNase B levels are elevated.
H Serum complement levels are low.
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H Urinalysis shows red blood cells, white blood cells,
mixed cell casts, protein, fibrin-degradation products, and C3 protein.

Imaging
H Kidney-ureter-bladder X-ray shows bilateral kidney
enlargement (acute glomerulonephritis).
H Chest X-ray reveals congestion caused by fluid retention.
H Renal biopsy confirms diagnosis.
Treatment
Patient teaching
Be sure to cover:
H taking prescribed drugs
H how to assess ankle edema
H reporting signs of infection
H recording daily weight
H following a low-sodium diet.
Discharge planning
H Refer the patient to social services, as appropriate.
H Refer the patient to renal disease support group.
General
H Treatment of the primary disease
H Bed rest
H Fluid restriction
H Sodium-restricted diet
H Correction of electrolyte imbalance
H Dialysis
H Plasmapheresis
Medications
H Antibiotics, according to the infective agent
H Anticoagulants such as heparin
H Diuretics such as furosemide
H Vasodilators such as hydralazine
H Corticosteroids, such as methylprednisolone and
prednisone
Surgery
H Kidney transplantation
Key outcomes
The patient will:
H identify risk factors that exacerbate the condition,
and modify lifestyle accordingly
H have laboratory values return to normal.
H Provide appropriate skin care and oral hygiene.
H Encourage the patient to express his feelings about
the disorder.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Renal function
Glomerulonephritis
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Goiter
Overview
Description
or the use of goitrogenic drugs (such as propylthiouracil, methimazole, iodides, and lithium)
Incidence
H Decreases with age
H Thyroid gland enlargement not caused by inflamma-
tion or a neoplasm
H Commonly classified as toxic (associated with hyperthyroidism) or nontoxic (not associated with hyperthyroidism or hypothyroidism)
H Mildly enlarged gland to a massive, multinodular
Pathophysiology
H Thyroid gland cant produce enough thyroid hor-
mone to meet metabolic requirements.
goiter
Complications
H Tracheal compression
H Hyperthyroidism
H Lymphoma
H Abscess
H Thyroid gland enlarges to compensate for inadequate
hormone synthesis.
Causes
H Thyroid growth-stimulating immunoglobulins
H Inherited defects
H Inadequate dietary intake of iodine
H Ingestion of large amounts of goitrogenic foods
(such as rutabagas, cabbage, soybeans, peanuts,

peaches, peas, strawberries, spinach, and radishes)
Assessment
History
H Dysphagia
Physical findings
H Swelling and distention of the neck, which may be
mildly to massively enlarged (see Understanding

simple goiter)
Understanding simple goiter

A simple (nontoxic) goiter is any enlargement of the thyroid gland not caused by inflammation or neoplasm. The
thyroid mass increases to compensate for inadequate hormone synthesis. Its most common in females, occurring
when thyroid hormone secretion fails to meet metabolic
needs.
Sporadic goiter follows ingestion of goitrogenic drugs
(such as propylthiouracil) and iodides or foods (such as
rutabagas and cabbage). Endemic goiter results from
geographically related nutritional factors such as iodinedepleted soil. Inherited defects may contribute to either
type of goiter.
The patient may report respiratory distress and dysphagia from compression of the trachea and esophagus and
dizziness or syncope when raising her arms over her
head. A firm, irregular enlargement and stridor caused by
tracheal compression may be found.
Diagnostic tests reveal normal serum thyroid hormone
levels; abnormalities rule out this diagnosis. Thyroid antibody titers are usually normal. Iodine 131 uptake is usually normal but may increase with iodine deficiency or a
biosynthetic defect. Urinalysis may show low urinary excretion of iodine.
Treatment to reduce thyroid hyperplasia involves thyroid
hormone replacement. Iodide administration commonly
relieves goiters caused by iodine deficiency. Sporadic goiter requires avoidance of goitrogenic drugs and food. Radioiodine ablation therapy aids some patients. Rarely, partial thyroidectomy is needed to relieve pressure on the
surrounding structures.
318
Goiter
Test results
Laboratory
H Thyroid-stimulating hormone level is high or normal.
H Serum thyroxine concentrations are low-normal or
normal.
H Iodine-131 uptake is normal or increased (50% of
the dose at 24 hours).
Other
H Patient history and physical examination help to confirm the diagnosis.
Treatment
General
H Avoidance of known goitrogenic drugs and foods
Medications
H Thyroid hormone such as levothyroxine
H Small doses of iodine
Surgery
H Subtotal thyroidectomy
Key outcomes
The patient will:
H have a reduced goiter
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H not demonstrate respiratory or swallowing difficulty.
H Encourage the patient to express feelings and con-
cerns.
Monitoring
H Vital signs
H Neck circumference
Patient teaching
Be sure to cover:
H symptoms of thyroid toxicosis
H use of iodized salt.
Goiter
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Gonadotropin deficiency
Overview
Description
H Lack of hormones (follicle-stimulating hormone
[FSH] and luteinizing hormone [LH]) that stimulate

the sex glands, primarily the testes and ovaries
H If chronic and untreated, can cause infertility and osteopenia
Pathophysiology
H Gonadotropin-releasing hormone (Gn-RH) is secret-
ed by the hypothalamus and causes the anterior pituitary to secrete the gonadotropins testosterone,
estrogen, FSH, and LH.
H Estrogen, progesterone, and testosterone, produced
by the gonads, function in a negative-feedback loop
that regulates Gn-RH secretion.
H Mechanisms that cause Gn-RH deficiency include:
pituitary tumor producing another hormone that
impinges on the gonadotropin-producing cells and
physically impairs Gn-RH biosynthesis
medical treatments such as radiation (impairs
Gn-RHproducing cells)
oversecretion of estrogen, progesterone, or testosterone by dysfunctional target glands, causing
Gn-RH inhibition through the negative-feedback
loop
prolactin (inhibits pituitary secretion of Gn-RH;
prolactin-secreting tumors can cause Gn-RH deficiency)
reduced Gn-RH secretion due to response of hypothalamus to physical stress, obesity, or starvation.
Causes
H Pituitary tumor or hemorrhage
H Oversecretion of target gland hormone, such as es-
trogen, progesterone, or testosterone

H Prolactin-secreting tumor
H Hypothalamic suppression of Gn-RH during periods
of physical or emotional stress, obesity, and starvation
H Genetics
Incidence
H Decreased libido, strength, and body hair, and fine
wrinkles around the eyes and lips (adults)

H Amenorrhea; vaginal, uterine, and breast atrophy;
clitoral enlargement; voice deepening; and beard
growth (females)
H Testicular atrophy, reduction in beard growth, and
erectile dysfunction (males)
H Mood and behavior changes
H Anosmia
320
H Depending on age of onset: inadequate sexual differ-
entiation, microphallus and partial or complete lack

of testicular descent, poor secondary sex characteristics and muscle development
Complications
H Infertility
Assessment
History
H Illness that affects testes
H Underdeveloped secondary sex characteristics
H Mood and behavior changes
H Infertility
Physical findings
H Underdeveloped secondary characteristics
H Decreased body hair
H Fine wrinkles around eyes and lips
Test results
Laboratory
H Testosterone level is low, and Gn-RH level is high in
primary testicular failure.
H Estrogen level is low, and Gn-RH level is high in primary ovarian failure.
H Gn-RH and testosterone or estrogen levels are low in
hypothalamic or pituitary dysfunction.
H Human chorionic gonadotropin stimulation test results are abnormal.
H Gn-RH stimulation test reveals insufficient elevation
of LH or FSH levels.
Treatment
General
H Stress reduction
H Weight gain or loss
Medications
H Gonadotropin, estrogen, or testosterone replacement
Surgery
H Removal of tumors
Key outcomes
The patient will:
H relate an understanding of the disorder and its treatment
H express positive feelings regarding body image
H seek appropriate support measures.
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Monitoring
Patient teaching
Be sure to cover:
H taking prescribed drugs.
Discharge planning
H Stress to the patient the importance of obtaining on-
going follow-up care.
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Gonorrhea
H Pneumonia
H Acute respiratory distress syndrome
Overview
Assessment
Description
History
H Common sexually transmitted disease (STD) that
H Unprotected sexual contact (vaginal, oral, or anal)
usually starts as infection of the genitourinary tract;

can also begin in rectum, pharynx, or eyes
H Left untreated, spreads through the blood to the
joints, tendons, meninges, and endocardium
H In females, can lead to chronic pelvic inflammatory
disease (PID) and sterility
with an infected person, an unknown partner, or

multiple sex partners
H History of STD
Pathophysiology
H Gonococci infect mucus-secreting epithelial surfaces
and penetrate through or between the cells to the

connective tissue.
H Inflammation and spread of the infection results.
Causes
H Transmission of Neisseria gonorrhoea, the causative
organism, through sexual contact with an infected

person
H For a child born to an infected mother, acquisition of
gonococcal ophthalmia neonatorum during passage
through the birth canal
H Acquisition of gonococcal conjunctivitis by touching
the eyes with a contaminated hand
Risk factors
Incidence
H Among sexually active individuals, incidence highest
in those with multiple partners, teenagers, nonwhites, the poor, the poorly educated, city dwellers,
and unmarried people who live alone
H Reinfection common
H Possible dysuria in males
H Possible absence of symptoms (in both sexes) or
symptoms related to the area infected
Physical findings
H Fever
H Purulent discharge from urethral meatus
H Female urethral meatus possibly red and edematous
H Friable cervix and a greenish yellow discharge
H Engorged, red, swollen vagina with profuse purulent
discharge
H Rectal infection
H Ocular infection
H Pharyngeal infection
H Papillary skin lesions on hands and feet
H PID
H Perihepatitis
H Pain and a cracking noise when moving an involved
joint
Test results
Laboratory
H Culture from the infection site of the urethra, cervix,
rectum, or pharynx reveals N. gonorrhea.
H Culture of conjunctival scrapings confirms gonococcal conjunctivitis.
H In males, a Gram stain showing gram-negative diplococci may confirm gonorrhea.
H Identification of gram-negative diplococci on smear
from joint fluid and skin lesions indicates gonococcal arthritis.
H Complement fixation and immunofluorescent assays
of serum reveal antibody titers four times the normal
rate.
H Venereal Disease Research Laboratory test may be reactive.
H Rapid plasma reagin test may be reactive.
H Vagina most common site in female children older
than age 1
Complications
H PID
H Acute epididymitis
H Proctitis
H Salpingitis
H Septic arthritis
H Dermatitis
H Perihepatitis
H Corneal ulceration
H Blindness
H Meningitis
H Osteomyelitis
Treatment
General
H Follow-up cultures 4 to 7 days after treatment and
again in 6 months
H For a pregnant patient, final follow-up before delivery
H Effective therapy (ends communicability within
hours)
H Abstinence from sexual activity until infection is
treated
Medications
H Antibiotics, such as ceftriaxone, doxycycline, and
azithromycin
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Prevention
Monitoring
Preventing gonorrhea
H Complications
H Follow-up culture results
To prevent gonorrhea, provide the following patient teaching:

H Tell the patient to avoid sexual contact until cultures
prove negative and infection is eradicated.
H Advise the patients partner to receive treatment even if
the partner doesnt have a positive culture. Recommend that the partner avoid sexual contact with anyone
until treatment is complete because reinfection is extremely common.
H Counsel the patient and all sexual partners to be tested
for the human immunodeficiency virus and hepatitis B
infection.
H Instruct the patient to be careful when coming into
contact with any bodily discharges to avoid contaminating the eyes.
H Tell the patient to take anti-infectives for the entire time
prescribed.
H To prevent reinfection, tell the patient to avoid sexual
contact with anyone suspected of being infected, to
use condoms during intercourse, to wash genitalia
with soap and water before and after intercourse, and
to avoid sharing washcloths or douche equipment.
H Advise the patient to return for follow-up testing.
Patient teaching
Be sure to cover:
H informing all sexual partners of the infection so that
they can seek treatment
H avoiding sexual contact until cultures are negative
and infection is eradicated
H being careful when coming into contact with any
bodily discharges to avoid contaminating the eyes
H safer sex practices
H taking anti-infectives for the time prescribed
H the importance of returning for follow-up testing
(see Preventing gonorrhea).
H 1% silver nitrate drops or erythromycin ointment in
neonates to prevent gonococcal ophthalmia neonatorum
Key outcomes
The patient will:
H express concern about self-concept, esteem, and
body image
H identify signs and symptoms of infection
H practice safer sex.
H Isolate the patient if his eyes are infected.
H With gonococcal arthritis, apply moist heat to ease
pain in affected joints.

H Report all cases of gonorrhea to the local public
health authorities as required.

H Report all cases of gonorrhea in children to child
abuse authorities.
H Routinely instill prophylactic drugs, according to fa-
cility protocol, in the eyes of all neonates on admission to the nursery.

H Check the neonate of an infected mother for signs of
infection, and obtain specimens for culture from the
neonates eyes, pharynx, and rectum.
Gonorrhea
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Goodpastures
syndrome
Overview
Description
H Pulmonary renal syndrome characterized by hemop-
tysis and rapidly progressive glomerulonephritis
Pathophysiology
H Abnormal production and deposition of antibodies
against glomerular basement membrane (GBM) and

alveolar basement membrane activate the complement and inflammatory responses.
H This results in glomerular and alveolar tissue damage.
Causes
H Immunofluorescence of GBM shows linear deposi-
tion of immunoglobulins.
H Serum anti-GBM antibody test reveals circulating
anti-GBM antibodies, which distinguish Goodpastures syndrome from other pulmonary-renal syndromes, such as Wegeners granulomatosis, polyarteritis, and systemic lupus erythematosus.
H Serum creatinine and blood urea nitrogen (BUN)
levels typically two to three times normal.
H Urinalysis may reveal red blood cells and cellular
casts, which typify glomerular inflammation; may
also show granular casts and proteinuria.
Imaging
H Chest X-rays reveal pulmonary infiltrates in a diffuse,
nodular pattern.
H Lung biopsy shows interstitial and intra-alveolar
hemorrhage with hemosiderin-laden macrophages.
H Renal biopsy usually shows focal necrotic lesions and
cellular crescents.
H Unknown
H May be associated with exposure to hydrocarbons or
Treatment
with type II hypersensitivity reaction

H Possible genetic predisposition
General
Incidence
H Occurs at any age; most commonly in males between
ages 20 and 30
H Plasmapheresis
H Dialysis
H Low-protein, low-sodium diet
Medications
H Hemoptysis
H Rapidly progressive glomerulonephritis
H High-dose I.V. corticosteroids such as methylpred-
Complications
Surgery
H Renal failure
H Pulmonary edema and hemorrhage
H Kidney transplantation
Assessment
History
H Possible complaint of malaise, fatigue, and pallor
H Possible pulmonary bleeding for months or years be-
fore developing overt hemorrhage and signs of renal

disease
nisolone
Key outcomes
The patient will:
Physical findings
H Hematuria
H Dyspnea, tachypnea, orthopnea
H Restlessness
H Hemoptysis, ranging from a cough with blood-tinged
H Elevate the head of the bed at least 30 degrees, and
sputum to frank pulmonary hemorrhage

H Pulmonary crackles and rhonchi
Test results
Laboratory
H Immunofluorescence of alveolar basement membrane shows linear deposition of immunoglobulins
as well as C3 and fibrinogen.
324
Goodpastures syndrome
administer humidified oxygen, as ordered.

H Encourage the patient to conserve his energy.
H Assist with activities of daily living, and provide fre-
quent rest periods.

H Transfuse blood and administer corticosteroids, as
ordered. Watch closely for signs and symptoms of

adverse reactions.
spirometer use.
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Monitoring
H Vital signs
H Intake and output
H Daily weight
H Creatinine clearance, BUN, and serum creatinine
levels
H Hematocrit and coagulation studies
Patient teaching
Be sure to cover:
H the importance of conserving energy
H an explanation that fluid intake may be restricted
H the name, dosage, purpose, and adverse effects of all
medications
H how to effectively deep-breathe and cough
H how to recognize the signs of respiratory or genitourinary bleeding and the need to report such signs
to the practitioner at once.
Discharge planning
H If dialysis or kidney transplantation is required, refer
the patient to a renal support group.

H Encourage regular follow-up care.
Goodpastures syndrome
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Gout
Overview
Description
H Coronary thrombosis
H Hypertension
H Infection when tophi rupture
Assessment
H Inflammatory arthritis caused by uric acid and crystal
History
deposits
H Red, swollen, and acutely painful joints
H Mostly affects feet, great toe, ankle, and midfoot
H Primary gout: patient symptom-free for years between attacks
H Sudden strike and quick peak in first acute attack
H Delayed attacks associated with olecranon bursitis
H Chronic polyarticular gout the final, unremitting
stage of the disease marked by persistent painful
polyarthritis
H Hypertension
H Renal calculi
H Waking during the night with pain in great toe
H Initial moderate pain that grows intense
H Chills; mild fever
Pathophysiology
H Uric acid crystallizes in blood or body fluids, and the
precipitate accumulates in connective tissue (tophi).

H Crystals trigger an immune response.
H Neutrophils secrete lysosomes for phagocytosis.
H Lysosomes damage tissue and exacerbate the im-
mune response.
Causes
H Decreased renal excretion of uric acid
H Genetic defect in purine metabolism (hyper-
uricemia)
H Secondary gout that develops with other diseases:
Obesity
Diabetes mellitus
Hypertension
Polycythemia
Leukemia
Myeloma
Sickle cell anemia
Renal disease
H Secondary gout that follows treatment with drugs
(hydrochlorothiazide or pyrazinamide)
Incidence
H Primary gout typically in males older than age 30 and
postmenopausal females taking diuretics
H Extreme pain in affected joints
H Redness and swelling in joints
H Tophi in great toe, ankle, or pinna of ear
H Elevated skin temperature
Complications
H Renal calculi
H Atherosclerotic disease
H Cardiovascular lesions
H Stroke
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Gout
Physical findings
H Swollen, dusky red or purple joint
H Limited movement of joint
H Tophi, especially in the outer ears, hands, and feet
(see Recognizing gouty tophi)

H Skin over tophi that may ulcerate and release chalky
white exudate or pus

H Secondary joint degeneration
H Erosions, deformity, and disability
H Warmth over joint
H Extreme tenderness
H Fever
H Hypertension
Test results
Laboratory
H Serum uric acid levels are elevated with a gout attack.
H White blood cell count is elevated in an acute attack.
H Urine uric acid level is elevated in 20% of patients.
Imaging
H X-ray of the articular cartilage and subchondral bone
shows evidence of chronic gout.
H Needle aspiration of synovial fluid shows needlelike
intracellular crystals.
Treatment
General
H Termination of acute attack
H Protection of inflamed, painful joints
H Treatment for hyperuricemia
H Local application of cold
H Prevention of recurrent gout
H Prevention of renal calculi
H Weight loss program, if indicated
H Sparing use of purine-rich foods (such as anchovies,
liver, and sardines)

H Bed rest (in acute attack)
H Immobilization of joint
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Recognizing gouty tophi
Monitoring
In advanced gout, urate crystal deposits develop into

hard, irregular, yellow-white nodules called tophi. These
bumps commonly protrude from the great toe and ear.
H Intake and output

H Serum uric acid levels
H Acute gout attacks 24 to 96 hours after surgery
H Pain control
Patient teaching
Tophus
Be sure to cover:
H the need to drink plenty of fluids (up to 2 qt [2 L]
per day)
H compliance with the prescribed medication regimen
H dietary adjustments
H the need to control hypertension.
Discharge planning
Tophi
appropriate.
Medications
H Analgesics such as oxycodone
H Nonsteroidal anti-inflammatory drugs, such as sundi-
lac and naproxen

H Antigout drugs, such as allopurinol, colchicine,
probenecid, and sulfinpyrazone
Key outcomes
The patient will:
pain
H perform activities of daily living within confines of
the disease
H demonstrate knowledge of the condition and treatment regimen.
H Allow adequate time for self-care.
H Institute bed rest.
H Use a bed cradle, if appropriate.
H Give pain medication, as needed.
H Apply cold packs to affected areas.
H Identify techniques and activities that promote rest
and relaxation.
H Administer anti-inflammatories, as prescribed.
H Provide a purine-poor diet.
Gout
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Graft rejection
syndrome
Assessment
History
H Signs and symptoms that vary markedly, depending
Overview
on type of rejection, underlying illnesses, and type of

organ transplanted
Description
Physical findings
H Rejection of a donated organ occurring when the
H Oliguria and increasing serum creatinine and blood
hosts immune responses are directed against the

graft
H Three subtypes based on time of onset and mechanisms involved:
Hyperacute rejection
Acute rejection
Chronic rejection
Pathophysiology
H Hyperacute rejection occurs within minutes to hours
after graft transplantation.

H Circulating host antibodies recognize and bind to
graft antigens.
H Binding of these antibodies leads to initiation of the
complement cascade, recruitment of neutrophils,

platelet activation, damage to graft endothelial cells,
and stimulation of coagulation reactions.
H Acute rejection may occur several hours to days
(even weeks) after transplantation.
H Alloantigen-reactive T cells from the host infiltrate
the graft and are activated by contact with foreign,
graft-related proteins that are presented to them by
antigen-presenting cells.
H These T cells may cause graft tissue damage.
H Chronic rejection is characterized by the development of blood vessel luminal occlusion due to progressive thickening of the intimal layers of medium
and large arterial walls.
H Large amounts of intimal matrix are produced, leading to increasingly occlusive vessel wall thickening.
H A slowly progressing reduction in blood flow results
in regional tissue ischemia, cell death, and tissue fibrosis.
Causes
H Immune system response to a graft
Incidence
H Hyperacute rejection rare; affects less than 1% of
transplant recipients
H Acute rejection in 50% of transplant patients (only
10% progress to graft loss)

H Chronic rejection in 50% of transplant patients with-
in 10 years after transplantation
urea nitrogen levels with kidney transplant

H Elevated transaminase levels, decreased albumin lev-
els, and hypocoagulability with liver transplant

H Hypotension, heart failure, and edema with heart
transplant
Test results
H Biopsy of the transplanted tissue confirms rejection.
H Hyperacute rejection is characterized by large numbers of polymorphonuclear leukocytes in the graft
blood vessels, widespread microthrombi, platelet accumulation, and interstitial hemorrhage with little or
no interstitial inflammation.
Treatment
General
H Close monitoring of function of grafted organ
H Surveillance, with prophylactic measures against op-
portunistic infections
H Dietary restrictions based on organ system affected
H Hemodialysis
H Mechanical ventilation
Medications
H Immunosuppressants, such as azathioprine and
basiliximab
H Antirejection therapies such as cyclosporine
H Antibiotics, according to infective organism
Key outcomes
The patient will:
H not experience fever, chills, and other signs and
symptoms of illness
H express his feelings about the condition
H comply with the treatment regimen.
H Rapid or gradual progression of organ dysfunction

Complications
Monitoring
H Rapid thrombosis
H Loss of graft function
H Vital signs
H Function of the transplanted organ
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H Signs and symptoms of rejection
H Intake and output
Patient teaching
Be sure to cover:
H how to recognize signs and symptoms of organ dysfunction
H the need to immediately report fever, chills, and other symptoms of infection
H the need for lifelong medication compliance.
Discharge planning
H Refer the patient and his family to social support, in-
cluding psychological support services, as indicated.
Graft rejection syndrome
329
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Guillain-Barr
syndrome
H Aspiration
H Life-threatening respiratory and cardiac compromise
Assessment
History
Overview
H Minor febrile illness 1 to 4 weeks before current
symptoms
Description
H Tingling and numbness (paresthesia) in the legs

H Progression of symptoms to the arms, the trunk and,
H A form of polyneuritis
H Acute, rapidly progressive, and potentially fatal
H Three phases:
H Stiffness and pain in the calves
Acute: beginning from first symptom, ending in 1

to 3 weeks
Plateau: lasting several days to 2 weeks
Recovery: coincides with remyelination and axonal
process regrowth; extends over 4 to 6 months and
may take up to 2 to 3 years; recovery possibly not
complete
Pathophysiology
finally, the face
Physical findings
H Muscle weakness (the major neurologic sign)
H Sensory loss, usually in the legs (spreads to arms)
H Difficulty talking, chewing, and swallowing
H Paralysis of the ocular, facial, and oropharyngeal
muscles
H Loss of position sense
H Diminished or absent deep tendon reflexes
H Segmented demyelination of peripheral nerves oc-
Test results
curs, preventing normal transmission of electrical

impulses.
H Sensorimotor nerve roots are affected; autonomic
nerve transmission may also be affected. (See Understanding sensorimotor nerve degeneration.)
H Cerebrospinal fluid (CSF) analysis may show a normal white blood cell count, an elevated protein count
and, in severe disease, increased CSF pressure.
Other
H Electromyography may demonstrate repeated firing
of the same motor unit instead of widespread sectional stimulation.
H Nerve conduction studies show marked slowing of
nerve conduction velocities.
Causes
H Unknown
Risk factors
H Surgery
H Rabies or swine influenza vaccination
H Viral illness
H Hodgkins or some other malignant disease
H Lupus erythematosus
Incidence
H Occurs between ages 30 and 50
H Symmetrical muscle weakness initially in lower ex-
tremities and progressing to upper extremities

H Paresthesia
H Diplegia
H Dysphagia
H Hypotonia
H Areflexia
Complications
H Thrombophlebitis
H Pressure ulcers
H Contractures
H Muscle wasting
330
Guillain-Barr syndrome
Treatment
General
H Possible endotracheal intubation or tracheotomy
with mechanical ventilation

H Fluid volume replacement
H Plasmapheresis
H Possible tube feedings
H Adequate caloric intake
H Exercise program to prevent contractures
H Emotional support
H Maintenance of skin integrity
Medications
H Corticosteroids such as methylprednisolone
H I.V. immune globulin
Surgery
H Possible gastrostomy or jejunotomy feeding tube in-
sertion
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Understanding sensorimotor nerve

degeneration
Guillain-Barr syndrome attacks the peripheral nerves so
that they cant transmit messages to the brain correctly.
Heres what goes wrong:
The myelin sheath degenerates for unknown reasons.
This sheath covers the nerve axons and conducts electrical impulses along the nerve pathways. With degeneration
comes inflammation, swelling, and patchy demyelination.
As this disorder destroys myelin, the nodes of Ranvier (at
the junctures of the myelin sheaths) widen. This delays
and impairs impulse transmission along the dorsal and
ventral nerve roots.
Because the dorsal nerve roots handle sensory function,
the patient may experience sensations, such as tingling
and numbness, when the nerve root is impaired. Similarly,
because the ventral roots are responsible for motor function, impairment causes varying weakness, immobility,
and paralysis.
Patient teaching
Be sure to cover:
H effective means of communication
H the appropriate home care plan
H instructions about medications
H adverse medication reactions.
Discharge planning
H Refer the patient to physical rehabilitation sources,
as indicated.
H Refer the patient to occupational and speech rehabil-
itation resources, as indicated.

H Refer the patient to the Guillain-Barr Syndrome
Foundation.
Key outcomes
The patient will:
H develop an alternate means of communication
H maintain required caloric intake daily
H maintain joint mobility and range of motion (ROM).
H Establish a means of communication before intuba-
tion is required, if possible.

H Turn and reposition the patient.
spirometer use.
H Provide passive ROM exercises.
H In case of facial paralysis, provide eye and mouth
care.
Monitoring
H Vital signs
H Arterial blood gas values
H Neurologic status
H Pulse oximetry
H Signs of thrombophlebitis
H Signs of urine retention
H Skin integrity
Guillain-Barr syndrome
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Gynecomastia
Overview
Description
H Enlargement of breast tissue in males
H Usually bilateral, except in males older than age 50
when its usually unilateral

H Usually resolves spontaneously in 6 to 12 months
H Pseudogynecomastia: accumulation of fat deposits,
Special populations
In neonates, gynecomastia may be associated with
galactorrhea (witchs milk). This sign usually
disappears within a few weeks but may persist
until age 2.
Incidence
H Affects up to 65% of adolescent males
H True gynecomastia: affects 1% of adult males
not breast tissue.
Pathophysiology
H Disturbance in the normal ratio of active androgen to
estrogen results in proliferation of the fibroblastic

stroma and the duct system of the breast.
Causes
H Testicular tumors
H Obesity
H Pituitary tumors
H Some hypogonadism syndromes
H Liver disease causing inability to break down normal
male estrogen secretions

H Chronic obstructive lung disease
H Other causes (see Drugs and treatments causing
gynecomastia)
Drugs and treatments causing

gynecomastia
In addition to the common causes of gynecomastia, various drugs and treatments may also cause this disorder.
Drugs
When gynecomastia is an effect of drugs, its typically
painful and unilateral. Estrogens used to treat prostate
cancer, including diethylstilbestrol (DES), estramustine,
and chlorotrianisene, directly affect the estrogenandrogen ratio. Drugs that have an estrogen-like effect,
such as cardiac glycosides and human chorionic gonadotropin, may do the same.
Regular use of alcohol, marijuana, or heroin reduces
plasma testosterone levels, causing gynecomastia. Other
drugs such as flutamide, cyproterone, spironolactone,
cimetidine, and ketoconazole produce this sign by
interfering with androgen production or action. Some
common drugs, including phenothiazines, tricyclic antidepressants, and antihypertensives, produce gynecomastia,
but it isnt known how.
Treatments
Gynecomastia may develop within weeks of starting
hemodialysis for chronic renal failure. It may also follow
major surgery or testicular irradiation.
332
Gynecomastia
Special populations
Most males have physicologic gynecomastia at
some time during adolescence, usually around age
14. This gynecomastia is usually asymmetrical and
tender; it commonly resolves within 2 years and
rarely persists beyond age 20.
H Enlarged breast tissue (at least 2 cm in diameter),
either unilateral or bilateral, beneath the areola
Complications
H Malignancy
H Complications of surgery:
Infection
Scarring
Sensory change
Hematoma
Breast asymmetry
Assessment
History
H Causative tumor
H Change in size of breast tissue
H History of causative factors
H Breast pain
Physical findings
H Enlarged breast tissue beneath the areola
H Further physical findings depending on cause
Test results
Laboratory
H Estrogen levels are excessively high and testosterone
levels are normal in drug- and tumor-induced hyperestrogenism.
H Testosterone levels are very low and estrogen levels
are normal in hypergonadism.
H Biopsy rules out malignancy.
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Treatment
General
H Treatment of cause
Medications
H Androgens, such as testosterone and methyltestos-
terone
Surgery
H Resection of extra breast tissue for cosmetic reasons
H Liposuction-assisted mastectomy
Key outcomes
The patient will:
H express understanding of the condition and its cause
H express positive feelings concerning body image.
H Apply cold compresses.
H Encourage verbalization of feelings and concerns.
Monitoring
H Vital signs
H Breast size
After surgery
H Pain control
H Wound site
Patient teaching
Be sure to cover:
H cause of condition and related treatment
H preoperative teaching, if appropriate.
Gynecomastia
333
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Haemophilus
influenzae infection
Overview
Description
H Infection that most commonly attacks respiratory sys-
tem
H Common cause of epiglottiditis, laryngotracheobron-
chitis, pneumonia, bronchiolitis, otitis media, and

meningitis
H Infrequent cause of bacterial endocarditis, conjunctivitis, facial cellulitis, septic arthritis, and osteomyelitis
Pathophysiology
H Antigenic response occurs with invasion of bacteria.
H Systemic disease results from invasion and
hematogenous spread to distant sites (meninges,

bones, and joints).
H Local invasion occurs on the mucosal surfaces.
H Otitis media occurs when bacteria reach the middle
ear through the eustachian tube.
Causes
H H. influenzae, a gram-negative, pleomorphic aero-
bic bacillus
H Transmission by direct contact with secretions or air-
borne droplets
Incidence
H H. influenzae type B (Hib) infection incidence lower
when vaccine is administered at ages 2, 4, 6, and 15

months
H Occurs in fewer than 2 in 100,000 children in the
United States
H H. influenza epiglottiditis most common in children
between ages 3 and 7 but can occur at any age
H Higher incidence of meningitis due to Hib in black
children
H Ten times higher incidence in Native Americans, possibly due to exposure, socioeconomic conditions,
and genetic differences in immune response
H Cause of 5% to 10% of bacterial meningitis cases in
adults
H 3% to 5% mortality rate
H Pericarditis, pleural effusion

H Respiratory failure due to pneumonia
Assessment
History
H Possible report of recent viral infection
H Malaise
H Fatigue
H Fever
Physical findings
Epiglottiditis
H Restlessness and irritability
H Use of accessory muscles, inspiratory retractions,
stridor
H Sitting up, leaning forward with mouth open, tongue
protruding, and nostrils flaring
H Expiratory rhonchi; diminishing breath sounds as the
condition worsens
H Pharyngeal mucosa that may look reddened (rarely,
with soft yellow exudate)
H Epiglottis that appears cherry red with considerable
edema
H Severe pain that makes swallowing difficult or impossible
Pneumonia
H Shaking chills
H Tachypnea
H Productive cough
H Impaired or asymmetrical chest movement caused by
pleuritic pain
H Dullness over areas of lung consolidation
Meningitis
H Altered level of consciousness
H Seizures and coma as disease progresses
H Positive Brudzinskis and Kernigs signs
H Exaggerated and symmetrical deep tendon reflexes
H Nuchal rigidity
H Opisthotonos
Test results
Laboratory
H Isolation of the organism in blood culture confirms
infection.
H Hib meningitis is detected in cerebrospinal fluid
cultures.
Treatment
H Generalized malaise
H High fever
General
Complications
H Airway maintenance (critical in epiglottiditis)

H Diet based on respiratory status (possible need for
H Permanent neurologic sequelae from meningitis,
including hearing loss

H Complete upper airway obstruction from epiglottiditis
H Cellulitis
334
Haemophilus influenzae infection
small, frequent meals)

H Nothing by mouth with inability to swallow ade-
quately
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Medications
H Cephalosporin
H Chloramphenicol and ampicillin (alternate regimen)
H Glucocorticoids, such as dexamethasone, betametha-
sone, and methylprednisone
Key outcomes
The patient will:
H have no adventitious breath sounds
H maintain adequate gas exchange
H have arterial blood gas (ABG) levels that return to
normal
H have no pathogens appear in cultures
H Maintain respiratory isolation.
H Maintain adequate respiratory function through cool
humidification, oxygen, as needed, and croup or face

tents.
H Keep emergency resuscitation equipment readily
available.
H Suction, as needed.
H Maintain adequate nutrition and elimination.
Monitoring
H Pulse oximetry
H ABG results
H Complete blood count for signs of bone marrow de-
pression when therapy includes ampicillin or chloramphenicol

H Intake and output
H Neurologic status
H Vital signs
Patient teaching
Be sure to cover:
H the importance of continuing the prescribed antibiotic until the entire prescription is finished
H using a room humidifier or breathing moist air from
a shower or bath, as necessary, for home treatment
of a respiratory infection
H coughing and deep-breathing exercises to clear
secretions
H the safe disposal of secretions and use of proper
hand-washing technique.
Discharge planning
necessary.
H Encourage the patient to receive vaccinations to pre-
vent future infections.
Haemophilus influenzae infection
335
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Hantavirus pulmonary
syndrome
H Fever
H Headache
H Nausea
H Vomiting
H Cough
Overview
Complications
Description
H Death (in 80% of cases)
H Viral disease that causes flulike symptoms

H Rapidly progresses to respiratory failure
Pathophysiology
H Rodents shed virus in stool, urine, and saliva.
H Human infection occurs from inhalation, ingestion
(of contaminated food or water, for example), contact with rodent excrement, or rodent bites. (See Sin
Nombre virus.)
Causes
H Hantaviruses
H Transmission with exposure to infected rodents
Assessment
History
H Rodent exposure (2 weeks before symptoms)
H Fever
H Myalgia
H Dizziness
Physical findings
(deer mice, pinion mice, brush mice, and western

chipmunks)
H Farming, hiking, or camping in rodent-infested areas
and occupying rodent-infested dwellings
H Cough
H Hypotension
H Tachycardia
H Tachypnea
H Severe hypoxemia and respiratory failure
Incidence
Test results
H Occurs mainly in southwestern United States

H More commonly affects whites
H Affects males more than females
H The Centers for Disease Control and Prevention and
H Noncardiogenic pulmonary edema
H Myalgia
Sin Nombre virus

This illustration shows the Sin Nombre virus, the most
common cause of Hantavirus pulmonary syndrome in the
United States and Canada. It exists primarily in western
states and provinces.
state health departments can perform definitive testing for hantavirus exposure and antibody formation.
Laboratory
H White blood cell count is elevated with a predominance of neutrophils, myeloid precursors, and atypical lymphocytes.
H Hematocrit is elevated.
H Platelet count is decreased.
H Partial thromboplastin time is prolonged.
H Fibrinogen level is normal.
H Serum creatinine levels are no greater than
2.5 mg/dl.
Imaging
H Chest X-rays eventually show bilateral diffuse infiltrates in almost all patients (findings consistent with
acute respiratory distress syndrome).
Treatment
General
H Intubation and aggressive respiratory management
H Adequate oxygenation
H Stabilization of heart rate and blood pressure
H Cautious fluid volume replacement
H Nothing by mouth until recovery begins
H Activity, as tolerated, with frequent rest periods
Medications
H Vasopressors, such as dopamine, dobutamine, and
norepinephrine
H Ribavirin
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Hantavirus pulmonary syndrome
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Key outcomes
The patient will:
H maintain a respiratory rate within 5 breaths/minute
of baseline
H maintain adequate gas exchange
H cough effectively
H expectorate mucus.
H Maintain a patent airway by suctioning, if necessary.
H Ensure adequate humidification, and check mechani-
cal ventilator settings frequently.

H Provide I.V. fluid therapy based on results of hemody-
namic monitoring.
H Report cases of Hantavirus pulmonary syndrome to
your state health department.
Monitoring
H Neurologic status
Patient teaching
Be sure to cover:
H the need to immediately report signs or symptoms of
respiratory distress
H prevention guidelines, with a focus on rodent control.
Discharge planning
H Refer the patient for follow-up with a pulmonologist,
if indicated.
Hantavirus pulmonary syndrome
337
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Headache
Overview
Description
H Head pain that may be a symptom of an underlying
disorder
H Classified as primary (headaches having no organic
or structural cause) or secondary (indicative of an

underlying structural or organic disease)
Pathophysiology
Headache
H Sustained muscle contractions directly deform pain
receptors.
H Inflammation or direct pressure affects the cranial
nerves.
H Pain-sensitive structures respond, including the skin,
scalp, muscles, arteries, and veins; cranial nerves V,
VII, IX, and X; and cervical nerves 1, 2, and 3.
Migraine
H Biochemical abnormalities occur, including local
leakage of a vasodilator polypeptide through the dilated arteries and a decreased plasma level of serotonin.
Causes
Headache
H Underlying intracranial disorder
H Systemic disorder
H Psychological disorders
H Allergy
H Tension (muscle contraction)
H Emotional stress
H Fatigue
H Menstruation
H Environmental stimuli
H Glaucoma
H Hormone replacement therapy
H Inflammation of the eyes or mucosa of the nasal or
paranasal sinuses
H Disorder of the scalp, teeth, extracranial arteries, or
external or middle ear
H Muscle spasms of the face, neck, or shoulders
H Vasodilators
H Hypoxia
H Hypertension
H Head trauma and tumors
H Intracranial bleeding, abscess, or aneurysm
H Caffeine withdrawal
H Overuse of over-the-counter headache medications
(rebound headache)
Migraine
H Constriction and dilation of intracranial and extracranial arteries
H Associated with:
Epilepsy
Hereditary hemorrhagic telangiectasia
338
Headache
Tourettes syndrome
Ischemic stroke
Depression
Incidence
Headache
H Affects 60% to 80% of people in the United States at
any point in time
Migraine
H Appears in childhood or adolescence
H Recurs throughout adulthood
H Affects 17% of females and 6% of males in the United
States
H Strong familial incidence
H Pain thats aching or tight
H Hatbandlike pattern around head
H Nausea
H Photophobia
H Phonophobia
H Blurred vision
Complications
H Worsening of existing hypertension
H Photophobia
H Motor weakness
H Loss of work
Assessment
History
Headache
H Location (frontal, temporal, or cervical), characteristics (frequency and intensity), onset and duration
(continuous or intermittent)
H Precipitating factors: tension, menstruation, loud
noises, menopause, alcohol consumption, stress,
and food allergies
H Aggravating factors: coughing, sneezing, and sunlight
H Associated symptoms: nausea or vomiting, weakness,
facial pain, and scotomas
H Use of headache-inducing medications
H Familial history of headaches
Migraine
H Unilateral, pulsating pain gradually becoming more
generalized
H May be preceded by scintillating scotoma, hemianopsia, unilateral paresthesia, or speech disorders
H May be accompanied by irritability, anorexia, nausea
or vomiting, and photophobia
Physical findings
Headache
H Findings based on cause
H If no underlying problem, normal physical findings
H Possible crepitus or tender spots of the head and
neck
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Migraine
H Pallor
H Possible extraocular muscle palsies
H Possible ptosis
H Possible neurologic deficits
Test results
Imaging
H Skull X-rays may show skull fracture (with trauma).
H Sinus X-rays may show sinusitis.
H Computed tomography scan may show tumor or subarachnoid hemorrhage or other intracranial pathology; may show pathology of sinuses.
H Magnetic resonance imaging may also show tumor.
H Lumbar puncture may show increased intracranial
pressure, suggesting tumor, edema, or hemorrhage.
H EEG may show alterations in the brains electrical
activity, suggesting intracranial lesion, head injury,
meningitis, or encephalitis.
Other
H Patient questionnaire tool evaluates functional status
and quality of life.
H express an increased sense of well-being

H understand causative factors or triggers.
H Encourage the use of relaxation techniques.
H Keep the patients room dark and quiet.
H Place ice packs on the patients forehead or a cold
cloth over his eyes.

H Administer prescribed drugs for pain.
Monitoring
H Pain control
H Response to alternative treatment
H Vital signs, especially blood pressure
H Neurologic status
Patient teaching
General
Be sure to cover:
H avoidance of migraine triggers
H lifestyle changes
H nonpharmacologic strategies
H monitoring of headaches with headache diary
H appropriate use of preventive medications
H possible adverse reactions to prescribed drugs.
H Yoga, meditation, or other relaxation therapy

H Identification and elimination of causative factors
Discharge planning
Treatment
(including environmental)
H Psychotherapy, if emotional stress involved
H For migraine patient, adequate oral fluid intake and
H Refer the patient to the National Headache Founda-
tion.
avoidance of dietary triggers

H For migraine patient, bed rest in dark, quiet room
Medications
Headache
H Analgesics, such as acetaminophen, aspirin, and
ibuprofen
H Tranquilizers, such as alprazolam, diazepam, and
lorazepam
H Muscle relaxants, such as carisopradol and tizanidine
Migraine
H Ergotamine preparations
H Preventive drugs, such as clonidine, propranolol,
topiramate, and valproate
H Triptan agents, such as electriptan, sumatriptan, and
naratriptan
Key outcomes
The patient will:
pain
H demonstrate methods of promoting relaxation and
inner well-being
Headache
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Hearing loss
Overview
Description
H Mechanical or nervous impediment to the transmis-
sion of sound waves to the brain

H Classified as sensorineural, conductive, or mixed
H Presbycusis (age related): most common type of
sensorineural hearing loss

H Congenital hearing loss: may be conductive or sen-
sorineural
H Sudden hearing loss: may be conductive, senso-
rineural, or mixed; usually affects only one ear

H Depending on the cause, with prompt treatment
(within 48 hours), hearing possibly restored

H Noise-induced hearing loss possibly transient or
permanent
Pathophysiology
H In conductive hearing loss, sound wave transmission
is interrupted between the external canal and inner

ear (junction of the stapes and oval window).
H In sensorineural hearing loss, sound wave transmission is interrupted between the inner ear and brain,
and theres cochlea or acoustic nerve dysfunction.
H In mixed hearing loss, a combination of dysfunction
of conduction and sensorineural transmission is involved.
Causes
Conductive hearing loss
H Cerumen impaction
H Blockage of the external ear
H Tympanic membrane thickening, retraction, scarring,
or perforation
H Otitis media, otitis externa
H Otosclerosis
H Serous otitis
Sensorineural hearing loss
H Impairment of the cochlea, eighth cranial or acoustic
nerve
H Loss of hair cells and nerve fibers in the cochlea
H Drug toxicity
H Vascular occlusion of the anterior cerebellar artery
H Infectious diseases
H Arteriosclerosis
H Otospongiosis
H Head or ear trauma
H Organ of Corti degeneration
H Prolonged exposure to loud noise (85 to 90 dB)
H Perilymphatic fistula
H Brief exposure to extremely loud noise (greater than
90 dB)
H Acoustic neuroma
Congenital hearing loss
H Sensorineural or conductive
340
Hearing loss
H May be transmitted as a dominant, autosomal domi-
nant, autosomal recessive, or sex-linked recessive

trait
Hearing loss in neonates
H Trauma during delivery
H Toxicity
H Infection during pregnancy or delivery
H Hereditary disorders
H Maternal exposure to rubella or syphilis during pregnancy
H Use of ototoxic drugs during pregnancy
H Prolonged fetal anoxia during delivery
H Congenital abnormalities of the ears, nose, or throat
Sudden hearing loss
H Occlusion of internal auditory artery by spasm or
thrombosis
H Subclinical mumps
H Bacterial and viral infections
H Acoustic neuroma
H Mnires disease
H Metabolic, vascular, or neurologic disorders
H Blood dyscrasias
H Ototoxic drugs
Risk factors
Special populations
Premature or low-birth-weight neonates with
congenital hearing loss are most likely to have
structural or functional hearing impairments.
H Neonates with serum bilirubin levels greater than
20 mg/dl (toxic effects on the brain)

H Erythroblastosis fetalis
H Maternal infection or drug abuse
H Frequent ear infections
H Repeated exposure to very loud noise
Incidence
H Most common disability in the United States
H Third most prevalent disorder in adults older than
age 65
H Presbycusis prevalent in adults older than age 50
H Hearing loss
H Tinnitus
Complications
H Tympanic membrane perforation
H Cholesteatoma
H Permanent hearing loss
H Speech and language delay in children
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Assessment
History
Key outcomes
H Deficient response to auditory stimuli within 2 to 3
The patient will:

H express understanding of the condition and treatment
H exhibit adequate coping mechanisms
H regain hearing or develop alternate means of communication.
days after birth

H Older child with hearing loss that impairs speech development
H Use of ototoxic substances
Sudden deafness
H Recent exposure to loud noise
H Brief exposure to extremely loud noise
H Persistent tinnitus
H Transient vertigo
H Face the patient when speaking and enunciate words
clearly, slowly, and in a normal tone.

H Provide an alternative method of communication.
Physical findings
Monitoring
H Obvious hearing difficulty
H Progression of hearing loss
H Adaptation to hearing aid
Test results
Imaging
H Computed tomography scan shows vestibular and auditory pathways.
H Magnetic resonance imaging shows acoustic tumors
and brain lesions.
H Auditory brain response shows activity in auditory
nerve and brain stem.
H Pure tone audiometry shows presence and degree of
hearing loss.
H Electronystagmography shows vestibular function.
H Otoscopic or microscopic examination shows middle
ear disorders; removes debris.
H Rinne and Webers tests show whether hearing loss is
conductive or sensorineural.
Patient teaching
Treatment
Be sure to cover:
H hearing loss, its causes, and treatments
H tests and procedures
H preoperative and postoperative instructions
H operation and maintenance of a hearing aid
H lip-reading lessons, which may increase the effectiveness
H the danger of excessive noise exposure
H the use of protective devices in a noisy environment
H the danger of exposure to drugs, chemicals, and infection (with pregnancy)
H the proper technique for ear cleaning or irrigation
H how to instill otic medications
H medication use and possible adverse effects.
General
Discharge planning
H Varies with the type and cause of impairment

H Hearing aids or other effective means of aiding com-
H If hearing deteriorates, refer the patient for speech
munication
H Avoidance of activities that allow water to enter ear, if
eardrum perforated
H Refer a child to an audiologist or otolaryngologist for
and hearing rehabilitation.

further evaluation, as indicated.
H Refer to community resources, as appropriate.
Medications
H Antibiotics as appropriate for infecting organism
H Agents to dissolve cerumen such as triethanolamine
polypeptide oleate-condensate
Surgery
H Correction of tympanic membrane perforation
H Cochlear implants
Hearing loss
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Heart failure
Complications
H Pulmonary edema
H Organ failure, especially the brain and kidneys
H MI
Assessment
Overview
Description
H Fluid buildup in the heart from myocardium that
cant provide sufficient cardiac output

H Usually occurs in a damaged left ventricle but may
occur in right ventricle either primarily or secondary

to left-sided heart failure
Pathophysiology
Left-sided heart failure
H Pumping ability of the left ventricle fails and cardiac
output falls.
H Blood backs up into the left atrium and lungs, causing pulmonary congestion.
Right-sided heart failure
H Ineffective contractile function of the right ventricle
leads to blood backing up into the right atrium and
the peripheral circulation, which results in peripheral edema and engorgement of the kidneys and other
organs.
Causes
H Mitral stenosis secondary to rheumatic heart disease,
constrictive pericarditis, or atrial fibrillation

H Mitral or aortic insufficiency
H Arrhythmias
H Hypertension
H Atherosclerosis with myocardial infarction (MI)
H Myocarditis
H Ventricular and atrial septal defects
H Constrictive pericarditis
H Pregnancy
H Thyrotoxicosis
H Infections
H Anemia
H Emotional stress
H Increased sodium or water intake
Incidence
H Affects 1% of people older than age 50
H Affects 10% of people older than age 80
H Reduced cardiac output
H Peripheral edema
342
Heart failure
History
H A disorder or condition that can precipitate heart
failure
H Dyspnea or paroxysmal nocturnal dyspnea
H Peripheral edema
H Fatigue
H Weakness
H Insomnia
H Anorexia
H Nausea
H Sense of abdominal fullness (particularly in right-
sided heart failure)

H Substance abuse (alcohol,
drugs, tobacco)
Physical findings
H Cough that produces pink, frothy sputum
H Cyanosis of the lips and nail beds
H Pale, cool, clammy skin
H Diaphoresis
H Ascites
H Tachycardia
H Pulsus alternans
H Hepatomegaly and, possibly, splenomegaly
H Decreased pulse pressure
H S3 and S4 heart sounds
H Moist, bibasilar crackles, rhonchi, and expiratory
wheezing
H Decreased pulse oximetry
H Peripheral edema
H Decreased urinary output
Test results
Laboratory
H B-type natriuretic peptide immunoassay is elevated.
Imaging
H Chest X-rays show increased pulmonary vascular
markings, interstitial edema, or pleural effusion and
cardiomegaly.
H Electrocardiography reflects heart strain or enlargement or ischemia. It may also reveal atrial enlargement, tachycardia, extrasystole, or atrial fibrillation.
H Pulmonary artery pressure monitoring typically
shows elevated pulmonary artery and pulmonary
artery wedge pressures, left ventricular end-diastolic
pressure in left-sided heart failure, and elevated right
atrial or central venous pressure in right-sided heart
failure.
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Treatment
General
H Antiembolism stockings
H Elevation of lower extremities
H Fluid restriction
H Calorie restriction, if indicated
H Low-fat diet, if indicated
H Walking program
Medications
H Oxygen
H Diuretics, such as furosemide, bumetanide, torse-
mide, and metolazone

H Inotropic drugs, such as digoxin, dobutamine, and
dopamine
H Vasodilators, such as nitrates, isosorbide, and nesiritide
H Angiotensin converting enzyme inhibitors, such as
captopril, enalapril, and lisinopril
H Angiotensin receptor blockers, such as losartan, valsartan, and irbesartan
H Calcium channel blockers such as amiodipine
H Beta-adrenergic blockers, such as atenolol, metoprolol, and carvedilol
Surgery
H For valvular dysfunction with recurrent acute heart
failure, surgical replacement

H Ventricular assist device
H Stent placement
Monitoring
H Daily weight for peripheral edema and other signs
and symptoms of fluid overload

H Cardiac rhythm
H Intake and output
H Vital signs
H Mental status
H Peripheral edema
ALERT
Auscultate for abnormal heart and breath sounds,
and report changes immediately.
H Blood urea nitrogen and serum creatinine, potassi-
um, sodium, chloride, and magnesium levels

H Prothrombin time and INR
Patient teaching
Be sure to cover:
H signs and symptoms of worsening heart failure
H the importance of follow-up care
H the need to avoid high-sodium foods
H the need to avoid fatigue
H instructions about fluid restrictions
H the need to weigh himself every morning, at the same
time, before eating, and after urinating; keeping a
record of his weight, and reporting a weight gain of
3 to 5 lb (1.5 to 2.5 kg) in 1 week
H the importance of smoking cessation, if appropriate
H weight reduction, as needed
H medication administration, dosage, possible adverse
effects, and monitoring needs.
Discharge planning
Key outcomes

H Refer the patient to a smoking-cessation program,
The patient will:

H carry out activities of daily living without excess
fatigue or decreased energy
H maintain adequate fluid balance.
if appropriate.
H Place the patient in Fowlers position, and give sup-
plemental oxygen.
H Provide continuous cardiac monitoring during acute
and advanced stages.

H Assist the patient with range-of-motion exercises.
H Apply antiembolism stockings. Check for calf pain
and tenderness.
Heart failure
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Heat syndrome
Overview
Description
H Temperature in excess of 105.8 F (41 C)
H Tachycardia (greater than 130 beats/minute)
H Widened pulse pressure
H Changes in level of consciousness (LOC)
H Tonic-dystonic contractions of the muscles
H Coma
H Tachypnea
H Hypoxia
H Heat exhaustion: acute heat injury with hyperthermia
Complications
caused by dehydration
H Heat stroke: extreme hyperthermia with thermoregulatory failure
H Hypovolemic shock
H Cardiogenic shock
H Renal failure
H Hepatic failure
Pathophysiology
H Normal regulation of temperature is by evaporation
(30% of bodys heat loss) or vasodilation. When heat

is generated or gained by the body faster than it can
dissipate, the thermoregulatory mechanism is
stressed and eventually fails.
H Hyperthermia accelerates.
H Cerebral edema and cerebrovascular congestion occur.
H Cerebral perfusion pressure increases and cerebral
perfusion decreases.
H Tissue damage occurs when temperature exceeds
107.6 F (42 C), resulting in tissue necrosis, organ
dysfunction, and failure.
Causes
H Illness
H Heart disease
H Endocrine disorders
H Neurologic disorder
H Infection (fever)
H Dehydration
H Behavior
H Excessive physical activity
H Excessive clothing
H Lack of acclimatization
H Hot environment without ventilation
H Inadequate fluid intake
H Drugs, such as phenothiazines, anticholinergics, and
amphetamines
H Sudden discontinuation of Parkinsons disease med-
ications
Risk factors
H Obesity
H Sodium and water depletion
H Alcohol use
H Poor physical condition
H Age
H Socioeconomic status
Incidence
H Increased incidence among elderly patients and
neonates during excessively hot summer days
344
Heat syndrome
Assessment
History
Heat exhaustion
H Prolonged activity in a very warm or hot environment
H Muscle cramps
H Thirst
H Weakness
H Headache
H Fatigue
Heat stroke
H Exposure to high temperature and humidity without
air circulation
H Same signs as heat exhaustion
H Blurred vision
H Confusion
H Hallucinations
H Decreased muscle coordination
H Syncope
Physical findings
Heat exhaustion
H Rectal temperature greater than 100 F (37.8 C)
H Pale skin
H Thready, rapid pulse
H Cool, moist skin
H Irritability
H Syncope
H Impaired judgment
H Hyperventilation
Heat stroke
H Rectal temperature of at least 104 F (40 C)
H Red, diaphoretic, hot skin in early stages
H Gray, dry, hot skin in later stages
H Tachycardia
H Slightly elevated blood pressure in early stages
H Decreased blood pressure in later stages
H Signs of central nervous system dysfunction
H Altered mental status
H Hyperpnea
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H Cheyne-Stokes respirations
H Anhydrosis (late sign)
Test results
Laboratory
H Abnormal serum electrolytes may show hyponatremia and hypokalemia.
H Arterial blood gas levels may show respiratory alkalosis.
H Complete blood count may show leukocytosis and
thrombocytopenia.
H Coagulation studies may show increased bleeding
and clotting times.
H Urinalysis may show concentrated urine and proteinuria with tubular casts and myoglobinuria.
H Blood urea nitrogen level may be elevated.
H Serum calcium level may be decreased.
H Serum phosphorus level may be decreased.
Patient teaching
Be sure to cover:
H how to avoid reexposure to high temperatures
H the need to maintain adequate fluid intake
H limiting activity in hot weather
H steps to prevent recurrence. (See Preventing heat
illness.)
Discharge planning
H Refer the patient to social services, if appropriate.
Treatment
General
Heat exhaustion
H Cool environment
H Oral or I.V. fluid administration
Heat stroke
H Lowering the body temperature as rapidly as possible
H Evaporation, hypothermia blankets, and ice packs to
the groin, axillae, and neck
H Supportive respiratory and cardiovascular measures
H Increased hydration; cool liquids only
H Avoidance of caffeine and alcohol
Key outcomes
The patient will:
H maintain a normal body temperature
H prevent recurrent episodes of hyperthermia
H express understanding of the need to maintain adequate fluid intake.
H Perform rapid cooling procedures.
H Provide supportive measures.
H Provide adequate fluid intake.
Monitoring
H Vital signs
H Pulse oximetry readings
H Complications
H LOC
H Cardiac rhythm
H Intake and output
H Myoglobin test results
Prevention
Preventing heat illness

Heat illness can occur insidiously if precautions arent
taken. The patient should follow these guidelines:
H Drink plenty of fluids during outdoor activities, especially on hot days. (Water and sports drinks are the
drinks of choice; avoid tea, coffee, soda, and alcohol
because these can lead to dehydration. He should attempt to take in more than hes losing.)
H Take frequent breaks for drinks and to mist himself
with a spray bottle of water to help with cooling.
H Wear lightweight, tightly woven, loose-fitting clothing
in light colors.
H Schedule vigorous activity and sports for cooler times
of the day.
H Protect himself from direct sun exposure by wearing a
hat, sunglasses, and using an umbrella.
H Gradually increase time spent outdoors to get his body
acclimated to the heat.
H Try to spend as much time as possible in a cooled or
air conditioned environment on very hot and humid
days.
H Discuss chronic conditions with his practitioner for
disease specific precautions.
Heat syndrome
345
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Hemophilia
H Pain and swelling in a weight-bearing joint, such as
the hip, knee, or ankle

H With mild hemophilia or after minor trauma, lack of
Overview
Description
H Hereditary bleeding disorder
H Characterized by greatly prolonged coagulation time
H Results from deficiency of specific clotting factors
H Hemophilia A (classic hemophilia): affects more
than 80% of hemophiliacs; results from factor VIII

deficiency
H Hemophilia B (Christmas disease): affects 15% of
hemophiliacs; results from factor IX deficiency
H Incurable
Pathophysiology
H Low level or absence of the blood protein necessary
for clotting causes disruption of normal intrinsic coagulation cascade.

H Abnormal bleeding, which may be mild, moderate,
or severe, depending on the degree of protein factor
deficiency, occurs.
H A platelet plug forms at the bleeding site, but the lack
of clotting factors impairs formation of a stable fibrin
clot.
H Immediate hemorrhage isnt prevalent; delayed
bleeding is common.
Causes
H Hemophilia A and B usually inherited as X-linked
recessive traits
H Spontaneous mutation
H Acquired immunologic process
Incidence
H Most common X-linked genetic disease
H Occurs in about 400 live male births in the United
States each year; rare in females
spontaneous bleeding, but prolonged bleeding with

major trauma or surgery
H Moderate hemophilia producing only occasional
spontaneous bleeding episodes
H Severe hemophilia causing spontaneous bleeding
H Prolonged bleeding after surgery or trauma or joint
pain in spontaneous bleeding into muscles or joints
H Signs of internal bleeding, such as abdominal, chest,
or flank pain; episodes of hematuria or hematemesis;
and tarry stools
H Activity or movement limitations and need for assistive devices, such as splints, canes, or crutches
Physical findings
H Hematomas on extremities, torso, or both
H Joint swelling in episodes of bleeding into joints
H Limited and painful joint range of motion in episodes
of bleeding into joints
Test results
Laboratory
HEMOPHILIA A
H Factor VIII assay is 0% to 25% of normal.
H Partial thromboplastin time (PTT) is prolonged.
H Platelet count and function, bleeding time, and pro-
thrombin time are normal.

HEMOPHILIA B
H Factor IX assay is deficient.
H Baseline coagulation results are similar to those of
hemophilia A, with normal factor VIII.

HEMOPHILIA A OR B
H Degree of factor deficiency defines severity:
Mild hemophilia factor levels are 5% to 25% of

normal.
Moderate hemophilia factor levels are 1% to
5% of normal.
Severe hemophilia factor levels are less than
1% of normal.
H Abnormal tendency to bleed

H Painful and swollen joints
Treatment
Complications
General
H Pain, swelling, extreme tenderness, and permanent
H Correct treatment to quickly stop bleeding by in-
joint and muscle deformity

H Peripheral neuropathies, pain, paresthesia, and muscle atrophy
H Ischemia and gangrene
H Shock and death
creasing plasma levels of deficient clotting factors

H Diet consisting of foods high in vitamin K
H Activity guided by degree of factor deficiency
Medications
H Aminocaproic acid
Assessment
History
H Familial history of bleeding disorders
H Prolonged bleeding with circumcision
H Concomitant illness
346
Hemophilia
Hemophilia A
H Cryoprecipitated antihemophilic factor (AHF),
lyophilized AHF, or both
H Desmopressin
Hemophilia B
H Factor IX concentrate
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Key outcomes
The patient will:
H have peripheral pulses that remain palpable and
strong
pain
H maintain range of motion (ROM) and joint mobility
H demonstrate adequate coping skills
H verbalize understanding of disease process and treatment regimen.
H Provide emotional support and reassurance when in-
dicated.
During bleeding episodes
H Apply pressure to bleeding sites.
H Administer the deficient clotting factor or plasma, as
ordered, until bleeding stops.
H Apply cold compresses or ice bags, and elevate the
injured part.
H To prevent recurrence of bleeding, restrict activity for
48 hours after bleeding is under control.
H Control pain with prescribed analgesics.
H Avoid I.M. injections.
H Avoid aspirin and aspirin-containing drugs.
During bleeding into a joint
H Immediately elevate the joint.
H To restore joint mobility, begin ROM exercises at
least 48 hours after the bleeding is controlled.
H Restrict weight bearing until bleeding stops and
swelling subsides.
H Apply ice packs and elastic bandages to alleviate
pain.
H the need to notify the physician immediately after
even a minor injury

H the need for parents to watch for signs of internal
bleeding
H the importance of avoiding aspirin, combination
medications that contain aspirin, and over-thecounter anti-inflammatory agents (use acetaminophen instead)
H the importance of good dental care and the need to
check with the physician before dental extractions or
surgery
H the need to wear medical identification jewelry at all
times
H how to administer blood factor components at home,
if appropriate
H the need to keep blood factor concentrate and infusion equipment available at all times
H adverse reactions that can result from replacement
factor procedures
H signs, symptoms, and treatment of anaphylaxis
H the need for the patient or parents to watch for early
signs of hepatitis
H the need to follow standard precautions.
Discharge planning
H Refer new patients to a hemophilia treatment center
for evaluation.
H For more information, refer the patients family to the
National Hemophilia Foundation.
Monitoring
H PTT
H Adverse reactions to blood products
H Signs and symptoms of decreased tissue perfusion
H Vital signs
H Bleeding from the skin, mucous membranes, and
wounds
Patient teaching
Be sure to cover:
H the benefits of regular isometric exercises
H how parents can protect their child from injury while
avoiding unnecessary restrictions that impair normal
development
H the need to avoid contact sports
H if an injury occurs, directions for parents to apply
cold compresses or ice bags and to elevate the injured part or apply light pressure to bleeding
Hemophilia
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Hemorrhoids
Overview
Description
H Pregnancy
H Obesity
Incidence
H Occur in both sexes
H Most cases occurring in people ages 20 to 50
H Varicosities found in the superior or inferior hemor-
rhoidal venous plexus

H Classified as first, second, third, or fourth degree,
depending on their severity
H First-degree hemorrhoids: confined to the anal canal
H Second-degree hemorrhoids: prolapse during straining but reduce spontaneously
H Third-degree hemorrhoids: prolapsed hemorrhoids
requiring manual reduction after each bowel movement
H Fourth-degree hemorrhoids: irreducible
H Painless, intermittent bleeding during defecation
Pathophysiology
History
H Dilation and enlargement of the superior plexus of
H Bright red blood on stool or toilet tissue

H Anal itching
H Vague feeling of anal discomfort
H Pain
the superior hemorrhoidal veins above the dentate

line cause internal hemorrhoids.
H Enlargement of the plexus of the inferior hemorrhoidal veins below the dentate line causes external
hemorrhoids, which may protrude from the rectum.
(See Comparing types of hemorrhoids.)
Causes
Complications
H Constipation
H Local infection
H Thrombosis of hemorrhoids
H Secondary anemia from severe or recurrent bleeding
Assessment
Physical findings
H Prolapse of rectal mucosa
H Anal tenderness on palpation
H Internal hemorrhoids (with digital examination)
H Prolonged sitting
H Straining at defecation
H Constipation, low-fiber diet
Comparing types of hemorrhoids

Covered by mucosa, internal hemorrhoids bulge into the rectal lumen and may prolapse during defecation. Covered by skin,
external hemorrhoids protrude from the rectum and are more likely to thrombose than internal hemorrhoids. The illustrations below show both frontal and cross-sectional views.
INTERNAL HEMORRHOIDS
348
Hemorrhoids
EXTERNAL HEMORRHOIDS
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Test results
H Anoscopy and flexible sigmoidoscopy visualize internal hemorrhoids.
Treatment
General
H High-fiber diet, increased fluid intake
H Avoidance of prolonged sitting
H Warm sitz baths to relieve pain
Medications
H Local anesthetic agents
H Hydrocortisone cream and suppositories
Surgery
H Injection sclerotherapy or rubber band ligation
H Hemorrhoidectomy by cauterization or excision
Key outcomes
The patient will:
H have reduced occurrence of hemorrhoids
regimen.
H Administer enemas preoperatively.
H Keep the wound site clean.
H Provide sitz baths.
Monitoring
H Bleeding
H Pain
Patient teaching
Be sure to cover:
H avoiding stool softeners after surgery
H the importance of regular bowel habits and good
anal hygiene
H avoiding too-vigorous wiping with washcloths and
use of harsh soaps
H the use of medicated astringent pads and white, unscented toilet paper.
Hemorrhoids
349
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Hemothorax
Overview
Description
H Blood in the pleural cavity
H May result in lung collapse
Pathophysiology
H Anxiety
H Cyanosis
H Stupor
H Affected side may expand and stiffen
H Unaffected side may rise with gasping respirations
H Dullness over affected side
H Decreased or absent breath sounds over affected side
H Symptoms associated with blunt trauma
H Tachycardia
H Hypotension
H Damaged intercostal, pleural, mediastinal, and some-
Test results
times lung parenchymal vessels cause blood to enter

the pleural cavity.
H The amount of bleeding and the cause is associated
with varying degrees of lung collapse and mediastinal
shift.
Laboratory
H Pleural fluid analysis shows hematocrit greater than
50% of serum hematocrit.
H Arterial blood gas (ABG) analysis may show increased partial pressure of carbon dioxide and
decreased partial pressure of oxygen.
H Serum hemoglobin level may be decreased, depending on blood loss.
Imaging
H Chest X-rays and computed tomography scan of the
thorax show the presence and extent of hemothorax
and help to evaluate treatment.
H Thoracentesis may yield blood or serosanguineous
fluid.
Causes
H Blunt or penetrating chest trauma
H Pulmonary infarction
H Necrotizing infections
H Pulmonary arteriovenous fistulas
H Hereditary hemorrhagic telangiectasis
H Heart or thorax surgery
H Neoplasm
H Dissecting thoracic aneurysm
H Anticoagulant therapy
H Thoracic endometriosis
H Central venous catheter insertion
H Tuberculosis
Incidence
H Occurs in about 30% of patients with chest trauma
H Chest pain
H Sudden shortness of breath
Complications
H Mediastinal shift
H Ventilatory compromise
H Lung collapse
H Cardiopulmonary arrest
H Pneumothorax
H Empyema
Assessment
History
H Recent trauma
H Recent thoracic surgery
H Metastatic disease
Physical findings
H Tachypnea
H Dusky skin color
H Diaphoresis
H Hemoptysis
H Restlessness
350
Hemothorax
Treatment
General
H Stabilization of the patients clinical condition
H Stoppage of bleeding
H Thoracentesis
H Insertion of chest tube
H Blood transfusion, or autotransfusion if blood loss
approaches or exceeds 1 L (see Using autotransfusion for chest wounds)

H I.V. therapy
Medications
H Oxygen
H Analgesics
Surgery
H Thoracotomy if chest tube doesnt improve condition
Key outcomes
The patient will:
H maintain fluid volume balance
pain
H verbalize understanding of the illness.
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Using autotransfusion for chest wounds

Autotransfusion is used most commonly in patients with
chest wounds, especially those that involve hemothorax.
Through autotransfusion, a patients own blood is collected,
filtered, and reinfused. The procedure may also be used
when two or three units of pooled blood can be recovered,
such as in cardiac or orthopedic surgery.
Autotransfusion eliminates the patients risk of transfusion
reaction or blood-borne disease, such as cytomegalovirus,
hepatitis, and human immunodeficiency virus. Its contraindicated in patients with sepsis or cancer.
How autotransfusion works

A large-bore chest tube connected to a closed drainage system is used to collect the patients blood from a wound or
chest cavity. This blood passes through a filter, which
catches most potential thrombi, including clumps of fibrin
and damaged red blood cells (RBCs). The filtered blood
passes into a collection bag. From the bag, the blood is reinfused immediately, or it may be processed in a commercial
cell washer that reduces anticoagulated whole blood to
washed RBCs for later infusion.
Assisting with autotransfusion

Set up the blood collection system as you would any closed
chest drainage system. Attach the collection bag according
to the manufacturers instructions.
If ordered, inject an anticoagulant, such as heparin or
acid-citrate-dextrose solution, into the self-sealing port on
the connector of the patients drainage tubing.
During reinfusion, monitor the patient for complications,
such as blood clotting, hemolysis, coagulopathies, thrombocytopenia, particulate and air emboli, sepsis, and citrate toxicity (from the acid-citrate-dextrose solution).
Drainage tube
From patient
To suction
Locking connectors to
collection bag
Self-sealing
ports
Microfilter
Water-seal chamber
Autotransfusion
collection bag
H Promote comfort and relaxation.
H Administer prescribed oxygen.
H Administer prescribed I.V. fluids and blood transfu-
sions.
H Assist with thoracentesis.
H Prepare the patient for surgery, if needed.
H Change the chest tube dressing, and provide chest
tube care, as needed.
Patient teaching
Be sure to cover:
H prescribed drugs and possible adverse effects
H preoperative and postoperative care, if needed
H mechanical ventilation, if needed
H deep-breathing exercises
H smoking cessation, if appropriate.
Monitoring
H Vital signs
H Intake and output
H ABG results
H Complete blood count results
H Complications
Hemothorax
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Hepatic encephalopathy
Overview
Description
H A neurologic syndrome that develops as a complica-
tion of aggressive fulminant hepatitis or chronic hepatic disease

H Most common in patients with cirrhosis
H In advanced stages, prognosis extremely poor despite
vigorous treatment
H Acute form occurring with acute fulminant hepatic
failure; possibly fatal
H Chronic form occurring with chronic liver disease;
usually reversible
H Also called hepatic coma
Pathophysiology
H Normally, the ammonia produced by protein break-
down in the bowel is metabolized to urea in the liver.

When portal blood shunts past the liver, ammonia directly enters the systemic circulation and is carried
to the brain.
H Such shunting may result from the collateral venous
circulation that develops in portal hypertension or
from surgically created portal-systemic shunts.
H Cirrhosis further compounds this problem because
impaired hepatocellular function prevents conversion of ammonia that reaches the liver.
Causes
H Ammonia intoxication of the brain
Risk factors
H Excessive protein intake
H Sepsis
H Excessive accumulation of nitrogenous body wastes
(from constipation or GI hemorrhage)

H Bacterial action on protein and urea to form ammo-
nia
H Hepatitis
H Diuretic therapy
H Alcoholism
H Fluid and electrolyte imbalance (especially metabolic
alkalosis)
H Hypoxia
H Azotemia
H Impaired glucose metabolism
H Infection
H Use of sedatives, opioids, and general anesthetics
Incidence
H Occurs in about 4 of 100,000 people
H Observed in 70% of patients with cirrhosis
352
H Changes in mental status and personality
H Jaundice
H Muscle tremors
H Fruity breath odor
Complications
H Irreversible coma
H Death
Assessment
History
Prodromal stage
H Slight personality changes, such as agitation, belligerence, disorientation, and forgetfulness
H Difficulty concentrating or thinking clearly
H Fatigue
H Mental changes, such as confusion and disorientation
H Sleep-wake reversal
Impending stage
H Mental changes, such as confusion and disorientation
Stuporous stage
H Marked mental confusion
Comatose stage
H Unable to arouse
Physical findings
Prodromal stage
H Slurred or slowed speech
H Slight tremor
Impending stage
H Tremors that have progressed to asterixis
H Lethargy
H Aberrant behavior
H Apraxia
H Possible incontinence
Stuporous stage
H Drowsy and stuporous
H Noisy and abusive when aroused
H Hyperventilation
H Muscle twitching
H Asterixis
Comatose stage
H Obtunded
H Seizures
H Hyperactive reflexes
H Positive Babinskis sign
H Fetor hepaticus (musty, sweet breath odor)
Test results
Laboratory
H Serum ammonia levels are elevated and, together
with characteristic clinical features, strongly suggest
hepatic encephalopathy.
H Serum bilirubin level is elevated and prothrombin
time is prolonged.
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H EEG shows slowing waves as the disease progresses.
Patient teaching
Treatment
Be sure to cover:
H signs of complications or worsening symptoms
General
H Elimination of underlying cause
H I.V. fluid administration
H Control of GI bleeding
H Life-support measures, if appropriate
H Bowel cleansing
H Limited protein intake
H Nothing by mouth with decreased responsiveness
H Parenteral or enteric feedings, if appropriate
H No alcohol use
Discharge planning
H Refer the patient to social services, as indicated.
Medications
H Lactulose
H Neomycin
H Salt-poor albumin
H Sorbitol-induced catharsis
Surgery
H Possible liver transplant
Key outcomes
The patient will:
H maintain orientation to environment
H Promote rest, comfort, and a quiet atmosphere.
H Use appropriate safety measures to protect the pa-
tient from injury.

H Maintain skin integrity.
Monitoring
H Level of consciousness and neurologic status
H Intake and output
H Weight and abdominal girth
H Signs of anemia, alkalosis, GI bleeding, and infection
H Serum ammonia level
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Hepatitis, nonviral
Overview
Description
H Inflammation of the liver
H Classified as toxic or drug-induced (idiosyncratic)
Pathophysiology
H Hepatocellular damage and necrosis are usually
caused by toxins and is dose-dependent.

H Nonvrial hepatitis occurs primarily in connection
with acetaminophen overdose.
Causes
H Acetaminophen overdose
H Alcohol overuse
H Aspirin and nonsteroidal anti-inflammatory drugs
H Direct hepatotoxicity
H Lack of bile excretion
H Possibly direct hepatotoxicity from hormonal contra-
ceptives or anabolic steroids

H Hypersensitivity to phenothiazine derivatives such as
chlorpromazine
H Statin drugs
H Inhaled anesthetics such as halothane
H Antifungal medications, such as ketoconazole and
amphotericin B
H Herbal supplements, such as cascava, kava, and
ma-huang
H Industrial chemicals such as for cleaning use or
herbicidals
H Antibiotics
H Thyroid medications
H Antidiabetic drugs
H Cytotoxic drugs
H Cholestatic reactions
H Metabolic and autoimmune disorders
H Infectious agents
Incidence
H Can affect males and females (autoimmune affects
females more commonly)
arthralgias, lymphadenopathy, and epigastric or

right upper quadrant pain.
Complications
H Fulminant hepatic failure
H Renal failure
H Liver fibrosis
H Cirrhosis
Assessment
History
H Exposure to causative agent
H Anorexia
H Nausea
H Vomiting
H Possibly abdominal pain
H Pruritus
Physical findings
H Jaundice
H Dark-colored urine
H Hepatomegaly
H Clay-colored stools
Test results
Laboratory
H Serum aspartate aminotransferase and alanine
aminotransferase levels are elevated.
H Total and direct bilirubin (with cholestasis) levels
are elevated.
H Alkaline phosphatase level is elevated.
H White blood cell count is elevated.
H Eosinophil count is elevated (possible in the druginduced type).
H Liver biopsy may help identify the underlying pathology.
Treatment
General
H Removal of causative agent by lavage, catharsis, or
H Nutritious diet and adequate fluid intake

H Clinical features of toxic and drug-induced hepatitis
vary with the severity of liver damage and the causative agent
H Symptoms resemble those of viral hepatitis
hyperventilation, depending on the route of exposure
Medications
H Acetylcysteine (acetaminophen poisoning)
H Corticosteroids (drug-induced hepatitis)
ALERT
Carbon tetrachloride poisoning also produces
headache, dizziness, drowsiness, and vasomotor
collapse; halothane-related hepatitis produces
fever, moderate leukocytosis, and eosinophilia;
chlorpromazine produces a rash, abrupt fever,
354
Hepatitis, nonviral
Key outcomes
The patient will:
H demonstrate an understanding of the disorder and
treatment regimen
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H remain free from complications

Monitoring
H Laboratory values
H Vital signs
H Complications
Patient teaching
Be sure to cover:
H proper handling of cleaning agents and solvents.
Discharge planning
Hepatitis, nonviral
355
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Hepatitis, viral
Overview
Description
H Infection and inflammation of the liver caused by a
virus
H Six types recognized (A, B, C, D, E, and G), and a
seventh suspected
H Marked by hepatic cell destruction, necrosis, and autolysis, leading to anorexia, jaundice, and hepatomegaly
H In most patients, hepatic cells eventually regenerate
with little or no residual damage, allowing recovery
H Complications more likely with old age and serious
underlying disorders
H Prognosis poor if edema and hepatic encephalopathy
develop
Pathophysiology
H Hepatic inflammation caused by virus leads to diffuse
injury and necrosis of hepatocytes.
H Malaise, fatigue
H Dark-colored urine, clay-colored stools
H Fever
H Jaundice
H Nausea; loss of appetite
Complications
H Life-threatening fulminant hepatitis
H Chronic active hepatitis (in hepatitis B)
H Syndrome resembling serum sickness, characterized
by arthralgia or arthritis, rash, and angioedema; can

lead to misdiagnosis of hepatitis B as rheumatoid
arthritis or lupus erythematosus
H Primary liver cancer (in hepatitis B or C)
H In hepatitis D, mild or asymptomatic form of hepatitis B that flares into severe, progressive chronic active hepatitis and cirrhosis
Assessment
History
H Hypertrophy and hyperplasia of Kupffer cells and
H 50% to 60% of people with hepatitis B have no signs
sinusoidal lining cells occurs.

H Bile obstruction may occur.
H 80% of people with hepatitis C have no signs or
Causes
H Revelation of a source of transmission
H Infection with the causative viruses for each of six
Prodromal stage
H Patient easily fatigued, with generalized malaise
H Anorexia, mild weight loss
H Depression
H Headache, photophobia
H Weakness
H Arthralgia, myalgia (hepatitis B)
H Nausea or vomiting
H Changes in the senses of taste and smell
Clinical jaundice stage
H Pruritus
H Abdominal pain or tenderness
H Indigestion
H Anorexia
H Possible jaundice of sclerae, mucous membranes,
and skin
Posticteric stage
H Most symptoms decreasing or subsided
major forms of viral hepatitis

Type A
H Transmittal by the fecal-oral or parenteral route
H Ingestion of contaminated food, milk, or water
Type B
H Transmittal by contact with contaminated human
blood, secretions, and stool
Type C
H Transmittal primarily by sharing of needles by I.V.
drug users, through blood transfusions, or tattoo
needles
Type D
H Found only in patients with an acute or a chronic
episode of hepatitis B
Type E
H Transmittal by parenteral route and commonly waterborne
Type G
H Thought to be blood-borne, with transmission similar to that of hepatitis B and C
Incidence
Hepatitis A
H Approximately 4 new cases per 100,000 annually
H May occur as an epidemic outbreak
Hepatitis B
H Estimated 1.25 million chronically infected Americans
H Highest rate of disease occurs in people ages 20
to 49
Hepatitis C
H Estimated 3.9 million chronically infected Americans
356
Hepatitis, viral
or symptoms
symptoms
Physical findings
Prodromal stage
H Fever (100 to 102 F [37.8 to 38.9 C])
H Dark-colored urine
H Clay-colored stools
Clinical jaundice stage
H Rashes, erythematous patches, or hives
H Abdominal tenderness in the right upper quadrant
H Enlarged and tender liver
H Splenomegaly
H Cervical adenopathy
Posticteric stage
H Decrease in liver enlargement
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Test results
Medications
Laboratory
H In suspected viral hepatitis, hepatitis profile routinely
performed; results identify antibodies specific to the
causative virus and establishing the type of hepatitis:
Type A detection of an antibody to hepatitis A
confirms the diagnosis.
Type B presence of hepatitis B surface antigens
and hepatitis B antibodies confirm the diagnosis.
Type C diagnosis depends on serologic testing
for the specific antibody 1 or more months after
the onset of acute illness; until then, diagnosis is
principally established by obtaining negative test
results for hepatitis A, B, and D.
Type D detection of intrahepatic delta antigens
or immunoglobulin (Ig) M antidelta antigens in
acute disease (or IgM and IgG in chronic disease)
establishes the diagnosis.
Type E detection of hepatitis E antigens supports the diagnosis; however, diagnosis may also
rule out hepatitis C.
Type G detection of hepatitis G ribonucleic acid
supports the diagnosis.
H Additional findings from liver function studies support the diagnosis:
Serum aspartate aminotransferase and serum alanine aminotransferase levels are increased in the
prodromal stage of acute viral hepatitis.
Serum alkaline phosphatase levels are slightly increased.
Serum bilirubin levels are elevated; levels may remain elevated late in the disease, especially with
severe disease.
Prothrombin time (PT) is prolonged. (PT more
than 3 seconds longer than normal, indicates
severe liver damage.)
White blood cell counts commonly reveal transient
neutropenia and lymphopenia followed by lymphocytosis.
H Liver biopsy shows chronic hepatitis.
H Standard immunoglobulin
H Vaccine (hepatitis A and B)
H Alfa-2b interferon (hepatitis B, C, and D)
H Cholestyramine
H Lamivudine (hepatitis B)
H Ribavirin (hepatitis C)
Treatment
General
For hepatitis A
H Supportive care
For hepatitis B
H Supportive care
For hepatitis C
H Aimed at clearing hepatitis C from the body, stopping
or slowing of hepatic damage, and symptom relief
H Symptomatic
H Small, high-calorie, high-protein meals (reduced
protein intake if signs of precoma lethargy, confusion, mental changes develop)
H Parenteral feeding, if appropriate
H Alcohol cessation
H Avoidance of contact sports and strenuous activity
Surgery
H Possible liver transplant (hepatitis C)
Key outcomes
The patient will:
H perform activities of daily living within the confines
of the disease process
regimen.
H Observe standard precautions to prevent transmis-
sion of the disease.

H Provide rest periods throughout the day.
Monitoring
H Daily weight
H Intake and output
H Stool for color, consistency, amount, and frequency
H Signs of complications
Patient teaching
Be sure to cover:
H measures to prevent the spread of disease
H the importance of rest and a proper diet
H the need to abstain from alcohol
H the need to avoid over-the-counter medications unless approved by the physician
H the need for follow-up care.
Discharge planning
H Refer the patient to Alcoholics Anonymous, if indi-
cated.
H Refer the patient to social services as needed.
Hepatitis, viral
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Hereditary hemorrhagic
telangiectasia
Overview
Description
H Inherited vascular disorder of the blood vessels that
can cause excessive bleeding

H Also called Osler-Weber-Rendu disease
Pathophysiology
H Venules and capillaries dilate to form fragile masses
of thin convoluted vessels (telangiectases), resulting

in an abnormal tendency to hemorrhage.
Causes
H Transmitted by autosomal dominant inheritance
Incidence
ecchymoses, and spider hemangiomas of varying size

(see Typical lesions of hereditary hemorrhagic
telangiectasia)
H Clubbing of the digits
Test results
Laboratory
H Platelet count may be abnormal.
H Complete blood count and anemia panel may show
hypochromic, microcytic anemia
H Arterial blood gas analysis shows hypoxia.
Imaging
H Chest X-rays may show lesions in the lungs.
H Echocardiography may show high-output cardiac
failure.
Typical lesions of hereditary

hemorrhagic telangiectasia
The illustrations below show the commonly encountered
lesions of hereditary hemorrhagic telangiectasia.
Dilated capillaries, either flat or raised, appear in localized aggregations, as on the fingers.
H Affects both sexes but may cause less severe bleeding
in females
H Occurs in 5,000 to 10,000 people
H Recurrent epistaxis
H Telangiectases
Complications
H Secondary iron deficiency anemia
H Vascular malformation causing pulmonary arteriove-
nous (AV) fistulas (rare)

H Recurring cerebral embolism and brain abscess
H Hemorrhagic shock
Assessment
History
H Established familial pattern of bleeding disorders
H Epistaxis, hemoptysis, or tarry stools
H Appearance of telangiectasia during late childhood
or adolescence
Physical findings
H Localized aggregations of dilated capillaries on the
skin of the face, ears, tongue, lips, conjunctivae,

scalp, hands, arms, and feet and under the nails
H Characteristic telangiectases: violet, bleed spontaneously, flat or raised, blanch on pressure, and nonpulsatile
H Signs of capillary fragility (may exist without overt
telangiectasia): spontaneous bleeding, petechiae,
358
On the face, spider hemangiomas reflect capillary

fragility.
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H Endoscopy may show bleeding tendency and may
rule out other disorders.

H Bone marrow aspiration shows depleted iron stores
and confirms secondary iron deficiency anemia.
H Genetic testing confirms the disorder in most cases.
Treatment
General
H Supportive therapy, including blood transfusions and
supplemental iron administration

H Ancillary treatment consisting of applying pressure
and topical hemostatic agents to bleeding sites, cauterizing bleeding sites not readily accessible, and
protecting the patient from trauma and unnecessary
bleeding
H Avoidance of activities with the potential for trauma
H Air humidification to keep mucuous membranes
moist
Patient teaching
Be sure to cover:
H the disorder, signs and symptoms, and treatment
H iron supplements, including the importance of following dosage instructions and of taking oral iron
with meals to minimize GI irritation
H a warning that iron turns stools dark green or black
and may cause constipation
H the management of constipation
H the management of minor bleeding episodes, especially recurrent epistaxis
H how to recognize major bleeding episodes that require emergency intervention.
Discharge planning
H Refer the patient for genetic counseling, as appro-
priate.
Medications
H Parenteral iron
H Antipyretics or antihistamines
H Laser treatment to destroy vessel
Other
H Embolization
H Endoscopic procedures to address GI bleeding
Key outcomes
The patient will:
H have laboratory values that return to normal
H demonstrate positive signs of coping
H exhibit no signs or symptoms of infection.
H Administer prescribed blood transfusions.
H Encourage fluid intake if the patient is bleeding or
hypovolemic.
H Provide meticulous skin care and hygiene.
H Use aseptic technique when caring for the patient.
Monitoring
H Vital signs
H Intake and output
H Signs of febrile or allergic transfusion reaction
H Indications of GI bleeding
H Laboratory values to detect possible renal, hepatic,
or respiratory failure
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Hernia, hiatal
Overview
Description
H Defect in the diaphragm that permits a portion of the
stomach to pass through the diaphragmatic opening

into the chest
H Three types: sliding hernia, paraesophageal (rolling)
hernia, and mixed hernia (sliding and rolling hernia)
Esophageal ulceration and perforation

Hemorrhage
Peritonitis
Mediastinitis
Aspiration
Strangulation and gangrene of herniated portion of
stomach
H Iron deficiency anemia
H Chronic cough
H Dysphagia
Assessment
Pathophysiology
History
Sliding hernia
H The muscular collar around the esophageal and diaphragmatic junction loosens.
H Increased intra-abdominal pressure causes the lower
portion of the esophagus and the upper portion of
the stomach to rise into the chest.
Paraesophageal hernia
H The stomach isnt properly anchored below the diaphragm.
H Increased intra-abdominal pressure causes the upper portion of the stomach to slide through the
esophageal hiatus.
H Heartburn 1 to 4 hours after eating; aggravated by re-
Causes
Physical findings
Sliding hernia
H Normal aging
H Secondary to esophageal carcinoma, kyphoscoliosis,
trauma, or surgery
H Diaphragmatic malformations that can cause congenital weakness
H Chronic esophagitis
Paraesophageal hernia
H Not fully understood
H Possibly none
H Dysphagia
Risk factors
H Obesity
H Smoking
H Pregnancy
H Presence of ascites
Incidence
H Sliding hernia 3 to 10 times more common than
paraesophageal and mixed hernias combined

H Increases with age
H 60% of people have hiatal hernias by age 60
H Higher prevalence in females than in males
H Heartburn
Complications
H Incarceration (with paraesophageal hernia)
H In association with gastroesophageal reflux disease:
Esophagitis
360
Hernia, hiatal
clining, belching, or conditions that increase intraabdominal pressure

H Regurgitation or vomiting
H Retrosternal or substernal chest pain (typically after
meals or at bedtime)
H Feeling of fullness after eating
H Feeling of breathlessness or suffocation
H Chest pain resembling angina pectoris
H Reflux
H Chronic cough
H Belching
Test results
Laboratory
H Serum hemoglobin level and hematocrit are decreased in patients with paraesophageal hernia, if
bleeding from esophageal ulceration is present.
H Fecal occult blood test may be positive.
H Analysis of gastric contents may reveal blood.
Imaging
H Chest X-rays reveal an air shadow behind the heart in
a large hernia; lower lobe infiltrates with aspiration.
H Barium swallow with fluoroscopy detects a hiatal
hernia and diaphragmatic abnormalities.
H Endoscopy and biopsy results identify the mucosal
junction and the edge of the diaphragm indenting the
esophagus; differentiate hiatal hernia, varices, erosions, ulcers, Barretts esophagus, and other small
gastroesophageal lesions; and rule out malignant tumors.
H Esophageal motility studies reveal esophageal motor
or lower esophageal pressure abnormalities before
surgical repair of the hernia.
H pH studies identify reflux of gastric contents.
H Acid perfusion (Bernstein) test identifies esophageal
reflux.
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Treatment
Patient teaching
General
Be sure to cover:
H the development of a dietary plan
H the need to sit upright after meals and snacks
H situations or activities that increase intra-abdominal
pressure
H desired drug actions and potential adverse effects
H the need to sleep with the head of the bed elevated
about 6 (15 cm).
H Smoking cessation (smoking stimulates gastric acid
production)
H Six small meals per day
H No fluids or food 1 to 2 hours before bedtime
H Elimination of spicy or irritating foods, alcohol, and
coffee
H Weight reduction, as appropriate
H Upright posture for 2 to 3 hours after eating
H Restriction of activities that increase intra-abdominal
pressure
Medications
H Antacids, such as aluminum hydroxide and calcium
carbonate
Discharge planning
appropriate.
appropriate.
H Histamine-2 receptor antagonists, such as cimeti-
dine, famotidine, and ranitidine

H Anticholinergic agents, such as glycopyrrolate and
hyoscyamine
H Motility agent, such as metoclopramide and
urecholine
H Cough suppressants, such as benzonatate and dex-
tromethorphan
H Proton pump inhibitors, such as omeprazole, lanso-
prazole, and rabeprazole
Surgery
H Hernia repair (rare)
Key outcomes
The patient will:
H show no evidence of aspiration
regimen.
H Prepare the patient for diagnostic tests.
H Teach positional therapy.
H If surgery is necessary, provide appropriate preoper-
ative and postoperative care.
Monitoring
ALERT
After endoscopy, watch for signs of perforation, including decreasing blood pressure, rapid pulse,
shock, and sudden pain.
H Patient response to prescribed antacids and other
drugs
Hernia, hiatal
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Herniated
intervertebral disk
H Paresthesia
H Motor weakness
Overview
H Bowel and bladder dysfunction
Description
H Rupture of fibrocartilaginous material that surrounds
the intervertebral disk, allowing protrusion of the nucleus pulposus

H Results in pressure on spinal nerve roots or spinal
cord that causes back pain and other symptoms of
nerve root irritation
H Most common site for herniation is L4-L5 disk space;
other sites include L5-S1, L2-L3, L3-L4, C6-C7, and
C5-C6
H Clinical manifestations determined by:
Location and size of the herniation into the spinal
canal
Amount of space that exists inside the spinal canal
H Also known as herniated nucleus pulposus, slipped
disk, or ruptured disk
Pathophysiology
Complications
Assessment
History
H Previous traumatic injury or back strain
H Unilateral, lower back pain
H Pain possibly radiating to the buttocks, legs, and feet
H Pain possibly beginning suddenly, subsiding in a few
days, and then recurring at shorter intervals with

progressive intensity
H Sciatic pain beginning as a dull ache in the buttocks,
worsening with Valsalvas maneuver, coughing, sneezing, or bending
H Pain possibly subsiding with rest
H Muscle spasms
H Chronic repetitive injury
H The ligament and posterior capsule of the disk are
Physical findings
usually torn, allowing the nucleus pulposus to extrude, compressing the nerve root.
H Occasionally, the injury tears the entire disk loose,
causing protrusion onto the nerve root or compression of the spinal cord.
H Large amounts of extruded nucleus pulposus or
complete disk herniation of the capsule and nucleus
pulposus may compress the spinal cord.
H Limited ability to bend forward

H Posture favoring the affected side
H Muscle atrophy, in later stages
H Tenderness over the affected region
H Radicular pain with straight-leg raising in lumbar
Causes
H Improper lifting or twisting
H Direct injury
H Degenerative disk disease
Risk factors
H Advanced age
H Congenitally small lumbar spinal canal
H Osteophytes along the vertebrae
H Work environment
Incidence
H About 90% affect lumbar (L) and lumbosacral spine;
8% in cervical (C) spine; 1% to 2% in thoracic (T)

spine
H Lumbar herniation more common in people ages
20 to 45
H Cervical herniation more common in people ages
45 and older
H Herniated disks more common in males than in
females
H Pain
H Limited range of motion (ROM)
362
Herniated intervertebral disk
herniation
H Increased pain with neck movement in cervical her-
niation
H Referred upper trunk pain with cervical neck com-
pression
Test results
Imaging
H X-rays of the spine show degenerative changes.
H Myelography shows the level of the herniation.
H Computed tomography scan shows bone and softtissue abnormalities; can also show spinal canal
compression.
H Magnetic resonance imaging shows soft-tissue abnormalities.
Other
H Electromyography measures muscle response to
nerve stimulation.
H Nerve conduction studies show sensory and motor
loss.
Treatment
General
H Initial treatment conservative and symptomatic, un-
less neurologic impairment progresses rapidly

H Possible traction
H Supportive devices such as a brace
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H Heat or ice applications

H Transcutaneous electrical nerve stimulation
H Chemonucleolysis
H Avoidance of repetitive activity
H Bed rest, initially
H Prescribed exercise program
H Physical therapy
Medications
ibuprofen, ketorolac, and naproxen

H Corticosteroids
H Muscle relaxants, such as methocarbamol, cariso-
prodol, and cyclobenzaprine

H Analgesics, such as codeine, hydromorphone, oxy-
codone, and acetaminophen
Surgery
H Laminectomy
H Spinal fusion
H Microdiskectomy
Key outcomes
The patient will:
H demonstrate adequate joint mobility and ROM
of the disorder
H achieve the highest level of mobility possible
H demonstrate strategies to prevent self-injury.
H Plan a pain-control regimen.
H Offer supportive care.
H Provide encouragement.
H Help the patient cope with chronic pain and im-
paired mobility.
H Include the patient and his family in all phases of his
care.
H Encourage the patient to express his concerns.
H Encourage performance of self-care.
H Help the patient identify activities that promote rest
and relaxation.
H Prepare the patient for myelography, if indicated.
H Periodically remove traction to inspect the skin.
H Prevent deep vein thrombosis.
H Prevent footdrop.
H Ensure a consistent regimen of leg- and back-
ALERT
During conservative treatment, watch for a deterioration in neurologic status, especially during the
first 24 hours after admission, which may indicate
an urgent need for surgery.
After surgery
H Enforce bed rest, as ordered.
H Use the logrolling technique to turn the patient.
H Assist the patient during his first attempt to walk.
H Provide a straight-backed chair for the patient to sit
in, as allowed.
Monitoring
H Vital signs
H Intake and output
H Pain control
H Mobility
H Motor strength
H Deep vein thrombosis
H Bowel and bladder function
After surgery
H Blood drainage system
H Drainage
H Incisions
H Dressings
H Neurovascular status
H Bowel sounds and abdominal distention
Patient teaching
Be sure to cover:
H bed rest
H traction
H heat application
H the exercise program
H myelography, if indicated
H preoperative and postoperative care, if indicated
H proper body mechanics
H skin care.
Discharge planning
H Refer the patient to physical therapy, if indicated.
H Refer the patient to occupational therapy, if indi-
cated.
appropriate.
strengthening exercises.
H Encourage adequate oral fluid intake.
H Encourage coughing and deep-breathing exercises.
H Provide a fracture bedpan for the patient on complete bed rest.
Herniated intervertebral disk
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Herpes simplex
Overview
Description
H Common viral infection that may be latent for years
H After initial herpes simplex virus (HSV) infection, pa-
tient becomes carrier susceptible to recurrent attacks

H Recurrent infections may be provoked by fever,
menses, stress, heat, cold, lack of sleep, sun exposure, and contact with reactivated disease (kissing,
sharing cosmetics, sexual intercourse)
Pathophysiology
H Virus enters mucosal surfaces or abraded skin sites
and initiates replication in cells of the epidermis and

dermis.
H Replication continues to permit infection of sensory
or autonomic nerve endings.
H Virus enters the neuronal cell and is transported
intra-axonally to nerve cell bodies in ganglia (where
the virus establishes latency) and spreads by the peripheral sensory nerves. (See Understanding the
genital herpes cycle.)
Causes
H Type 1 (HSV-1) Herpesvirus hominis transmitted
primarily by contact with oral secretions; mainly affects oral, labial, ocular, or skin tissues
H Type 2 (HSV-2) Herpesvirus hominis transmitted
primarily by contact with genital secretions; mainly
affects genital structures
Incidence
H Occurs worldwide and equally in males and females
H Lower socioeconomic groups infected more com-
monly, probably due to crowded living conditions

H Infection with HSV-1 more common, occurring earli-
er in life than infection with HSV-2
H Fever, malaise, and headache
H Tender inguinal adenopathy
H Typical primary lesions erupting after prodromal tin-
gling and itching

H Ruptured vesicles producing painful ulcers followed
by yellow crusting
Complications
H Primary (or initial) HSV infection during pregnancy
leading to spontaneous abortion, premature labor,

microcephaly, and intra-uterine growth retardation
H Congenital herpes transmitted during vaginal birth,
producing a subclinical neonatal infection or severe
infection with seizures, chorioretinitis, skin vesicles,
and hepatosplenomegaly
H HSV-1 causing life-threatening nonepidemic encephalitis in infants
364
Herpes simplex
H Gingivostomatitis in children ages 1 to 3

H Blindness from ocular infection
H Increased risk for cervical cancer
H Urethral stricture from recurrent genital herpes
H Perianal ulcers
H Colitis
H Esophagitis (more frequent in the impaired host)
H Pneumonitis
H Neurologic disorders
H Uremia with multiple organ involvement
Assessment
History
H Oral, vaginal, or anal sexual contact with an infected
person or other direct contact with lesions

H With recurrent infection, various precipitating factors
identified
Physical findings
Primary perioral HSV
H Sore throat, fever, anorexia, adenopathy
H Increased salivation
H Severe mouth pain, halitosis
H Small vesicles on an erythematous base possibly present on pharyngeal and oral mucosa
Primary genital HSV
H Malaise
H Tender inguinal adenopathy
H Dysuria, leukorrhea
H Dyspareunia
H Fluid-filled vesicles on the cervix, labia, perianal
skin, vulva, and vagina; glans penis, foreskin, and
penile shaft
H Extragenital lesions possibly seen on the mouth or
anus
Primary ocular infection
H Photophobia, excessive tearing
H Follicular conjunctivitis, chemosis
H Blepharitis, vesicles on eyelids
H Lethargy and fever
H Regional adenopathy
Test results
Laboratory
H Tissue culture shows isolation of virus (gold standard).
H Staining of scrapings from the base of the lesion
demonstrate characteristic giant cells or intranuclear
inclusions of herpes virus infection.
H Tissue analysis shows HSV antigens or deoxyribonucleic acid in scrapings from lesions.
Treatment
General
H Symptomatic and supportive therapy
H Ophthalmologist treatment for eye infections
H Avoidance of acidic foods (with stomatitis)
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H Abstinence from sexual activity during active phase
(with genital lesions)
Medications
H Antipyretics and analgesics such as acetominophen
H Anesthetic mouthwashes
H Bicarbonate-based mouth rinse
H Drying agents such as astringents
H Ophthalmic drugs
H Antivirals, such as acyclovir, valacyclovir, and famci-
clovir
Understanding the genital herpes cycle

After a patient is infected with genital herpes, a latency period follows. The virus takes up permanent residence in
the nerve cells surrounding the lesions, and intermittent
viral shedding may take place.
Repeated outbreaks may develop at any time, again followed by a latent stage during which the lesions heal
completely. Outbreaks may recur as often as three to eight
times yearly.
Although the cycle continues indefinitely, some people
remain symptom-free for years.
H Docosanol
INITIAL INFECTION
Highly infectious period marked by fever, aches,
adenopathy, pain, and ulcerated skin
and mucous membranes
Key outcomes
The patient will:
pain
H exhibit no complications related to trauma to oral
mucous membranes
H voice feelings about potential or actual changes in
sexuality.
H Observe standard precautions.
H Encourage the patient to express his feelings, and
provide support.
Monitoring
H Adverse reactions to medications
H Complications
H Lesions
LATENCY
Intermittently infectious period marked by viral domancy
or viral shedding and no disease symptoms
RECURRENT INFECTION
Highly infectious period similar to initial infection with
milder symptoms that resolve faster
Discharge planning
H Refer the patient with an eye infection to an ophthal-
mologist.
H Refer the patient to a support group such as the Her-
pes Resource Center, as appropriate.

H If child abuse is suspected, make a report to local
authorities and social services.
Patient teaching
Be sure to cover:
H the recommended use of lip balm with sunscreen
(with oral lesions)
H instructions to keep lesions dry, except for applying
prescribed topical drugs
H the use of sunscreen to prevent skin-induced recurrences
H the recommendation that sexual partners be
screened for sexually transmitted diseases (with genital herpes)
H for a patient with genital herpes, the recommendation to use warm compresses or take sitz baths several times per day and avoid all sexual contact during
outbreaks of active infection.
Herpes simplex
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Herpes zoster
Overview
H Possibly more prevalent in people who had chicken-
pox at a young age
H Localized vesicular skin lesions, confined to a der-
sal root ganglia that remains in people who have had

chickenpox
H Also called shingles
matome; thoracic, cervical and ophthalmic dermatomes most commonly involved

H Severe neuralgic pain in peripheral areas innervated
by the nerves arising in the inflamed root ganglia
H Pain generally precedes rash by 2 to 3 days
H Lesions pustulate, crust, and heal in 3 to 4 weeks
Pathophysiology
Complications
H Herpes zoster erupts when the virus reactivates after
H Deafness
H Bells palsy
H Secondary skin infection
H Postherpetic neuralgia
H Meningoencephalitis
H Cutaneous dissemination
H Ocular involvement with facial zoster
H Hepatitis
H Pneumonitis
H Peripheral motor weakness
H Cranial nerve syndrome
Description
H Acute unilateral and segmental inflammation of dor-
dormancy in the cerebral ganglia (extramedullary

ganglia of the cranial nerves) or the ganglia of posterior nerve roots.
H The virus may multiply as it reactivates, and antibodies remaining from the initial infection may neutralize it.
H Without opposition from effective antibodies, the
virus continues to multiply in the ganglia, destroys
neurons, and spreads down the sensory nerves to the
skin, causing localized vascular eruptions.
Causes
H Dormant varicella-zoster virus (herpesvirus that also
causes chickenpox) that reactivates
Assessment
Incidence
History
H Most common in adults ages 50 and older

H Bone marrow transplant patients especially at risk
H Typically no history of exposure to others with the
A look at herpes zoster

These characteristic herpes zoster lesions are fluid-filled
vesicles that dry and form scabs after about 10 days. Unilateral vesicular lesions in a dermatomal pattern should
rapidly lead to a diagnosis of herpes zoster.
varicella-zoster virus
H Fever
H Malaise
H Pain that mimics appendicitis
H Pleurisy
H Musculoskeletal pain
H Severe, deep pain
H Pruritus
H Paresthesia or hyperesthesia (usually affecting the
trunk and occasionally the arms and legs)
Physical findings
H Small, red, vesicular skin lesions spread unilaterally
around the thorax or vertically over the arms or legs

H May see vesicles filled with clear fluid or pus
H Vesicles drying, forming scabs or even becoming
gangrenous (see A look at herpes zoster)

H Enlarged regional lymph nodes
Geniculate involvement
H Vesicle formation in the external auditory canal and
ipsilateral facial palsy
H Hearing loss, dizziness, and loss of taste
Trigeminal involvement
H Eye pain
H Corneal and scleral damage and impaired vision
H Conjunctivitis, extraocular weakness, ptosis, and paralytic mydriasis
H Secondary glaucoma
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Herpes zoster
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Test results
Laboratory
H Vesicular fluid and infected tissue analyses show
eosinophilic intranuclear inclusions and varicella
virus.
H Staining antibodies from vesicular fluid and identification under fluorescent light aid differentiation of
herpes zoster from herpes simplex virus.
H Specific antibody immune globulin measurement of
varicella antibodies is elevated.
H Cerebrospinal fluid analysis demonstrates increased
protein levels and, possibly, pleocytosis.
H Lumbar puncture indicates increased pressure.
Treatment
General
H Transcutaneous peripheral nerve stimulation for
postherpetic neuralgia
H Soothing baths
H Cold compresses
Medications
H Lesions
Patient teaching
Be sure to cover:
H the use of a soft toothbrush, eating soft foods, and
using a saline- or bicarbonate-based mouthwash and
oral anesthetics to decrease discomfort from oral lesions
H the need for meticulous hygiene to prevent spreading
infection to other body parts
H that the virus can be transmitted if the blisters break
H the need to avoid scratching lesions
H advice to apply a cold compress if vesicles rupture
H local treatment of vesicles.
Discharge planning
H Refer the patient to an ophthalmologist for ocular in-
volvement.
H Refer the patient to a pain management specialist for
postherpetic neuralgia.
H Antivirals, such as acyclovir, valacyclovir, and fami-
clovir
H Antipruritics, such as hydroxyzine and diphenhy-
dramine
H Analgesics, such as acetominophen and ibuprofen
imipramine
H Systemic antibiotic as appropriate for infecting
organisms
H Corticosteroids, topical and oral, such as betametha-
sone, dexamethasone, and hydrocortisone

H Tranquilizers and sedatives, such as diazepam and
lorazepam
H Patient-controlled analgesia
H Vaccine for at-risk people age 60 or older
Key outcomes
The patient will:
pain
H remain free from complications.
H Maintain meticulous hygiene to prevent spreading the
infection to other parts of the patients body.

H With open lesions, follow contact isolation precau-
tions to prevent the spread of infection.
Monitoring
H Adverse reaction to medications
Herpes zoster
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Hip fracture
Overview
Description
H Break in the head or neck of the femur (usually the
head)
H Most common fall-related injury resulting in hospi-
talization
H Leading cause of disability among older adults
H May permanently change level of functioning and
independence
H Almost 25% of patients die within 1 year after hip
fracture
Pathophysiology
H With bone fracture, the periosteum and blood vessels
in the marrow, cortex, and surrounding soft tissues

are disrupted.
H This results in bleeding from the damaged ends of
the bone and from the neighboring soft tissue.
H Clot formation occurs within the medullary canal, between the fractured bone ends, and beneath the periosteum.
H Bone tissue immediately adjacent to the fracture dies,
and the necrotic tissue causes an intense inflammatory response.
H Vascular tissue invades the fracture area from surrounding soft tissue and marrow cavity within 48
hours, increasing blood flow to the entire bone.
H Bone-forming cells in the periosteum, endosteum,
and marrow are activated to produce subperiosteal
procallus along the outer surface of the shaft and
over the broken ends of the bone.
H Collagen and matrix, which become mineralized to
form callus, are synthesized by osteoblasts within the
procallus.
H During the repair process, remodeling occurs; unnecessary callus is resorbed, and trabeculae are
formed along stress lines.
H New bone, not scar tissue, is formed over the healed
fracture.
Causes
H Falls
H Trauma
H Cancer metastasis
H Osteoporosis
H Skeletal disease
Incidence
H Affects more than 300,000 people each year
H Occurs in one of five females by age 80
H More common in white females
368
Hip fracture
H Impaired function
H Deformity
H Edema
H Muscle spasm
H Pain and tenderness
H Impaired sensation
Complications
H Pneumonia
H Venous thrombosis
H Pressure ulcers
H Social isolation
H Depression
H Bladder dysfunction
H Pulmonary embolus
H Hip dislocation
H Death
Assessment
History
H Falls or trauma to the bones
H Pain in the affected hip and leg
H Pain exacerbated by movement
Physical findings
H Outward rotation of affected extremity
H Affected extremity possibly appearing shorter
H Limited or abnormal range of motion (ROM)
H Edema and discoloration of the surrounding tissue
H In an open fracture, bone protruding through the
skin
Test results
Imaging
H X-rays show the location of the fracture.
H Computed tomography scan shows abnormalities in
complicated fractures.
Treatment
General
H Depends on age, comorbidities, cognitive function-
ing, support systems, and functional ability

H Possible skin traction
H Physical therapy
H Nonweight-bearing transfers
H Foods rich in vitamin A and C, calcium, and protein
H Adequate vitamin D
H Bed rest, initially
H Ambulation as soon as possible after surgery
Medications
H Analgesics, such as butorphanol, meperidine, and
ketorolac initially, then acetaminophen and ibuprofen
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ALERT
H Anticoagulants, such as warfarin, for deep vein
thrombosis prophylaxis
Surgery
H Total hip arthroplasty
H Hemiarthroplasty
H Percutaneous pinning
H Internal fixation using a compression screw and
After surgery, assess the patient for complications,

such as deep vein thrombosis, pulmonary embolus,
and hip dislocation.
Patient teaching
plate
Key outcomes
The patient will:
H identify factors that increase the potential for injury
H maintain muscle strength and tone and joint ROM
H verbalize feelings of increased comfort
the confines of the injury
H Administer prescribed prophylactic anticoagulation
after surgery.
H Maintain traction.
H Maintain proper body alignment.
H Use logrolling techniques to turn the patient in bed.
H Maintain nonweight-bearing status.
H Increase the patients activity level, as prescribed.
H Consult physical therapy as early as possible.
H Assist with active ROM exercises to unaffected limbs.
H Keep the patients skin clean and dry.
H Prevent skin breakdown.
H Encourage good nutrition; offer high-protein, high-
calorie snacks.
H Perform daily wound care.
H Provide antiembolism stockings.
ALERT
Dont massage the patients legs and feet to promote circulation because this could increase the
risk of thromboembolism.
Monitoring
H Vital signs
H Intake and output
H Pain
H Mobility and ROM
H Incision and dressings
H Complications
H Coagulation study results
H Signs of bleeding
H Neurovascular status
H Skin integrity
Be sure to cover:
H ROM exercises
H meticulous skin care
H proper body alignment
H wound care
H signs of infection
H coughing and deep-breathing exercises and incentive
spirometry
H assistive devices
H activity restrictions and lifestyle changes
H safe ambulation practices
H nutritious diet and adequate fluid intake
H decreasing risk for additional injury. (See Preventing hip fracture.)
Discharge planning
H Refer the patient to physical and occupational thera-
py programs, as indicated.
H Refer the patient to home health or intermediate
care.
Prevention
Preventing hip fracture

Hip fractures are debilitating, with only 25% of those
treated making a complete recovery. Its important to discuss prevention, especially with aging patients. Steps that
can be taken to minimize the risk of hip fracture include
the following:
H Obtain a baseline bone density test at menopause to
assess bone status.
H Ensure proper dietary calcium and vitamin D intake and
take supplements as appropriate.
H Perform weight-bearing exercises, such as walking, to
encourage increased bone density, strength, and balance.
H Avoid smoking and excessive alcohol intake which
decrease bone density.
H Take prescribed medication for osteoporosis, such as
alendronate, risedronate, raloxifene, or calcitonin.
H Assess the home environment for fall risks, such as
electrical cords, throw rugs, and unlighted stairs.
H Install grab bars in the bathroom and non-slip mats in
the tub or shower.
H Wear flat, slip-resistant shoes.
H Avoid heavy lifting and climbing on step ladders or
chairs.
H Wear glasses as prescribed and follow-up with routine
vision screenings.
H Be aware of adverse effects of medications that might
cause dizziness or weakness.
Hip fracture
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Hirschsprungs disease
Overview
Description
H Congenital disorder of the large intestine character-
ized by the absence or marked reduction of parasympathetic ganglion cells in the colorectal wall
H Usually coexists with other congenital anomalies,
particularly trisomy 21 and anomalies of the urinary
tract such as megaloureter
H Also called congenital megacolon and congenital
aganglionic megacolon
Pathophysiology
H Parasympathetic ganglion cells in the colorectal wall
are absent or markedly reduced in number.

H The aganglionic bowel segment contracts without the
reciprocal relaxation needed to propel feces forward.

H Impaired intestinal motility causes severe, intractable
constipation.
H Colonic obstruction can ensue, causing bowel dilation and subsequent occlusion of surrounding blood
and lymphatic vessels.
H Ensuing mucosal edema, ischemia, and infarction
draw large amounts of fluid into the bowel, causing
copious amounts of liquid stool.
H Continued infarction and destruction of the mucosa
can lead to infection and sepsis.
H Overflow diarrhea caused by increased water secre-
tion into bowel with bowel obstruction

In children
H Intractable constipation caused by decreased GI
motility
H Abdominal distention caused by retention of stool
H Easily palpated fecal masses caused by retention of
stool
H Wasted extremities (in severe cases) caused by impaired intestinal motility and its effects on nutrition
and intake
H Loss of subcutaneous tissue (in severe cases) caused
by malnutrition
H Large protuberant abdomen caused by retention of
stool and consequent changes in fluid and electrolyte
homeostasis
In adults
H Abdominal distention from decreased bowel motility
and constipation
H Chronic intermittent constipation caused by impaired
intestinal motility
Complications
H Bowel perforation
H Nutritional deficiencies
H Enterocolitis
H Hypovolemic shock
H Sepsis
Assessment
Causes
History
H Familial congenital defect
H Familial history of difficult stool passage

H Failure to pass meconium within the first 24 to 48
Incidence
H Occurs in 1 in 2,000 to 1 in 5,000 live births
H Up to seven times more common in males than in fe-
males (although the aganglionic segment is usually

shorter in males)
H Most prevalent in whites
H Both sexes equally affected by total aganglionosis
H Females with Hirschsprungs disease at higher risk
for having affected children
In neonates
H Failure to pass meconium within 24 to 48 hours because of inability to propel intestinal contents forward
H Bile-stained or fecal vomiting as a result of bowel obstruction
H Abdominal distention caused by to retention of intestinal contents and bowel obstruction
H Irritability caused by resultant abdominal distention
H Feeding difficulties and failure to thrive caused by
retention of intestinal contents and abdominal distention
H Dehydration caused by subsequent feeding difficulties and inability to ingest adequate fluids
370
hours after birth

H Vomiting of bile-stained or fecal contents
H Anorexia
H Nausea
H Lethargy
H Constipation
Physical findings
H Distended abdomen
H Tachypnea
H Rectum without stools
Test results
Imaging
H Barium enema reveals a narrowed segment of distal
colon with a saw-toothed appearance and a funnelshaped segment above it.
H Upright plain abdominal X-rays show marked colonic
distention.
H Rectal biopsy confirms diagnosis by showing the absence of ganglion cells.
H Rectal manometry detects failure of the internal anal
sphincter to relax and contract.
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Treatment
General
H Daily colonic lavage (to empty the infants bowel until
the time of surgery)

H Oral feeding with breast milk or predigested formula
when bowel sounds return (infants)
H that complete continence may take several years to
develop and that constipation may recur at times

H with parents, participation in the childs care as
much as possible, if appropriate.
Discharge planning
H Refer the parents to an enterostomal therapist for
information on ostomy care.
ALERT
Without prompt treatment, an infant with colonic
obstruction may die within 24 hours from enterocolitis that leads to severe diarrhea and hypovolemic shock.
Surgery
H Corrective surgery to pull the normal ganglionic seg-
ment through to the anus (usually delayed until the

infant is at least age 10 months)
H Temporary colostomy or ileostomy to compress the
colon in instances of total bowel obstruction
Key outcomes
The patient will:
H have bowel function return to normal patterns
H maintain fluid balance.
H Maintain fluid and electrolyte balance and prevent
shock.
H Provide adequate nutrition and hydrate with I.V. flu-
ids, as needed.
H Relieve respiratory distress by keeping the patient in
an upright position.
After colostomy or ileostomy
H Place the infant in a heated incubator, with the temperature set at 98 to 99 F (36.7 to 37.2 C), or in
a radiant warmer.
Monitoring
H Vital signs
H Signs of sepsis and enterocolitis
H Intake and output
H Laboratory values
Patient teaching
Be sure to cover:
H recognizing the signs of fluid loss, dehydration, and
enterocolitis
H withholding foods that have increased the number of
stools previously
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Histoplasmosis
Overview
Description
H Fungal infection
H Three forms in the United States
Primary acute histoplasmosis

Progressive disseminated histoplasmosis (acute
disseminated or chronic disseminated disease)
Chronic pulmonary (cavitary) histoplasmosis
H Also known as Ohio Valley disease, Central Mississippi Valley disease, Appalachian Mountain disease, and Darlings disease
Pathophysiology
H Spores reach alveoli and are transformed into bud-
ding forms, carried to regional lymphatics, and then

disseminated throughout the body.
H Intense granulomatous reaction occurs and caseation necrosis or calcification (resembling tuberculosis) occurs.
H Transient dissemination can leave granulomas in the
spleen.
Causes
H Caused by Histoplasma capsulatum, which is found
in the stool of birds and bats and in soil contaminated by their stool (near roosts, chicken coops, barns,
caves, and underneath bridges)
H Transmitted to humans by inhalation of H. capsulatum or H. capsulatum var. duboisii spores or invasion of spores after minor skin trauma
Incidence
H Occurs worldwide, but especially in temperate areas
of Asia, Africa, Europe, and North and South America

H In the United States, most prevalent in southeastern,
mid-Atlantic, and central states

H Primary acute histoplasmosis most common in in-
fants, young children, and immunocompromised

patients
H Incubation period ranges from 3 to 17 days, al-
though chronic pulmonary histoplasmosis may

progress slowly for many years
H Chronic pulmonary infections occur more commonly
in males older than age 40, particularly with a history
of cigarette smoking or chronic lung disease
Complications
H Vascular or bronchial obstruction
H Acute pericarditis
H Pleural effusion
H Mediastinal fibrosis or granuloma
H Intestinal ulceration
372
Histoplasmosis
H Addisons disease
H Endocarditis
H Meningitis
Assessment
History
H Possible history of an immunocompromised condi-
tion
H Exposure to contaminated soil in an endemic area
Physical findings
H Fever, which may rise as high as 105
F (40.6 C)
Primary acute histoplasmosis
H Usually no characteristic signs
H Mild respiratory illness, cough
H Malaise, headache, myalgia, anorexia
H Chest pain
Progressive disseminated histoplasmosis
H Pain
H Hoarseness, tachypnea in later stages
H Ulceration of the oropharynx, dysphagia
H Pallor from anemia
H Jaundice and ascites
H Lymphadenopathy
Chronic pulmonary histoplasmosis
H Productive cough, dyspnea, hemoptysis
H Shortness of breath, cyanosis
H Extreme weakness, weight loss
H Upper lobe fibrocavitary pneumonia
Test results
Laboratory
H Blood cultures done by lysis-centrifugation technique
reveal organism causing the infection.
H In disseminated forms, culture of bone marrow, mucosal lesions, liver, and bronchoalveolar lavage help
show organisms in disseminated histoplasmosis.
H Sputum cultures are preferred in chronic pulmonary
histoplasmosis, may take 2 to 4 weeks to culture, and
show growth of the organism.
H Radioactive assay for histoplasma antigen in blood or
urine shows presence of histoplasma antigen.
Imaging
H Chest X-rays show lung damage.
Treatment
General
H Oxygen for respiratory distress
H Parenteral fluids for dysphagia caused by oral or la-
ryngeal ulcerations
H Smoking cessation
H Cool mist humidifier
H Soft, bland foods (with oropharyngeal ulceration)
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Medications
H Antifungal therapy, such as amphotericin B and
itraconazole
H Glucocorticoids
H Refer the patient with chronic pulmonary or dissemi-
nated histoplasmosis for psychological support to

cope with long-term treatment, if needed.
H Refer the patient to a social worker or an occupational therapist, as needed.
H Help the parents of a child with this disease arrange
for a visiting teacher.
Surgery
H Lung resection to remove pulmonary nodules
H Shunt for increased intracranial pressure
H Cardiac repair for constrictive pericarditis
H Laser surgery (photo coagulation) for ocular
histoplasmosis syndrome
Key outcomes
The patient will:
H be free from pain
H express feelings of increased comfort in maintaining
air exchange
H experience no further weight loss
H Provide oxygen therapy, if needed.
H Plan rest periods.
H Consult with a dietitian and the patient concerning
food preferences.
Monitoring
H Hypoglycemia and hyperglycemia, which indicate
adrenal dysfunction
H Neurologic status
Patient teaching
Be sure to cover:
adverse effects
H cardiac and pulmonary signs that could indicate
effusions
H the need to watch for early signs of this infection and
to seek treatment promptly to help prevent histoplasmosis for people in endemic areas
H the need for patients who risk occupational exposure
to contaminated soil to wear face masks.
Discharge planning
H Stress the need for follow-up care on a regular basis
for at least 1 year.
Histoplasmosis
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Hodgkins disease
Overview
Description
H Neoplastic disorder characterized by painless, pro-
gressive enlargement of lymph nodes, spleen, and

other lymphoid tissue
H With appropriate treatment, 5-year survival rate
about 90%
Pathophysiology
H Enlarged lymphoid tissue results from proliferation
of lymphocytes, histiocytes, eosinophils, and

Reed-Sternberg cells.
H Untreated Hodgkins disease follows a variable but
relentlessly progressive and ultimately fatal course.
Causes
Risk factors
H Enlarged, rubbery lymph nodes in the neck (which
enlarge during periods of fever and then revert to

normal size)
Test results
Laboratory
H Hematologic tests show mild to severe normocytic
anemia, normochromic anemia in 50% of patients,
and elevated, normal, or reduced white blood cell
count and differential show any combination of
neutrophilia, lymphocytopenia, monocytosis, and
eosinophilia.
H Serum alkaline phosphatase levels are elevated, indicating liver or bone involvement.
H Tests must first rule out other disorders that enlarge
the lymph nodes.
H Lymph node biopsy confirms the presence of ReedSternberg cells, abnormal histiocyte proliferation,
and nodular fibrosis and necrosis. Lymph node biopsy is also used to determine lymph node and organ
involvement.
H A staging laparotomy is necessary for patients
younger than age 55 and for those without obvious
stage III or IV disease, lymphocyte predominance
subtype histology, or medical contraindications.
H Genetic factors
H Viral factors
H Environmental factors
Treatment
H For patient with stage I or IIA disease, radiation ther-
General
H Painless swelling of lymph nodes

H Fever, night sweats
H For patient with stage IIB or III disease, radiation
Incidence
H For patient with stage IV disease, chemotherapy
H Occurs in all races; slightly more common in whites

H Peaks in two age-groups: ages 15 to 38 and people
alone (or chemotherapy and radiation therapy to involved sites), sometimes inducing complete remission
H Autologous bone marrow transplantation or autologous peripheral blood sternal transfusions and immunotherapy
older than age 50

H Most common in young adults, except in Japan (ex-
clusively in people older than age 50)

H Greater incidence in males than in females
Complications
H Multiple organ failure
apy alone
therapy and chemotherapy
Medications
Assessment
H Chemotherapy
H Antiemetics, such as prochlorperazine and metoclo-
History
H Sedatives, such as alprazolam and lorazepam

H Antidiarrheals, such as loperamide/simethicone and
H Painless swelling of one of the cervical, axillary, or
inguinal lymph nodes

H Persistent fever and night sweats
H Weight loss despite an adequate diet, with resulting
fatigue and malaise

H Increasing susceptibility to infection
Physical findings
H Edema of the face and neck and jaundice
374
Hodgkins disease
pramide
diphenoxylate/atropine
Key outcomes
The patient will:
H have no further weight loss
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H demonstrate adequate skin integrity
pain.
H Provide a well-balanced, high-calorie, high-protein
diet.
H Provide for periods of rest.
Monitoring
H Pain control
H Lymph node enlargement
H Body temperature
H Fatigue
H Daily weight
Patient teaching
Be sure to cover:
H the importance of maintaining good nutrition
H the pacing of activities to counteract therapy-induced
fatigue
H the importance of good oral hygiene
H the avoidance of crowds and people with known
infection
H the importance of checking the lymph nodes
Discharge planning
Hodgkins disease
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Hookworm disease
Overview
Description
H Infection of the upper intestine caused by Ancy-
lostoma duodenale (found in the Eastern Hemisphere) or Necator americanus (in the Western
Hemisphere)
H Occurs mostly in tropical and subtropical climates
H Also called uncinariasis or ground itch
Pathophysiology
H Disease is transmitted to humans through direct skin
penetration (usually in the foot) by hookworm larvae

in soil contaminated with feces containing hookworm ova.
H These ova develop into infectious larvae in 1 to 3
days.
H The larvae travel through the lymphatics to the pulmonary capillaries, where they penetrate alveoli and
move up the bronchial tree to the trachea and
epiglottis. There they are swallowed and enter the GI
tract.
H When they reach the small intestine, they mature, attach to the jejunal mucosa, and suck blood, oxygen,
and glucose from the intestinal wall.
H These mature worms then deposit ova, which are excreted in the stool, starting the cycle anew. Hookworm larvae mature in about 5 to 6 weeks.
Causes
H Transmission of A. duodenale (found in the Eastern
Hemisphere) or N. americanus (in the Western

Hemisphere)
Incidence
H Affects one billion people worldwide
H More common in whites
H Children more at risk because of playing or walking
barefoot in contaminated soil
H Irritation, pruritus, and edema at the site of entry
H Secondary bacterial infection with pustule formation
H Pneumonitis and hemorrhage with fever, sore throat,
crackles, and cough (larvae in lungs)

H Fatigue, nausea, weight loss, dizziness, melena, and
uncontrolled diarrhea (larvae in intestines)
Complications
H Anemia
H Cardiomegaly
H Heart failure
H Generalized massive edema
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Hookworm disease
Assessment
History
H Recent walking (barefoot) in an area with contami-
nated soil
H Irritation and pruritus at entry site
H Fatigue
H Cough, hoarseness
H Abdominal pain
H Fever
H Nausea
H Weight loss
H Dizziness
H Diarrhea
Physical findings
H Papulovasicular rash
H Crackles (with lung involvement)
H Irregular respirations
H Bloody sputum
H Black, tarry stools
H Edema
Test results
Laboratory
H Stool specimen reveals larvae.
H Hemoglobin level is decreased to as low as 5 to
9 g/dl (in severe case).
H Leukocyte count is increased to as high as 47,000/l.
H Eosinophil count is increased to as high as 500 to
700/l.
Treatment
General
H Blood transfusions (if anemia severe)
H Nutritious high-protein, high-iron diet
H Activity, as tolerated, with frequent rest periods
Medications
H Mebendazole
H Pyrantel pamoate
H Albendazole
H Iron supplements
H Topical thiabendazole (cutaneous larva migrans)
Key outcomes
The patient will:
H report having increased energy levels
H have decreased episodes of diarrhea
H maintain a normal respiratory rate.
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H Isolate the incontinent patient.
H Teach proper hand-washing technique.
H For severe anemia, administer oxygen, as ordered.
H Allow frequent rest periods.
H Reposition frequently.
H Assess family members for symptoms.
Monitoring
H Intake and output
H Quantity and frequency of stools
H Daily weight
H Skin integrity
Patient teaching
Be sure to cover:
H the need to wear shoes when outdoors
H nutritious diet
H proper hygiene after toileting
H use of prescribed iron supplements and how this
treatment affects stools
H the need to start another course of treatment if stool
examination remains positive for larvae
adverse effects.
Hookworm disease
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Human papillomavirus
H More than 50% of sexually active people becoming
infected during their lifetimes

H About 80% of females infected by age 50
Overview
Description
H Sexually transmitted disease (STD)
H Group of viruses with more than 100 different strains
H About 30 types spread through sexual contact
H Low-risk and high-risk types
H Primarily infects genital area; mouth and throat pos-
sible but rare
H Most infected individuals having no symptoms and
clearing the infection on their own

H Symptoms (if they develop) that occur 2 to 3 months
after infection; possibly developing as early as 3

weeks and as late as many years after infection
H For 90% of females, cervical HPV infection becoming
undetectable within 2 years
H Causes benign papillomas (warts)

H Affects both sexes
Complications
Pathophysiology
H Pregnant females passing HPV to neonate during
H Human papillomavirus is very contagious.

H It may produce proteins that interfere with cell func-
H Large vaginal papillomas that cause excessive bleed-
tions that normally prevent excessive cell growth.

H Its contracted during oral, vaginal, or anal sex with
an infected person.
H High-risk HPV possibly leading to cancer of the
mouth, cervix, vulva, vagina, anus, or penis

vaginal delivery (rare)
ing with vaginal birth
H Associated with an increased risk of anal cancer in
males receiving anal sex
H About two-thirds of those who have sexual contact
with an infected person develop papillomas, usually

within 3 months of contact.
Papillomas can be single or multiple cauliflowerlike growths or may be flat and white or barely visible areas commonly producing no symptoms.
These growths affect the penis, scrotum, vulva,
anus, and the linings of the vagina, cervix, or rectum.
H Initial growths may spread to other areas of the genitals or to the anal area.
Assessment
Causes
Physical findings
H Human papillomavirus (HPV)

H HPV 6 and HPV 11
H Genital warts
History
H Sexual partner with HPV or genital warts
H May exhibit no signs or symptoms
H Possible discharge from the vagina or penis
H Previous STD
H Abnormal Papanicolaou (Pap) test
Low-risk viruses
Most commonly associated with genital warts
Cause most visible genital warts
H HPV 16 and HPV 18
Most common high-risk viruses
Growths usually flat and nearly invisible
Majority resolving on their own
Soft, moist, pink, or flesh-colored swellings

Raised or flat; possibly cauliflower-shaped
Individual or grouped
Small or large
Location: groin, thigh, vulva, vagina, anus, urethra,
cervix, penis, or scrotum
H HPV 16 and HPV 18: no visible genital warts
H Patient possibly unaware of warts
Risk factors
Test results
H Impaired immune system

H Partner with multiple sex partners or HPV-infected
Genital warts are typically diagnosed by visual inspection.

Laboratory
H Pap tests (most common means of diagnosis for females) are abnormal.
H Confirmatory follow-up test for HPV deoxyribonucleic acid can identify 13 of the high-risk types of HPV
associated with the development of cervical cancer.
H No testing is available for males.
sex partners
H Possibly, uncircumcised males
H Sexual activity before age 18
H Unprotected sexual contact
Incidence
H About 20 million people currently infected
H About 6.2 million new infections in United States
each year
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Treatment
Patient teaching
General
Be sure to cover:
H need to inform sexual partners about the risk of
genital warts
H need for regular Pap testing and careful medical
follow-up
H reasons for not using nonprescription wart removal
products
H use of female condoms
H limitations of male and female condoms
H that podophyllin and fluorouracil cream cant be
used during pregnancy
H availability of HPV vaccine, Gardasil, which blocks
HPV 6, 11, 16, and 18, recommended for females
ages 9 to 26 before first sexual contact.
H No cure for HPV infection; wart removal doesnt
eliminate infection or communicability

H Geared toward warts and precancerous cervical
changes
H Genital warts possibly disappearing without treatment
H 20% to 50% of people experiencing recurrence of
warts
H Treatment varying based on size and location of
warts; can be painful and may cause scarring
Medications
H Topical, applied by physician, such as podophyllin
resin, trichloroacetic acid, and fluorouracil cream

H Interferon injection into wart
H Topical, prescriptions applied at home, such as im-
iquimod cream and podofilox lotion or gel
Surgery
H Cryosurgery
H Electrocautery
H Laser treatment
H Surgical excision
H Loop electrosurgical excision procedure
Key outcomes
The patient will:
H verbalize an understanding of the disease
H remain free from complications
H express feelings of comfort after treatment
H communicate feelings about changes in body image
H voice feelings about the need for changes in sexual
activity.
H Use standard precautions when theres a risk of con-
tact with genital secretions.

H Administer pain medication as ordered.
H Provide a nonthreatening, nonjudgmental atmo-
sphere that encourages the patient to verbalize feelings about perceived changes in sexual identity and
behavior.
Monitoring
H Sites treated with topical medication
H Surgical sites
H Pap test results
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Huntingtons disease
Overview
Description
H Degenerative disease of the brain causing dementia
H Death usually 10 to 15 years after onset
H Also called Huntingtons chorea, hereditary chorea,
chronic progressive chorea, and adult chorea
Pathophysiology
H Degeneration in the cerebral cortex and basal gan-
glia leads to chronic progressive chorea (dancelike

movements).
H The final stage is mental deterioration, which ends in
dementia.
Causes
H Genetic link
H Transmitted as autosomal dominant trait (either sex
can transmit and inherit it)
Incidence
H 2% of cases in children
H 5% of cases as late as age 60
H Each child of a parent with this disease: 50% chance
of inheritance
H Cant be passed on by child who doesnt inherit it
H Chorea
H Emotional changes, irritability
H Clumsiness, bradykinesia
H Incontinence
H Increased appetite
H Bouts of anger
H Purposeless movements
H Grimacing
H Dysarthria
H Writhing and twitching
H Loss of motor control; rigidity
H Dysphagia
H Oral apraxia, aprosody
Assessment
History
Findings vary depending on disease progression.
H Familial history
H Emotional and mental changes
H Insidious onset
H Total dependency through:
Intellectual decline
Emotional disturbances
Loss of musculoskeletal control
H Described as clumsy, irritable, or impatient
H Subject to fits of anger
H Periods of suicidal depression, apathy, or elation
H Ravenous appetite, especially for sweets
H Loss of bladder and bowel control in later stages
Physical findings
H Choreic movements
H Rapid, usually violent, and purposeless movements
H Cognitive decline
Early stages
H Mild fidgeting
H Grimacing, tongue smacking
H Dysarthria
H Athetoid movements related to emotional state
H Torticollis
H Deficits in short-term memory
Later stages
H Constant writhing and twitching
H Unintelligible speech
H Ambulation impossible
H Appears emaciated and exhausted
Test results
Laboratory
H Deoxyribonucleic acid analysis may show disease.
Imaging
H Positron-emission tomography may show disease.
H Magnetic resonance imaging shows characteristic
butterfly dilation of the brains lateral ventricles.
H Computed tomography scan shows brain atrophy.
Treatment
Complications
General
H Choking and aspiration

H Pneumonia
H Heart failure
H Infections
H Suicide
H No known cure
H Supportive and symptomatic treatment
H Psychotherapy
H Possibly soft diet
H Safety measures
H Electroconvulsive therapy
Medications
H Tranquilizers such as clonazepam
H Dopamine agonists such as haloperidol
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Huntingtons disease
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H Neuroleptics, such as chlorpromazine and tetra-
benazine
H Selective serotonin reuptake inhibitors, such as flu-
oxetine and sertraline

H Tricyclic antidepressants, such as nortriptyline and
imipramine
Key outcomes
The patient will:
H maintain a patent airway without evidence of aspiration
H develop alternative means of communication to
express self.
H Identify self-care deficits.
H Encourage the patient to be independent.
H Provide communication aids.
H Help the patient with difficulty walking.
H Maintain a turning schedule.
H Elevate the head of the bed during eating.
H Protect the patient from infections.
Monitoring
H Response to prescribed drugs
H Possible suicide ideation
H Temperature
H White blood cell count
Patient teaching
Be sure to cover:
H aspiration precautions
H communication strategies.
Discharge planning
H Refer the patient to the Huntingtons Disease Society
of America.
H Refer the patient to appropriate community organiza-
tions.
H Refer the family for genetic counseling.
H Refer the patient for psychotherapy, as appropriate.
Huntingtons disease
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Hydrocele
Overview
Description
H A collection of fluid between the visceral and parietal
layers of the testicles tunica vaginalis or along the

spermatic cord
H The most common cause of scrotal swelling
H Described as communicating or noncommunicating
Pathophysiology
Communicating
H A patency between the scrotal sac and the peritoneal
cavity allows peritoneal fluids to collect in the scrotum.
Noncommunicating
H Fluid accumulation may be caused by infection, trauma, tumor, an imbalance between the secreting and
absorptive capacities of scrotal tissue, or an obstruction of lymphatic or venous drainage in the spermatic
cord.
H This leads to a displacement of fluid in the scrotum,
outside the testes.
H Subsequent swelling results, leading to reduced
blood flow to the testes.
Causes
Physical findings
H Soft, nontender fullness within the hemiscrotum
H Transillumination of the scrotum revealing a ho-
mogenous glow without internal shadows
Test results
Imaging
H Abdominal X-rays distinguish acute hydrocele from
an incarcerated hernia.
H Ultrasound distinguishes spermatoceles from hydroceles and identifies torsion or tumor.
Other
H Transillumination to distinguish fluid-filled from solid mass (a tumor doesnt transilluminate).
Treatment
General
H Frequently resolves spontaneously
H Scrotal elevation
H Postoperatively avoidance of vigorous activity for
short time
Medications
ibuprofen and naproxen

H Nonopioid analgesics, such as acetaminophen, as-
H Congenital malformation (infants)

H Trauma to the testes or epididymis
H Infection of the testes or epididymis
H Testicular tumor
Surgery
Incidence
H Surgical repair to avoid strangulation of the bowel
H Apparent in 6% of full-term male neonates

H Incidence in adult males unknown
H Aspiration of fluid and injection of sclerosing drug
H Scrotal swelling and feeling of heaviness
H Inguinal hernia (commonly present in congenital
hydrocele)
pirin, and diflunisal

H Operative exploration if underlying pathology sus-
pected
(inguinal hernia with bowel present in the sac)
into the scrotal sac for a tense hydrocele impeding
blood circulation or causes pain
H Excision of tunica vaginalis for recurrent hydroceles
H Suprainguinal excision for testicular tumor detected
by ultrasound
H Size varying from slightly larger than the testes to the
size of a grapefruit or larger

H Fluid collection with either flaccid or tense mass
H Pain with acute epididymal infection or testicular
torsion
H Scrotal tenderness due to severe swelling
Complications
H Epididymitis
Assessment
History
H Scrotal tenderness
H Inguinal hernia
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Hydrocele
Key outcomes
The patient (or his parents) will:
H express feeling or demonstrate behavior of comfort
and relief from pain
H express understanding of disorder, diagnosis, and
treatment.
H Place a rolled towel between the patients legs and el-
evate the scrotum to help reduce severe swelling.

H Apply heat or ice packs to the scrotum.
H Provide preoperative teaching.
H Provide postoperative wound care, if appropriate.
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Monitoring
H Swelling
H Worsening of condition
Patient teaching
Be sure to cover:
H the need to wear a loose-fitting athletic supporter
lined with soft cotton dressings
H how to take a sitz bath
H the need to avoid tub baths postoperaively for 5 to
7 days
H the possibility that the hydrocele may reaccumulate
for 1 month postoperatively because of edema.
Discharge planning
H Follow-up visits may be required biweekly, monthly,
or every 2 to 3 months, depending on recovery rate.
Hydrocele
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Hydrocephalus
Overview
Description
H A variety of conditions characterized by an excess of
fluid within the cranial vault, subarachnoid space, or

both
H Occurs because of interference with cerebrospinal
fluid (CSF) flow caused by increased fluid production, obstruction within the ventricular system, or defective reabsorption of CSF
H Types include:
Noncommunicating hydrocephalus: obstruction
within the ventricular system
Communicating hydrocephalus: impaired absorption of CSF
H Enlargement of head clearly disproportionate to
growth
H Distended scalp veins
H Thin, shiny, fragile-looking scalp skin
H Underdeveloped neck muscles
H Depressed orbital roof
H Downward displacement of eyes
H High-pitched, shrill cry; irritability
H Projectile vomiting
H Skull widening
Complications
H Impaired motor function
H Vision loss
H Death (increased intracranial pressure [ICP])
H Infection and malnutrition (more common in
infants)
Assessment
Pathophysiology
History
H The obstruction of CSF flow associated with hydro-
Infants
H History that may disclose cause
H High-pitched, shrill cry; irritability
H Anorexia
H Episodes of projectile vomiting
Adults and older children
H Frontal headaches
H Nausea and vomiting (may be projectile)
H Symptoms causing wakening or occurring on awakening
H Diplopia
H Restlessness
cephalus produces dilation of the ventricles proximal

to the obstruction.
H The obstructed CSF is under pressure, causing atrophy of the cerebral cortex and degeneration of the
white matter tracts, with selective preservation of
gray matter.
H When excess CSF fills a defect caused by atrophy, a
degenerative disorder, or a surgical excision, the fluid isnt under pressure, and atrophy and degenerative changes arent induced.
Causes
Noncommunicating hydrocephalus
H Congenital abnormalities in the ventricular system
H Mass lesions such as a tumor that compresses one of
the structures of the ventricular system
H Aqueduct stenosis
H Arnold-Chiari malformation
Communicating hydrocephalus
H Adhesions from inflammation, such as with meningitis or subarachnoid hemorrhage
H Compression of the subarachnoid space by a mass
such as a tumor
H Congenital abnormalities of the subarachnoid space
H High venous pressure within the sagittal sinus
H Head injury
H Cerebral atrophy
Incidence
H Rare cases of congenital hydrocephalus
H Noncommunicating hydrocephalus more common in
children
H Communicating hydrocephalus more common in
adults
384
Hydrocephalus
Physical findings
Infants
H Enlarged head clearly disproportionate to the infants
growth
H Head possibly appearing normal in size with bulging
fontanels
H Distended scalp veins
H Thin, fragile, and shiny scalp skin
H Underdeveloped neck muscles
H Depression of the roof of the eye orbit
H Displacement of the eyes downward
H Prominent sclera (sunset sign)
H Abnormal leg muscle tone
Adults and older children
H Decreased level of consciousness (LOC)
H Ataxia
H Impaired intellect
H Incontinence
H Signs of increased ICP
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Test results
Monitoring
Imaging
H Skull X-rays show thinning of the skull with separation of sutures and widening of the fontanels in infants.
H Angiography, computed tomography scan, and magnetic resonance imaging show differentiation between hydrocephalus and intracranial lesions and
Arnold-Chiari deformity.
H Fontanels for tension or fullness

H Head circumference
H Signs and symptoms of increased ICP
H Complications
H Neurologic status
H Intake and output
Treatment
General
After surgery
H Signs and symptoms of meningitis
H Redness, swelling, and other signs and symptoms of
local infection
H Dressing for drainage
H Response to analgesics
H Shunting of CSF directly from the ventricular system
to some point beyond the obstruction

H Small, frequent feedings
H Slow feeding of infant
H Decreased movement during and immediately after
ALERT
Monitor the patient for vomiting, which may be an
early sign of shunt malfunction.
meals
Medications
Patient teaching
H Possible preoperative and postoperative antibiotics
Surgery
H Surgical correction (the only treatment for hydro-
cephalus):
Removal of obstruction to CSF flow
Implantation of a ventriculoperitoneal shunt to divert CSF flow from the brains lateral ventricle into
the peritoneal cavity
With concurrent abdominal problem, ventriculoatrial shunt to divert CSF flow from the brains lateral ventricle into the right atrium of the heart
Key outcomes
Be sure to cover:
H shunt surgery: hair loss and the visibility of a mechanical device
H postoperative shunt care
H signs and symptoms of increased ICP or shunt malfunction
H signs and symptoms of paralytic ileus
H the need for periodic shunt surgery to lengthen the
shunt as the child grows older.
Discharge planning
H Refer the patient to special education programs, as
appropriate.
The patient will:

H develop no signs and symptoms of infection
H maintain and improve current LOC
H develop no signs and symptoms of increased ICP.
H Elevate the head of the bed to 30 degrees or put an
infant in an infant seat.

H Administer prescribed oxygen, as needed.
H Provide small, frequent feedings.
H Decrease the patients movement during and immedi-
ately after meals.

After shunt surgery

H Place the patient on the side opposite the operative
site.
H Administer prescribed I.V. fluids.
Hydrocephalus
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Hydronephrosis
Overview
Description
H Abnormal dilation of the renal pelvis and calyces of
one or both kidneys

H Caused by obstruction of urine flow in the genitouri-
nary tract
Pathophysiology
H With obstruction in the urethra or bladder, hydro-
nephrosis is usually bilateral.

H With obstruction in a ureter, hydronephrosis is usu-
ally unilateral.
H Obstructions distal to the bladder cause the bladder
to dilate, acting as a buffer zone, delaying hydronephrosis.

H Total obstruction of urine flow with dilation of the
collecting system ultimately causes complete cortical
atrophy and glomerular filtration ceases.
Causes
H Benign prostatic hyperplasia (BPH)
H Urethral strictures
H Renal calculi
H Strictures or stenosis of the ureter or bladder outlet
H Congenital abnormalities
H Bladder, ureteral, or pelvic tumors
H Blood clots
H Neurogenic bladder
H Ureterocele
H Tuberculosis
H Gram-negative infection
Incidence
H About 1 in 100 people affected by unilateral hydro-
nephrosis
H About 1 in 200 people affected by bilateral hydro-
nephrosis
H Flank pain
Complications
H Renal calculi
H Sepsis
H Renovascular hypertension
H Obstructive nephropathy
H Infection
H Pyelonephritis
H Paralytic ileus
H Renal failure
386
Hydronephrosis
Assessment
History
H Possibly no initial symptoms, but increasing pressure
behind the obstruction eventually resulting in renal

dysfunction
H Varies depending on cause of obstruction
H No symptoms or complaint of only mild pain and
slightly decreased urine flow
H Severe, colicky renal pain or dull flank pain that radiates to the groin
H Hematuria
H Pyuria
H Dysuria
H Alternating oliguria and polyuria, anuria
H Nausea
H Vomiting
H Abdominal fullness
H Pain on urination
H Dribbling
H Urinary hesitancy
H Change in voiding pattern
Physical findings
H Hematuria
H Pyuria
H Urinary tract infection
H Palpable kidney
H Lower extremity edema
H Distended bladder
H Costovertebral angle tenderness
Test results
Laboratory
H Renal function study results are abnormal.
H Urine studies confirm inability to concentrate urine,
glomerular filtration rate is decreased, and pyuria
occurs if infection is present.
H Leukocytosis indicates infection.
Imaging
H Excretory urography, retrograde pyelography, and renal ultrasonography confirm diagnosis.
H I.V. urogram may show site of obstruction.
H Nephrogram may show delayed appearance time.
H Radionuclide scan may show site of obstruction.
H Computed tomography scan may indicate cause.
Treatment
General
H For inoperable obstructions, decompression and
drainage of the kidney, using a nephrostomy tube

placed temporarily or permanently in the renal pelvis
H If renal function affected, low-protein, low-sodium,
and low-potassium diet
H Urinary catheterization
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Medications
H Antibiotic therapy as appropriate for infecting
organism
H Analgesics
H Oral alkalinization therapy (for uric acid calculi)
such as allopurinol
H Steroid therapy (for retroperitoneal fibrosis)
Surgery
H Dilatation for urethral stricture
H Prostatectomy for BPH
H Placement of percutaneous nephrostomy tube
Key outcomes
The patient will:
H avoid or have minimized complications
H demonstrate skill in managing urinary elimination.
H Allow the patient to express his fears and anxieties.
Monitoring
H Intake and output
H Vital signs
H Fluid and electrolyte status
H Nephrostomy tube function and drainage, if appro-
priate
H Wound site (postoperatively)
Patient teaching
Be sure to cover:
H the procedure and postoperative care, if surgery is
scheduled
H nephrostomy tube care, if appropriate
H dietary changes
H hydronephrosis symptom recognition and reporting.
Discharge planning
H Follow-up imaging studies may be required to evalu-
ate recovery.
H Follow-up laboratory studies may be needed to as-
sess renal function.
Hydronephrosis
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Hyperaldosteronism
Overview
Description
H Hypersecretion of the mineralocorticoid aldosterone
by the adrenal cortex

H Causes excessive reabsorption of sodium and water
H Fatigue
H Headache
H Paresthesia
H Possibly tetany (resulting from metabolic alkalosis)
Complications
H Neuromuscular irritability, tetany, paresthesia
H Seizures
H Left ventricular hypertrophy, heart failure, death
H Metabolic alkalosis, nephropathy, azotemia
and excessive renal excretion of potassium

H May be primary (uncommon) or secondary
Pathophysiology
In primary hyperaldosteronism
(Conns syndrome)
H Chronic excessive secretion of aldosterone is independent of the renin-angiotensin system and suppresses plasma renin activity.
H This aldosterone excess enhances sodium and water
reabsorption and potassium loss by the kidneys,
which leads to mild hypernatremia and, simultaneously, hypokalemia and increased extracellular fluid
volume.
H Expansion of intravascular fluid volume also occurs
and results in volume-dependent hypertension and
increased cardiac output.
ALERT
Excessive ingestion of English black licorice or
licorice-like substances can produce a syndrome
similar to primary hyperaldosteronism because of
the mineralocorticoid action of glycyrrhizic acid.
In secondary hyperaldosteronism
H Secondary hyperaldosteronism results from an extraadrenal abnormality that stimulates the adrenal gland
to increase aldosterone production.
Causes
H Benign aldosterone-producing adrenal adenoma (in
70% of patients)
H Bilateral adrenocortical hyperplasia (in children) or
carcinoma (rarely)
H Conditions that reduce renal blood flow and extracel-
lular fluid volume (renal artery stenosis)

H Conditions that produce a sodium deficit (Wilms
tumor)
H Nephrotic syndrome
H Bartters syndrome
H Hepatic cirrhosis with ascites
H Heart failure
Assessment
History
H Nocturnal polyuria
H Polydipsia
H Fatigue
H Headaches
Physical findings
H Muscle weakness
H Intermittent, flaccid paralysis
H Paresthesia
H High blood pressure
Test results
Laboratory
H Serum potassium levels are persistently low.
H Plasma renin level is low and fails to increase appropriately during volume depletion (upright posture,
sodium depletion) and plasma aldosterone level is
high during volume expansion by salt loading (confirm primary hyperaldosteronism in a hypertensive
patient without edema).
H Serum bicarbonate level is elevated.
H Urine aldosterone levels are markedly increased.
H Plasma aldosterone levels are increased.
H Plasma renin levels are increased (secondary).
H Suppression test differentiates between primary and
secondary hyperaldosteronism.
Imaging
H Chest X-rays show left ventricular hypertrophy caused
by chronic hypertension.
H Adrenal angiography or computed tomography scan
localizes tumor.
H Electrocardiography shows signs of hypokalemia
(ST-segment depression and U waves).
Treatment
Incidence
General
H Three times more common in females than in males

H Treatment of underlying cause (secondary)

H Low-sodium, high-potassium diet
H Muscle weakness
H Intermittent, flaccid paralysis
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Medications
H Potassium-sparing diuretics (primary) such as
spironolactone
Surgery
H Unilateral adrenalectomy (primary)
Key outcomes
The patient will:
H express understanding of the condition and treatment modalities.
H Watch for signs of tetany (muscle twitching,
Chvosteks sign, Trousseaus sign).

H Administer potassium replacement, and keep I.V. cal-
cium gluconate available.

H After adrenalectomy, watch for weakness, hypona-
tremia, rising serum potassium levels, and signs of

adrenal hypofunction, especially hypotension.
Monitoring
H Intake and output
H Vital signs
H Weight
Patient teaching
Be sure to cover:
H adverse effects of spironolactone, including hyperkalemia, impotence, and gynecomastia, if appropriate
H the importance of wearing medical identification
jewelry while taking steroid hormone replacement
therapy.
Hyperaldosteronism
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Hyperbilirubinemia,
unconjugated
Overview
Description
H Excessive serum bilirubin levels and mild jaundice
H The result of hemolytic processes in the neonate
H Can be physiologic (with jaundice the only symptom)
or pathologic (resulting from an underlying disease)

H Also called neonatal jaundice
Pathophysiology
H As erythrocytes break down at the end of their neo-
natal life cycle, hemoglobin separates into globin

(protein) and heme (iron) fragments.
Causes of hyperbilirubinemia
The infants age at onset of hyperbilirubinemia may provide clues as to the sources of this jaundice-causing disorder.
Day 1
H Blood type incompatibility (Rh, ABO, other minor blood

groups)
H Intrauterine infection (rubella, cytomegalic inclusion
body disease, toxoplasmosis, syphilis and, occasionally, bacteria such as Escherichia coli, Staphylococcus,
Pseudomonas, Klebsiella, Proteus, and Streptococcus)
Day 2 or 3
H Infection (usually from gram-negative bacteria)

H Polycythemia
H Enclosed hemorrhage (skin bruises, subdural
hematoma)
H Respiratory distress syndrome (hyaline membrane disease)
H Heinz body anemia from drugs and toxins (vitamin K3,
sodium nitrate)
H Transient neonatal hyperbilirubinemia
H Abnormal red blood cell morphology
H Red cell enzyme deficiencies (glucose-6-phosphate
dehydrogenase, hexokinase)
H Physiologic jaundice
H Blood group incompatibilities
Days 4 and 5
H Breast-feeding, respiratory distress syndrome, maternal diabetes

H Crigler-Najjar syndrome (congenital nonhemolytic
icterus)
H Gilbert syndrome
Day 7 and later
H Herpes simplex
H Pyloric stenosis
H Hypothyroidism
H Neonatal giant cell hepatitis
H Infection (usually acquired in neonatal period)
H Bile duct atresia
H Galactosemia
H Choledochal cysts.
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Hyperbilirubinemia, unconjugated
H Heme fragments form unconjugated (indirect)
bilirubin, which binds with albumin for transport to

liver cells to conjugate with glucuronide, forming direct bilirubin.
H Because unconjugated bilirubin is fat-soluble and
cant be excreted in the urine or bile, it may escape
to extravascular tissue, especially fatty tissue and the
brain, resulting in hyperbilirubinemia.
H Hyperbilirubinemia may develop when:
certain factors disrupt conjugation and usurp
albumin-binding sites, including drugs (such as
aspirin, tranquilizers, and sulfonamides) and
conditions (such as hypothermia, anoxia, hypoglycemia, and hypoalbuminemia)
decreased hepatic function results in reduced
bilirubin conjugation
increased erythrocyte production or breakdown
results from hemolytic disorders or Rh or ABO incompatibility
biliary obstruction or hepatitis results in blockage
of normal bile flow
maternal enzymes present in breast milk inhibit
the infants glucuronyl-transferase conjugating
activity.
Causes
See Causes of hyperbilirubinemia.
Incidence
H Common in neonates
H Less common in Black infants than in White infants
H Jaundice
Complications
H Kernicterus
H Cerebral palsy
H Epilepsy
Assessment
History
H Previous sibling with neonatal jaundice
H Familial history of anemia, bile stones, splenectomy,
liver disease
H Maternal illness suggestive of viral or other infection
H Maternal drug intake
H Delayed cord clamping
H Birth trauma with bruising
Physical findings
H Yellowish skin, particularly in the sclerae
Test results
Laboratory
H Serum bilirubin levels are elevated.
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Treatment
General
H Phototherapy
H Exchange transfusions
Medications
H Albumin
H Phenobarbital (rarely used)
H Rh (D) immune globulin (human) (to Rh-negative
o
mother)
Key outcomes
The patient will:
H exhibit normal body temperature
H maintain normal fluid balance
H have a reduced bilirubin level.
H Reassure parents that most infants experience some
degree of jaundice.
H Keep emergency equipment available when transfus-
ing blood.
H Administer Rh
o(D) immune globulin (human), to an

Rh-negative mother after amniocentesis, or to
prevent hemolytic disease in subsequent infants to
an Rh-negative mother during the third trimester, after the birth of an Rh-positive infant, or after spontaneous or elective abortion.
Monitoring
H Jaundice
H Bilirubin levels
H Body temperature
H Intake and output
H Bleeding and complications
Patient teaching
Be sure to cover:
H that the infants stool contains some bile and may be
greenish.
Hyperbilirubinemia, unconjugated
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Hypercalcemia
Overview
Description
H Excessive levels of serum calcium
Pathophysiology
H Together with phosphorus, calcium is responsible for
the formation and structure of bones and teeth.

H Calcium helps to maintain cell structure and func-
tion.
H It plays a role in cell membrane permeability and impulse transmission.
H It affects the contraction of cardiac muscle, smooth
muscle, and skeletal muscle.
H It participates in the blood-clotting process.
H Hypercalcemia leads to multiple-organ system dysfunction.
Causes
H Anorexia
H Constipation
H Nausea, vomiting
H Polyuria
Physical findings
H Confusion
H Muscle weakness
H Hyporeflexia
H Decreased muscle tone
Test results
Laboratory
H Serum calcium levels are greater than 10.5 mg/dl.
H Ionized calcium levels are greater than 5.8 mg/dl.
H Albumin level is elevated.
H Electrocardiography shows shortened QT interval
and ventricular arrhythmias.
Treatment
H Hyperparathyroidism
H Hypervitaminosis D
H Certain cancers
H Multiple fractures and prolonged immobilization
H Certain drugs (see Drugs causing hypercalcemia)
General
Incidence
H Normal saline solution

H Loop diuretics, such as furosemide, bumetamide,
H Considerably higher in females than in males

H No gender predominance in elevated calcium levels

H Hemodialysis with kidney failure
Medications
and torsemide
related to cancer
H Corticosteroids to counter effects of excess vitamin D
See Clinical effects of hypercalcemia.
Complications
H Renal calculi
H Coma
H Cardiac arrest
Assessment
History
H Underlying cause
H Lethargy
H Weakness
Key outcomes
The patient will:
H express an understanding of the disorder and treatment regimen.
Clinical effects of hypercalcemia

Dysfunction
Effects
Cardiovascular
Signs of heart block, cardiac arrest, hypertension
Gastrointestinal
Anorexia, nausea, vomiting, constipation, dehydration, polydipsia
Musculoskeletal
Weakness, muscle flaccidity, bone

pain, pathologic fractures
Neurologic
Drowsiness, lethargy, headaches,

depression or apathy, irritability,
confusion
Other
Renal polyuria, flank pain and,

eventually, azotemia
Drugs causing hypercalcemia

These drugs can cause or contribute to hypercalcemia:
H antacids that contain calcium
H calcium preparations (oral or I.V.)
H lithium
H thiazide diuretics
H vitamin A
H vitamin D.
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Hypercalcemia
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H Provide safety measures and institute seizure precau-
tions, if appropriate.
H Watch for signs of heart failure.
Monitoring
H Cardiac rhythm
H Seizures
H Calcium levels
Patient teaching
Be sure to cover:
H avoiding nonprescription drugs high in calcium
H increasing fluid intake
H following a low-calcium diet.
Discharge planning
H Refer the patient to a dietitian and social services, if
indicated.
Hypercalcemia
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Hyperchloremia
Overview
Complications
H Hypervolemia
H Coma
Description
Assessment
H Excessive serum levels of the chloride anion

H Usually accompanied by sodium and water retention
History
Pathophysiology
H Risk factors for high chloride level

H Chloride accounts for two-thirds of all serum anions.

H Chloride is secreted by stomach mucosa as hydro-
Physical findings
chloric acid; it provides an acid medium that aids digestion and activation of enzymes.
H Chloride helps maintain acid-base and body water
balances, influences the osmolality or tonicity of extracellular fluid, plays a role in the exchange of oxygen and carbon dioxide in red blood cells, and helps
activate salivary amylase (which, in turn, activates the
digestive process).
H An inverse relationship exists between chloride and
bicarbonate. When the level of one goes up, the level
of the other goes down. (See Anion gap and metabolic acidosis.)
H Chloride imbalanace can lead to metabolic acidosis
and altered fluid balance if left untreated.
Causes
H Hyperparathyroidism
H Renal tubular acidosis
H Hypernatremia
H Prolonged diarrhea
H Loss of pancreatic secretion
H Certain drugs (see Drugs causing hyperchloremia)
H Agitation
H Pitting edema
H Dyspnea
H Rapid deep breathng (Kussmauls respirations)
H Weakness
H Tachypnea
H Hypertension
Test results
H Serum chloride level is greater than 108 mEq/L.
H With metabolic acidosis, serum pH is less than
7.35 and serum carbon dioxide level is less than

22 mEq/L and anion gap is normal.
H Serum sodium level is greater than 145 mEq/L.
Treatment
General
H Restoring fluid, electrolyte, and acid base balance
H Restricted sodium and chloride intake
Incidence
Medications
H Associated with other acid-base disorders and rarely
H Sodium bicarbonate I.V.

H Lactated Ringers solution
H Diuretics, such as furosemide, bumetanide, and
occurs alone.
hydrochlorothiazide
H Agitation, tachycardia, hypertension, pitting edema,
dyspnea
H Deep, rapid breathing; weakness; diminished cogni-
tive ability; and, ultimately, coma (if in metabolic acidosis)
Key outcomes
Anion gap and metabolic acidosis
The patient will:

Hyperchloremia increases the likelihood that a patient will

develop hyperchloremic metabolic acidosis.
Drugs causing hyperchloremia
How it happens
If a patient with metabolic acidosis has a normal anion
gap, the acidosis is probably caused by a loss of bicarbonate ions by the kidneys or the GI tract. In such cases,
a corresponding increase in chloride ions also occurs.
Acidosis can also result from an accumulation of chloride ions in the form of acidifying salts. A corresponding
decrease in bicarbonate ions occurs at the same time.
394
Hyperchloremia
These drugs can cause or contribute to hyperchloremia:

H acetazolamide
H ammonium chloride
H phenylbutazone
H sodium polystyrene sulfonate (Kayexalate)
H salicylates (overdose)
H triamterene.
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H Provide a safe environment.
H Evaluate muscle strength and adjust activity level.
H Reorient the confused patient when necessary.
Monitoring
H Signs of metabolic alkalosis
H Intake and output
H Neurologic status
H Cardiac rhythm
Patient teaching
Be sure to cover:
H dietary or fluid restrictions, as indicated
Hyperchloremia
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Hyperkalemia
Overview
Description
H Excessive serum levels of the potassium anion
H Commonly induced by other treatments
Pathophysiology
H Potassium facilitates contraction of both skeletal and
smooth muscles, including myocardial contraction.
Complications
H Cardiac arrhythmia
H Cardiac arrest
Assessment
History
H Irritability
H Paresthesia
H Muscle weakness
H Nausea
H Abdominal cramps
H Diarrhea
H Potassium figures prominently in nerve impulse con-
Physical findings
duction, acid-base balance, enzyme action, and cell

membrane function.
H Slight deviation in serum levels can produce profound clinical consequences.
H Potassium imbalance can lead to muscle weakness
and flaccid paralysis due to an ionic imbalance in
neuromuscular tissue excitability.
H Hypotension
H Irregular heart rate
H Cardiac arrhythmia (possible)
Causes
H Renal dysfunction or failure
H Use of potassium-sparing diuretics such as triam-
terene by patients with renal disease

H Burns
H Crushing injuries
H Adrenal gland insufficiency
H Dehydration
H Diabetic acidosis
H Increased intake of potassium
H Decreased urinary excretion of potassium
H Severe infection
H Large quantities of blood transfusions
H Certain drugs (see Drugs causing hyperkalemia)
Incidence
H Diagnosed in up to 8% of hospitalized patients in the
United States
See Clinical effects of hyperkalemia.
Test results
Laboratory
H Serum potassium levels are greater than 5 mEq/L.
H Arterial pH is decreased.
H Electrocardiography shows a tall, tented T wave.
Treatment
General
H Hemodialysis or peritoneal dialysis
Clinical effects of hyperkalemia

Dysfunction
Effects
Acid-base
balance
Metabolic acidosis
Cardiovascular
Tachycardia and later bradycardia,

electrocardiogram changes (tented
and elevated T waves, widened
QRS complex, prolonged PR interval, flattened or absent P waves,
depressed ST segment), cardiac
arrest (with levels > 7 mEq/L)
Gastrointestinal
Nausea, diarrhea, abdominal

cramps
Genitourinary
Oliguria, anuria
Musculoskeletal
Muscle weakness, flaccid paralysis
Neurologic
Hyperreflexia progressing to weakness, numbness, tingling, flaccid

paralysis
Drugs causing hyperkalemia

These drugs may increase potassium levels:
H angiotensin-converting enzyme inhibitors
H antibiotics
H beta-adrenergic blockers
H chemotherapeutic drugs
H nonsteroidal anti-inflammatory drugs
H potassium (in excessive amounts)
H spironolactone.
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Avoiding false results

When a patient receives a laboratory test result indicating
a high potassium level, and the result doesnt make sense,
make sure its a true result. If the sample was drawn using
poor technique, the results may be falsely high. These are
some of the causes of falsely high potassium levels:
H drawing the sample above an I.V. infusion containing
potassium
H using a recently exercised arm or leg for the venipuncture site
H causing hemolysis (cell damage) as the sample is
obtained.
Medications
H Rapid infusion of 10% calcium gluconate (decreases
myocardial irritability)
H Insulin and 10% to 50% glucose I.V.
H Sodium polystyrene sulfonate with 70% sorbitol
Key outcomes
The patient will:
H maintain a normal potassium level
H understand potential adverse effects of prescribed
drugs.
H Check the serum sample. (See Avoiding false
results.)
H Implement safety measures.
H Be alert for signs of hypokalemia after treatment.
Monitoring
H Serum potassium levels
H Cardiac rhythm
H Intake and output
Patient teaching
Be sure to cover:
H monitoring intake and output
H preventing future episodes of hyperkalemia
H need for potassium-restricted diet.
Hyperkalemia
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Hyperlipoproteinemia
Overview
Description
H Increased plasma concentrations of one or more
lipoproteins
H Primary form: at least five distinct and inherited
metabolic disorders
H May occur secondary to other conditions such as di-
abetes mellitus
H Clinical changes ranging from relatively mild symp-
toms, managed by diet, to potentially fatal pancreatitis
Pathophysiology
H Low-density lipoprotein (LDL) level is increased and
high-density lipoprotein (HDL) level is decreased.

H Development of atherosclerosis is accelerated.
Causes
H Primary hyperlipoproteinemia
Types I and III transmitted as autosomal recessive

traits
Types II, IV, and V transmitted as autosomal dominant traits
H Secondary hyperlipoproteinemia
Diabetes mellitus
Pancreatitis
Hypothyroidism
Renal disease
Incidence
Type I
H Relatively rare; present at birth
Type II
H Onset between ages 10 and 30
Type III
H Uncommon; usually occurring after age 20
Type IV
H Relatively common, especially in middle-aged males
Type V
H Uncommon; usually occurring in late adolescence or
early adulthood
H Increased plasma concentrations of one or more
lipoproteins
Complications
H Coronary artery disease (CAD)
H Pancreatitis
Assessment
History
Type I
H Recurrent attacks of severe abdominal pain
H Abdominal pain usually preceded by fat intake
H Malaise and anorexia
Type II
H History of premature and accelerated coronary
atherosclerosis
H Symptoms that typically develop in 20s or 30s
Type III
H No clinical symptoms until after age 20
H Aggravating factors, such as obesity, hypothyroidism,
and diabetes mellitus
Type IV
H Atherosclerosis
H Early CAD
H Excessive alcohol consumption
H Poorly controlled diabetes mellitus
H Birth control pills containing estrogen (can precipitate severe hypertriglyceridemia)
H Hypertension
H Hyperuricemia
Type V
H Abdominal pain associated with pancreatitis
H Complaints related to peripheral neuropathy
Physical findings
Type I
H Papular or eruptive xanthomas over pressure points
and extensor surfaces
H Ophthalmoscopic examination: lipemia retinalis
(reddish white retinal vessels)
H Abdominal spasm, rigidity, or rebound tenderness
H Hepatosplenomegaly, with liver or spleen tenderness
H Fever possibly present
Type II
H Tendinous xanthomas on the Achilles tendons and
tendons of the hands and feet
H Tuberous xanthomas, xanthelasma
H Juvenile corneal arcus
Type III
H Tuberoeruptive xanthomas over elbows and knees
H Palmar xanthomas on the hands, particularly the fingertips
Type IV
H Obesity
H Xanthomas possibly noted during exacerbations
Type V
H Eruptive xanthomas on extensor surface of arms and
legs
H Ophthalmoscopic examination: lipemia retinalis
Test results
Laboratory
H Serum lipid profiles show elevated levels of total cholesterol, triglycerides, very low-density lipoproteins,
LDLs, or HDLs.
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Treatment
General
Key outcomes
H Weight reduction
H Elimination or treatment of aggravating factors, such
The patient will:

H verbalize understanding of the disorder and treatment regimen.
as diabetes mellitus, alcoholism, and hypothyroidism

H Reduction of risk factors for atherosclerosis
H Smoking cessation
H Treatment of hypertension
H Avoidance of hormonal and estrogen-containing
contraceptive drugs
H Restriction of cholesterol and saturated animal fat
intake
H Avoidance of alcoholic beverages to decrease plasma
triglyceride levels
H Inclusion of polyunsaturated vegetable oils (reduces
plasma LDLs)
H Maintenance of exercise and physical fitness program
Type I
H Restricted fat intake (less than 20 g/day); 20- to
40-g/day, medium-chain triglyceride diet to supplement calorie intake
Type II
H Restriction of cholesterol intake to less than 300 mg/
day for adults and less than 150 mg/day for children;
restricted triglyceride intake (to less than 100 mg/
day for children and adults); and diet high in polyunsaturated fats
Type III
H Restricted cholesterol intake (to less than 300 mg/
day) and carbohydrates; increased polyunsaturated
fats
Type IV
H Restricted cholesterol intake; increased polyunsaturated fats
Type V
H Long-term maintenance of a low-fat diet; 20- to 40-g/
day medium-chain triglyceride diet
Medications
H Statins, such as rosuvastatin, atorvastatin, and sim-
vastatin
H Nicotinic acid (niacin)
H Bile acid resins, such as cholestyramine-sucrose and
colestipol
H Fibrates, such as gemfibrozil and fenofibrate
Surgery
H If unable to tolerate drug therapy, surgical creation
of an ileal bypass
H For severely affected homozygote children, portacav-
H Administer prescribed antilipemics.
H Prevent or minimize adverse reactions.
H Urge the patient to adhere to the prescribed diet.
H Assist the patient with additional lifestyle changes.
H Encourage verbalization of fears related to premature
CAD.
Monitoring
H Vital signs
H Adverse reactions
H Serum lipoproteins
H Signs and symptoms related to CAD or its sequelae
Patient teaching
Be sure to cover:
H the need to maintain a steady weight and strictly adhere to the prescribed diet (for the 2 weeks preceding serum cholesterol and serum triglyceride tests),
and to fast for 12 hours before the test
H the need to avoid excessive sugar intake and alcoholic beverages
H minimized intake of saturated fats (higher in meats
and coconut oil)
H increased intake of polyunsaturated fats (vegetable
oils)
H avoidance of hormonal contraceptives or drugs that
contain estrogen
H foods high in cholesterol and saturated fats
H the prescribed medication regimen and possible
adverse effects
H signs and symptoms requiring medical evaluation.
Discharge planning
H Refer the patient for a medically supervised exercise
program.
indicated.
H Refer the patient to a dietitian, if necessary.
al shunt as a last resort to reduce plasma cholesterol

levels
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Hypermagnesemia
Overview
Incidence
H Rarely occurs in the United States
See Clinical effects of hypermagnesemia.
Description
Complications
H Excessive serum levels of the magnesium cation
H Respiratory depression
H Cardiac arrest
Pathophysiology
H Magnesium enhances neuromuscular integration and
stimulates parathyroid hormone secretion, thus regulating intracellular fluid calcium levels.
H Magnesium may also regulate skeletal muscles
through its influence on calcium utilization by depressing acetylcholine release at synaptic junctions.
H Magnesium activates many enzymes for proper carbohydrate and protein metabolism, aids in cell metabolism and the transport of sodium and potassium
across cell membranes, and influences sodium,
potassium, calcium, and protein levels.
H About one-third of magnesium taken into the body is
absorbed through the small intestine and is eventually excreted in the urine; remaining unabsorbed magnesium is excreted in the stool.
Causes
H Chronic renal insufficiency
H Use of magnesium-containing laxatives, especially
with renal insufficiency (see Drugs and supplements

causing hypermagnesemia)
H Overuse of magnesium-containing antacids
H Severe dehydration (resulting oliguria can cause
magnesium retention)
H Overcorrection of hypomagnesemia
H Addisons disease
H Adrenocortical insufficiency
H Untreated diabetic ketoacidosis
Risk factors
H Advanced age
H Pregnancy
H Neonates whose mothers received magnesium sulfate
during labor
H Patients receiving magnesium sulfate to control
seizures
Assessment
History
H Nausea
H Vomiting
H Drowsiness
H Confusion
Physical findings
H Flushed appearance
H Hypotension
H Weak pulse
H Muscle weakness
H Hyporeflexia (see Testing the patellar reflex)
Test results
Laboratory
H Serum magnesium levels are greater than 2.5 mEq/L.
H Electrocardiography shows prolonged PR interval,
widened QRS complex, and tall T waves.
Treatment
General
H Identification and correction of the underlying cause
H Peritoneal dialysis or hemodialysis
Medications
H Loop diuretics, such as furosemide, with impaired
renal function
H Calcium gluconate (10%)
Clinical effects of hypermagnesemia

Drugs and supplements causing
hypermagnesemia
Monitor your patients magnesium level closely if hes
receiving:
H an antacid (Di-Gel, Gaviscon, Maalox)
H a laxative (milk of magnesia, Haleys M-O, magnesium
citrate)
H a magnesium supplement (magnesium oxide, magnesium sulfate).
400
Hypermagnesemia
Dysfunction
Effects
Cardiovascular
Bradycardia, weak pulse, hypotension, heart block, cardiac arrest
Neurologic
Drowsiness, flushing, lethargy,

confusion, diminished sensorium
Neuromuscular
Diminished reflexes, muscle weakness, flaccid paralysis, respiratory

muscle paralysis that may cause
respiratory embarrassment
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Testing the patellar reflex

One way to gauge your paSitting
tients magnesium status is to Have the patient sit on the side of the
test his patellar reflex, one of bed with his legs dangling freely, as
the deep tendon reflexes that shown below. Then test the reflex.
the magnesium level affects.
To test the reflex, strike the
patellar tendon just below
the patella with the patient
sitting or lying in a supine
position, as shown. Look for
leg extension or contraction
of the quadriceps muscle in
the front of the thigh.
If the patellar reflex is absent, notify the physician
immediately. This finding
may mean the patients magnesium level is 7 mEq/L or
higher.
Supine position
Flex the patients knee at a 45-degree angle, and
place your nondominant hand behind it for support
(as shown below). Then test the reflex.
Patient teaching
Key outcomes
Be sure to cover:
H avoidance of abusing laxatives and antacids containing magnesium, particularly in elderly patients or
those patients with compromised renal function
H hydration requirements
The patient will:

H attain and maintain a normal magnesium level
H understand the causes of high magnesium levels
H have a normal electrocardiogram.
H Provide sufficient fluids for adequate hydration and
maintenance of renal function.

H Report abnormal serum electrolyte levels imme-
diately.
H Watch patients receiving a cardiac glycoside and
calcium gluconate simultaneously because calcium

excess enhances the cardiac glycoside.
Monitoring
H Vital signs
H Magnesium levels
H Intake and output
H Cardiac rhythm
H Neuromuscular system
Hypermagnesemia
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Hypernatremia
Incidence
Overview
H Occurs in about 1% of hospitalized patients (usually
elderly patients)
Description
H Excessive serum levels of the sodium cation relative
to body water
Pathophysiology
H Pulmonary edema
H Circulatory disorders
H Decreased level of consciousness (see Clinical
effects of hypernatremia)
H Sodium is the major cation (90%) in extracellular
Complications
fluid; potassium, the major cation in intracellular

fluid.
H During repolarization, the sodium-potassium pump
continually shifts sodium into the cells and potassium
out of the cells; during depolarization, it does the reverse.
H Sodium cation functions include maintaining tonicity
and concentration of extracellular fluid, acid-base
balance (reabsorption of sodium ion and excretion
of hydrogen ion), nerve conduction and neuromuscular function, glandular secretion, and water balance.
H Increased sodium causes high serum osmolality (increased solute concentrations in the body), which
stimulates the hypothalmus and intiates the sensation
of thirst.
H Seizures
H Coma
H Permanent neurologic damage
Causes
H Decreased water intake
H Excess adrenocortical hormones, as in Cushings syn-
drome
H Antidiuretic hormone deficiency (diabetes insipidus)
H Salt intoxication (less common), which may be pro-
duced by excessive table salt ingestion

H Excessive I.V. administration of sodium solutions
H Certain drugs (see Drugs causing hypernatremia)
Risk factors
H People unable to drink voluntarily
Assessment
History
H Fatigue
H Restlessness, agitation
H Weakness
H Disorientation
H Lethargy
Physical findings
H Flushed skin
H Dry, swollen tongue
H Sticky mucous membranes
H Low-grade fever
H Twitching
H Hypertension, dyspnea (with hypervolemia)
H Orthostatic hypotension and oliguria (with hypo-
volemia)
Test results
Laboratory
H Serum sodium level is greater than 145 mEq/L.
H Urine sodium level is less than 40 mEq/24 hours,
with high serum osmolality.
Clinical effects of hypernatremia
Drugs causing hypernatremia

Ask the patient if hes taking any of these drugs that can
elevate his sodium level:
H antacids with sodium bicarbonate
H antibiotics such as ticarcillin disodium-clavulanate
potassium (Timentin)
H salt tablets
H sodium bicarbonate injections (such as those given
during cardiac arrest)
H I.V. sodium chloride preparations
H sodium polystyrene sulfonate (Kayexalate).
402
Hypernatremia
Dysfunction
Effects
Cardiovascular
Hypertension, tachycardia, pitting

edema, excessive weight gain
Cutaneous
Flushed skin; dry, sticky membranes
Gastrointestinal
Rough, dry tongue; intense thirst
Genitourinary
Oliguria
Neurologic
Fever, agitation, restlessness,

seizures
Respiratory
Dyspnea, respiratory arrest, death

(from dramatic rise in osmotic
pressure)
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Treatment
General
H Administration of sodium-free solutions (such as
dextrose in water) followed by infusion of halfnormal saline solution to prevent hyponatremia

H Discontinuation of drugs that promote sodium
retention
Key outcomes
The patient will:
H maintain a normal sodium level
H remain alert and oriented to his environment.
H Obtain a drug history to check for drugs that pro-
mote sodium retention.

H Assist with oral hygiene.
H Observe for signs of cerebral edema during fluid
replacement therapy.
Monitoring
H Serum sodium levels
H Intake and output
H Neurologic status
Patient teaching
Be sure to cover:
H the importance of sodium restriction
H low-sodium diet
H prescribed drugs
H signs and symptoms of hypernatremia
H avoiding over-the-counter medications that contain
sodium.
Hypernatremia
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Hyperparathyroidism
Overview
Description
H Characterized by a greater than normal secretion of
parathyroid hormone (PTH)

H Classified as either primary or secondary
Pathophysiology
H In primary hyperparathyroidism, one or more of the
parathyroid glands enlarges, increasing PTH secretion and elevating serum calcium levels or an adenoma secretes PTH, unresponsive to negative feedback
of serum calcium.
H In secondary hyperparathyroidism, excessive compensatory production of PTH stems from a hypocalcemia-producing abnormality outside the parathyroid gland, which isnt responsive to PTH such as
decreased intestinal absorption of calcium or vitamin D.
H Increased PTH levels act directly on the bone and the
kidney tubules, resulting in an increase in extracellular calcium.
H Renal excretion and uptake into the soft tissues or
skeleton cant compensate for increased calcium.
Causes
H Adenoma
H Genetic disorders
H Multiple endocrine neoplasia
H Dietary vitamin D or calcium deficiency
H Decreased intestinal absorption of vitamin D or
calcium
H Osteomalacia
H Ingestion of drugs such as phenytoin
H Laxative ingestion
H Idiopathic
Incidence
H Increased incidence in postmenopausal females
H Onset usually between ages 35 and 65
H Bone pain and tenderness
H Renal calculi
H Abdominal distress
H Anxiety and depression
Complications
H Osteoporosis
H Subchondral fractures
H Traumatic synovitis
H Renal calculi and colic
H Renal insufficiency and failure
H Peptic ulcers
H Cholelithiasis
404
Hyperparathyroidism
H Vascular damage
H Heart failure
H Muscle atrophy
H Depression
Assessment
History
H Recurring nephrolithiasis
H Polyuria
H Hematuria
H Chronic lower back pain
H Easy fracturing
H Osteoporosis
H Constant, severe epigastric pain that radiates to the
back
H Abdominal pain
H Anorexia, nausea, and vomiting
H Constipation
H Polydipsia
H Muscle weakness, particularly in the legs
H Lethargy
H Personality disturbances
H Depression
H Overt psychosis
H Cataracts
H Anemia
Physical findings
H Muscle weakness and atrophy
H Psychomotor disturbances
H Stupor and, possibly, coma
H Skin necrosis
H Subcutaneous calcification
Test results
Laboratory
IN PRIMARY DISEASE
H Alkaline phosphatase level is increased.
H Osteocalcin level is increased.
H Tartrate-resistant acid phosphatase level is increased.
H Serum PTH level is increased.
H Serum phosphorus level is decreased.
H Urine and serum calcium and serum chloride levels
are increased.
H Creatinine levels may be increased.
H Basal acid secretion may be increased.
H Serum amylase may be increased.
IN SECONDARY DISEASE
H Serum calcium level is normal or slightly decreased.
H Serum phosphorus level is variable.
H Serum PTH level is increased.
Imaging
H X-rays show diffuse bone demineralization, bone
cysts, outer cortical bone absorption, and subperiosteal erosion of the phalanges and distal clavicles in
primary disease.
H X-ray spectrophotometry shows increased bone
turnover in primary disease.
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H Esophagography, thyroid scan, parathyroid thermog-
raphy, ultrasonography, thyroid angiography, computed tomography scan, and magnetic resonance
imaging may show location of parathyroid lesions.
Treatment
General
H In primary disease, treatment to decrease calcium
levels
H In renal failure, dialysis
H In secondary disease, treatment to correct underlying
cause of parathyroid hypertrophy
H Increased oral fluid intake
Medications
Primary disease
H Bisphosphonates
H Oral sodium or potassium phosphate
H Calcitonin
H Plicamycin, if primary disease is metastatic
Secondary disease
H Vitamin D therapy
H Aluminum hydroxide
H Glucocorticoids
Postoperatively
H I.V. magnesium and phosphate
H Sodium phosphate
H Supplemental calcium
H Vitamin D or calcitriol
Surgery
H With primary hyperparathyroidism, removal of ade-
noma or all but one-half of one gland
Key outcomes
The patient will:
H maintain current weight
H maintain balanced fluid volume status
H perform activities of daily living without excessive
fatigue
H express positive feelings about self.
After parathyroidectomy
H Keep a tracheotomy tray and endotracheal tube setup
at the bedside.
H Maintain seizure precautions.
H Place the patient in semi-Fowlers position.
H Support the patients head and neck with sandbags.
H Have the patient ambulate as soon as possible.
ALERT
Watch for complaints of tingling in the hands and
around the mouth. If these symptoms dont subside
quickly, they may be prodromal signs of tetany, so
keep I.V. calcium gluconate or calcium chloride
available for emergency administration.
Monitoring
H Vital signs
H Intake and output
H Serum calcium levels
After parathyroidectomy
H Increased neuromuscular irritability
H Complications
H Neck edema
H Chvosteks sign
H Trousseaus sign
Patient teaching
Be sure to cover:
H the signs and symptoms of tetany, respiratory distress, and renal dysfunction
H the need for periodic blood tests
H avoidance of calcium-containing antacids and thiazide diuretics
H the need to wear medical identification jewelry.
H Obtain baseline serum potassium, calcium, phos-
phate, and magnesium levels before treatment.

H Provide at least 3 qt (3 L) of fluid per day.
H Schedule frequent rest periods.
H Provide comfort measures.
H Help the patient turn and reposition every 2 hours.
H Support affected extremities with pillows.
Hyperparathyroidism
405
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Hyperphosphatemia
Overview
Complications
Description
H Excessive serum levels of phosphate
H Reflects the kidneys inability to excrete excess phos-
phorus
Pathophysiology
H Usually remains asymptomatic

H May result in hypocalcemia with tetany and seizures
H Soft tissue calcifications

H Hypocalcemia
H Bone fractures
Assessment
H Phosphorus exists primarily in inorganic combina-
History
tion with calcium in teeth and bones.

H In extracellular fluid, the phosphate ion supports
several metabolic functions: utilization of B vitamins,
acid-base homeostasis, bone formation, nerve and
muscle activity, cell division, transmission of hereditary traits, and metabolism of carbohydrates, proteins, and fats.
H Renal tubular reabsorption of phosphate is inversely
regulated by calcium levels an increase in phosphorus causes a decrease in calcium. An imbalance
causes hypophosphatemia or hyperphosphatemia.
H Anorexia
H Decreased mental status
Causes
H Hypocalcemia
H Hypervitaminosis D
H Renal failure
H Overuse of laxatives with phosphates or phosphate
enemas
H Certain drugs (see Drugs and supplements causing
hyperphosphatemia)
H Acid-base imbalance
Risk factors
H Muscle necrosis
H Infection
H Heat stroke
H Trauma
H Chemotherapy
Incidence
H Occurs most commonly in children, who tend to
consume more phosphorus-rich foods and beverages

than adults
H Greater incidence in children and adults with renal
insufficiency
Physical findings
H Hyperreflexia
H Hypocalcemic electrocardiogram changes
H Muscle weakness and cramps
H Papular eruptions
H Paresthesia
H Presence of Chvosteks or Trousseaus sign
H Abdominal spasm
H Tetany
H Visual impairment
H Conjunctivitis
Test results
Laboratory
H Serum phosphorus level is greater than 4.5 mg/dl.
H Serum calcium level is less than 8.9 mg/dl.
H Blood urea nitrogen and creatinine levels are increased.
Imaging
H X-ray studies may reveal skeletal changes caused by
osteodystrophy in chronic hyperphosphatemia.
H Electrocardiography may show changes characteristic of hypercalcemia.
Treatment
General
H Peritoneal dialysis or hemodialysis (if severe)
H Discontinuation of drugs associated with hyperphos-
phatemia
Drugs and supplements causing

hyperphosphatemia
These drugs may cause hyperphosphatemia:
H enemas such as Fleet enemas
H laxatives containing phosphorus or phosphate
H oral phosphorus supplements
H parenteral phosphorus supplements (sodium phosphate, potassium phosphate)
H vitamin D supplements.
406
Hyperphosphatemia
H Low-phosphorus diet
H I.V. saline solution
Medications
H Aluminum
H Magnesium
H Calcium gel
H Phosphate-binding antacids
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Foods high in phosphorus

These foods have a high phosphorus content:
H beans
H lentils
H bran
H milk
H cheese
H nuts
H chocolate
H peanut butter
H dark-colored sodas
H seeds
H ice cream
H yogurt.
Key outcomes
The patient will:
H maintain adequate vital signs
H have a normal phosphorus level
H express understanding of condition and treatment
H maintain a low-phosphorus diet.
H Provide safety measures.
H Be alert for signs of hypocalcemia.
H Give phosphate-binding antacids with meals to in-
crease their effectiveness.

H Prepare the patient for dialysis, if appropriate.
H Assist with selecting a low-phosphorus diet.
Monitoring
H Vital signs
H Phosphorus and calcium levels
H Intake and output
H Renal studies
Patient teaching
Be sure to cover:
H prescribed medications
H avoidance of preparations that contain phosphorus
H avoidance of high-phosphorus foods. (See Foods
high in phosphorus.)
Discharge planning
indicated.
Hyperphosphatemia
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Hyperpituitarism
Overview
Description
H Glucose intolerance
H Diabetes mellitus
H Severe psychological stress
Assessment
H Chronic, progressive disease marked by hormonal
History
dysfunction and startling skeletal overgrowth

H Prognosis dependent on cause
H Life expectancy usually reduced
H Appears in two forms: acromegaly and gigantism
H Also referred to as growth hormone (GH) excess
H Gradual onset of acromegaly

H Relatively abrupt onset of gigantism
H Soft-tissue swelling
H Hypertrophy of the face and extremities
H Diaphoresis, oily skin
H Fatigue, sleep disturbances
H Weight gain
H Headaches, decreased vision
H Decreased libido, impotence
H Oligomenorrhea, infertility
H Joint pain
H Hypertrichosis
H Irritability, hostility, and other psychological distur-
Pathophysiology
H Progressive excessive secretion of pituitary GH
occurs.
H Acromegaly occurs after epiphyseal closure, causing
bone thickening and transverse growth and visceromegaly.

H Gigantism occurs before epiphyseal closure with excess GH, causing proportional overgrowth of all body
tissues.
H A large tumor may cause loss of other trophic hormones, such as thyroid-stimulating hormone,
luteinizing hormone, follicle-stimulating hormone,
and corticotropin, which may cause dysfunction of
target organs.
Causes
H GH-producing adenoma of the anterior pituitary
gland
H Excessive GH secretion
H Excessive GH-releasing hormone
H Possible genetic cause
Incidence
Acromegaly
H Usually occurs between ages 30 and 50
Gigantism
H Affects infants and children
H Progressive enlargement of the face, hands and feet,
thorax, and soft tissue

H Coarsening of features
H Headache
H Menstrual disturbances
Complications
H Arthritis
H Carpal tunnel syndrome
H Osteoporosis
H Kyphosis
H Hypertension
H Arteriosclerosis
H Cardiomegaly and heart failure
H Blindness
H Severe neurologic disturbances
408
Hyperpituitarism
bances
Physical findings
H Enlarged jaw, thickened tongue
H Enlarged and weakened hands
H Coarsened facial features
H Oily or leathery skin
H Prominent supraorbital ridge
H Deep, hollow-sounding voice
H Cartilaginous and connective tissue overgrowth
H Skeletal abnormalities
Special populations
In infants, inspection reveals a highly arched
palate, muscular hypotonia, slanting eyes, and
exophthalmos.
Test results
Laboratory
H GH radioimmunoassay shows increased plasma GH
levels and levels of insulin-like growth factor I.
H Glucose suppression test fails to suppress the hormone level to below the accepted norm of 2 ng/ml.
Imaging
H Skull X-rays, computed tomography scan, or magnetic resonance imaging shows location of pituitary tumor.
H Bone X-rays show a thickening of the cranium and
long bones and osteoarthritis in the spine.
Treatment
General
H Treatment to curb overproduction of GH
H Pituitary radiation therapy
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Medications
H Replacement of thyroid, cortisone, and gonadal hor-
mones postoperatively if entire pituitary removed

H GH synthesis inhibitor
H Long-acting analogue of somatostatin
Surgery
H Transsphenoidal hypophysectomy
Key outcomes
H avoidance of activities that increase ICP

H deep breathing through the mouth if nasal packing is
in place postoperatively
H hormone replacement therapy, if ordered
H the need to wear a medical identification bracelet
H follow-up examinations
H possible tumor recurrence.
Discharge planning
H Refer the patient for psychological counseling to help
deal with body image changes and sexual dysfunction, as needed.
The patient will:

the extent possible
H maintain joint mobility and range of motion (ROM).
H Provide reassurance that mood changes result from
hormonal imbalances and can be reduced with treatment.

H Perform or assist with ROM exercises.
H Evaluate muscle weakness.
H Assist with early postoperative ambulation.
ALERT
Report large increases in urine output after
surgery, which may indicate diabetes insipidus.
Monitoring
H Vital signs
H Intake and output
H Serum glucose levels
H Signs and symptoms of hyperglycemia
After surgery
H Signs and symptoms of increased intracranial pressure (ICP) and intracranial bleeding
H Surgical incisions and dressings
H Complications
H Signs and symptoms of hormonal deficiency
Patient teaching
Be sure to cover:
Hyperpituitarism
409
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Hypersplenism
Overview
Description
H Exaggerated splenic activity and, possibly, spleno-
Assessment
History
H Frequent bacterial infection
H Frequent bruising
H Spontaneous hemorrhaging from the mucous mem-
branes and GI or genitourinary tract
megaly
H Results in peripheral blood cell deficiency as the
spleen traps and destroys peripheral blood cells
H May be primary or secondary
H Fever
H Weakness
H Palpitations
H Weight loss
Pathophysiology
Physical findings
H The spleens normal filtering and phagocytic func-
H Ulcerations of the mouth, legs, and feet

H Bruising
H Splenomegaly
H Jaundice
H Pallor
tions accelerate indiscriminately, automatically removing antibody-coated, aging, and abnormal cells,
even though some cells may be functionally normal.
H The spleen may also temporarily sequester normal
platelets and red blood cells (RBCs), withholding
them from circulation. In this manner, the enlarged
spleen may trap as many as 90% of the bodys
platelets and up to 45% of its RBC mass.
Causes
H Idiopathic (see Causes of splenomegaly)
H An extrasplenic disorder, such as chronic malaria,
polycythemia vera, or rheumatoid arthritis
Incidence
H Affects all ages
H Anemia
H Leukopenia
H Thrombocytopenia
H Splenomegaly
H Easy bruising
Test results
Laboratory
H Hemoglobin level is decreased (as low as 4 g/dl).
H White blood cell count is decreased (less than
4,000/l).
H Platelet count is decreased (less than 125,000/l).
H Reticulocyte count is elevated (more than
75,000/l).
Imaging
H Ultrasound or splenic scan shows enlarged spleen or
possible underlying cause such as a tumor.
H A high spleen-liver ratio of radioactivity indicates
splenic destruction or sequestration.
Treatment
General
Complications
H Treatment of underlying disease (secondary)

H Limited activity
H Nothing by mouth if surgery indicated
H Bleeding
H Postsplenectomy infection and thromboembolic
Medications
disease
H Antibiotics if infection present

H Pneumococcal vaccine (after splenectomy)
Surgery
Causes of splenomegaly
Congestive
H Cirrhosis, thrombosis
Cystic or neoplastic
H Cysts, leukemia, lymphoma, myelofibrosis
Hyperplastic
H Hemolytic anemia, polycythemia
Infectious
H Acute (abscesses, subacute infective endocarditis),

chronic (tuberculosis, malaria, Feltys syndrome)
Infiltrative
H Gauchers disease, Niemann-Pick disease
410
Hypersplenism
H Splenectomy only in transfusion-dependent patients
refractory to medical therapy
Key outcomes
The patient will:
H understand restrictions imposed by illness
H not show signs of bleeding.
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H If splenectomy is scheduled, administer preoperative
transfusions of blood or blood products (fresh

frozen plasma and platelets) to replace deficient
blood elements, as ordered.
H Treat symptoms or complications of any underlying
disorder.
Monitoring
H Vital signs
H Signs of bleeding
H Complete blood cell count
After surgery
H Pain control
H Wound site
Patient teaching
Be sure to cover:
H activity restrictions.
Hypersplenism
411
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Hypertension
Overview
Description
H Intermittent or sustained elevation of diastolic or sys-
tolic blood pressure
H Serial blood pressure measurements:
prehypertension: systolic blood pressure (SBP)

120 to 139 mm Hg or diastolic blood pressure
(DBP) 80 to 89 mm Hg
stage 1: SBP 140 to 159 mm Hg or DBP 90 to
99 mm Hg
stage 2: SBP 160 mm Hg or DBP 100 mm Hg
H Usually begins as benign disease, slowly progressing
Complications
to accelerated or malignant state

H Two major types: essential (also called primary or
idiopathic) hypertension and secondary hypertension, which results from renal disease or another
identifiable cause
H Malignant hypertension, a medical emergency: a severe, fulminant form commonly arising from both
types
H Cardiac disease
H Renal failure
H Blindness
H Stroke
Pathophysiology
H In many cases, no symptoms, and disorder revealed
Several theories
H Changes in arteriolar bed cause increased peripheral
vascular resistance.
H Abnormally increased tone in the sympathetic nervous system originating in the vasomotor system centers causes increased peripheral vascular resistance.
H Increased blood volume results from renal or hormonal dysfunction.
H Increase in arteriolar thickening caused by genetic
factors leads to increased peripheral vascular resistance.
H Abnormal renin release results in the formation of
angiotensin II, which constricts the arterioles and
increases blood volume.
Causes
H Unknown, in most cases
H 5% to 10% due to underlying condition, certain
medications, or illicit drugs
Risk factors
H Family history
H Blacks in the United States
H Stress
H Obesity
H High-sodium, high-saturated fat diet
H Use of tobacco
H Use of hormonal contraceptives
H Excess alcohol intake
H Aging
Incidence
H Affects about 33% of adults in the United States
H Essential hypertension: 90% to 95% of cases
412
Hypertension
Assessment
History
incidentally during evaluation for another disorder
or during a routine blood pressure screening program
H Symptoms that reflect the effect of hypertension on
the organ systems
H Awakening with a headache in the occipital region,
which subsides spontaneously after a few hours
H Dizziness, fatigue, confusion
H Palpitations, chest pain, dyspnea
H Epistaxis
H Hematuria
H Blurred vision
Physical findings
H Bounding pulse
H S4
H Peripheral edema in late stages
H Hemorrhages, exudates, and papilledema of the eye
in late stages if hypertensive retinopathy present

H Pulsating abdominal mass, suggesting an abdominal
aneurysm
H Elevated blood pressure on at least two consecutive
occasions after initial screenings

H Bruits over the abdominal aorta and femoral arteries
or the carotids
Test results
Laboratory
H Urinalysis may show protein, red blood cells, or
white blood cells, suggesting renal disease, or glucose, suggesting diabetes mellitus.
H Serum potassium levels less than 3.5 mEq/L may indicate adrenal dysfunction (primary hyperaldosteronism).
H Blood urea nitrogen levels normal or elevated to
more than 20 mg/dl and serum creatinine levels normal or elevated to more than 1.5 mg/dl suggest renal
disease.
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Imaging
H Excretory urography may reveal renal atrophy, indicating chronic renal disease; one kidney more than
5
8(1.6 cm) shorter than the other suggests unilateral renal disease.
H Chest X-rays may demonstrate cardiomegaly.
H Renal arteriography may show renal artery stenosis.
H Electrocardiography may show left ventricular hypertrophy or ischemia.
H An oral captopril challenge may be done to test for
renovascular hypertension.
H Ophthalmoscopy reveals arteriovenous nicking and,
in hypertensive encephalopathy, edema.
Treatment
General
H Lifestyle modification, such as weight control, limit-
ing alcohol, regular exercise, and smoking cessation

H For a patient with secondary hypertension, correc-
tion of the underlying cause and control of hypertensive effects

H Low-saturated fat and low-sodium diet
H Adequate calcium, magnesium, and potassium in diet
Medications
H Diuretics, such as furosemide, hydrochlorothiazide,
and indapamide
H Beta-adrenergic blockers, such as atenolol and
metoprolol
H Help the patient identify risk factors and modify his
lifestyle, as appropriate.
Monitoring
H Signs and symptoms of target end-organ damage
H Complications
H Risk factor modification
H Adverse effects of antihypertensive agents
Patient teaching
Be sure to cover:
H how to use a self-monitoring blood pressure cuff and
to record the reading in a journal for review by the
physician
H the importance of compliance with antihypertensive
therapy and establishing a daily routine for taking
prescribed drugs
H the need to report adverse effects of drugs
H the need to avoid high-sodium antacids and overthe-counter cold and sinus medications containing
harmful vasoconstrictors
H examining and modifying lifestyle, including diet
H the need for a routine exercise program, particularly
aerobic walking
H the importance of follow-up care.
H Calcium channel blockers, such as felodipine and
Discharge planning
nisoldipine
benazepril, captopril, and enalapril
H Alpha-blockers, such as doxazosine and prazosin
H Vasodilators, such as hydralazine and minoxidil
H Angiotensin-receptor blockers, such as olmesartan,
candesartan, and irbesartan
H Aldosterone antagonists, such as eplerenone and
spironolactone
H Combination alpha- and beta-blockers, such as
carvedilol and labetalol
H Alpha-receptor antagonist such as clonidine
H Refer the patient to stress-reduction therapies or
support groups, as needed.
Key outcomes
The patient will:
H develop no arrhythmias
H comply with the therapy regimen.
H Encourage dietary changes, as appropriate.
Hypertension
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Hyperthyroidism
Overview
Description
H An alteration in thyroid function in which thyroid
hormones (TH) exert greater than normal responses

H Management determined by cause
H Hyperthyroidism: a form of thyrotoxicosis in which
excess thyroid hormones are secreted by the thyroid

gland
H Thyrotoxicoses not associated with hyperthyroidism:
subacute thyroiditis, ectopic thyroid tissue, and ingestion of excessive TH
H Graves disease: also known as toxic diffuse goiter;
an autoimmune disease, the most common form of
hyperthyroidism
H Also known as thyrotoxicosis
Pathophysiology
H In Graves disease, thyroid-stimulating antibodies
bind to and stimulate the thyroid-stimulating hormone (TSH) receptors of the thyroid gland.
H The trigger for this autoimmune disease is unclear.
H Its associated with the production of autoantibodies
possibly caused by a defect in suppressor-T-lymphocyte function that allows the formation of these autoantibodies.
Causes
H Diseases that can cause hyperthyroidism:
Graves disease
Toxic multinodular goiter
Thyroid cancer
Increased TSH secretion
Genetic and immunologic factors
Excessive iodine intake
Stress
Surgery
Infection
Toxemia of pregnancy
Diabetic ketoacidosis
Incidence
H Graves disease: most common between ages 30 and
60; more common in females than in males

H Increased among monozygotic twins
H More common with family history of thyroid abnor-
malities
H Only 5% of hyperthyroid patients younger than age 15
H Increased metabolic rate
H Heat intolerance
H Increased tissue sensitivity to sympathetic nervous
system stimulation
H Goiter (almost always present)
H Exophthalmos
414
Hyperthyroidism
Complications
H Arrhythmias
H Heart failure
H Muscle weakness and atrophy
H Paralysis
H Osteoporosis
H Vitiligo
H Skin hyperpigmentation
H Corneal ulcers
H Myasthenia gravis
H Impaired fertility
H Decreased libido
H Gynecomastia
H Thyrotoxic crisis or thyroid storm
H Hepatic or renal failure
Assessment
History
Graves disease
H Nervousness, tremor
H Heat intolerance
H Weight loss despite increased appetite
H Sweating
H Frequent bowel movements
H Palpitations
H Poor concentration
H Shaky handwriting
H Clumsiness
H Emotional instability and mood swings
H Thin, brittle nails
H Hair loss
H Oligomenorrhea or amenorrhea
H Fertility problems
H Diminished libido
H Diplopia
Physical findings
Graves disease
H Enlarged thyroid (goiter)
H Exophthalmos
H Tremor
H Smooth, warm, flushed skin
H Fine, soft hair
H Premature graying and increased hair loss
H Friable nails and onycholysis
H Pretibial myxedema
H Thickened skin
H Accentuated hair follicles
H Tachycardia at rest
H Full, bounding pulses
H Arrhythmias, especially atrial fibrillation
H Possible systolic murmur
H Dyspnea
H Hepatomegaly
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H Weakness, especially in proximal muscles, and
atrophy
H Possible generalized or localized paralysis
H Gynecomastia
H Increased tearing
Test results
Laboratory
H Radioimmunoassay shows increased serum triiodothyronine and thyroxine concentrations.
H Serum protein-bound iodine is increased.
H Serum cholesterol and total lipid levels are
decreased.
H TSH level is decreased.
Imaging
H Thyroid scan shows increased uptake of radioactive
iodine (131I).
H Ultrasonography shows subclinical ophthalmopathy.
Treatment
General
H Adequate caloric intake
Medications
H Treatment with 131I: a single oral dose; treatment of
choice for females past reproductive age or males

and females not planning to have children
H Thyroid hormone antagonists, such as methimazole
and propylthiouracil (PTU)
metoprolol
H Corticosteroids
H Sedatives, such as diazepam and lorazepam
Surgery
H Subtotal (partial) thyroidectomy
H Surgical decompression
Key outcomes
The patient will:
H have normal bowel movements
H remain normothermic.

H Reassure the patient and his family that mood swings
and nervousness usually subside with treatment.

H Help the patient identify and develop coping strate-
gies.
H Avoid excessive palpation of the thyroid.
After thyroidectomy
H Change dressings and perform wound care, as ordered.
H Keep the patient in semi-Fowlers position.
H Support the patients head and neck with sandbags.
Monitoring
H Vital signs
H Daily weight
H Intake and output
H Daily neck circumference
H Hyperglycemia and glycosuria
H Electrocardiogram for arrhythmias and ST-segment
changes
H Complete blood count results
H Frequency and characteristics of stools
After thyroidectomy
H Dressings
H Signs and symptoms of hemorrhage into the neck
H Surgical incision
H Dysphagia or hoarseness
H Signs and symptoms of hypocalcemia
Patient teaching
Be sure to cover:
H the need for regular medical follow-up visits
H the need for lifelong thyroid hormone replacement
jewelry
H precautions with 131I therapy
H signs and symptoms of hypothyroidism and hyperthyroidism
H eye care for ophthalmopathy.
H Minimize physical and emotional stress.
H Balance rest and activity periods.
H Keep the patients room cool and quiet and the
lights dim.
H Encourage the patient to dress in loose-fitting, cotton
clothing.
H Consult a dietitian to ensure a nutritious diet with ad-
equate calories and fluids.
Hyperthyroidism
415
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Hypocalcemia
H Respiratory arrest
Overview
Assessment
Description
History
H Deficient serum levels of calcium
H Underlying cause
H Anxiety
H Irritability
H Seizures
H Muscle cramps
H Diarrhea
Pathophysiology
H Together with phosphorous, calcium is responsible
for the formation and structure of bones and teeth.

H Calcium helps maintain cell structure and function.
H It plays a role in cell membrane permeability and im-
pulse transmission.
H It affects the contraction of cardiac muscle, smooth
muscle, and skeletal muscle.

H It also participates in the blood-clotting process.
H Decreased calcium levels can result in multi-system
dysfunction.
Causes
Incidence
H Affects persons of all ages
See Clinical effects of hypocalcemia.
Complications
Test results
Laboratory
H Serum calcium levels are less than 8.5 mg/dl.
H Ionized calcium levels are less than 4.5 mg/dl.
H Electrocardiography shows lengthened QT interval,
prolonged ST segment, and arrhythmias.
Treatment
General
H Diet high in calcium and vitamin D
Medications
H Laryngeal spasm
H Seizures
H Oral calcium and vitamin D supplements

H Calcium gluconate I.V.
Clinical effects of hypocalcemia

Dysfunction
Effects
Cardiovascular
Arrhythmias, hypotension
Gastrointestinal
Increased GI motility, diarrhea
Musculoskeletal
Paresthesia, tetany or painful tonic

muscle spasms, facial spasms, abdominal cramps, muscle cramps,
spasmodic contractions
Neurologic
Anxiety, irritability, twitching around

mouth, laryngospasm, seizures,
Chvosteks sign, Trousseaus sign
416
H Twitching
H Carpopedal spasm
H Tetany
H Hypotension
H Confusion
H Positive Chvosteks and Trousseaus sign (see Elicit-
ing signs of hypocalcemia)
H Inadequate dietary intake of calcium and vitamin D

H Malabsorption or loss of calcium from the GI tract
H Severe infections or burns
H Overcorrection of acidosis
H Pancreatic insufficiency
H Renal failure
H Hypomagnesemia
Other
Physical findings
Blood-clotting abnormalities
Hypocalcemia
Key outcomes
The patient will:
H express an understanding of the disorder and treatment.
H Provide safety measures; institute seizure precau-
tions, if appropriate.
H Administer prescribed calcium replacement.
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Eliciting signs of hypocalcemia

When the patient complains of muscle spasms and paresthesia in his limbs, try eliciting Chvosteks and Trousseaus signs indications of tetany associated with calcium deficiency.
Follow the procedures described here, keeping in mind
the discomfort they typically cause. If you detect these
signs, notify the physician immediately. During these
tests, watch the patient for laryngospasm, monitor his
cardiac status, and have resuscitation equipment nearby.
Chvosteks sign
To elicit this sign, tap the patients facial nerve just in front
of the earlobe and below the zygomatic arch or between
the zygomatic arch and the corner of the mouth, as shown
below.
H Assess I.V. sites if administering calcium I.V. (infiltra-
tion causes sloughing).
Monitoring
H Cardiac rhythm
H Seizures
H Calcium levels
Patient teaching
Be sure to cover:
H proper administration of calcium supplements
H the need to follow a high-calcium diet.
Discharge planning
indicated.
A positive response (indicating latent tetany) ranges

from simple mouth-corner twitching to twitching of all facial muscles on the side tested. Simple twitching may be
normal in some patients. However, a more pronounced response usually confirms Chvosteks sign.
Trousseaus sign
In this test, occlude the brachial artery by inflating a blood
pressure cuff on the patients upper arm to a level between
diastolic and systolic blood pressure. Maintain this inflation for 3 minutes while observing the patient for carpal
spasm (shown below), which is Trousseaus sign.
Hypocalcemia
417
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Hypochloremia
Overview
Description
H Deficient serum levels of the chloride anion
Pathophysiology
H Chloride accounts for two-thirds of all serum anions.
H Chloride is secreted by the stomachs mucosa as hy-
drochloric acid; it provides an acid medium that aids

digestion and activation of enzymes.
H It participates in maintaining acid-base and body water balances, influences the osmolality or tonicity of
extracellular fluid, plays a role in the exchange of
oxygen and carbon dioxide in red blood cells, and
helps activate salivary amylase (which, in turn, activates the digestive process).
H When serum chloride levels drop, levels of sodium,
potassium, calcium, and other electrolytes may be affected.
H When chloride levels decrease, bicarbonate levels
rise to compensate.
Causes
H Untreated diabetic ketoacidosis
H Addisons disease
H Chloride-deficient formula (for infants)
H Sodium-restricted diets
H Prolonged use of mercurial diuretics
H Administration of dextrose I.V. without electrolytes
H Prolonged diarrhea or diaphoresis
H Loss of hydrochloric acid in gastric secretions due to
vomiting, gastric suctioning, or gastric surgery

H Certain drugs (see Drugs causing hypochloremia)
Risk factors
H Cystic fibrosis
H Pyloric obstruction
H Draining fistula
H Ileostomy
H Heart failure
Complications
H Seizures
H Coma
Assessment
History
H Risk factors for low chloride levels
H Agitation
H Irritability
Physical findings
H Muscle weakness
H Twitching
H Tetany
H Shallow, depressed breathing
H Muscle cramps
Test results
Laboratory
H Serum chloride level is less than 98 mEq/L.
H Serum sodium level is less than 135 mEq/L.
H Supportive values in metabolic alkalosis, include:
serum pH greater than 7.45
serum carbon dioxide level greater than
32 mEq/L.
Treatment
General
H Treatment of underlying condition
H High-sodium diet
H Treatment of associated metabolic acidosis or elec-
trolyte imbalances
Medications
H Normal saline I.V. solution
H Ammonium chloride
H Potassium chloride (for metabolic acidosis)
H Muscle weakness and twitching

H Muscle hypertonicity
H Tetany
H Shallow, depressed breathing (if metabolic alkalosis
occurs)
Drugs causing hypochloremia

These kinds of diuretics may cause hypochloremia:
H loop (such as furosemide)
H osmotic (such as mannitol)
H thiazide (such as hydrochlorothiazide).
418
Hypochloremia
Dietary sources of chloride

These foods provide chloride:
H fruits
H vegetables
H table salt
H salty foods
H processed meats
H canned vegetables.
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Key outcomes
The patient will:
H Offer foods high in chloride. (See Dietary sources of
chloride.)
H Provide environmental safety.
H Administer prescribed I.V. fluids and drugs.
Monitoring
H Muscle strength and movement
H Cardiac rhythm
H Signs of metabolic alkalosis
Patient teaching
Be sure to cover:
H signs and symptoms of electrolyte imbalance
H dietary supplements
Hypochloremia
419
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Incidence
H Affects up to 20% of hospitalized patients (significant
in only about 4% to 5% of these patients)
Hypokalemia
H Affects up to 14% of outpatients mildly

H Approximately 80% of patients who receive diuretics
Overview
H Males and females affected equally
become hypokalemic
Description
H Deficient serum levels of the potassium anion
H Normal range for a serum potassium level narrow
(3.5 to 5 mEq/L); a slight decrease can have a profound consequence
Pathophysiology
H Potassium facilitates contraction of both skeletal and
smooth muscles, including myocardial contraction.

H Potassium figures prominently in nerve impulse con-
duction, acid-base balance, enzyme action, and cell

membrane function.
H A slight deviation in serum levels can produce profound clinical consequences.
H Potassium imbalance can lead to muscle weakness
and flaccid paralysis due to an ionic imbalance in
neuromuscular tissue excitability.
Causes
See Clinical effects of hypokalemia.
Complications
H Cardiac arrest
H Rhabdomyolysis
Assessment
History
H Muscle weakness
H Paresthesia
H Abdominal cramps
H Anorexia
H Nausea, vomiting
H Constipation
H Polyuria
H Excessive GI or urinary losses, such as vomiting,
Physical findings
gastric suction, diarrhea, dehydration, anorexia,

or chronic laxative abuse
H Trauma (injury, burns, or surgery)
H Chronic renal disease, with tubular potassium
wasting
H Certain drugs, especially potassium-wasting diuretics,
steroids, and certain sodium-containing antibiotics
(carbenicillin) (see Drugs causing hypokalemia)
H Acid-base imbalances
H Prolonged potassium-free I.V. therapy
H Hyperglycemia
H Cushings syndrome
H Primary hyperaldosteronism
H Excessive ingestion of licorice
H Severe serum magnesium deficiency
H Low-potassium diet
H Hyporeflexia
H Weak, irregular pulse
H Decreased bowel sounds
Clinical effects of hypokalemia

Dysfunction
Cardiovascular
Dizziness, hypotension, arrhythmias,

electrocardiogram changes (flattened T waves, elevated U waves,
decreased ST segments), cardiac
arrest (with levels < 2.5 mEq/L)
Gastrointestinal
Nausea, vomiting, anorexia, diarrhea,

abdominal distention, paralytic ileus
or decreased peristalsis
Genitourinary
Polyuria
Musculoskeletal
Muscle weakness and fatigue, leg

cramps
Neurologic
Malaise, irritability, confusion, mental depression, speech changes, decreased reflexes, respiratory paralysis
Drugs causing hypokalemia

These drugs can deplete potassium and cause hypokalemia:
H adrenergics, such as albuterol and epinephrine
H antibiotics, such as amphotericin B, carbenicillin, and
gentamicin
H cisplatin
H corticosteroids
H diuretics, such as furosemide and thiazide
H insulin
H laxatives (when used excessively).
420
Hypokalemia
Effects
Acid-base balance Metabolic alkalosis
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Test results
Laboratory
H Serum potassium levels are less than 3.5 mEq/L.
H pH and bicarbonate levels are elevated.
H Serum glucose level is slightly elevated.
H Characteristic electrocardiography changes, such as
flattened T wave, depressed ST segment and U wave,
are present.
Treatment
Patient teaching
Be sure to cover:
H monitoring intake and output
H preventing future episodes of hypokalemia
H need for a high-potassium diet (see Dietary sources
of potassium)
H warning signs and symptoms to report to the physician.
General
H High-potassium diet
Medications
H Potassium chloride (I.V. or orally)
ALERT
A patient taking a diuretic may be switched to a
potassium-sparing diuretic to prevent excessive
urinary loss of potassium.
Key outcomes
The patient will:
H maintain a normal potassium level
H understand potential adverse effects of medications
H express an understanding of high-potassium foods.
H Implement safety measures.
H Be alert for signs of hyperkalemia after treatment.
H Administer I.V. fluids.
Monitoring
H Serum potassium levels
H Cardiac rhythm
H Intake and output
H Vital signs
ALERT
A patient taking a cardiac glycoside, especially if
hes also taking a diuretic, should be monitored
closely for hypokalemia, which can potentiate the
action of the cardiac glycoside and cause toxicity.
Dietary sources of potassium

These foods provide potassium:
H avocados
H molasses
H bananas
H oranges
H cantaloupe
H peaches
H citrus juices
H potatoes
H dried apricots
H prunes
H fresh fish and meat
H tomato or prune juice
H grapefruit
H tomatoes
H honeydew melons
H whole grains.
Hypokalemia
421
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Hypomagnesemia
Overview
Description
H Deficient serum levels of the magnesium cation
H Relatively common imbalance
Pathophysiology
H Magnesium enhances neuromuscular integration and
stimulates parathyroid hormone secretion, thus regulating intracellular fluid calcium levels.
H Magnesium may also regulate skeletal muscles.
H It activates many enzymes for proper carbohydrate
and protein metabolism, aids in cell metabolism and
the transport of sodium and potassium across cell
membranes, and influences sodium, potassium, calcium, and protein levels.
H About one-third of magnesium taken into the body is
absorbed through the small intestine and is eventually excreted in the urine; the remaining unabsorbed
magnesium is excreted in the stool.
H Decreased serum levels of magnesium, primarily
lead to dysfunction of the central nervous system and
neuromuscular, GI, and cardiac systems.
H Hypercalcemia
H Excessive release of adrenocortical hormones
H Certain drugs (see Drugs causing hypomagne-
semia)
Risk factors
H Sepsis
H Serious burns
H Wounds requiring debridement
Incidence
H Occurs in 10% to 20% of hospitalized patients (50%
to 60% of patients in the intensive care unit)

H Occurs in 25% of outpatients with diabetes
H Occurs in 30% to 80% of alcoholics
See Clinical effects of hypomagnesemia.
Complications
H Laryngeal stridor
H Seizures
H Respiratory depression
H Cardiac arrest
Assessment
Causes
History
H Malabsorption syndrome
H Chronic diarrhea
H Postoperative complications after bowel resection
H Prolonged diuretic therapy
H Nasogastric suctioning
H Administration of parenteral fluids without magne-
H Dysphagia
H Nausea
H Vomiting
H Drowsiness
H Confusion
H Leg and foot cramps
sium salts
H Starvation or malnutrition
H Severe dehydration
H Diabetic acidosis
H Hyperaldosteronism
Physical findings
H Tachycardia
H Hypertension
H Muscle weakness, tremors, twitching
Drugs causing hypomagnesemia

Monitor the patients magnesium level if hes taking any of
these drugs that can cause or contribute to hypomagnesemia:
H aminoglycoside antibiotic, such as amikacin, gentamicin, streptomycin, or tobramycin
H amphotericin B
H cisplatin
H cyclosporine
H insulin
H laxative
H loop or thiazide diuretic, such as bumetanide,
furosemide, and torsemide
H pentamidine isethionate.
422
Hypomagnesemia
Clinical effects of hypomagnesemia

Dysfunction
Effects
Cardiovascular
Arrhythmias, vasomotor changes

(vasodilation and hypotension) and,
occasionally, hypertension
Neurologic
Confusion, delusions, hallucinations,

seizures
Neuromuscular
Hyperirritability, tetany, leg and foot

cramps, Chvosteks sign (facial muscle spasms induced by tapping the
branches of the facial nerve)
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H Chvosteks and Trousseaus signs

Test results
Laboratory
H Serum magnesium levels are less than 1.5 mEq/L.
H Other electrolyte abnormalities, such as below-normal serum potassium or calcium level, are present.
H Electrocardiography shows abnormalities, such as
prolonged QT interval and atrioventricular block.
Patient teaching
Be sure to cover:
H prescribed drugs
H avoidance of drugs that deplete magnesium, such as
diuretics and laxatives
H the need to adhere to a high-magnesium diet
H danger signs and when to report them.
Discharge planning
H Refer the patient to Alcoholics Anonymous if appro-
Treatment
priate.
General
H Dietary replacement of magnesium
Medications
H Magnesium oxide
H Magnesium sulfate (I.M. or I.V.)
Key outcomes
The patient will:
H maintain a normal magnesium level
H understand the causes of high magnesium levels.
H Report abnormal serum electrolyte levels
immediately.
ALERT
A low magnesium level may increase the bodys retention of a cardiac glycoside. Be alert for signs of
digoxin toxicity if your patient is taking digoxin.
H Ensure patient safety.
H Reorient the patient as needed.
Monitoring
H Vital signs
H Magnesium levels
H Intake and output
H Cardiac rhythm
Hypomagnesemia
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Hyponatremia
H Trauma, surgery (wound drainage), or burns

H Adrenal gland insufficiency (Addisons disease) or
Overview
H Cirrhosis of the liver with ascites

H Syndrome of inappropriate antidiuretic hormone
hypoaldosteronism
Description
H Deficient serum levels of the sodium cation in rela-
tion to body water
Pathophysiology
(SIADH), resulting from brain tumor, stroke, pulmonary disease, or neoplasm with ectopic antidiuretic hormone production
H Certain drugs, such as chlorpropamide and clofibrate (see Drugs causing hyponatremia)
H Sodium is the major cation (90%) in extracellular
Incidence
fluid; potassium, the major cation in intracellular

fluid.
H During repolarization, the sodium-potassium pump
continually shifts sodium into the cells and potassium
out of the cells; during depolarization, it does the reverse.
H Sodium cation functions include maintaining tonicity
and concentration of extracellular fluid, acid-base
balance (reabsorption of sodium ion and excretion
of hydrogen ion), nerve conduction and neuromuscular function, glandular secretion, and water balance.
H Sodium depletion causes dysfunction of multiple
organ systems.
H Occurs in about 1% of hospitalized patients (30% of
Causes
H Vomiting
H Suctioning
H Diarrhea
H Excessive perspiration or fever
H Use of potent diuretics
H Tap water enemas
H Excessive water intake
H Infusion of I.V. dextrose in water without other
solutes
H Malnutrition or starvation
H Low-sodium diet, usually in combination with one of
patients in intensive care unit)

H More common in the very young and very old
H Pulmonary edema
H Circulatory disorders
H Decreased level of consciousness (LOC) (see Clini-
cal effects of hyponatremia)
Complications
H Seizures
H Coma
H Permanent neurologic damage
Assessment
History
H Altered LOC
H Nausea
H Headache
H Muscle weakness
H Abdominal cramps
Physical findings
H Poor skin turgor
the other causes
Drugs causing hyponatremia

Drugs can contribute to the development of hyponatremia
by potentiating the action of antidiuretic hormone, by
causing syndrome of inappropriate antidiuretic hormone,
or by inhibiting sodium reabsorption in the kidney (diuretics).
Anticonvulsants
H carbamazepine
H chlorpropamide
H tolbutamide (rarely)
Antineoplastics
Sedatives
H cyclophosphamide
H vincristine
Antipsychotics
H fluphenazine
H thioridazine
H thiothixene
424
Hyponatremia
Dysfunction
Effects
Cardiovascular
Hypotension; tachycardia; with

severe deficit, vasomotor collapse,
thready pulse
Gastrointestinal
Nausea, vomiting, abdominal

cramps
Genitourinary
Oliguria or anuria
Integumentary
Cold, clammy skin; decreasing skin

turgor
Neurologic
Anxiety, headaches, muscle twitching and weakness, seizures
Respiratory
Cyanosis with severe deficiency
Diuretics
H bumetanide
H ethacrynic acid
H furosemide
H thiazides
Antidiabetics
Clinical effects of hyponatremia
H barbiturates
H morphine
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H Rapid, bounding pulse

H Muscle twitching
Test results
Laboratory
H Serum sodium level is less than than 135 mEq/L.
H Urine specific gravity is less than 1.010.
H Serum osmolality is less than 280 mOsm/kg (dilute
blood).
H Urine specific gravity is increased and urine sodium
level is elevated (0.20 mEq/L) in patients with
SIADH.
Treatment
General
H Restricted fluid intake
H High-sodium diet
Medications
H Oral sodium supplements
H Demeclocycline or lithium
H Administration of normal saline solution
H Hypertonic (3% or 5%) saline solutions (with serum
sodium levels less than 110 mEq/L)
Key outcomes
The patient will:
H maintain a normal sodium level
H remain alert and oriented to his environment.
H Restrict fluid intake.
Monitoring
H Vital signs
H Serum sodium levels
H Intake and output
H Neurologic status
Patient teaching
Be sure to cover:
H drug therapy and possible adverse effects
H dietary changes and fluid restrictions
H monitoring daily weight
H signs and symptoms to report to the physician.
Hyponatremia
425
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Hypoparathyroidism
Overview
Description
H Deficiency in parathyroid hormone (PTH) secretion
by the parathyroid glands or the decreased action of

PTH in the periphery
H Because parathyroid glands primarily regulate calcium balance, neuromuscular symptoms range from
paresthesia to tetany
H Classified as idiopathic, acquired, or reversible
Pathophysiology
H PTH normally maintains serum calcium levels by in-
creasing bone resorption and by stimulating renal

conversion of vitamin D to its active form, which enhances GI absorption of calcium and bone resorption.
H PTH also maintains the inverse relationship between
serum calcium and phosphate levels by inhibiting
phosphate reabsorption in the renal tubules and enhancing calcium reabsorption.
H Abnormal PTH production in hypoparathyroidism
disrupts this delicate balance.
Causes
H Autoimmune genetic disorder
H Congenital absence or malformation of the parathy-
roid glands
H Accidental removal of or injury to one or more
parathyroid glands during surgery

H Ischemia or infarction of the parathyroid glands dur-
ing surgery
H Hemochromatosis
H Sarcoidosis
H Amyloidosis
H Tuberculosis
H Neoplasms
H Trauma
H Massive thyroid irradiation
H Hypomagnesemia-induced impairment of hormone
secretion
H Suppression of normal gland function due to hyper-
calcemia
H Delayed maturation of parathyroid function
H Abnormalities of the calcium-sensor receptor
Incidence
H Muscle spasms
H Hyperreflexia
H Neuromuscular excitability
Complications
H Heart failure
H Cataracts
H Tetany
H Increased intracranial pressure
H Irreversible calcification of basal ganglia
H Bone deformities
H Laryngospasm, respiratory stridor, anoxia
H Vocal cord paralysis
H Seizures
H Death
Special populations
Hypoparathyroidism that develops during childhood results in malformed teeth.
Assessment
History
H Neck surgery or irradiation
H Malabsorption disorders
H Alcoholism
H Tingling in the fingertips, around the mouth and,
occasionally, in the feet

H Muscle tension and spasms
H Feeling like throat is constricted
H Dysphagia
H Difficulty walking and a tendency to fall
H Nausea, vomiting, abdominal pain
H Fatigue
Physical findings
H Brittle nails
H Dry skin
H Coarse hair, alopecia
H Transverse and longitudinal ridges in the fingernails
H Loss of eyelashes and fingernails
H Stained, cracked, and decayed teeth
H Tetany
H Positive Chvosteks and Trousseaus signs
H Increased deep tendon reflexes
H Irregular, slow or rapid pulse
H Idiopathic and reversible forms most common in
Test results
children
H Acquired form most common in older patients who
have undergone thyroid gland surgery
Laboratory
H Radioimmunoassay for PTH is decreased.
H Serum and urine calcium levels are decreased.
H Serum phosphate levels are increased.
H Urine creatinine levels are decreased.
426
Hypoparathyroidism
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Imaging
H Computed tomography scan may show frontal lobe
and basal ganglia calcifications.
H X-rays may show increased bone density and bone
malformation.
H Electrocardiography shows a prolonged QT interval.
Treatment
General
H To restore the calcium and associated mineral bal-
ance within the body
H Electrocardiogram for QT interval changes and
arrhythmias
H Signs and symptoms of decreased cardiac output
H Chvosteks sign
H Trousseaus sign
ALERT
Closely monitor the patient receiving digoxin and
calcium because calcium potentiates the effect of
digoxin. Stay alert for signs of digoxin toxicity.
Patient teaching
H Supportive care necessary for an acute, life-
threatening attack or hypoparathyroid tetany

H High-calcium, low-phosphorus diet
Medications
H Vitamin D
H Supplemental calcium
H Calcitriol
Acute, life-threatening tetany

H I.V. administration of 10% calcium gluconate, 10%
calcium glucepate, or 10% calcium chloride
H Sedatives
H Anticonvulsants
Be sure to cover:
H follow-up care
H complications
H periodic checks of serum calcium levels.
Discharge planning
H Refer the patient to an alcoholism treatment program
for additional counseling, if necessary.
Surgery
H To treat underlying cause such as tumor
Key outcomes
The patient will:
H maintain intact skin integrity
H verbalize an understanding of the disorder and treatment regimen.
H Maintain a patent I.V. line.
H Keep emergency equipment readily available.
H Encourage the patient to express his feelings.
Monitoring
H Vital signs
H Intake and output
H Serum calcium and phosphorus levels
Hypoparathyroidism
427
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Hypophosphatemia
Overview
Description
H Deficient serum phosphate levels
Pathophysiology
H Phosphorus exists primarily in inorganic combina-
tion with calcium in teeth and bones.

H In extracellular fluid, the phosphate ion supports
several metabolic functions: utilization of B vitamins,

acid-base homeostasis, bone formation, nerve and
muscle activity, cell division, transmission of hereditary traits, and metabolism of carbohydrates, proteins, and fats.
H Renal tubular reabsorption of phosphate is inversely
regulated by calcium levels an increase in phosphorus causes a decrease in calcium. An imbalance
causes hypophosphatemia or hyperphosphatemia.
Causes
H Inadequate dietary intake
H Commonly related to malnutrition resulting from a
prolonged catabolic state or chronic alcoholism

H Intestinal malabsorption
H Chronic diarrhea
H Hyperparathyroidism with resultant hypercalcemia
H Hypomagnesemia
H Vitamin D deficiency
H Chronic use of antacids containing aluminum hy-
droxide
H Arrhythmias
H Rhabdomyolysis
H Seizures
H Coma
Assessment
History
H Anorexia
H Memory loss
H Muscle and bone pain
H Fractures
H Chest pain
Physical findings
H Tremor and weakness in speaking voice
H Confusion
H Bruising and bleeding
Test results
H Serum phosphorus levels are less than 2.5 mg/dl.
Treatment
General
H Discontinuation of drugs that may cause hypophos-
phatemia (see Drugs that may cause hypophosphatemia)

H High-phosphorus diet
H Use of parenteral nutrition solution with inadequate
Medications
phosphate content
H Renal tubular defects
H Tissue damage in which phosphorus is released by
injured cells
H Diabetic acidosis
H Phosphate salt tablets or capsules

H Potassium phosphate I.V.
Incidence
Key outcomes
H Varies according to the underlying cause

H Occurs in about 1% to 5% of hospitalized patients
H Patients with alcoholism, diabetic ketoacidosis, or
The patient will:

H maintain adequate vital signs
H maintain a normal phosphorus level.
sepsis: 40% to 80% incidence
H More than 50% of renal transplant patients experi-
encing low phosphate levels; many chronically
H Anorexia
H Muscle weakness
H Tremor
H Paresthesia
H Osteomalacia (when persistent)
H Peripheral hypoxia
Complications
H Heart failure
H Shock
428
Hypophosphatemia
Drugs that may cause hypophosphatemia

The following drugs may cause hypophosphatemia:
H acetazolamide, thiazide diuretics (chlorothiazide and
hydrochlorothiazide), loop diuretics (bumetanide and
furosemide), and other diuretics
H antacids, such as aluminum carbonate, aluminum hydroxide, calcium carbonate, and magnesium oxide
H insulin
H laxatives.
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H Provide safety measures.
H Administer prescribed phosphorus replacement.
H Assist with ambulation and activities of daily living.
Monitoring
H Neurologic status
H Phosphorus and calcium levels
H Intake and output
Patient teaching
Be sure to cover:
H proper administration of phosphorus supplements
H the need to adhere to a high-phosphorus diet. (See
Foods high in phosphorus, page 407.)
Discharge planning
indicated.
Hypophosphatemia
429
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Hypopituitarism
Overview
Description
H Partial or complete failure of the anterior pituitary
gland to produce its vital hormones: corticotropin,

thyroid-stimulating hormone (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH),
growth hormone (GH), and prolactin
H May be primary or secondary, resulting from dysfunction of the hypothalamus
H Development of clinical features typically slow and
not apparent until 75% of the pituitary gland is destroyed
H Total loss of all hormones fatal without treatment
H Prognosis good with adequate replacement therapy
and correction of the underlying causes
H Panhypopituitarism: absence of all hormones
Pathophysiology
H The pituitary gland is extremely vulnerable to is-
chemia and infarction because its highly vascular.

H Any event that leads to circulatory collapse and com-
pensatory vasospasm may result in gland ischemia,

tissue necrosis, or edema.
H Expansion of the pituitary within the fixed compartment of the sella turcica further impedes blood supply to the pituitary.
Causes
H Tumor
H Pituitary gland hypoplasia or aplasia
H Pituitary infarction
H Partial or total hypophysectomy by surgery, irradia-
tion, or chemical agents

H Granulomatous disease
H Deficiency of hypothalamus releasing hormones
H Idiopathic
H Infection
H Trauma
Incidence
H Relatively rare
H Occurs in adults and children
H Metabolic dysfunction
H Sexual immaturity
H Fatigue
Complications
H Any combination of deficits in the production of the
six major hormones

H GH deficiency
H TSH deficiency
430
Hypopituitarism
H Corticotropin deficiency
H Gonadotropin and prolactin deficiency
H Pituitary apoplexy (a medical emergency)
H High fever, shock, coma, and death
H Diabetes insipidus
Special populations
In children, hypopituitarism can cause dwarfism
and pubertal delay.
Assessment
History
H Signs and symptoms dependent on which pituitary
hormones are deficient, patients age, and severity of

disorder
Gonadotropin (FSH and LH) deficiency
in females
H Amenorrhea
H Dyspareunia
H Infertility
H Reduced libido
Gonadotropin (FSH and LH) deficiency in
males
H Impotence
H Reduced libido
TSH deficiency
H Cold intolerance
H Constipation
H Menstrual irregularity
H Lethargy
H Severe growth retardation in children despite treatment
Corticotropin deficiency
H Fatigue
H Nausea, vomiting, anorexia
H Weight loss
Prolactin deficiency
H Absent postpartum lactation
H Amenorrhea
Physical findings
GH deficiency
H Physical signs possibly not apparent in neonate
H Growth retardation usually apparent at age 6 months
In children:
H Chubbiness from fat deposits in the lower trunk
H Short stature
H Delayed secondary tooth eruption
H Delayed puberty
H Average height of 4 (1.2 m), with normal proportions
H More subtle signs in adults (fine wrinkles near the
mouth and eyes)
Gonadotropin (FSH and LH) deficiency
in women
H Breast atrophy
H Sparse or absent axillary and pubic hair
H Dry skin
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Gonadotropin (FSH and LH) deficiency in men

H Decreased muscle strength
H Testicular softening and shrinkage
H Retarded secondary sexual hair growth
TSH deficiency
H Dry, pale, puffy skin
H Slow thought processes
H Bradycardia
Corticotropin deficiency
H Depigmentation of skin and nipples
H Hypothermia and hypotension during periods of
stress
Prolactin deficiency
H Sparse or absent growth of pubic and axillary hair
Panhypopituitarism
H Mental abnormalities, including lethargy and psychosis
H Physical abnormalities, including orthostatic hypotension and bradycardia
Test results
Laboratory
H Serum thyroxin levels are decreased in diminished
thyroid gland function due to lack of TSH.
H Radioimmunoassay shows decreased plasma levels of
some or all of the pituitary hormones.
H Increased prolactin levels may indicate a lesion in
the hypothalamus or pituitary stalk.
H Oral administration of metyrapone may show the
source of low hydroxycorticosteroid levels in serum
or urine.
H Insulin administration shows low levels of corticotropin, indicating pituitary or hypothalamic failure.
H Dopamine antagonist administration evaluates prolactin secretory reserve.
H I.V. administration of gonadotropin-releasing hormone may distinguish pituitary and hypothalamic
causes of gonadotropin deficiency.
H Provocative testing shows persistently low GH and
insulin-like growth factor-1 levels, confirming GH
deficiency.
Imaging
H Computed tomography scans, magnetic resonance
imaging, or cerebral angiography may show the presence of intrasellar or extrasellar tumors.
Treatment
General
H If caused by a lesion or tumor, removal, radiation, or
both, followed by possible lifelong hormone replacement therapy

H Endocrine substitution therapy for affected organs
H Regular exercise program
H Rest periods for fatigue
Special populations
Children with hypopituitarism may also need
adrenal and thyroid hormone replacement and, as
they approach puberty, sex hormones.
Surgery
H For pituitary tumor
Key outcomes
The patient will:
H maintain body weight
H maintain normal body temperature
H demonstrate age-appropriate skills and behavior to
the extent possible
H verbalize feelings of positive self-esteem.
H Encourage maintenance of adequate calorie intake.
H Keep the patient warm.
Monitoring
H Laboratory tests for hormonal deficiencies
H Calorie intake
H Daily weight
H Vital signs
H Neurologic status
H Signs and symptoms of pituitary apoplexy, a medical
emergency
H Signs and symptoms of hypoglycemia
Patient teaching
Be sure to cover:
H long-term hormonal replacement therapy and adverse reactions
H regular follow-up appointments
H energy-conservation techniques
H the need for adequate rest
H the need for a balanced diet.
Discharge planning
H Refer the parents for psychological counseling or to
community resources.
Medications
H Hormone replacement, appropriate to deficiency
Hypopituitarism
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Hypothermia
Overview
Description
H Lowering of the core body temperature to below
95 F (35 C)
H Systemic reaction, rather than localized
H Produces chemical changes in body
H Can be fatal
Pathophysiology
H Low core body temperature

H Rigid muscles
H Irregular heart and respiratory rates
H Unconsciousness
Complications
H Fatal coagulation disorders
H Renal failure
H Cardiorespiratory arrest
Assessment
H Exposure to cold temperatures slows the actions of
History
enzymes throughout body.

H The body attempts to generate heat by inducing shivering (involuntary contraction and expansion of
muscle tissue).
H Muscle action creates heat through friction.
H Body is unable to generate sufficient heat.
H Metabolic changes slow the functions of most major
organ systems, including decreased renal flow and
glomerular filtration.

H Exposure to cold temperatures
Causes
H Interference with the bodys temperature regulation
by alterations in heat production, conduction, convection, radiation, evaporation, or respiration

H Examples:
Cold-water near drowning
Prolonged exposure to cold temperatures
Administration of blood products
Disease processes
Risk factors
H Youth
H Increased age
H Lack of insulating subcutaneous body fat
H Wet or inadequate clothing
H Drug abuse
H Cardiac disease
H Hypothyroidism
H Fatigue
H Malnutrition
H Excessive alcohol intake
H Smoking
H Certain medications
Incidence
H About 600 elderly people in the United States dying
each year from hypothermia

H One study shows about 12,000 people dying during
one 15-year period; about 50% of these deaths were

in people older than age 65; males were affected
more than females; and whites were affected less frequently than people of other races
H Uncontrollable shivering
432
Hypothermia
Physical findings
H Mild core body temperature between 90 and
95 F (32.2 and 35 C)
Cool skin
Fatigue
Slow gait
Apathy
Slurred speech
Confusion
Shivering
Muscle weakness
H Moderate core body temperature between 82
and 86 F (27.8 and 30 C)
Cold skin
Cyanosis
Bradycardia
Atrial and ventricular arrhythmias
Hypotension
Stupor or coma
Muscular rigidity
Generalized edema
Slowed reflexes
Poorly reactive pupils
Oliguria
H Severe core body temperature below 82 F
(27.8 C)
Very cold skin
Muscle rigidity
Apnea
Ventricular fibrillation
Unresponsiveness
Fixed pupils
Test results
Laboratory
H Complete blood count may indicate hemoconcentration or anemia from blood loss or cell damage.
H Liver enzyme studies may be increased due to organ
damage.
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Treatment
Patient teaching
General
Be sure to cover:
H ways to prevent recurrence
H effects of alcohol, smoking, and drugs that increase
risks
H diseases that may predispose patient to recurrence.
H Protecting the patient from further heat loss

H Insulation to conserve body heat
H Dry clothing if necessary
H Passive rewarming
No external methods used

Body regains heat slowly
H Active rewarming
Heating blankets and other objects
Warm-water immersion
Radiant heat
H Active core rewarming
Heated I.V. fluids
Genitourinary tract irrigation
Peritoneal, gastric, and mediastinal lavage
Hemodialysis
H Cardiopulmonary resuscitation (CPR) and defibrillation, if necessary
H Oxygen and controlled ventilation
Medications
H Antiarrhythmic agents such as lidocaine, if indicated
Key outcomes
The patient will:
H show signs of adequate cardiac output
H express feelings of comfort and warmth
H verbalize an understanding of the condition and how
to prevent recurrence
H attain and maintain normal body temperature
H Administer CPR if necessary.
H Assist with rewarming procedures, as ordered.
H Provide supportive environment for anxious patient
and family.
Monitoring
H Vital signs
H Temperature
H Cardiac and ventilatory status
H Neurologic status
H Intake and output
H Skin integrity during rewarming due to possible
burns
H Complete blood count
H Coagulation and liver enzyme study results
H Urinalysis test results
H Serum amylase, glucose, electrolyte, and blood urea
nitrogen levels
Hypothermia
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Hypothyroidism
H Cardiomegaly
H Heart failure
H Pleural and pericardial effusion
Overview
GI complications
H Achlorhydria
H Anemia
H Dynamic colon
H Megacolon
Other complications
H Conductive or sensorineural deafness
H Psychiatric disturbances
H Benign intracranial hypertension
H Impaired fertility
H Myxedema coma
Description
H Clinical condition characterized by either decreased
circulating levels of or resistance to free thyroid hormone (TH)

H Classified as primary or secondary
H Severe hypothyroidism known as myxedema
Pathophysiology
H In primary hypothyroidism, a decrease in TH pro-
duction is a result of the loss of thyroid tissue.

H This results in an increased secretion of thyroid-
stimulating hormone (TSH) that leads to a goiter.

H In secondary hypothyroidism, the pituitary typically
fails to synthesize or secrete adequate amounts of

TSH, or target tissues fail to respond to normal blood
levels of TH.
H Either type may progress to myxedema, which is clinically more severe and considered a medical emergency.
Causes
H Autoimmune thyroiditis (Hashimotos) (most com-
mon cause)
H Thyroid gland surgery
H Radioactive iodine therapy
H Inflammatory conditions
H Endemic iodine deficiency
H Antithyroid drugs
H Amyloidosis
H Sarcoidosis
H External radiation to the neck
H Drugs, such as iodides and lithium
H Pituitary failure to produce TSH
H Hypothalamic failure to produce thyrotropin-
releasing hormone
H Postpartum pituitary necrosis
H Pituitary tumor
H Idiopathic
Incidence
H Most prevalent in females
H In the United States, increased incidence in people
older than age 40
H Decreased energy metabolism
H Decreased heat production
Complications
Cardiovascular complications
H Arteriosclerosis
H Ischemic heart disease
H Peripheral vascular disease
434
Hypothyroidism
Assessment
History
H Vague and varied symptoms that developed slowly
over time
H Energy loss, fatigue
H Forgetfulness
H Sensitivity to cold
H Unexplained weight gain
H Constipation
H Anorexia
H Decreased libido
H Menorrhagia
H Paresthesia
H Joint stiffness
H Muscle cramping
Physical findings
H Slight mental slowing to severe obtundation
H Thick, dry tongue
H Hoarseness; slow, slurred speech
H Dry, flaky, inelastic skin
H Puffy face, hands, and feet
H Periorbital edema; drooping upper eyelids
H Dry, sparse hair with patchy hair loss
H Loss of outer third of eyebrow
H Thick, brittle nails with transverse and longitudinal
grooves
H Ataxia, intention tremor; nystagmus
H Doughy skin that feels cool
H Weak pulse and bradycardia
H Muscle weakness
H Sacral or peripheral edema
H Delayed reflex relaxation time
H Possible goiter
H Absent or decreased bowel sounds
H Hypotension
H A gallop or distant heart sounds
H Adventitious breath sounds
H Abdominal distention or ascites
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Test results
Laboratory
H Radioimmunoassay shows decreased serum levels of
T3 and T4.
H Serum TSH level is increased with thyroid insufficiency and decreased with hypothalamic or pituitary
insufficiency.
H Serum cholesterol, alkaline phosphatase, and triglycerides levels are elevated.
H Serum electrolytes show low serum sodium levels in
myxedema coma.
H Arterial blood gas analysis shows decreased pH and
increased partial pressure of carbon dioxide in
myxedema coma.
Imaging
H Skull X-rays, computed tomography scan, and magnetic resonance imaging may show pituitary or hypothalamic lesions.
H Thyroid scan and uptake evaluates structure and
function.
Treatment
General
H To restore and maintain a normal thyroid state
H Need for long-term thyroid replacement
H Low-fat, low-cholesterol, high-fiber, low-sodium diet
H Possibly fluid restriction
Medications
H Synthetic hormone levothyroxine
H Synthetic liothyronine
Surgery

Monitoring
H Vital signs
H Intake and output
H Daily weight
H Pulmonary status
H Edema
H Bowel sounds, abdominal distention, frequency of
bowel movements
H Mental and neurologic status
H Signs and symptoms of hyperthyroidism
Patient teaching
Be sure to cover:
H physical and mental changes
H signs and symptoms of myxedema
H the need for lifelong hormone replacement therapy
H the need to wear a medical identification bracelet
H the importance of keeping accurate records of daily
weight
H the need to adhere to a well-balanced, high-fiber,
low-sodium diet
H energy-conservation techniques.
Discharge planning
H Refer the patient and family members to a mental
health professional for additional counseling, if

needed.
H For underlying cause such as pituitary tumor
Key outcomes
The patient will:
H demonstrate normal laboratory values
H maintain balanced fluid volume status
H consume adequate daily calorie requirements
H Maintain fluid restrictions and a low-sodium diet.
H Provide a high-bulk, low-calorie diet.
H Reorient the patient, as needed.
H Offer support and encouragement.
H Keep the patient warm, as needed.
Hypothyroidism
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Idiopathic
thrombocytopenic
purpura
Overview
Description
H A deficiency of platelets occurring when the immune
system destroys the bodys own platelets

H May be acute, as in postviral thrombocytopenia, or
chronic, as in essential thrombocytopenia or autoimmune thrombocytopenia

H Excellent prognosis for acute form; recovery in nearly four of five patients without treatment
H Good prognosis for chronic form; remissions commonly lasting weeks or years, especially among females
Pathophysiology
H Circulating immunoglobulin (Ig) G molecules react
with host platelets, which are then destroyed in the

spleen and, to a lesser degree, in the liver.
H Normally, the life span of platelets in circulation is 7
to 10 days. In idiopathic thrombocytopenic purpura
(ITP), platelets survive 1 to 3 days or less.
Causes
H Viral infection
H Immunization with a live virus vaccine
H Immunologic disorders
H Drug reactions
Incidence
Special populations
Acute ITP usually affects children between ages 2
and 6; chronic ITP mainly affects adults younger
than age 50, especially women between ages 20
and 40.
H Epistaxis
H Bleeding gums
H Hemorrhages into the skin, mucous membranes, and
other tissues causing red discoloration of skin (purpura)

H Small, purplish hemorrhagic spots on skin (petechiae)
H Excessive menstrual bleeding
Complications
H Hemorrhage
H Cerebral hemorrhage
H Purpuric lesions of vital organs (such as the brain
and kidney)
436
Idiopathic thrombocytopenic purpura
Assessment
History
H Epistaxis
H Bleeding gums
H Menorrhagia
H Recent viral illness
Physical findings
H Petechiae or ecchymosis
H Bleeding into mucous membranes
H Splenomegaly
Test results
Laboratory
H Platelet count is less than 20,000/l.
H Platelets are of abnormal size and appearance.
H Hemoglobin level is decreased (if bleeding occurred).
H Bone marrow studies show abundant megakaryocytes (platelet precursor cells) and a circulating
platelet survival time of only several hours to a few
days.
H Humoral tests measure platelet-associated IgG (onehalf of all patients with ITP display elevated IgG
levels).
Treatment
General
H Rest periods between activities
H Complete bed rest during active bleeding
Medications
Acute
H Glucocorticoids to prevent further platelet destruction by immunosuppression
H IgG or Rho immunoglobulin
H Rituximab
H Chemotherapy
Chronic
H Vitamin K
H Corticosteroids such as prednisone
Surgery
H Splenectomy (when splenomegaly accompanies the
initial thrombocytopenia)
Other
H Platelet transfusion with profuse bleeding
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Key outcomes
The patient will:
H demonstrate the use of protective measures, including conserving energy, maintaining a balanced diet,
and getting plenty of rest
H Administer prescribed platelets.
H Protect all areas of petechia and ecchymoses from
further injury.
Monitoring
H Signs of bleeding
H Platelet count
H Intake and output
H Vital signs
When receiving immunosuppressants

H Bone marrow depression
H Infection
H Mucositis
H GI ulcers
H Severe diarrhea or vomiting
Patient teaching
Be sure to cover:
H how to observe for petechiae, ecchymoses, and other
signs of recurrence
H avoiding aspirin and ibuprofen
H avoiding straining during defecation and coughing
H bleeding precautions.
Discharge planning
H Advise the patient to carry medical identification to
alert others about the condition.
Idiopathic thrombocytopenic purpura
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Impetigo
Overview
Description
H Contagious, superficial bacterial skin infection
H Nonbullous and bullous forms
H May complicate chickenpox, eczema, and other skin
disorders marked by open lesions

H Most commonly appears on face, arms, and legs
Pathophysiology
Nonbullous impetigo
H Eruption occurs when bacteria inoculate traumatized
skin cells.
H Lesions begin as small vesicles, which rapidly erode.
H Honey-colored crusts surrounded by erythema are
formed.
Bullous impetigo
H Eruption occurs in nontraumatized skin via bacterial
toxin or exotoxin.
H Lesions begin as thin-walled bullae and vesicles.
H Lesions contain clear to turbid yellow fluid; some
crusting exists. (See Recognizing impetigo.)
Risk factors
H Poor hygiene
H Untreated minor trauma
H Overcrowded living conditions
H Lesions of preexisting eczema, chickenpox, scabies
H Other skin rashes
H Anemia
H Malnutrition
Incidence
H Most common among infants, children, and young
adults
H More common in warm ambient temperatures
H Predominant during late summer and early fall
H Painlessness
H Tender, red macule or papule
H Pustules
Complications
H Acute glomerulonephritis
H Ecthyma (see Comparing ecthyma and impetigo)
H Exfoliative eruption (staphylococcal scalded-skin
syndrome)
Causes
Assessment
H Spread by autoinoculation through scratching
History
Recognizing impetigo
In impetigo, when the vesicles break, crust forms from the
exudate. This infection is especially contagious among
young children.

H Absence of pain
H Possible pruritus
Physical findings
Nonbullous impetigo
H Small, red macule or vesicle becoming pustular within a few hours
H Characteristic thick, honey-colored crust forming
from the exudate
H Satellite lesions due to autoinoculation
Bullous impetigo
H Thin-walled vesicle
H Thin, clear crust forming from exudate
H Lesion appearing as a central clearing circumscribed
by an outer rim
Test results
Laboratory
H Gram stain of vesicular fluid shows infecting
organism.
H Culture and sensitivity testing of exudate or denuded
crust shows infecting organism.
H White blood cell count is elevated.
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Impetigo
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Treatment
General
H Removal of exudate by washing lesions two to three
times per day with soap and water

H Warm soaks or compresses of normal saline solution
or a diluted soap solution for stubborn crusts

H Prevention with use of benzoyl peroxide soap
Medications
H Antihistamines
Comparing ecthyma and impetigo

Ecthyma is a superficial skin infection that usually causes
scarring. It generally results from infection by group A
beta-hemolytic streptococci.
Ecthyma differs from impetigo in that its characteristic
ulcer results from deeper penetration of the skin by the infecting organism (involving the lower epidermis and dermis), and the overlying crust tends to be raised (38 to
114) [1 to 3 cm]).
These lesions are usually found on the legs after a
scratch or an insect bite. Autoinoculation can transmit ecthyma to other parts of the body, especially to sites that
have been scratched open.
Therapy for ecthyma is basically the same as for impetigo, beginning with removal of the crust, but the patients response may be slower. Parenteral antibiotics are
also used.
Key outcomes
The patient will:
H demonstrate proper skin care regimen
H verbalize feelings about changed body image.
Discharge planning
H Encourage the patient to schedule follow-up appoint-
ments as recommended by his physician.
H Remove crusts by gently washing with bactericidal
soap and water.

H Soften stubborn crusts with cool compresses.
H Encourage verbalization of feelings about body
image.
H Comply with local public health standards and
guidelines.
Monitoring
H Complications
Patient teaching
Be sure to cover:
H prevention techniques (see Preventing the spread of
impetigo)
H trimming fingernails short
H regular bathing with bactericidal soap
H identification of characteristic lesions
H completion of prescribed medications
H possible adverse reactions
H lesion care.
Prevention
Preventing the spread of impetigo

The spread of impetigo can be prevented by following
these guidelines:
H Practice meticulous hand-washing techniques after
touching linens.
H Use a clean towel and washcloth with each bath if
impetigo is present.
H Avoid sharing clothes and linens.
H Avoid sharing razors, towels, and washcloths.
H Clean all minor cuts and scrapes with soap and water.
Impetigo
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Infectious
mononucleosis
Assessment
History
H Contact with a person having infectious mononu-
Overview
Description
H An acute infectious disease that causes fever, sore
throat, and cervical lymphadenopathy
Pathophysiology
H Virus enters and replicates in epithelial cells of the
oropharynx and B cells of tonsillar tissue, causing alteration of shape and function of the infected cells.
H Infected B cells activate cell-mediated immunity with
proliferation of abnormal cytotoxic T cells in lymphoid tissues.
H Lymphoproliferation stops when cytotoxic T cells are
able to destroy infected B cells.
Causes
cleosis
H Headache
H Malaise
H Fatigue
H Sore throat
H Fever
H Loss of appetite
H Muscle aches or stiffness
Physical findings
H Exudative tonsillitis, pharyngitis
H Palatal petechiae
H Periorbital edema
H Maculopapular rash that resembles rubella
H Cervical adenopathy; possible inguinal and axillary
adenopathy
H Splenomegaly, hepatomegaly, jaundice
H Epstein-Barr virus (EBV), a member of the herpes
Test results
group
H Spread by contact with oral secretions (kissing)
H Also transmitted during bone marrow transplantation
and blood transfusion
Laboratory
H White blood cell (WBC) count is increased 10,000 to
20,000/l during the second and third weeks of illness; lymphocytes and monocytes account for 50% to
70% of the total WBC count; 10% of the lymphocytes
are atypical.
H Fourfold increase in heterophil antibodies (agglutinins for sheep red blood cells) during the acute
phase and at 3- to 4-week intervals.
H Antibodies to EBV and cellular antigens are shown by
indirect immunofluorescence.
H Liver function studies are abnormal.
Incidence
H Primarily affects young adults and children
H Common and widespread in early childhood in de-
veloping countries and socioeconomically depressed

populations
H Incubation period of about 4 to 6 weeks in young
adults
H Prodromal symptoms include headache, malaise,
and profound fatigue

H After 3 to 5 days, triad of symptoms, including sore
throat, cervical lymphadenopathy, and temperature
fluctuations, with an evening peak of 101 to 102 F
(38.3 to 38.9 C)
Complications
H Splenic enlargement or rupture
H Aseptic meningitis
H Encephalitis
H Hemolytic anemia
H Pericarditis
H Secondary bacterial throat infection
H Hepatitis
440
Infectious mononucleosis
Treatment
General
H Essentially supportive
H Nutritious diet
H Soft food (with throat soreness)
H Avoidance of strenuous activity or contact sports until
fully recovered
Medications
H Acetaminophen or ibuprofen
H Steroids such as prednisone
Surgery
H Splenectomy for splenic rupture
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Key outcomes
The patient will:
H maintain temperature within normal limits
H conserve energy while performing daily activities to
tolerance level
H identify factors that intensify pain and change behavior accordingly
H express needs and communicate whether needs are
met.
Prevention
Preventing the spread of infectious

mononucleosis
The spread of infectious mononucleosis can be limited by
teaching the patient to follow these guidelines:
H Avoid sharing food, dishes, glasses, and utensils.
H Avoid kissing for several days after fever has subsided.
H Use good hand-washing techniques.
H Dont donate blood for at least 6 months from onset of
illness.
H Provide warm saline gargles for symptomatic relief of
sore throat.
H Provide adequate fluids and nutrition.
H Plan care to provide frequent rest periods.
Monitoring
H Fatigue
H Liver function tests
H Complications
Patient teaching
Be sure to cover:
H expectation that convalescence may take several
weeks
H need for bed rest during the acute illness
H explanation that theres a period of prolonged communicability
H prevention techniques (see Preventing the spread of
infectious mononucleosis)
H benefits of bland foods, milk shakes, fruit juices, and
broths to minimize throat discomfort.
Discharge planning
H Refer the patient to an otolaryngologist for marked
tonsillar swelling or a neurologist for a central nervous system complication.
Infectious mononucleosis
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Influenza
Overview
Description
H An acute, highly contagious infection of the respirato-
ry tract
H Has capacity for antigenic variation (ability to mutate
into different strains so that no immunologic resistance is present in those at risk)

H Antigenic variation characterized as antigenic drift
(minor changes occurring yearly or every few years)
and antigenic shift (major changes that lead to pandemics)
H Also called the grippe or the flu
Pathophysiology
H The virus invades the epithelium of the respiratory
tract, causing inflammation and desquamation.

H After attaching to the host cell, viral ribonucleic acid
enters the cell and uses host components to replicate

its genetic material and protein, which are then assembled into new virus particles.
H Newly produced viruses burst forth to invade other
healthy cells.
H Viral invasion destroys host cells, impairing respiratory defenses (especially mucociliary transport system) and predisposing the patient to secondary bacterial infection.
Causes
H Type A, most prevalent; strikes annually with new
serotypes causing epidemics every 3 years

H Type B also annual; causes epidemics only every 4
to 6 years
H Type C endemic; causes only sporadic cases
H Infection transmitted by inhaling a respiratory
droplet from an infected person or by indirect contact (drinking from a contaminated glass)
Incidence
H Affects all age-groups; highest incidence among
school-age children
H Greatest severity (may lead to death) in young chil-
dren, elderly people, and those with chronic diseases

H Occurs sporadically or in epidemics (usually during
colder months) with peak within 2 to 3 weeks after

initial cases and lasting 2 to 3 months
H Flu symptoms after incubation period of 24 to
Complications
H Pneumonia
H Myositis
H Exacerbation of chronic obstructive pulmonary
disease
H Reyes syndrome
H Myocarditis
H Pericarditis
H Transverse myelitis
H Encephalitis
Assessment
History
H Usually, recent exposure (typically within 48 hours)
to a person with influenza

H Patient not receiving influenza vaccine during the
past season
H Headache
H Malaise
H Myalgia
H Fatigue, listlessness, weakness
Physical findings
H Fever (usually higher in children)
H Signs of croup, dry cough
H Red, watery eyes; clear nasal discharge
H Erythema of the nose and throat without exudate
H Tachypnea, shortness of breath, cyanosis
H With bacterial pneumonia, purulent or bloody
sputum
H Cervical adenopathy and tenderness
H Breath sounds may be diminished in areas of con-
solidation
H Nausea, vomiting, and diarrhea possibly occurring,
but more common in children than adults
Test results
H After an epidemic is confirmed, diagnosis requires
only observation of clinical signs and symptoms.

Laboratory
H Inoculation of chicken embryos with nasal secretions
from infected patients shows influenza virus.
H Throat swabs, nasopharyngeal washes, or sputum
culture shows isolation of the influenza virus.
H Immunodiagnostic techniques show viral antigens in
tissue culture or in exfoliated nasopharyngeal cells
obtained by washings.
H Leukocyte counts are elevated in secondary bacterial
infection.
H Leukocyte counts are decreased in overwhelming
viral or bacterial infection.
48 hours
H Sudden onset of chills, fever (101 to 104 F [38.3
to 40 C]), headache, malaise, myalgia (particularly

in the back and limbs), photophobia, a nonproductive cough and, occasionally, laryngitis, hoarseness,
rhinitis, and rhinorrhea
442
Influenza
Treatment
General
H Fluid and electrolyte replacements
H Oxygen and assisted ventilation, if indicated
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Medications
H Acetaminophen
H Guaifenesin or expectorant
H Amantadine for influenza A
Key outcomes
The patient will:
H report increased energy level
H maintain a normal temperature
pain
H maintain respiratory rate within 5 breaths/minute of
baseline.
Prevention
Preventing the spread of influenza

The spread of influenza can be limited by teaching the patient to follow these guidelines:
H Wash hands frequently and use good hand-washing
techniques.
H Cover mouth and nose when coughing or sneezing.
H Dispose of tissues properly.
H Avoid touching eyes, nose, and mouth.
H Avoid close contact with others.
H Stay home and rest when sick.
H Get plenty of sleep, fluids, and nutritious foods.
H High-risk patients should take antiviral drugs as
prescribed.
H Get the influenza vaccine yearly.
H Administer oxygen therapy, if warranted.
Monitoring
H Temperature
H Complications
Patient teaching
Be sure to cover:
H mouthwash or warm saline gargles to ease sore
throat
H importance of increased fluids to prevent dehydration
H warm bath or a heating pad to relieve myalgia
H prevention techniques. (See Preventing the spread
of influenza.)
Influenza
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Inguinal hernia
Overview
Description
H Protrusion of part of an internal organ through an
abnormal opening in the wall of the cavity that surrounds it

H The most common type of hernia (see Common
sites of hernia)
H May be direct or indirect
H Also called rupture
Pathophysiology
H In an inguinal hernia, the large or small intestine,
omentum, or bladder protrudes into the inguinal

canal.
H In an indirect hernia, abdominal viscera leave the
abdomen through the inguinal ring and follow the
spermatic cord (in males) or round ligament (in females); they emerge at the external ring and extend
down into the inguinal canal, typically into the scrotum or labia.
H In a direct inguinal hernia, instead of entering the
canal through the internal ring, the hernia passes
through the posterior inguinal wall, protrudes directly through the transverse fascia of the canal (in an
area known as Hesselbachs triangle), and comes
out at the external ring.
Causes
H Direct hernias: more common in middle-aged and
elderly people
H A lump that appears over the herniated area when
the patient stands or strains and that disappears

when the patient is in a supine position
H Tension on the herniated contents possibly causing a
sharp, steady pain in the groin that fades when the
hernia is reduced
H Strangulation that produces severe pain possibly
leading to partial or complete bowel obstruction and
intestinal necrosis
Complications
H Strangulation
H Infection (after surgery)
Assessment
History
H Sharp or catching pain when lifting or straining
Physical findings
H Obvious swelling or lump in the inguinal area (large
hernia) (see Identifying a hernia)
Test results
Laboratory
H White blood cell count is elevated (with intestinal
obstruction).
H Indirect
weakness in fascial margin of internal

inguinal ring
H Direct weakness in fascial floor of inguinal canal
H Either weak abdominal muscles (caused by congenital malformation, trauma, or aging) or increased
intra-abdominal pressure (caused by heavy lifting,
pregnancy, obesity, or straining)
Incidence
H Indirect hernias: more common; may develop at any
age; three times more common in males; especially

prevalent in infants
Identifying a hernia
Palpation of the inguinal area while the patient is performing Valsalvas maneuver confirms the diagnosis of inguinal hernia. To detect a hernia in a male patient, ask the patient to stand with his ipsilateral leg slightly flexed and his
weight resting on the other leg. Insert an index finger into
the lower part of the scrotum and invaginate the scrotal
skin so the finger advances through the external inguinal
ring to the internal ring (about 12 to 2 [1 to 5 cm]
through the inguinal canal). Tell the patient to cough. If
pressure is felt against the fingertip, an indirect hernia exists; if pressure is felt against the side of the finger, a direct hernia exists.
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Inguinal hernia
Treatment
General
H Manual reduction
H Truss
H Nothing by mouth if surgery necessary
Medications
H Analgesics
H Electrolyte replacement
Surgery
H Herniorrhaphy
H Hernioplasty
H Bowel resection (with strangulation or necrosis)
Key outcomes
The patient will:
H have normal bowel function
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Common sites of hernia

There are four common sites of hernia: umbilical, incisional,
inguinal, and femoral. Here are descriptions of each type
with an illustration demonstrating where each type is located.
Umbilical
Umbilical hernia results from abnormal muscular structures
around the umbilical cord. This hernia is quite common in
neonates but also occurs in females who are obese or who
have had several pregnancies. Because most umbilical hernias in infants close spontaneously, surgery is warranted
only if the hernia persists for more than 4 to 5 years. Taping
or binding the affected area or supporting it with a truss may
relieve symptoms until the hernia closes. A severe congenital umbilical hernia, which allows the abdominal viscera to
protrude outside the body, must be repaired immediately.
Incisional
Incisional (ventral) hernia develops at the site of previous
surgery, usually along vertical incisions. This hernia may result from a weakness in the abdominal wall, caused by an
infection, impaired wound healing, inadequate nutrition, extreme abdominal distention, or obesity. Palpation of an inci-
sional hernia may reveal several defects in the surgical scar.

Effective repair requires pulling the layers of the abdominal
wall together without creating tension or, if this isnt possible, the use of Teflon, Marlex mesh, or tantalum mesh to
close the opening.
Inguinal
Inguinal hernia can be direct or indirect. An indirect inguinal
hernia causes the abdominal viscera to protrude through the
inguinal ring and follow the spermatic cord (in males) or
round ligament (in females). A direct inguinal hernia results
from a weakness in the fascial floor of the inguinal canal.
Femoral
Femoral hernia occurs where the femoral artery passes into
the femoral canal. Typically, a fatty deposit within the femoral canal enlarges and eventually creates a hole big enough
to accommodate part of the peritoneum and bladder. A femoral hernia appears as a swelling or bulge at the pulse point
of the large femoral artery. Its usually a soft, pliable, reducible, nontender mass but commonly becomes incarcerated or strangulated.
Umbilical
Incisional
Inguinal
Femoral
H Apply a truss after a hernia has been reduced.
Monitoring
H Vital signs
H Pain control
H Signs of strangulation or incarceration
Patient teaching
Be sure to cover:
H avoidance of lifting heavy objects or straining during
bowel movements
H signs and symptoms of infection (oozing, tenderness,
warmth, and redness) at the incision site
H wound care
H after surgery, not resuming normal activity or returning to work without the surgeons permission.
Discharge planning
H Encourage the patient to schedule follow-up appoint-
ments as recommended by the surgeon.
Inguinal hernia
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Insect bites and stings

Overview
Description
H Bite or sting from an insect or other arthropod, such
as a tick, brown recluse spider, black widow spider,

scorpion, bee, wasp, yellow jacket, or fire ant, that
causes pain or a local systemic reaction
Pathophysiology
H A bite or sting can injure the skin, and secretions re-
leased from a bite or sting can cause a physiologic

response specific to the insect or arthropod.
H Reactions to secretion exposure range from barely
noticeable to life-threatening.
H Transmission of disease may result from a bite or
sting.
H Mouth parts of an insect or arthropod are classified
as piercing-sucking, sponging, or biting-chewing.
Causes
H Toxic effects of venom
H Hypersensitivity response
Incidence
H Unknown
Local reaction
H Mild discomfort to moderate or severe pain
H Erythema and warmth
H Tenderness
H Edema of surrounding tissues
H Severe local reaction
H Generalized erythema
H Urticaria
H Pruritic edema
Systemic response
H All of the above symptoms
H Anxiety, disorientation
H Weakness
H GI disturbances
H Dizziness
H Hypotension
H Stridor
H Dyspnea and cough
H Cardiovascular collapse
Complications
H Anaphylaxis
H Hemolytic anemia
H Rarely, thrombocytopenia (brown recluse spider
only)
446
Assessment
History
Tick bite
H Itching at the affected site
H Tick observed at lesion
Brown recluse spider bite
H Minimal initial pain that increases over time
H Fever, chills, malaise, weakness
H Nausea, vomiting
H Joint pain
Black widow spider bite
H Pinprick sensation, followed by dull, numbing pain
H Leg bite: severe pain and large-muscle cramping
H Vertigo
H Chills and sweats
Bee, wasp, or yellow jacket sting
H Pain and pruritus
H Generalized weakness
H Chest tightness
H Dizziness
H Abdominal cramps
H Throat constriction
Fire ant sting
H Immediate pain, itching, and burning
Physical findings
Tick bite
H Tick paralysis
H Expanding skin lesion, erythema migrans
H Bleb (blister)
H Bluish ring around bite
H Joint pain
H Seizures
H Petechiae
H Rigid, painful abdomen
H Rigidity and pain in the chest, shoulders, and back
(if arm bite)
H Extreme restlessness (systemic)
H Pallor
H Seizures, especially in children
H Hypertension
H Tachycardia with thready pulse
H Raised, reddened wheal, possibly with a protruding
stinger from the bee, wasp, or yellow jacket
H Wheezing
H Hypotension
Fire ant sting
H Clear vesicles with surrounding erythema
H Pustule
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Test results
Surgery
Laboratory
H Urinalysis shows hematuria (black widow spider
bite).
H White blood cell count is increased (black widow
spider bite).
H Anemia panel shows hemolytic anemia (brown
recluse spider bite).
H Platelet count shows thrombocytopenia (brown
recluse spider bite).
Other
H Identification of the insect is difficult unless stung by
a honeybee or bumblebee, which typically leaves a
stinger with a venom sac in the lesion.
H Lesion excision for brown recluse spider bite
Treatment
General
Tick bite
H Tick removal
H Symptomatic therapy for severe symptoms
H Cool compresses and elevation of extremity
H I.V. fluids
H Ice packs
Bee, wasp, yellow jacket, or fire ant sting
H Ice application
H Elevation of affected extremity
H Supportive treatment
H Nothing by mouth if severe, systemic reaction
H Rest to limit toxic effects of venom
Medications
Tick bite
H Antipruritics
H Antibiotics
Doxycycline, amoxicillin, or cefuroxime axetil for
Lyme disease
Doxycycline for Rocky Mountain spotted fever
H Corticosteroids
H Antibiotic ointment
H Antihistamines
H Tranquilizers
H Tetanus prophylaxis
H Antivenin I.V.
H Calcium gluconate I.V.
H Muscle relaxants
H Adrenaline or antihistamines
H Tetanus immunization
H Oxygen for respiratory difficulty
Bee, wasp, yellow jacket, or fire ant sting
H Antihistamines such as diphenhydramine
H Steroids for severe reactions
H Bronchodilator such as epinephrine
Key outcomes
The patient will:
H maintain adequate ventilation and a patent airway
H regain skin integrity
H Keep the affected part immobile.
H Clean the bite or sting site with antiseptic.
H Apply ice.
H Provide emergency resuscitation.
Tick bite
H Remove the tick promptly and carefully.
H Use tweezers to grasp the tick near its head or
mouth, and gently pull to remove the whole tick without crushing it.
H If possible, seal the tick in a plastic bag and keep it
in case the patient needs to see a physician. Otherwise, flush the tick down the toilet or burn it.
H Clean the lesion with a 1:20 Burows aluminum
acetate solution.
H Apply antibiotic ointment, as ordered.
H Remove all jewelry.
H Apply cool compresses.
H Avoid cutting into the wound or applying suction.
H Scrape stinger off; dont pull or squeeze it, which
releases more toxin.
Fire ant sting
H Apply cool compresses.
H Gently wash the bite area, leaving the blister intact.
H Be prepared to intervene for an acute severe allergic
reaction (rare).
Monitoring
H Vital signs
H General appearance
H Changes at the bite or sting site
Patient teaching
Be sure to cover:
H avoidance of insect bites and stings
H examination of the body for ticks after being outdoors
H removal of ticks
H medical identification jewelry or card
H anaphylaxis kit use
H insect repellent use.
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Intestinal obstruction
Overview
Description
H Partial or complete blockage of the lumen of the
H Abdominal pain
H Change in bowel habits
Complications
H Perforation
H Peritonitis
H Septicemia
H Metabolic alkalosis or acidosis
H Death
small or large bowel

H Usually a medical emergency
H Most likely after abdominal surgery or with congeni-
tal bowel deformities

H Without treatment, complete obstruction in any part
of bowel causing death within hours from shock and

vascular collapse
Pathophysiology
H Mechanical or nonmechanical (neurogenic) block-
age of the lumen occurs.

H Fluid, air, or gas collects near the site.
H Peristalsis increases temporarily in an attempt to
break through the blockage.

H Intestinal mucosa is injured, and distention at and
above the site of obstruction occurs.

H Venous blood flow is impaired, and normal absorp-
tive processes cease.

H Water, sodium, and potassium are secreted by the
bowel into the fluid pooled in the lumen.
Causes
Mechanical obstruction
H Adhesions
H Strangulated hernias
H Carcinomas
H Foreign bodies
H Compression of the bowel wall from stenosis,
intussusception, volvulus of the sigmoid or cecum,
tumors, and atresia
Nonmechanical obstruction
H Paralytic ileus
H Toxicity, such as that associated with uremia or
generalized infection
H Neurogenic abnormalities
H Thrombosis or embolism of mesenteric vessels
Risk factors
H Abdominal surgery
H Radiation therapy
H Gallstones
H Inflammatory bowel disease
Incidence
H Diagnosed in about 20% of hospital admissions for
abdominal illness
448
Assessment
History
H Recent change in bowel habits
H Hiccups
H Colicky pain
H Nausea, vomiting
H Constipation
H Diffuse abdominal discomfort
H Frequent vomiting
H Severe abdominal pain (if obstruction results from
vascular insufficiency or infarction)
Physical findings
H Distended abdomen
H Borborygmi and rushes (occasionally loud enough to
be heard without a stethoscope)
H Rebound tenderness
H Decreased bowel sounds (early), then absent bowel
sounds
Test results
Laboratory
H Serum sodium, chloride, and potassium levels are
decreased.
H White blood cell counts are elevated.
H Serum amylase level is elevated if pancreas is irritated by a bowel loop.
H Blood urea nitrogen level is increased (with dehydration).
Imaging
H Abdominal X-rays reveal the presence and location of
intestinal gas or fluid. In small-bowel obstruction, a
typical stepladder pattern emerges, with alternating
fluid and gas levels apparent in 3 to 4 hours.
H Barium enema reveals a distended, air-filled colon or
a closed loop of sigmoid with extreme distention (in
sigmoid volvulus).
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Treatment
Patient teaching
General
Be sure to cover:
H the disorder (focusing on the patients type of intestinal obstruction), diagnosis, and treatment
H techniques for coughing and deep breathing, and use
of an incentive spirometer
H colostomy or ileostomy care, if appropriate
H incision care
H postoperative activity limitations and why these restrictions are necessary
H importance of following a structured bowel regimen,
particularly if the patient had a mechanical obstruction due to fecal impaction.

H Decompression of the bowel to relieve vomiting and
distention
H Treatment of shock and peritonitis
H Nothing by mouth if surgery planned
H Parenteral nutrition until bowel is functioning
H High-fiber diet when obstruction relieved
H Bed rest during acute phase
H Postoperatively, avoidance of lifting and contact
sports
Medications
H Broad-spectrum antibiotics
H Analgesics
H Blood replacement
Surgery
Discharge planning
H Refer the patient to an enterostomal therapist, if
indicated.
H Usually the treatment of choice (exception is paralyt-
ic ileus in which nonoperative therapy is usually attempted first)

H Type of surgery depends on cause of blockage
Key outcomes
The patient will:
H return to normal bowel function
H maintain caloric requirement
H maintain stable vital signs.
H Insert a nasogastric (NG) tube and attach to
low-pressure, intermittent suction.

H Maintain the patient in semi-Fowlers position.
H Provide mouth and nose care.
H Begin and maintain I.V. therapy, as ordered.
Monitoring
H Vital signs
H Signs and symptoms of shock
H Bowel sounds and signs of returning peristalsis
H NG tube function and drainage
H Pain control
H Abdominal girth measurement to detect progressive
distention
H Electrolytes and signs and symptoms of metabolic de-
rangements
H Wound site (postoperatively)
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Intussusception
Overview
Description
H Lymphoid hyperplasia
H Meckels diverticulum
H Alterations in intestinal motility
In adults
H Benign or malignant tumors (65% of patients)
H Polyps
H Meckels diverticulum
H Gastroenterostomy with herniation
H Appendiceal stump
H Condition in which a portion of the bowel telescopes
Incidence
or invaginates into an adjacent bowel portion (see

Understanding intussusception)
H Can be fatal if treatment delayed more than 24 hours
H Pediatric emergency
H Most common in infants

H Three times more common in males than in females
H About 87% of children with intussusception younger
Pathophysiology
H A bowel section invaginates and is propelled by peri-
stalsis.
H More bowel is pulled in, causing edema, obstruction,
and pain.
Causes
than age 2; about 70% of these children between

ages 4 and 11 months
H Seasonal peaks in late spring and early summer
H Intermittent attacks of colicky pain
H Vomiting
H Abdominal guarding
H Intussusception may be linked to viral infections due
Complications
to seasonal peaks.
In infants
H Unknown
In older children
H Polyps
H Hemangioma
H Lymphosarcoma
H Strangulation of the intestine

H Gangrene of the bowel
H Shock
H Bowel perforation
H Peritonitis
H Death
Assessment
Understanding intussusception
In intussusception, a bowel section invaginates and is propelled along by peristalsis, pulling in more bowel. This illustration shows intussusception of a portion of the transverse colon. Intussusception typically produces edema,
hemorrhage from venous engorgement, incarceration, and
obstruction.
Invaginated bowel
History
H Intermittent attacks of colicky pain
H Pain that causes the child to scream, draw his legs up
to his abdomen, turn pale and diaphoretic and, possibly, grunt

H Vomiting, initially stomach contents; later,
bile-stained or fecal material
H Currant jelly stools, which contain mixture of
blood and mucus
Physical findings
H Distended, tender abdomen
H Guarding over the intussusception site
H Palpable sausage-shaped abdominal mass in the right
Cecum
upper quadrant or in the midepigastric area if transverse colon involved

H Bloody mucus on rectal examination
H In adults, abdominal pain localized in right lower
quadrant, radiating to the back, and increasing with
eating
Test results
Laboratory
H White blood cell count up to 15,000/l indicates
obstruction; more than 15,000/l, strangulation;
and more than 20,000/l, bowel infarction.
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Intussusception
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Imaging
H Barium enema confirms colonic intussusception
when it shows the characteristic coiled-spring sign;
it also delineates the extent of intussusception.
H Upright abdominal X-rays may show a soft-tissue
mass and signs of complete or partial obstruction,
with dilated loops of bowel.
Treatment
General
H Hydrostatic reduction
H Bowel decompression
H Nothing by mouth until bowel functions properly
H Bed rest until condition is resolved
Patient teaching
Be sure to cover:
H wound care
H parental participation in their childs care to minimize the stress of hospitalization (visiting hours
should be flexible).
Discharge planning
H Encourage the patients family to make follow-up ap-
pointments as recommended by his physician.
Medications
H Analgesics
H Antibiotics if infection occurs
Surgery
H Indicated for children with recurrent intussuscep-
tion, those who show signs of shock or peritonitis,

and those in whom symptoms present longer than
24 hours
H In adults, always the treatment of choice
Key outcomes
The patient will:
H have family members who understand the disorder
and treatment regimen.
H Offer reassurance and emotional support to the pa-
tient and, if the patient is a child, to his parents.

Monitoring
H Vital signs
H Intake and output
H Hydration status
H Bowel sounds, stools, abdominal distention
H Wound site (after surgery)
H For recurrence in the first 36 to 48 hours after
reduction
Intussusception
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Irritable bowel
syndrome
Overview
Description
H Contributing psychological factors, such as a recent
stressful life change, that may have triggered or aggravated symptoms

H Anxiety and fatigue
Physical findings
H Normal bowel sounds
H Tympany over a gas-filled bowel
H Common condition marked by chronic or periodic
Test results
diarrhea alternating with constipation

H Accompanied by straining and abdominal cramps
H Initial episodes early in life and late teens to twenties
H Prognosis good
H Also known as spastic colon, spastic colitis, mucous colitis
H Assessment involves studies to rule out other, more
Pathophysiology
H Precise etiology unclear
H Involves a change in bowel motility, reflecting an ab-
normality in the neuromuscular control of intestinal

smooth muscle
Causes
H Anxiety and stress
H Dietary factors, such as fiber, raw fruits, coffee, alco-
hol, and foods that are cold, highly seasoned, or laxative in nature
Other possible triggers
H Hormones
H Laxative abuse
H Allergy to certain foods or drugs
Incidence
H Occurs mostly in females, with symptoms first emerg-
ing before age 40
serious disorders.
Laboratory
H Stool examination is negative for occult blood, parasites, and pathogenic bacteria.
H Complete blood count, serologic tests, serum albumin, and erythrocyte sedimentation rate are normal.
Imaging
H Barium enema may reveal colonic spasm and a tubular appearance of the descending colon. Its also
used to rule out certain other disorders, such as diverticula, tumors, and polyps.
H Sigmoidoscopy may disclose spastic contractions.
Treatment
General
H Stress management
H Lifestyle modifications
H Diet based on the patients symptoms
H Initially, an elimination diet
H Avoidance of sorbitol, nonabsorbable carbohydrates,
and lactose-containing foods

H Increased dietary bulk
H Regular exercise
H Chronic constipation or diarrhea

H Lower abdominal pain
Medications
Complications
H Anticholinergics and antispasmodics

H Antidiarrheals such as loperamide
H Antiemetics
H Simethicone
H Mild tranquilizers
H Tricyclic antidepressants, such as impiramine and
H Diverticulitis and colon cancer

H Chronic inflammatory bowel disease
Assessment
History
H Chronic constipation, diarrhea, or both
H Lower abdominal pain (typically in the left lower
quadrant) usually relieved by defecation or passage

of gas
H Small stools with visible mucus or pasty, pencil-like
stools instead of diarrhea
H Dyspepsia
H Abdominal bloating
H Heartburn
H Faintness and weakness
452
Irritable bowel syndrome
H Bulk-forming laxatives/fiber supplements, such as
psyllium and methylcellulose
amitriptyline
H 5HT3-receptor antagonist such as alosetron
Key outcomes
The patient will:
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H maintain normal laboratory values

H understand the disease process and treatment
regimen.
H Because the patient generally isnt hospitalized for ir-
ritable bowel syndrome, nursing interventions almost

always focus on patient teaching.
Monitoring
H Weight
H Diet
H Bowel movements
Patient teaching
Be sure to cover:
H dietary plans and implementation
H need to drink 8 to 10 glasses of water or other compatible fluids daily
H proper use of prescribed medication, reviewing desired effects and possible adverse reactions
H need to implement lifestyle changes that reduce
stress
H smoking cessation
H need for regular physical examinations. (For patients
older than age 40, emphasize the need for colorectal
cancer screening, including annual proctosigmoidoscopy and rectal examinations.)
Irritable bowel syndrome
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Juvenile rheumatoid
arthritis
Overview
Description
H Several inflammatory conditions characterized by
chronic synovitis and joint swelling, pain, and tenderness

H Major types systemic (Stills disease or acute
febrile type), polyarticular, and pauciarticular
Pathophysiology
H If juvenile rheumatoid arthritis (JRA) isnt arrested,
the inflammatory process in the joints occurs in four

stages:
Synovitis develops from congestion and edema of
the synovial membrane and joint capsule.
Pannus covers and invades cartilage and eventually
destroys the joint capsule and bone.
Fibrous tissue and ankylosis occludes the joint
space.
Fibrous tissue calcifies, resulting in bony ankylosis
and total immobility.
Physical findings
Systemic JRA
H Mild, transient arthritis or frank polyarthritis with
fever and rash
H Behavior may clearly suggest joint pain and fatigue
H Painful breathing and nonspecific abdominal pain
H Fatigue, shortness of breath, palpitations, and fever
H Resting or exertional tachycardia; arrhythmias; jugular vein distention; heart murmurs
H Hepatic, splenic, and lymph node enlargement
H Friction rub associated with pericarditis
Polyarticular JRA
H Pain in the wrists, elbows, knees, ankles, and small
joints of the hands and feet
H Pain in larger joints, including the temporomandibular, cervical spine, hips, and shoulders
H Tenderness, stiffness, and swelling of joints
H Possible low-grade fever with daily peaks
H Weight loss
H Noticeable developmental retardation
H Hepatic, splenic, and lymph node enlargement
H Subcutaneous nodules on the elbows or heels
Pauciarticular JRA
H Pain in the hips, knees, heels, feet, ankles, and elbows
H Eye redness, blurred vision, and photophobia
H Lower back pain
Causes
Test results
H Unknown
H Suggested link to genetic factors or an abnormal im-
Laboratory
H Serum hemoglobin levels are decreased, and neutrophil (neutrophilia) and platelet (thrombocytosis)
levels are increased; other findings include elevated
erythrocyte sedimentation rate and elevated C-reactive protein, serum haptoglobin, immunoglobulin,
and C3 complement levels.
H Antinuclear antibody test is positive in patients with
polyarticular JRA and in those with pauciarticular
JRA with chronic iridocyclitis.
H Rheumatoid factor (RF) appears in about 15% of patients with JRA. (In contrast, about 85% of patients
with rheumatoid arthritis test positive for RF; patients
with polyarticular JRA may test positive for RF.)
H Human leukocyte antigen-B27 forecasts later development of ankylosing spondylitis.
Imaging
H X-ray studies demonstrate early structural changes
associated with JRA. These include soft-tissue
swelling, effusion, and periostitis in affected joints.
Later evidence includes osteoporosis and accelerated
bone growth followed by subchondral erosions,
joint-space narrowing, bone destruction, and fusion.
mune response
H Viral or bacterial (streptococcal) infection, trauma,
and emotional stress
Incidence
H May occur as early as age 6 weeks but seldom before
age 6 months; peak onset between ages 1 and 3 and

8 and 12
H Occurs in an estimated 150,000 to 250,000 children
in United States; affects twice as many girls as boys
H Joint stiffness in the morning
Complications
H Flexion contractures
H Ocular damage and loss of vision
H Retarded growth and development
Assessment
History
H Common complaint of joint stiffness in morning or
after periods of inactivity

H In young children, typically irritability and listlessness
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Juvenile rheumatoid arthritis
Treatment
General
H Physical therapy
H Splints
H Heat application during passive exercises
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H Adequate iron, protein, calcium, and caloric intake

Medications
H Analgesic such as acetaminophen
H Nonsteroidal anti-inflammatory drugs (NSAIDs)
H Disease-modifying antirheumatic drugs, such as
methotrexate, penicillamine, gold salts, and the antimalarial drug hydroxychloroquine.
H signs and symptoms of exacerbation, and the need to
notify the pediatrician about these symptoms

H need for proper nutrition and caloric consumption
H childs special needs (telling teachers and the school
principal).
Discharge planning
H Consult an occupational therapist to assess the pa-
tients home care needs.
Surgery
H Soft-tissue releases to improve mobility
H Joint replacement (delayed until child matures physi-
cally and can tolerate vigorous rehabilitation)
Key outcomes
The patient will:
pain
H recognize and express feelings about limitations due
to illness
H identify factors that increase risk for injury
H maintain optimum mobility.
H Focus nursing care on reducing pain and promoting
mobility.
H During inflammatory exacerbations, administer
NSAIDs or prescribed medication on a regular

schedule.
H Allow the patient to rest frequently throughout the
day to conserve energy for times when she must be
mobile.
H Arrange the patients environment for participation in
activities of daily living so that she feels capable of
accomplishing tasks.
Monitoring
H Pain level
H Signs and symptoms of bleeding
H Joint mobility
Patient teaching
Be sure to cover:
H need to encourage the child to be as independent as
possible
H need for regular slit-lamp examinations to enable
early diagnosis and treatment of iridocyclitis
H signs and symptoms of bleeding caused by NSAID
therapy (instructing the patient to take these medications with meals or milk to reduce adverse GI reactions)
Juvenile rheumatoid arthritis
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Kaposis sarcoma
H Untreated lesions that may appear as large, ulcerative
masses
Overview
H Dyspnea
H Edema from lymphatic obstruction
H Wheezing and hypoventilation
Description
Test results
H Most common acquired immunodeficiency syndrome
H Tissue biopsy shows the type and stage of the lesion.
(See Laubensteins stages in Kaposis sarcoma.)
(AIDS)related cancer
H Characterized by obvious, colorful lesions
H Most common internal sites: lungs and GI tract
(esophagus, oropharynx, and epiglottis)
Pathophysiology
Treatment
H Kaposis sarcoma causes structural and functional
General
damage.
H When associated with AIDS, it progresses aggressively, involving the lymph nodes, the viscera and, possibly, GI structures.
H Radiation therapy for palliation of symptoms (pain
Causes
Risk factors
from obstructing lesions in the oral cavity or extremities and edema caused by lymphatic blockage); also
for cosmetic improvement
H Small meals
H Limited activity
H Males, especially white

H Immunosuppression and immune deficiency
H People of Mediterranean or Middle Eastern descent
H Africans
Medications
Incidence
H Removal of lesion from skin (especially if lesion is
H Originally affected 35% of AIDS patients; now declin-
ing with earlier detection of AIDS

H 1 in 200 transplant patients in the United States
H Chemotherapy
H Biological response modifier
Surgery
small), using local excision, electrodesiccation and
curettage, or cryotherapy
H History of AIDS
H Lesions of various shapes, sizes, and colors
Complications
H Severe pulmonary involvement, resulting in respira-
tory distress
H GI involvement, leading to digestive problems
Assessment
History
H Possible history of AIDS
H Pain (in advanced cases)
Physical findings
H Several lesions of various shapes, sizes, and colors
(ranging from red-brown to dark purple) on the

skin, buccal mucosa, hard and soft palates, lips,
gums, tongue, tonsils, conjunctiva, and sclera (the
most common sites)
H In advanced disease, lesions that may merge, becoming one large plaque
456
Kaposis sarcoma
Laubensteins stages in Kaposis

sarcoma
L.J. Laubenstein proposed this staging system to evaluate
and treat patients with acquired immunodeficiency syndrome and Kaposis sarcoma:
H Stage I locally indolent cutaneous lesions
H Stage II locally aggressive cutaneous lesions
H Stage III mucocutaneous and lymph node
involvement
H Stage IV visceral involvement.
Within each stage, a patient may have different symptoms further classified as stage subtype A or B, which are:
H Subtype A no systemic signs or symptoms
H Subtype B one or more systemic signs and
symptoms, including 10% weight loss, fever of
unknown origin that exceeds 100 F (37.8 C) for
longer than 2 weeks, chills, lethargy, night sweats,
anorexia, and diarrhea.
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Key outcomes
The patient will:
H exhibit no signs and symptoms of infection.
H Encourage verbalization and offer support.
H Inspect the skin for new lesions and skin breakdown.
H Provide rest periods.
Monitoring
H Adverse effects of treatment
H Vital signs
H Pain control
Patient teaching
Be sure to cover:
H infection prevention techniques and, if necessary, basic hygiene measures to prevent infection (especially
if the patient also has AIDS)
H the need for ongoing treatment and care.
Discharge planning
H Refer the patient to available resources and support
services.
Kaposis sarcoma
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Kawasaki syndrome
H Skin desquamation, especially in the groin, on the
palms, and soles

H Possible aneurysms leading to sudden death
Overview
Description
H A noncontagious, febrile, self-limited disorder of un-
known origin
H Affects the mucus membranes, lymph nodes, blood
vessels, and heart

H Occurs in stages: acute, subacute, and convalescent
H Cardiac complications most serious sequelae
H Full recovery expected
H Also known as mucocutaneous lymph node syndrome and infantile polyarteritis
Pathophysiology
H An infection results in altered immune function.
H Antibodies increase as a result of the infection and
cause inflammation of blood vessels.

H Blood vessel inflammation increases platelet accu-
mulation and results in thrombi.

H Thrombi result in obstruction of heart and systemic
blood vessels.
Causes
H Possible genetic role after exposure to an unknown
virus, bacteria, or other pathogen
Risk factors
H None known
H No known preventive measures
Incidence
H Peak incidence in boys younger than age 4, but can
occur up to puberty
H Affects boys 112 times more commonly than girls
H Occurs more commonly in late winter and spring
H Most common in Japan or in Japanese or Korean
children living elsewhere

H Commonly occurs in clusters within a geographic
location
H Rarely occurs twice in the same household
Acute phase
H High fever for 5 days or more (up to 106.5 F
[41.4 C]) unresponsive to antipyretics
H Lethargy and irritability
H Reddened, swollen hands and feet
H Inflamed mucous membrane of eyes
H Strawberry tongue with red, cracked lips
H Rash in trunk area
H Enlarged cervical lymph nodes
H Abdominal pain, anorexia, and diarrhea resulting
from internal lymph node swelling
H Reddened, swollen joints
Subacute phase
H Begins about 10 days after the onset of symptoms
458
Kawasaki syndrome
Convalescent phase
H Occurs between the 25th and 40th days
H May continue beyond 40 days without distinguishing
features
Complications
H Vasculitis leading to aneurysm and myocardial infarc-
tion
H Death (2% of patients with Kawasaki syndrome dying
from coronary vasculitis)

H Future coronary bypass surgery if coronary artery
disease develops
H Myocarditis
H Pericarditis
H Abnormal valve functioning
Assessment
History
H Fever of 5 days or more, unresponsive to antipyretics
H Occurrence of characteristic symptoms
Physical findings
H Reddened, swollen hands and feet
H Inflamed mucous membrane of eyes
H Strawberry tongue with red, cracked lips
H Rash in trunk area
H Reddened, swollen joints
H Possible enlarged gallbladder
Test results
Laboratory
rate are elevated in acute phase.
H Platelet count is elevated in the subacute phase.
H Culture results are all negative.
H Liver function test results are elevated.
H Urinalysis may show pyuria or proteinuria.
Imaging
H Sequential echocardiograms detect artery disease.
H Chest X-ray rules out cardiomegaly or subclinical
pneumonitis.
Treatment
General
H Hospitalization
H Symptomatic
H Prevention of complications
H Soft, nonirritating foods
H Avoidance of citrus (mouth sores)
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Medications
H I.V. gamma globulin
H Aspirin
Key outcomes
The patient will:
H maintain adequate tissue perfusion
H have normal vital signs
H have a capillary refill time of less than 5 seconds
H experience a tolerable pain level
H experience increased comfort
H maintain adequate nutrition.
H Observe for signs of heart failure, such as tachycar-
dia, dyspnea, crackles, and edema.

H Inspect the extremities for color, temperature, and
capillary refill.
H Observe and report joint swelling and redness.
H Observe and report nature of rash.
H Keep clothing from constricting or irritating rash.
H Moisten lips with lip balm to prevent cracking.
H Offer frequent fluids.
H Observe for signs of GI upset, such as nausea and
vomiting.
H Avoid pressure on the extremities with edema.
Monitoring
H Complications such as chest pain, arrhythmias, and
electrocardiogram changes
H Edema changes
H Intake and output
H Adverse effects of I.V. immunoglobulin: allergic reac-
tions, fever, chills, headache, transfusion reactions,

and pulmonary edema
Patient teaching
Be sure to cover:
H the disorder, diagnosis and treatment
H aspirin therapy during and after hospitalization
H reporting exposure to viral illnesses, such as influenza or chickenpox, while taking aspirin, in order to
prevent Reyes syndrome
H possibility of long-term management if cardiac complications exist
H need to delay immunizations (especially the measlesmumps-rubella and chickenpox vaccines) when immunoglobulin is given.
Discharge planning
H Encourage the patient to schedule a follow-up exami-
nation in 2 to 3 weeks.
Kawasaki syndrome
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Keratitis
Overview
Description
H Infection of the cornea
H Usually affects only one eye
Pathophysiology
H Photophobia
H Pain
H Lacrimation
Complications
H Blindness
H Corneal scarring or perforation
Assessment
H Inflammation of the cornea results from corneal
History
infection.
H Inflammation may be deep or superficial.
H Recent upper respiratory tract infection, accompa-
Causes
H Viral, bacterial, or fungal infection
H Congenital syphilis
Risk factors
H Tear deficiency
H Denervation
H Immune reactions
H Ischemia
H Trauma
H Contact lenses
Incidence
H Fairly common
H May develop at any age
nied by cold sores

H Eye pain
H Central vision loss
H Sensitivity to light
H Sensation of a foreign body in eye
H Blurred vision
Physical findings
H Cornea lacks normal luster
H Characteristic branched lesion of the cornea with
herpes simplex virus type 1
Test results
H Slit-lamp examination with sodium fluorescein staining may show corneal inflammation or abrasion;
small branchlike (dendritic) lesions indicate possible herpes simplex virus infection. (See Examining
the eye with a slit lamp.)
Treatment
Examining the eye with a slit lamp
An ophthalmologist uses the slit lamp, an instrument
equipped with a special lighting system and a binocular
microscope, to view the eyelids, eyelashes, conjunctiva,
sclera, cornea, tear film, anterior chamber, iris, crystalline
lens, and vitreous face. The examiner may adjust the size,
shape, intensity, and depth of the light source as well as
the magnification of the microscope, to evaluate normally
transparent or near-transparent ocular fluids and tissues.
If he notes abnormalities, he can attach special devices to
the slit lamp to allow more detailed investigation.
Preparing the patient
H Tell the patient that the slit-lamp examination evaluates

the front portion of the eyes and that it requires that he
remain still. Reassure him that the examination is
painless.
H If the patient wears contact lenses, tell him to remove
them for the test, unless the test is being performed to
evaluate the fit of the lens.
H If the test calls for dilating eyedrops, check the
patients history for adverse reactions to mydriatics
and for the presence of angle-closure glaucoma before
giving the drops. Dilating eyedrops arent used in
routine eye examinations, but some diseases require
pupillary dilation before slit-lamp examination.
460
Keratitis
General
H Eye shield or patch
Medications
Acute dendritic keratitis
H Trifluridine eyedrops
H Vidarabine ophthalmic ointment
H Broad-spectrum antibiotic
Chronic dendritic keratitis
H Vidarabine therapy
H Long-term topical therapy may be necessary
Fungal keratitis
H Natamycin
Surgery
H Corneal transplantation for severe ulcerations with
residual scarring
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Key outcomes
The patient will:
ALERT
Watch for keratitis in patients predisposed to cold
sores. Corneal infection is commonly caused by a
virus, such as adenovirus or herpes simplex, the
same viruses that cause cold sores. Be sure to tell
patients never to touch their eyes after touching
their mouths.
Prevention
Preventing the spread of keratitis

The spread of keratitis can be prevented by following
these guidelines:
H Use meticulous hand-washing techniques.
H Avoid touching the eyes after touching the mouth,
especially in patients with cold sores.
H Dont share eyedrops or ointment.
H Dont touch the eyedropper or ointment tip to the eye.
H Wash hands before and after administering eyedrops.
H Follow the providers directions and complete antibiotic
or antifungal treatment course as prescribed.
H Take antiviral as prescribed.
H Keep follow-up appointments.
H Use artificial tears as directed.
H Wear protective eye wear to prevent further injury.
H Wear gloves when in contact with eyes or ocular
drainage with herpes simplex virus.

H Dim the lights in case of photophobia.
Monitoring
H Visual acuity
Patient teaching
Be sure to cover:
H how stress, traumatic injury, fever, colds, and sun
overexposure can trigger flare-up
H wearing sunglasses for photophobia
H preventing spread of infection. (See Preventing the
spread of keratitis.)
Keratitis
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Kidney cancer
Overview
Description
H Proliferation of cancer cells in the kidney
H 85%: originate in kidneys; 15%: metastasize from
various primary-site carcinomas

H Also called nephrocarcinoma, renal carcinoma,
hypernephroma, and Grawitzs tumor
Causes
H Unknown
Risk factors
H Heavy cigarette smoking
H Regular hemodialysis treatments
Incidence
H More common after age 40
H Renal pelvic tumors and Wilms tumor most common
in children
Pathophysiology
H Most kidney tumors are large, firm, nodular, encap-
H Hematuria
H Flank pain
sulated, unilateral, and solitary.

H Kidney cancer may affect either kidney; occasionally
tumors are bilateral or multifocal. (See Unilateral
kidney tumor.)
H Renal cancers arise from the tubular epithelium.
H Tumor margins are usually clearly defined.
H Tumors can include areas of ischemia, necrosis, and
focal hemorrhage.
H Tumor cells may be well differentiated to anaplastic.
H Kidney cancer can be separated histologically into
clear cell, granular cell, and spindle cell types.
H The prognosis is better for patients with the clear cell
type than for the other types; in general, however, the
prognosis depends more on the cancers stage than
on its type. The overall prognosis has improved considerably, with a 5-year survival rate of about 50%.
Complications
H Hemorrhage
H Metastasis
Assessment
History
H Hematuria
H Dull, aching flank pain
H Weight loss (rare)
H Fatigue
H Intermittent fever
Physical findings
H Palpable smooth, firm, nontender abdominal mass
Unilateral kidney tumor

In kidney cancer, tumors such as this one in the upper
kidney pole usually occur unilaterally.
Test results
Laboratory
H Alkaline phosphatase, bilirubin, and transaminase
levels are increased.
H Prothrombin time is prolonged.
Imaging
H Renal ultrasonography and computed tomography
scan can be used to verify renal cancer.
H Excretory urography, nephrotomography, and
kidney-ureter-bladder radiography are used to aid
diagnosis and help in staging.
Treatment
General
H Because of radiation resistance, radiation used only
when cancer has spread into perinephric region or

lymph nodes or when primary tumor or metastatic
sites cant be completely excised
H Low-protein diet
H Postoperatively, no heavy lifting or contact sports for
6 to 8 weeks
Medications
H Chemotherapy
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H Biotherapy with lymphokine-activated killer cells
plus recombinant interleukin-2

H Interferon
Surgery
H Radical nephrectomy, with or without regional lymph
node dissection
Key outcomes
The patient will:
H communicate understanding of medical regimen,
medications, diet, and activity restrictions
H maintain ventilation
H utilize support services.
Monitoring
H Wound site
H Intake and output
H Complete blood count; serum chemistry results
H Pain control
Patient teaching
Be sure to cover:
H need for a healthy, well-balanced diet and regular exercise
H importance of checking with the physician before
taking vitamins or other dietary supplements
H importance of follow-up care.
Discharge planning
indicated.
Kidney cancer
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Klinefelter syndrome
Overview
Description
H Relatively common genetic abnormality that results
from an extra X chromosome, creating an XXY sex

chromosome constitution
H Affects only males and usually becomes apparent at
puberty, when secondary sex characteristics develop
H Failure of the testicles to mature and degenerative
testicular changes that eventually result in irreversible infertility
Pathophysiology
H The extra chromosome responsible for Klinefelter
syndrome probably results from either meiotic

nondisjunction during parental gametogenesis or
from mitotic nondisjunction in the zygote.
H The incidence of meiotic nondisjunction increases
with maternal age.
Causes
H One extra X chromosome creating 47,XXY comple-
ment instead of the normal 46,XY

H In the rare mosaic form, some cells containing extra
X chromosomes; others containing normal XY complement

H Turners syndrome, the lack of one X chromosome
(45,X), possibly being a cause (see Turners syndrome)
Incidence
H In the United States, approximately 1 in 500 to 1,000
males born with an extra sex chromosome; over

3,000 affected males born yearly
H Prevalence: 5 to 20 times higher in neonates with
mental retardation
H May not be apparent until puberty (or later in mild
cases)
Turners syndrome
In Turners syndrome, one of the X chromosomes (or part
of the second X chromosome) may be lost from either the
ovum or sperm through nondisjunction or chromosome
lag. Mixed aneuploidy may result from mitotic nondisjunction.
This disorder occurs in 1 in 2,500 to 7,000 births; up to
95% of affected fetuses are spontaneously aborted.
H Behavioral problems in adolescence

H Infertility
Complications
H Aspermatogenesis and infertility
H Learning disabilities and behavioral problems
H Osteoporosis
H Breast cancer due to the extra X chromosome
Signs and symptoms

In utero, the fetus may have a cystic hygroma, seen on ultrasound; however, these may also be seen in fetuses that
dont have Turners syndrome. The mother may have elevated or low levels of serum alpha-fetoprotein.
At birth, 50% of infants with this syndrome measure
below the third percentile in length. Many have swollen
hands and feet, a wide chest with laterally displaced nipples, and a low hairline that becomes more obvious as
they grow. They may have webbing of the neck and
coarse, enlarged, prominent ears. Gonadal dysgenesis is
seen at birth and typically causes sterility in adult females
(unless they have the mosaic form).
Cardiovascular defects, such as a bicuspid aortic valve
and coarctation of the aorta, occur in 10% to 40% of patients. Short stature (usually under 59 [150 cm]) is the
most common adult sign.
Most patients have average or slightly below-average
intelligence; they commonly exhibit spatial defects,
rightleft disorientation for extrapersonal space, and defective figure drawing.
Assessment
Diagnosis and treatment
H Abnormal body build (long legs with short, obese
Turners syndrome can be diagnosed by chromosome

analysis. Differential diagnosis should rule out mixed gonadal dysgenesis, Noonans syndrome, and other similar
disorders.
Treatment should begin in early childhood and may include hormonal therapy (androgens, human growth hormone and, possibly, small doses of estrogen). Later, progesterone and estrogen can induce sexual maturation, but
most patients remain sterile.
464
History
H Sexual dysfunction (impotence, lack of libido)
H In some individuals, behavioral problems beginning
in adolescence
H Increased incidence of pulmonary disease and vari-
cose veins
Physical findings
H Small penis and prostate gland
H Small testicles
H Sparse facial and abdominal hair
H Feminine distribution of pubic hair (triangular
shape)
H In fewer than 50% of patients, gynecomastia
H In the mosaic form, delay of pathologic changes and
resulting infertility
trunk)
H Tall stature
Test results
Laboratory
H A karyotype (chromosome analysis) is determined by
culturing lymphocytes from the patients peripheral
blood.
H Urinary 17-ketosteroid levels are decreased.
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H Follicle-stimulating hormone excretion is increased.

H Plasma testosterone levels are decreased after
puberty.
Treatment
General
Medications
H Supplemental testosterone
Surgery
H Mastectomy in patients with persistent gynecomastia.
Key outcomes
The patient will:
H express feelings about the disorder
H comply with prescribed treatment.
H Encourage the patient to discuss his feelings of con-
fusion and rejection that may arise, and try to reinforce his male identity.
Monitoring
Patient teaching
Be sure to cover:
H the potential benefits and adverse effects of testosterone administration.
Discharge planning
H Send the fertile patient with the mosaic form of the
syndrome for genetic counseling.
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Labyrinthitis
Overview
Complications
H Meningitis
H Permanent balance disability
H Permanent hearing loss
Description
Assessment
H Inflammation of the labyrinth of the inner ear

H Typically produces severe vertigo with head move-
History
ment and sensorineural hearing loss

H Viral labyrinthitis most prevalent form
Pathophysiology
H Lesion within vestibular pathways (inner ear to cere-
bral cortex) results in an imbalance in the vestibular

system.
Causes
H Viral or bacterial infections
H Cholesteatoma
H Drug toxicity
H Head injury
H Tumor
H Vasculitis
H Allergies
Risk factors
H Current or recent viral infection, especially
respiratory
H Allergies
H Smoking
H Excess alcohol intake
H Stress
Incidence
H Affects all ages beyond infancy
H Severe vertigo with head movement
H Sensorineural hearing loss
H Tinnitus
H Severe vertigo from any movement of the head

H Unilateral or bilateral hearing loss
H Loss of balance and falling in the direction of the af-
fected ear
Physical findings
H Spontaneous nystagmus
H Jerking movements of eyes toward unaffected ear
H Purulent drainage
Test results
Laboratory
H Culture and sensitivity tests show the infecting
organism.
Imaging
H Computed tomography scanning results rule out
brain lesion.
H Audiometric testing reveals sensorineural hearing
loss.
H A flat tympanogram may suggest fluid in the middle
ear, a perforated tympanic membrane, or impacted
cerumen. Fluctuations on the tympanogram, synchronous with the patients pulse, suggest a glomangioma in the middle ear.
H Electronystagmography may show decreased velocity
from one side that indicates hypofunction or canal
paresis. An inability to induce nystagmus with ice
water denotes a dead labyrinth.
Treatment
General
Managing labyrinthitis
H Tell the patient to avoid sudden position changes.
H Help the patient assess how much this disability will affect his daily life.
H Work with the patient to identify hazards in the home,
such as throw rugs and dark stairways.
H Discuss the patients anxieties and concerns about vertigo attacks and decreased hearing.
H Stress the importance of maintaining and resuming
normal diversions or social activities when balance disturbance is absent.
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Labyrinthitis
H Based on relieving symptoms

H Increased oral fluids
H During acute attacks, bed rest in darkened room
with head immobilized between pillows
Medications
H Meclizine to relieve vertigo
H Benzodiazepines such as valium
H I.V. fluids for severe dehydration
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Surgery
H Surgical excision of cholesteatoma
H Drainage of middle and inner ear infected areas
H Labyrinthectomy
Key outcomes
The patient will:
H maintain normal fluid volumes
H be free from injury
H verbalize understanding of the condition and treatment.
H Offer the patient reassurance when appropriate.
H Maintain bed rest in a darkened room with his head
immobilized during acute attacks.

For the patient with hearing loss

H Encourage expression of concerns about hearing
loss.
H Give clear, concise explanations.
H Face him when speaking.
H Enunciate words clearly, slowly, and in a normal
tone.
H Provide a pencil and paper to aid communication.
H Alert staff to communication needs.
Monitoring
H Vital signs
H Intake and output
H Auditory acuity
H Complications
Patient teaching
Be sure to cover:
H limitation of activities to avoid danger from vertigo
H recovery time (up to 6 weeks)
H prompt treatment of upper respiratory tract and systemic infections
H controlling use of salicylates and other potentially
toxic substances
H completion of the prescribed medication regimen
H preoperative and postoperative instructions, as indicated
H management of labyrinthitis (see Managing
labyrinthitis).
Labyrinthitis
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Lactose intolerance
Overview
Description
H Inability to digest and absorb lactose, the main car-
bohydrate in milk
H Stems from an insufficiency of the enzyme lactase
H May be congenital (rare) or acquired
H Deficiency continues for life
Pathophysiology
See Understanding lactase insufficiency.
Causes
Incidence
H High incidence among certain ethnic groups, includ-
ing Blacks, Asians, Native Americans, Greek Cypriots,

and some Ashkenazic Jews
H Abdominal pain and distention after ingesting dairy
products
Complications
H Dehydration
Assessment
History
H GI signs and symptoms, such as diarrhea, abdominal
H Genetic basis
H Medical conditions that disrupt the intestinal mucosa
(secondary)
H Medications that cause GI disturbances
H Ionizing radiation to the abdomen and abdominal
surgery
cramping, discomfort, distention, flatulence, and

borborygmus (intestinal rumbling), following ingestion of milk products
H History of a medical disorder or treatment that disrupts the GI mucosa
Physical findings
H Nonverbal signs of patient distress, such as doubling
Understanding lactase insufficiency

Normally, the enzyme lactase hydrolyzes dietary lactose in
the jejunum and proximal ileus. The hydrolysis splits lactose into glucose and galactose, which bind to glucose
carriers and eventually pass into the portal vein. If lactase
levels are insufficient to split the lactose, a chain of effects
is triggered.
Available lactase is insufficient to

hydrolyze dietary lactose.
Unsplit lactose remains as unabsorbed glucose

in the small intestine.
Unabsorbed glucose acts osmotically

to draw in and retain intraluminal fluid,
leading to diarrhea.
Intestinal bacteria ferment the lactose,

breaking it down into hydrogen, carbon dioxide,
water, and organic acids.
Accumulation of gases causes discomfort,

flatulence, and distention.
468
Lactose intolerance
over or holding the abdomen

H Rectal tissue irritation and excoriation related to di-
arrhea
Test results
Laboratory
H Lactose tolerance testing: A blood sample is taken after the patient has fasted overnight. Then the patient
ingests a specified oral lactose load. Serum glucose
levels are taken on blood samples drawn at specified
intervals following lactose ingestion and on the fasting blood sample. A minimal increase (less than
20 mg/dl) in the serum glucose level and GI symptoms (cramping, flatulence and, perhaps, diarrhea)
confirm lactase deficiency.
H Breath hydrogen analysis measures excess hydrogen
exhalation resulting from bacterial fermentation of
lactose in the colon. (Hydrogen from the colon passes to the blood and then to the lungs.) Increased hydrogen content of expired air confirms lactose intolerance.
Other
H Lactose challenge test produces diarrhea and bloating within minutes to hours.
H Lactose-free diet testing eliminates lactose from the
patients diet for a period of time such as 5 days. If
he becomes asymptomatic, the diagnosis is upheld.
H Small-bowel biopsy (rarely used) determines
whether lactose intolerance is primary or secondary.
Only the secondary form shows abnormal epithelium.
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Treatment
General
H Lactose-free diet
Medications
H checking product labels carefully for lactose content
and avoiding products that list milk solids, milk sugars, whey, or casein
H the need to eliminate all sources of lactose from his
diet until he is symptom free
H how to use lactase enzyme products
H avoiding vitamin D and calcium deficiencies.
H Lactase enzyme products available as chewable
tablets, tablets, and capsules

H Antidiarrheal agents, such as loperamide and bis-
muth subsalicylate
H Calcium supplement
Key outcomes
The patient will:
H have fluid volume within normal parameters
H maintain adequate caloric intake.
H Administer prescribed antidiarrheal agents.
H Administer prescribed lactase enzyme products.
H Assess the patient for abdominal discomfort.
H Encourage relaxation and diversion techniques to
relieve discomfort.
H Initiate patient care measures to protect the rectal
skin and mucous membranes.

H Assess the patient for signs of dehydration.
H Provide patient privacy.
Monitoring
H Elimination pattern
H Diet
H Skin integrity
Patient teaching
Be sure to cover:
H lactose intolerance and its associated signs and
symptoms, risks, and treatment, especially dietary
management
H avoiding foods that contain lactose, such as milk
(whole, low-fat, skim, evaporated, condensed, buttermilk, cream), ice cream, cheese, sour cream, custards, milk-based puddings, butter, drinks prepared
with chocolate or malted milk powder, cream sauces
and gravies, cream-based soups, chocolate candy, instant potatoes, baked products made with milk, and
frozen or canned fruits and vegetables containing
lactose
Lactose intolerance
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Laryngeal cancer
Overview
Description
H Malignant cells in the tissues of the larynx or voice
box
H Squamous cell carcinoma: most common form (95%
of cases)
H Adenocarcinoma and sarcoma: rare (5% of cases)
H Tumor intrinsic (located on the true vocal cords;
tends not to spread because underlying connective

tissues lack lymph nodes), or extrinsic (located on
another part of the larynx; tends to spread easily)
Pathophysiology
Assessment
History
Stage I
H Complaints of local throat irritation
H 2-week history of hoarseness
Stages II and III
H Hoarseness
H Sore throat
H Voice volume reduced to whisper
Stage IV
H Pain radiating to ears
H Dysphagia
H Dyspnea
Physical findings
supraglottic (on the false vocal cords)

glottic (on the true vocal cords)
subglottic (rare downward extension from the
vocal cords).
H Malignant cells that proliferate can cause swallowing
and breathing impairment.
H A tumor can decrease mobility of the vocal cords.
Stage I
H None
Stage II
H Possible abnormal movement of vocal cords
Stage III
H Abnormal movement of vocal cords; possible lymphadenopathy
Stage IV
H Neck mass or enlarged cervical nodes
Causes
Test results
H Unknown
Imaging
H Xeroradiography, laryngeal tomography, computed
tomography scan, and laryngography confirm the
presence of a mass.
H Chest X-ray rules out metastasis.
H Laryngoscopy allows definitive staging by obtaining
multiple biopsy specimens to establish a primary diagnosis, to determine the extent of the disease, and
to identify additional premalignant lesions or second
primaries.
Other
H Biopsy identifies cancer cells.
H Laryngeal cancer is classified by its location:
Risk factors
H Smoking
H Alcoholism
H Chronic inhalation of noxious fumes
H Familial disposition
H History of gastroesophageal reflux disease
Incidence
H About nine times more common in males than
females
H Most victims between ages 50 and 65
Intrinsic laryngeal cancer
H Hoarseness lasting longer than 3 weeks
Extrinsic laryngeal cancer
H Lump in the throat
H Pain or burning of the throat when drinking hot liquid or citrus drinks
With metastasis
H Dysphagia
H Dyspnea
H Cough
H Pain, most commonly radiating to the ear
Complications
H Increased swallowing difficulty and pain
H Metastasis
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Laryngeal cancer
Treatment
General
H Precancerous lesions laser surgery
H Early lesions laser surgery or radiation therapy
H Advanced lesions radiation therapy and
chemotherapy
H Speech preservation
H Speech rehabilitation (when speech preservation im-
possible) esophageal speech, prosthetic devices,

or experimental surgical reconstruction of the voice
box
H Diet based on treatment options
H May require enteral feeding
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Medications
Discharge planning
H Chemotherapeutic agents
H Analgesics
H Arrange for rehabilitation measures (including laryn-
Surgery
H Cordectomy
H Partial or total laryngectomy
H Supraglottic laryngectomy or total laryngectomy with
geal speech, esophageal speech, an artificial larynx,

and various mechanical devices).
H Refer the patient to local resources and support services.
laryngoplasty
Key outcomes
The patient will:
H express feelings regarding illness
H utilize available support systems.
H Provide supportive psychological, preoperative, and
postoperative care.
H Assist with establishing a method of communication.
H Prepare the patient for functional losses (inability to
smell, blow his nose, whistle, gargle, sip, or suck on

a straw).
H Suction when needed.
H After total laryngectomy, elevate the head of the bed
30 to 45 degrees and support the back of the neck to
prevent tension on sutures and, possibly, wound dehiscence.
Monitoring
After partial laryngectomy
H Tracheostomy tube care
H Use of voice
After total laryngectomy
H Laryngectomy tube care
H Vital signs
H Pain control
H Nasogastric (NG) tube placement and function
Patient teaching
Be sure to cover:
H appropriate oral hygiene practices (before partial or
total laryngectomy)
H postoperative procedures, such as suctioning, NG
tube feeding, and laryngectomy tube care
H preparation for any functional losses.
Laryngeal cancer
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Laryngitis
Overview
Description
H Acute or chronic inflammation of vocal cords
H Isolated infection or part of a generalized bacterial
or viral upper respiratory tract infection

H Typical viral infection mild, with limited duration
H Inflammatory changes caused by repeated attacks
(associated with chronic laryngitis)
Pathophysiology
H Inflammatory response to cell damage by viruses re-
sults in hyperemia and fluid exudation.

H Irritant receptors are triggered.
H Kinins and other inflammatory mediators may induce
spasm of upper airway smooth muscle.
Special populations
Developmental differences in the upper airway
structures of young children may result in severe
narrowing of the upper airways with inflammation, to the degree that respiratory failure may result from hypoventilation.
Assessment
History
H Hoarseness ranging from mild to complete loss of
voice
H Feeling of throat rawness
H Throat pain
H Dry cough
H Malaise
H Difficulty swallowing
Physical findings
H Cough
H Fever
H Regional lymphadenopathy
H Stridor (in children)
Test results
Laboratory
H White blood cell count is elevated in bacterial
infection.
H Indirect laryngoscopy reveals red, inflamed and,
occasionally, hemorrhagic vocal cords exudate.
Treatment
Causes
General
H Infection
H Overuse of the voice
H Inhalation of smoke or fumes
H Aspiration of caustic chemicals
H Chronic laryngitis
H Chronic upper respiratory tract disorders
H Mouth breathing
H Smoking
H Constant exposure to dust or other irritants
H Alcohol abuse
H Gastroesophageal reflux
H Symptom-based
H Elimination of underlying cause
H Resting the voice (primary treatment)
H Humidification
H Avoidance of smoking
H Avoidance of whispering
H Cold fluids
H Rest during febrile period, with head of bed elevated
Incidence
Medications
H Analgesics
H Throat lozenges
H Antibiotics as appropriate (bacterial infection)
H Common disorder
H Affects all ages
Surgery
H Hoarseness
H Dry cough
Key outcomes
Complications
H Chronic hoarseness
H Permanent laryngeal tissue changes
472
Laryngitis
H Tracheotomy in chronic laryngitis
The patient will:

H exhibit an adequate breathing pattern
H express understanding of the condition and treatment.
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H Encourage discussion of concerns.
H Keep tracheotomy tray at bedside.
H Encourage modification of predisposing factors.
H Restrict verbal communication.
H Anticipate needs.
Monitoring
ALERT
In severe, acute laryngitis, monitor the patient for
signs and symptoms of airway obstruction.
Patient teaching
Be sure to cover:
H why the patient shouldnt talk
H alternate methods of communication
H speaking softly rather than whispering
H maintenance of adequate humidification
H smoking cessation
H medication and possible adverse reactions
H importance of completing prescribed antibiotics
H avoidance of occupational hazards.
Discharge planning
indicated.
Laryngitis
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Latex allergy
Overview
Description
H An immunoglobulin (Ig) Emediated immediate hy-
persensitivity reaction to products that contain natural latex

H Can range from local dermatitis to life-threatening
anaphylactic reaction
Pathophysiology
H Mast cells release histamine and other secretory
products.
H Vascular permeability increases and vasodilation and
bronchoconstriction occur.
H Chemical sensitivity dermatitis is a type IV delayed hypersensitivity reaction to the chemicals used in processing rather than the latex itself.
H In a cell-mediated allergic reaction, sensitized T lymphocytes are triggered, stimulating the proliferation
of other lymphocytes and mononuclear cells, resulting in tissue inflammation and contact dermatitis.
Causes
H Frequent contact with latex-containing products (see
Products that contain latex)
Risk factors
H Medical and dental professionals
H Workers in latex companies
H Patients with spina bifida or other conditions that re-
quire multiple surgeries involving latex material

H History of:
Asthma or other allergies, especially to bananas,

avocados, tropical fruits, or chestnuts
Multiple intra-abdominal or genitourinary surgeries
Frequent intermittent urinary catheterization
Incidence
H Present in 1% to 5% of population of the United
States
H Affects 10% to 30% of health care workers
H Most prevalent (20% to 68%) in patients with spina
bifida and urogenital abnormalities

H Hypotension
H Tachycardia
H Urticaria and pruritus
H Difficulty breathing, bronchospasm, wheezing, and
stridor
H Angioedema
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Latex allergy
Complications
H Respiratory obstruction
H Systemic vascular collapse
H Death
Assessment
History
H Exposure to latex
Physical findings
H Signs of anaphylaxis
H Rash
H Angioedema
H Conjunctivitis
H Wheezing, stridor
Test results
Diagnosis of latex allergy is based mainly on history and
physical assessment.
Laboratory
H Radioallergosorbent test shows specific IgE antibodies to latex (safest for use in patients with history of
type I hypersensitivity).
Products that contain latex

Medical products
H Adhesive bandages
H Airways, Levin tube
H Blood pressure cuff, tubing, and bladder
H Catheter leg straps
H Catheters
H Dental dams
H Elastic bandages
H Electrode pads
H Fluid-circulating hypothermia blankets
H Handheld resuscitation bags
H Hemodialysis equipment
H I.V. catheters
H Latex or rubber gloves
H Medication vials
H Pads for crutches
H Protective sheets
H Reservoir breathing bags
H Rubber airways and endotracheal tubes
H Tape
H Tourniquets
Nonmedical products
H Adhesive tape
H Balloons (excluding Mylar)
H Cervical diaphragms
H Condoms
H Disposable diapers
H Elastic stockings
H Glue
H Latex paint
H Nipples and pacifiers
H Rubber bands
H Tires
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Other
H Patch test results in hives with itching or redness as a
positive response.
Treatment
General
H Prevention of exposure, including use of latex-free
products to decrease possible exacerbation of hypersensitivity

H Maintenance of patent airway
Medications
H Use before and after possible exposure to latex
H Corticosteroids
H Antihistamines
H Histamine-2 receptor blockers
Acute treatment
H Epinephrine 1:1,000
H Oxygen therapy
H Volume expanders
H I.V. vasopressors
H Aminophylline and albuterol
Key outcomes
The patient will:
H identify latex products in order to avoid exposure.
H Maintain airway, breathing, and circulation.
ALERT
When adding medication to an I.V. bag, inject the
drug through the spike port, not the rubber latex
port.
H Keep the patients environment latex free.
Monitoring
H Vital signs
Patient teaching
Be sure to cover:
H potential for life-threatening reaction
H wearing medical identification jewelry that identifies
allergy
H how to use an epinephrine autoinjector.
Latex allergy
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Lead poisoning
Incidence
Overview
H About 4.4% of children in the United States having an
H Sharp decline for the past 30 years due to education
and regulations
Description
H Toxicity from repeated or excessive exposure to lead
which occurs naturally in the environment

H Present in:
Lead-based paint
Soil and dust
Drinking water
Air
Food
H Major worldwide health hazard
Pathophysiology
H Lead replaces calcium in the bones, affecting rapidly
growing bones; it appears as lines on X-rays.

H Substances, such as sodium citrate, ascorbate, amino
acids, vitamin D, protein and fat, and lactose, bind to
lead and enhance its absorption.
H Lead is metabolized in blood, skeleton, soft tissues,
and bile, and other body fluids.
H It affects every body system but primarily red blood
cell chemistry, the kidneys, and the nervous system.
H Brain damage occurs at low lead levels and isnt reversible.
Causes
H Inhalation of lead dust or fumes
H Ingestion of lead
Risk factors
H Children with pica or iron deficiency anemia
H Living where more than 27% of the housing was built
before 1950
H Exposure to leaded-paint surfaces
H Dust from clothing of lead worker
H Water from lead or lead-soldered plumbing
H Lead-glazed ceramics
H Soil and dust near lead industries and roads
H Hobbies
Glazed pottery making

Target shooting at firing ranges
Painting
Stained glass making
H Home remodeling
H Occupational exposuremore than 900 occupations, including:
Plumbers
Auto mechanics
Glass manufacturers
Printers
Construction workers
H Herbal folk remedies
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Lead poisoning
elevated lead level

H Black, non-Hispanic children at greatest risk
H Highest between ages 1 and 5 and adult workers
H Anemia
H Anorexia
H Constipation
Complications
H Renal failure
H Encephalopathy
H Exposure during pregnancy associated with low birth
weight and premature birth
Assessment
History
H Commonly produces no symptoms until severe
H Possible myalgia or paresthesia
H Fatigue or lethargy
H Irritability
H Difficulty concentrating
H Headache
H Tremors
H Vomiting
H Weight loss
H Seizures
H Delayed developmental milestones
Physical findings
H Typically normal
H Abdominal tenderness, possibly severe
H Possible symptoms of neuropathy or encephalopathy
Test results
Laboratory
H Serum lead levels are elevated.
H Complete blood count may show microcytic anemia.
H Free erythrocyte protoporphyrin level is elevated.
H Zinc protoporphyrin level is elevated.
H Provocative chelation test estimates the total body
burden of lead and the efficacy of treatment.
Imaging
H Abdominal X-rays
H Long-bone X-rays may show growth retardation.
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Treatment
General
H Based on blood lead level
H Separate individual from source of exposure
H Possibly intestinal irrigation
H Chelation therapy to promote lead excretion
Medications
H Calcium disodium edetate, usually I.V. but may be
given I.M.
H Dimercaprol given I.M.
H Oral agents
D-penicillamine (used for about 30 years but still

not FDA approved for chelation therapy)
Succimer (DMSA)
H Diazepam for initial seizure control, if indicated
Key outcomes
The patient (or parent) will:
H verbalize understanding of the disease and its treatment
H express understanding of preventive measures
H eliminate sources of lead from the home.
The patient will:
H verbalize reduced or absent pain
H show age-appropriate skills and activities
H show developmental progress
H demonstrate increased energy.
H Provide the prescribed diet, and encourage dietary
Prevention
Preventing lead poisoning

Lead poisoning can be prevented by following these
guidelines:
H Discuss screening family members for lead with health
care provider.
H Identify sources of lead in the home, such as in tap
water, handmade pots or pottery, imported cans of
food, and lead paint.
H Keep children away from lead paint and other sources
of lead in the home.
H Eat foods high in iron, calcium, and vitamin C, which
limit lead absorption.
H Wash hands after playing or working outside, before
eating, and before bed.
H Have the home inspected before doing major
remodeling and repairs, and reside elsewhere while the
lead source is being removed.
H If family members work with lead, they should change
their clothes before coming home from work, take off
shoes before entering the home, and shower before
playing with children.
H Discard toys that may contain lead paint.
H Dont let children play near major roadways or bridges.
H Run cold water for at least 1 minute before using.
H Dont use hot water for drinking, mixing formula, or
cooking.
Patient teaching
Be sure to cover:
H importance of follow-up care and monitoring lead
levels
H lead poisoning prevention. (See Preventing lead
poisoning.)
changes.
H Encourage activities that can be completed in short
periods.
H Help the patient (or parent) identify risk factors and
modify lifestyle, as appropriate.

H Facilitate screening of all family members.
Monitoring
H Adverse reactions to prescribed drugs
H Level of pain
H Laboratory values
H Urine output
H Complications
H Risk factor and lifestyle modifications
Lead poisoning
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Legg-Calv-Perthes
disease
H Slight shortening of the leg

H Severely restricted abduction and internal rotation of
Overview
H Permanent disability
H Premature osteoarthritis
Description
H Ischemic necrosis leading to eventual flattening of
the head of the femur due to vascular interruption

H Typically unilateral, occurs bilaterally in 20% of patients
H Also called coxa plana
H Usually runs its course in 3 to 4 years
H May lead to premature osteoarthritis later in life from
misalignment of the acetabulum and flattening of the
femoral head
Pathophysiology
H The first stage, synovitis, is characterized by synovial
inflammation and increased joint fluid, and typically

lasts 1 to 3 weeks.
H In the second (avascular) stage, vascular interruption causes necrosis of the ossification center of the
femoral head (usually in several months to 1 year).
H In the third stage, revascularization, a new blood
supply causes bone resorption and deposition of immature bone cells. New bone replaces necrotic bone
and the femoral head gradually reforms.
H The final, or residual stage, involves healing and
regeneration. Immature bone cells are replaced by
normal bone cells, thereby fixing the joints shape.
There may be residual deformity, based on the
degree of necrosis that occurred in stage two.
Causes
H Exact vascular obstructive changes that initiate dis-
the hip
Complications
Assessment
History
H Family history
H Limp that becomes progressively worse
H Persistent pain in the groin, anterior thigh, or knee
aggravated by activity and relieved by rest
Physical findings
H Muscle atrophy
H Slight shortening of the affected leg
H Restricted hip abduction and internal rotation
H Adductor muscle spasm in the affected hip
Test results
Imaging
H Hip X-rays taken every 3 to 4 months confirm the diagnosis, with findings that vary according to the stage
of the disease.
H Anterior-posterior X-rays and magnetic resonance
imaging enhance early diagnosis of necrosis and
visualization of articular surface.
Treatment
General
H Protection of the femoral head from further stress
and damage by containing it within the acetabulum
ease unknown
H Current etiologic theories:
Venous obstruction with secondary intraepiphyseal
thrombosis
Trauma to retinacular vessels
Vascular irregularities (congenital or developmental)
Vascular occlusion secondary to increased intracapsular pressure from acute transient synovitis
Increased blood viscosity resulting in stasis and
decreased blood flow
H Reduced weight bearing by means of bed rest in bilat-
Incidence
Surgery
H Occurs most frequently in boys ages 4 to 10

H Tends to occur in families
H For a young child in the early stages of the disease,
H Persistent thigh pain or limp that becomes progres-
sively more severe

H Mild pain in the hip, thigh, or knee aggravated by
activity and relieved by rest

H Muscle spasm
H Atrophy of muscles in the upper thigh
478
Legg-Calv-Perthes disease
eral split counterpoised traction, then application of

hip abduction splint or cast, or weight bearing while
a splint, cast, or brace holds the leg in abduction
(braces remaining in place for 6 to 18 months)
H Physical therapy with passive and active range-ofmotion (ROM) exercises after cast removal
Medications
H Analgesics
osteotomy and subtrochanteric derotation providing

maximum confinement of the epiphysis within the
acetabulum allowing return of the femoral head to
normal shape and full ROM; proper placement of
the epiphysis thus allowing remolding with ambulation; postoperatively, requiring a hip-spica cast for
about 2 months
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Key outcomes
The patient will:
pain
of the disease
regimen.
H Provide cast care.
Monitoring
H Intake and output
H Neurovascular status of affected extremity
H Skin integrity
Patient teaching
Be sure to cover:
H proper cast care and monitoring of skin integrity.
Legg-Calv-Perthes disease
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Legionnaires disease
Overview
Description
H Hypotension
H Delirium
H Seizures
H Heart failure
H Arrhythmias
H Renal failure
H Shock
H An acute bronchopneumonia produced by a gram-
negative bacillus
H Illness ranging from mild (with or without pneu-
monitis) to serious multilobed pneumonia with mortality as high as 15%

H Outbreaks (usually in late summer and early fall)
epidemic or confined to a few cases
Pathophysiology
Assessment
History
H Presence at a suspected source of infection
H Prodromal symptoms, including anorexia, malaise,
myalgia, and headache
H The legionella enter the lungs after aspiration or in-
Physical findings
halation.
H Although alveolar macrophages phagocytize the legionella, the organisms arent killed and proliferate
intracellularly.
H The cells rupture, releasing the legionella, and the
cycle starts again.
H Lesions develop a nodular appearance, and alveoli
become filled with fibrin, neutrophils, and alveolar
macrophages.
H Rapidly rising fever with chills

H Grayish or rust-colored, nonpurulent, occasionally
Causes
H Legionella pneumophila, an aerobic, gram-negative
bacillus most likely transmitted by air

H Water distribution systems (such as whirlpool spas
and decorative fountains): a primary reservoir for

the organism
Risk factors
H Smoking
H Diabetes
H Cancer, especially hematologic or pulmonary
H End-stage renal disease
H Chronic cardiopulmonary disease
H Advanced age
H Alcohol abuse
H Recent surgery
Incidence
H Most likely to affect males more than females
H Others at increased risk:
Elderly patients
Immunocompromised patients
Patients with chronic underlying disease such as
diabetes
Alcoholics
Cigarette smokers
blood-streaked sputum
H Tachypnea
H Bradycardia (in about 50% of patients)
H Neurologic signs (altered level of consciousness
[LOC])
H Dullness over areas of secretions and consolidation
or pleural effusions
H Fine crackles that develop into coarse crackles as the
disease progresses
Test results
Laboratory
H Gram staining reveals numerous neutrophils but no
organism.
H Definitive method of diagnosis involves isolation of
the organisms from respiratory secretions or bronchial washings or through thoracentesis.
H Definitive tests include direct immunofluorescence of
L. pneumophila and indirect fluorescent serum antibody testing.
H Leukocytosis and increased erythrocyte sedimentation rate are present.
H Partial pressure of arterial oxygen is decreased, and
partial pressure of arterial carbon dioxide is initially
decreased.
H Serum sodium level less than 131 mg/L indicates
hyponatremia.
Imaging
H Chest X-ray typically shows patchy, localized infiltration, which progresses to multilobed consolidation
(usually involving the lower lobes) and pleural effusion.
H In fulminant disease, chest X-ray reveals opacification of the entire lung.
Treatment
H Nonspecific prodromal symptoms

H Initial nonproductive cough that becomes productive
General
Complications
H Fluid replacement
H Hypoxia and acute respiratory failure
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Medications
H Antibiotics, such as levofloxacin and azithromycin
H Antipyretics such as acetominophen
Key outcomes
The patient will:
H cough effectively
H expectorate sputum effectively
H express feelings of increased comfort in maintaining
air exchange
H regain and maintain normal fluid and electrolyte balance
H have normal breath sounds.
H Give tepid sponge baths or use hypothermia blankets
to lower fever.
H Provide frequent mouth care. If necessary, apply
soothing cream to irritated nostrils.

Monitoring
H Vital signs
H Respiratory status and arterial blood gas values
H LOC
Patient teaching
Be sure to cover:
H importance of disinfection of water supply
H purpose of postural drainage, and how to perform
coughing and deep-breathing exercises
H proper hand washing and disposal of soiled tissues
to prevent disease transmission.
Discharge planning
H Refer the patient to a pulmonologist, if necessary.
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Leukemia, acute
Overview
Description
H Malignant proliferation of white blood cell (WBC)
precursors, or blasts, in bone marrow or lymph tissue; blasts accumulate in peripheral blood, bone
marrow, and body tissues
H Most common form of cancer among children
H Common forms:
Acute lymphoblastic (lymphocytic) leukemia
(ALL), characterized by abnormal growth of lymphocyte precursors (lymphoblasts)
Acute myeloblastic (myelogenous) leukemia
(AML); causes rapid accumulation of myeloid precursors (myeloblasts)
Acute monoblastic (monocytic) leukemia, or
Schillings type; results in marked increase in
monocyte precursors (monoblasts)
H ALL: treatment induces remissions in 90% of children (average survival time: 5 years) and 65% of
adults (average survival time: 1 to 2 years); children
ages 2 to 8 have best survival rate about 50%
with intensive therapy
H AML: average survival time is only 1 year after diagnosis, even with aggressive treatment (remissions
lasting 2 to 10 months in 50% of children; adult survival, only about 1 year after diagnosis, even with
treatment)
H Without treatment, invariably fatal
Pathophysiology
H Immature, nonfunctioning WBCs appear to accumu-
late first in the tissue where they originate, such as

lymphocytes in lymph tissue and granulocytes in
bone marrow.
H The immature, nonfunctioning WBCs spill into the
bloodstream and overwhelm red blood cells (RBCs)
and platelets; from there, they infiltrate other tissues.
Causes
H Unknown
Risk factors
H Radiation (especially prolonged exposure)
H Certain chemicals and drugs
H Viruses
H Genetic abnormalities
H Chronic exposure to benzene
In children
H Down syndrome
H Ataxia
H Telangiectasia
482
Leukemia, acute
H Congenital disorders, such as albinism and congeni-
tal immunodeficiency syndrome
Incidence
H More common in whites (especially of Jewish ances-
try)
H More common in children between ages 2 and 5
(80% in this age-groupALL), and those who live in

urban and industrialized areas
H Sudden onset of high fevers
H Night sweats
H Malaise
H Bone and joint pain
H Shortness of breath during physical activity
H Excessive bleeding or bruises
Complications
H Infection
H Organ malfunction through encroachment or hemor-
rhage
Assessment
History
H Sudden onset of high fever
H Abnormal bleeding
H Fatigue and night sweats
H Weakness, lassitude, recurrent infections, and chills
H Abdominal or bone pain in patients with ALL, AML,
or acute monoblastic leukemia
Physical findings
H Tachycardia, palpitations, and a systolic ejection
murmur
H Decreased ventilation
H Pallor
H Lymph node enlargement
H Liver or spleen enlargement
Test results
Laboratory
H Blood counts show thrombocytopenia and neutropenia, and a WBC differential shows the cell type.
Imaging
H Computed tomography scan shows the affected organs, and cerebrospinal fluid analysis shows abnormal WBC invasion of the central nervous system.
H Bone marrow aspiration that shows a proliferation of
immature WBCs confirms acute leukemia; if the aspirate is dry or free from leukemic cells but the patient
has other typical signs of leukemia, a bone marrow
biopsy, usually of the posterior superior iliac spine,
must be performed.
H Lumbar puncture is used to detect meningeal involvement.
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Treatment
General
H Transfusions of platelets to prevent bleeding
H Transfusions of RBCs to treat anemia
H Bone marrow transplantation in some patients
H Radiation therapy in case of brain or testicular infil-
tration
H Chemotherapeutic and radiation treatment, depending on diagnosis
Medications
For meningeal infiltration
H Intrathecal instillation of methotrexate or cytarabine
with cranial radiation
For ALL
H Vincristine, prednisone, high-dose cytarabine, and
daunorubicin
H Intrathecal methotrexate or cytarabine because ALL
carries 40% risk of meningeal infiltration
For AML
H Combination of I.V. daunorubicin and cytarabine (if
these fail to induce remission, treatment with some
or all of the following drugs: a combination of cyclophosphamide, vincristine, prednisone, or methotrexate; high-dose cytarabine alone or with other drugs;
amsacrine; etoposide; and 5-azacytidine and mitoxantrone)
For acute monoblastic leukemia
H Cytarabine and thioguanine with daunorubicin or
doxorubicin
H Anti-infectives, such as antibiotics, antifungals, antivirals and granulocyte injections
Monitoring
H Complications from treatment
H Urine pH (should be above 7.5)
H Vital signs
Patient teaching
Be sure to cover:
H use of a soft toothbrush and avoidance of hot, spicy
foods and commercial mouthwashes
H signs and symptoms of abnormal bleeding
H planned rest periods during the day.
Discharge planning
services.
Key outcomes
The patient will:
H exhibit intact mucous membranes
H experience no chills, fever, or other signs and symptoms of illness
H Encourage verbalization and provide comfort.
H After bone marrow transplantation, keep the patient
in a sterile room, administer antibiotics, and transfuse packed RBCs as necessary.

H Control mouth ulceration by checking often for obvious ulcers and gum swelling and by providing frequent mouth care and saline rinses.
Leukemia, acute
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Leukemia, chronic
granulocytic
H Hemorrhage
H Pain
Assessment
Overview
History
Description
H Renal calculi or gouty arthritis

H Fatigue, weakness, dyspnea, decreased exercise tol-
H Type of leukemia characterized by abnormal over-
growth of granulocytic precursors (myeloblasts,

promyelocytes, metamyelocytes, and myelocytes) in
bone marrow, peripheral blood, and body tissues
H Always fatal (average survival time 3 to 4 years after
onset of chronic phase and 3 to 6 months after onset
of acute phase)
H Clinical course in two distinct phases:
insidious chronic phase (characterized by anemia
and bleeding abnormalities)
acute phase (blast crisis, or myeloblasts, the most
primitive granulocytic precursors, proliferating
rapidly)
H During acute phase, may develop either lymphoblastic or myeloblastic disease (despite vigorous treatment, chronic granulocytic leukemia rapidly advancing after onset of acute phase)
H Also called chronic myelogenous (or myelocytic)
leukemia (CML)
Pathophysiology
H CML is a myeloproliferative disorder, originating in a
progenitor stem cell.

H Malignant transformation is identified in erythroid,
megakaryocytic, and macrophage cell lines.

H Malignant transformation arises from pluripotential
stem cells or lymphoid stem cells.
Causes
Risk factors
H Presence of the Philadelphia chromosome (found in
almost 90% of patients)

H Myeloproliferative diseases
Incidence
H Most common in young and middle-aged adults
H Slightly more common in males than in females, and
rare in children
H In United States, 3,000 to 4,000 cases annually
erance, and headache

H Recent weight loss and anorexia
Physical findings
H Evidence of bleeding and clotting disorders
H Low-grade fever and tachycardia
H Pallor
H Difficulty breathing
H Retinal hemorrhage
H Hepatosplenomegaly with abdominal discomfort and
pain
H Sternal and rib tenderness
Test results
Laboratory
H Chromosomal studies of peripheral blood or bone
marrow show the Philadelphia chromosome.
H Low leukocyte alkaline phosphatase levels confirm
chronic granulocytic leukemia.
H Complete blood count reveals:
white blood cell (WBC) abnormalities, including
leukocytosis (WBC count over 50,000/l, rising
as high as 250,000/l), occasionally leukopenia
(WBC count under 5,000/l), and neutropenia
(neutrophil count under 1,500/l) despite high
WBC count
increased circulating myeloblasts
decreased hemoglobin level (below 10 g/dl), and
low hematocrit (less than 30%)
thrombocytosis (more than 1 million thrombocytes/l).
H Serum uric acid level may exceed 8 mg/dl.
Imaging
H Computed tomography scan may show the affected
organs.
H Bone marrow aspirate or biopsy (performed only if
the aspirate is dry) may be hypercellular, characteristically showing bone marrow infiltration by a significantly increased number of myeloid elements; in the
acute phase, myeloblasts predominate.
(about 20% of all leukemias)
H Fatigue
H Weakness
H Weight loss
H History of gouty arthritis or renal calculi
Complications
H Infection
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Leukemia, chronic granulocytic
Treatment
General
H Bone marrow transplantation (chronic phase, more
than 60% of patients who receive transplant achieving remission)

H Local splenic radiation
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H Leukapheresis (selective leukocyte removal) to re-
Discharge planning
duce WBC count

services.
Medications
H Antineoplastics, such as hydroxyurea or imatinib
Surgery
H Splenectomy
Key outcomes
The patient will:
H have intact mucous membranes
H experience no chills, fever, or other signs and symptoms of illness
H express feelings of increased comfort and energy
H Plan care to minimize fatigue.
H Regularly check skin and mucous membranes for
pallor, petechiae, and bruising.

H Encourage deep-breathing and coughing exercises.
H Encourage verbalization and provide comfort.
H After bone marrow transplantation, keep the patient
in a sterile room and give prescribed antibiotics and

packed red blood cells.
Monitoring
H Complete blood count
H Vital signs
Patient teaching
Be sure to cover:
H how to minimize bleeding and infection risks (such
as by using a soft-bristled toothbrush, an electric razor, and other safety devices)
H high-calorie, high-protein diet
H reinforcement of the physicians explanation of the
procedure, possible outcome, and potential adverse
effects (if the patient will undergo bone marrow
transplantation)
adverse effects
H signs and symptoms of infection and thrombocytopenia.
Leukemia, chronic granulocytic
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Leukemia, chronic
lymphocytic
Physical findings
H Macular or nodular eruptions and evidence of skin
infiltration
H Enlarged lymph nodes, liver, and spleen
H Bone tenderness and edema from lymph node ob-
struction
Overview
H Pallor, dyspnea, tachycardia, bleeding, and infection
Description
H Signs of opportunistic fungal, viral, or bacterial in-
H The most benign and the most slowly progressive
form of leukemia
H Prognosis poor if anemia, thrombocytopenia, neutropenia, bulky lymphadenopathy, and severe lymphocytosis develop
Pathophysiology
H Chronic lymphocytic leukemia is a generalized, pro-
gressive disease marked by an uncontrollable spread

of abnormal, small lymphocytes in lymphoid tissue,
blood, and bone marrow.
H Once these cells infiltrate bone marrow, lymphoid
tissue, and organ systems, clinical signs begin to
appear.
H Gross bone marrow replacement by abnormal lymphocytes is the most common cause of death, usually
within 4 to 5 years of diagnosis.
Causes
Risk factors
H Hereditary factors
H Undefined chromosomal abnormalities
H Certain immunologic defects, such as acquired
from bone marrow involvement

fections
Test results
Laboratory
H Miscellaneous blood tests reveal the disease. (Typically, chronic lymphocytic leukemia is an incidental
finding during a routine complete blood count that
reveals numerous abnormal lymphocytes.)
In the early stages, white blood cell (WBC) count
is mildly but persistently elevated; granulocytopenia is the rule, although WBC count climbs as disease progresses.
Hemoglobin level is less than 11 g/dl.
WBC differential shows neutropenia (less than
1,500/l) and lymphocytosis (more than
10,000/l).
Platelet count shows thrombocytopenia (less than
150,000/l).
Serum protein electrophoresis shows hypogammaglobulinemia.
Imaging
H Computed tomography scan shows affected organs.
H Bone marrow aspiration and biopsy show lymphocytic invasion.
agammaglobulinemia or ataxia-telangiectasia
Incidence
H Most common in elderly people; nearly all afflicted
are males older than age 50
Treatment
General
H Chronic lymphocytic leukemia almost one-third of
H Radiation therapy to relieve symptoms (generally for
new leukemia cases annually

H Higher incidence recorded within families
H Fever, malaise, weakness
patient with enlarged lymph nodes, painful bony lesions, or massive splenomegaly)
H Avoidance of hot and spicy foods for patient with
impaired oral membranes
Complications
Medications
H Infection
H In end-stage disease: anemia, progressive spleno-
H Systemic chemotherapy, such as fludarabine, chlo-
megaly, leukemic cell replacement of the bone marrow, and profound hypogammaglobulinemia, which
usually terminates with fatal septicemia
Assessment
History
H Fatigue, malaise, fever, weight loss, and frequent in-
fections
H Weakness, palpitations
486
Leukemia, chronic lymphocytic
rambucil, and cyclophosphamide

H Other antineoplastics, such as rituximab and alem-
tuzumab
Key outcomes
The patient will:
H have intact mucous membranes
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H experience no chills, fever, or other signs and symp-
toms of illness
H express feelings of increased comfort and energy
H Help establish an appropriate rehabilitation program
during remission.
H Place in reverse isolation, if necessary.
H Administer blood component therapy, as necessary.
Monitoring
H Signs and symptoms of bleeding and thrombo-
cytopenia
H Pain control
H Vital signs
Patient teaching
Be sure to cover:
H use of a soft toothbrush and avoidance of commercial mouthwashes to prevent irritating the mouth
ulcers that result from chemotherapy
adverse effects
H signs and symptoms of infection, bleeding, and
recurrence
H staying away from anyone with an infection
H signs and symptoms of recurrence.
Discharge planning
services.
Leukemia, chronic lymphocytic
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Listeriosis
Overview
Description
by coming in contact with infected animals, contaminated sewage or mud, or soil contaminated with
feces organism. (See Preventing listeriosis.)
Causes
H Contamination with L. monocytogenes
H An infection caused by the weakly hemolytic, gram-
Risk factors
positive bacillus Listeria monocytogenes

H Occurs most commonly in fetuses, in neonates (during the first 3 weeks of life), and in older or immunosuppressed adults; infected fetus usually stillborn or born prematurely
H Infection producing milder illness in pregnant females and varying degrees of illness in older and immunosuppressed patients; prognoses dependent on
severity of underlying illness
H Age extremes
H Pregnancy
H Weakened immune system
H Handling or eating uncooked or undercooked meat,
Pathophysiology
H L. monocytogenes is a nonspore producing, motile
gram-positive bacillus with aerobic and anaerobic

characteristics.
H It grows best at neutral to slightly alkaline pH.
H Transmission occurs:
in utero (through the placenta) or during passage
through an infected birth canal
by inhaling contaminated dust
by drinking contaminated, unpasteurized milk
soft cheese, and unpasturized milk

H Occupations involving contact with animals, such as
butchers, veterinarians, and farmers
Incidence
H 7.4 cases per million population
H Affects females of childbearing age
H Transient asymptomatic carrier state
H Bacteremia and a febrile, generalized illness
H In a pregnant female, especially during the third
trimester: a mild illness with malaise, chills, fever,

and back pain (possibly also severe uterine infection,
abortion, premature delivery, or stillbirth)
H Transplacental infection possibly causing early
neonatal death or granulomatosis infantiseptica,
which produces organ abscesses in infants
Complications
Preventing listeriosis
Follow these general guidelines to prevent listeriosis:
H Thoroughly cook raw food from animal sources, such
as beef, pork, or poultry.
H Wash raw vegetables thoroughly before eating.
H Keep uncooked meats separate from vegetables and
from cooked foods and ready-to-eat foods.
H Avoid unpasteurized (raw) milk or foods made from
unpasteurized milk.
H Wash hands, knives, and cutting boards after handling
uncooked foods.
Patients at high risk, such as those with weakened immune systems and pregnant women, should follow the
general guidelines, plus:
H Avoid hot dogs, luncheon meats, and deli meats, unless they are reheated until steaming hot.
H Avoid cross-contaminating other foods, utensils, and
food preparation surfaces with fluid from hot dog packages, and wash hands after handling hot dogs, luncheon meats, and deli meats.
H Dont eat soft cheeses, such as feta, Brie, Camembert,
blue-veined cheeses, and Mexican-style cheeses such
as queso blanco fresco.
H Dont eat refrigerated pts or meat spreads. Canned or
shelf-stable pts and meat spreads may be eaten.
H Dont eat refrigerated smoked seafood, such as
salmon, trout, whitefish, cod, tuna, or mackerel, unless
its in a cooked dish such as a casserole.
488
Listeriosis
H Stillbirth
H Meningitis
H Septic arthritis
H Endocarditis
Assessment
History
H Ingestion of infected food
H Eye or skin exposure to laboratory animals or ani-
mals seen in veterinary practice
Physical findings
H Back pain and malaise
H Fever
H Nausea and diarrhea
H Headache, stiff neck
H Confusion, loss of balance, seizures
H Skin lesions on trunk and extremities
H Signs of sepsis
Test results
Laboratory
H L. monocytogenes is identified by its diagnostic tumbling motility on a wet mount of the culture.
H Positive culture of blood, spinal fluid, drainage from
cervical or vaginal lesions, or lochia from a mother
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with an infected neonate is present; isolation of the

organism from these specimens is generally difficult.
Treatment
General
H Symptomatic
Medications
H Antibiotics, such as penicillin G and ampicillin
Key outcomes
The patient will:
H show improvement in signs and symptoms.
H Provide adequate nutrition by total parenteral nutri-
tion, nasogastric tube feedings, or a soft diet, as

ordered.
Monitoring
H Neurologic status
H Fontanels (in neonates)
H Vital signs
H Intake and output
Patient teaching
Be sure to cover:
H how to avoid infective materials on farms where
listeriosis is endemic among livestock.
Listeriosis
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Liver cancer
Overview
Description
H Malignant cells growing in the tissues of the liver
H Rapidly fatal, usually within 6 months
H After cirrhosis, the leading cause of fatal hepatic dis-
ease
H Liver metastasis occurring as solitary lesion (the first
sign of recurrence after a remission)
Pathophysiology
H Most (90%) primary liver tumors originate in the
parenchymal cells and are hepatomas. Others originate in the intrahepatic bile ducts (cholangiomas).
H Approximately 30% to 70% of patients with hepatomas also have cirrhosis.
H Rare tumors include a mixed-cell type, Kupffer cell
sarcoma, and hepatoblastoma.
H The liver is one of the most common sites of metastasis from other primary cancers. Cells metastasize to
gallbladder, mesentery, peritoneum, and diaphragm
by direct extension.
Causes
H Immediate cause unknown
H Environmental exposure to carcinogens
H Possibly androgens and oral estrogens
H Hepatitis B virus
H Hepatitis C virus
H Hepatitis D virus
Risk factors
H Cirrhosis
H Excessive alcohol intake
H Malnutrition
Incidence
H Most prevalent in males older than age 60
H Primary liver cancer roughly 2% of all cancers in
North America and 10% to 50% of cancers in Africa

and parts of Asia

H Initially, dull aching abdominal pain
H Severe pain in the epigastrium or right upper
quadrant
Physical findings
H Jaundice
H Dependent edema
H Abdominal bruit, hum, or rubbing sound
H Tender, nodular, enlarged liver
H Ascites
H Palpable mass in the right upper quadrant
Test results
Laboratory
H Liver function studies are abnormal.
H Alpha-fetoprotein levels are greater than
500 mcg/ml.
H Electrolyte study results are abnormal.
Imaging
H Liver scan may show filling defects and lesions in
the liver.
H Arteriography may define large tumors.
H Ultrasound and computed tomography scans may
reveal lesions in the liver.
H Liver biopsy by needle or open biopsy reveals cancerous cells.
Treatment
General
H Radiation therapy (alone or with chemotherapy)
H High-calorie, low-protein diet
H Postoperative avoidance of heavy lifting and contact
sports
Medications
H Chemotherapeutics, such as doxorubicin, 5-fluo-
rouracil, and cisplatin
Surgery
H Resection (lobectomy or partial hepatectomy)
H Liver transplantation
H Right upper quadrant pain

H Fatigue
Complications
Key outcomes
H GI hemorrhage
H Progressive cachexia
H Liver failure
Assessment
The patient will:

H maintain stable hemodynamic status
H exhibit adequate coping behaviors
History
H Weight loss
H Weakness, fatigue, and fever

490
Liver cancer
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Monitoring
H Vital signs
H Weight
H Pain control
H Neurologic status
H Complete blood count; liver function tests
H Wound site
Patient teaching
Be sure to cover:
adverse effects.
Discharge planning
H Refer the patient and family to support services.
Liver cancer
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Liver failure
Overview
Description
H Inability of the liver to function properly, usually as
the end result of any liver disease

H Causes a complex syndrome involving the impair-
ment of many different organs and body functions

(see Understanding liver functions)
H Two conditions occurring in liver failure hepatic
encephalopathy and hepatorenal syndrome
H Liver transplantation only cure
Pathophysiology
H Manifestations of liver failure include hepatic en-
cephalopathy and hepatorenal syndrome.

H The liver cant detoxify the blood.
H Liver dysfunction and collateral vessels that shunt
blood around the liver to the systemic circulation
permit toxins absorbed from the GI tract to circulate
freely to the brain.
H The normal liver transforms ammonia (a by-product
of protein metabolism) to urea, which the kidneys
excrete.
H When the liver cant transform ammonia to urea, ammonia blood levels rise, and the ammonia is delivered to the brain.
H Short-chain fatty acids, serotonin, tryptophan, and
false neurotransmitters may also accumulate in the
blood.
Hepatorenal syndrome
H Renal failure is concurrent with liver disease; the
kidneys appear to be normal but abruptly cease functioning.
H Blood volume expands, hydrogen ions accumulate,
and electrolyte disturbances occur.
Understanding liver functions

To understand how liver disease affects the body, you
need to understand its main functions. The liver:
H detoxifies poisonous chemicals, including alcohol, and
drugs (prescribed and over-the-counter as well as illegal substances)
H makes bile to help digest food
H stores energy by stockpiling sugar (carbohydrates, glucose, and fat) until needed
H stores iron reserves as well as vitamins and minerals
H manufactures new proteins
H produces important plasma proteins necessary for
blood coagulation, including prothrombin and fibrinogen
H serves as a site for hematopoiesis during fetal development.
492
Liver failure
H The cause may be the accumulation of vasoactive
substances that cause inappropriate constriction of

renal arterioles, leading to decreased glomerular filtration and oliguria.
H The vasoconstriction may also be a compensatory response to portal hypertension and the pooling of
blood in the splenic circulation.
Causes
H Viral hepatitis
H Nonviral hepatitis
H Cirrhosis
H Liver cancer
H Acetaminophen toxicity
H Malnutrition
H Long-term alcohol abuse
H Hemochromatosis
H Ingestion of wild, poisonous mushrooms
Risk factors
H Obesity
H Diabetes
H Hyperlipidemia
H Abdominal surgery removing large sections of the
small intestines
Incidence
H Patients younger than age 10 and older than age 40
faring poorly
H Jaundice
H Abdominal pain or tenderness
H Nausea and anorexia
H Fatigue
H Weight loss
H Pruritus
H Oliguria
H Splenomegaly
H Ascites
H Peripheral edema
H Varices of the esophagus, rectum, and abdominal
wall
H Petechia
H Amenorrhea
H Gynecomastia (in males)
Complications
H Variceal bleeding
H GI hemorrhage
H Coma
H Death
Assessment
History
H Liver disorder
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H Fatigue
H Weight loss
H Nausea
H Anorexia
H Pruritus
Physical findings
H Jaundice
H Splenomegaly
H Ascites
H Peripheral edema
Test results
Laboratory
H Liver function tests reveal elevated levels of aspartate
aminotransferase, alanine aminotransferase, alkaline
phosphatase, and bilirubin.
H Blood studies reveal anemia, impaired red blood cell
production, elevated bleeding and clotting times, low
blood glucose levels, and increased serum ammonia
levels.
H Urine osmolarity is increased.
Monitoring
H Vital signs
H Laboratory values
H Intake and output
H Weight and abdominal girth
Patient teaching
Be sure to cover:
H signs of complications and when to notify the
physician
H importance of following a low-protein diet
H importance of avoiding alcohol.
Discharge planning
H Refer the patient to available support services, as
appropriate.
Treatment
General
H Paracentesis to remove ascitic fluid
H Balloon tamponade to control bleeding varices
H Low-protein, high-carbohydrate diet
Medications
H Lactulose
H Potassium-sparing diuretics (for ascites)
H Vasoconstrictors (for variceal bleeding)
H Vitamin K
Surgery
H Sclerosis to stop bleeding varices
H Shunt placement
H Liver transplantation
Key outcomes
The patient will:
H stabilize fluid status
H remain oriented to his surroundings.
H Reorient patient, as needed.
Liver failure
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Lung cancer
Overview
Description
H Malignant tumors arising from the respiratory epithe-
lium
H Most common types are epidermoid (squamous
cell), adenocarcinoma, small-cell (oat cell), and

large-cell (anaplastic)
H Most common site is wall or epithelium of bronchial
tree
H For most patients, poor prognosis, depending on extent of cancer when diagnosed and cells growth rate
(only about 13% of patients with lung cancer surviving 5 years after being diagnosed)
Pathophysiology
H Individuals with lung cancer demonstrate bronchial
epithelial changes progressing from squamous cell

alteration or metaplasia to carcinoma in situ.
H Tumors originating in the bronchi are thought to be
more mucus producing.
H Partial or complete obstruction of the airway occurs
with tumor growth, resulting in lobar collapse distal
to the tumor.
H Early metastasis occurs to other thoracic structures,
such as hilar lymph nodes or the mediastinum.
H Distant metastasis occurs to the brain, liver, bone,
and adrenal glands.
Causes
Risk factors
H Smoking
H Exposure to carcinogenic and industrial air pollu-
tants (asbestos, arsenic, chromium, coal dust, iron

oxides, nickel, radioactive dust, and uranium)
H Radon exposure
Incidence
H Family susceptibility
Special populations
Lung cancer is the most common cause of death
from cancer for men and women ages 50 to 75.
H 15% of new cancer cases
H 29% of all cancer deaths
Epidermoid and small-cell
H Smokers cough
H Hoarseness
H Wheezing
494
Lung cancer
H Dyspnea
H Hemoptysis
H Chest pain
H Cushings and carcinoid syndromes
H Hypercalcemia
Adenocarcinoma and large-cell

H Fever
H Weakness
H Weight loss
H Anorexia
H Shoulder pain
H Gynecomastia
H Hypertrophic pulmonary osteoarthropathy
Complications
H Spread of primary tumor to intrathoracic structures
H Tracheal obstruction
H Esophageal compression with dysphagia
H Phrenic nerve paralysis with hemidiaphragm eleva-
tion and dyspnea

H Sympathetic nerve paralysis with Horners syndrome
H Spinal cord compression
H Lymphatic obstruction with pleural effusion
H Hypoxemia
H Anorexia and weight loss, sometimes leading to
cachexia, digital clubbing, and hypertrophic osteoarthropathy

H Neoplastic and paraneoplastic syndromes, including
Pancoasts syndrome and syndrome of inappropriate
antidiuretic hormone
Assessment
History
H Exposure to carcinogens
H Coughing
H Hemoptysis
H Hoarseness
H Fatigue
Physical findings
H Finger clubbing
H Edema of the face, neck, and upper torso
H Dilated chest and abdominal veins (superior vena
cava syndrome)
H Weight loss
H Enlarged liver
H Wheezing
H Pleural friction rub
Test results
Laboratory
H Cytologic sputum analysis shows diagnostic evidence
of pulmonary malignancy.
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H Liver function studies are abnormal especially with
metastasis.
Imaging
H Chest X-rays show advanced lesions and can show a
lesion up to 2 years before signs and symptoms appear; findings may indicate tumor size and location.
H Contrast studies of the bronchial tree (chest tomography, bronchography) demonstrate size and location as well as spread of lesion.
H Bone scan is used to detect metastasis.
H Computed tomography (CT) scan of the chest is used
to detect malignant pleural effusion.
H CT scan of the brain is used to detect metastasis.
H Positron-emission tomography aids in the diagnosis
of primary and metastatic sites.
H Bronchoscopy can be used to identify the tumor site.
Bronchoscopic washings provide material for cytologic and histologic study.
H Needle biopsy of the lungs (relies on biplanar fluoroscopic visual control to locate peripheral tumors before withdrawing a tissue specimen for analysis) allows firm diagnosis in 80% of patients.
H Tissue biopsy of metastatic sites (including supraclavicular and mediastinal nodes and pleura) is used
to assess disease extent. Based on histologic findings,
staging describes the diseases extent and prognosis
and is used to direct treatment.
H Thoracentesis allows chemical and cytologic examination of pleural fluid.
H Gallium scans of the liver and spleen help detect
metastasis.
H Exploratory thoracotomy is performed to obtain
biopsy.
Key outcomes
The patient will:
pain.
H Encourage verbalization.
Monitoring
H Chest tube function and drainage
H Wound site
H Vital signs
H Sputum production
H Hydration and nutrition
H Oxygenation
H Pain control
Patient teaching
Treatment
Be sure to cover:
H postoperative procedures and equipment
H exercises to prevent shoulder stiffness
adverse effects
H risk factors for recurrent cancer.
General
Discharge planning
H Various combinations of surgery, radiation therapy,
H Refer smokers to local branches of the American
and chemotherapy to improve prognosis

H Palliative (most treatments)
H Preoperative and postoperative radiation therapy
H Laser therapy
H Activity, as tolerated per breathing capacity
Cancer Society or Smokenders.

H Provide information about group therapy, individual
counseling, and hypnosis.

services.
Medications
H Chemotherapy combinations
H Erletin
H Biologicals such as bevacizumab
Surgery
H Partial removal of lung (wedge resection, segmental
resection, lobectomy, radical lobectomy)

H Total removal of lung (pneumonectomy, radical
pneumonectomy)
Lung cancer
495
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Lupus erythematosus
Overview
Description
H Chronic inflammatory disorder of the connective tis-
sues appearing in two forms: discoid lupus erythematosus, which affects only the skin, and systemic
lupus erythematosus (SLE), which affects multiple
organ systems as well as the skin and possibly fatal
H Characterized by recurring remissions and exacerbations, especially common during the spring and summer
H Prognosis improving with early detection and treatment but remaining poor for patients who develop
cardiovascular, renal, or neurologic complications,
or severe bacterial infections
Assessment
History
H History of contributing factor
H Fever
H Weight loss
H Malaise
H Fatigue
H Polyarthralgia
H Abdominal pain
H Headaches, irritability, and depression (common)
H Nausea, vomiting, diarrhea, constipation
H Irregular menstrual periods or amenorrhea during
the active phase of SLE
Physical findings
H Rashes
H Joint involvement, similar to rheumatoid arthritis (al-
though the arthritis of lupus usually nonerosive)
Pathophysiology
H Skin lesions, most commonly an erythematous rash
H Autoimmunity is believed to be the prime mechanism
in areas exposed to light (classic butterfly rash over

the nose and cheeks in less than 50% of patients) or
a scaly, papular rash (mimics psoriasis), especially
in sun-exposed areas
H Vasculitis (especially in the digits), possibly leading
to infarctive lesions, necrotic leg ulcers, or digital
gangrene
H Patchy alopecia and painless ulcers of the mucous
membranes
H Lymph node enlargement (diffuse or local, and nontender)
involved with SLE.

H The body produces antibodies against components of
its own cells such as the antinuclear antibody (ANA),
and immune complex disease follows.
H Patients with SLE may produce antibodies against
many different tissue components, such as red blood
cells (RBCs), neutrophils, platelets, lymphocytes, or
almost any organ or tissue in the body.
Causes
Risk factors
H Physical or mental stress
H Streptococcal or viral infections
H Exposure to sunlight or ultraviolet light
H Immunization
H Pregnancy
H Abnormal estrogen metabolism
H Treatment with certain drugs, such as procainamide
(Pronestyl), hydralazine (Apresoline), and anticonvulsants
Incidence
H Affects 14 to 50 people per 100,000 in the United
States
H Affects females more than males
H Affects all ages, but peak incidence is young adult-
hood
See Signs of systemic lupus erythematosus.
Complications
H Concomitant infections
H Urinary tract infections
H Renal failure
H Osteonecrosis of hip from long-term steroid use
496
Lupus erythematosus
Test results
Laboratory
H Antidouble-stranded deoxyribonucleic acid antibody, the most specific test for SLE, correlates with
disease activity, especially renal involvement, and
helps monitor response to therapy; it may be low or
absent in remission.
H Complete blood count with differential may show
anemia and a decreased white blood cell (WBC)
count.
H Platelet count is decreased.
H Erythrocyte sedimentation rate is elevated.
H Serum hypergammaglobulin is elevated.
H ANA and lupus erythematosus cell tests show positive
results in active SLE.
H Urine studies may show RBCs and WBCs, urine casts
and sediment, and significant protein loss (more
than 0.5 g/24 hours).
H Serum complement blood studies show decreased
serum complement (C3 and C4) levels indicating
active disease.
H Lupus anticoagulant and anticardiolipin tests may be
positive in some patients (usually in patients prone to
antiphospholipid syndrome of thrombosis, abortion,
and thrombocytopenia).
Imaging
H Chest X-ray may show pleurisy or lupus pneumonitis.
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H Electrocardiography may show a conduction defect
with cardiac involvement or pericarditis.
H Kidney biopsy determines disease stage and extent of
renal involvement.
Treatment
General
H Symptomatic
H Dialysis or kidney transplant for renal failure
H Diet restrictions based on extent of disorder
Medications
H Nonsteroidal anti-inflammatory drugs, including
aspirin
H Topical corticosteroid creams, such as hydrocorti-
sone buteprate and triamcinolone

H Intralesional corticosteroids or antimalarials such as
hydroxychloroquine sulfate
H Systemic corticosteroids
Key outcomes
The patient will:
H express understanding of disease and treatment.
Signs of systemic lupus erythematosus

Systemic lupus erythematosus (SLE) often mimics other
diseases, making it difficult to diagnose. Symptoms may
be vague and vary greatly among patients.
For these reasons, the American Rheumatism Association issued a list of criteria for classifying SLE to be used
primarily for consistency in epidemiologic surveys. Usually, four or more of these signs are present at some time
during the course of the disease:
H malar or discoid rash
H photosensitivity
H oral or nasopharyngeal ulcerations
H nonerosive arthritis (of two or more peripheral joints)
H pleuritis or pericarditis
H profuse proteinuria (more than 0.5 g/day) or excessive
cellular casts in the urine
H seizures or psychoses
H hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia
H antidouble-stranded deoxyribonucleic acid or positive
findings of antiphospholipid antibodies (elevated immunoglobulin [Ig] G or IgM anticardiolipin antibodies,
positive test result for lupus anticoagulant, or falsepositive serologic test results for syphilis)
H abnormal antinuclear antibody titer.
Discharge planning
H Arrange for physical therapy and occupational coun-
seling, as appropriate.
H Refer the patient to the Lupus Foundation of America
and the Arthritis Foundation, as necessary.
H Provide a balanced diet. Renal involvement may man-
date a low-sodium, low-protein diet.

H Urge the patient to get plenty of rest. Schedule diag-
nostic tests and procedures to allow adequate rest.

H Explain all tests and procedures.
H Apply heat packs to relieve joint pain and stiffness.
H Encourage regular exercise to maintain full range of
motion (ROM) and prevent contractures.
Monitoring
H Signs and symptoms
H Vital signs
H Intake and output
H Laboratory reports
Patient teaching
Be sure to cover:
H ROM exercises as well as body alignment and postural techniques
H expected benefit of prescribed medications as well as
adverse effects
H cosmetic tips, such as suggesting the use of hypoallergenic makeup and referral to a hairdresser who
specializes in scalp disorders.
Lupus erythematosus
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Lyme disease
Overview
Description
H A multisystem disorder caused by a spirochete
Pathophysiology
H A tick injects spirochete-laden saliva into the blood-
stream or deposits fecal matter on the skin.

H After incubating for 3 to 32 days, the spirochetes mi-
grate outward on the skin, causing a rash, and disseminate to other skin sites or organs through the
bloodstream or lymph system.
H Spirochetes may survive for years in the joints or die
after triggering an inflammatory response in the host.
Causes
H The spirochete Borrelia burgdorferi, carried by the
minute tick Ixodes dammini (also called I. scapularis) or another tick in the Ixodidae family
Risk factors
H Outdoor occupations
H Outdoor activities, such as camping and hunting
H Geographic location with tick infestation
Incidence
H Affects all ages and both sexes
H Onset during the summer months
H Occurs in geographic ranges of ixodid ticks
H Typically begins with classic skin lesion, erythema
migrans (EM)
H Skin lesions with bright red outer rims and white
centers appearing on axilla, thigh, and groin

H Initial reported symptoms, such as fatigue, malaise,
migratory myalgia, and arthralgia

H Cardiac, neurologic, or joint abnormalities possibly
developing weeks or months later
Complications
H Myocarditis
H Pericarditis
H Arrhythmias
H Meningitis
Differentiating Lyme disease

Lyme disease, or chronic neuroborreliosis, needs to be
differentiated from chronic fatigue syndrome or fibromyalgia, which is difficult late in the disease because of
chronic pain and fatigue. The other diseases produce
more generalized and disabling symptoms; also, patients
lack evidence of joint inflammation, have normal neurologic tests, and have a greater degree of anxiety and depression than patients with Lyme disease.
498
Lyme disease
If untreated in acute phase

H Encephalitis
H Cranial or peripheral neuropathies
H Arthritis
Assessment
History
H Recent exposure to ticks
H Onset of symptoms in warmer months
H Severe headache and stiff neck with rash eruption
H Fever (up to 104 F [40 C]) and chills
Physical findings
H Regional lymphadenopathy
H Tenderness in the skin lesion site or the posterior
cervical area
Early stage
H Tachycardia or irregular heartbeat
H Mild dyspnea
H EM
H Headache
H Myalgia
H Arthralgia
Later stage
H Neurologic signs such as memory impairment
H Bells palsy
H Intermittent arthritis (see Differentiating Lyme disease)
H Cardiac symptoms, such as heart failure, pericarditis,
and dyspnea
H Neurologic symptoms, such as memory impairment
and myelitis
H Fibromyalgia
H Ocular signs such as conjunctivitis
Test results
Laboratory
H Assays for anti-B. burgdorferi show evidence of previous or current infection.
H Enzyme-linked immunosorbent assay or indirect immunofluorescence microscopy shows immunoglobulin (Ig) M levels peak 3 to 6 weeks after infection,
IgG antibodies are detected several weeks after infection and may continue to develop for several months
and generally persist for years.
H Positive Western blot assay shows serologic evidence.
of past or current infection with B. burgdorferi
H Polymerase chain reaction is used when joint and
cerebrospinal fluid involvement are present.
ALERT
Serologic testing isnt useful early in the course of
Lyme disease because of its low sensitivity. However, it may be more useful in later disease stages,
when sensitivity and specificity of the test are improved.
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H Lumbar puncture with analysis of cerebrospinal fluid
may show antibodies to B. burgdorferi.
H Skin biopsy may be used to detect B. burgdorferi.
Treatment
General
H Prompt tick removal using proper technique
H Rest periods when needed
Medications
H I.V. or oral antibiotics (initiated as soon as possible
after infection), such as doxycycline, amoxicillin,

ceftriaxone, and cefuroxime axetil
Prevention
Preventing lyme disease

Lyme disease can be prevented by following these guidelines:
H Avoid tick-infested areas.
H Cover the skin with light-colored clothing to make ticks
more visible.
H Wear long sleeves and pants and tuck pant legs into
socks.
H Use insect repellants, such as DEET or permethricin
(on clothing only).
H Inspect the body and scalp for attached ticks at least
every 4 hours and remove. Lyme disease is less likely
if the tick is removed in less than 48 hours.
H Check pets for ticks.
Key outcomes
The patient will:
H express relief from pain
H attain the highest degree of mobility possible.
H Plan care to provide adequate rest.
H Assist with range-of-motion and strengthening exer-
cises (with arthritis).

Monitoring
H Skin lesions
H Complications
Patient teaching
Be sure to cover:
H importance of follow-up care and reporting recurrent or new symptoms to the physician
H prevention of Lyme disease (see Preventing Lyme
disease)
H information about the vaccine for persons at risk for
contracting Lyme disease.
Discharge planning
H If the patient is in the late stages of the disease, refer
him to a dermatologist, neurologist, cardiologist, or

infectious disease specialist, as indicated.
Lyme disease
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Lymphocytic
choriomeningitis
Overview
Description
H A mild, biphasic, febrile illness lasting about 2 weeks
H Asymptomatic in one-third of individuals and re-
solves without serious sequelae in most cases

H Rarely fatal (less than 1% mortality rate)
H Also known as LCM or lymphocytic meningitis
Pathophysiology
H Infected mice or other hosts excrete lymphocytic
choriomeningitis virus (LCMV) in saliva, urine, and

feces.
H Human infection is through inhalation of infectious
aerosolized particles of host urine, feces, or saliva;
food contaminated with virus; or contamination of
mucous membranes, skin lesions, or cuts with infected body fluids.
H The incubation period is 8 to13 days and is followed
by a biphasic, febrile illness.
H The initial viremia extensively seeds extra-central
nervous system tissue and sometimes cortical tissue.
H The leptomeninges are infiltrated mainly by lymphocytes and histiocytes, with few neutrophils.
H The hosts immune response to the infected cells
produces various symptoms.
H Natural killer cells are first to respond, then cytotoxic T cells respond with interferon.
H Meningeal symptoms appear in 15 to 21 days.
Causes
H LCMV
H Arenavirus
Risk factors
H Handling infected animals or their excreta
Incidence
H Prevalence of LCM in humans: 2% to 10%, but im-
portant to note that LCM historically underreported

H Individuals of all ages susceptible, but more common
in young adults
H Cases reported in Europe, North America, South
America, Australia, and Japan, but most cases occurring in the northeast and eastern seaboard areas of
the United States
H More common during fall and winter
H Infection occurring equally in males and females
H Early: fever, malaise, anorexia, weakness, muscle
aches, retro-orbital headache, nausea, and vomiting

(other symptoms appearing less commonly include
500
Lymphocytic choriomeningitis
sore throat, nonproductive cough, joint pain, chest

pain, testicular pain, and parotid [salivary gland]
pain)
H Late: include alopecia and signs and symptoms of
meningitis (fever, increased headache, and stiff
neck) or encephalitis (drowsiness, confusion, sensory disturbances, and motor abnormalities such as
paralysis)
Complications
H Temporary or permanent neurologic damage possi-
ble (meningitis, paralysis, coma)

H Possible maternal transmission (Pregnancy-related
infection associated with abortion, congenital hydrocephalus, chorioretinitis, and mental retardation)
H Myelitis presenting with muscle weakness, paralysis,
or changes in body sensation
H Guillain-Barrtype syndrome
H Orchitis (usually unilateral) or parotitis
H Cardiac involvement such as myocarditis
H Psychosis
H Joint pain and arthritis during convalescence, especially in the metacarpophalangeal and proximal interphalangeal joints
H Prolonged convalescence, with continuing dizziness,
somnolence, and fatigue
Assessment
History
H Exposure to rodents, hamsters, or their excreta 1 to
3 weeks before symptom onset
Physical findings
H Lymphadenopathy
H Maculopapular rash
H Fever
H Cough
H Possible bradycardia
Test results
Laboratory
PHASE I
H White blood cell (WBC) count is decreased (leuko-
penia).
H Platelet count is decreased (thrombocytopenia).
H Liver enzymes are mildly elevated.
PHASE II
H Protein levels are increased.
H WBC count is increased.
H Glucose levels in cerebrospinal fluid (CSF) are
decreased.
H Enzyme-linked immunosorbent assay detects immunoglobulin M antibodies from serum or CSF (the
preferred diagnostic test).
H Lumbar puncture: In patients with meningeal signs,
CSF is typically abnormal, consisting of an increased
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Prevention
opening pressure, increased protein levels, and a

lymphocytic pleocytosis, usually in the range of
several hundred WBCs.
Treatment
General
H Hospitalization and supportive treatment based on
severity
Medications
Preventing lymphocytic
choriomeningitis
Lymphocytic choriomeningitis can be prevented by following these guidelines:
H Use meticulous hand-washing techniques using soap
and water after handling pet rodents.
H Clean cages in a well-ventilated area.
H Use a liquid disinfectant, such as diluted household
bleach, to clean up rodent droppings.
H Avoid putting rodents near your face.
H Closely supervise children and make sure they follow
good hand-washing practices after touching rodents.
H No specific treatment
H Anti-inflammatory drugs possibly useful
H Ribavirin (effective against LCMV in vitro)
H Analgesics (for symptom relief)
Surgery
H Acute hydrocephalus possibly requiring surgical
shunting to relieve increased intracranial pressure
H Refer paralyzed or comatose patients to physical
therapy or occupational therapy, as needed.

H Refer psychotic patients for follow-up with a psychia-
trist.
Key outcomes
The patient will:
H report acute symptom relief
H use precautions in handling rodents in the future
H have a plan to manage potential complications during convalescence
H understand the importance of follow-up appointments.
H Encourage rest and fluids after lumbar puncture.
H Administer total care if the patient is paralyzed or in
a coma.
H Encourage diet and activity, as tolerated.
Monitoring
H Vital signs
H Acute hydrocephalus
H Cardiac signs and symptoms
H Skin integrity
H If lumbar puncture, complications
Patient teaching
Be sure to cover:
H prevention techniques (see Preventing lymphocytic
choriomeningitis)
H use of a personal respirator.
Discharge planning
H Refer pregnant patients to an obstetrician for moni-
toring.
Lymphocytic choriomeningitis
501
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Lymphoma,
non-Hodgkins
H Meningitis
H Anemia
H Liver, kidney, and lung problems (with tumor
growth)
H Central nervous system involvement possibly leading
Overview
Description
H Heterogeneous group of malignant diseases that orig-
inate in lymph glands and other lymphoid tissue

H Usually classified according to histologic, anatomic,
and immunomorphic characteristics developed by

the National Cancer Institute (Rappaport histologic
and Lukes and Collins classifications also used in
some facilities)
H New categories of non-Hodgkins lymphoma, called
mantle zone lymphoma and marginal zone lymphoma
H Also called malignant lymphoma and lymphosarcoma
Pathophysiology
H Non-Hodgkins lymphoma seems to be similar to
Hodgkins disease, but Reed-Sternberg cells arent

present, and the lymph node destruction is different.
H Lymphoid tissue is defined by the pattern of infiltration as diffuse or nodular. Nodular lymphomas yield
a better prognosis than the diffuse form, but in both
the prognosis is less hopeful than in Hodgkins disease.
Causes
Risk factors
H History of autoimmune disease
Incidence
H Three times more common than Hodgkins disease
H Incidence increasing, especially in patients with au-
toimmune disorders and those receiving immunosuppressant treatment or those with acquired immunodeficiency syndrome
Special populations
Males older than age 60 have the highest incidence
of non-Hodgkins lymphoma.
to increased intracranial pressure
Assessment
History
H Symptoms mimicking those of Hodgkins disease
H Painless, swollen lymph glands (swelling that may
have appeared and disappeared over several

months)
H Complaints of fatigue, malaise, weight loss, fever, and
night sweats
H Trouble breathing, cough (usually children)
Physical findings
H Enlarged tonsils and adenoids
H Rubbery nodes in the cervical and supraclavicular
areas
Test results
Laboratory
H Uric acid levels are normal or elevated.
H Calcium level is elevated due to bone lesions.
Imaging
H Miscellaneous scans (chest X-rays; lymphangiography; liver, bone, and spleen scans; a computed tomography scan of the abdomen; and excretory urography) show disease progression.
H Biopsies of lymph nodes; of tonsils, bone marrow,
liver, bowel, or skin; or, as needed, of tissue removed
during exploratory laparotomy help to differentiate
non-Hodgkins lymphoma from Hodgkins disease.
H The same staging system used for Hodgkins disease
is used for non-Hodgkins lymphomas.
Treatment
General
H Radiation therapy mainly during the localized stage
of the disease
H Total nodal irradiation usually effective in nodular
and diffuse lymphomas

H Enlarged, painless lymph nodes
H Fever, malaise
H Weight loss
H Well-balanced, high-calorie, high-protein diet

H Limited activity
Complications
Medications
H Hypercalcemia
H Hyperuricemia
H Lymphomatosis
H Chemotherapy in combinations
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Surgery
H Total or subtotal gastrectomy to treat perforation
(common in patients with gastric lymphomas) before

chemotherapy
Key outcomes
The patient will:
pain.
H Provide time for rest periods.
Monitoring
H Vital signs
H Pain control
Patient teaching
Be sure to cover:
H preoperative and postoperative procedures
H dietary plan
H mouth care using a soft-bristled toothbrush and
avoidance of commercial mouthwashes
H relaxation and comfort measures
adverse effects
H symptoms that require immediate attention.
Discharge planning
services.
Lymphoma, non-Hodgkins
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Major depression
Overview
Description
H Patient appearing unhappy and apathetic
Complications
H Profound alteration of social, family, and occupation-
al functioning
H Suicide
Assessment
H Persistent sad, dysphoric mood; may be life-
History
threatening
H Unipolar depressive disorder with onset in early
adulthood and recurrences throughout life (at least
two more episodes in 50% to 60% of patients)
H Recurrences possible after protracted symptom-free
period or occurring sporadically, increasing in frequency, or occurring in clusters
H Profound loss of pleasure in all enjoyable activities
Pathophysiology
for a full month to 1 or more years

H Life problems or losses
H Physical disorder
H Use of prescription, nonprescription, or illicit drugs
H Change in eating and sleeping patterns
H Lack of interest in sex
H Changes occur in the receptor-neurotransmitter rela-
Physical findings
tionships in the limbic system.

H Changes in the hypothalamic-pituitary-adrenal regulation system may be an adaptive deregulation of the
stress response.
H Theres a possible defect on chromosome II or X.
H Difficulty concentrating or thinking clearly

H Easily distracted
H Indecisiveness
H Delusions of persecution or guilt
H Agitation
Causes
H Genetic, familial, biochemical, physical, psychologi-
cal, and social causes

H Many physical causes result in secondary depression
H Seasonal depression
Risk factors
H Female sex
H Family history of major depression or bipolar disor-
der
H Chronic illness
H Chronic pain
H Substance abuse
H Adverse reaction to medication such as beta-
adrenergic blockers
Incidence
H Affects about 17.6 million Americans each year
H Affects 5% to 20% of general population at some
time in their lives

H 6% to 8% of patients in care settings meet diagnostic
criteria
H Incidence increases with age
H Twice as common in females as in males, regardless
of age
H Depressed mood daily for 2 weeks or longer
H History of personal loss or severe stress
H Patient expressing doubts about self-worth or ability
to cope
504
Major depression
DSM-IV-TR criteria
A diagnosis is confirmed when five or more of the following symptoms present during the same 2-week period and represent a change from previous functioning:
H Depressed mood (irritable mood in children and
adolescents) most of the day, nearly every day, as indicated by either subjective account or observation
by others
H Markedly diminished interest or pleasure in all, or
almost all, activities most of the day, nearly every day
H Significant weight loss or weight gain (greater than
5% of the patients body weight in a month) when not
dieting, or a change in appetite nearly every day
H Insomnia or hypersomnia nearly every day
H Psychomotor agitation or retardation nearly every
day
H Fatigue or loss of energy nearly every day
H Feelings of worthlessness and excessive or inappropriate guilt nearly every day
H Diminished ability to think or concentrate, or indecisiveness, nearly every day
H Recurrent thoughts of death, recurrent suicidal
ideation without a specific plan, or suicide attempt or
a specific plan for committing suicide (see Suicide
prevention guidelines)
H Symptoms not due to a mixed episode, a medical
condition, the effects of a medication or other substance, or bereavement
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Test results
Laboratory
H Toxicology screening suggests a drug-induced
depression.
H Dexamethasone suppression test may show a failure
to suppress cortisol secretion.
Other
H Beck Depression Inventory shows the onset, severity,
duration, and progression of depressive symptoms.
Suicide prevention guidelines

To help deter potential suicide in the patient with major
depression, keep in mind these guidelines.
Assess for clues to suicide

Watch for such clues as communicating suicidal
thoughts, threats, and messages; hoarding medication;
talking about death and feelings of futility; giving away
prized possessions; describing a suicide plan; and changing behavior, especially as depression begins to lift.
Provide a safe environment
Treatment
Check patient areas and correct dangerous conditions,

such as exposed pipes, windows without safety glass, and
access to the roof or open balconies.
General
Remove dangerous objects
H Electroconvulsive therapy
H Short-term psychotherapy (a combination of individ-
ual, family, or group psychotherapy)

H Scheduled activities of daily living
Medications
H Selective serotonin-reuptake inhibitors, such as flu-
oxetine, paroxetine, and sertraline

H Maprotiline
desipramine
H Monoamine oxidase inhibitors such as phenelzine
Remove such objects as belts, razors, suspenders, light

cords, glass, knives, nail files, and clippers from the patients environment.
Consult with staff

Recognize and document verbal and nonverbal suicidal
behaviors, keep the physician informed, share data with
all staff, clarify the patients specific restrictions, assess
risk and plan for observation, and clarify day and night
staff responsibilities and frequency of consultation.
Observe the suicidal patient

Be alert when the patient is using a sharp object (shaving), taking medication, or using the bathroom (to prevent
hanging or other injury). Assign the patient to a room near
the nurses station and with another patient. Continuously
observe the acutely suicidal patient.
Maintain personal contact
Key outcomes
The patient will:
H voice feelings related to self-esteem
H make a verbal contract not to harm self
H engage in social interactions with others
H verbally and behaviorally demonstrate a positive selfevaluation.
H Encourage participation in individual and group
therapy.
H Encourage verbalization and expression of feelings.
H Listen attentively and respectfully.
H Provide a structured routine.
H Encourage interaction with others.
H Document observations and significant conversa-
Help the suicidal patient feel that he isnt alone or without

resources or hope. Encourage continuity of care and consistency of primary nurses. Building emotional ties to others is the ultimate technique for preventing suicide.
Patient teaching
Be sure to cover:
H depression and its effects on daily living
H need for adherence to medication regimen
H medication administration, dosage, and possible adverse effects and interactions with other substances.
Discharge planning
H Refer the patient to available support services and
community assistance.
tions.
H Assume an active role in initiating communication.
H Plan activities for when the patients energy levels are
highest.
H Provide distraction from self-absorption.
Monitoring
H Suicidal ideations
H Self-care
H Functioning level
Major depression
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Malabsorption
Overview
Description
H Defect in the GI tract in which the intestinal mucosa
fails to absorb single or multiple nutrients efficiently

H Absorption of amino acids, fat, sugar, or vitamins
possibly impaired
H Resulting inadequate movement of nutrients from the
small intestine to the bloodstream or lymphatic system

H Manifestations primarily dependent on what isnt
being absorbed
Pathophysiology
H The mechanism of malabsorption depends on the
cause.
H In celiac sprue, dietary gluten a product of wheat,
barley, rye, and oats is toxic to the patient, causing injury to the mucosal villi. The mucosa appears
Causes of malabsorption
Many disorders from systemic to organ-specific diseases may lead to malabsorption.
Diseases of the small intestine

Primary small-bowel disease
H Bacterial overgrowth from stasis in afferent loop after
Billroth II gastrectomy
H Massive bowel resection
H Nontropical sprue (celiac disease)
H Regional enteritis
H Tropical sprue
Ischemic small-bowel disease
H Chronic heart failure
H Mesenteric atherosclerosis
Systemic disease involving small bowel
H Acute enteritis
H Giardiasis
Drug-induced malabsorption
H Calcium carbonate
H Neomycin
Hepatobiliary disease
H Biliary fistula
H Biliary tract obstruction
H Cirrhosis and hepatitis
Hereditary disorder
H Primary lactase deficiency
Pancreatic disorders
H Chronic pancreatitis
H Cystic fibrosis
H Pancreatic cancer
H Pancreatic resection
H Zollinger-Ellison syndrome
Previous gastric surgery

H Billroth II gastrectomy
H Pyloroplasty
H Total gastrectomy
H Vagotomy
506
Malabsorption
flat and has lost absorptive surface. Symptoms generally disappear when gluten is removed from the diet.
H Lactase deficiency is a disaccharide deficiency syndrome. Lactase is an intestinal enzyme that splits
nonabsorbable lactose (a disaccharide) into the absorbable monosaccharides glucose and galactose.
Production may be deficient, or another intestinal
disease may inhibit the enzyme.
H After gastrectomy, poor mixing of chyme with gastric
secretions is the cause of postsurgical malabsorption.
H In Zollinger-Ellison syndrome, increased acidity in
the duodenum inhibits release of cholecystokinin,
which stimulates pancreatic enzyme secretion. Pancreatic enzyme deficiency leads to decreased breakdown of nutrients and malabsorption.
H Bacterial overgrowth in the duodenal stump (loop
created in the Billroth II procedure) causes malabsorption of vitamin B12.
Causes
H Prior gastric surgery
H Pancreatic disorders
H Hepatobiliary disease
H Disease of the small intestine
H Hereditary disorders
H Drug toxicity (see Causes of malabsorption)
Incidence
H Depends on cause of malabsorption
H Weight loss and generalized malnutrition
H Diarrhea
H Steatorrhea
H Flatulence and abdominal distention
H Nocturia
H Edema
H Amenorrhea
H Anemia
H Glossitis, cheilosis
H Bruising, bleeding tendency
H Bone pain, skeletal deformities, fractures
H Tetany, paresthesia
Complications
H Fractures
H Anemias
H Bleeding disorders
H Tetany
H Malnutrition
Assessment
History
H Fatigue
H Diarrhea
H Steatorrhea
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Physical findings
H Signs of weight loss or muscle wasting
H Pallor
H Ecchymosis
H Peripheral edema
Test results
Laboratory
H Stool specimen for fat reveals excretion of greater
than 6 g of fat per day.
H D-xylose absorption test shows less than 20% of 25 g
of D-xylose in the urine after 5 hours (reflects disorders of proximal bowel).
H Schilling test reveals deficiency of vitamin B12 absorption.
H Culture of duodenal and jejunal contents confirms
bacterial overgrowth in the proximal bowel.
Imaging
H GI barium studies show characteristic features of the
small intestine.
H Small intestine biopsy reveals the atrophy of mucosal
villi.
H Intake and output

H Laboratory values
Patient teaching
Be sure to cover:
H following a gluten-free diet.
Discharge planning
H Encourage follow-up visits, as ordered.
Treatment
General
H Identification of cause and appropriate correction
H Gluten-free diet to stop progression of celiac disease
and malabsorption
H Lactose-free diet to treat lactase deficiency
Medications
H Dietary supplementation
H Vitamin B12 injections
Key outcomes
The patient will:
H have improved absorption of nutrients
H express understanding of cause of disorder.
H Watch for signs of dehydration, such as dry skin and
mucous membranes and poor skin turgor.

H Protect patients with osteomalacia from injury by
keeping the side rails up and assisting with ambulation, as necessary.
Monitoring
H Calorie intake
H Weight
Malabsorption
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Malaria
Overview
Description
H An acute infectious disease: caused by protozoa of
the genus Plasmodium: P. falciparum, P. vivax, P.

malariae, and P. ovale
H Mosquito vectors transmitting the disease to humans
H Falciparum malaria: the most severe form of the disease
H Untreated primary attacks: last from 1 week to 1
month or longer
H Relapses common and possibly recurring sporadically for several years
H Hepatic parasites (P. vivax, P. ovale, and P. malariae) possibly persisting for years in the liver; responsible for the chronic carrier state
Pathophysiology
H Plasmodium sporozoites are injected by the bite of a
mosquito vector.
H The infective sporozoites migrate by blood circulation to parenchymal cells of the liver; there they form
Special considerations for

antimalarial drugs
Chloroquine
H Perform baseline and periodic ophthalmologic examinations, and report blurred vision, increased sensitivity
to light, and muscle weakness to the physician.
H Consult with the physician about altering therapy if
muscle weakness appears in a patient on long-term
therapy.
H Monitor the patient for tinnitus and other signs of ototoxicity, such as nerve deafness and vertigo.
H Caution the patient to avoid excessive exposure to the
sun to prevent exacerbating drug-induced dermatoses.
Primaquine
H Give with meals or antacids.

H Discontinue administration if you observe a sudden fall
in hemoglobin concentration or in erythrocyte or leukocyte count or marked darkening of the urine, suggesting impending hemolytic reaction.
Pyrimethamine
H Give with meals to minimize GI distress.

H Check blood counts (including platelets) twice a week.
If signs of folic or folinic acid deficiency develop, reduce or discontinue dosage while patient receives parenteral folinic acid until blood counts become normal.
Quinine
H Use with caution in patients with cardiovascular conditions, asthma, hemolytic anemia, and granulocytosis,
in a severe reaction.
H Monitor blood pressure frequently while administering
quinine I.V. infusion. Rapid administration causes
marked hypotension.
508
Malaria
cystlike structures containing thousands of merozoites.

H Upon release, each merozoite invades an erythrocyte
and feeds on hemoglobin.
H Eventually, the erythrocyte ruptures, releasing heme
(malaria pigment), cell debris, and more merozoites, which, unless destroyed by phagocytes, enter
other erythrocytes.
Causes
H Bite of female Anopheles mosquitoes
Risk factors
H Resident of, or travel to, an endemic area
H Pregnancy
H Lack of immunity
H Poverty
H Lack of access to health care
Incidence
H 300 to 500 million cases annually (internationally)
H Since 1940, few cases of malaria contracted in the
United States; most of these transmitted by blood

transfusions or the use of contaminated needles by
drug addicts
H Chills
H Fever
H Headache
H Myalgia
H Interspersed periods of well-being (the hallmark of
the benign form of malaria)

Acute attack
H Occurs when erythrocytes rupture
H Three stages:
cold stage, lasting 1 to 2 hours, ranging from
chills to extreme shaking
hot stage, lasting 3 to 4 hours, characterized by
high fever up to 107 F (41.7 C)
wet stage, lasting 2 to 4 hours, characterized by
profuse sweating
Falciparum malaria
H Persistent high fever
H Red blood cell (RBC) sludging that leads to capillary
obstruction at various sites
Complications
H Renal failure
H Liver failure
H Heart failure
H Pulmonary edema
H Severe normocytic anemia
H Seizures
H Hypoglycemia
H Splenic rupture
H Cerebral dysfunction
H Death
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Assessment
History
Key outcomes
H Travel to endemic area

H Recent blood transfusion
H I.V. drug abuse
H Chills, fever
H Headache, backache
The patient will:

H have adequate fluid volume
H express feelings and fears about current situation.
Physical findings
H Obtain a detailed patient history.

H Follow proper hand-washing and aseptic techniques.
H Record symptom pattern, fever, type of malaria, and
H Pale skin
H Urticaria
H Jaundice
H Petechial rash
H Hepatosplenomegaly (P. vivax and P. ovale)
Test results
Laboratory
H Peripheral blood smears identify parasites in RBCs.
H Hemoglobin levels are decreased.
H Leukocyte count may be decreased (as low as
3,000/l).
H Protein and leukocytes are present in urine sediment.
FALCIPARUM MALARIA
H Platelet numbers are reduced (20,000 to 50,000/l).
H Prothrombin time is prolonged (18 to 20 seconds).
H Partial thromboplastin time is prolonged (60 to
100 seconds).
systemic signs.
H Report all cases of malaria to local public health
authorities.
Monitoring
H Vital signs
H Intake and output
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and potential for relapse
H Plasma fibrinogen is decreased.
Treatment
General
H Symptomatic
H Activity, as tolerated (bed rest during acute phase)
Medications
H Oral chloroquine (for all forms except chloroquine-
resistant P. falciparum)
H Oral quinine (for malaria caused by P. falciparum)
given concurrently with pyrimethamine and a sulfonamide, such as sulfadiazine

H Primaquine phosphate (for hepatic phase) (see
Special considerations for antimalarial drugs)
H Other antimalarials, such as doxycycline and
hydroxycholorquine sulfate
H Antipyretics
Malaria
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Mastitis
Overview
Description
H Inflammation of the breast tissue
H Lactating breast infection
H Good prognosis
Pathophysiology
H A pathogen (typically originating in nursing infants
nose or pharynx) invades the breast tissue, entering

through a fissured or abraded nipple.
H The result is parenchymatous inflammation of the
mammary glands, which disrupts normal lactation.
H Systemic manifestations of inflammation may result.
Causes
H Occurs occasionally in nonlactating females

H Rare in males
H Red, swollen, warm, and tender breasts
H Nipple cracks or fissures
H Enlarged axillary lymph nodes
Complications
H Abscess
Assessment
History
H Fever
H Malaise
H Flulike symptoms
H Tenderness
H Most common pathogen Staphylococcus aureus;
Physical findings
less frequently, S. epidermidis or beta-hemolytic

streptococci
H Disseminated tuberculosis (rare)
H Mumps virus (rare)
H Nipple abrasion or fissure

H Enlarged axillary lymph nodes
H Involved breast red, edematous, warm, and hard
Risk factors
H Fissure or abrasion of the nipple
H Blocked milk ducts
H Incomplete letdown reflex
H Tight bra
H Prolonged intervals between breast-feedings
Incidence
Test results
Laboratory
H Cultures of expressed milk confirm generalized
mastitis.
H Cultures of breast skin confirm localized mastitis.
Treatment
H Usually occurring in first 3 months postbirth but
General
possibly occurring at any time during breast-feeding

H More common in breast-feeding primiparas
H Warm soaks
H Avoidance of tight bras and clothing
H Continuation of breast-feeding in both breasts to pre-
vent engorgement, with proper infant sucking and

changing of feeding positions to drain the milk
Preventing mastitis
To help your patient prevent mastitis from recurring, follow these guidelines:
H Stress to the patient the importance of emptying the
breasts completely because milk stasis can cause infection and mastitis.
H Teach the patient to alternate feeding positions and to
rotate pressure areas on the nipples.
H Remind the patient to position the infant properly on
the breast with the entire areola in his mouth.
H Advise the patient to expose sore nipples to the air as
often as possible.
H Teach the patient proper hand-washing technique and
personal hygiene.
H Instruct the patient to get plenty of rest and consume
sufficient fluids and a balanced diet to enhance
breast-feeding.
H Suggest that the patient apply a warm, wet towel to the
affected breast or take a warm shower to relax and improve breast-feeding.
510
Mastitis
Medications
H Antibiotics according to infecting organism
H Analgesics
Surgery
H Breast abscess incision and drainage
Key outcomes
The patient will:
H exhibit no signs or symptoms of infection
H resume breast-feeding without further complications
H Provide warm soaks.
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Monitoring
H Abscess development
H Breast engorgement
H Skin integrity
H Breast-feeding
Patient teaching
Be sure to cover:
H reassurance that breast-feeding wont harm the infant
because hes the source of the infection
H offering the infant the unaffected breast first to promote complete emptying and prevent clogged ducts
H need to stop breast-feeding with abscessed breast
H use of a breast pump until abscess heals
H continuation of breast-feeding on the unaffected side
H prevention of mastitis. (See Preventing mastitis.)
Discharge planning
H Refer the patient to a lactation specialist, if indicated.
Mastitis
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Melanoma, malignant
Overview
Description
H Neoplasm that arises from melanocytes
H Potentially the most lethal of the skin cancers
H Common sites: head and neck in males, legs and
chest in females, and backs of people exposed to

excessive sunlight
H Four types:
Superficial spreading melanoma most common
type; usually develops between ages 40 and 50
Nodular melanoma grows vertically, invades the
dermis, and metastasizes early; usually develops
between ages 40 and 50
Acral-lentiginous melanoma occurs on the
palms and soles and under the tongue; most common among Hispanics, Asians, and Blacks
Lentigo maligna melanoma relatively rare; most
benign, slowest growing, and least aggressive of
the four types; most commonly occurs in areas
heavily exposed to the sun; arises from a lentigo
maligna on an exposed skin surface; usually occurs between ages 60 and 70
Pathophysiology
H Melanomas arise as a result of malignant degenera-
tion of melanocytes located either along the basal

layer of the epidermis or in a benign melanocytic
nevus.
H Up to 70% of malignant melanomas arise from a preexisting nevus.
H Malignant melanoma spreads through the lymphatic
and vascular systems and metastasizes to the regional
lymph nodes, skin, liver, lungs, and central nervous
system.
H Malignant melanoma follows an unpredictable
course; recurrence and metastasis may not appear
for more than 5 years after resection of the primary
lesion.
Causes
H Ultraviolet rays from the sun that damage the skin
Risk factors
H Excessive exposure to sunlight
H Skin type (blond or red hair, fair skin, and blue
eyes; prone to sunburn; and Celtic or Scandinavian

ancestry)
H Hormonal factors (pregnancy)
H Family history
H Past history of melanoma
H Preexisting pigmented mole or nevus
Incidence
H Lifetime U.S. incidence: 1 in 60 people
H Most common cancer in females ages 25 to 29
H Unusual in children
512
Melanoma, malignant
H Peak incidence between ages 50 and 70, but inci-
dence in younger age-groups increasing
H Nonhealing sore
H Preexisting lesion or nevus that enlarges
H Signs of melanoma:
Asymmetrical lesion
Border irregularity
Color varied
Diameter larger than 6 mm
Complications
H Metastasis to the lungs, liver, or brain
Assessment
History
H A sore that doesnt heal, a persistent lump or
swelling, and changes in preexisting skin markings,

such as moles, birthmarks, scars, freckles, or warts
H Preexisting skin lesion or nevus that enlarges,
changes color, becomes inflamed or sore, itches, ulcerates, bleeds, changes texture, or shows signs of
surrounding pigment regression
Physical findings
H Lesions on the ankles or the inside surfaces of the
knees
H Uniformly discolored nodule on knee or ankle
H Small, elevated tumor nodules that may ulcerate and
bleed
H Palpable polypoid nodules that resemble the surface
of a blackberry
H Pigmented lesions on the palms and soles or under
the nails
H Long-standing lesion that has ulcerated
H Flat nodule with smaller nodules scattered over the
surface
Test results
Laboratory
H Complete blood count with differential shows
anemia.
H Platelet count is abnormal if metastasis has occurred.
H Liver function studies are abnormal if metastasis has
occurred.
Imaging
H Chest X-rays and computed tomography scan help in
staging.
H Excisional biopsy and full-depth punch biopsy with
histologic examination can show tumor thickness
and disease stage.
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Treatment
General
H Close long-term follow-up care to detect metastasis
and recurrences
H Radiation therapy (usually for metastatic disease)
H Avoidance of sun exposure
Medications
H Chemotherapy
H Biotherapy
H Immunotherapy such as interferon
Surgery
H Surgical resection to remove tumor and 3- to 5-cm
margin
H Regional lymphadenectomy
Key outcomes
The patient will:
H maintain weight
H experience healing of wound without signs of
infection
Prevention
Preventing malignant melanoma

Malignant melanoma can be prevented by following these
guidelines:
H Apply sunscreen and protective lip balm every day at
least 30 minutes before going outside, even on cloudy
days.
H Use sun protective factor (SPF) of 15 or greater.
H Reapply sunscreen every 2 to 3 hours and after
sweating or swimming.
H Wear protective clothing, such as long-sleeved shirts,
hats, and sunglasses with UV protection.
H Avoid lying in the sun.
H Avoid sun exposure between the hours of 10 a.m. and
4 p.m.
H Avoid sunbeds and tanning salons.
H Have health care provider check suspicious spots or
moles and have them removed if needed.
H Perform monthly self skin examinationespecially if
theres a family history of skin cancer.
Discharge planning
services.
H Provide a high-protein, high-calorie diet.
Monitoring
H Pain control
H Wound site
Patient teaching
Be sure to cover:
H need for close follow-up care to detect recurrences
early
H signs and symptoms of recurrence
H detrimental effects of overexposure to solar radiation
and benefits of regular use of a sunblock or a sunscreen and protective clothing. (See Preventing malignant melanoma.)
Melanoma, malignant
513
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Mnires disease
Overview
Description
H History of smoking
H Alcohol use
ALERT
In some females, premenstrual edema may precipitate outbreaks of Mnires disease.
H Inner ear disease that results from a labyrinthine
dysfunction
H Causes severe vertigo, sensorineural hearing loss,
and tinnitus
H Usually, only one ear involved
H After multiple attacks over several years, possibly
incapacitating residual tinnitus and hearing loss
H Also known as endolymphatic hydrops
Pathophysiology
H Mnires disease may result from overproduction or
decreased absorption of endolymphthe fluid contained in the labyrinth of the ear.

H Accumulated endolymph dilates the semicircular
canals, utricle, and saccule and causes degeneration
of the vestibular and cochlear hair cells.
H Overstimulation of the vestibular branch of cranial
nerve VIII impairs postural reflexes and stimulates
the vomiting reflex. (See Normal vestibular function.)
H Perception of sound is impaired as a result of this excessive cranial nerve stimulation, and injury to sensory receptors for hearing may affect auditory acuity.
Causes
H Unknown, but possibly associated with:
Family history
Immune disorder
Migraine headaches
Middle ear infection
Head trauma
Autonomic nervous system dysfunction
Premenstrual edema
Risk factors
H Recent viral infection
H Stress
H Fatigue
H Allergies
Normal vestibular function

The three semicircular canals and the vestibule of the inner
ear are responsible for equilibrium and balance. Each of
the semicircular canals lies at a 90-degree angle to the others. Head movement in one direction causes the endolymph inside each semicircular canal to move in the opposite direction and causes vestibular otoliths (crystals of
calcium salts) to shift in their gel medium. This movement
stimulates hair cells, sending electrical impulses to the
brain through the vestibular portion of cranial nerve VIII.
Together, these organs help detect the bodys present position as well as any change in its direction or motion.
514
Mnires disease
Incidence
H Usually affects adults between ages 30 and 60; rare in
children
H Sudden severe spinning, whirling vertigo, lasting
from 10 minutes to several hours

H Tinnitus
H Hearing impairment
H Feeling of fullness or blockage in the affected ear
preceding an attack
H Severe nausea, vomiting, sweating, and pallor during
an acute attack
H Nystagmus
H Loss of balance and falling to the affected side
Complications
H Continued tinnitus
H Hearing loss
H Injury
Assessment
History
H Vertigo
H Nausea
H Tinnitus
H Falls
Physical findings
H Inability to maintain upright posture
H Unsteady gait
H Diplopia
H Hypotension
Test results
Imaging
imaging rule out acoustic neuroma as a cause of
symptoms.
H Audiometric testing shows a sensorineural hearing
loss and loss of discrimination and recruitment.
H Electronystagmography shows normal or reduced
vestibular response on the affected side.
H Cold caloric testing shows impairment of oculovestibular reflex.
H Electrocochleography shows increased ratio of summating potential to action potential.
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H Brain stem evoked response audiometry test rules
out acoustic neuroma, brain tumor, and vascular

lesions in the brain stem.
H avoidance of sudden position changes and any tasks
that vertigo makes hazardous

H restriction of caffeine, nicotine, and alcohol.
Treatment
General
H Lying down to minimize head movement, and avoid-
ing sudden movements and glaring lights to reduce

dizziness (during an attack)
H Sodium restriction
Medications
H Promethazine or prochlorperazine
H Atropine
H Dimenhydrinate
H Central nervous system depressants, such as lo-
razepam and diazepam during an acute attack

H Antihistamines, such as meclizine and diphenhy-
dramine
For long-term management
H Diuretics
H Betahistine dihydrochloride
H Vasodilators
H Antihistamines or mild sedatives
H Systemic streptomycin (chemical ablation)
Surgery
H Endolymphatic drainage and shunt procedures
H Vestibular nerve resection
H Labyrinthectomy
H Cochlear implantation
Key outcomes
The patient will:
H remain safe from injury
H seek appropriate support to assist with coping.
H Maintain a safe environment; provide assistance
when necessary.
Monitoring
H Intake and output
H Frequency of attacks
Patient teaching
Be sure to cover:
H avoidance of reading and exposure to glaring lights
to reduce dizziness
Mnires disease
515
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Meningitis
Overview
Description
H Inflammation of brain and spinal cord meninges
H May affect all three meningeal membranes (dura
mater, arachnoid membrane, and pia mater)

H Usually follows onset of respiratory symptoms
H Sudden onset, causing serious illness within 24
hours
H Prognosis usually good; complications rare
H Bacterial meningitis: acute infection in the subarachnoid space
Incidence
H Infants, children, and elderly people at highest risk
H Nuchal rigidity
H Headache
H Fever
H Meningismus, typically with signs of cerebral
dysfunction
H Seizures
Complications
H Visual impairment; optic neuritis
H Cranial nerve palsies; deafness
H Paresis or paralysis
H Endocarditis
H Coma
H Vasculitis
H Cerebral infarction
H Seizures
Special populations
Prognosis is poor for infants and elderly people.
Pathophysiology
H Inflammation of pia-arachnoid and subarachnoid
space progresses to congestion of adjacent tissues.

H Nerve cells are destroyed.
H Intracranial pressure (ICP) increases due to exu-
dates.
H Results can include:
engorged blood vessels

disrupted blood supply
edema of the brain tissue
thrombosis
rupture
acute hydrocephalus.
Causes
H Bacterial infection, usually from Neisseria meningi-
tidis and Streptococcus pneumoniae (Before the

1990s, Haemophilus influenzae type b [Hib] was
the leading cause of bacterial meningitis. However,
new vaccines have reduced its occurrence in children.)
H Viruses
H Protozoa
H Fungi
H Secondary to another bacterial infection such as
pneumonia
H May follow skull fracture, penetrating head wound,
lumbar puncture, or ventricular shunting procedures
Risk factors
H I.V. drug abuse
H Age older than 60 or younger than 5
H Diabetes
H Alcoholism or cirrhosis
516
Meningitis
Assessment
History
H Headache
H Fever
H Nausea, vomiting
H Weakness
H Myalgia
H Photophobia
H Confusion, delirium
H Seizures
Physical findings
H Meningismus
H Rigors
H Profuse sweating
H Kernigs and Brudzinskis signs (elicited in only 50%
of adults)
H Declining level of consciousness (LOC)
H Rash (with meningococcemia)
H Focal neurologic deficits such as visual field defects
H Signs of increased ICP (in later stages)
Special populations
Meningismus and fever are commonly absent in
neonates and the only clinical clues may be nonspecific, such as refusal to feed, high-pitched cry,
and irritability.
Special populations
Elderly patients may experience an insidious onset,
exhibiting lethargy and variable signs of meningismus and no fever.
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Test results
Monitoring
Laboratory
H White blood cell count shows leukocytosis.
H Blood cultures are positive in bacterial meningitis,
depending on the pathogen.
Imaging
H Chest X-rays may reveal a coexisting pneumonia.
H Neuroimaging techniques, such as computed tomography scanning and magnetic resonance imaging,
may detect complications and a parameningeal
source of infection.
H Lumbar puncture and cerebrospinal fluid analysis
shows:
increased opening pressure
neutrophilic pleocytosis
elevated protein
hypoglycorrhachia
positive Gram stain
positive culture.
H Neurologic status
H Vital signs
H Signs and symptoms of cranial nerve involvement
H Signs and symptoms of increased ICP
H LOC
H Seizures
H Fluid balance
H Complications
Treatment
General
Patient teaching
Be sure to cover:
H contagion risks for close contacts
H signs and symptoms of meningitis
H polysaccharide meningococcal vaccine, pneumococcal vaccine, and Hib vaccine.
H Hypothermia
H Fluid therapy
H Pain control
H Bed rest (in acute phase)
Medications
H Antibiotics, such as vancomycin and meropenem
H Antiarrhythmics
H Osmotic diuretics
H Anticonvulsants
H Aspirin or acetaminophen
Key outcomes
The patient will:
H have normal temperature
H express feelings of increased comfort and pain relief
H have intact skin.
H Maintain respiratory isolation for first 24 hours (with
meningococcal meningitis).
H Position the patient in proper body alignment.
H Encourage active range-of-motion (ROM) exercises
when appropriate.
H Provide passive ROM exercises when appropriate.
H Maintain adequate nutrition.
H Administer prescribed laxatives or stool softeners.
H Provide meticulous skin and mouth care.
Meningitis
517
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Metabolic syndrome
Overview
Description
H A cluster of symptoms triggered by insulin resistance:
abdominal fat; obesity; high blood pressure; and high

levels of blood glucose, triglycerides, and cholesterol
H Increased risk of diabetes, heart disease, and stroke
H Commonly unrecognized
H Also known as syndrome X, insulin resistance syndrome, dysmetabolic syndrome, and multiple
metabolic syndrome
Pathophysiology
H The body breaks down food into basic components,
one of which is glucose.

H Glucose provides energy for cellular activity.
H Excess glucose is stored in cells for future use. Its
guided into storage cells by insulin, which is secreted

by the pancreas.
H In those with metabolic syndrome, glucose doesnt
respond to insulins attempt to guide it into storage
cells. This is called insulin resistance.
H To overcome this resistance, the pancreas produces
excess insulin, which causes damage to arterial
lining.
H Excessive insulin secretion also promotes fat storage
deposits and prevents fat breakdown.
H This series of events can lead to diabetes, blood
clots, and coronary events.
Causes
H Acquired
Risk factors
H Obesity
H Improper diet
H Insufficient physical activity
H Aging
H Hyperinsulinemia/impaired glucose tolerance
H Previous myocardial infarction
Incidence
H Affects an estimated 47 million Americans
H Most common in Mexican Americans (highest rate at
32%)
H In Black and Mexican American populations, females
more susceptible than males; otherwise, males and

females equally affected
H Waist size: more than 40
(101.6 cm) in men; more

than 35 (88.9 cm) in women (see Why abdominal
obesity is dangerous)
H Lethargy, especially after eating
518
Metabolic syndrome
Complications
H Coronary artery disease
H Diabetes
H Hyperlipidemia
H Premature death
Assessment
History
H Familial history
H Hypertension
H High low-density lipoproteins (LDL) and triglyceride
levels
H Low high-density lipoproteins (HDL) levels
H Abdominal obesity
H Poor diet
Physical findings
H Abdominal obesity
Test results
Laboratory
H Blood glucose levels are high.
H LDL and triglyceride levels are high.
H HDL levels are low.
H Hyperinsulinemia is present.
H Serum uric acid level is elevated.
Other
H Blood pressure is greater than 130/85 mm/Hg.
Treatment
General
H Weight-reduction program
H Low alcohol intake
H Low-cholesterol diet
H Diet high in complex carbohydrates (grains, beans,
vegetables, fruit) and low in refined carbohydrates

(soda, table sugar, high fructose corn syrup)
H Daily physical activity of at least 20 minutes
Medications
H Oral antidiabetic agents
H Antihypertensives
H Statins
Key outcomes
The patient will:
H maintain a healthy weight
H increase his level of activity
H consume a proper diet.
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Why abdominal obesity is dangerous

People with excess weight around the waist have a greater
risk of developing metabolic syndrome than people with
excess weight around the hips. Thats because intraabdominal fat tends to be more resistant to insulin than
fat in other areas of the body. Insulin resistance increases
the release of free fatty acid into the portal system, leading to increased apolipoprotein B, increased low-density
lipoprotein, decreased high-density lipoprotein, and increased triglyceride levels. As a result, the risk of cardiovascular disease increases.
H Promote lifestyle changes and provide appropriate
support.
Monitoring
H Blood pressure
H Ordered laboratory tests
Patient teaching
Be sure to cover:
H principles of healthy diet
H relationship of diet, inactivity, and obesity to metabolic syndrome
H benefits of increased physical activity
Discharge planning
H Refer the patient to a dietitian and an exercise
program, as appropriate.
H Stress the importance of follow-up.
Metabolic syndrome
519
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Methicillin-resistant
Overview
Description
H A mutation of a very common bacterium easily
spread by direct person-to-person contact

H Also known as MRSA
Pathophysiology
H 90% of Staphylococcus aureus isolates or strains
are penicillin-resistant, and about 27% of all S. aureus isolates are resistant to methicillin, a penicillin
derivative. These strains may also resist cephalosporins, aminoglycosides, erythromycin, tetracycline,
and clindamycin.
H When natural defense systems break down (after invasive procedures, trauma, or chemotherapy), the
usually benign bacteria can invade tissue, proliferate,
and cause infection.
H The most frequent colonization site is the anterior
nares (40% of adults and most children become
transient nasal carriers). The groin, armpits, and intestines are less common colonization sites.
Assessment
History
H Possible risk factors for MRSA
H Carrier patient typically asymptomatic
Physical findings
H In symptomatic patients, signs and symptoms related
to the primary diagnosis (respiratory, cardiac, or

other major system symptoms)
Test results
Laboratory
H Cultures from suspicious wounds, skin, urine, or
blood show MRSA.
Treatment
General
H Transmission precautions: contact isolation for
wound, skin, and urine infection; respiratory isolation for sputum infection
H No treatment needed for patient with colonization
only
H High-protein diet
Causes
Medications
H MRSA that enters a health care facility through an in-
H Vancomycin and imipenem
fected or colonized patient (symptom-free carrier of

the bacteria) or colonized health care worker
H Transmitted mainly by health care workers hands
(MRSA possibly remaining viable for days on surfaces and clothing)
Risk factors
H Immunosuppression
H Prolonged facility stays
H Extended therapy with multiple or broad-spectrum
antibiotics
Key outcomes
The patient will:
H attain hemodynamic stability
H remain afebrile
H have an adequate fluid volume.
H Proximity to others colonized or infected with MRSA

H Invasive devices such as indwelling catheters
Incidence
H Provide emotional support to the patient and family.

H Consider grouping infected patients together and
H Endemic in nursing homes, long-term care facilities,
and community facilities
H Dependent on body system affected
Complications
H Sepsis
H Death
520
Methicillin-resistant Staphylococcus aureus
having the same nursing staff care for them.

H Use proper hand-washing technique.
H Use contact and standard precautions.
Monitoring
H Vital signs
H Culture results
H Complications
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Patient teaching
Be sure to cover:
H difference between MRSA and colonization
H prevention of MRSA spread
H need for family and friends to wear protective garb
(and to dispose of it properly) when they visit the
patient
adverse effects
H need to take antibiotics for the full prescription period, even if the patient begins to feel better.
Discharge planning
indicated.
Methicillin-resistant Staphylococcus aureus
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Complications
Mitral stenosis
H Cardiac arrhythmias, especially atrial fibrillation

H Thromboembolism
Overview
Assessment
Description
H Narrowing of the mitral valve orifice, which is nor-
History
mally 3 to 6 cm
H Mild mitral stenosis: valve orifice of 2 cm
H Severe mitral stenosis: valve orifice of 1 cm
Mild mitral stenosis

H Asymptomatic
Moderate to severe mitral stenosis
H Gradual decline in exercise tolerance
H Dyspnea on exertion; shortness of breath
H Orthopnea
H Weakness
H Fatigue
H Palpitations
H Cough
Pathophysiology
H Valve leaflets become diffusely thickened by fibrosis
and calcification.
H The mitral commissures and the chordae tendinae
fuse and shorten, the valvular cusps become rigid,

and the valves apex becomes narrowed.
H This obstructs blood flow from the left atrium to the
left ventricle, resulting in incomplete emptying.
H Left atrial volume and pressure increase, and the
atrial chamber dilates.
H Increased resistance to blood flow causes pulmonary
hypertension, right ventricular hypertrophy and,
eventually, right-sided heart failure and reduced cardiac output.
Causes
H Rheumatic fever
H Congenital anomalies
H Atrial myxoma
H Endocarditis
H Rheumatoid arthritis
murmur of mitral stenosis)
rhythm
Test results
H Two-thirds of all mitral stenosis patients female

H Occurs in approximately 40% of patients with
rheumatic heart disease
H Gradual decline in exercise tolerance
H Chest pain, palpitations
Identifying the murmur of mitral stenosis

A low, rumbling crescendo-decrescendo murmur in the
mitral valve area characterizes mitral stenosis.
SYSTOLE
522
H Hemoptysis
H Peripheral and facial cyanosis
H Malar rash
H Ascites
H Peripheral edema
H Hepatomegaly
H A loud S1 or opening snap
H A diastolic murmur at the apex (see Identifying the
H Crackles over lung fields
H Right ventricular lift
H Resting tachycardia; irregularly irregular heart
Incidence
S1
Physical findings
DIASTOLE
S2
Mitral stenosis
SYSTOLE
S1
S2
Imaging
H Chest X-rays show left atrial and ventricular enlargement (in severe mitral stenosis), straightening of the
left border of the cardiac silhouette, enlarged pulmonary arteries, dilation of the upper lobe pulmonary
veins, and mitral valve calcification.
H Echocardiography discloses thickened mitral valve
leaflets and left atrial enlargement.
H Cardiac catheterization shows a diastolic pressure
gradient across the valve, elevated pulmonary artery
wedge pressure (greater than 15 mm Hg), and pulmonary artery pressure in the left atrium with severe
pulmonary hypertension.
H Electrocardiography reveals left atrial enlargement,
right ventricular hypertrophy, right axis deviation,
and (in 40% to 50% of cases) atrial fibrillation.
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Treatment
Patient teaching
General
Be sure to cover:
H need to plan for periodic rest in daily routine
H how to take the pulse
H signs and symptoms to report
H use of prophylactic antibiotics for procedures.
H Synchronized electrical cardioversion to correct atri-
al fibrillation
Medications
H Digoxin
H Diuretics
H Oxygen
H Calcium channel blockers such as diltiazem
H Infective endocarditis antibiotic prophylaxis
H Nitrates
Surgery
H Commissurotomy or valve replacement
H Percutaneous balloon valvuloplasty
Key outcomes
The patient will:
fatigue
H maintain hemodynamic stability and adequate cardiac output
H have no complications due to fluid excess
H exhibit adequate coping mechanisms.
H Check for hypersensitivity reaction to antibiotics.
H If the patient needs bed rest, stress its importance.
H Provide a bedside commode to encourage energy
conservation.
H Allow the patient to express concerns over her inabil-
ity to meet responsibilities due to activity restrictions.

H Place the patient in an upright position to relieve dys-
pnea, if needed.
H Provide a low-sodium diet.
Monitoring
H Intake and output
H Signs and symptoms of heart failure and pulmonary
edema
H Signs and symptoms of thromboembolism
H Postoperatively: hypotension, arrhythmias, and
thrombus formation
Mitral stenosis
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Mitral valve
insufficiency
H Papillary muscle disorders such as coronary artery
disease
Incidence
H Affects both sexes equally
Overview
Description
H Valvular disease of the mitral valve that allows the
backflow of blood from the left ventricle to the left

atrium
H May be acute (sudden volume overload of the left
ventricle), chronic compensated (left ventricle compensates and left ventricular enlargement occurs), or
chronic decompensated (left ventricle unable to sustain forward cardiac output)
H Also known as mitral regurgitation
Pathophysiology
H Blood from the left ventricle flows back into the left
atrium during systole, causing the atrium to enlarge

to accommodate the backflow.
H As a result, the left ventricle dilates to accommodate
the increased volume of blood from the atrium and
to compensate for diminishing cardiac output.
H Ventricular hypertrophy and increased end-diastolic
pressure result in increased pulmonary artery pressure, eventually leading to left- and right-sided heart
failure.
H Dyspnea
H Peripheral edema
H Tachycardia
Complications
H Heart failure
H Pulmonary edema
H Thromboembolism
H Endocarditis
H Arrhythmias
H Shock
Assessment
History
H Causal occurrence
H Orthopnea
H Dyspnea
H Fatigue
H Angina
H Palpitations
Causes
Physical findings
H Trauma
H Rheumatic fever
H Scleroderma
H Hypertrophic cardiomyopathy
H Severe left-sided heart failure
H Ruptured chordae tendineae
H Associated with congenital anomalies such as trans-
H Tachycardia
H Crackles in the lungs
H Hepatomegaly (right-sided failure)
H Holosystolic murmur at the apex (see Identifying
position of the great arteries
Identifying the murmur of mitral

valve insufficiency
A high-pitched, rumbling pansystolic murmur that radiates from the mitral area to the left axillary line characterizes mitral valve insufficiency.
SYSTOLE
S1
524
DIASTOLE
S2
SYSTOLE
S1
Mitral valve insufficiency
S2
the murmur of mitral valve insufficiency)

H Possible split S2
H S3
Test results
Imaging
H Chest X-ray reveals left atrial and ventricular enlargement and pulmonary congestion.
H Echocardiography shows abnormal valve leaflet motion and left atrial enlargement.
H Cardiac catheterization reveals mitral insufficiency
with increased left ventricular end-diastolic volume
and pressure, increased atrial pressure and pulmonary artery wedge pressure, and decreased cardiac
output.
H Electrocardiography may show left atrial and ventricular hypertrophy, sinus tachycardia, or atrial fibrillation.
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Treatment
General
H Treat underlying cause appropriately
H Low-sodium diet
Medications
H Diuretics, such as furosemide and spironolactone
H Inotropic agents, such as digoxin and milrinone
H Angiotensin-converting enzyme inhibitors
H Oxygen
H Prophylactic antibiotics before and after surgery or
dental care to prevent endocarditis

H Antiarrhythmics, such as amiodarone and digoxin, to
treat atrial fibrillation or atrial flutter

H Vasodilators such as nitroprusside
Surgery
H Annuloplasty or valvuloplasty to reconstruct or repair
the valve
H Valve replacement with a prosthetic valve
Key outcomes
The patient will:
fatigue
H Watch for signs of heart failure or pulmonary edema.
Monitoring
H Cardiac rhythm
H Pulmonary artery catheter readings
H Intake and output
H Adverse effects of drug therapy
Patient teaching
Be sure to cover:
H dietary restrictions and medication
Mitral valve insufficiency
525
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Mitral valve prolapse

Overview
Description
H Portion of the mitral valve (MV) prolapses into the
left atrium during ventricular contraction (systole)
Pathophysiology
Test results
Imaging
H Echocardiography may reveal mitral valve prolapse
(MVP) with or without mitral insufficiency.
H Electrocardiography is usually normal but may reveal
atrial or ventricular arrhythmia.
H Signal-averaged electrocardiography may show ventricular and supraventricular arrhythmias.
H Holter monitor worn for 24 hours may show an arrhythmia.
H Myxomatous degeneration of MV leaflets with redun-
dant tissue leads to prolapse of the MV into the left

atrium during systole.
H In some patients, this results in leakage of blood into
the left atrium from the left ventricle.
Causes
H Connective tissue disorders, such as systemic lupus
erythematosus and Marfan syndrome

H Congenital heart disease
H Acquired heart disease, such as coronary artery dis-
ease and rheumatic heart disease
Incidence
H More prevalent in females than males
H Usually detected in young adulthood
H Affects 2.5% to 5% of the general population
Special populations
Mitral valve prolapse is most common in females
ages 20 to 40.
H Palpitations
H Atypical chest pain
H Dyspnea
Complications
Treatment
General
H Usually requires no treatment; only regular monitor-
ing
H Decreased caffeine intake
H Fluid intake to maintain hydration
Medications
metoprolol
H Antiarrhythmics as appropriate
Key outcomes
The patient will:
H carry out activities of daily living without fatigue or
decreased energy
H maintain adequate cardiac output, without arrhythmias
H exhibit adequate coping mechanisms.
H Provide reassurance and comfort if the patient expe-
riences anxiety.
H Arrhythmias
H Mitral insufficiency from chordal rupture
H Mitral regurgitation
H If fatigue is a concern, plan rest periods.

H Discuss the patients drug therapy including dosage,
Assessment
Monitoring
History
H Usually asymptomatic
H Possible fatigue, syncope, palpitations, chest pain, or
dyspnea on exertion
Physical findings
H Mid-to-late systolic click and late systolic murmur
526
adverse reactions, and when to notify the physician if

a problem arises.
H Discuss the importance of adequate hydration.
H Vital signs
H Blood pressure while lying, sitting, and standing
H Heart sounds
H Signs and symptoms of mitral insufficiency
H Serial echocardiograms
H Electrocardiograms for arrhythmias
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Patient teaching
Be sure to cover:
H need to perform the most important activities of the
day when energy levels are highest
H need for antibiotic prophylaxis therapy before dental
or surgical procedures as indicated (not all patients
with MVP require antibiotic prophylaxis)
H avoidance of foods and beverages high in caffeine
H taking medications as prescribed
H using caution with over-the-counter medications that
contain stimulants.
Discharge planning
H If the patient is being discharged with a Holter moni-
tor, make sure she understands the importance of

documenting her activities throughout the monitoring process.
H Refer the patient to an MVP support group.
H Refer the patient to a planned exercise program.
527
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Motion sickness
Overview
Assessment
History
Visual receptors
Vestibular receptors
Body proprioceptors
H Also induced when patterns of motion differ from
those previously experienced
H Nervous system affected
H Recent travel
H Exposure to smoke, carbon monoxide, or fumes
H Recent illness, such as cold or ear infection
H Anxiety
H Panic attack
H Malaise
H Fatigue
H Weakness
H Confusion
H Vertigo
Pathophysiology
Physical findings
H Central cholinergic pathways, possibly in the vestibu-
lar nuclei, may play a role in motion sickness.

H Motion sickness may be mediated by vasopressin released from the pituitary.
H Associated with increases in blood levels of epinephrine and norepinephrine; levels are also increased in
certain brain regions.
H Nausea
H Vomiting
H Diaphoresis
H Pallor
H Hypersalivation
H Yawning
H Hyperventilation
Causes
Test results
H Body, inner ear, and the eyes sending conflicting sig-
Laboratory
H Blood tests rule out other disorders.
Imaging (with frequent episodes)
imaging rule out other disorders.
H Possible EEG, if prolonged episode, rules out other
disorders.
Description
H Sensory conflict about body motion
H Involvement of:
nals to the brain

H Anticipating movement possibly producing anxiety
and symptoms
Risk factors
H Motion (automobile, plane, boat, amusement rides)
H Travel
H Visual stimuli (such as a moving horizon)
H Poor ventilation (fumes, smoke, carbon monoxide)
H Emotions (fear, anxiety)
H Illness or poor health
Incidence
H Unknown
H Children ages 2 to 12 affected more commonly than
adults
H Occurs during or after motion or visual stimuli
H GI disturbances
H Nervous system disturbances
Complications
H Hypotension
H Dehydration
H Depression
H Panic
H Syncope
528
Motion sickness
Treatment
General
H Removing triggers
H Minimizing exposure
H Improving ventilation
H Acupressure on point 2 cm proximal from transverse
crease of palmar side of wrist, between tendons

(Pericardium 6 [P6])
H Diet
Decrease oral intake; frequent small meals
Avoidance of alcohol
H Semirecumbent seating
H Fix vision at 45-degree angle above horizon
H Avoidance of fixation of vision on moving objects
such as waves
H Avoidance of reading while in moving automobile or
boat
H Mind-body practices, such as cognitive-behavioral
therapy and biofeedback
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Medications
Prevention
H Scopolamine
H Promethazine
H Cyclizine
H Dimenhydrinate
H Meclizine
H Ginger
Preventing motion sickness
Key outcomes
The patient will:
H express reduced levels of anxiety
H verbalize understanding of the disorder and its treatment
H express improvement in symptoms
H maintain adequate hydration.
Motion sickness can be prevented by following these

guidelines:
H Avoid reading.
H Choose seating with good ventilation.
H Sit in a semirecumbent position.
H Sit in a place with the least possible movement, such
as the middle of the plane or boat or in the front of the
car.
H Fix vision at 45 degrees above the horizon on a
stationary object.
H Avoid alcohol.
H Dont smoke.
H Decrease dietary intake or eat small, frequent meals.
H Premedicate with over-the-counter or prescription
drugs as advised.
H Engage in distracting mental activities.
H Remove triggers or noxious stimuli.
H Help the patient identify risk factors and make modi-
fications to reduce symptoms, as appropriate.

H Provide reassurance and support.
Monitoring
H Intake and output
H Risk-factor modification
Patient teaching
Be sure to cover:
H use of acupressure to reduce symptoms
H prevention techniques. (See Preventing motion
sickness.)
Motion sickness
529
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Multiple myeloma
H History of repeated pneumonia, bladder or kidney
infections, or sinusitis
H Pain on movement or weight bearing, especially in
Overview
Description
H Disseminated neoplasm of marrow plasma cells
H Prognosis usually poor because by diagnosis, the ver-
tebrae, pelvis, skull, ribs, clavicles, and sternum infiltrated

H With early diagnosis and treatment, life commonly
prolonged by 3 to 5 years
H Without treatment, fatal in 52% of patients within 3
months of diagnosis; in 90% within 2 years
H Also called malignant plasmacytoma, plasma cell
myeloma, and myelomatosis
Pathophysiology
H Infiltration of the bone produces osteolytic lesions
throughout the skeleton.

H In late stages, the malignant plasma cells infiltrate
the lymph nodes, liver, spleen, and kidneys.

H Infiltrates prevent normal function.
Causes
Risk factors
H Genetic factors
H Occupational exposure to radiation
H Obesity
Incidence
H More common in blacks
the thoracic and lumbar vertebrae
Physical findings
H Noticeable thoracic deformities and reduction in
body height of 5 (12.7 cm)
Test results
Laboratory
H Complete blood count shows moderate or severe
anemia; the differential may show 40% to 50% lymphocytes but seldom more than 3% plasma cells;
Rouleau formation, commonly the first clue, is seen
on differential smear and results from elevation of
the erythrocyte sedimentation rate.
H Urine studies may show protein urea, Bence Jones
protein, and hypercalciuria; absence of Bence Jones
protein doesnt rule out multiple myeloma, but its
presence almost invariably confirms the disease.
H Serum electrophoresis shows an elevated globulin
spike thats electrophoretically and immunologically
abnormal.
H Serum calcium level is elevated.
Imaging
H X-rays during the early stages may reveal only diffuse
osteoporosis. Eventually, they show the characteristic
lesions of multiple myeloma: multiple, sharply circumscribed osteolytic, or punched out lesions, particularly on the skull, pelvis, and spine.
H Bone marrow aspiration reveals myelomatous cells
and abnormal number of immature plasma cells
(10% to 95% instead of the normal 3% to 5%).
Treatment
H History of neoplastic fractures

H Joint and back pain
General
Complications
H Adjuvant local radiation

H Dialysis (if renal complications develop)
H Plasmapheresis to remove the M protein from the
H Infections (such as pneumonia)

H Pyelonephritis, renal calculi, and renal failure
H Hematologic imbalance
H Fractures
H Hypercalcemia
H Hyperuricemia
H Dehydration
Assessment
History
H History of neoplastic fractures
H Severe, constant back pain, which may increase with
exercise
H Arthritic symptoms
H Peripheral paresthesia
H Progressive weakness and fatigue
530
Multiple myeloma
blood and return the cells to the patient (temporary

effect)
H Peripheral blood stem cell transplantation
Medications
H Bisphosphonates
H Analgesics
H Chemotherapeutics, such as melphalan, cyclophos-
phamide, and vincristine

H Thalidomide or lenalidomide
H Immunotherapy
H Proteasome inhibitor such as bortezomib
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Surgery
H Laminectomy if the patient develops vertebral com-
pression
Key outcomes
The patient will:
H express feelings regarding illness
pain
H demonstrate effective coping skills.
H Encourage fluid intake (3 to 4 qt [3 to 4 L] daily).
After surgery
H Encourage mobilization.
Monitoring
H Signs and symptoms of severe anemia and fractures
H Proper positioning (alignment)
H Pain control
Patient teaching
Be sure to cover:
H importance of deep breathing and changing position
every 2 hours after surgery
H appropriate dress for weather conditions (because
the patient may be sensitive to cold)
H avoidance of crowds and people with infections
adverse effects
H safety precautions to prevent falls.
Discharge planning
services.
Multiple myeloma
531
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Multiple sclerosis
Overview
Description
H Progressive demyelination of white matter of brain
Complications
H Injuries from falls
H Urinary tract infections
H Constipation
H Contractures
H Pressure ulcers
H Pneumonia
H Depression
and spinal cord

H Characterized by exacerbations and remissions
H May progress rapidly, causing death within months
H Prognosis varies (70% of patients with multiple scle-
rosis lead active lives with prolonged remissions)

H Also known as MS
Pathophysiology
H Sporadic patches of demyelination occur in the cen-
tral nervous system, resulting in widespread and varied neurologic dysfunction.
Causes
H Slow-acting viral infection
H An autoimmune response of the nervous system
H Allergic response
H Events that precede the onset:
emotional stress
overwork
fatigue
pregnancy
acute respiratory tract infections
H Genetic factors possibly also involved
Risk factors
H Trauma
H Anoxia
H Toxins
H Vascular lesions
H Anorexia nervosa
Incidence
H Highest in females
H Highest among people in northern urban areas
H Highest in higher socioeconomic groups
H Low incidence in Japan
H Family history increases incidence
H Increased incidence with living in a cold, damp cli-
mate
H Major cause of chronic disability in young adults
ages 20 to 40
H Dependent on the extent and site of myelin destruc-
tion
H Sensory impairment
H Muscle dysfunction
H Bladder and bowel disturbances
H Speech problems
H Fatigue
532
Multiple sclerosis
Assessment
History
H Symptoms related to extent and site of myelin de-
struction, extent of remyelination, and adequacy of

subsequent restored synaptic transmission
H Symptoms possibly transient or last for hours or
weeks
H Chronic, progressive loss or deterioration
H Symptoms unpredictable and difficult to describe
H Visual problems and sensory impairment (the first
signs)
H Blurred vision or diplopia
H Urinary problems (such as urgency, frequency,
incontinence)
H Dysphagia
H Bowel disturbances (involuntary evacuation or
constipation)
H Fatigue (typically the most disabling symptom)
Physical findings
H Poor articulation
H Muscle weakness of the involved area
H Spasticity; hyperreflexia
H Intention tremor
H Gait ataxia
H Paralysis, ranging from monoplegia to quadriplegia
H Nystagmus; scotoma
H Optic neuritis
H Ophthalmoplegia
Test results
H Years of testing and observation may be required for
diagnosis.
Laboratory
H Cerebrospinal fluid analysis shows mononuclear cell
pleocytosis, an elevation in the level of total immunoglobulin (Ig) G, and presence of oligoclonal Ig.
Imaging
H Magnetic resonance imaging is the most sensitive
method of detecting multiple sclerosis focal lesions.
Other
H EEG abnormalities occur in one-third of patients with
MS.
H Evoked potential studies show slowed conduction of
nerve impulses.
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Treatment
General
H Symptomatic treatment for acute exacerbations and
related signs and symptoms

H High fluid diet and fiber intake in case of constipa-
tion
Medications
H Antineoplastics such as mitoxantrone
H Muscle relaxants, such as baclofen and tizandine
H I.V. steroids followed by oral steroids
H Biological response modifiers, such as glatiramer,
interferon beta-1a, and interferon beta-1b

H Natalizumab (use restricted to special distribution
programs)
Key outcomes
Describing multiple sclerosis

Various terms are used to decribe multiple sclerosis (MS).
H Elapsing-remitting: clear relapses (or acute attacks or
exacerbations) with full recovery and lasting disability.
Between attacks, the disease doesnt worsen.
H Primary progressive: steadily progressing or worsening with minor recovery or plateaus. This form is uncommon and may involve different brain and spinal
cord damage from other forms.
H Secondary progressive: beginning as a pattern of clearcut relapses and recovery but becoming steadily progressive and worsening between acute attacks.
H Progressive-relapsing: steadily progressing from the
onset but also has clear, acute attacks. This form is
rare. In addition, differential diagnosis must rule out
spinal cord compression, foramen magnum tumor
(which may mimic the exacerbations and remissions of
MS), multiple small strokes, syphilis or another infection, thyroid disease, and chronic fatigue syndrome.
Patient teaching
The patient will:

fatigue
H develop regular bowel and bladder habits
H use available support systems and coping mechanisms.
Be sure to cover:
H disease process (see Describing multiple sclerosis)
H avoidance of stress, infections, and fatigue
H maintaining independence
H avoiding exposure to bacterial and viral infections
H nutritional management
H adequate fluid intake and regular urination.
Discharge planning

H Assist with physical therapy program.
H Promote emotional stability.
H Keep the bedpan or urinal readily available because
H Refer the patient to the National Multiple Sclerosis
Society.
H Refer the patient to physical and occupational reha-
bilitation programs, as indicated.

H Refer the patient for counseling.
the need to void is immediate.

H Provide bowel and bladder training, if indicated.
Monitoring
H Muscle dysfunction
H Energy level
H Speech
H Elimination patterns
H Vision changes
Multiple sclerosis
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Mumps
Overview
Description
H An acute inflammation of one or both parotid glands,
and sometimes the sublingual or submaxillary glands

H Also called infectious or epidemic parotitisan
Pathophysiology
H Virus replication occurs in the epithelium of the up-
per respiratory tract, leading to viremia.

H Infection of the central nervous system (CNS) or
glandular tissues (or both) occurs, resulting in

perivascular and interstitial mononuclear cell infiltrates with edema.
H Necrosis of acinar and epithelial duct cells occurs in
the salivary glands and germinal epithelium of the
seminiferous tubules.
Causes
H A paramyxovirus found in the saliva of an infected
person
H Transmitted by droplets or by direct contact with the
saliva of an infected person
Risk factors
H Travel outside the United States
H Unvaccinated status
Incidence
Assessment
History
H Inadequate immunization and exposure to someone
with mumps within the preceding 2 to 3 weeks

H Myalgia, headache
H Malaise, fever
H Earache aggravated by chewing
Physical findings
H Swelling and tenderness of the parotid glands
H Simultaneous or subsequent swelling of one or more
other salivary glands (see Parotid inflammation in

mumps)
Test results
H Glandular swelling confirms the diagnosis.
Laboratory
H Serologic testing shows mumps antibodies.
Treatment
General
H Rest
H Cold compresses for swollen glands
H Use of athletic supporter if testicles are tender
H Liquid to mechanical soft diet until able to swallow
H Bed rest until fever resolves
H Seldom occurring in infants younger than age 1 be-
Medications
cause of passive immunity from maternal antibodies

H About 50% of cases in young adults; remainder in
young children or immunocompromised adults
H Peak incidence during late winter and early spring
H Analgesics
H Antipyretics
H Usually begins with prodromal symptoms that last for
Key outcomes
24 hours
H Myalgia, anorexia, malaise, headache, an earache aggravated by chewing, and pain when drinking sour or
acidic liquids; may have a fever of 101 to 104 F
(38.3 to 40 C)
The patient will:

H remain afebrile
pain
H achieve adequate nutritional intake.
Complications
H Epididymoorchitis
H Sterility
H Pancreatitis
H Transient sensorineural hearing loss
H Arthritis
H Nephritis
H Spontaneous abortion (with contact during the first
trimester)
534
Mumps
H Apply warm or cool compresses to the neck area to
relieve pain.
H Provide scrotal support, if needed.
H Report all cases of mumps to local public health au-
thorities.
H Disinfect articles soiled with nose and throat secre-
tions.
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Parotid inflammation in mumps

The mumps virus (paramyxovirus) attacks the parotid glands the main salivary glands. Inflammation causes characteristic
swelling and discomfort with eating, drinking, swallowing, and talking.
Parotid gland
Monitoring
H Signs of CNS involvement
H Auditory acuity
H Complications
Patient teaching
Be sure to cover:
H need to stay away from school or work from days 12
through 25 after exposure
H importance of having children immunized with live
attenuated mumps vaccine at age 15 months or
older, if applicable
H if epididymoorchitis occurs, reassurance that it wont
cause impotence and sterility (occurs only with bilateral orchitis)
H need for bed rest during febrile period
H need to avoid spicy, irritating foods, and those that
require much chewing; advise a soft, bland diet
H need for family members to follow respiratory isolation precautions until symptoms subside.
Discharge planning
H Refer the patient to a urologist for orchitis, if indi-
cated.
Mumps
535
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Muscular dystrophy
Overview
Description
H Hereditary disorder characterized by progressive
symmetrical wasting of skeletal muscles

H No neural or sensory defects
H Four main types: Duchennes (pseudohypertrophic),
Beckers (benign pseudohypertrophic), LandouzyDejerine (facioscapulohumeral) dystrophy, and Erbs

(limb-girdle) dystrophy
H Duchennes beginning during early childhood, death
occurring within 10 to 15 years
Pathophysiology
H Muscle fibers necrotize and regenerate in various
states.
H Regeneration slows and degeneration dominates.
H Fat and connective tissue replace muscle fibers.
H Weakness results.
Causes
H Various genetic mechanisms (band Xp 21)
H Duchennes and Beckers X-linked recessive
H Landouzy-Dejerine autosomal dominant
H Erbs usually autosomal recessive
Duchennes
H Onset insidious
H Pelvic muscle weakness
H Interferes with childs ability to run, climb, and walk
Beckers
H Onset after age 5
H Symptoms the same as Duchennes, but slower progression
Landouzy-Dejerine
H Onset before age 10
H Weakness of eye, face, and shoulder muscles
H Inability to raise arms over head
H Inability to close eyes
H Inability to pucker lips or whistle
H Abnormal facial movements
H Absence of facial movements when laughing or crying
H Pelvic muscles weaken as disease progresses
Erbs
H Symptoms the same as in Landouzy-Dejerine but
slower progression
H Less of a disability than in Landouzy-Dejerine
H Muscle weakness of upper arm and pelvic muscles
Physical findings
Assessment
Duchennes and Beckers

H Wide stance and waddling gait
H Gowers sign when rising from a sitting or supine
position
H Muscle hypertrophy and atrophy
H Calves enlarged due to fat infiltration into the muscle
H Posture changes
H Lordosis and a protuberant abdomen
H Scapular winging or flaring when raising arms
H Contractures
H Tachypnea and shortness of breath
Landouzy-Dejerine
H Pendulous lower lip
H Possible disappearance of nasolabial fold
H Diffuse facial flattening leading to a masklike expression
H Inability to suckle (infants)
H Scapulae with a winglike appearance; inability to
raise arms above head
Erbs
H Apparent effects of muscle weakness
H Muscle wasting
H Winging of the scapulae
H Lordosis with abdominal protrusion
H Waddling gait
H Poor balance
H Inability to raise the arms
History
Test results
H Evidence of genetic transmission

H Progressive muscle weakness
Laboratory
H Urine creatinine, serum creatine kinase, lactate dehydrogenase, alanine aminotransferase, and aspartate
aminotransferase levels are elevated.
Incidence
H Duchennes and Beckers: affect males almost exclu-
sively
H Landouzy-Dejerine and Erbs: affect both sexes about
equally
H Waddling gait
H Toe walking
H Lumbar lordosis
H Frequent falls
H Dyspnea
H Dysphagia
Complications
H Crippling disability
H Contractures
H Pneumonia
H Arrhythmias
H Cardiac hypertrophy
H Dysphagia
536
Muscular dystrophy
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H Muscle biopsy result confirms the diagnosis.
H Immunologic and biological results facilitate prenatal
and postnatal diagnosis.
H Electromyography shows abnormal muscle movements.
H Amniocentesis detects sex of fetus for high-risk
family.
Other
H Genetic testing may be used to detect the gene defect
that leads to muscular dystrophy in some families.
Treatment
General
H No known treatment to stop progression
H Orthopedic appliances
H Low-calorie, high-protein, high-fiber diet
H Tube feedings, as needed
H Exercise, as tolerated
H Physical therapy
Patient teaching
Be sure to cover:
H maintenance of peer relationships
H how to maintain mobility and independence
H possible complications and prevention
H signs and symptoms of respiratory tract infections
H need for a low-calorie, high-protein, high-fiber diet
H need to avoid long periods of bed rest and inactivity.
Discharge planning
H Refer the patient for sexual counseling, if indicated.
H Refer the patient for physical therapy, vocational re-
habilitation, social services, and financial assistance.

H Refer the patient to the Muscular Dystrophy Associa-
tion.
H Refer the patient for genetic counseling.
Medications
H Stool softeners
H Possible steroids
Surgery
H Surgery to correct contractures
H Spinal fusion
Key outcomes
The patient will:
H perform activities of daily living without muscle
fatigue or intolerance
H maintain muscle strength, joint mobility, and range of
motion
H show no evidence of complications
baseline.
H Take steps to prevent muscle atrophy.
H Use splints, braces, grab bars, and overhead slings.
H Use a footboard or high-topped shoes and a foot
cradle.
H Provide a low-calorie, high-protein, high-fiber diet.
Monitoring
H Intake and output
H Joint mobility
H Muscle weakness
H Complications
Muscular dystrophy
537
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Myasthenia gravis

H Jaw hanging open (especially when tired)
H Head bobbing
H Symptoms milder on awakening; worsen as the day
progresses
H Short rest periods that temporarily restore muscle
Overview
Description
H An acquired autoimmune disorder characterized by
abnormal fatigability of striated (skeletal) muscles

H Sporadic but progressive weakness
H Muscle weakness exacerbated by exercise and repeti-
tive movement
H Initial symptoms related to cranial nerves
H With respiratory system involvement, may be life-
threatening
H Spontaneous remissions in about 25% of patients
Pathophysiology
H Blood cells and thymus gland produce antibodies
that block, destroy, or weaken neuroreceptors

(which transmit nerve impulses).
H The result is failure in transmission of nerve impulses at the neuromuscular junction.
Causes
H Autoimmune disorder associated with the thymus
gland
H Accompanies other immune and thyroid disorders
Incidence
H Occurs at any age
H Three times more common in females than males
H Highest in females ages 18 to 25
H Highest in males ages 50 to 60
H Transient myasthenia in about 20% of infants born to
myasthenic mothers
H Weak eye closure; ptosis
H Diplopia
H Skeletal muscle weakness; paralysis
Complications
H Pneumonia
H Aspiration
Assessment
History
H Varying assessment findings
H Progressive muscle weakness
H Extreme muscle weakness and fatigue (cardinal
symptoms)
H Ptosis and diplopia (the most common sign and
symptom)
538
Myasthenia gravis
function
H Symptoms that become more intense during menses,
after emotional stress, after prolonged exposure to

sunlight or cold, and with infections
Physical findings
H Sleepy, masklike expression
H Drooping jaw
H Ptosis
H Decreased tidal volume
H Respiratory distress and myasthenic crisis
Test results
Laboratory
H Serum acetylcholine receptor antibodies are
elevated.
Imaging
H Chest X-rays or computed tomography scan shows
thymoma.
Other
H Positive Tensilon test shows temporary improved
muscle function and confirms the diagnosis.
H Electrodiagnostic testing shows a rapid reduction
of more than 10% in the amplitude of evoked
responses.
Treatment
General
H Plasmapheresis
H Emergency airway and ventilation management
H Activity, as tolerated (exercise possibly exacerbating
symptoms; planned rest periods possibly retarding

symptoms)
Medications
H Anticholinesterase drugs, such as neostigmine and
pyridostigmine
H I.V. immune globulin
H Immunosuppressants such as cyclosporine
Surgery
H Thymectomy
Key outcomes
The patient will:
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baseline
H maintain range of motion and joint mobility
H Maintain nutritional management program.
H Maintain social activity.
Monitoring
H Neurologic and respiratory function
ALERT
Monitor patient for signs of impending myasthenic
crisis, including increased muscle weakness, respiratory distress, and difficulty talking or chewing.
Patient teaching
Be sure to cover:
H surgery (preoperative and postoperative teaching)
H energy conservation techniques
H avoidance of strenuous exercise, stress, infection,
needless exposure to the sun or cold weather
H nutritional management program
H swallowing therapy program.
Discharge planning
H Refer the patient to the Myasthenia Gravis Founda-
tion.
Myasthenia gravis
539
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Myocardial infarction
Overview
Description
H Reduced blood flow through one or more coronary
Complications
H Arrhythmias
H Cardiogenic shock
H Heart failure causing pulmonary edema
H Pericarditis
H Rupture of the atrial or ventricular septum, ventricu-
lar wall
H Ventricular aneurysm
H Cerebral or pulmonary emboli
H Extensions of the original infarction
H Mitral insufficiency
arteries causing myocardial ischemia and necrosis

H Infarction site depends on the vessels involved
H Also called MI and heart attack
Assessment
Pathophysiology
History
H One or more coronary arteries become occluded.

H If coronary occlusion causes ischemia lasting longer
H Possible CAD with increasing anginal frequency,
than 30 to 45 minutes, irreversible myocardial cell

damage and muscle death occur.
H Every MI has a central area of necrosis surrounded
by an area of hypoxic injury. This injured tissue is
potentially viable and may be salvaged if circulation
is restored, or it may progress to necrosis.
H Cardinal symptom of MI: persistent, crushing sub-
Causes
H Atherosclerosis
H Thrombosis
H Platelet aggregation
H Coronary artery stenosis or spasm
Risk factors
H Increased age (40 to 70)
H Diabetes mellitus
H Elevated serum triglyceride, low-density lipoprotein,
and cholesterol levels, and decreased serum highdensity lipoprotein levels

H Excessive intake of saturated fats, carbohydrates, or
salt
H Hypertension
H Obesity
H Positive family history of coronary artery disease
(CAD)
H Smoking
H Stress or a type A personality
H Use of drugs, such as amphetamines or cocaine
Incidence
H Males more susceptible than premenopausal females
H Increasing among females who smoke and take hor-
monal contraceptives
H In postmenopausal females, similar to incidence in
males
H Substernal chest pain or pressure with radiation
H Shoulder or jaw pain
H Dyspnea
H Atypical symptoms such as nausea
540
severity, or duration
sternal pain or pressure possibly radiating to the left
arm, jaw, neck, and shoulder blades, and possibly
persisting for 12 or more hours
H In elderly patient or one with diabetes, pain possibly
absent; in others, pain possibly mild and confused
with indigestion
H A feeling of impending doom, fatigue, nausea, vomiting, and shortness of breath
H Sudden death (may be the first and only indication
of MI)
Physical findings
H Extreme anxiety and restlessness
H Dyspnea
H Diaphoresis
H Tachycardia
H Hypertension
H Bradycardia and hypotension, in inferior MI
H An S4, an S3, and paradoxical splitting of S2 with ven-
tricular dysfunction
H Systolic murmur of mitral insufficiency

H Pericardial friction rub with transmural MI or peri-
carditis
H Low-grade fever during the next few days
Test results
Laboratory
H Serum creatine kinase (CK) level is elevated, especially the CK-MB isoenzyme.
H Serum lactate dehydrogenase (LD) level is elevated;
higher LD1 isoenzyme (found in cardiac tissue) than
LD2 (in serum).
H Elevated white blood cell count usually appears on
the second day and lasts 1 week.
H Myoglobin (the hemoprotein found in cardiac and
skeletal muscle) thats released with muscle damage
as soon as 2 hours after MI is detected.
H Troponin levels increase within 4 to 6 hours of myocardial injury and may remain elevated for 5 to 11
days.
H Complete blood count may show amenia.
H Serum C-reactive protein level is elevated.
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H Chemistry profile may show abnormal electrolyte
levels.
Imaging
H Nuclear medicine scans can identify acutely damaged
muscle by picking up accumulations of radioactive
nucleotide, which appear as a hot spot on the film.
Myocardial perfusion imaging reveals a cold spot
in most patients during the first few hours after a
transmural MI.
H Echocardiography shows ventricular wall dyskinesia
with a transmural MI and helps to evaluate the ejection fraction.
H Serial 12-lead electrocardiography readings may be
normal or inconclusive during the first few hours after an MI. Characteristic abnormalities include serial
ST-segment depression in subendocardial MI and
ST-segment elevation and Q waves, representing scarring and necrosis, in transmural MI.
H Pulmonary artery catheterization may be performed
to detect left- or right-sided heart failure and to monitor response to treatment.
H develop no complications of fluid volume excess

pain
H exhibit adequate coping skills.
H Assess pain and administer prescribed analgesics.
Treatment
Record the severity, location, type, and duration of

pain. Avoid I.M. injections.
H Check the patients blood pressure before and after
giving nitroglycerin.
H During episodes of chest pain, obtain electrocardiogram.
H Organize patient care and activities to provide periods of uninterrupted rest.
H Provide a low-cholesterol, low-sodium diet with
caffeine-free beverages.
H Provide emotional support, and help to reduce stress
and anxiety.
H If the patient has undergone percutaneous transluminal coronary angioplasty, sheath care is necessary.
Watch for bleeding. Keep the leg with the sheath insertion site immobile. Maintain strict bed rest. Check
peripheral pulses in the affected leg frequently.
General
Monitoring
H For arrhythmias, a pacemaker or electrical car-
H Serial electrocardiograms
H Vital signs and heart and breath sounds
dioversion
H Intra-aortic balloon pump for cardiogenic shock
H Low-fat, low-cholesterol diet
H Calorie restriction, if indicated
H Bed rest with bedside commode
H Gradual increase in activity, as tolerated
Medications
H I.V. thrombolytic therapy, such as streptokinase and
alteplase, started within 3 hours of symptom onset

H Vasodilators such as nitroglycerin
H Platelet aggregation inhibitors such as clopidogrel
H Aspirin
H Antiarrhythmics
H Heparin
H Morphine I.V.
H Inotropic drugs such as dopamine
H Angiotensin-converting inhibitors such as captopril
H Stool softeners
H Oxygen
Surgery
H Surgical revascularization
H Percutaneous revascularization
ALERT
Watch for crackles, cough, tachypnea, and edema,
which may indicate impending left-sided heart
failure.
H Daily weight; intake and output
H Cardiac enzyme levels; coagulation studies
H Cardiac rhythm for reperfusion arrhythmias (treat
according to facility protocol)
Patient teaching
Be sure to cover:
H procedures
H medication administration, dosage, and psosible adverse reactions
H progressive resumption of sexual activity
H appropriate responses to new or recurrent symptoms
H typical or atypical chest pain to report.
Discharge planning
H Refer the patient to a cardiac rehabilitation program.

Key outcomes
The patient will:

H develop no arrhythmia
needed.
needed.
541
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Myocarditis
H Nonspecific symptoms, such as fatigue, dyspnea, pal-
pitations, persistent tachycardia, and persistent fever

H Mild, continuous pressure or soreness in the chest
Overview
Description
H Focal or diffuse inflammation of the myocardium typ-
ically uncomplicated and self-limiting

H Recovery usually spontaneous and without residual
defects
Pathophysiology
H An infectious organism triggers an autoimmune, cel-
lular, and humoral reaction.

H Inflammation may lead to hypertrophy, fibrosis, and
inflammatory changes of the myocardium and conduction system.

H Heart muscle weakens, and contractility is reduced.
Causes
H Viruses
H Bacteria
H Fungi
H Ricettsial
H Hypersensitive immune reactions such as acute
rheumatic fever
H Radiation therapy
H Parasitic infections
H Helminthic infections such as trichinosis
Physical findings
H S3 and S4 gallops, muffled S1
H Pericardial friction rub
H Crackles
H Arrhythmia
Test results
Laboratory
H Cardiac enzyme levels, including creatine kinase
(CK), CK-MB, aspartate aminotransferase, and lactate
dehydrogenase are elevated.
rate are elevated.
H Antibody titers, such as antistreptolysin-O titer in
rheumatic fever, are elevated.
H Cultures of stool, throat, pharyngeal washings, or
other body fluids show the causative bacteria or
virus.
H Endomyocardial biopsy can be used to confirm diagnosis.
H Electrocardiography typically shows diffuse STsegment and T-wave abnormalities as in pericarditis,
conduction defects (prolonged PR interval), and ventricular and supraventricular ectopic arrhythmias.
Treatment
Risk factors
General
H Recent viral or bacterial infection

H Human immunodeficiency syndrome
H Connective tissue diseases
H For patient with signs and symptoms of heart failure,
hospitalization until stabilized
H Oxygen therapy, if indicated

H Low-sodium diet
H Modified bed rest
Medications
H Mild, continuous chest soreness or pressure
H Anti-infectives as appropriate
H Antiarrhythmics
H Anticoagulants
H Anti-inflammatory agents, such as steroids and non-
Incidence
Complications
H Cardiomyopathy
H Chronic valvulitis (when it results from rheumatic
fever)
captoril
H Arrhythmias
H Thromboembolism
Assessment
History
H Possible recent upper respiratory tract infection with
fever, viral pharyngitis, or tonsillitis
542
steroidal anti-inflammatory drugs

H Angiotensin-converting enzyme inhibitors such as
Myocarditis
H Diuretics
H Inotropic agents
Surgery
H Pacemaker implantation
H Ventricular assist device
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Key outcomes
The patient will:
H carry out activities of daily living without weakness
or fatigue
H maintain hemodynamic stability and adequate
cardiac output without arrhythmia
H Stress the importance of bed rest. Provide a bedside
commode.
H Allow the patient to express his concerns about the
effects of activity restrictions on his responsibilities

and routines.
H Administer prescribed parenteral anti-infectives and
other drugs.
Monitoring
H Vital signs
H Intake and output
H Possible digoxin toxicity
H Cardiac rhythm
H Daily weight
Patient teaching
Be sure to cover:
H prevention of myocarditis
H for a patient taking cardiac glycosides at home, how
to check the pulse for 1 full minute before taking the
dose, and the need to withhold the dose and notify
the physician if the heart rate falls below the predetermined rate (usually 60 beats/minute)
H when to notify the physician.
Myocarditis
543
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Assessment
Near drowning
History
Overview
Physical findings
Description
H Victim survives physiologic effects of submersion

H Primary problems: hypoxemia and acidosis
H Dry near drowning: fluid not aspirated; respiratory
obstruction or asphyxia
H Wet near drowning: fluid aspirated; asphyxia or
secondary changes from fluid aspiration

H Secondary near drowning: recurrence of respira-
tory distress
Pathophysiology
H Immersion stimulates hyperventilation.
H Voluntary apnea occurs.
H Laryngospasm develops.
H Hypoxemia develops and can lead to brain damage
and cardiac arrest.
Causes
H Inability to swim
H Panic
H Boating accident
H Sudden acute illness
H Seizures
H Blow to the head while in the water
H Venomous stings from aquatic animals
H Excessive alcohol consumption before swimming
H Decompression sickness from deep-water diving
H Dangerous water conditions
H Suicide attempt
H Victim found in water
H Fever or hypothermia
H Rapid, slow, or absent pulse
H Shallow, gasping, or absent respirations
H Altered LOC
H Seizures
H Cyanosis or pink, frothy sputum or both
H Crackles, rhonchi, wheezing, or apnea
H Tachycardia
H Irregular heartbeat
Test results
Laboratory
H Arterial blood gas (ABG) level shows degree of hypoxia, intrapulmonary shunt, and acid-base balance.
H Electrolyte levels are imbalanced.
H Complete blood count shows hemolysis.
H Blood urea nitrogen and creatinine levels reveal
impaired renal function.
H Urinalysis shows signs of impaired renal function.
Imaging
H Cervical spine X-ray may show evidence of fracture.
H Serial chest X-rays may show pulmonary edema.
Other
H Electrocardiography may show myocardial ischemia
or infarct or cardiac arrhythmias.
Treatment
General
H Incidence greater in males
H Stabilizing neck
H Establishing airway and providing ventilation
H Correcting abnormal laboratory values
H Warming measures, if hypothermic
H Nothing by mouth until swallowing ability has re-
H Activity based on extent of injury and success of re-
Incidence
H Most common cause of injury and death in children
ages 1 month to 14 years
H Altered vital signs

H Dyspnea
H Hypoxia
H Cardiopulmonary arrest
Complications
H Neurologic impairment
H Seizure disorder
H Pulmonary edema
H Renal damage
H Bacterial aspiration
H Pulmonary complications
H Cardiac complications
544
Near drowning
turned
suscitation
Medications
H Bronchodilators such as albuterol
H Cardiac drug therapy if appropriate
Key outcomes
The patient will:
H have a patent airway at all times
H develop effective coping mechanisms.
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Prevention
H Perform cardiopulmonary resuscitation as indicated.

H Perform active external rewarming and passive re-
Preventing near drowning
warming measures for mild hypothermia (93.2 to

96.8 F [34 to 36 C]); for active external rewarming of truncal areas only and passive rewarming measures for moderate hypothermia (86 F [30 C] to
93.2 F); for active internal rewarming measures for
severe hypothermia (less than 86 F).
H Protect the cervical spine.
Monitoring
Near drowning can be prevented by following these guidelines:

H Surround swimming pools with adequate fencing.
H Lock all entrances to pool area.
H Constantly supervise children near water, including
areas where water level is only a few inches.
H Dont swim after ingesting drugs or drinking alcohol.
H Monitor adults and children near water if they have a
history of seizures.
H Never swim alone.
H Always wear a life jacket in a boat.
H Dont dive into shallow water.
H Electrolyte and ABG measurement results

H Cardiac rhythm
H Vital signs
H Neurologic status
H Core body temperature
H Psychological state
Patient teaching
Be sure to cover:
H the need to avoid using alcohol or drugs before
swimming
H water safety measures. (See Preventing near drowning.)
Discharge planning
H Recommend a water safety course given by the Red
Cross, YMCA, or YWCA.

H Refer the patient or family for psychological coun-
seling if appropriate.
H Refer the patient or family to resource and support
services.
Near drowning
545
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H Myonecrosis
H Amputation
Necrotizing fasciitis
Assessment
Overview
History
Description
H A progressive, rapidly spreading inflammatory infec-
tion of the deep fascia

H Mortality rate: 70% to 80%
H Most commonly called flesh-eating bacteria
H Also called hemolytic streptococcal gangrene,
acute dermal gangrene, suppurative fasciitis, and

synergistic necrotizing cellulitis
Pathophysiology
H Infecting bacteria enter the host through a local
tissue injury or a breach in a mucous membrane

barrier.
H Organisms proliferate in an environment of tissue hypoxia caused by trauma, recent surgery, or a medical
condition that compromises the patient.
H Necrosis of the surrounding tissue results, accelerating the disease process by creating a favorable environment for organisms.
H The fascia and fat tissues are destroyed, with secondary necrosis of subcutaneous tissue.
Causes
H Group A beta-hemolytic Streptococcus (GAS) and
Staphylococcus aureus, alone or together: the most

common primary infecting bacteria (More than 80
types of the causative bacteria, Streptococcus pyogenes, makes epidemiology of GAS infections complex.)
Risk factors
H Advanced age
H Chronic illness such as diabetes
H Steroid use
Incidence
H Three times more likely in males than females
H Rarely occurs in children except in countries with
poor hygiene practices

H Mean age: 38 to 44
H Pain out of proportion to the size of the wound or
injury
H Rapid deterioration in overall clinical status
Complications
H Renal failure
H Septic shock
H Scarring with cosmetic deformities
H Myositis
546
H Associated risk factors

H Pain
H Tissue injury
Physical findings
H Rapidly progressing erythema at the site of insult
H Fluid-filled blisters and bullae (indicate rapid pro-
gression of the necrotizing process)

H By days 4 and 5, large areas of gangrenous skin
H By days 7 to 10, extensive necrosis of the subcuta-
neous tissue
H Fever
H Sepsis
H Hypovolemia
H Hypotension
H Respiratory insufficiency
H Deterioration in level of consciousness
H Signs of sepsis
Test results
Laboratory
H Tissue biopsy shows infiltration of the deep dermis,
fascia, and muscular planes with bacteria and polymorphonuclear cells, and necrosis of fatty and muscular tissue.
H Cultures of microorganisms from the periphery of
the spreading infection or from deeper tissues during
surgical debridement identify the causative organism.
H Gram stain and culture of biopsied tissue identify the
causative organism.
Imaging
H Radiographic studies may pinpoint the presence of
subcutaneous gases.
H Computed tomography scans may show the anatomic
site of involvement by locating necrosis.
H Magnetic resonance imaging shows areas of necrosis
and areas that require surgical debridement.
Treatment
General
H Wound care
H Bed rest until treatment effective
Medications
H Antimicrobials, such as penicillin, clindamycin, and
metronidazole
H Analgesics
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Surgery
H Immediate surgical debridement, fasciectomy, or
amputation
Key outcomes
The patient will:
H remain afebrile
H Provide supportive care and supplemental oxygen,
as appropriate.
Monitoring
H Vital signs
H Mental status
H Wound status
H Pain control
Patient teaching
Be sure to cover:
H importance of strict sterile technique and proper
hand-washing technique for wound care
adverse effects
H importance of recognizing and reporting signs and
symptoms of complications.
Discharge planning
H Refer the patient for follow-up with an infectious dis-
ease specialist and surgeon, as indicated.

H Refer the patient to physical rehabilitation, if indi-
cated.
H For education and support, refer the patient to orga-
nizations such as the National Necrotizing Fasciitis

Foundation.
547
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Nephrotic syndrome
Incidence
Overview
H In children, 1 in 50,000 new cases per year

H In adults, 1 or 2 in 50,000 new cases per year
H In children, peak incidence between ages 2 and 3
Description
H Kidney disorder characterized by marked protein-
H Fluid retention
H Anorexia
H Hypertension
uria, hypoalbuminemia, hyperlipidemia, increased

coagulation, and edema
H Results from a glomerular defect that affects permeability, indicating renal damage
H Prognosis highly variable, depending on underlying
cause
H Some forms possibly progressing to end-stage renal
failure
Pathophysiology
H Glomerular protein permeability increases.
H Urinary excretion of protein, especially albumin,
increases.
H Hypoalbuminemia develops and causes decreased
colloidal oncotic pressure.
Complications
H Malnutrition
H Infection
H Coagulation disorders
H Thromboembolic vascular occlusion
H Accelerated atherosclerosis
H Acute renal failure
Assessment
H Leakage of fluid into interstitial spaces leads to acute,
History
generalized edema.
H Vascular volume loss leads to increased blood viscosity and coagulation disorders.
H The renin-angiotensin system is triggered, causing
tubular reabsorption of sodium and water and contributing to edema.
H Lethargy
H Depression
H Anorexia
H Underlying cause
H Presence of risk factor
Causes
Physical findings
H Primary (idiopathic) glomerulonephritis (about 75%
H Periorbital edema
H Mild to severe dependent edema
H Ascites
H Swollen external genitalia
H Signs of pleural effusion
H Pallor
of cases)
H Lipid nephrosis (main cause in children younger
than age 8)
H Membranous glomerulonephritis (most common
lesion in adult idiopathic nephrotic syndrome)
H Focal glomerulosclerosis (can develop spontaneously at any age, occur after kidney transplantation, or
result from heroin injection; develops in about 10%
of childhood cases and up to 20% of adult cases)
H Membranoproliferative glomerulonephritis (may follow infection, particularly streptococcal infection;
occurs primarily in children and young adults)
H Metabolic diseases such as diabetes
H Collagen-vascular disorders
H Circulatory diseases
H Certain neoplastic diseases such as multiple myeloma
H Viral infections
H Drugs, such as nonsteroidal anti-inflammatory drugs
and penicillamine
H Certain allergies such as to bee stings
Risk factors
H Nephrotoxins
H Infection
H Allergic reactions
H Pregnancy
H Hereditary nephritis
H Chronic analgesic abuse
548
Nephrotic syndrome
Test results
Laboratory
H Urinalysis reveals an increased number of hyaline,
granular, waxy, fatty casts and oval fat bodies; consistent, heavy proteinuria (levels greater than 3.5 mg/dl
for 24 hours) strongly suggests nephrotic syndrome.
H Serum cholesterol, serum phospholipid, serum
triglyceride levels are increased; serum albumin
H Renal biopsy allows histologic identification of the
lesion.
Treatment
General
H Correction of the underlying cause if possible
H Diet consisting of 0.6 g of protein per kilogram of
body weight
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Page 549
H Restricted sodium intake

Medications
H Diuretics
H Antibiotics for infection
H Glucocorticoids
H Possible alkylating agents
H Possible cytotoxic agents
Key outcomes
The patient will:
H identify risk factors that worsen tissue perfusion, and
modify lifestyle appropriately
H Offer the patient reassurance and support, especially
during the acute phase, when severe edema changes

body image.
H Provide information regarding dietary restrictions
and fluid restriction.
Monitoring
H Urine for protein
H Intake and output
H Daily weight
H Plasma albumin and transferrin levels
H Edema
Patient teaching
Be sure to cover:
H signs of infection that should be reported
H adherence to diet
adverse effects.
Discharge planning
H Refer the patient to social services as needed.
Nephrotic syndrome
549
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Neural tube defects

Overview
Assessment
History
H Maternal history revealing factors that cause defect
Description
Physical findings
H Birth defects that involve the spine or skull

H Result from neural tubes failure to close approxi-
Spina bifida
H Possibly a depression or dimple, tuft of hair, soft fatty
deposit, port wine nevi, or a combination of these
abnormalities on the skin over the spinal area
H Saclike protrusion over the spinal cord
H Flaccid or spastic paralysis
Anencephaly
H Part or entire top of skull missing
Encephalocele
H Saclike protrusion through a defective opening in the
skull
H Paralysis
mately 28 days after conception

H Different forms including spina bifida (50% of cas-
es), anencephaly (40%), and encephalocele (10%)
Pathophysiology
H Spina bifida occulta, the least severe neural tube de-
fect (NTD), is characterized by incomplete closure of

one or more vertebrae without protrusion of the
spinal cord or meninges. More severe forms have incomplete closure of one or more vertebrae, causing
protrusion of the spinal contents in an external sac
or cystic lesion (spina bifida cystica). (See Types of
spinal cord defects.)
H In anencephaly, the closure defect occurs at the cranial end of the neuroaxis and, as a result, part or the
entire top of the skull is missing, severely damaging
the brain. Portions of the brain stem and spinal cord
may also be missing. This condition is fatal.
H In encephalocele, a saclike portion of the meninges
and brain protrudes through a defective opening in
the skull. Usually it occurs in the occipital area, but it
may also occur in the parietal, nasopharyngeal, or
frontal area.
Causes
H Exposure to a teratogen
H Part of a multiple malformation syndrome such as
trisomy 18 or 13 syndrome
H A combination of genetic and environmental factors;
possibly a lack of folic acid in the mothers diet
Incidence
H Spina bifida occulta most common NTD
H At least twice the incidence in North Carolina and
South Carolina than in the rest of the United States

H More common in Whites than in Blacks
H
Some degree of neurologic dysfunction
Complications
H Paralysis below the level of the defect
H Infection such as meningitis
H Hydrocephalus
H Death
H Urinary tract disorders
H Learning disabilities
H Latex allergy
550
Neural tube defects
Test results
Laboratory
H Elevated maternal alpha-fetoprotein (AFP), amniotic
fluid AFP, and amniotic fluid acetylcholinesterase
levels indicate further testing is needed.
H Fetal karyotype detects chromosomal abnormalities
(present in 5% to 7% of NTDs).
H Maternal serum AFP screening in combination with
other serum markers, such as human chorionic gonadotropin (hCG), free beta-hCG, or unconjugated
estriol (for patients with a lower risk of NTDs and
those who will be younger than age 3412 at the time
of delivery) estimates a fetus risk of NTD as well as
possible increased risk for perinatal complications,
such as premature rupture of membranes, abruptio
placentae, or fetal death.
Imaging
H Prenatal ultrasound reveals defect (performed when
an increased risk of open NTD exists, based on family history or abnormal serum screening results; not
conclusive for open NTDs or ventral wall defects).
H Spinal X-rays reveal spina bifida occulta.
H Myelography differentiates spina bifida occulta from
other spinal abnormalities, especially spinal cord tumors.
H Skull X-rays, cephalic measurements, and computed
tomography (CT) scan demonstrate associated hydrocephalus.
H X-rays show a basilar bony skull defect (CT scan and
ultrasonography further define the defect [with encephalocele]).
Other
H Transillumination of the protruding sac distinguishes
between myelomeningocele (typically doesnt transilluminate) and meningocele (typically transilluminates).
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Types of spinal cord defects

There are three major types of spinal cord defects. Spina bifida occulta is characterized by a depression or raised area and a
tuft of hair over the defect. In myelomeningocele, an external sac contains meninges, cerebrospinal fluid, and a portion of the
spinal cord or nerve roots. In meningocele, an external sac contains only meninges and cerebrospinal fluid.
SPINA BIFIDA OCCULTA
MYELOMENINGOCELE
Treatment
General
H Symptomatic according to neurologic effects of
defect
H Assessment of growth and development throughout
lifetime
H Physical therapy
Medications
H Antibiotics, as indicated
Surgery
H Surgical closure of the protruding sac
H Shunt to relieve associated hydrocephalus
H Surgery during infancy to place protruding tissues
back in the skull, excise the sac, and correct associated craniofacial abnormalities (encephalocele)
MENINGOCELE
After surgery
H Change the dressing regularly, as ordered, and check
and report signs of drainage, wound rupture, and
infection.
H Place the infant in a prone position to protect and
assess the site.
H If leg casts have been applied, watch for signs that
the child is outgrowing the cast. Regularly check
distal pulses to ensure adequate circulation.
Monitoring
Before surgery
H Neurologic status
H Feeding ability
After surgery
H Signs of increased intracranial pressure
H Intake and output
H Vital signs
Patient teaching
Key outcomes
The patient will:
H maintain intact skin
H attain age-appropriate growth and development.
Be sure to cover:
H how to prevent contractures, pressure ulcers, and
urinary tract infections
H prevention; folic acid before and during pregnancy.
Discharge planning
H When an NTD has been diagnosed prenatally, refer
Before surgery
H Clean the defect gently with sterile saline solution or
other solutions, as ordered.
H Handle the infant carefully, and dont apply pressure
to the defect.
H Provide adequate time for parent-child bonding, if
possible.
the prospective parents to a genetic counselor.

H Refer the family for psychological and support
services.
Neural tube defects
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Neurogenic bladder
Overview
Description
H All types of bladder dysfunction caused by an inter-
ruption of normal bladder innervation by the nervous

system
H Can be hyperreflexic (hypertonic, spastic, or automatic) or flaccid (hypotonic, atonic, or autonomous)
H Also known as neuromuscular dysfunction of the
lower urinary tract, neurologic bladder dysfunction, and neuropathic bladder
Pathophysiology
H Reflux of urine into kidneys

H Urinary tract infections (UTIs)
H Calculus formation
H Renal failure
Assessment
History
H Frequent UTIs
H Hyperactive autonomic reflexes (autonomic dysre-
flexia) when the bladder is distended and the lesion

is at upper thoracic or cervical level
H Involuntary or frequent, scant urination without a
feeling of bladder fullness
H Overflow incontinence and diminished anal sphincter
tone, due to flaccid neurogenic bladder
H An upper motor neuron lesion (at or above T12)
Physical findings
causes spastic neurogenic bladder, with spontaneous

contractions of detrusor muscles, increased intravesical voiding pressure, bladder wall hypertrophy with
trabeculation, and urinary sphincter spasms.
H A lower motor neuron lesion (at or below S2 to S4)
affects the spinal reflex that controls micturition. The
result is a flaccid neurogenic bladder with decreased
intravesical pressure, and increased bladder capacity, residual urine retention, and poor detrusor contraction. The bladder may not empty spontaneously.
H Interruption of the efferent nerves at the cortical level results in loss of voluntary control. Higher centers
also control micturition, and voiding may be incomplete. Sensory neuron interruption leads to dribbling
and overflow incontinence. (See Types of neurogenic bladder.)
H Severe hypertension, bradycardia, and vasodilation
Causes
H Cerebral disorders
H Spinal cord disease
H Trauma
H Metabolic disturbances
H Acute infectious diseases
H Heavy metal toxicity
H Collagen diseases
H Vascular diseases
H Herpes zoster
H Sacral agenesis (absence of a completely formed
sacrum)
Incidence
H Based on type of neurogenic bladder disorder
H Some degree of incontinence
H Changes in initiation or interruption of micturition
H Inability to completely empty the bladder
Complications
H Incontinence
H Residual urine retention
552
Neurogenic bladder
(blotchy skin) above the level of the lesion

H Piloerection and profuse sweating above the level of
the lesion
H Spontaneous spasms (caused by voiding) of the arms
and legs
H Increased anal sphincter tone
H Greatly distended bladder without feeling of bladder
fullness, due to sensory impairment
Test results
Laboratory
H Urine culture is positive for infection.
Imaging
H Retrograde urethrography shows strictures and
diverticula.
H Voiding cystourethrography evaluates bladder neck
function, vesicoureteral reflux, and continence.
H Urodynamic studies evaluate how urine is stored in
the bladder, how well the bladder empties urine, and
urines movement out of the bladder during voiding.
H Urine flow study (uroflow) shows diminished or impaired urine flow.
H Cystometry evaluates bladder nerve supply, detrusor
muscle tone, and intravesical pressures during bladder filling and contraction.
H Urethral pressure profile determines urethral function with respect to the urethras length and outlet
pressure resistance.
H Sphincter electromyelography correlates neuromuscular function of the external sphincter with bladder
muscle function during bladder filling and contraction; it also evaluates how well the bladder and urinary sphincter muscles work together.
H Videourodynamic studies correlate visual documentation of bladder function with pressure studies.
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Types of neurogenic bladder

Neural lesion
Type
Cause
Upper motor
Uninhibited
Lack of voluntary control in infancy

Multiple sclerosis
Reflex or automatic
Spinal cord transaction

Cord tumors
Multiple sclerosis
Autonomous
Sacral cord trauma

Tumors
Herniated disk
Abdominal surgery with transection of pelvic parasympathetic
nerves
Motor paralysis
Lesions at levels S2, S3, S4

Poliomyelitis
Trauma
Tumors
Sensory paralysis
Posterior lumbar nerve roots

Diabetes mellitus
Tabes dorsalis
Lower motor
Treatment
General
H Absorbent products
H Urethral occlusive devices
H Catheterization of the bladder
H Avoidance of dietary stimulants, such as spicy foods,
citrus fruits, and chocolate

H Avoidance of excessive fluid intake
H Avoidance of caffeinated and carbonated products
H Pelvic muscle exercises
H Bladder training program
Medications
H Anticholinergics such as darifenacin
H Alpha-adrenergic stimulators
H Antispasmodics such as oxybutynin
Surgery
H External sphincterotomy, urethral dilation, urinary
diversion, or transurethral resection of the bladder

neck to correct structural impairment
H Possible implantation of an artificial urinary sphincter if permanent incontinence follows surgery
H Catheterize the patient, as appropriate.
H Provide emotional support, as appropriate.
Monitoring
H Intake and output
Patient teaching
Be sure to cover:
H dietary adjustments
H pelvic exercises
H bladder evacuation techniques
Discharge planning
H Refer the patient to rehabilitation program as neces-
sary.
Key outcomes
The patient will:
H regain normal voiding habits
H express positive feelings regarding self-image
H follow bladder training program, as indicated.
Neurogenic bladder
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Nocardiosis
Overview
Description
H Acute, subacute, or chronic bacterial infection
caused by a weakly gram-positive species of the

genus Nocardia usually Nocardia asteroides
Pathophysiology
H Pericarditis
H Endocarditis
H Peritonitis
H Mediastinitis
H Septic arthritis
H Keratoconjunctivitis
H Purulent meningitis
H Seizures
Assessment
H Nocardia are aerobic gram-positive bacteria with
History
branching filaments resembling fungi.

H Normally found in soil, these organisms cause occasional sporadic disease in humans and animals
throughout the world.
H Their incubation period is unknown but probably
lasts several weeks.
H The usual mode of transmission is inhalation of organisms suspended in dust. Transmission by direct
inoculation through puncture wounds or abrasions is
less common.
H Immunocompromising condition
H Chills
H Night sweats
H Anorexia
H Malaise
H Weight loss
H Dyspnea
H Pleural pain
H Puncture wound or abrasion
Causes
H Fever
H Cellulitis
H Productive cough
H Subcutaneous abscesses that lack induration
H Crackles
H Inhalation or inoculation of Nocardia bacteria
Risk factors
H Alcoholism
H Pulmonary alveolar proteinosis
H Male gender
Incidence
H About 500 to 1,000 cases annually in the United
States
H More common in males (3:1), especially those with a
compromised immune system

H In patients with brain infection, mortality exceeds
80%; in other forms, mortality is 50%
Cutaneous infection
H Cellulitis
H Erythematous nodule at site of inoculation
Pulmonary infection
H Cough producing thick, tenacious, purulent,
mucopurulent and, possibly, blood-tinged sputum
H Fever
Disseminated infection
H Confusion and disorientation
H Dizziness and nausea
H Headache
H Seizures
Complications
H Pleurisy
H Intrapleural effusions
H Empyema
H Tracheitis
H Bronchitis
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Nocardiosis
Physical findings
Test results
Laboratory
H Culture of sputum or pleural fluid shows causative
organism.
Imaging
H Chest X-rays vary and may show fluffy or interstitial
infiltrates, nodules, or abscesses.
H In brain infection with meningitis, lumbar puncture
shows nonspecific changes such as increased opening pressure; cerebrospinal fluid shows increased
white blood cell count and protein levels and decreased glucose levels compared to serum glucose.
Treatment
General
H Activity, as tolerated (during acute phase, bed rest)
H Safety measures
Medications
H Antimicrobial therapy for at least 6 to 12 months
H Combination drug therapy (sulfonamide, ceftri-
axone) and amikacin

H Antipyretics
Surgery
H Drainage of abscesses and excision of necrotic tissue
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Key outcomes
The patient will:
H cough effectively
H have normal breath sounds.
H Provide adequate nourishment.
H Give tepid sponge bath to reduce fever.
Monitoring
H Vital signs
H Sputum production and character
H Compliance with treatment
H Allergic reaction to antibiotics
Patient teaching
Be sure to cover:
H need for long-term antibiotic therapy
H signs of worsening infection
H allergic reaction to antibiotics.
Discharge planning
H Encourage follow-up care, as indicated.
Nocardiosis
555
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O
Obesity
Overview
Description
H An excess of body fat, generally 20% above ideal
body weight
H BMI of 30 or greater (see BMI measurements)

H Morbid obesity: 50% to 100%; or 100 or more
pounds above ideal weight; or body mass index

(BMI) greater than 40
H Second-leading cause of preventable deaths in the
United States
Pathophysiology
H Hypertension
H Hyperlipidemia
H Stroke
H Breast cancer
H Colon cancer
H Degenerative joint disease
H Sleep apnea
H Diabetes mellitus
H Renal disease
H Gallbladder disease
H Psychosocial difficulties
H Premature death
Assessment
H Fat cells increase in size in response to dietary
History
intake.
H When the cells can no longer expand, they increase
in number.
H With weight loss, the size of the fat cells decreases,
but the number of cells doesnt.
H Increasing weight
H Complications of obesity
Causes
Test results
H Excessive caloric intake combined with inadequate
Other
H Comparison of height and weight to a standard table
shows elevation.
H Measurement of the thickness of subcutaneous fat
folds with calipers approximates excess total body
fat. (See Taking anthropometric arm measurements.)
H BMI is 30 or greater.
H Waist to hip ratio: patient is overweight when ratio
for males is greater than 1 and females is greater
than 0.8.
energy expenditure
H Theories that explain obesity:
Hypothalamic dysfunction of hunger and satiety
centers
Genetic predisposition
Abnormal absorption of nutrients
Impaired action of GI and growth hormones and
of hormonal regulators such as insulin
Socioeconomic status
Environmental factors
Psychological factors
Physical findings
H Visible excess weight
Incidence
Treatment
H More than 50% of United States residents overweight

H Obesity affecting one in five children
General
H BMI of 30 or greater
Complications
BMI measurements
Use these steps to calculate body mass index (BMI):
H Multiply weight in pounds by 705.
H Divide this number by height in inches.
H Then divide this by height in inches again.
H Compare results to these standards:
18.5 to 24.9: normal
25.0 to 29.9: overweight
30 to 39.9: obese
40 or greater: morbidly obese.
H Hypnosis and behavior modification techniques

H Reduction in daily caloric intake
H Increase in daily activity level
H Treatment of organic cause
Medications
H Appetite suppressants such as sibutramine
H Lipase inhibitors such as orlistat
Surgery
H Vertical banded gastroplasty
H Gastric bypass
Key outcomes
The patient will:
H reduce BMI to normal level
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Obesity
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Taking anthropometric arm measurements

Follow these steps to determine triceps skinfold thickness, midarm circumference, and midarm muscle circumference.
Triceps skinfold thickness
H Use the tape measure to find the midpoint between the

shoulder and the elbow. Grasp the patients skin with
your thumb and forefinger, about 38 (1 cm) above the
midpoint, as shown below.
H Place calipers at the midpoint, and squeeze for 3 seconds.
H Record the measurement to the nearest millimeter.
H Take two more readings, and use the average.
Midarm circumference and midarm muscle

circumference
H At the midpoint, measure the midarm circumference, as

shown below. Record the measurement in centimeters.
H Calculate the midarm muscle circumference by multiplying the triceps skinfold thickness measured in millimeters by 3.14.
H Subtract this number from the midarm circumference.
Recording the measurements

Record all three measurements as a percentage of the standard measurements (see table below), using this formula:
Actual measurement
___________________
100%
Standard measurement
Remember, a measurement
less than 90% of the standard indicates caloric deprivation. A measurement over
90% indicates adequate or
more-than-adequate energy
reserves.
Measurement
Standard
90%
Triceps skinfold thickness
Males: 12.5 mm
Females: 16.5 mm
Males: 11.3 mm
Females : 14.9 mm
Midarm circumference
Males: 29.3 cm
Females : 28.5 cm
Males: 26.4 cm
Females : 25.7 cm
Midarm muscle circumference
Males: 25.3 cm
Females : 23.3 cm
Males: 22. 8 cm
Females : 20.9 cm
H safely reduce weight

H demonstrate effective coping mechanisms to deal
with long-term compliance.
H Obtain an accurate diet history to identify the pa-
tients eating patterns and the importance of food

to his lifestyle.
H Promote increased physical activity as appropriate.
Monitoring
H Diet
H Intake and output
H Vital signs
H Weight and BMI
Patient teaching
Be sure to cover:
H need for long-term maintenance after desired weight
is achieved
H dietary guidelines
H safe weight loss practices.
Discharge planning
H Refer the patient to a weight-reduction program.
H Refer the patient to a long-term cognitive behavior
modification program.
Obesity
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Obsessive-compulsive
disorder
Overview
Description
H Obsessive thoughts and compulsive behaviors that
impair everyday functioning

H May be simple or complex and ritualized
H Also known as OCD
Pathophysiology
H This anatomic-physiologic disturbance is thought to
involve an alteration in the frontal-subcortical neural

circuitry of the brain.
H Dysregulation of serotonin neurotransmission may
also be a factor.
Causes
H Decrease in caudate nucleus volume
Risk factors
H Coexisting mental disorder
H Tic disorders
Incidence
H Affects 1 in 50 U.S. residents
H More common in males and first-born children
H Repetitive behaviors and activities for more than
1 hour per day.

H Activities alleviate anxiety triggered by a core fear.
Complications
H Impairment of occupational and social functioning
H Endangerment of health and safety
H Depression
Assessment
History
H Presence of obsessive thoughts, words, or mental im-
ages that persistently and involuntarily invade the

consciousness
H Moderate to severe impairment of social and occupational functioning
H Patient usually rigid and conscientious, with great
aspirations
H Patient who takes responsibility seriously and finds
decision-making difficult
H Patient who lacks creativity and the ability to find
alternate solutions to problems
558
Obsessive-compulsive disorder
Physical findings
H Formal, reserved manner
H Patient is accurate and complete, carefully qualifying
statements and anticipating every move and gesture

of person to whom he speaks
H Flat and unemotional affect, except for controlled
anxiety
H Self-awareness is intellectual, without accompanying
emotion or feeling
DSM-IV-TR criteria
Diagnosis is confirmed when the patient meets these
criteria:
Obsessions
H Patient experiences recurrent and persistent ideas,
thoughts, impulses, or images as intrusive and senseless.
H Patient attempts to ignore or suppress such thoughts
or impulses or to neutralize them with some other
thought or action.
H Patient recognizes that the obsessions are products
of his mind, not externally imposed.
H Patients obsession is unrelated to another Axis I disorder.
Compulsions
H Patient performs repetitive, purposeful, and intentional behaviors in response to an obsession or according to certain rules or in a stereotypical manner.
H Behavior is intended to neutralize or prevent discomfort or some dreaded event or situation, but the behavior isnt connected in a realistic way with intended outcome, or is clearly excessive.
H Patient recognizes that the behavior is excessive or
unreasonable.
Test results
Imaging
H Positron-emission tomography shows abnormal
metabolism of frontal cortex and caudate nuclei.
Other
H Yale-Brown scale rates severity of obsessivecompulsive disorder.
H Maudsley Obsessive-Compulsive Inventory identifies
obsessive thoughts and behaviors.
Treatment
General
H Behavioral therapy
H Increasing exposure to stressful situations
H Keeping a diary of daily stressors
H Substituting new activities for compulsive behavior
Medications
H Selective serotonin-reuptake inhibitors, such as flu-
voxamine, fluoxetine, and sertraline

H Tricyclic antidepressants such as clomipramine
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Key outcomes
The patient will:
H reduce the amount of time spent each day on obsessing and ritualizing
H produce no harmful effects from ritualistic behavior
H express feelings of anxiety as they occur
H cope with stress without excessive obsessivecompulsive behavior.
H Provide an accepting patient atmosphere.
H Allow time for ritualistic behavior (unless its danger-
ous) until distraction occurs.

H Provide for basic needs.
H Make reasonable demands and set reasonable limits;
make the patients purpose clear.

H Explore patterns leading to the behavior or recurring
problems.
H Encourage active diversional resources.
H Assist with individualized problem-solving.
H Identify insight and improved behavior.
Monitoring
H Behavioral changes
H Disturbing topics of conversation
H Effective interventions
H Effects of pharmacologic therapy
Patient teaching
Be sure to cover:
H how to identify progress
H importance of realistic expectations of self and
others
H stress relief by channeling emotional energy
H relaxation and breathing techniques.
Discharge planning
H Refer the patient to social services and support
services.
H Stress the importance of follow-up care.
Obsessive-compulsive disorder
559
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Oral and pharyngeal

cancer
Overview
Description
H Malignant tumors that start in the mouth or in the
throat behind the mouth

H Involves several types of tissue and cells, resulting in
different types of cancers, which influences treatment

options and prognosis
H 90% of tumors, squamous cell carcinomas
H Others include:
Lymphomas, melanomas, and adenocarcinomas
originating in the minor salivary glands, tonsils,
and base of the tongue
Sarcomas
Pathophysiology
H Damage to cell deoxyribonucleic acid causes rapid
growth and repair.

H Growth is unrestrained and cells lose characteristics
H A nonhealing sore in the mouth
H Unrelieved pain in the mouth
H A persistent lump or thickening in the cheek or neck
H A persistent white or red patch on the gums, tongue,
tonsil, or lining of the mouth

H A persistent sore throat or a feeling that something is
caught in the throat

H Difficulty or pain while chewing or swallowing
H Difficulty moving the jaw or tongue
H Numbness of the tongue or other area of the mouth
H Swelling of the jaw causing dentures to fit poorly or
become uncomfortable
H Loosening of the teeth or pain around the teeth or
jaw
H Voice changes
H Weight loss
Complications
H Recurrence
H Metastasis to larynx, lymph nodes, and other organs
H Functional and cosmetic disabilities
H Persistent dysphagia secondary to surgery or radia-
tion therapy
H Persistent problems with articulation
of original tissue type.
Causes
H Tobacco, alcohol, ultraviolet (UV) light, virus, or oth-
er carcinogen
H Believed to be a combination of biologic, genetic,
and lifestyle factors
Risk factors
H Use of any tobacco (cigarettes, cigars, pipes, snuff,
or chewing tobacco)
H Excessive alcohol consumption
H Exposure to UV light
H Long-term irritation to the lining of the mouth
H Plummer-Vinson syndrome
H Human papillomavirus infection
H Immune system suppression
H Betel nut or betel leaf chewing
Incidence
H Account for 4% of all cancers occurring in males and
2% in females
H About two-thirds of cases occurring in people older
than age 55; rare in children

H Males affected more commonly than females
H Highest incidence in Asia, related to the habit of
chewing betel nut, fresh betel leaf, and habitual reverse smoking (lighted end held within the oral
cavity)
H Most common sites:
Tongue: 28%
Lip: 23%
Floor of the mouth: 16%
Minor salivary glands: 11%
560
Oral and pharyngeal cancer
Assessment
History
H Complaints of difficulty or pain when swallowing
H Persistent sore throat
H Change in speech patterns
H Weight loss
Physical findings
H Mouth sores
H Lump or thickening in the cheek or neck, or any-
where in the mouth

H White or red patch on the gums, tongue, tonsil, or
lining of the mouth

H Swollen jaw
H Loose teeth
Test results
Imaging
H Chest X-ray rules out metastasis to the lungs.
H Bone scans if theres pain in the bones suggest bone
metastasis.
imaging identifies possible intracranial or liver
metastasis.
H Biopsy confirms diagnosis.
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Treatment
General
H Varies depending on location of cancer
H Unresectable lesions usually treated with radiation
therapy, chemotherapy, or both

H A soft diet or nasogastric or gastrostomy feedings
possibly needed
Medications
H Opioid analgesics for pain
H Chemotherapy if indicated
H importance of preventing aspiration

H importance of oral hygiene
H need to report adverse drug effects
H importance of restricting alcohol use
H importance of not smoking or using smokeless to-
bacco
Discharge planning
H Refer the patient to home care or social services as
appropriate.
H Refer the patient to a dietitian as needed.
Surgery
H Primary tumor resection
H Wide resection, with or without radiation therapy,
chemotherapy, or a combination of both

H Full or partial mandible or maxilla resection
H Micrographic surgery for lip resections
H Laryngectomy or tracheostomy if necessary
Key outcomes
The patient will:
H verbalize understanding of the disease process
H be free from mouth lesions
H be free from signs and symptoms of bleeding
H verbalize reduced or absent pain
H maintain or gain weight
H have clear breath sounds.
H Provide care before and after chemotherapy, radia-
tion therapy, or surgery, as appropriate.

H Take precautions to reduce the risk of aspiration
with oral feedings.

H Provide interventions to reduce the risk of infection.
H Encourage activity as tolerated.
Monitoring
H Adverse effects of drugs
H Breath sounds
H Vital signs
Patient teaching
Be sure to cover:
H signs and symptoms that require prompt medical attention
H importance of adequate nutrition and fluids
H care of the mouth and skin after chemotherapy, radiation therapy, or surgery
Oral and pharyngeal cancer
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Osgood-Schlatter
disease
Overview
Description
H Partial separation of the epiphysis of the tibial tuber-
H Pain that worsens from running, jumping, squatting,
and ascending or descending stairs

H Symptoms relieved with rest
H Precipitating trauma
Physical findings
H Soft-tissue swelling
H Localized heat and tenderness
H Decreased flexibility and restriction in the ham-
strings, triceps surae, and quadriceps muscle
cle from the tibial shaft, leading to tendinitis

H Affects one or both knees
H Also known as osteochondrosis
H Pain at 30-degree flexion with tibia starting at
Pathophysiology
Test results
H Bone growth is faster than soft tissue growth.

H Muscle tendon tightness occurs across the joint.
H Flexibility is decreased.
H When the large quadricep muscle contracts, the
Imaging
H X-rays and ultrasound show epiphyseal closings, soft
tissue swelling, and bone fragmentation.
H Bone scan may reveal increased uptake in the area of
the tibial tuberosity.
patellar tendons pull away from the tibia and fibia

causing pain.
H Tendinitis of the knee results.
Causes
90 degrees in internal rotation

H Palpable firm mass
Treatment
H Traumatic avulsion of the proximal tibial tuberosity at
General
the patellar tendon insertion

H Locally deficient blood supply
H Genetic factors
H Exercise
H Ice application for 20 minutes every 2 to 4 hours

H Reinforced elastic knee support, plaster cast, or
Risk factors
H Male gender
H Age 11 to 18 years
H Rapid skeletal growth
H Repetitive jumping sports
Incidence
H Most common in active adolescent boys after under-
going a rapid growth spurt
splint
H Reduction of sports activities or exercise
H Avoidance of exercises that demand quadriceps
contraction
H In severe cases, immobilization for 6 to 8 weeks
H Rehabilitation exercises
Medications
H Nonsteroidal anti-inflammatory drugs
H Analgesics
Surgery
H Removal or fixation of the epiphysis
H Frequent fractures
H Pain at inferior aspect of patella
Complications
Key outcomes
H Irregular growth of the proximal tibial epiphysis

H Partial avascular necrosis of the proximal tibial
The patient will:

pain
H exhibit developmental milestones
epiphysis
H Chronic pain
H Patellar tendon avulsion
H Degenerative arthritis
H Chrondromalacia
Assessment
History
H Intermittent aching, pain, swelling, and tenderness
below the kneecap
562
Osgood-Schlatter disease
H Administer prescribed analgesics and assess re-
sponse.
H Ensure proper application of knee support or splint.
H Provide the patient with crutches if needed.
H Promote and allow adequate time for self-care.
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Monitoring
H Limitation of movement
H Muscle atrophy
H After surgery: circulation, sensation, and pain
H Excessive bleeding
Patient teaching
Be sure to cover:
H prescribed exercise program
H use of crutches if needed
H protection of the injured knee
H avoidance of activities that require deep knee bending for 2 to 4 months.
Discharge planning
H Refer the patient for occupational and physical
therapy as appropriate.
Osgood-Schlatter disease
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Osteoarthritis
Overview
Assessment
History
H Chronic degeneration of joint cartilage

H Most common form of arthritis
H Disability from minor limitation to near immobility
H Most commonly affects the hips and knees
H Varying progression rates
H Predisposing traumatic injury

H Deep, aching joint pain
H Pain after exercise or weight bearing
H Pain possibly relieved by rest
H Stiffness in morning and after exercise
H Aching during changes in weather
H Grating feeling when the joint moves
H Limited movement
Pathophysiology
Physical findings
H Deterioration of the joint cartilage occurs.

H Reactive new bone forms at the margins and sub-
H Contractures
H Joint swelling
H Muscle atrophy
H Deformity of the involved areas
H Gait abnormalities
H Hard nodes that may be red, swollen, and tender on
Description
chondral areas.
H Breakdown of chondrocytes occurs.
H Cartilage flakes irritate synovial lining.
H The cartilage lining becomes fibrotic.
H Joint movement is limited.
H Synovial fluid leaks into bone defects, causing cysts.
H Unknown, may be a combination of factors
the distal and proximal interphalangeal joints (see

Signs of osteoarthritis)
H Loss of finger dexterity
H Muscle spasms, limited movement, and joint instability
Risk factors
Test results
H Advancing age
H Hereditary, possibly
H Muscle weakness
H Traumatic injury
H Congenital abnormality
H Endocrine disorders such as diabetes mellitus
H Metabolic disorders such as chondrocalcinosis
Laboratory
H Synovial fluid analysis rules out inflammatory
arthritis.
Imaging
H X-rays of the affected joint may show a narrowing of
the joint space or margin, cystlike bony deposits in
the joint space and margins, sclerosis of the subchondral space, joint deformity or articular damage,
bony growths at weight-bearing areas, and possible
joint fusion.
H Radionuclide bone scan may be used to rule out inflammatory arthritis by showing normal uptake of the
radionuclide.
H Magnetic resonance imaging shows affected joint, adjacent bones, and disease progression.
H Neuromuscular tests may show reduced muscle
strength.
Other
H Arthroscopy shows internal joint structures and identifies soft-tissue swelling.
Causes
Incidence
H Occurs after age 40
H Deep, aching joint pain
H Stiffness, especially in morning and after exercise
H Crepitus of the joint during motion
H Heberdens nodes (bony enlargements of distal inter-
phalangeal joints)
H Altered gait
H Decreased range of motion (ROM)
H Localized headaches
Complications
H Flexion contractures
H Subluxation
H Deformity
H Ankylosis
H Bony cysts
H Gross bony overgrowth
H Central cord syndrome
H Nerve root compression
H Cauda equina syndrome
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Osteoarthritis
Treatment
General
H Relieve pain
H Improve mobility
H Minimize disability
H Physical therapy
H Assistive mobility devices
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Signs of osteoarthritis
Heberdens nodes appear on the dorsolateral aspect of the
distal interphalangeal joints. These bony and cartilaginous
enlargements are usually hard and painless. They typically
occur in middle-aged and elderly patients with osteoarthritis.
HEBERDENS NODES
Medications
H Analgesics
H Intra-articular injections with corticosteroids
Surgery
H Arthroplasty (partial or total)
H Arthrodesis
H Osteoplasty
H Osteotomy
Key outcomes
The patient will:
pain
the disease
H achieve the highest level of mobility
H Allow adequate time for self-care.
H Adjust pain medications to allow maximum rest.
H Identify techniques that promote rest and relaxation.
H Administer prescribed anti-inflammatories.
H For affected hand joints, use hot soaks and paraffin
dips.
H For affected lumbosacral spinal joints, provide a firm
mattress.
H For affected cervical spinal joints, apply a cervical
collar.
Bouchards nodes are similar to Heberdens nodes but are

less common and appear on the proximal interphalangeal
joints.
BOUCHARDS NODES
H For an affected hip, apply moist heat pads and ad-
minister antispasmodics.
H For an affected knee, help with ROM exercises.
H Apply elastic supports or braces.
H Check crutches, cane, braces, or walker for prop-
er fit.
Monitoring
H Pain pattern
H Response to analgesics
H ROM
Patient teaching
Be sure to cover:
H need for adequate rest during the day, after exertion,
and at night
H energy conservation methods
H need to take medications exactly as prescribed
H adverse reactions to drugs
H wearing support shoes that fit well and repairing
worn heels
H installation of safety devices at home
H ROM exercises, performing them as gently as
possible
H need to maintain proper body weight
H use of crutches or other orthopedic devices.
Discharge planning
H Refer the patient to occupational or physical thera-
pist as indicated.
Osteoarthritis
565
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Osteogenesis imperfecta
Overview
Description
H Genetic disease in which bones are thin, poorly de-
Complications
H Deafness
H Stillbirth or death within the first year of life
(autosomal-recessive disorder)
H Hyperplastic callus formation
H Repeated respiratory infections
H Cerebral hemorrhage caused by birth trauma
veloped, and fracture easily

H Expression varies, depending on whether the defect
is carried as a trait or is clinically obvious

H Also called brittle bone disease
H Categorized into four main types
Type I: mild
Type II: most severe with multiple fractures, hearing loss, and may be lethal at birth
Type III and IV: high survival rate and benefits
from treatment
Pathophysiology
H The pathogenesis begins when mutations in the genes
change the structure of collagen.

H Possible mutations in other genes may cause varia-
tions in the assembly and maintenance of bone and

other connective tissues.
H Collectively or alone, these mutated genes lead to
pathologic fractures and impaired healing.
Causes
H Genetic disease, typically autosomal dominant (char-
acterized by a defect in the synthesis of connective

tissue)
H Autosomal recessive carriage of gene defects producing osteogenesis imperfecta in homozygotes (osteoporosis in some)
Incidence
H Affects between 20,000 and 50,000 U.S. residents
Assessment
History
H Fractures early in life
H Hearing loss
H Easy bruising
Physical findings
H Blue sclerae, showing that mutation is expressed in
more than one connective tissue

H Short trunk
H Hearing loss
H Fractures
H Kyphoscoliosis
Test results
Laboratory
H Serum alkaline phosphatase levels are elevated during periods of rapid bone formation and cellular injury.
H Skin culture shows reduced quantity of fibroblasts.
Imaging
H Echocardiography may show mitral insufficiency or
floppy mitral valves.
H Prenatal ultrasound (during second trimester) reveals bowing of long bones, fractures, limb shortening, and decreased skull echogenicity.
H Skull, long bone, and pelvis X-rays reveal thin bones,
fractures with deformities, beaded ribs, and osteopenia.
Special populations
Age of onset of presentation ranges from in utero
to infancy.
H Frequent fractures caused by falls as toddler begins
to walk; poor healing

H Short stature due to multiple fractures caused by mi-
nor physical stress
Treatment
General
H Prevention of fractures
H Nutritious, well-balanced diet
H Safety during periods of activity
H Physical therapy
H Pain management
H Deformed cranial structure and limbs due to multi-
Medications
ple fractures
H Thin skin and bluish sclera of the eyes; thin collagen
fibers of the sclera allowing the choroid layer to be
seen
H Abnormal tooth and enamel development due to improper deposition of dentin
H Middle ear deafness
H Antibiotics (when infection occurs)

H Biphosphates and calcium supplements for types III
and IV
Surgery
H Internal fixation of fractures to ensure stabilization
and prevent deformities

H Spinal fusion for scoliosis
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Key outcomes
The patient (and his family) will:
H follow safety measures to prevent fractures
H understand the disorder and its treatment
H Ensure a safe environment.
H Encourage activities based on ability.
Monitoring
H Environment
H Bone condition
Patient teaching
Be sure to cover:
H safe handling of the infant
H how to recognize fractures and correctly splint them
H how to protect the child during diapering, dressing,
and other activities of daily living
H encouraging interests that dont require strenuous
physical activity
H the importance of good nutrition to heal bones and
promote growth
H use of shock-absorbing footwear
H importance of not letting infants younger than age 1
year sit upright.
Discharge planning
H Refer the child and his parents for genetic counseling
to assess the recurrence risk.

H Instruct the parents to provide their child with med-
ical identification jewelry.
567
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Osteomalacia and
rickets
Overview
Description
H Vitamin D deficiency that doesnt allow bone to cal-
cify normally
H Also called rickets in infants and young children;
osteomalacia in adults
H Prognosis good with treatment
H Possible disappearance of bone deformities in adults;
usually persist in children
Pathophysiology
H Vitamin D regulates the absorption of calcium ions
from the intestine.

H When vitamin D is lacking, falling serum calcium
concentration stimulates synthesis and secretion of

parathyroid hormone.
H This causes the release of calcium from bone, decreasing renal calcium excretion and increasing renal phosphate excretion.
H When the concentration of phosphate in the bone decreases, osteoid may be produced but mineralization
cant proceed normally.
H This causes large quantities of osteoid to accumulate,
coating the trabeculae and linings of the haversian
canals and areas beneath the periosteum.
H When bone matrix mineralization is delayed or inadequate, bone is disorganized in structure and lacks
density. The result is gross deformity of both spongy
and compact bone.
Causes
H Inadequate dietary intake of vitamin D
H Malabsorption of vitamin D
H Inadequate exposure to sunlight
H Inherited impairment of renal tubular reabsorption
of phosphate (from vitamin D insensitivity) in vitamin

Dresistant rickets (refractory rickets, familial
hypophosphatemia)
H Conditions reducing the absorption of fat-soluble vitamin D
H Hepatic or renal disease
H Malfunctioning parathyroid gland contributing to calcium deficiency and interfering with vitamin D activation in the kidneys
Incidence
H Rare in the United States
H Does appear occasionally in breast-fed infants not re-
ceiving a vitamin D supplement or in infants being

fed a formula with a nonfortified milk base
H Occurs in overcrowded urban areas where smog limits sunlight penetration
568
Osteomalacia and rickets
ALERT
Incidence of rickets is highest in children with
darkly pigmented skin who, because of their pigmentation, absorb less sunlight.
H May be asymptomatic until a fracture occurs
H Leg and lower back pain due to vertebral collapse
H Bowed legs
H Knock-knees
H Rachitic rosary (beading of ends of ribs)
H Enlarged wrists and ankles
H Pigeon breast (protruding ribs and sternum)
H Delayed closing of fontanels
H Softening skull
H Bulging forehead
H Poorly developed muscles (pot belly)
H Difficulty walking and climbing stairs
H Kyphoscoliosis
Complications
H Spontaneous multiple fractures
H Tetany in infants
H Bone deformities
Assessment
History
H Poor diet
H Leg and lower back pain
Physical findings
H Bowed legs
H Knock-knees
H Enlarged wrists and ankles
H Pigeon breast (protruding ribs and sternum)
H Bulging forehead
H Poorly developed muscles (pot belly)
H Kyphoscoliosis
Test results
Laboratory
H Serum calcium concentration is less than 7.5 mg/dl.
H Serum inorganic phosphorus concentration is less
than 3 mg/dl.
H Serum citrate level is less than 2.5 mg/dl.
H Alkaline phosphatase level is less than 4 Bodansky
units/dl.
Imaging
H X-rays show characteristic bone deformities and abnormalities such as Loosers transformation zones
(radiolucent bands perpendicular to the surface of
the bones indicating reduced bone ossification confirm the diagnosis).
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Treatment
General
H Sufficient sun exposure
H Diet high in vitamin D (fortified milk, fish liver oils,
herring, liver, and egg yolks)

H Treatment of bone deformities or fractures
Medications
H Oral supplements of vitamin D, calcium, and phos-
phorus, depending on underlying cause

H For rickets refractory to vitamin D, or in rickets
accompanied by hepatic or renal disease, 25hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, or a synthetic-analogue of active vitamin D
Surgery
H Possible surgical intervention for intestinal disease
H Appropriate repair of bone fractures
Key outcomes
The patient will:
H have increased vitamin D intake
H remain free from fractures
H express understanding of the disorder and its treatment.
H Obtain a dietary history to assess the patients vitamin
D intake.
H Administer prescribed supplements or medications.
Monitoring
H Dietary intake
H Bone integrity
Patient teaching
Be sure to cover:
H symptoms of vitamin D toxicity (headache, nausea,
constipation and, after prolonged use, renal calculi)
H safety and sun exposure.
Discharge planning
H If the patients vitamin D deficiency appears to be
linked to adverse socioeconomic conditions, refer

him to an appropriate community agency.
H Refer the patient to a weight-bearing exercise program.
Osteomalacia and rickets
569
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Osteomyelitis
Overview
H Sudden pain in affected bone

H Tenderness, heat, swelling
H Restricted movement
H Chronic infection
Description
Complications
H Pyogenic bone infection

H Infecting microorganisms invading by indirect or di-
H Chronic infection
H Skeletal deformities
H Joint deformities
H Disturbed bone growth in children
H Differing leg lengths
H Impaired mobility
rect entry
H Chronic or acute
H Good prognosis for acute form (with prompt treat-
ment)
H Poor prognosis for chronic form
Pathophysiology
H Organisms settle in a hematoma or weakened area
and spread directly to bone.

H Pus is produced and pressure builds within the rigid
medullary cavity.
H Pus is forced through the haversian canals.
H Subperiosteal abscess forms.
H Bone is deprived of its blood supply.
H Necrosis results and new bone formation is stimulated.
H Dead bone detaches and exits through an abscess or
the sinuses.
H Osteomyelitis becomes chronic.
Causes
H Traumatic injury
H Acute infection originating elsewhere in the body
H Streptococcus pyogenes
H Pseudomonas aeruginosa
H Escherichia coli
H Proteus vulgaris
H Fungi or viruses
H Salmonella
H Open bone injury
H Diminished blood supply to bone as with atheroscle-
rosis
Risk factors
H Diabetes
H Hemodialysis
H Sickle cell disease
H I.V. drug abuse
H Advanced age
Incidence
H Incidence of both types declining, except in drug
abusers
Special populations
The acute form affects rapidly growing children,
especially boys.
570
Osteomyelitis
Assessment
History
H Previous injury, surgery, or primary infection
H Sudden, severe pain in the affected bone
H Pain unrelieved by rest and worse with motion
H Related chills, nausea, and malaise
H Refusal to use the affected area
Physical findings
H Tachycardia and fever
H Swelling and restricted movement over the infection
site
H Tenderness and warmth over the infection site
H Persistent pus drainage from an old pocket in a sinus
tract
Test results
Laboratory
H White blood cell count shows leukocytosis.
H Blood culture identifies the pathogen.
H Bone or soft tissue biopsy sample is cultured to identify the pathogen.
Imaging
H X-rays may show bone involvement.
H Bone scans may detect early infection.
imaging can show extent of infection.
Treatment
General
H Decrease internal bone pressure
H Prevent bone necrosis
H Free tissue transfers
H I.V. fluids, as needed
H High-protein diet rich in vitamin C
H Bed rest
H Immobilization of involved bone and joint with a cast
or traction
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Medications
H I.V. antibiotics
H Analgesics
H Intracavitary instillation of antibiotics for open
wounds
Surgery
H Surgical drainage
H Local muscle flaps
H Sequestrectomy
H Amputation for chronic and unrelieved symptoms
Key outcomes
The patient will:
H experience increased comfort and decreased pain
H exhibit adequate fluid volume
H exhibit adequate tissue perfusion and pulses distally
H Control infection.
H Protect the bone from injury.
H Promote and allow adequate time for self-care.
H Encourage activities that promote rest and relaxation.
H With skeletal traction, cover the pin insertion points
with small, dry dressings.

H Provide firm pillows.
H Provide thorough skin care.
H Provide complete cast care.
Monitoring
H Vital signs
H Wound appearance and healing
H Pain control
H Drainage and suctioning equipment
H Sudden malpositioning of the limb
Patient teaching
Be sure to cover:
adverse effects
H techniques for promoting rest and relaxation
H wound site care
H signs of recurring infection
H importance of follow-up examinations.
Discharge planning
H Refer the patient for occupational therapy, as appro-
priate.
H Refer the patient to home care for I.V. antibiotic ther-
apy as appropriate.
Osteomyelitis
571
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Osteoporosis
Overview
Description
H Loss of calcium and phosphate from bones causing
increased vulnerability to fractures

H Primary or secondary to underlying disease
H Types of primary osteoporosis: postmenopausal os-
H Sudden pain associated with bending or lifting
H Back pain (if vertebral collapse occurs)
H Increasing deformity
H Kyphosis
H Loss of height
H Decreased exercise tolerance
H Spontaneous wedge fractures
Complications
H Bone fractures (vertebrae, femoral neck, and distal
teoporosis (type I) and age-associated osteoporosis

(type II)
H Secondary osteoporosis: caused by an identifiable
agent or disease
Assessment
Pathophysiology
History
H The rate of bone resorption accelerates as the rate of
H Postmenopausal patient
H Condition known to cause secondary osteoporosis
H Snapping sound or sudden pain in lower back when
bone formation decelerates.

H Decreased bone mass results and bones become
porous and brittle.
Causes
radius)
bending down to lift something

H Possible slow development of pain (over several
years)

H Prolonged therapy with steroids, heparin, or anti-
H With vertebral collapse, backache and pain radiating
seizure drugs
H Bone immobilization
H Alcoholism
H Malnutrition
H Liver disease
H Malabsorption
H Scurvy
H Hyperthyroidism
H Osteogenesis imperfecta
H Sudecks atrophy (localized in hands and feet, with
recurring attacks)
H Low calcium intake
H Pain aggravated by movement or jarring
Risk factors
H Mild, prolonged negative calcium balance
H Declining gonadal adrenal function
H Female gender
H Increasing age
H Family history
H European descent
H Early menopause
H Cigarette smoking
H Alcoholism
H Breast cancer and chemotherapy
H Faulty protein metabolism (caused by estrogen defi-
around the trunk
Physical findings
H Humped back
H Markedly aged appearance
H Loss of height
H Muscle spasm
H Decreased spinal movement with flexion more limit-
ed than extension
Test results
Laboratory
H Serum calcium, phosphorus, and alkaline levels are
normal.
H Parathyroid hormone level is elevated.
Imaging
H X-ray studies show characteristic degeneration in the
lower thoracolumbar vertebrae.
H Computed tomography scan assesses spinal bone
loss.
H Bone scans show injured or diseased areas.
H Bone biopsy shows thin, porous, but otherwise normal bone.
Other
H Dual or single photon absorptiometry (measurement
of bone mass) shows loss of bone mass.
ciency)
Incidence
H Idiopathic affects children and adults
H Type I (or postmenopausal): affects women ages 51
to 75
H Type II (or senile): most common between ages 70
and 85
572
Osteoporosis
Treatment
General
H Control bone loss
H Prevent additional fractures
H Control pain
H Reduction and immobilization of fractures
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H Diet rich in vitamin D, calcium, and protein

H Physical therapy program of gentle exercise and
activity
H Supportive devices
Medications
H Estrogen
H Sodium fluoride
H Calcium and vitamin D supplements
H Biphosphates, such as alendronate, risedronate, and
H sleeping on a firm mattress

H avoiding excessive bed rest
H use of a back brace, if appropriate
H proper body mechanics
H home safety devices
H diet rich in calcium.
Discharge planning
H Refer the patient for physical and occupational thera-
py, as appropriate.
ibandronate
H Teriparatide
H Strontium ranelate
H Calcitonin
H Analgesics
Surgery
H Open reduction and internal fixation for femur
fractures
Key outcomes
The patient will:
H demonstrate measures to prevent injury
H Encourage careful positioning, ambulation, and pre-
scribed exercises.
H Promote self-care while allowing adequate time.
H Encourage mild exercise.
H Assist with walking.
H Perform passive ROM exercises.
H Promote physical therapy sessions.
H Use safety precautions.
H Apply heat.
Monitoring
H Skin for redness, warmth, and new pain sites
H Height
H Exercise tolerance
H Joint mobility
Patient teaching
Be sure to cover:
adverse effects
H performing monthly breast self-examination while
on estrogen therapy
H need to report vaginal bleeding promptly
H need to report new pain sites immediately
Osteoporosis
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Otitis externa
Overview
Description
H Acute or chronic inflammation of the external ear
canal
H With treatment, usually subsides within 7 days
H Tends to recur and may become chronic
H If severe and chronic, may reflect underlying dia-
betes mellitus, hypothyroidism, or nephritis

H Also known as external otitis and swimmers ear
Pathophysiology
H External ear canal inflammation results from inva-
sion by infecting organisms.
Causes
H Traumatic injury or excessive moisture that predis-
poses canal to infection

H Bacteria (common) and fungi (less common)
H Occasionally, dermatologic conditions, such as seb-
orrhea or psoriasis
Risk factors
H Swimming in contaminated water
H Cleaning ear canal with cotton-tipped applicator,
bobby pin, finger, or other object
Assessment
History
H Repeated exposure to ear trauma, water, use of ear-
phones, or allergic response to hair spray, dye, or

other hair-care products
H Mild to severe ear itching or pain aggravated by jaw
motion, clenching the teeth, opening the mouth, or
chewing
H Fungal otitis externa possibly asymptomatic
Physical findings
H Swollen, inflamed ear canal
H Ear discharge that may be foul-smelling and yellow to
green in color
H Thick red epithelium in canal with chronic otitis
externa
H Increased pain or itching on palpation or manipula-
tion
Test results
Laboratory
H Microscopic examination shows the causative organism.
H Audiometric testing may reveal a partial hearing loss.
H Otoscopy reveals a swollen external ear canal, periauricular lymphadenopathy and, occasionally, regional cellulitis.
H Exposure to dust, hair-care products, or other irri-
tants
H Regular use of earphones, earplugs, or earmuffs
H Chronic drainage from a perforated tympanic mem-
brane
Incidence
H Most common during summer, but can occur any
time of the year
Treatment
General
H Cleaning of debris from canal under direct visualiza-
tion
H With mild, chronic otitis externa, use of specially
fitted earplugs for showering or swimming
Medications
H Swollen, inflamed ear canal

H Mild to severe itching or pain aggravated by jaw
H Analgesics
H Antibiotic drops
H Oral antibiotics if lymphadenopathy present, or if
motion, clenching the teeth, opening the mouth, or

chewing
external ear swollen
Complications
Surgery
H Complete closure of the ear canal

H Significant hearing loss
H Otitis media
H Cellulitis
H Abscesses
H Disfigurement of the pinna
H Lymphadenopathy
H Osteitis
H Septicemia
H Stenosis
H Excision and abscess drainage
574
Otitis externa
Key outcomes
The patient will:
H show no signs or symptoms of infection
H regain hearing function or develop other ways to
communicate.
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Prevention
Preventing otitis externa

H To prevent recurrence, tell the patient to avoid potential
irritants, such as hair-care products and earrings.
H Warn against cleaning the ears with cotton-tipped applicators or other objects.
H Dry ears thoroughly with a towel after swimming,
showering, or bathing.
H Turn head to each side and pull earlobes to help water
run out.
H Use a hair dryer set to the coolest setting and lowest
speed to help dry ears.
H Dont use earplugs.
H Instill alcohol-based over-the-counter ear product according to manufacturers directions.
H Clean and dry the ear gently and thoroughly.
H Use wet soaks on infected skin.
With hearing loss

H Encourage discussion of concerns.
H Reassure the patient that hearing loss from an external ear infection is temporary.
H Face the patient when speaking.
H Enunciate words clearly, slowly, and in a normal
tone.
H Allow adequate time to grasp what was said.
H Alert staff to the communication problem.
Monitoring
H Auditory acuity
H Type and amount of aural drainage
H Complications
Patient teaching
Be sure to cover:
H proper hand washing and daily ear cleaning
H administration of ear drops, ointment, and ear wash
H antibiotics, as prescribed
H recognizing and reporting adverse reactions
H preventing recurrence. (See Preventing otitis externa.)
Otitis externa
575
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Otitis media
Overview
Complications
Description
H Inflammation of the middle ear associated with fluid
accumulation
H Acute, chronic, suppurative, or secretory
Pathophysiology
H The disease process differs with otitis media type.
Suppurative form
H Nasopharyngeal flora reflux through the eustachian
tube and colonize the middle ear.
H Respiratory tract infections, allergic reactions, and
position changes allow reflux of nasopharyngeal flora
through the eustachian tube and colonization in the
middle ear.
Secretory form
H Obstruction of the eustachian tube promotes transudation of sterile serous fluid from blood vessels in
the middle ear membrane.
Causes
H Suppurative otitis media: bacterial infection with
pneumococci, group A beta-hemolytic streptococci,

staphylococci, and gram-negative bacteria
H Chronic suppurative otitis media: inadequate treatment of acute otitis episodes or infection by resistant
strains of bacteria
H Secretory otitis media: viral infection, allergy, or
barotrauma
H Chronic secretory otitis media: adenoidal tissue overgrowth, edema, chronic sinus infection, or inadequate treatment of acute suppurative otitis media
Risk factors
H Young age
H Congenital abnormalities
H Immune deficiency
H Exposure to cigarette smoke
H Family history
H Recent upper respiratory infection
H Allergies
Incidence
H Most common in infants and children
Special populations
Acute otitis media is an emergency in an immunocompromised child.
H Peaks between ages 6 and 24 months
H Subsides after age 3 years
H Most common during winter months
H More common in boys
576
Otitis media
H Severe, deep, throbbing ear pain

H Mild to high fever
H Spontaneous rupture of the tympanic membrane

H Persistent perforation
H Chronic otitis media
H Mastoiditis
H Meningitis
H Cholesteatomas
H Abscesses, septicemia
H Lymphadenopathy, leukocytosis
H Permanent hearing loss and tympanosclerosis
H Vertigo
Assessment
History
H Upper respiratory tract infection
H Allergies
H Severe, deep, throbbing ear pain
H Dizziness
H Nausea, vomiting
Acute secretory otitis media

H Sensation of fullness in the ear
H Popping, crackling, or clicking sounds on swallowing or moving the jaw
H Describes hearing an echo when speaking
Tympanic membrane rupture
H Pain that suddenly stops
H Recent air travel or scuba diving
Physical findings
H Sneezing and coughing with upper respiratory tract
infection
H Mild to high fever
H Painless, purulent discharge in chronic suppurative
otitis media
H Obscured or distorted bony landmarks of the tym-
panic membrane in acute suppurative otitis media

H Tympanic membrane retraction in acute secretory
otitis media
H Clear or amber fluid behind the tympanic membrane
H Blue-black tympanic membrane with hemorrhage
into the middle ear

H Pulsating discharge with tympanic perforation
H Conductive hearing loss (varies with size and type of
tympanic membrane perforation and ossicular destruction)

Chronic otitis media
H Thickening and scarring of tympanic membrane
H Decreased or absent tympanic membrane mobility
H Cholesteatoma
Test results
Laboratory
H Culture and sensitivity tests of exudate show the
causative organism.
H Complete blood count shows leukocytosis.
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Imaging
H X-ray studies demonstrate mastoid involvement.
H Tympanometry detects hearing loss and evaluates the
condition of the middle ear.
H Audiometry shows degree of hearing loss.
H Pneumatic otoscopy may show decreased tympanic
membrane mobility.
ALERT
In adults, unilateral serous otitis media should
always be evaluated for a nasopharyngealobstructing lesion such as carcinoma.
Treatment
General
H In acute secretory otitis media, Valsalvas maneuver
several times per day (may be the only treatment

required)
H Concomitant treatment of the underlying cause
H Elimination of eustachian tube obstruction
Medications
H Antibiotic therapy such as amoxicillin
H Analgesics, such as aspirin or acetaminophen
H Sedatives (small children)
H Nasopharyngeal decongestant therapy
Surgery
H Myringotomy and aspiration of middle ear fluid, fol-
lowed by insertion of a polyethylene tube into the

tympanic membrane
H Myringoplasty
H Tympanoplasty
H Mastoidectomy
H Cholesteatoma excision
H Stapedectomy for otosclerosis
Key outcomes
The patient will:
H exhibit no signs or symptoms of infection
H verbalize understanding of the disorder and treatment regimen
H regain hearing or develop compensatory mechanisms
H experience no injury or harm.
H Encourage discussion of concerns about hearing
loss.
With hearing loss
H Offer reassurance, when appropriate, that hearing
loss caused by serious otitis media is temporary.
H Face the patient when speaking and enunciate clearly
and slowly.
Prevention
Preventing otitis media

For a patient recovering from otitis media at home, instruct the patient or his family to follow these guidelines
to help prevent a recurrence:
H Teach the patient how to recognize upper respiratory
tract infections, and encourage early treatment of
them.
H Instruct parents not to feed an infant in a supine position and not to put him to bed with a bottle. Explain
that doing so could cause reflux of nasopharyngeal
flora.
H If appropriate, teach the patient to promote eustachian
tube patency by performing Valsalvas maneuver several times per day, especially during airplane travel.
H After tympanoplasty, advise the patient not to blow his
nose or get his ear wet when bathing.
H Explain adverse reactions to the prescribed medication,
emphasizing those that require immediate medical attention.
H Allow time for the patient to grasp what was said.

H Alert staff to the patients communication problem.
After myringotomy
H Wash hands before and after ear care.
H Place sterile cotton loosely in the external ear to absorb drainage and prevent infection. Change the cotton when damp. Avoid placing cotton or plugs deep
in ear canal.
H Administer antiemetics after tympanoplasty and reinforce dressings.
Monitoring
H Pain level
H Excessive bleeding or discharge
H Auditory acuity
H Complications
Patient teaching
Be sure to cover:
H proper instillation of ointment, drops, and ear wash,
as ordered
adverse effects
H importance of taking antibiotics
H adequate fluid intake
H correct instillation of nasopharyngeal decongestants
H use of fitted earplugs for swimming after myringotomy and tympanostomy tube insertion
H notification of the physician if tube falls out and for
ear pain, fever, or pus-filled discharge
H preventing recurrence. (See Preventing otitis
media.)
Otitis media
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Otosclerosis
Overview
Description
Test results
H Rinne test result shows bone-conducted tone is
heard longer than air-conducted tone.
H Webers test result shows that sound lateralizes to the
more damaged ear.
H Audiometric testing reveals hearing loss.
H Bone disease that occurs only in the middle ear and
results in an overgrowth of abnormal bone, usually

involving the stapes
H Most common cause of conductive hearing loss
H With surgery, prognosis good
H Also known as hardening of the ear and otospongiosis
Treatment
Pathophysiology
Medications
H Normal bone of otic capsule is gradually replaced
H Sodium fluoride (may prevent further worsening of
with highly vascular spongy bone.

H Spongy bone immobilizes the footplate of the normally mobile stapes.
H Conduction of vibrations from the tympanic membrane to the cochlea is disrupted, and conductive
hearing loss results.
H If the inner ear is involved, sensorineural hearing
loss may develop.
Causes
H Genetic factor transmitted as an autosomal dominant
trait
H Pregnancy (may trigger onset)
Incidence
H Occurs in at least 10% of whites
H Twice as common in females as in males
H Usually occurs between ages 15 and 50
H Slow, progressive hearing loss in one ear, with pro-
gression to both ears, without middle ear infection

H Tinnitus
Complications
H Bilateral conductive hearing loss
H Taste disturbance
Assessment
History
H Family history of hearing loss (excluding presbycu-
sis)
H Tinnitus
H Ability to hear a conversation better in a noisy envi-
ronment than in a quiet one (paracusis of Willis)

H Vertigo, especially after bending over
Physical findings
H Tympanic membrane that appears normal
H Schwartzes sign (faint pink blush throughout the
tympanic membrane from vascularity of active otosclerotic bone)
578
Otosclerosis
General
H Hearing aids
H Avoidance of activities that provoke dizziness
hearing)
Surgery
H Stapedectomy
H Prosthesis insertion to restore partial or total hearing
H Fenestration
H Stapes mobilization
Key outcomes
The patient will:
H show no evidence of infection
H experience no injury or harm
H express needs and feelings
H regain hearing or develop other ways of communicating
H express understanding of illness and treatment.
H Encourage discussion of concerns about hearing
loss.
H Offer reassurance with hearing loss, when appro-
priate.
H Provide clear, concise explanations.
H Face the patient when speaking.
H Enunciate clearly and slowly, in a normal tone.
H Allow adequate time to grasp what was said.
H Alert the staff to communication problem.
After surgery
H Position as ordered.
H Assist with ambulation when indicated.
H Reassure the patient that taste disturbance is common and usually subsides in a few weeks.
Monitoring
H For vertigo
H Hearing loss
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ALERT
Watch for and report postoperative facial drooping,
which may indicate swelling of or around the facial nerve.
Patient teaching
Be sure to cover:
H preoperative and postoperative teaching, if indicated
H slow movement to prevent vertigo
adverse effects
H importance of protecting ears against the cold
H need to avoid activities that provoke dizziness
H avoidance of anyone with an upper respiratory tract
infection
H changing external ear dressing and incision care
H completion of prescribed drug regimen
H need for follow-up care
H how hearing may be masked by packing, dressing,
and postoperative edema
H why hearing may not be noticeably improved for 1 to
4 weeks after surgery
H avoidance of loud noises and sudden pressure
changes until healing is complete
H avoidance of blowing nose for at least 1 week to prevent contaminated air and bacteria from entering the
eustachian tube
H avoidance of sudden movements
H avoidance of wetting head in shower or swimming
for about 6 weeks
H avoidance of getting water in the ear for an additional
4 weeks
H prevention of constipation and avoidance of straining
while defecating.
Discharge planning
H Refer the patient to an audiologist for hearing aids as
appropriate.
H Refer the patient to a speech and language therapist
as needed.
H Refer the patient for lip reading or sign language
instruction as appropriate.
Otosclerosis
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Ovarian cancer
Overview
Description
H Malignancy arising from the ovary; a rapidly pro-
gressing cancer; difficult to diagnose

H Prognosis varying with histologic type and stage
H 90% primary epithelial tumors
H Stromal and germ cell tumors also important tumor
types
Assessment
History
H Symptoms of bloating, pelvic or abdominal pain, dif-
ficulty eating or feeling full quickly, and urinary

symptoms possibly persistent; a change from normal
H May have lack of obvious signs, or signs and symptoms that vary with tumor size and extent of metastasis (disease usually metastasized before diagnosis is
made)
H In later stages: urinary frequency, constipation, pelvic
discomfort, distention, weight loss, abdominal pain
Pathophysiology
Physical findings
H Ovarian cancer spreads rapidly intraperitoneally by
H Gaunt appearance
H Grossly distended abdomen accompanied by ascites
H Palpable abdominal mass with rocky hardness or
local extension or surface seeding and, occasionally,

through the lymphatics and the bloodstream.
H Metastasis to the ovary can occur from breast, colon,
gastric, and pancreatic cancers.
Causes
Risk factors
H Infertility problems or nulliparity
H Celibacy
H Exposure to asbestos and talc
H History of breast or uterine cancer
H Family history of ovarian cancer
H Diet high in saturated fat
H Gene mutation BRCA1 and BRCA2
Incidence
H After lung, breast, and colon cancer, primary ovarian
cancer is the most common cause of cancer death

among females in the United States (about 40% survive for 5 years)
H More common after age 50
H Females in industrialized nations at greater risk
H Metastatic ovarian cancer: more common than
cancer at any other site in females with previously
treated breast cancer
H Bloating
H Pelvic or abdominal pain
H Difficulty eating or feeling full quickly
H Urinary urgency or frequency
Complications
H Fluid and electrolyte imbalance
H Leg edema
H Ascites
H Profound cachexia
H Recurrent malignant effusions
rubbery or cystlike quality
Test results
Laboratory
H Deoxyribonucleic acid testing indicates an inherited
gene mutation.
H Laboratory tumor marker studies (such as ovarian
carcinoma antigen, carcinoembryonic antigen, and
human chorionic gonadotropin) show abnormalities
that may indicate complications.
Imaging
H Abdominal ultrasonography, computed tomography
scan, or X-rays delineate tumor size.
H Aspiration of ascitic fluid can reveal atypical cells.
Other
H Exploratory laparotomy, including lymph node evaluation and tumor resection, is required for accurate
diagnosis and staging.
Treatment
General
H Radiation therapy (not commonly used because it
causes myelosuppression, which limits effectiveness

of chemotherapy)
H Radioisotopes as adjuvant therapy
H High-protein diet
Medications
H Chemotherapy after surgery
H Immunotherapy
H Hormone replacement therapy in prepubertal girls
who had bilateral salpingo-oophorectomy
Surgery
H Total abdominal hysterectomy and bilateral
salpingo-oophorectomy with tumor resection

H Omentectomy, appendectomy, lymph node palpation
with probable lymphadenectomy, tissue biopsies, and

peritoneal washings
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Ovarian cancer
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H Resection of involved ovary

H Biopsies of omentum and uninvolved ovary
H Peritoneal washings for cytologic examination of
pelvic fluid
Key outcomes
The patient will:
H show no further evidence of weight loss
H express feelings about the potential loss
pain
H establish effective coping mechanisms.
H Provide abdominal support, and be alert for abdomi-
nal distention.
Monitoring
H Vital signs
H Intake and output
H Wound site
H Pain control
H Hydration and nutrition status
Patient teaching
Be sure to cover:
H dietary needs
H importance of preventing infection, emphasizing
proper hand-washing technique
adverse effects.
Discharge planning
Ovarian cancer
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Ovarian cysts
Causes
Overview
H Theca-lutein cysts
H Hydatidiform mole
H Choriocarcinoma
H Hormone therapy
H Granulosa-lutein cysts (excessive accumulation of
blood during menstruation)
Description
H Non-neoplastic sacs on an ovary that contain fluid or
semisolid material
H Usually small and nonsymptomatic
H May be single or multiple (polycystic ovary syn-
drome)
H Include follicular cysts, theca-lutein cysts, and corpus luteum cysts
H Can develop any time between puberty and menopause, including during pregnancy
H Excellent prognosis for non-neoplastic ovarian cysts
(The risk for ovarian malignancy isnt increased with
a functional [physiologic] ovarian cyst.)
Pathophysiology
H Follicular cysts are generally very small and arise
from follicles that overdistend, either because they

havent ruptured or have ruptured and resealed before their fluid was reabsorbed. (See Follicular
cyst.)
H Luteal cysts develop if a mature corpus luteum persists abnormally and continues to secrete progesterone. They consist of blood or fluid that accumulates in the cavity of the corpus luteum and are
typically more symptomatic than follicular cysts.
H When luteal cysts persist into menopause, they secrete excessive amounts of estrogen in response to
the hypersecretion of follicle-stimulating hormone
and luteinizing hormone that normally occurs during
menopause.
Follicular cyst
A common type of ovarian cyst, a follicular cyst is usually
semitransparent and overdistended, with watery fluid visible through its thin walls.
Incidence
H Can occur at any age, but occurring more commonly
in females of reproductive age
H Possibly no symptoms (small ovarian cysts such as
follicular cysts)
H Mild pelvic discomfort, lower back pain, dyspareu-
nia, or abnormal uterine bleeding, secondary to a

disturbed ovulatory pattern (large or multiple cysts)
H Acute abdominal pain similar to that of appendicitis
(ovarian cysts with torsion)
H Unilateral pelvic discomfort (from granulosa-lutein
cysts appearing early in pregnancy and growing as
large as 2 to 212 [5 to 6 cm] in diameter)
H Delayed menses, followed by prolonged or irregular
bleeding (granulosa-lutein cysts in nonpregnant females)
Complications
H Torsion or rupture of cyst
H Infertility
H Amenorrhea
H Secondary dysmenorrhea
H Oligomenorrhea
Assessment
History
H Mild pelvic discomfort
H Urinary urgency
H Lower back pain
H Dyspareunia
H Irregular bleeding
Physical findings
H Rigid abdomen
H Enlarged ovaries
Test results
Laboratory
H Human chorionic gonadotropin (HCG) titer is elevated (theca-lutein cyst).
H Urine 17-ketosteroid level is slightly elevated (polycystic ovary syndrome).
Imaging
H Ultrasound reveals cyst.
Other
H Laparoscopy (usually for another condition) reveals
cyst.
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Ovarian cysts
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Treatment
General
H Follicular cysts: no treatment because cysts common-
ly disappear spontaneously within one to two menstrual cycles (excision of persistent cysts to rule out
malignancy)
H Theca-lutein cysts: discontinuation of HCG or
clomiphene citrate therapy
H Ruptured cysts: culdocentesis to drain intraperitoneal fluid
Medications
H Gonadotropin-releasing hormonal agonists, such as
leuprolide and goserelin

H Analgesics
Surgery
H Laparoscopy or exploratory laparotomy with possible
ovarian cystectomy or oophorectomy for persistent

or suspicious ovarian cyst
After surgery
Monitoring
H Signs of rupture
H Vital signs
H Vaginal bleeding
Patient teaching
Be sure to cover:
H perioperative instructions
H need to report increased menstrual bleeding
H need to report abdominal mass.
Ovarian cysts
583
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Pagets disease
Overview
Kyphosis
Asymmetrical bowing of the tibia and femur
Waddling gait
Pathologic fractures
Muscle weakness
Description
Complications
Bone disorder that causes an irregular bone forma-
Fractures
Paraplegia
Blindness and hearing loss with tinnitus and vertigo
Osteoarthritis
Sarcoma
Hypertension
Renal calculi
Hypercalcemia
Gout
Heart failure
tion
Affects one or several skeletal areas (spine, pelvis,
femur, and skull)
Slow and progressive
Causes malignant bone changes in about 5% of
patients
Can be fatal, particularly when associated with heart
failure, bone sarcoma, or giant cell tumors
Also known as osteitis deformans
ALERT
Pagets disease of the breast, a form of breast cancer, is a different disorder than Pagets disease.
(See Pagets disease of the breast.)
Pathophysiology
In the initial phase (osteoclastic phase), excessive
bone resorption occurs.
Assessment
History
Severe, persistent pain
Impaired mobility
Pain that worsens with weight bearing
Increased hat size
Headaches
The second phase (osteoblastic phase) involves
Physical findings
excessive abnormal bone formation.

Affected bones enlarge and soften.
New bone structure is chaotic, fragile, and weak.
Causes
Cranial enlargement over frontal and occipital areas

Kyphosis
Barrel-shaped chest
Asymmetrical bowing of the tibia and femur
Warmth and tenderness over affected sites
Exact cause unknown

Theory: slow or dormant viral infection (possibly
Test results
mumps)
Incidence
More common after age 40
More common in males
More common in people of European, Austrailian,
and New Zealand descent

Familial
Severe, persistent pain
Pain worsened by weight-bearing activities
Cranial enlargement
Barrel-shaped chest
Laboratory
Red blood cell count shows anemia.
Serum alkaline phosphatase level is elevated.
24-hour urine hydroxyproline level is elevated.
Imaging
X-ray studies show bone expansion and increased
bone density.
Bone scans clearly show early pagetic lesions.
Bone biopsy shows a characteristic mosaic pattern of
bone tissue.
Treatment
General
Pagets disease of the breast

Commonly misdiagnosed as a dermatologic problem, this
rare type of breast cancer appears as a red, scaly crust on
the nipple, causing itchiness and burning. Biopsy confirms the diagnosis. Treatment should be started to prevent spread of malignancy to the lymph nodes and other
parts of the body.
584
Pagets disease
Heat therapy
Massage
Well-balanced diet
Activity, as tolerated
Pacing of activities
Use of assistive devices
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Medications
Calcitonin
Nonsteroidal anti-inflammatory drugs
Biphosphonates, such as zoledronic acid,
pamidronate, and edidronate

Calcium supplements
Vitamin D
Surgery
Reduction of pathologic fractures
Correction of secondary deformities
Relief of neurologic impairment
Key outcomes
The patient will:
express feelings of increased comfort and decreased
pain
perform activities of daily living to the extent possible
maintain adequate skin integrity
demonstrate measures to prevent self-injury
maintain joint mobility and range of motion.
Take measures to prevent pressure ulcers.
Instruct the patient with footdrop to wear high-
topped sneakers or use a footboard.
Monitoring
Pain level, response to analgesic therapy
New areas of pain
New movement restrictions
Sensory and motor disturbances
Serum calcium and alkaline phosphatase levels
Intake and output
Patient teaching
Be sure to cover:
the disorder, diagnosis, and treatment
pacing of activities
use of assistive devices
exercise program
use of a firm mattress or a bed board
home safety measures
how to take prescribed drugs
adverse reactions to report.
Discharge planning
Refer the patient to community resource and support
sources, as appropriate.
Refer the patient to physical and occupational
therapy.
Pagets disease
585
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Pancreatic cancer
Overview
Description
Proliferation of cancer cells in the pancreas
Fifth most lethal type of carcinoma
Poor prognosis (most patients die within 1 year of
diagnosis)
Pathophysiology
Pancreatic cancer is almost always adenocarcinoma.
Nearly two-thirds of tumors appear in the head of the
pancreas; islet cell tumors are rare.

Two main tissue types form fibrotic nodes. Cylinder
cells arise in ducts and degenerate into cysts; large,
fatty, granular cells arise in parenchyma.
A high-fat or excessive protein diet induces chronic
hyperplasia of the pancreas, with increased cell
turnover.
Causes
Possible link to inhalation or absorption of carcino-
gens (such as cigarette smoke, excessive fat and protein, food additives, and industrial chemicals), which
the pancreas then excretes
Risk factors
Chronic pancreatitis
Diabetes
Chronic alcohol abuse
Smoking
Occupational exposure to chemicals
Overweight
Incidence
Three to four times more common in smokers than
nonsmokers
Highest in black males ages 35 to 70
Highest in Israel, United States, Sweden, and Canada;
lowest in Switzerland, Belgium, and Italy
Intermittent epigastric pain
Weight loss
Anorexia, nausea, and vomiting
Jaundice
Complications
Nutrient malabsorption
Type 1 diabetes
Liver and GI problems
Mental status changes
Hemorrhage
Pulmonary congestion
Assessment
History
Colicky, dull, or vague intermittent epigastric pain,
which may radiate to the right upper quadrant or

dorsolumbar area; unrelated to posture or activity
and aggravated by meals
Rapid, profound weight loss
Physical findings
Jaundice
Large, palpable, well-defined mass in the subumbili-
cal or left hypochondrial region

Abdominal bruit or pulsation
Test results
Laboratory
Pancreatic enzymes are absent.
Serum bilirubin level is increased.
Serum lipase and amylase levels may be increased.
Thrombin time is prolonged.
Aspartate aminotransferase and alanine aminotransferase levels are elevated if liver cell necrosis is present.
Alkaline phosphatase level is markedly elevated in
biliary obstruction.
Serum insulin level is measureable if islet cell tumor
is present.
Hypoglycemia or hyperglycemia is present.
Specific tumor markers for pancreatic cancer,
including carcinoembryonic antigen, pancreatic
oncofetal antigen, alpha-fetoprotein, and serum
immunoreactive elastase I, are elevated.
Imaging
Barium swallow, retroperitoneal insufflation, cholangiography, and scintigraphy locate the neoplasm and
detect changes in the duodenum or stomach.
Ultrasonography and computed tomography scan
identify masses.
Magnetic resonance imaging discloses tumor location and size.
Angiography reveals tumor vascularity.
Endoscopic retrograde cholangiopancreatography
allows tumor visualization and specimen biopsy.
Percutaneous fine-needle aspiration biopsy may detect tumor cells.
Laparotomy with biopsy allows definitive diagnosis.
Treatment
General
Mainly palliative
May involve radiation therapy as adjunct to fluo-
rouracil chemotherapy
Well-balanced diet, as tolerated
Small, frequent meals
586
Pancreatic cancer
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Postoperative avoidance of lifting and contact sports

After recovery, no activity restrictions
expected postoperative care

information about diabetes, including signs and
Medications
adverse effects of radiation therapy and chemo-
Chemotherapy, such as fluorouracil, gemcitabine,
and erlotinib
Antibiotics
Anticholinergics
Antacids
Diuretics
Insulin
Analgesics
Pancreatic enzymes, such as pancreatin or pancrelipase
symptoms of hypoglycemia and hyperglycemia

therapy.
Discharge planning
Refer the patient to community resource and support
services.
Refer the patient to hospice care, if indicated.
Refer the patient to the American Cancer Society.
Surgery
Total pancreatectomy
Cholecystojejunostomy, choledochoduodenostomy,
and choledochojejunostomy
Gastrojejunostomy
Whipples operation or radical pancreatoduodenec-
tomy
Key outcomes
The patient will:
maintain an adequate weight
maintain normal fluid volume status
maintain skin integrity
verbalize increased comfort and pain relief
avoid injury.
Administer prescribed drugs and blood transfusions.
Provide small, frequent meals.
Ensure adequate rest and sleep.
Assist with range-of-motion and isometric exercises,
as appropriate.
Perform meticulous skin care.
Apply antiembolism stockings.
Encourage verbalization and provide emotional
support.
Monitoring
Fluid balance and nutrition
Abdominal girth, metabolic state, and daily weight
Blood glucose levels
Complete blood count
Pain control
Bleeding
Patient teaching
Be sure to cover:
end-of-life issues
medication administration, dosage, and possible
adverse effects
Pancreatic cancer
587
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Pancreatitis
Overview
Description
Inflammation of the pancreas
Occurs in acute and chronic forms; 10% mortality in
acute form
Atelectasis and pleural effusion

Pneumonia
Paralytic ileus
GI bleeding
Pancreatic abscess and cancer
Pseudocysts
Assessment
Irreversible tissue damage with chronic form, tend-
History
ing to progress to significant pancreatic function loss

Can be idiopathic but sometimes associated with biliary tract disease, alcoholism, trauma, and certain
drugs
Intense epigastric pain centered close to the umbili-
Pathophysiology
Enzymes normally excreted into the duodenum by
the pancreas are activated in the pancreas or its

ducts and start to autodigest pancreatic tissue.
Consequent inflammation causes intense pain, third
spacing of large fluid volumes, pancreatic fat necrosis with consumption of serum calcium and, occasionally, hemorrhage.
Causes
Biliary tract disease
Alcoholism
Abnormal organ structure
Metabolic or endocrine disorders
Pancreatic cysts or tumors
Penetrating peptic ulcers
Penetrating trauma
Viral or bacterial infection
Risk factors
Use of glucocorticoids, sulfonamides, thiazides, and
hormonal contraceptives
Renal failure and kidney transplantation
Endoscopic retrograde cholangiopancreatography
(ERCP)
Heredity
Emotional or neurogenic factors
Incidence
Acute form: 2 of every 10,000 people
Chronic form: 2 of every 25,000 people
Affects more males than females
Affects Blacks four times more than Whites
Intense epigastric pain
History of predisposing factors
Foul-smelling foamy stools
Complications
Diabetes mellitus
Massive hemorrhage
Diabetic acidosis
Shock and coma
588
Pancreatitis
cus and radiating to the back, between the 10th thoracic and 6th lumbar vertebrae
Pain aggravated by fatty foods, alcohol consumption,
or recumbent position
Weight loss with nausea and vomiting
Predisposing factor
Physical findings
Hypotension
Tachycardia
Fever
Dyspnea, orthopnea
Generalized jaundice
Cullens sign (bluish periumbilical discoloration)
Turners sign (bluish flank discoloration)
Steatorrhea (with chronic pancreatitis)
Abdominal tenderness, rigidity, and guarding
Test results
Laboratory
Serum amylase and lipase levels are elevated.
White blood cell count is elevated.
Serum bilirubin level is elevated.
Transient hyperglycemia and glycosuria may occur.
Urinary amylase level is increased.
In chronic pancreatitis: serum alkaline phosphatase,
amylase, and bilirubin levels are elevated; serum glucose level shows transient elevation; and lipid and
trypsin level in stool is elevated.
Imaging
Abdominal and chest X-rays differentiate pancreatitis
from other diseases that cause similar symptoms;
they also detect pleural effusions.
Computed tomography scan and ultrasonography
show increased pancreatic diameter, pancreatic
cysts, and pseudocysts.
ERCP shows pancreatic anatomy, identifies ductal
system abnormalities, and differentiates pancreatitis
from other disorders.
Treatment
General
Emergency treatment of shock, as needed; vigorous
I.V. replacement of fluid, electrolytes, and proteins

Blood transfusions (for hemorrhage)
Nasogastric suctioning
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Nothing by mouth
Once crisis starts to resolve, oral low-fat, low-protein
Discharge planning
Refer the patient to social services, as needed.
feedings implemented gradually

Alcohol and caffeine abstention
Medications
Analgesics
Antacids
Histamine antagonists
Antibiotics as appropriate
Anticholinergics
Total parenteral nutrition
Pancreatic enzymes such as pancrelipase
Insulin
Albumin
Surgery
Not indicated in acute pancreatitis unless complica-
tions occur
For chronic pancreatitis: sphincterotomy
Pancreaticojejunostomy
Key outcomes
The patient will:
maintain normal fluid volume
maintain a patent airway
verbalize feelings of increased comfort
avoid complications
maintain skin integrity
initiate lifestyle changes.
Administer prescribed drugs and I.V. therapy.
Encourage the patient to express his feelings.
Provide emotional support.
Monitoring
Vital signs
Nasogastric tube function and drainage
Respiratory status
Acid-base balance
Serum glucose level
Fluid and electrolyte balance
Daily weight
Pain control
Nutritional status and metabolic requirements
Patient teaching
Be sure to cover:
identification and avoidance of acute pancreatitis
triggers, such as alcohol abuse and smoking
dietary needs
adverse effects.
Pancreatitis
589
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Panic disorder
Overview
Description
Assessment
History
Repeated episodes of unexpected apprehension or
fear
Anxiety in its most severe form, characterized by re-
Physical findings
current episodes of intense apprehension, terror,

and impending doom
May be associated with specific situations or tasks
Commonly exists concurrently with agoraphobia
May be triggered by severe separation anxiety experienced during early childhood
Can persist for years without treatment, with alternating exacerbations and remissions
During a panic attack:
Trembling
Digestive disturbances
Hyperventilation
Tachycardia
Profuse sweating
DSM-IV-TR criteria
biochemistry, especially in norepinephrine, serotonin, and gamma-aminobutyric acid activity

Possibly related to stressful events or unconscious
conflicts that occur early in childhood
Diagnosis of panic disorder is confirmed when the patient meets the following criteria:
recurrent, unexpected panic attacks with at least one
of the attacks having been followed by 1 month (or
more) of one (or more) of the following:
persistent concern about having additional attacks
worry about the attacks implications or consequences
significant change in behavior related to the attack
agoraphobia
attacks not due to the direct physiologic effects of a
substance or a general medical condition
attacks not better accounted for by another mental
disorder, such as social phobia, specific phobia,
obsessive-compulsive disorder, posttraumatic stress
disorder, or separation anxiety.
Risk factors
Test results
Close family member with the disorder
Laboratory
Urine and serum toxicology tests may reveal the presence of psychoactive substances that can precipitate
panic attacks, including barbiturates, caffeine, and
amphetamines.
Other
Various tests may be ordered to rule out an organic
basis for the symptoms.
Pathophysiology
Increased sensitivity to adrenergic central nervous
system discharges occurs, with hypersensitivity of

presynaptic alpha-2 receptors.
Causes
Combination of physiologic and psychological factors
Temporal lobe dysfunction
May develop as a persistent pattern of maladaptive
behavior acquired by learning

Possible contributing factors: alterations in brain
Incidence
Males and females affected equally
Panic disorder with agoraphobia about twice as com-
mon in females than in males

Typical onset in late adolescence or early adulthood,
commonly in response to a sudden loss
Repeated episodes of unexpected apprehension, fear,
and intense discomfort that may last for minutes or

hours and leave the patient shaken, fearful, and exhausted
Attacks that occur several times a week, sometimes
daily
Hyperventilation
Tachycardia
Trembling
Profuse sweating
Digestive disturbances
Chest pain
Complications
Psychoactive substance use disorder
590
Panic disorder
Treatment
General
Behavioral therapy
Supportive psychotherapy
Medications
Antianxiety agents, such as diazepam and lorazepam
Antidepressants such as paroxetine
Buspirone
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Key outcomes
The patient will:
experience reduced anxiety by identifying internal
precipitating situation
identify current stressors
set limits and compromises on behavior when ready
develop effective coping mechanisms.
Stay with the patient until the attack subsides.
Speak in short, simple sentences and slowly give one
direction at a time. Avoid giving lengthy explanations

and asking too many questions.
Administer prescribed drugs.
Monitoring
Response to therapy
Vital signs during an attack
Patient teaching
Be sure to cover:
relaxation techniques such as focusing on slow, deep
breathing
adverse effects
the importance of follow-up care.
Discharge planning
Encourage the patient and his family to use commu-
nity resources such as the Anxiety Disorders Association of America.
Panic disorder
591
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Parkinsons disease
Overview
Excessive sweating
Decreased GI motility
Orthostatic hypotension
Oily skin
Eyes fixed upward
Description
Complications
Brain disorder causing progressive deterioration,
Injury from falls

Food aspiration
Urinary tract infections
Skin breakdown
with muscle rigidity, akinesia, and involuntary

tremors
Usual cause of death: aspiration pneumonia
One of the most common crippling diseases in the
United States
Pathophysiology
Assessment
Dopaminergic neurons degenerate, causing loss of
History
available dopamine.
Dopamine deficiency prevents affected brain cells
from performing their normal inhibitory function.
Excess excitatory acetylcholine occurs at synapses.
Nondopaminergic receptors are also involved.
Motor neurons are depressed. (See Understanding
Parkinsons disease.)
Muscle rigidity
Akinesia
Insidious (unilateral pill-roll) tremor, which increas-
Causes
Usually unknown
Exposure to such toxins as manganese dust and car-
bon monoxide
Type A encephalitis
Drug-induced (Haldol, methyldopa, reserpine)
Risk factors
Heredity
Expose to pesticides and herbicides
Reduced estrogen levels
Incidence
More common in males than females
Occurs in middle age or later
Rare in blacks
Muscle rigidity
Tremor
Resistance to passive muscle stretching
Akinesia
High-pitched, monotonous voice
Drooling
Loss of posture control
Dysarthria
Understanding Parkinsons disease

Research on the pathogenesis of Parkinsons disease focuses on damage to the substantia nigra from oxidative
stress. Oxidative stress is believed to:
alter the brains iron content
impair mitochondrial function
alter antioxidant and protective systems
reduce glutathione
damage lipids, proteins, and deoxyribonucleic acid.
592
Parkinsons disease
es during stress or anxiety and decreases with purposeful movement and sleep
Dysphagia
Fatigue with activities of daily living (ADLs)
Muscle cramps of legs, neck, and trunk
Oily skin
Increased perspiration
Insomnia
Mood changes
Dysarthria
Physical findings
High-pitched, monotonous voice
Drooling
Masklike facial expression
Difficulty walking
Lack of parallel motion in gait
Loss of posture control with walking
Oculogyric crises (eyes fixed upward, with involun-
tary tonic movements)

Muscle rigidity causing resistance to passive muscle
stretching
Difficulty pivoting
Loss of balance
Test results
Imaging
Computed tomography scan or magnetic resonance
imaging rules out other disorders such as intracranial tumors.
Treatment
General
High-bulk foods
Physical therapy and occupational therapy
Assistive devices to aid ambulation
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Medications
Levodopa and carbidopa
Anticholinergics such as trihexyphenidyl
Antihistamines such as diphenhydramine
Antiviral agents such as amantadine
Tricyclic antidepressants
Dopamine agonist, such as bromocriptine, apomor-
phine, and pramipexole

Coenzyme Q10
Catechol-O-methyltransferase inhibitors such as tolcapone
household safety measures

importance of daily bathing
methods to improve communication
swallowing therapy regimen (aspiration precau-
tions).
Discharge planning
Refer the patient for occupational and physical reha-
bilitation, as indicated.
Surgery
Used when drug therapy fails
Stereotaxic neurosurgery
Destruction of ventrolateral nucleus of thalamus
Key outcomes
The patient will:
perform ADLs
avoid injury
maintain adequate caloric intake
express positive feelings about himself
develop adequate coping behaviors
seek support resources.
Take measures to prevent aspiration.
Protect the patient from injury.
Stress the importance of rest periods between
activities.
Ensure adequate nutrition.
Provide frequent warm baths and massage.
Encourage the patient to enroll in a physical therapy
program.
Provide emotional and psychological support.
Encourage the patient to be independent.
Assist with ambulation and range-of-motion
exercises.
Monitoring
Vital signs
Intake and output
Drug therapy
Adverse reactions to medications
Postoperatively: signs of hemorrhage and increased
intracranial pressure
Swallowing
Patient teaching
Be sure to cover:
adverse effects
measures to prevent pressure ulcers and contractures
Parkinsons disease
593
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Patent ductus arteriosus

Overview
Description
Heart condition in which the lumen of the ductus (fe-
tal blood vessel that connects the pulmonary artery to

the descending aorta) remains open after birth
Initially may produce no clinical effects, but in time
can precipitate pulmonary vascular disease, causing
symptoms to appear by age 40
Good prognosis if the shunt is small or surgical repair is effective; otherwise, may advance to intractable heart failure, possibly fatal
Pathophysiology
Respiratory distress
Assessment
History
Prematurity
Rubella
Difficulty breathing
Physical findings
Gibson murmur during systole and diastole
Thrill at the left sternal border
Prominent left ventricular impulse
Bounding peripheral arterial pulses (Corrigans
pulse)
Widened pulse pressure
The lumen of the ductus remains open after birth
Test results
and creates a left-to-right shunt of blood from the

aorta to the pulmonary artery, resulting in recirculation of arterial blood through the lungs.
Prevalent in premature neonates, probably as a result
of abnormalities in oxygenation or the relaxant action of prostaglandin E, which prevents ductal spasm
and contracture necessary for closure.
Imaging
Chest X-rays may show increased pulmonary vascular
markings, prominent pulmonary arteries, and enlargement of the left ventricle and aorta.
Echocardiography detects and helps estimate the size
of a patent ductus arteriosus (PDA). It also reveals
an enlarged left atrium and left ventricle or right ventricular hypertrophy from pulmonary vascular disease.
Electrocardiogram may be normal or may indicate
left atrial or ventricular hypertrophy and, in pulmonary vascular disease, biventricular hypertrophy.
Cardiac catheterization shows pulmonary arterial
oxygen content higher than right ventricular content
due to the influx of aortic blood.
Causes
May be a combination of genetics and environmental
factors
Prematurity
Rubella syndrome
Associated with other congenital defects, such as
coarctation of the aorta, ventricular septal defect,

and pulmonary and aortic stenoses
Risk factors
Poorly controlled maternal diabetes
Drug or alcohol use during pregnancy
Exposure to chemicals or radiation during pregnancy
Incidence
Twice as common in females than in males
The most common congenital heart defect found in
adults
Infants
Signs and symptoms of heart failure
Heightened susceptibility to respiratory tract infections
Slow motor development
Failure to thrive
Adults
Pulmonary vascular disease
Fatigability and dyspnea on exertion
Complications
Chronic pulmonary hypertension
Intractable left-sided heart failure
594
Treatment
General
No immediate treatment (if asymptomatic)
Fluid restriction
Medications
Diuretics
Cardiac glycosides
Antibiotics (preoperatively)
Nonsteroidal anti-inflammatory drugs such as
ibuprofen for premature neonates
Surgery
Ligation of the ductus
Special populations
If symptoms are mild, surgical correction is usually
delayed until at least age 1. Before surgery, children
with PDA require antibiotics to protect against infective endocarditis.
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Cardiac catheterization to deposit a plug in the duc-
tus to stop shunting or for administration of indomethacin I.V. (a prostaglandin inhibitor that is an
alternative to surgery in premature neonates) to induce ductus spasm and closure
Key outcomes
The patient will:
maintain adequate ventilation
maintain hemodynamic stability
remain free from signs and symptoms of infection
utilize support groups to help cope effectively.
Provide emotional support to the patient and family.
Monitoring
Respiratory status
Vital signs
Cardiac rhythm
Intake and output
Patient teaching
Be sure to cover:
activity restrictions based on the childs tolerance
and energy levels
importance of informing any physician who treats the
child about his history of surgery for PDA even if
the child is being treated for an unrelated medical
problem.
Discharge planning
Stress the need for regular medical follow-up exami-
nations.
Refer the patient to community resources and social
services.
595
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Pediculosis
Overview
Description
Infestation of human parasitic lice, which feed exclu-
sively on human blood and lay eggs (nits) on body

hairs or clothing fibers; after nits hatch, lice must
feed within 24 hours or die (see Types of lice)
Pediculosis capitis (head lice): confined to scalp
and, occasionally, eyebrows, eyelashes, and beard
Pediculosis corporis (body lice): found next to skin
in clothing seams; move to the host only to feed on
blood
Pediculosis pubis (crab lice): found primarily in pubic hairs; may extend to eyebrows, eyelashes, and axillary or body hair
Pathophysiology
Nits
Pruritus
Skin excoriation
Complications
Skin excoriation
Secondary bacterial infections
Hyperpigmentation or residual scarring
Assessment
History
Exposure to causative organism
Headache
Fever
Malaise
Pruritus
Cutaneous changes
Lice crawl and attach superficially to the epidermis
Physical findings
and hair. One female louse deposits approximately

60 to 150 nits to hair shafts. Nits survive by ingesting
blood from the human host.
A louse bite injects a toxin into the skin. Mild irritation and a purpuric spot result.
Repeated bites cause sensitization to the toxin, leading to more serious inflammation. In severe cases,
sensitization causes wheals or a rash on the trunk.
Scratching may result in secondary bacterial infection.
Pediculosis capitis
Visible lice
Skin excoriation on the scalp and neck
Matted, lusterless hair (in severe cases)
Occipital and cervical lymphadenopathy
Oval, gray-white nits visible on hair shafts
Pediculosis corporis
Red papules or macules, usually on the shoulders,
trunk, or buttocks
Excoriations from scratching
Nits on clothing seams
Pediculosis pubis
Visible brownish-gray lice
Erythematous papules
Small macules on the thighs, buttocks, or lower abdomen
Coarse, grainy-feeling, white-gray nits attached to
pubic hairs
Causes
Pediculosis capitis
Pediculus humanus var. capitis, P. humanus var.
corporis
Spreads through shared clothing, hats, combs, and
hairbrushes
P. humanus var. corporis
Spreads through shared clothing and bedding, especially with environmental overcrowding, prolonged
wearing of same clothing, or poor personal hygiene
Pediculosis pubis
Phthirus pubis
Spreads through sexual intercourse or contact with
clothing, bedding, or towels harboring lice
Incidence
Pediculosis capitis
More common in children
More common in girls
More common in warmer months
More common in Whites and Asians, less common in
Blacks
Pediculosis pubis
More common in adults
More common in cooler months
596
Pediculosis
Test results
Direct inspection with hand lens shows visible lice or
nits.
Woods light examination shows fluorescence of live
nits (dead nits dont fluoresce).
Treatment
General
Use of fine-toothed comb dipped in vinegar
Hair-washing with ordinary shampoo
Laundering of potentially contaminated clothing and
bed linen
Bathing with soap and water
Petroleum jelly applied to eyebrows or eyelashes
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Types of lice
Head louse
Body louse
Pubic louse
Pediculus humanus var. capitis (head

louse) resembles P. humanus var. corporis (body louse).
Pediculus humanus var. corporis

(body louse) has a long abdomen, and
its legs are all about the same length.
Phthirus pubis (pubic, or crab, louse)

is slightly translucent. Its first set of
legs is shorter than its second and
third sets.
Medications
Monitoring
Pediculosis capitis
Permethrin or pyrethrins
Pediculicide cream (for severe infestation)
Pediculosis pubis
Pediculicide shampoo
Adverse reactions to insecticide treatment

Complications
Response to treatment
Be sure to cover:
how to inspect for lice, eggs, and lesions
how to decontaminate infestation sources
how to apply insecticidal agents
removal of nits and lice
importance of not sharing personal articles
adverse reactions to treatment, including when to notify the physician
notification and treatment of sexual contacts within
previous 30 days.
Key outcomes
The patient will:
exhibit resolution of the infestation
report feelings of increased comfort
demonstrate understanding of the treatment regimen
verbalize feelings about changed body image.
Patient teaching

Use personal protective equipment when administer-
ing delousing treatment.

Notify the school if infestation occurs in a child.
Encourage the patient to express feelings about the
infestation.
Pediculosis
597
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Pelvic inflammatory
disease
Overview
Description
Umbrella term referring to any acute, subacute, re-
current, or chronic infection of the oviducts and

ovaries, with adjacent tissue involvement
Includes inflammation of the cervix (cervicitis),
uterus (endometritis), fallopian tubes (salpingitis),
and ovaries (oophoritis)
Possible extension of the inflammation to connective
tissue lying between the broad ligaments (parametritis)
Commonly called PID
Pathophysiology
Various conditions, procedures, or instrumentation
can alter or destroy the cervical mucus, which normally serves as a protective barrier.
As a result, bacteria enter the uterine cavity, causing
inflammation of various structures.
Causes
Aerobic or anaerobic organisms (commonly, over-
growth of one or more of the bacterial species found

in the cervical mucus)
Sexually transmitted infections (Neisseria gonorrhoeae and Chlamydia trachomatis)
Septicemia
Infected drainage from a chronically infected fallopian tube
Ruptured appendix
Diverticulitis of the sigmoid colon
Pelvic abscess
Use of intrauterine device
Risk factors
Multiple sex partners
Conditions or procedures that alter or destroy cervi-
cal mucus
Procedures that risk transfer of contaminated cervi-
cal mucus into the endometrial cavity by an instrument

Infection during or after pregnancy
Cigarette smoking
Multiparity
Douching
Intercourse during menses
Therapeutic abortion
Incidence
Primarily affects females ages 16 to 40
598
Pelvic inflammatory disease
Special populations
Adolescents are at high risk for sexually transmitted diseases, including PID.
Profuse, purulent vaginal discharge
Lower abdominal pain
Vaginal bleeding
Complications
Septicemia (potentially fatal)
Pulmonary embolism
Infertility
Peritonitis
Shock
Death
Ectopic pregnancy
Assessment
History
Profuse, purulent vaginal discharge
Low-grade fever
Malaise
Lower abdominal pain
Vaginal bleeding
Physical findings
Pain with cervical movement or adnexal palpation
Vaginal discharge
Unilaterally or bilaterally tender adnexal mass
Test results
Laboratory
Culture and sensitivity and Gram stain of endocervix
or cul-de-sac secretions show the causative agent.
Urethral and rectal secretions show the causative
agent.
C-reactive protein level is elevated.
Imaging
Transvaginal ultrasonography may show the presence
of thickened, fluid-filled fallopian tubes.
Computed tomography scan may show complex tuboovarian abscesses and is useful in diagnosing PID.
Magnetic resonance imaging provides images of soft
tissue; useful not only for establishing the diagnosis
of PID but also for detecting other processes responsible for symptoms.
Culdocentesis obtains peritoneal fluid or pus for culture and sensitivity testing.
Diagnostic laparoscopy identifies cul-de-sac fluid,
tubal distention, and masses in pelvic abscess.
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Prevention
Treatment
General
Frequent perineal care if vaginal discharge occurs
Bed rest
Medications
Antibiotics
Analgesics
I.V. fluids, as needed
Surgery
Drainage of pelvic abscess
Preventing PID
Pelvic inflammatory disease (PID) can be prevented by
following these guidelines:
Use latex condoms.
Have yearly tests for Chlamydia done for sexually
active females with multiple sex partners.
Abstain from sexual intercourse.
Have partners tested and treated for sexually
transmitted diseases (STDs).
See a physician as soon as symptoms of PID or STD
appear.
Avoid multiple sex partners.
Avoid douching.
ALERT
A ruptured pelvic abscess is a life-threatening condition. The patient may need a total abdominal hysterectomy with bilateral salpingo-oophorectomy.
causes of PID, such as dyspareunia and sexual activ-
ity
signs and symptoms of infection after a minor gyne-
cologic procedure
Key outcomes
The patient will:
express feelings of increased comfort
remain free from signs or symptoms of infection
exhibit stable vital signs
maintain fluid balance
express feelings about having PID.
Administer prescribed antibiotics and analgesics.
Provide frequent perineal care.
Use meticulous hand-washing technique.
Encourage the patient to discuss her feelings, and of-
ALERT
Tell the patient to immediately report fever, increased vaginal discharge, or pain especially
after a minor gynecologic procedure.
avoidance of douching or intercourse for at least 7
days after a minor gynecologic procedure.
Discharge planning
Refer the patient to infertility counseling, if indicated.
Refer the patient to a smoking-cessation program, if
indicated.
fer emotional support.

Help the patient develop effective coping strategies.
Monitoring
Vital signs
Fluid intake and output
Signs and symptoms of dehydration
Vaginal discharge
Pain control
ALERT
Watch for and report abdominal rigidity and distention. These signs may indicate development of
peritonitis.
Patient teaching
Be sure to cover:
ways to prevent a recurrence (see Preventing PID)
Pelvic inflammatory disease
599
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Peptic ulcer
Overview
Description
Circumscribed lesion in the mucosal membrane of
the lower esophagus, stomach, duodenum, or jejunum

Occurs in two major forms: duodenal ulcer and gastric ulcer (both forms chronic)
Duodenal ulcers: represent about 80% of peptic ulcers; affect the proximal part of the small intestine
and follow a chronic course characterized by remissions and exacerbations (about 5% to 10% of patients with duodenal ulcers developing complications
that necessitate surgery)
Pathophysiology
Helicobacter pylori releases a toxin that promotes
mucosal inflammation and ulceration.

In a peptic ulcer resulting from H. pylori, acid isnt
the dominant cause of bacterial infection but contributes to the consequences.

Ulceration stems from inhibition of prostaglandin
synthesis, increased gastric acid and pepsin secretion, reduced gastric mucosal blood flow, or decreased cytoprotective mucus production.
Complications
GI hemorrhage
Abdominal or intestinal infarction
Ulcer penetration into attached structures
Assessment
History
Periods of symptom exacerbation and remission,
with remissions lasting longer than exacerbations

History of predisposing factor
Left epigastric pain described as heartburn or indi-
gestion, accompanied by feeling of fullness or distention

Gastric ulcer
Recent weight or appetite loss
Nausea or vomiting
Pain triggered or worsened by eating
Duodenal ulcer
Pain relieved by eating; may occur 112 to 3 hours after food intake
Pain that awakens the patient from sleep
Weight gain
Physical findings
Pallor
Epigastric tenderness
Hyperactive bowel sounds
Causes
Test results
H. pylori
Use of nonsteroidal anti-inflammatory drugs
Laboratory
Complete blood count shows anemia.
Occult blood is present in stools.
Venous blood sample shows H. pylori antibodies.
Urea breath test shows low levels of exhaled carbon
13 (13C).
Fasting serum gastrin level rules out Zollinger-Ellison
syndrome.
Imaging
Barium swallow or upper GI and small-bowel series
may reveal the ulcer.
Upper GI tract X-rays reveal mucosal abnormalities.
Upper GI endoscopy or esophagogastroduodenoscopy confirm the ulcer and permit cytologic
studies and biopsy to rule out H. pylori or cancer.
Gastric secretory studies show hyperchlorhydria.
(NSAIDs) or glucocorticoids
Pathologic hypersecretory states
Risk factors
Type A blood (for gastric ulcer)
Type O blood (for duodenal ulcer)
Other genetic factors
Exposure to irritants
Cigarette smoking
Trauma
Psychogenic factors and stress
Normal aging
Excessive alcohol consumption
Incidence
Gastric ulcers: most common in middle-aged and el-
derly males, especially those who are poor and undernourished; prevalence higher in chronic users
of aspirin or alcohol
Duodenal ulcers: most common in males ages 20
to 50
Left epigastric or abdominal pain with exacerbations
and remissions
History of predisposing factor
600
Peptic ulcer
Treatment
General
Symptomatic
Iced saline lavage, possibly containing norepineph-
rine
Laser or cautery during endoscopy
Stress reduction
Smoking cessation
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Avoidance of dietary irritants

Nothing by mouth if GI bleeding evident
Medications
For H. pylori
Amoxicillin and biaxin
Proton pump inhibitors, such as omeprazole and
lansoprazole
For gastric or duodenal ulcer
Proton pump inhibitors
Antacids
Histamine-receptor antagonists or gastric acid pump
inhibitor, such as cimetidine and famotidine
Coating agents (for duodenal ulcer) such as sucralfate
Sedatives and tranquilizers (for gastric ulcer)
Anticholinergics such as dicyclomine (for duodenal
ulcers; usually contraindicated in gastric ulcers)
Prostaglandin analogs such as misoprostol
Patient teaching
Be sure to cover:
adverse effects
warnings against over-the-counter medications, especially aspirin, aspirin-containing products, and
NSAIDs, unless the physician approves
warnings against caffeine and alcohol intake during
exacerbations
appropriate lifestyle changes
dietary modifications.
Discharge planning
indicated.
Surgery
Indicated for perforation, lack of response to conser-
vative treatment, suspected cancer, or other complications

Type varies with ulcer location and extent; major
operations: bilateral vagotomy, pyloroplasty, and
gastrectomy
Key outcomes
The patient will:
maintain adequate fluid volume
verbalize an understanding of the illness
comply with the treatment regimen.
Provide six small meals or small hourly meals, as
ordered.
Offer emotional support.
Monitoring
Medication effects
Vital signs
Signs and symptoms of bleeding
Pain control
If patient had surgery

Nasogastric tube function and drainage
Bowel function
Fluid and nutritional status
Wound site
Signs and symptoms of metabolic alkalosis or perforation
Peptic ulcer
601
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Perforated eardrum
Overview
Description
Rupture of the tympanic membrane
May cause hearing loss
Typically heals spontaneously
Pathophysiology
Pressure on the tympanic membrane causes a trau-
Perforated tympanic membrane seen on otoscopic
examination
Test results
Laboratory
Ear drainage culture identifies causative organism or
determines if an infection caused the rupture.
Imaging
Skull and temporal lobe X-rays may reveal an associated fracture, especially when a bad fall caused the
eardrum rupture.
Audiometric testing evaluates middle ear function.
matic opening that allows release of pressure.

The rupture may be central or marginal.
The hole exposes the middle and inner ear to dam-
age or infection.
Causes
Bacterial infection (acute or chronic suppurative
otitis media)
Treatment
General
May heal spontaneously
No dietary restrictions unless nausea occurs; in that
case, clear liquids until nausea passes
Trauma
Puncture
Skull fracture
Burns
Excessive change in pressure
Safety precautions if the patient has vertigo
Incidence
Surgery
More common in children
Myringoplasty
Tympanoplasty
Ear pain
Ear discharge
Vertigo (may be transient)
Tinnitus
Hearing loss
Fever or chills
Nausea or vomiting
Complications
Mastoiditis
Meningitis
Permanent hearing loss
Assessment
History
Mild or severe ear trauma
Recent airline flight during an upper respiratory in-
fection
Sudden onset of severe earache and bleeding
from ear
Hearing loss
Tinnitus
Vertigo
Physical findings
Signs of hearing loss
Outer ear drainage
602
Perforated eardrum
Medications
Analgesics such as acetaminophen
Antibiotics if perforation resulted from infection
Key outcomes
The patient (or parents) will:
express an understanding of hearing changes
demonstrate appropriate use of pain relief methods
express an understanding of the potential causes of
ear injury
remain free from infection.
Insert a sterile wick.
When talking, face the patient and speak distinctly
and slowly.
Monitoring
Hearing ability
Ear drainage
Safety
Signs of complications
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Patient teaching
Be sure to cover:
importance of avoiding swimming or use of ear plugs
care during hair washing
the need to complete the course of antibiotic therapy
as prescribed.
use of safety equipment in the workplace and at
home to prevent injury to the ear
prevention techniques. (See Preventing a perforated
eardrum.)
Prevention
Preventing a perforated eardrum

A perforated eardrum can be prevented by following these
guidelines:
Avoid irrigating the ear or cleaning the middle ear canal
with a cotton-tipped applicator.
Dont insert a foreign object into the ear.
Treat ear infections promptly.
Use safety equipment in the workplace and at home to
prevent ear injury.
Prevent ear popping from excess pressure during flight
by chewing gum during ascent and descent.
Dont fly or scuba dive with a cold or active allergies.
Protect ears from loud noises.
Perforated eardrum
603
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Pericarditis
Overview
Description
Complications
Pericardial effusion
Cardiac tamponade
Assessment
Inflammation of the pericardium the fibroserous
History
sac that envelops, supports, and protects the heart

Occurs in acute and chronic forms
Acute form: can be fibrinous or effusive; characterized by serous, purulent, or hemorrhagic exudate
Chronic form: characterized by dense fibrous pericardial thickening
Chronic form called constrictive pericarditis
Delayed form known as Dresslers syndrome: May
occur weeks after heart attack or heart surgery
Predisposing factor
Sharp, sudden pain, usually starting over the sternum
Pathophysiology
Pericardial tissue is damaged by bacteria or other
substance that releases chemical mediators of inflammation into surrounding tissue.

Friction occurs as the inflamed layers rub against
each other.
Chemical mediators dilate blood vessels and increase
vessel permeability.
Vessel walls leak fluids and proteins, causing extracellular edema.
Dresslers syndrome may be caused by autoimmune
response.
Causes
Bacterial, fungal, or viral infection (in infectious
pericarditis)
Neoplasms (primary or metastatic)
High-dose chest radiation
Uremia
Hypersensitivity or autoimmune disease
Drugs, such as hydralazine or procainamide
Idiopathic factors
Myocardial infarction (MI)
Chest trauma
Aortic aneurysm with pericardial leakage
Myxedema with cholesterol deposits in pericardium
Radiation
Rheumatologic conditions
Tuberculosis
Incidence
Affects males more than females
Most common in males ages 20 to 50
Pericardial friction rub
Chest pain
Breathing difficulty in a supine position
Fatigue
Dry cough
Abdominal or leg swelling
604
Pericarditis
and radiating to the neck, shoulders, back, and arms

Pleuritic pain, increasing with deep inspiration and de-
creasing when the patient sits up and leans forward

Dyspnea
Chest pain (may mimic MI pain)
Physical findings
Pericardial friction rub
Diminished apical impulse
Fluid retention, ascites, hepatomegaly (resembling
those of chronic right-sided heart failure)

With pericardial effusion: tachycardia
With cardiac tamponade: pallor, clammy skin, hypo-
tension, pulsus paradoxus, jugular vein distention,

and dyspnea
Test results
Laboratory
White blood cell count is elevated, especially in infectious pericarditis.
Erythrocyte sedimentation rate is elevated.
Serum CK-MB levels are slightly elevated with associated myocarditis.
Pericardial fluid culture may identify a causative organism in bacterial or fungal pericarditis.
Blood urea nitrogen level is elevated in uremia.
Elevated antistreptolysin-O titers may indicate
rheumatic fever.
Positive reaction in purified protein derivative skin
test indicates tuberculosis.
Imaging
Echocardiography showing an echo-free space between the ventricular wall and the pericardium indicates pericardial effusion.
High-resolution computed tomography scan and
magnetic resonance imaging reveals pericardial
thickness.
Electrocardiography shows initial ST-segment elevation across the precordium.
Treatment
General
Management of rheumatic fever, uremia, tuberculo-
sis, or other underlying disorder

Dietary restrictions based on underlying disorder
Bed rest as long as fever and pain persist
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Medications
Discharge planning

Corticosteroids
Refer the patient to home care or social services, as
needed.
Surgery
Surgical drainage
Pericardiocentesis
Partial pericardectomy (for recurrent pericarditis)
Total pericardectomy (for constrictive pericarditis)
Key outcomes
The patient will:
maintain hemodynamic stability and adequate cardiac output
avoid arrhythmias
verbalize feelings of increased comfort and decreased pain.
Administer prescribed analgesics and oxygen.
Administer prescribed antibiotics on time.
Stress the importance of bed rest. Provide a bedside
commode.
Place the patient upright to relieve dyspnea and chest
pain.
ALERT
Keep a pericardiocentesis set readily available
whenever you suspect pericardial effusion.
Encourage the patient to express concerns about the
effects of activity restrictions on responsibilities and

routines.
Review the patients allergy history.
Provide appropriate postoperative care.
Monitoring
Vital signs
Heart rhythm
Heart sounds
Hemodynamic values
Patient teaching
Be sure to cover:
the disorder, diagnosis, and treatments
how to perform deep-breathing and coughing exercises
the need to resume daily activities slowly and to
schedule rest periods in daily routine, as instructed
by the physician.
Pericarditis
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Peritonitis
Overview
Description
Inflammation of the peritoneum; may extend
throughout the peritoneum or localize as an abscess

Commonly decreases intestinal motility and causes
intestinal distention with gas

Fatal in 10% of cases, with bowel obstruction the
usual cause of death
Can be acute or chronic
Pathophysiology
Bacteria invade the peritoneum after inflammation
and perforation of the GI tract.

Fluid containing protein and electrolytes accumulates
in the peritoneal cavity; normally transparent, the

peritoneum becomes opaque, red, inflamed, and
edematous.
Infection may localize as an abscess rather than disseminate as a generalized infection.
Causes
Bacterial or chemical inflammation
Risk factors
Peritoneal dialysis
History of peritonitis
GI tract perforation (from appendicitis, diverticulitis,
peptic ulcer, or ulcerative colitis)

Ruptured ectopic pregnancy
Incidence
With progression
Increasingly severe and constant abdominal pain that
increases with movement and respirations
Possible referral of pain to shoulder or thoracic area
Inability to pass stools and flatus
Hiccups
Physical findings
Fever
Tachycardia
Hypotension
Shallow breathing
Signs of dehydration
Positive bowel sounds (early); absent bowel sounds
(later)
Abdominal rigidity
General abdominal tenderness
Rebound tenderness
Typical patient positioning: lying very still with knees
flexed
Test results
Laboratory
Complete blood count shows leukocytosis.
Imaging
Abdominal X-rays show edematous and gaseous distention of the small and large bowel. With perforation of a visceral organ, X-rays show air in the abdominal cavity.
Chest X-rays may reveal elevation of the diaphragm.
Computed tomography scan reveals fluid and inflammation.
Paracentesis shows the exudates nature and permits
bacterial culture testing.
More common in males
Treatment
Abdominal pain
Fever
Rebound tenderness
General
Complications
Abscess
Septicemia
Respiratory compromise
Bowel obstruction
Shock
I.V. fluids
Nasogastric (NG) intubation
Nothing by mouth until bowel function returns
Gradual increase in diet
Parenteral nutrition, if necessary
Bed rest until condition improves
Semi-Fowlers position
Avoidance of lifting for at least 6 weeks postopera-
tively
Assessment
Medications
History
Antibiotics, depending on infecting organism

Electrolyte replacement
Analgesics
Early phase
Vague, generalized abdominal pain
If localized: pain over a specific area (usually the inflammation site)
If generalized: diffuse pain over the abdomen
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Peritonitis
Surgery
Treatment of choice; procedure varies with the cause
of peritonitis
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Key outcomes
The patient will:
regain normal vital signs
show no signs or symptoms of infection.
Encourage early postoperative ambulation.
Monitoring
Pain control
Vital signs
NG tube function and drainage
Bowel function
Wound site
Signs and symptoms of dehiscence
ALERT
Watch for signs and symptoms of abscess formation, including persistent abdominal tenderness
and fever.
Patient teaching
Be sure to cover:
preoperatively, coughing and deep-breathing techniques
postoperative care procedures
signs and symptoms of infection
proper wound care
adverse effects
dietary and activity limitations (depending on type of
surgery).
Discharge planning
Refer the patient to home care services as needed.
Peritonitis
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Pertussis
Overview
Risk factors
Incomplete immunization
Incidence
50% of cases seen in underimmunized children
younger than age 1
Description
Commonly occurs in schools, nursing homes, and
Highly contagious respiratory infection

Typically causes an irritating cough that becomes
Epidemics occurring every 3 to 5 years without sea-
paroxysmal and ends in a high-pitched, inspiratory

whoop
Follows a 6- to 8-week course that includes three
2-week stages with varying symptoms
Also called whooping cough
residential facilities
sonal variation
ysmal coughing, which enhances disease transmission.

Various toxins produced during the infection impair
local defenses and cause local tissue damage. Toxins
may cause direct central nervous system injury.
Catarrhal (first) stage

Hacking nocturnal cough
Anorexia
Sneezing, lacrimation, and rhinorrhea
Paroxysmal (second) stage
Spasmodic, recurrent coughing (usually at night)
with tenacious mucus; cough typically ends in a loud,
crowing, inspiratory whoop
Vomiting if the patient chokes on mucus
Convalescent (third) stage
Gradual subsidence of paroxysmal coughing and
vomiting
Causes
Complications
Nonmotile, gram-negative coccobacillus B. pertussis;
Increased venous pressure

Anterior eye chamber hemorrhage
Detached retina and blindness
Rectal prolapse
Inguinal or umbilical hernia
Encephalopathy, seizures
Atelectasis, pneumonitis, or pneumonia
In infants: apnea, anoxia
Otitis media
Pneumonia
Pathophysiology
The infecting organism adheres to ciliated epithelial
cells and multiplies.

The resulting local mucosal damage induces parox-
occasionally, B. parapertussis or B. bronchiseptica

(see Bordetella pertussis)
Typically transmitted by direct inhalation of contaminated droplets from someone in the acute disease
stage
Spreads indirectly through soiled linen and other articles contaminated by respiratory secretions
Bordetella pertussis
This microscopic enlargement shows Bordetella pertussis,
the nonmotile, gram-negative coccobacillus that
commonly causes whooping cough. After entering the tracheobronchial tree, pertussis causes mucus to become increasingly tenacious. The classic 6-week course of
whooping cough follows.
Assessment
History
Possible lack of immunization coupled with exposure
to pertussis during previous 3 weeks
Physical findings
Low or normal body temperature
Mild conjunctivitis
Listlessness
Engorged neck veins
Epistaxis during paroxysmal coughing
Exhaustion and cyanosis after coughing spell
Diminished breath sounds, upper airway wheezing
Test results
Laboratory
White blood cell count and differential show lymphocytosis.
B. pertussis is found in nasopharyngeal swabs and
sputum culture in early disease stages.
Direct immunofluorescence shows antigen.
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Pertussis
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Treatment
General
importance of immunization and vaccinations and
the need to notify the physician of adverse reactions

to the vaccine.
For infants and elderly patients: hospitalization with
Discharge planning
vigorous supportive therapy and fluid and electrolyte

replacement
Oxygen therapy, as warranted
Adequate nutrition with small, frequent meals
Increased fluid intake
Rest periods when fatigued
Refer the patient to a pulmonologist for follow-up
care, as indicated.
Medications
Antitussives
Antibiotics, such as erythromycin, azithromycin, and
clarithromycin
Key outcomes
The patient will:
remain free from adventitious breath sounds
regain normal arterial blood gas levels
show no evidence of pathogens in cultures.
Maintain respiratory isolation (mask only) for 5 to
7 days after antibiotic therapy begins.

Provide oxygen and moist air, as ordered; if needed,
assist respiration.
Suction secretions, as necessary. Elevate the head of
the bed to ease breathing.

Create a quiet environment to decrease coughing
stimulation.
Assess for complications caused by excessive
coughing.
Provide emotional support to the patient and parents,
as appropriate.
Report pertussis cases to local public health authori-
ties.
Monitoring
Respiratory status
Acid-base balance
Fluid and electrolyte balance
Patient teaching
Be sure to cover (with the patient or parents, as appropriate):
the disease process and medical procedures
need for the patients close contacts to get medical
care
when to notify the physician
Pertussis
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Pharyngitis
Overview
Description
Acute or chronic inflammation of the pharynx
Most common throat disorder
Usually subsides in 3 to 10 days unless complications
occur
Physical findings
Mild fever
Fiery red appearance of the posterior pharyngeal
wall
Swollen, exudate-flecked tonsils
Lymphoid follicles
Bacterial pharyngitis
Acutely inflamed throat, with patches of white and
yellow follicles
Strawberry-red tongue
Enlarged, tender cervical lymph nodes
Pathophysiology
Test results
Cellular damage caused by a virus or bacteria causes
Laboratory
Throat culture identifies the causative organism.
Rapid strep test shows group A beta-hemolytic streptococcal infection.
White blood cell count and differential show atypical
lymphocytes.
Imaging
Computed tomography scan identifies abscesses.
an inflammatory response.
Hyperemia and fluid exudation result.
Causes
Viral or bacterial infection
Beta-hemolytic streptococci (15% to 20% of acute
pharyngitis cases)
Mononucleosis
In children
Streptococcal bacteria infections
Gonococcal pharyngitis
Release of a toxin produced by Corynebacterium
diphtheria
Fungal pharyngitis
Prolonged antibiotic use (in immunosuppressed
patients)
Incidence
Widespread among adults who:
live or work in dusty or dry environments
use their voices excessively
use tobacco or alcohol habitually
suffer from chronic sinusitis, persistent coughs, or
allergies
Treatment
General
Warm saline gargles
Hospitalization for dehydration
Elimination of the underlying cause
Adequate humidification
Adequate fluid intake
Avoidance of citrus juices
Bed rest while febrile
Medications
Anesthetic throat lozenges

Analgesics as needed
Antifungal agents (for fungal pharyngitis)
Equine antitoxins (for diphtherial pharyngitis)
Sore throat
Pharyngeal edema
Surgery
Complications
Otitis media
Sinusitis
Mastoiditis
Rheumatic fever
Nephritis
Assessment
History
Sore throat
Slight difficulty swallowing (swallowing saliva more
painful than swallowing food)

Sensation of a lump in the throat
Constant, aggravating urge to swallow
Headache
Muscle and joint pain
610
Pharyngitis
Abscess drainage
Key outcomes
The patient will:
maintain intact mucous membranes
achieve adequate daily calorie intake.
Obtain throat cultures, as ordered.
Instruct the patient to use warm saline gargles.
Encourage adequate oral fluid intake.
Perform meticulous mouth care.
Maintain a restful environment.
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Monitoring
Intake and output
Signs and symptoms of dehydration
ALERT
Examine the patients skin twice per day for rashes
caused by drug sensitivity or rashes that could indicate a communicable disease.
Patient teaching
Be sure to cover:
importance of completing prescribed antibiotic
therapy
adverse effects
preventive measures, such as hand washing and
avoiding close contact with people who are sick
avoidance of excessive exposure to air conditioning
smoking cessation
ways to minimize environmental sources of throat
irritation
importance of throat cultures for all family members
if the patient has a streptococcal infection.
Discharge planning
indicated.
Pharyngitis
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Pheochromocytoma
Overview
Description
ALERT
Pheochromocytoma may occur during pregnancy
when uterine pressure on the tumor causes more
frequent hypertensive crises. These crises carry a
high risk for spontaneous abortion and can be fatal for both the mother and fetus.
Catecholamine-producing tumor, typically benign;
usually derived from adrenal medullary cells

Most common cause of adrenal medullary hyper-
secretion
Usually produces norepinephrine; large tumors secrete both epinephrine and norepinephrine
Potentially fatal, but with treatment carries a good
prognosis
Also known as chromaffin tumor
Assessment
History
Unpredictable episodes of hypertensive crisis
Paroxysmal symptoms suggesting a seizure disorder
or anxiety attack
Hypertension that responds poorly to conventional
treatment
Pathophysiology
Hypotension or shock after surgery or diagnostic
Pheochromocytoma causes excessive catecholamine
procedures
During paroxysms or crises
Throbbing headache
Palpitations
Visual blurring
Nausea and vomiting
Severe diaphoresis
Feelings of impending doom
Precordial or abdominal pain
Moderate weight loss
Dizziness or light-headedness when moving to an
upright position
production from autonomous tumor functioning.

The tumor stems from a chromaffin cell tumor of the
adrenal medulla or sympathetic ganglia (more commonly in the right adrenal gland than in the left).
Extra-adrenal pheochromocytomas may occur in the
abdomen, thorax, urinary bladder, and neck and in
association with the 9th and 10th cranial nerves.
Causes
May be inherited as an autosomal dominant trait
Incidence
Rare; seen in about 0.5% of newly diagnosed hyper-
Physical findings
tensive patients
Seen in all races
Affects both sexes equally
Typically familial
Most common in patients ages 30 to 50
During paroxysms or crises

Hypertension
Tachypnea
Pallor or flushing
Profuse sweating
Tremor
Seizures
Tachycardia
Paroxysmal or sustained hypertension
Hypertensive crises triggered by conditions that dis-
place the abdominal contents or by use of opiates,

histamine, glucagon, or corticotropin
Headache
Flushing
Diaphoresis
Tachycardia
Retinal changes
Complications
Stroke
Retinopathy
Irreversible kidney damage
Acute pulmonary edema
Cholelithiasis
Cardiac arrhythmias
Heart failure
Test results
Laboratory
Vanillylmandelic acid and metanephrine levels in a
24-hour urine specimen are increased.
Total plasma catecholamine levels are 10 to 50 times
higher than normal on direct assay.
Imaging
Computed tomography (CT) scan or magnetic resonance imaging of adrenal glands may show intraadrenal lesions.
CT scan, chest X-rays, or abdominal aortography may
reveal extra-adrenal pheochromocytoma.
Treatment
General
High-protein diet with adequate calories
Rest during acute attacks
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Pheochromocytoma
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Medications
Alpha-adrenergic blockers such as phenoxybenza-
mine
Catecholamine-synthesis antagonists
Beta-adrenergic blockers such as atenolol
Calcium channel blockers
I.V. phentolamine or nitroprusside during paroxysms
After adrenalectomy
Vital signs
Bowel sounds
Wound dressings
Incision
Signs and symptoms of hemorrhage
Pain
or crises
ALERT
Because severe and occasionally fatal paroxysms
have been induced by opiates, histamines, and other drugs, all medications should be considered
carefully and administered cautiously in patients
with known or suspected pheochromocytoma.
Surgery
Removal of pheochromocytoma
Key outcomes
Patient teaching
Be sure to cover:
adverse effects
way to prevent paroxysmal attacks
signs and symptoms of adrenal insufficiency
importance of wearing medical identification jewelry
how to monitor his own blood pressure.
Discharge planning
Refer family members for genetic counseling if auto-
somal dominant transmission of pheochromocytoma

is suspected.
The patient will:

maintain stable vital signs
maintain normal cardiac output
avoid complications.
Take orthostatic blood pressures.
Ensure the reliability of urine catecholamine mea-
surements.
Provide comfort measures.
Consult a dietitian, as needed.
Tell the patient to report symptoms of an acute
attack.
After adrenalectomy
ALERT
Be aware that postoperative hypertension is common because the stress of surgery and adrenal
gland manipulation stimulate catecholamine secretion.
Monitoring
Vital signs, especially blood pressure
Serum glucose level
Daily weight
Neurologic status
Renal function
Cardiovascular status
Adverse reactions to medications
Pheochromocytoma
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Pituitary tumors
Complications
Overview
Diabetes insipidus from tumor compression of the
Endocrine abnormalities throughout the body, unless
lost hormones are replaced
Description
Nonmalignant intracranial tumor; accounts for 10%
of all intracranial neoplasms

Most common tumor tissue types: chromophobe adenoma (90%), basophil adenoma, and eosinophil
adenoma
Most common site: anterior pituitary (adenohypophysis)
Considered a neoplastic condition because of the
tumors invasive growth
Carries a fair to good prognosis, depending on how
far the tumor spreads beyond the sella turcica
Pathophysiology
As a pituitary adenoma grows, it replaces normal
glandular tissue and enlarges the sella turcica (which

houses it).
Chromophobe adenoma may be associated with production of corticotropin, melanocyte-stimulating hormone, growth hormone, and prolactin.
Basophil adenoma may be associated with excess
corticotropin production and, consequently, Cushings syndrome.
Eosinophil adenoma may be associated with excessive growth hormone.
Causes
Unknown
Risk factors
Autosomal dominant trait
Incidence
Affects adults of both sexes between ages 30 and 50
Twice as common in females as in males
Headache, visual changes, double vision, and droop-
ing eyelids
Nipple discharge
Gynecomastia
Menses cessation
Decreased libido, male impotence
Cold intolerance
Nausea, vomiting, and constipation
Personality changes
Skin changes
Hair loss
Fatigue
Seizures
Hypotension
614
Pituitary tumors
hypothalamus
Assessment
History
Neurologic and endocrine abnormalities
Personality changes or dementia
Amenorrhea
Decreased libido
Impotence
Lethargy, weakness, increased fatigability
Sensitivity to cold
Constipation
Seizures
With cranial nerve involvement: diplopia and dizzi-
ness
Physical findings
Rhinorrhea
Head tilting during physical examination
Skin changes
Strabismus
Test results
Laboratory
Cerebrospinal fluid analysis shows an increased protein level.
Imaging
Skull X-rays with tomography may show an enlarged
sella turcica or erosion of its floor; if growth hormone secretion predominates, X-rays show enlargement of the paranasal sinuses and mandible, thickened cranial bones, and separated teeth.
Carotid angiography may identify displacement of the
anterior cerebral and internal carotid arteries from
tumor enlargement and may rule out intracerebral
aneurysm.
Computed tomography scan may confirm an adenoma and accurately depict its size.
Magnetic resonance imaging scan differentiates
healthy, benign, and malignant tissues and blood
vessels.
Treatment
General
Radiation therapy used for small, nonsecretory tu-
mors confined to the sella turcica or for patients

considered poor surgical risks
Individualized diet according to tumor manifestations; possible sodium or caloric restriction
In initial postoperative period, avoidance of coughing, sneezing, bending, and other movements that
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may increase intracranial pressure (ICP) or cause

cerebrospinal fluid leakage
Medications
Corticosteroids or thyroid or sex hormones
Insulin
Bromocriptine and cabergoline for prolactin-
producing tumors
Octreotide acetate and pegvisomant for growth hormone producing tumors
medication administration, dosage, and possible ad-
verse effects
importance of immediately reporting persistent post-
nasal drip or constant swallowing.
Discharge planning
Encourage the patient to wear medical identification
that indicates his medical condition and its proper

treatment.
Surgery
Transfrontal removal of a large tumor impinging on
the optic apparatus

Transsphenoidal resection for a smaller tumor con-
fined to the pituitary fossa

Cryohypophysectomy
Key outcomes
The patient will:
remain free from injury
express positive feelings about himself
report an increased sense of well-being
exhibit increased energy
participate in care and prescribed therapies (along
with family members).
Maintain patient safety.
Provide rest periods to avoid fatigue.
Establish a supportive, trusting relationship with the
patient.
Monitoring
After supratentorial or transsphenoidal
hypophysectomy
Proper positioning (head of the bed elevated 30 degrees)
Intake and output
Signs and symptoms of infection
Blood glucose level
After craniotomy
Vital signs
Neurologic status
Signs and symptoms of increased ICP
Patient teaching
Be sure to cover:
preoperative instructions on surgery, treatments, and
postoperative course
avoidance of coughing, sneezing, and bending
Pituitary tumors
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Placenta previa
Overview
Description
Placental implantation in the lower uterine segment,
encroaching on the internal cervical os

Common cause of bleeding during the second half of
pregnancy (Among patients who develop placenta
previa during the second trimester, less than 15%
have persistent previa at term.)
Carries good maternal prognosis if hemorrhage can
be controlled
Usually necessitates pregnancy termination if bleeding is heavy
Fetal prognosis dependent on gestational age and
amount of blood lost; risk for death greatly reduced
by frequent monitoring and prompt management
Pathophysiology
The placenta covers all or part of the internal cervi-
cal os. (See Three types of placenta previa.)
Assessment
History
Onset of painless, bright red, vaginal bleeding after
20th week of pregnancy

Vaginal bleeding before labor onset, typically episod-
ic and stopping spontaneously

May be asymptomatic
Physical findings
Soft, nontender uterus
Fetal malpresentation
Minimal descent of fetal presenting part
Good fetal heart tones
Test results
Laboratory
Maternal hemoglobin level is decreased.
Imaging
Transvaginal ultrasound scan determines placental
position.
Pelvic examination confirms diagnosis.
Causes
ALERT
Unknown
Risk factors
Defective vascularization of the decidua
Multiple pregnancy
Previous uterine surgery
Multiparity
Advanced maternal age
Endometriosis
Smoking
Incidence
About 1 in every 200 pregnancies
More common in multigravidas than primigravidas
Occurs more commonly after age 35
Pelvic examination isnt commonly performed because it increases maternal bleeding and can dislodge more of the placenta.
Treatment
General
Control of blood loss, blood replacement
Delivery of viable neonate
Prevention of coagulation disorders
With premature fetus, careful observation to give fe-
tus more time to mature

With complete placenta previa, hospitalization
Possible vaginal delivery (if bleeding is minimal and
placenta previa is marginal or when labor is rapid)
Painless, bright red, vaginal bleeding

Vaginal bleeding after 20th week of pregnancy
Complications
Anemia
Hemorrhage
Shock
Renal damage
Cerebral ischemia
Maternal or fetal death
ALERT
Because of possible fetal blood loss through the placenta, a pediatric team should be on hand during
delivery to immediately assess and treat neonatal
shock, blood loss, and hypoxia.
Nothing by mouth initially, then as guided by clinical
status
Bed rest
Medications
I.V. fluids, using large-bore catheter
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Three types of placenta previa

The degree of placenta previa depends largely on the extent of cervical dilation at the time of examination because the dilating cervix gradually uncovers the placenta, as shown below.
Marginal placenta previa
Partial placenta previa
Total placenta previa
If the placenta covers just a fraction of

the internal cervical os, the patient has
marginal, or low-lying, placenta previa.
The patient has the partial, or incomplete, form of the disorder if the placenta caps a larger part of the internal
os.
If the placenta covers all of the internal

os, the patient has total, complete, or
central placenta previa.
Surgery
Patient teaching
Immediate cesarean delivery in case of severe hem-
orrhage or as soon as fetus is sufficiently mature
Key outcomes
The patient will:
verbalize her feelings about her condition
use available support systems to aid coping.
Be sure to cover:
signs and symptoms of placenta previa
possibility of emergency cesarean delivery
possibility of the birth of a premature neonate
possibility of neonatal death
postpartum physical and emotional changes to
expect.
Discharge planning
Refer the patient for professional counseling if neces-
sary.
Obtain blood samples for complete blood count and
blood type and crossmatch.

Initiate external electronic fetal monitoring.
Administer prescribed I.V. fluids and blood products.
If the patient is Rh-negative, give Rho(D) immune
globulin (RhoGAM) after every bleeding episode, as

ordered.
Offer emotional support during labor.
Provide information about labor progress and the
condition of the fetus.
Encourage the patient to express her feelings.
Monitoring
Vital signs
Vaginal bleeding, including character of blood loss
Central venous pressure
Intake and output
Fetal heart tones
Signs and symptoms of hemorrhage and shock
Placenta previa
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Plague
Overview
Description
Acute, febrile, zoonotic infection caused by the gram-
negative, nonsporulating bacillus Yersinia pestis

Usually transmitted to humans through the bite of a
flea from an infected rodent host, such as a rat or

squirrel; occasional transmission from handling infected animals or their tissues (see Bubonic plague
carrier)
Potential bioterrorism and biological warfare agent
Forms of plague
Bubonic: most common form; causes swollen and
sometimes suppurating, lymph glands (buboes)
Septicemic: rapid, severe systemic form
Pneumonic: can be primary or secondary to the other two forms; highly contagious, with secondary
spread a serious concern (Primary pneumonic
plague is an acutely fulminant form causing acute
prostration, respiratory distress, and death, possibly
within 2 to 3 days after onset. Secondary pneumonic
plague is transmitted by contaminated respiratory
droplets.)
Without treatment, 60% mortality in bubonic plague
and nearly 100% in septicemic and pneumonic
plague; with treatment, 18% mortality
Incidence
Becoming more prevalent in the United States
Most common between May and September; in
hunters who skin wild animals, between October and

February
Fever
Chills
Weakness
Headache
Bubonic plague
Characteristic buboes
History of exposure to rodents
Complications
Peritoneal or pleural effusions
Septicemia
Fulminant pneumonia
Pericarditis
Seizures
Diffuse interstitial myocarditis
Multifocal hepatic necrosis
Diffuse hemorrhagic splenic necrosis
Respiratory failure
Cardiovascular collapse
Meningitis
Death
Assessment
Pathophysiology
History
Y. pestis is one of the most invasive bacterium
Milder form of bubonic plague

History of exposure to rodents
Malaise
Fever
Excruciatingly painful bubo
Severe form of bubonic plague
Sudden fever of 103 to 106 F (39.4 to 41.1 C)
Chills, myalgia, and headache
Restlessness, disorientation
Abdominal pain, nausea, and vomiting
Constipation followed by bloody diarrhea
known; mechanisms by which it causes disease

arent fully understood.
Once inoculated through the skin or mucous membranes, Y. pestis usually invades cutaneous lymphatic
vessels and regional lymph nodes; direct bloodstream inoculation may also occur.
Organisms are probably phagocytized by mononuclear phagocytes without being destroyed and are
then disseminated to distant sites in the body.
Plague can involve almost any organ and usually results in massive and widespread tissue destruction,
especially if left untreated.
Causes
Y. pestis
Risk factors
Rural areas
Urban areas with overcrowding, poor sanitation, and
large rat populations

Veterinarians
Cat owners
Hunters, campers, and hikers in outbreak areas
618
Plague
Physical findings
Milder form of bubonic plague
Fever
Pain or tenderness in regional lymph nodes
Painful, inflamed, and possibly suppurative buboes
(usually in the axillary, cervical, or inguinal areas)
Necrotization of hemorrhagic areas
Moribund state within hours after onset
Bubonic plague
Fever
Prostration
Restlessness, disorientation, delirium
Toxemia
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Staggering gait
Skin mottling, petechiae
Circulatory collapse
Coma
Bubonic plague carrier

Bubonic plague is usually transmitted to humans through
the bite of an infected flea (Xenopsylla cheopis), shown
here.
Test results
Laboratory
Y. pestis is found in capsular antigen testing, Wayson
stain, or fluorescent antibody stain.
White blood cell count is greater than 20,000/l,
with increased polymorphonuclear leukocytes and
hemoagglutination reaction.
Y. pestis is present in culture and Gram stain of skinlesion needle aspirate or lymph node aspirate, blood,
or sputum.
Imaging
Chest X-rays show fulminating pneumonia in pneumonic plague.
Treatment
General
Supportive management to control fever, shock, and
seizures and maintain fluid balance

Warm, moist compresses on buboes
Diet, as tolerated
Tube feedings or total parenteral nutrition, if re-
quired
Supplemental I.V. fluids
Bed rest during the acute phase
Medications
Antibiotics, such as streptomycin and gentamicin
Oxygen
Corticosteroids
Benzodiazepines
Anticonvulsants
Antipyretics
Surgery
Maintain a patent airway and adequate oxygenation.

Apply warm, moist compresses to buboes.
Provide meticulous skin care.
Prevent further injury to necrotic tissue areas.
Institute seizure precautions.
Report suspected plague cases to local public health
department.
Monitoring
Vital signs
Intake and output
Skin integrity
Pulmonary status
Cardiovascular status
Nutritional status
Seizures
Complications
Abnormal bleeding
Mentation
Incision and drainage of necrotic buboes
Key outcomes
The patient will:
maintain acceptable tissue perfusion and cellular
oxygenation
maintain effective ventilation
verbalize feelings of fear and anxiety
demonstrate effective coping mechanisms.
Administer drugs, I.V. fluids, and oxygen, as pre-
scribed and needed.

If pneumonic plague, use standard and droplet pre-
Patient teaching
Be sure to cover:
medication administration, dosage, and possible adverse effects
isolation procedures
personal protective measures
avoidance of contact with sick or dead wild animals
and the need to wear gloves when handling animal
carcasses
importance of insect and rodent population control
use of repellents, insecticides, and protective clothing when at risk for exposure to rodents fleas
elimination of rodent food and habitats
insecticide control of fleas.
cautions.
Provide adequate nutrition.
Plague
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Pleural effusion and

empyema
Overview
Description
Assessment
History
Underlying pulmonary disease
Shortness of breath
Chest pain
Malaise
Fluid accumulation in the pleural space; the fluid
Physical findings
may be extracellular, pus (empyema), blood (hemothorax), chyle (chylothorax), or bilious

Effusion classified as transudative or exudative
Fever
Trachea deviated away from the affected side
Dullness and decreased tactile fremitus over the effu-
Pathophysiology
Diminished or absent breath sounds

Pleural friction rub
Bronchial breath sounds
In empyema, foul-smelling sputum
Typically, fluid and other blood components migrate
through the walls of intact capillaries bordering the

pleura.
In transudative effusion, fluid is watery and diffuses
out of the capillaries if hydrostatic pressure increases
or capillary oncotic pressure decreases.
In exudative effusion, inflammatory processes increase capillary permeability. Exudative effusion is
less watery and contains high concentrations of white
blood cells and plasma proteins.
Empyema occurs when pulmonary lymphatics become blocked, leading to outpouring of contaminated lymphatic fluid into the pleural space.
Causes
Transudative pleural effusion
Cardiovascular disease
Hepatic disease
Renal disease
Hypoproteinemia
Exudative pleural effusion
Pleural infection
Pleural inflammation
Pleural malignancy
Empyema
Pulmonary infection
Lung abscess
Infected wound
Intra-abdominal infection
Thoracic surgery
Incidence
sion
Test results
Laboratory
PLEURAL FLUID ANALYSIS FINDINGS
In transudative effusion: specific gravity is less than
1.015 and protein level is less than 3 g/dl.

In exudative effusion: ratio of protein in pleural fluid
to protein in serum is 0.5 or higher; lactate dehydrogenase (LD) level is 200 IU or higher; ratio of LD in
pleural fluid to LD in serum is 0.6 or higher.
In empyema: microorganisms are present, white
blood cell count is increased, and glucose level is
decreased.
In esophageal rupture or pancreatitis: pleural fluid
amylase levels exceede serum amylase levels.
Imaging
Chest X-rays may show pleural effusions; lateral decubitus films may show loculated pleural effusions or
small pleural effusions not visible on standard chest
X-rays.
Computed tomography scan of the thorax shows
small pleural effusions.
Thoracentesis obtains pleural fluid specimens for
analysis.
Other
Tuberculin skin test may be positive for tuberculosis.
Pleural biopsy may be positive for carcinoma.
Can occur at any age

Treatment
General
Shortness of breath
Chest pain
Malaise
Nonproductive cough
Thoracentesis to remove fluid

Possible chest tube insertion
Possible chemical pleurodesis
High-calorie diet
Complications
Atelectasis
Infection
Hypoxemia
620
Pleural effusion and empyema
Medications
Antibiotics
Oxygen
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Surgery
Removal of thick coating over lung (decortication)
Key outcomes
The patient will:
consume the specified number of calories daily
express an understanding of the illness
Administer prescribed drugs and oxygen.
Assist during thoracentesis.
Encourage the patient to use an incentive spirometer.
Encourage deep-breathing exercises.
Provide meticulous chest tube care.
Ensure chest tube patency.
Keep petroleum gauze at the bedside.
Monitoring
Vital signs
Intake and output
Respiratory status
Pulse oximetry
Signs and symptoms of pneumothorax
Chest tube drainage
Patient teaching
Be sure to cover:
adverse effects
how thoracentesis is performed
chest tube insertion and drainage
signs and symptoms of infection
signs and symptoms of pleural fluid reaccumulation
when to notify the physician.
Discharge planning
Provide a home health referral for follow-up care.
indicated.
Pleural effusion and empyema
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Pleurisy
Physical findings
Overview
Coarse vibration on palpation of the affected area
Characteristic late-inspiration and early-expiration
pleural friction rub
Description
Inflammation of the visceral and parietal pleurae that
line the inside of the thoracic cage and envelop the

lungs
Also called pleuritis
Pathophysiology
The pleurae become swollen and congested.
As a result, pleural fluid transport is hampered, and
friction between the pleural surfaces increases.
Causes
Pneumonia
Tuberculosis
Viruses
Systemic lupus erythematosus
Rheumatoid arthritis
Uremia
Dresslers syndrome
Cancer
Pulmonary infarction
Chest trauma
Pathologic rib fractures
Pneumothorax
Sickle cell disease
Radiation therapy
Human immunodeficiency virus
Certain drugs, such as methotrexate or penicillin
Incidence
Test results
Imaging
Chest X-rays show absence of pneumonia.
Electrocardiography shows absence of ischemic
heart disease.
Treatment
General
Symptomatic
Possible intercostal nerve block
Diet, as tolerated
Bed rest
Medications
Anti-inflammatories
Analgesics
Surgery
Thoracentesis
Key outcomes
The patient will:
express feelings of increased comfort; relief of pain
demonstrate energy conservation techniques
demonstrate effective coping strategies.
Sudden dull, aching, burning, or sharp pain that
worsens on inspiration
Limited movement on the affected side during
breathing
Shortness of breath
Fever and chills

Encourage deep breathing and coughing.
Encourage the patient to use an incentive spirometer.
Assist the patient in splinting the affected side.
Position the patient in high Fowlers position.
Plan care to allow frequent rest periods.
Assist with passive range-of-motion (ROM) exercises.
Encourage active ROM exercises.
Assist with thoracentesis.
Encourage verbalization and provide emotional
Complications
Adhesions
Pleural effusion
Chronic pain or shortness of breath
Assessment
History
Sudden dull, aching, burning, or sharp pain that
worsens on inspiration
Predisposing factor
Cough
Shortness of breath
Fever
622
Pleurisy
support.
Monitoring
Vital signs
Intake and output
Pain control
Complications
Breath sounds
Respiratory status
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Patient teaching
Be sure to cover:
adverse effects
how to perform splinting and deep-breathing
exercises
importance of regular rest periods
signs and symptoms of possible complications
Pleurisy
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Pneumocystis carinii
pneumonia
Overview
Description
Communicable, opportunistic lung infection com-
monly associated with human immunodeficiency

virus (HIV)
A leading cause of opportunistic infection and death
among patients with acquired immunodeficiency syndrome (AIDS) in industrialized countries
Pathophysiology
The infecting organism invades the lungs bilaterally,
multiplies extracellularly, and fills alveoli with organisms and exudate.

As a result, gas exchange is impaired.
Alveoli hypertrophy and thicken, eventually leading to
extensive consolidation.
Causes
P. carinii; spreads mainly through the air (although
part of the normal flora in most healthy people, this

organism becomes an aggressive pathogen in immunocompromised patients)
Possible role of B-cell function defects
Physical findings
Low-grade, intermittent fever
Tachypnea
Dyspnea
Accessory muscle use for breathing
Cyanosis (with acute illness)
Dullness on percussion (with consolidation)
Crackles
Decreased breath sounds
Test results
Laboratory
P. carinii is found on histologic sputum specimen
studies.
Hypoxia and increased A-a gradient on arterial blood
gas (ABG) values are seen.
Imaging
Chest X-rays may show slowly progressing, fluffy infiltrates, occasional nodular lesions, or spontaneous
pneumothorax.
Gallium scan may show increased uptake over the
lungs.
Fiber-optic bronchoscopy
Transbronchial biopsy
Open lung biopsy
Treatment
General
HIV/AIDS
Immunosuppression
Immunodeficiency disorders
Oxygen therapy
Mechanical ventilation
High-calorie, high-protein diet
Nutritional supplements, as needed
Increased fluid intake
Rest periods when fatigued
Incidence
Medications
Most common in premature or malnourished infants,
Co-trimoxazole (may be given prophylactically to
Risk factors
children with primary immunodeficiency disease, patients receiving immunosuppressive therapy, and
those with HIV/AIDS
Insidious onset, with increasing shortness of breath
and nonproductive cough

Hypoxemia and hypercapnia (may not cause signifi-
cant clinical symptoms)
Complications
Disseminated infection
Pulmonary insufficiency and death
AIDS and other high-risk patients)

Pentamidine
Key outcomes
The patient will:
maintain normal vital signs
maintain adequate fluid volume
maintain normal breath sounds
regain normal ABG values
demonstrate correct bronchial hygiene techniques
verbalize fears, feelings, and concerns.
Assessment
History
Implement standard precautions.

Encourage ambulation, deep-breathing exercises,
Immunodepression, as from HIV infection, leukemia,
lymphoma, or organ transplantation
624
Pneumocystis carinii pneumonia
and use of an incentive spirometer.
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Provide adequate rest periods.

Encourage the patient to express fears, feelings, and
concerns.
Monitoring
Respiratory status
ABG values
Fluid and electrolyte status
Patient teaching
Be sure to cover:
adverse effects
energy conservation techniques
importance of taking prophylactic drugs to prevent
recurrence (for HIV-infected patients and other
immunocompromised individuals)
home oxygen therapy, if indicated.
Discharge planning
Refer the patient to a pulmonologist or an infectious
disease specialist for follow-up care, as needed.

If the patient has AIDS or HIV, provide information
about resources and support organizations.
Pneumocystis carinii pneumonia
625
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Pneumonia
Overview
Special populations
Incidence and mortality are highest in elderly
patients.
Description
Acute infection of the lung parenchyma impairing gas
Pleuritic chest pain

Cough
Excessive sputum production
Chills
exchange
May be classified by etiology, location, or type
Pathophysiology
A gel-like substance forms as microorganisms and
Complications
phagocytic cells break down.

This substance consolidates within the lower airway
structure.
Inflammation involves the alveoli, alveolar ducts, and
interstitial spaces surrounding the alveolar walls.
In lobar pneumonia, inflammation starts in one area
and may extend to the entire lobe. In bronchopneumonia, it starts simultaneously in several areas, producing patchy, diffuse consolidation. In atypical
pneumonia, inflammation is confined to the alveolar
ducts and interstitial spaces.
Septic shock
Hypoxemia
Respiratory failure
Empyema
Bacteremia
Endocarditis
Pericarditis
Meningitis
Lung abscess
Pleural effusion
Causes
Assessment
Bacterial or viral organism

Aspiration of foreign matter
History
Risk factors
Bacterial and viral pneumonia
Chronic illness and debilitation
Cancer
Abdominal and thoracic surgery
Atelectasis
Bacterial or viral respiratory infections
Chronic respiratory disease
Influenza
Smoking
Malnutrition
Sickle cell disease
Tracheostomy
Poor oral hygiene
Immunosuppressive therapy
Endotracheal intubation or mechanical ventilation
Aspiration pneumonia
Alcoholism
Exposure to noxious gases
Caustic substance entering airway
Advanced age
Debilitation
Nasogastric (NG) tube feedings
Impaired gag reflex
Decreased level of consciousness
Incidence
Affects both sexes and all ages
More than four million cases annually in the United
States
626
Pneumonia
Bacterial pneumonia
Sudden onset of:
Pleuritic chest pain
Cough
Purulent sputum production
Chills
Viral pneumonia
Nonproductive cough
Constitutional symptoms
Fever
Aspiration pneumonia
Fever
Weight loss
Malaise
Physical findings
Fever
Sputum production
Dullness over the affected area
Crackles, wheezing, or rhonchi
Decreased fremitus
Tachypnea
Use of accessory muscles
Test results
Laboratory
Complete blood count shows leukocytosis.
Blood cultures are positive for causative organism.
Arterial blood gas (ABG) values show hypoxemia.
Fungal or acid-fast bacilli cultures identify the etiologic agent.
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Assay for legionella soluble antigen in urine detects
presence of antigen.
Sputum culture, Gram stain, and smear reveal the
infecting organism.
Imaging
Chest X-rays generally show patchy or lobar infiltrates.
Bronchoscopy or transtracheal aspiration specimens
identify the etiologic agent.
Other
Pulse oximetry may reveal decreased oxygen saturation.
Treatment
General
Mechanical ventilation (positive end-expiratory pres-
sure) for respiratory failure

High-calorie, high-protein diet
Adequate fluids
Bed rest initially; progress as tolerated
Medications
Antibiotics
Humidified oxygen
Antitussives
Analgesics
Bronchodilators
Surgery
Drainage of parapneumonic pleural effusion or lung
abscess
Key outcomes
The patient will:
Administer prescribed I.V. fluids and electrolyte re-
placement.
Maintain a patent airway and adequate oxygenation.
Administer prescribed supplemental oxygen. Admin-
ister oxygen cautiously if the patient has chronic lung

disease.
Suction the patient, as needed.
Obtain sputum specimens, as needed.
Provide a high-calorie, high-protein diet of soft
foods.
Administer supplemental oral feedings, NG tube feedings, or parenteral nutrition, if needed.
Take steps to prevent aspiration during NG feedings.
Prevention
Preventing pneumonia
Urge bedridden and postoperative patients to perform
deep-breathing and coughing exercises frequently. Position these patients properly to promote full aeration
and secretion drainage.
Advise the patient to avoid using antibiotics indiscriminately for minor infections. Doing so could produce
upper airway colonization with antibiotic-resistant bacteria. If pneumonia develops, the causative organisms
may require treatment with more toxic antibiotics.
Encourage the high-risk patient to ask the physician
about an annual influenza vaccination and pneumococcal pneumonia vaccination. A single dose of pneumococcal vaccine is recommended for most patients age
54 and older; certain patients may need one booster
dose after 5 years.
Discuss ways to avoid spreading the infection to others. Remind the patient to sneeze and cough into tissues and to dispose of tissues in a waxed or plastic
bag. Advise the patient to wash his hands thoroughly
after handling contaminated tissues.
Dispose of secretions properly.

Provide a quiet, calm environment with frequent rest
periods.
Include the patient in care decisions whenever
possible.
Monitoring
Vital signs
Intake and output
Daily weight
Sputum production
Respiratory status
Breath sounds
Pulse oximetry
ABG values
Patient teaching
Be sure to cover:
adverse effects
need for adequate fluid intake
importance of adequate rest
deep-breathing and coughing exercises
chest physiotherapy
avoidance of irritants that stimulate secretions
home oxygen therapy, if required
ways to prevent pneumonia. (See Preventing pneumonia.)
Discharge planning
indicated.
Pneumonia
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Pneumothorax
Overview
Description
High positive end-expiratory pressures, causing rup-
ture of alveolar blebs

Chest tube occlusion or malfunction
Risk factors
Male gender
Smoking
Lung disease
History of pneumothorax
Accumulation of air or gas between the parietal and
Incidence
visceral pleurae, leading to lung collapse

Degree of lung collapse determined by amount of
trapped air or gas
Most common pneumothorax types: open, closed,
and tension
Occurs in 9,000 United States residents annually
Pathophysiology
Sudden, sharp, pleuritic pain
Pain exacerbated by chest movement
Shortness of breath
Air accumulates and separates the visceral and pari-
Complications
etal pleurae.
Negative pressure is eliminated, affecting elastic recoil forces.
The lung recoils and collapses toward the hilus.
In open pneumothorax, atmospheric air flows directly into the pleural cavity, collapsing the lung on the
affected side.
In closed pneumothorax, air enters the pleural space
from within the lung, increasing pleural pressure and
preventing lung expansion.
In tension pneumothorax, air in the pleural space is
under higher pressure than air in the adjacent lung.
Air enters the pleural space from a pleural rupture
only on inspiration. This air pressure exceeds barometric pressure, causing compression atelectasis. Increased pressure may displace the heart and great
vessels and cause mediastinal shift.
Fatal pulmonary and circulatory impairment
Causes
Open pneumothorax
Penetrating chest injury
Central venous catheter insertion
Chest surgery
Transbronchial biopsy
Thoracentesis
Percutaneous lung biopsy
Closed pneumothorax
Blunt chest trauma
Rib fracture
Clavicle fracture
Congenital bleb rupture
Emphysematous bullae rupture
Barotrauma
Erosive tubercular or cancerous lesions
Interstitial lung disease
Tension pneumothorax
Penetrating chest wound
Lung or airway puncture from positive-pressure ventilation
Mechanical ventilation after chest injury
628
Pneumothorax
Assessment
History
Possibly asymptomatic (with small pneumothorax)
Sudden, sharp, pleuritic pain
Pain that worsens with chest movement, breathing,
and coughing
Shortness of breath
Physical findings
Asymmetrical chest wall movement
Overexpansion and rigidity on the affected side
Possible cyanosis
Subcutaneous emphysema
Hyperresonance on the affected side
Decreased or absent breath sounds on the affected
side
Decreased tactile fremitus over the affected side
Tension pneumothorax
Distended jugular veins
Pallor
Anxiety
Tracheal deviation away from the affected side
Weak, rapid pulse
Hypotension
Tachypnea
Cyanosis
Test results
Laboratory
Arterial blood gas analysis may show hypoxemia.
Imaging
Chest X-rays may show air in the pleural space and,
possibly, a mediastinal shift.
Other
Pulse oximetry may show decreased oxygen saturation.
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Treatment
General
Conservative treatment of spontaneous pneumotho-
rax with no signs of increased pleural pressure, less

than 30% lung collapse, and no obvious physiologic
compromise
Diet, as tolerated
Bed rest
Chest tube insertion
Needle thoracostomy
Medications
Oxygen
Analgesics
Surgery
Thoracotomy, pleurectomy for recurring sponta-
neous pneumothorax
Repair of traumatic pneumothorax
Doxycycline or talc installation into pleural space
ALERT
Watch for signs and symptoms of tension pneumothorax, which can be fatal. These include
anxiety, hypotension, tachycardia, tachypnea,
and cyanosis.
Patient teaching
Be sure to cover:
adverse effects
chest tube insertion
deep-breathing exercises
signs and symptoms of recurrent spontaneous pneumothorax and when to notify the physician.
Discharge planning
appropriate.
Key outcomes
The patient will:
Assist with chest tube insertion.
ALERT
If the chest tube dislodges, immediately place a petroleum gauze dressing over the opening.
Encourage deep-breathing and coughing exercises.
Offer reassurance, as appropriate.
Include the patient and his family in care decisions
whenever possible.
Monitoring
Vital signs
Intake and output
Respiratory status
Breath sounds
Chest tube system
Complications
Pneumothorax recurrence
Pneumothorax
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Poisoning
Overview
Description
Contact with a harmful substance by inhalation, in-
gestion, injection, or skin contact

Prognosis varies with the amount of poison ab-
sorbed, its toxicity, and the time lapse between poisoning and treatment
Pathophysiology
The disorder process varies with the type of poison.
Causes
Accidental ingestion of medication
Improper cooking, canning, or storage of food
Suicide attempt
Homicide attempt
Risk factors
Cardiac arrhythmias
Acute renal failure
Liver failure
Test results
Laboratory
Lactate level is either increased or decreased.
Serum calcium level is increased.
Serum magnesium level is increased.
Toxicology studies show poison levels in the patients
mouth, vomitus, urine, feces, or blood, or on the patients hands or clothing.
Arterial blood gas values identify hypoxemia or metabolic derangements.
Imbalanced serum electrolyte levels such as hypokalemia may show anion-gap metabolic acidosis.
Imaging
Chest X-rays may show pulmonary infiltrates or edema in inhalation poisoning; may show aspiration
pneumonia in petroleum distillate inhalation.
Abdominal X-rays may show the presence of iron
pills or other radiopaque substances.
Electrocardiography may show arrhythmias or
QRS- and QT-interval prolongation.
Employment in chemical plant

Inappropriate storage of medications or chemicals
Inappropriate labeling
Treatment
Incidence
Emergency resuscitation, as needed

Recommendations of local poison control center
Symptomatic care
Airway and ventilation maintenance
Oxygen administration
Nothing by mouth until the episode resolves
Safety measures
Affects 1 million people annually; fatal in about 800
cases
Fourth most common cause of death in children
Hypotension
Altered neurologic status
Changes in skin temperature and color
Cardiopulmonary arrest
Complications
Cardiac arrhythmias
Seizures
Neurogenic shock
Cardiovascular collapse
Coma and death
General
Medications
Specific antidote, if available
Activated charcoal, if appropriate
Key outcomes
History
The patient will:

maintain orientation to time, place, and person
express feelings of increased comfort and pain relief
identify factors that increase the risk for injury.
Poison exposure
Drug overdose
Physical findings
Perform cardiopulmonary resuscitation, if needed.

Induce emesis, if recommended.
Perform gastric lavage and administer a cathartic as
Assessment
Vary with type of poison, possibly including:
630
Central nervous system depression or excitability

Respiratory depression
Cardiovascular depression
Cardiovascular excitation
Poisoning
ordered.
Provide supplemental oxygen as ordered and
needed.
Send vomitus and aspirate for analysis.
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In severe poisoning, provide peritoneal dialysis or
hemodialysis.
Monitoring
Vital signs
Level of consciousness
Respiratory status
Suicidal ideations, if indicated
Patient teaching
Be sure to cover:
prevention techniques (see Preventing poisoning)
importance of keeping poison control telephone
number readily available.
Prevention
Preventing poisoning
Poisoning can be prevented by following these guidelines:
Read all labels before taking medications or using
chemicals.
Store medication and chemicals away from children
and pets.
Dont take medication that has been prescribed for
someone else.
Dont transfer medications or chemicals from their
original container unless properly labeled.
Dont tell children that medication is candy.
Use childproof caps on medication containers.
Always close containers carefully.
Use well-marked pill-dispensing system to pre-pour
medications for elderly or visually impaired patients
who are unable to safely self-administer.
Discharge teaching
Refer the patient for psychological counseling in case
of suicide attempt.
Refer the patient to the proper authorities in case of
deliberate poisoning.
Poisoning
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Poliomyelitis
Overview
Vomiting
Lethargy
Irritability
Pains in neck, back, arms, legs, and abdomen
Muscle tenderness, weakness, and spasms in the ex-
Description
tensors of the neck and back and sometimes in the

hamstring and other muscles
An acute communicable disease caused by the polio
virus
Ranges in severity from inapparent infection to fatal
paralytic illness (mortality 5% to 10%)
Prognosis excellent if central nervous system (CNS)
spared
Also called polio or infantile paralysis
Pathophysiology
The poliovirus has three antigenically distinct sero-
types (types I, II, and III) that cause poliomyelitis.

Incubation period ranges from 3 to 35 days (7 to 14
days on average).
The virus usually enters the body through the alimen-
tary tract, multiplies in the oropharynx and lower intestinal tract, and then spreads to regional lymph
nodes and the blood.
Factors that increase the risk of paralysis include
pregnancy; advanced age; localized trauma, such as a
recent tonsillectomy, tooth extraction, or inoculation;
and unusual physical exertion at or just before the
clinical onset of poliomyelitis.
Causes
Contraction of the virus from direct contact with in-
fected oropharyngeal secretions or feces
Risk factors
Travel to polio oubtreak area
Lack of immunization
Compromised immune system
Poor sanitation
Pregnancy
Incidence
PARALYTIC
Symptoms similar to those of nonparalytic polio-
myelitis
Asymmetrical weakness of various muscles
Loss of superficial and deep reflexes
Paresthesia
Hypersensitivity to touch
Urine retention
Constipation
Abdominal distention
BULBAR PARALYTIC
Respiratory paralysis
Symptoms of encephalitis
Facial weakness
Diplopia
Dysphasia
Difficulty chewing
Inability to swallow or expel saliva
Regurgitation of food through the nasal passages
Dyspnea
Complications
Hypertension
Urinary tract infection
Urolithiasis
Atelectasis
Pneumonia
Myocarditis
Cor pulmonale
Skeletal and soft-tissue deformities
Paralytic ileus
Assessment
Minor polio outbreaks, usually among nonimmu-
History
nized groups
Onset during the summer and fall
Mostly occurs in people older than age 15
Adults and girls at greater risk for infection; boys, for
paralysis
Exposure to polio virus

Fever
Abortive infection
Slight fever
Malaise
Headache
Sore throat
Inflamed pharynx
Vomiting
Major poliomyelitis
NONPARALYTIC
Moderate fever
Headache
632
Poliomyelitis
Physical findings
Muscle weakness
Resistance to neck flexion (nonparalytic and paralyt-
ic poliomyelitis)
Patient tripods (extends his arms behind him for
support) when sitting up

Patients head falls back when supine and shoulders
are elevated (Hoynes sign)

Unable to raise legs 90 degrees when in a supine po-
sition
Kernigs and Brudzinskis signs (paralytic polio-
myelitis)
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Test results
Laboratory
Polio virus is isolated from throat washings early in
the disease, from stools throughout the disease, and
from cerebrospinal fluid cultures in CNS infection.
Convalescent serum antibody titers are four times
greater than acute titers.
Tests to rule out coxsackievirus and echovirus infections must be performed.
Treatment
General
Supportive
Moist heat applications
Well-balanced diet
Physical therapy
Assistive devices
Medications
Analgesics
Antipyretics
Key outcomes
The patient will:
demonstrate effective coping mechanisms
use available support systems.
Provide good skin care, reposition the patient often,
and keep the bed dry.

Maintain contact isolation.
Monitoring
Signs of paralysis
Respiratory status
Vital signs
Nutritional status
Patient teaching
Be sure to cover:
physical therapy
avoiding complications of limited mobility
proper hand-washing and contact isolation techniques
vaccination of unimmunized household members.
Discharge planning
Refer the patient to support services as appropriate.
Poliomyelitis
633
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Polycystic kidney
disease
Heart failure
Recurrent hematuria
Life-threatening retroperitoneal bleeding
Proteinuria
Overview
Assessment
Description
History
Growth of multiple, bilateral, grapelike clusters of
Adult polycystic disease

Family history
Polyuria
Urinary tract infections (UTIs)
Headaches
Pain in back or flank area
Gross hematuria
Abdominal pain, usually worsened on exertion and
eased by lying down
fluid-filled cysts in the kidneys

May progress slowly even after renal insufficiency
symptoms appear
Two distinct forms
infantile form: causes stillbirth or early neonatal
death
adult form: has insidious onset but usually becomes obvious between ages 30 and 50
Usually fatal within 4 years of uremic symptom onset,
unless dialysis begins
Carries a widely varying prognosis in adults
Also known as PKD
Pathophysiology
Cysts enlarge the kidneys, compressing and eventual-
ly replacing functioning renal tissue.

Renal deterioration results; deterioration is more
gradual in adults than in infants.

The condition progresses relentlessly to fatal uremia.
Causes
Familial
Infantile form: inherited as an autosomal recessive
trait
Adult form: inherited as an autosomal dominant trait
Risk factors
If one parent has autosomal dominant PKD: 50%
chance that the disease will pass to a child

parents not having the
disease possibly having a child with the disease if
both parents carriers of the abnormal gene and both
passing the gene to their child (one in four chance)
In autosomal recessive PKD:
Incidence
Infantile form: 1 in 6,000 to 40,000 infants
Adult form: 1 in 50 to 1,000 adults
Enlarged kidneys
Signs and symptoms of renal failure
Abdominal or flank pain
Hypertension
Nocturia
Complications
Hepatic failure
Renal failure
Respiratory failure
634
Polycystic kidney disease
Physical findings
Infantile form
Pronounced epicanthal folds
Pointed nose
Small chin
Floppy, low-set ears (Potter facies)
Huge, bilateral, symmetrical flank masses that are
tense and cant be transilluminated
Signs of respiratory distress, heart failure and, eventually, uremia and renal failure
Signs of portal hypertension (bleeding varices)
Adult form
Hypertension
Signs of an enlarging kidney mass
Grossly enlarged kidneys (in advanced stages)
Test results
Laboratory
Urinalysis may show hematuria or bacteria or protein.
Creatinine clearance test results may show renal insufficiency or failure.
Sodium loss or retention is possible.
Imaging
Excretory or retrograde urography reveals enlarged
kidneys, with pelvic elongation, flattening of the calyces, and indentations caused by cysts. In a neonate,
excretory urography shows poor excretion of contrast medium.
Ultrasonography, tomography, and radioisotopic
scans show kidney enlargement and cysts.
Tomography, computed tomography scan, and magnetic resonance imaging show multiple areas of cystic damage.
Treatment
General
Monitoring of renal function
Dialysis
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Low-protein and, possibly, low-sodium diet

Fluid restriction (in renal failure)
Avoidance of contact sports
Medications
Analgesics
Antibiotics for UTI
Antihypertensive agents
Surgery
Kidney transplantation
Surgical drainage for cystic abscess or retroperi-
toneal bleeding
Key outcomes
The patient will:
maintain urine specific gravity within designated
limits
identify risk factors that worsen decreased tissue perfusion, and modify lifestyle appropriately.
Provide supportive care to minimize symptoms.
Individualize patient care accordingly.
Monitoring
Urine (for blood, cloudiness, calculi, and granules)
Intake and output
Electrolyte levels
Vital signs
Access site for dialysis
Patient teaching
Be sure to cover:
adverse effects
follow-up with the physician for severe or recurring
headaches
signs and symptoms of UTI and prompt notification
of the physician
importance of blood pressure control
possible need for dialysis or transplantation.
Discharge planning
Refer a young adult patient or the parents of an infant
with polycystic kidney disease for genetic counseling.
Polycystic kidney disease
635
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Polycystic ovary
syndrome
Overview
Description
Metabolic disorder characterized by multiple ovarian
cysts
Prognosis good for ovulation and fertility with appropriate treatment
Pathophysiology
A general feature of all anovulation syndromes is a
lack of pulsatile release of gonadotropin-releasing

hormone.
Initial ovarian follicle development is normal.
Many small follicles begin to accumulate because
theres no selection of a dominant follicle.
These follicles may respond abnormally to the hormonal stimulation, causing an abnormal pattern of
estrogen secretion during the menstrual cycle.
Endocrine abnormalities may be the cause of polycystic ovary syndrome or cystic abnormalities; muscle and adipose tissue are resistant to the effects of
insulin, and lipid metabolism is abnormal.
Causes
Exact cause unknown; possible theories:
Abnormal enzyme activity triggering excess androgen secretion

Endocrine abnormalities
Incidence
Occurs in 6% to 10% of females in the United States;

50% to 80% of these females, obese
Among females who seek treatment for infertility,
more than 75% having some degree of polycystic
ovary syndrome, usually manifesting by anovulation
alone
Affects females of reproductive age
Mild pelvic discomfort
Lower back pain
Dyspareunia
Abnormal uterine bleeding secondary to disturbed
ovulatory pattern
Hirsutism
Acne
Male-pattern hair loss
Infertility
Obesity
Impaired glucose tolerance (by age 40)
Complications
Malignancy
636
Polycystic ovary syndrome
Increased risk for cardiovascular disease and type 2
diabetes mellitus
Secondary amenorrhea
Oligomenorrhea
Infertility
Addisons disease
Ovarian atrophy
Assessment
History
Diabetes
Mild pelvic discomfort
Lower back pain
Dyspareunia
Abnormal uterine bleeding secondary to disturbed
ovulatory pattern
Physical findings
Obesity
Hirsutism
Acne
Male-pattern hair loss
Hyperpigmentation of the skin
Test results
Laboratory
Urinary 17-ketosteroid levels are slightly elevated.
Estrogen action is unopposed during menstrual cycle
due to anovulation.
Ratio of luteinizing hormone to follicle-stimulating
hormone is elevated (usually 3:1 or greater).
Testosterone and androstenedione levels are elevated.
Imaging
Ultrasound permits visualization of the ovary.
Surgery
Surgery may confirm the presence of ovarian cysts.
Direct visualization by laparoscopy confirms the
presence of cysts.
Treatment
General
Lifestyle modifications
Weight-loss diet
Daily exercise program
Hair removal
Medications
Clomiphene
Medroxyprogesterone
Low-dose hormonal contraceptives
Metformin
Antiandrogens (for hirsutism)
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Surgery
Ovarian wedge resection
Laparoscopic surgery to create focal areas of damage
in the ovarian cortex and stoma
Key outcomes
The patient will:
express understanding of condition and treatment
Postoperatively, encourage frequent movement in bed
and early ambulation.
Provide emotional support

Encourage weight reduction, if appropriate.
Provide guidelines for exercise program.
Monitoring
Preoperatively
Signs of cyst rupture
Postoperatively
Vital signs
Signs of infection
Patient teaching
Be sure to cover:
diabetic diet, if appropriate
low-calorie diet
importance of regular follow-up care.
Discharge planning
Refer the patient to a reproductive endocrinologist.
Refer the patient to supportive services as appro-
priate.
637
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Polycythemia, secondary
Overview
Description
Excessive production of circulating red blood cells
(RBCs) due to hypoxia, tumor, or disease

Also called reactive polycythemia
Pathophysiology
Secondary polycythemia may result from increased
production of the hormone erythropoietin.

Bone marrow is stimulated to produce RBCs (in-
creased production of erythropoietin possibly an inappropriate pathologic response to renal, central

nervous system, or endocrine disorders or to certain
neoplasms).
Its a compensatory response to several conditions,
such as:
hypoxemia
hemoglobin abnormalities
heart failure
right-to-left shunting of blood in the heart
central or peripheral alveolar hypoventilation
low oxygen content at high altitudes.
It may be an inappropriate (pathologic) response to:
renal disease
central nervous system disease
neoplasms
endocrine disorders.
Causes
Increased production of erythropoietin
Conditions that cause prolonged tissue hypoxia, such
as shock or compression of major blood vessels

Recessive genetic trait
Risk factors
Smoking
Severe heart or lung disease
Long periods of time at high altitudes
Occupations such as pilots or mountaineers
Incidence
Assessment
History
Emphysema
Headaches
Lethargy
Physical findings
Clubbed fingers
Ruddy skin
Cyanosis
Splenomegaly
Shortness of breath
Hypoxemia
Test results
Laboratory
RBC mass is increased.
Hematocrit and hemoglobin level are elevated.
Mean corpuscular volume and mean corpuscularhemoglobin level are elevated.
Urinary erythropoietin count is elevated.
Blood histamine level is elevated.
Arterial oxygen saturation level is normal to low.
Bone marrow biopsy reveals hyperplasia confined to
the erythroid series.
Treatment
General
Correction of underlying disease or environmental
condition
Therapeutic phlebotomy
Plasmapheresis
Smoking cessation
Low-sodium diet
Medications
Analgesics
Low-flow oxygen therapy
Occurs in 2 of every 100,000 people living at or near
sea level
Greater incidence among those living at high altitude
Key outcomes
Ruddy, cyanotic skin
Emphysema
Hypoxemia without hepatomegaly or hypertension
(in the hypoxic patient)

Clubbing of the fingers (when underlying cause is
cardiovascular)
Complications
Hemorrhage
Thromboembolism secondary to hemoconcentration
638
The patient will:

maintain adequate gas exchange
maintain normal fluid balance
remain free from signs of infection.
Promote optimal activity.
Before and after therapeutic phlebotomy, check the
patients blood pressure with him lying down. After

the procedure, have the patient drink approximately
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24 oz (710 ml) of water or juice. To prevent syncope, have him sit up for about 5 minutes before
walking.
Encourage verbalization and provide support.
Monitoring
Signs of thrombosis
Respiratory status
Vital signs
Patient teaching
Be sure to cover:
symptoms of recurring polycythemia and the importance of reporting them promptly
the importance of regular blood studies (every 2 to
3 months), even after the disease is controlled
the need for relocation if altitude is a contributing
factor
dietary restrictions
using an electric razor
maintaining a safe environment
alternating rest periods and activity.
Discharge planning
Refer the patient to social services as appropriate.
639
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Polycythemia vera
Overview
Description
Night sweats
Epigastric and joint pain
Vision alterations, such as scotomas, double vision,
and blurred vision

Pruritus
Abdominal fullness
Chronic, myeloproliferative disorder of increased red
Physical findings
blood cell (RBC) mass, leukocytosis, thrombocytosis, and increased hemoglobin concentration
Also called primary polycythemia, erythema, polycythemia rubra vera, splenomegalic polycythemia,
and Vaquez-Osler disease
Congestion of the conjunctiva, retina, and retinal
Pathophysiology
Uncontrolled and rapid cellular reproduction and
maturation cause proliferation or hyperplasia of all

bone marrow cells.
Increased RBC mass makes the blood abnormally
viscous and inhibits blood flow to the microcirculation.
Diminished blood flow and thrombocytosis set the
stage for intravascular thrombosis.
veins
Oral mucous membrane congestion
Hypertension
Ruddy cyanosis
Ecchymosis
Hepatosplenomegaly
Test results
Risk factors
Laboratory
Uric acid level is increased.
Increased RBC mass and normal arterial oxygen saturation confirm diagnosis with splenomegaly or two
of the following:
platelet count above 400,000/l (thrombocytopenia)
white blood cell count above 10,000/l in adults
elevated leukocyte alkaline phosphatase level
elevated serum vitamin B12 levels or unbound B12binding capacity.
Bone marrow biopsy shows panmyelosis.
Male gender
Older than age 60
Family member with the disorder
Treatment
Incidence
General
Five new cases per million people each year

Rare in children and blacks
90% of patients have mutation JAK2
Therapeutic phlebotomy
Pheresis
Myelosuppressive agents, such as hydroxyurea and
Causes
Hyperplasia of all bone marrow cells (panmyelosis)
Mutation to deoxyribonucleic acid in a single cell in
the bone marrow; mutation in the protein JAK2
Joint pain
Hypertension
Complications
Hemorrhage
Vascular thromboses
Uric acid calculi
Myelofibrosis
Acute leukemia
Assessment
History
Vague feeling of fullness in the head or rushing in the
ears
Tinnitus
Headache
Dizziness, vertigo
Epistaxis
640
Polycythemia vera
Medications
anagrelide
Radioactive phosphorus
Chemotherapy
Key outcomes
The patient will:
maintain strong peripheral pulses
maintain normal skin color and temperature
remain free from evidence of infection
express feelings of increased comfort and decreased
pain.
Keep the patient active and ambulatory.
If bed rest is necessary, implement a daily program
of active and passive range-of-motion exercises.

Encourage additional fluid intake.
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If the patient has symptomatic splenomegaly, suggest
instructions on infection prevention for an outpatient
or provide small, frequent meals followed by a rest

period.
If the patient has pruritus, administer prescribed
drugs.
Encourage the patient to express concerns about the
disease and its treatment.
who develops leukopenia (including avoiding crowds

and watching for infection symptoms)
radioactive phosphorus administration procedure (if
scheduled) and the possible need for repeated phlebotomies
dental care
use of gloves when outdoors if temperature is below
50 F (10 C).
ALERT
Report acute abdominal pain immediately. It may
signal splenic infarction, renal calculus formation,
or abdominal organ thrombosis.
Discharge planning
Refer the patient to social services as needed.
During and after therapeutic phlebotomy

Make sure the patient is lying down comfortably. Stay
alert for tachycardia, clamminess, and complaints of
vertigo. If these effects occur, the procedure should
be stopped.
Immediately after phlebotomy, have the patient sit up
for about 5 minutes before letting him walk. Give
24 oz (710 ml) of juice or water.
During myelosuppressive chemotherapy
If nausea and vomiting occur, begin antiemetic therapy and adjust the patients diet.
If treating with radioactive phosphorus, obtain a
blood sample for complete blood cell (CBC) count
and platelet count before starting treatment. (Personnel who administer radioactive phosphorus should
take radiation precautions to prevent contamination.)
Have the patient lie down during I.V. administration
and for 15 to 20 minutes afterward.
Monitoring
Vital signs
Adverse reactions to drugs
CBC and platelet count before and during therapy
Complications
Signs and symptoms of impending stroke
Hypertension
Signs and symptoms of heart failure
Signs and symptoms of bleeding
Patient teaching
Be sure to cover:
importance of staying as active as possible
use of an electric razor to prevent accidental cuts
ways to minimize falls and contusions at home
avoidance of high altitudes
common bleeding sites, if the patient has thrombocytopenia
importance of reporting abnormal bleeding promptly
therapeutic phlebotomy procedure (if scheduled)
and its effects
symptoms of iron deficiency to report
possible adverse reactions to myelosuppressive
therapy
Polycythemia vera
641
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Polyps, intestinal
Overview
Description
A small, tumorlike growth that projects from a mu-
Complications
Anemia
Bowel obstruction
Rectal bleeding
Intussusception
Colorectal cancer (villous adenomas and familial
polyps)
Electrolyte imbalance
cous membrane surface

May develop in the colon or rectum, where they pro-
trude into the GI tract
Assessment
Pathophysiology
History
Masses of tissue resulting from unrestrained cell
Diarrhea
Bloody stools
Painful defecation
Changes in bowel habits
growth in the upper epithelium rise above the mucosal membrane and protrude into the GI tract.
They may be described by their appearance:
pedunculated: attached by a stalk to the intestinal
wall
sessile: attached to the intestinal wall with a broad
base and no stalk.
Polyps are classified according to tissue type:
adenomatous polyps, such as tubular adenoma,
tubulovillous adenoma, and villous adenoma
nonadenomatous polyps, such as hyperplastic
polyps, inflammatory polyps, and juvenile polyps.
Most polyps are benign. However, villous and familial
polyps show a marked inclination to become malignant.
ALERT
Familial polyposis is commonly linked to rectosigmoid adenocarcinoma.
Causes
Unknown
Risk factors
Heredity
Age
High-fat, low-fiber diet
Incidence
Villous adenomas most prevalent in males older than
age 55
Common polypoid adenomas most prevalent in white
females between ages 45 and 60

Incidence in both sexes increased after age 70
Juvenile polyps most common in children younger
than age 10
Rectal bleeding
Painful defecation
Changes in bowel habits
Physical findings
Polyp felt during digital rectal examination
Test results
Laboratory
Occult blood is present in stools.
Hemoglobin level is low.
Hematocrit is low with anemia.
Serum electrolyte imbalances are evident with villous
adenomas.
Imaging
Barium enema identifies polyps that are located high
in the colon.
Sigmoidoscopy, colonoscopy, and rectal biopsy identify polyps.
Treatment
General
Diet, as tolerated
Medications
Analgesics
Surgery
Polypectomy, commonly by fulguration (destruction
by high-frequency electricity) during endoscopy

Abdominoperineal resection, low anterior resection,
ileostomy, colostomy
Biopsy
Snare removal during colonoscopy
Key outcomes
The patient will:
return to normal bowel habits
express increased comfort
maintain electrolyte balance.
642
Polyps, intestinal
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Observe the amount and character of stools.
Prepare the patient with precancerous or familial le-
sions for abdominoperineal resection.

Monitoring
Electrolyte levels
Rectal bleeding
Vital signs
Intake and output
After surgery
Signs of bleeding
Wound condition
Patient teaching
Be sure to cover:
wound care, if appropriate
enterostomal therapy and care.
Discharge planning
If the patient has benign polyps, stress the need for
routine follow-up studies to check for new polypoid

growth.
Polyps, intestinal
643
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Porphyrias
Overview
Description
Umbrella term for a group of metabolic disorders
that affect the biosynthesis of heme (a hemoglobin

component), resulting in excessive porphyrin production
Classified by the site of excessive porphyrin production as erythropoietic, hepatic, or erythrohepatic
porphyria
Pathophysiology
Various metabolic disorders affect heme biosyn-
thesis.
This leads to excessive production and excretion of
porphyrins or their precursors.
Causes
Inherited as an autosomal dominant trait, except
Gnthers disease (inherited as an autosomal recessive trait) and toxic-acquired porphyria (which results from lead ingestion or exposure)
Incidence
More common in Whites than Blacks or Asians
Darkening of urine left in the light or air

Neurologic signs of wristdrop or footdrop
Muscle weakness
Fever (with an acute attack)
Splenomegaly (if hemolytic anemia present)
Wheezing and dyspnea (with acute intermittent por-
phyria)
Test results
Laboratory
The ion-exchange chromatography test shows urine
aminolevulinic acid.
In acute intermittent porphyria: urine porphobilinogen (as shown by the Watson-Schwartz test), leukocytosis, elevated bilirubin and alkaline phosphatase
levels, and hyponatremia are present.
In variegate porphyria: protoporphyrin and coproporphyrin is present in stools.
In hereditary coproporphyria: abundant coproporphyrin is present in stools and, to a lesser extent, in
urine.
In porphyria cutanea tarda: uroporphyrin excretion
is increased with varying amounts of fecal porphyrins.
In Gnthers disease: urine porphyrins are present.
In erythropoietic protoporphyria: protoporphyrin is
present in red blood cells.
In toxic acquired porphyria: urine lead level is
0.2 mg/L or higher.
In porphyria cutanea tarda: serum iron levels are
increased.
Neuropsychiatric, dermatologic, and abdominal
symptoms
Precipitating factors
Certain medications
Hormonal changes
Infection
Malnutrition
Complications
Treatment
General
High-carbohydrate diet
Fluid restriction
Avoidance of direct sun exposure
With hepatic porphyria: neurologic and hepatic dys-
Medications
function
With acute intermittent porphyria: flaccid paralysis,
respiratory paralysis, and death
With erythropoietic porphyria: hemolytic anemia
Beta-caotene supplements
Chlorpromazine I.V.
Analgesics
Hemin
Assessment
History
Mild or severe abdominal pain
Photosensitivity
Paresthesia
Neuritic pain
Physical findings
Wide variation, depending on the type of porphyria
Psychosis
Seizures
Skin lesions
644
Porphyrias
Surgery
In hemolytic anemia: splenectomy
Key outcomes
The patient will:
maintain intact skin integrity
avoid complications
regain normal bowel movements
express feelings of increased comfort.
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Drugs that aggravate porphyria

Make sure the patient with porphyria doesnt receive any
of the following drugs, which are known to trigger signs
and symptoms of porphyria:
barbiturates
carbamazepine
carisoprodol
chloramphenicol
chlordiazepoxide
danazol
diazepam
ergot alkaloids
estrogens
glutethimide
griseofulvin
imipramine
meprobamate
methsuximide
methyldopa
pentazocine
phenytoin
progesterones
sulfonamides
tolbutamide.
Discharge planning
For toxic-acquired porphyria, refer the patient and
family to resources that can help identify lead

sources in the home.
Check the patients history for use of medications that
can trigger an acute attack. (See Drugs that aggravate porphyria.)

Perform passive and active range-of-motion exercises.
Encourage the patient to express feelings and concerns about the disease.
Monitoring
Respiratory status
GI motility
Vital signs
Patient teaching
Be sure to cover:
avoidance of excessive sun exposure and use of sun
screen
importance of wearing medical identification
lead sources (if the patient has toxic-acquired porphyria)
precipitating factors, including crash diets, fasting,
and use of alcohol, estrogens, and barbiturates
stress-management techniques
ways to prevent infection
value of a high-carbohydrate diet.
Porphyrias
645
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Posttraumatic stress
disorder
Overview
Description
Development of psychological symptoms, such as in-
tense fear and feelings of hopelessness and loss of

control, after exposure to extreme trauma
Can be acute, chronic, or delayed
Pathophysiology
The alpha2-adrenergic receptor response that in-
hibits stress-induced release of norepinephrine is

impaired.
Progressive behavioral sensitization results, with generalization to stimulus cues from the original trauma.
Consequently, responses of increased sympathetic activity occur.
Causes
An event that the patient views as traumatic (typically
an event outside the range of usual human experience)
Risk factors
History of psychopathology
Neurotic and extroverted characteristics
History of child abuse or neglect
Incidence
Affects 30% of trauma victims
Occurs in up to 15% of Unites States residents at
some time in their lives

More common in females than males
Detachment and loss of emotional response
Feelings of depersonalization
Inability to recall specific aspects of the traumatic
event
Flashbacks within dreams or thoughts when cues to
the event occur

Nightmares of the traumatic event
Complications
Increased risk for other anxiety, mood, and sub-
stance-related disorders
Substance abuse
Feelings of detachment or estrangement, which may
damage interpersonal relationships
Assessment
History
Difficulty falling or staying asleep
Aggressive outbursts on awakening
646
Posttraumatic stress disorder
Panic attacks
Phobic avoidance of situations that arouse memories
of the traumatic event

Early life experiences, interpersonal factors, military
experiences, or other incidents that suggest the traumatic event

Symptoms that began immediately or soon after the
trauma (although in some cases, symptoms dont develop until months or years later)
Pangs of painful emotions and unwelcome thoughts
Traumatic re-experiencing of the traumatic event
Chronic anxiety
Rage and survivor guilt
Use of violence to solve problems
Depression and suicidal thoughts
Fantasies of retaliation
Physical findings
Emotional numbing (diminished or constricted re-
sponse)
Memory impairment
Difficulty concentrating
Signs of substance abuse
Physiologic reactivity on exposure to internal or ex-
ternal cues that symbolize or resemble an aspect of

the traumatic event
DSM-IV-TR criteria
Diagnosis is confirmed when the patient meets the following criteria:
Exposure to a traumatic event that included both of
the following:
actual or threatened death or serious injury or
threat to the physical integrity of self or others
a response of intense fear, helplessness, or horror.
Persistent reexperiencing of this traumatic event in at
least one of these ways:
recurrent and intrusive distressing recollections of
the event
recurrent distressing dreams of the event
flashbacks of the event
intense psychological distress at exposure to
events
physiologic reactivity on exposure to events.
Persistent avoidance of stimuli associated with the
trauma, or numbing of general responsiveness not
present before the trauma, as indicated by at least
three of these criteria:
efforts to avoid thoughts or feelings associated
with the traumatic event
efforts to avoid activities or situations that arouse
recollections of the traumatic event
inability to recall an important aspect of the event
sharply decreased interest in significant activities
feeling of detachment or estrangement from others
restricted range of effect
sense of a foreshortened future.
Persistent symptoms of increased arousal (not previously present) as indicated by two or more of these
criteria:
difficulty falling or staying asleep
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irritability or outbursts of anger

difficulty concentrating
hypervigilance
exaggerated startle response.
The disturbance must have lasted at least 1 month
and must cause significant distress or impairment of social, occupational, or other important areas of functioning.
importance of identifying and avoiding cues that
worsen symptoms
problem-solving skills
relaxation and breathing techniques
adverse effects.
Discharge planning
Treatment
Refer the patient to support services.

Refer the patient for psychotherapy.
Refer the patient to physical, social, and occupational
General
Refer the patient to drug treatment programs, as ap-
Supportive or expressive psychotherapy

Behavior therapies
Support groups
Rehabilitation programs in physical, social, and oc-
rehabilitation programs, as indicated.

propriate.
cupational areas
Treatment of alcohol or drug abuse, as needed
Active avoidance of stimuli that trigger memories of
the traumatic event
Medications
Benzodiazepines (short-term use)
Tricyclic antidepressants
Monoamine oxidase inhibitors
Selective serotonin-reuptake inhibitors
Sedating antidepressants
Anticonvulsants
Key outcomes
The patient will:
express feelings and fears related to the traumatic
event
use available support systems
use effective coping mechanisms
maintain or reestablish adaptive social interactions
with family members.
Encourage the patient to express feelings of grief,
mourning, and anger.

Practice crisis intervention techniques, as needed.
Assume a positive, consistent, honest, and nonjudg-
mental attitude.
Help the patient evaluate behavior.
Monitoring
Response to drug therapy
Patient teaching
Be sure to cover:
healing process
Posttraumatic stress disorder
647
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Precocious puberty
Overview
Description
Early sexual maturity
True precocious puberty: early maturation of the
hypothalamic-pituitary-gonadal axis, development of

secondary sex characteristics, gonadal development,
and spermatogenesis
Pseudoprecocious puberty: development of secondary sex characteristics without gonadal development
For males: physical changes occurring before age 9
and for females, before age 8
Pathophysiology
Special populations
Males as young as 7 with true precocious puberty
have fathered children.
In females
Rapid growth spurt
Breast development at early age
Pubic hair
Early menarche
Complications
Testicular tumor (males)
Ovarian or adrenal malignancy (females)
Assessment
In males, precocious puberty results from pituitary
History
or hypothalamic intracranial lesions that cause excessive secretion of gonadotropin.

In females, it results from early development and activation of the endocrine glands without corresponding abnormality.
Rapid growth spurt

Early muscle development (males)
Early menarche (females)
Causes
In males
TRUE PRECOCIOUS PUBERTY
Idiopathic
Genetically transmitted as a dominant gene
PSEUDOPRECOCIOUS PUBERTY
Testicular tumors
Congenital adrenogenital syndrome
In females
TRUE PRECOCIOUS PUBERTY
Idiopathic
Central nervous system (CNS) disorders
PSEUDOPRECOCIOUS PUBERTY
Ovarian and adrenocortical tumors
Estrogen or androgen ingestion
Increased end-organ sensitivity to low levels of circu-
lating sex hormones
Risk factors
Obesity
Exposure to sex hormones
McCune-Albright syndrome or congenital adrenal
hyperplasia
Incidence
Five times more common in females than in males
More common in blacks
In males
Early bone development; initial growth spurt
Early muscle development
Stunted adult stature
Adult hair pattern
Penile growth
Bilateral enlarged testes
648
Precocious puberty
Physical findings
Enlarged penis or testicles (males)
Enlarged breasts (females)
Pubic hair
Test results
Laboratory
IN MALES WITH TRUE PRECOCIOUS PUBERTY
Plasma testosterone levels are elevated.
Ejaculate shows live spermatozoa.
Luteinizing and follicle-stimulating hormones and
corticotropin levels are elevated.

IN MALES WITH PSEUDOPRECOCIOUS PUBERTY
Chromosomal karyotype analysis shows abnormal
pattern of autosomes and sex chromosomes.

24-hour urinary 17-ketosteroid and other steroid
levels are elevated.

IN FEMALES WITH PSEUDOPRECOCIOUS PUBERTY
Vaginal smear shows estrogen secretion.
Urinary tests for gonadotropic activity and excretion
of 17-ketosteroids are elevated.

Luteinizing and follicle-stimulating hormone levels
are elevated.
Imaging
X-rays of the hands, wrists, knees, and hips determine bone age and possibly premature epiphyseal
closure.
Ultrasound verifies suspected abdominal lesion.
X-rays possibly show CNS tumors.
Treatment
General
Aimed at underlying cause
Supportive psychological counseling
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Medications
Medroxyprogesterone (females)
Surgery
Removal of ovarian or adrenal tumors
Removal of thyroid gland
Key outcomes
The patient will:
demonstrate effective coping mechanisms
avoid complications.
Monitoring
Complications
Patient teaching
Be sure to cover:
adverse effects
the need to continue social and emotional support.
Discharge planning
Refer the patient to psychological counseling, as nec-
essary.
Precocious puberty
649
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Premenstrual syndrome
Overview
Description
Edema
Diarrhea or constipation
Appetite changes and food cravings
Fatigue
Exacerbations of skin, respiratory, or neurologic
problems
Group of somatic, behavioral, cognitive, and mood-
Physical findings
related symptoms occurring 1 to 14 days before

menses and usually subsiding with menses onset
Causes effects that range from minimal discomfort to
severe, disruptive symptoms
Also known as PMS and premenstrual dysphoric
disorder (PMDD)
Possible edema
Pathophysiology
PMS may result from a progesterone deficiency dur-
ing the luteal phase of the ovarian cycle.
Test results
Laboratory
Blood studies rule out anemia, thyroid disease, or
other hormonal imbalances.
Other
A daily symptom calendar aids diagnosis of PMS.
Psychological evaluation may be used to rule out or
detect an underlying psychiatric disorder.
Hormone levels and patterns in females with PMS
dont differ significantly from those in women who

dont experience PMS.
Treatment
Causes
General
Physiologic, psychological, and sociocultural factors

Possible progesterone deficiency in the luteal phase
Possible serotonin or norepinephrine deficiency
Possible low vitamin and mineral levels
Symptom relief
Stress reduction
Relaxation techniques
Diet low in simple sugars, caffeine intake, animal fat,
Incidence
Increased calcium and complex carbohydrate intake

Aerobic exercise
Affects 30% of females in the United States
Special populations
Moderate to severe symptoms occur in 14% to 88%
of adolescent girls
Usually occurs between ages 25 and 45
Affects women in their 40s most severely
PMS resolving completely at menopause
Anxiety
Irritability
Depression
Multiple somatic complaints
Complications
Psychosocial problems
Reduced self-esteem
Depression
Inability to function (in PMDD)
Assessment
History
Behavioral changes
Breast tenderness or swelling
Abdominal tenderness or bloating
Joint pain
Headache
650
and sodium
Medications
Antidepressants such as selective serotonin-reuptake
inhibitors
Vitamins such as B complex
Progestins and estrogens, such as drospirenone and
ethinyl estradiol and medroxyprogesterone acetate

Prostaglandin inhibitors
Monophasic birth control pills
Key outcomes
The patient will:
identify effective and ineffective coping techniques
use available support systems, such as family, friends,
and groups, to develop and maintain effective coping
skills
express positive feelings about herself.
Encourage adequate fluid intake.
Offer emotional support and reassurance.
Encourage the patient to express feelings.
Instruct the patient to chart symptoms daily for two
cycles.
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Monitoring
Coping skills
Patient teaching
Be sure to cover:
physiologic basis of PMS
beneficial lifestyle changes
relaxation and stress-reduction techniques
dietary management.
Discharge planning
Refer the patient to a self-help group for females with
PMS.
Refer the patient for psychological counseling, as in-
dicated.
Refer the patient to a dietitian as needed.
651
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Pressure ulcers
Overview
Assessment
History
One or more risk factors
Description
Physical findings
Localized areas of ischemic tissue caused by pres-
Shiny, erythematous superficial lesion (early)

Small blisters or erosions with progression of super-
sure, shearing, or friction

Most common over bony prominences, especially the
sacrum, ischial tuberosities, greater trochanter,
heels, malleoli, and elbows
May be superficial, caused by localized skin irritation
(with subsequent surface maceration), or deep, arising in underlying tissue (Deep lesions may go undetected until they penetrate the skin.)
Also called decubitus ulcers, pressure sores, or
bedsores
Pathophysiology
Impaired skin capillary pressure results in local tis-
sue anoxia.
Anoxia leads to edema and multiple capillary throm-
ficial erythema
Possible necrosis and ulceration with deeper ero-
sions and ulcerations

Malodorous, purulent discharge (suggesting sec-
ondary bacterial infection)

Black eschar around and over the lesion
Test results
Laboratory
Infecting organism is identified by wound culture and
sensitivity testing of exudate.
Total serum protein level is decreased.
Other
Diagnosis is typically made from inspection.
boses.
An inflammatory reaction results in ulceration and
necrosis of ischemic cells.
Treatment
Causes
General
Local tissue compression

Shearing force
Friction
Measures to prevent pressure ulcers

Relief of pressure on the affected area
Meticulous skin care
Devices, such as pads, mattresses, and special beds
Moist wound therapy dressings
Whirlpool baths
Diet high in protein, iron, and vitamin C (unless con-
Risk factors
Poor nutrition
Diabetes mellitus
Immobility or paralysis
Cardiovascular disorders
Advanced age
Incontinence
Obesity
Edema
Anemia
Poor hygiene
Exposure to chemicals
Steroids
Incidence
Affect roughly 10% of hospitalized patients and 20%
traindicated)
Active and passive range-of-motion (ROM) exercises
Frequent turning and repositioning
Medications
Enzymatic ointments
Healing ointments
Antibiotics, if indicated
Surgery
Debridement of necrotic tissue
Skin grafting (in severe cases)
to 40% of patients in long-term care facilities
Vary with the ulcer stage (see Stages of pressure ul-
cers)
Complications
Secondary bacterial infection
Septicemia
Gangrene
652
Pressure ulcers
Key outcomes
The patient will:
exhibit improved or healed lesions or wounds
maintain adequate daily caloric intake
maintain joint mobility and ROM
avoid infection and other complications.
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Stages of pressure ulcers

To protect the patient from pressure ulcer complications, learn to recognize the stages of ulcer formation.
Stage I
Stage III
The skin is red and intact and doesnt blanche with external
pressure. (A black persons skin may look purple.) The skin
feels warm and firm.
A hole develops and slough may be present. Undermining

may or may not be present.
Stage IV
Stage II
Skin breaks appear and discoloration may occur. Penetrating to the subcutaneous fat layer, the sore is painful and visibly swollen. Thulcer may be characterized as an abrasion,
blister, or shallow crater.
The ulcer destroys tissue from the skin to the bone. Findings include slough or eschar and deep tunnels that extend
from the ulcer.
Suspected deep tissue injury

The skin is purple or maroon but intact or a blood-filled blister may be present.
Unstageable
The ulcer destroys tissue from the skin to possibly the bone.
The base of the ulcer is covered by slough, eschar or both.
Until this is removed, the depth and stage cant be determined.
Apply dressings appropriate for the ulcer stage.
Encourage adequate food and fluid intake.
Reposition the bedridden patient at least every
2 hours.
Elevate the head of the bed 30 degrees or less.
Perform passive ROM exercises.
Encourage active ROM exercises, if possible.
Use pressure-relief aids on the bed.
Provide meticulous skin care.
Monitoring
Changes in skin color, turgor, temperature, sensa-
tion, and drainage

Change in the ulcer stage
Laboratory results
Complications
Intake and output
Patient teaching
Be sure to cover:
techniques for changing positions
active and passive ROM exercises
avoidance of skin-damaging agents
debridement procedures
skin graft surgery, if required
signs and stages of healing
importance of a well-balanced diet and adequate
fluid intake
adverse effects
importance of notifying the physician immediately of
signs and symptoms of infection.
Discharge planning
Refer the patient to a wound care specialist, if indi-
cated.
Pressure ulcers
653
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Proctitis
Overview
Description
An acute or chronic inflammation of the rectal mu-
cosa
Good prognosis unless massive bleeding occurs
Pathophysiology
Mucosal cell loss occurs along with acute inflamma-
tion of the lamina propria, eosinophilic crypt abscess, and endothelial edema of the arterioles
Rectal tissue ischemia occurs
Mucosal friability, ulcers, bleeding, and fistulas result
Causes
Crohns disease
Amebiasis
Immunodeficiency disorders
Neisseria gonorrhoeae
Chlamydia trachomatis
Herpes simplex virus 1 and 2
Syphilis
Radiation therapy
Papillomavirus
Ischemia
Toxins
Vasculitis
Risk factors
High-risk sexual practices
Homosexuality
Autoimmune disorders
Incidence
Assessment
History
Tenesmus
Abdominal cramping
Loose stool with or without abdominal pain
Pruritus
Rectal and anal pain
Physical findings
Bloody or mucoid stools
Superficial ulcers
Mucosal erythema
Painless chancres
Mucosal friability
Test results
Laboratory
Complete blood count evaluates blood loss.
C-reactive protein may be elevated.
Rectal swab identifies gonorrhea or chlamydia.
Venereal disease research laboratory test diagnoses
syphilis.
Culture of vesicular fluid identifies herpes simplex
virus.
In acute proctitis, sigmoidoscopy shows edematous,
bright-red, or pink rectal mucosa thats thick, shiny,
friable and, possibly, ulcerated.
In chronic proctitis, sigmoidoscopy shows thickened
mucosa, loss of vascular pattern, and stricture of the
rectal lumen.
Biopsy rules out carcinoma.
Treatment
Occurs in 5% to 20% of patients receiving radiation
General
therapy
More common in Jewish people
More common in males than females
Occurs predominantly in adults
Elimination of the underlying cause

Increased fluids
Activity as tolerated
Sitz baths
Medications
Tenesmus
Constipation
Feeling of rectal fullness
Left-sided abdominal pain
Enemas
Steroid (hydrocortisone) suppositories
Tranquilizers
Antibiotics (based on cause)
Antivirals
Complications
Ulcerations
Crypt abscesses
Bleeding
Fissures
Fistulas
Ulcerative colitis
654
Proctitis
Surgery
Diverting colostomy may be necessary.
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Key outcomes
The patient will:
understand the disease process and treatment
regimen
exhibit adequate coping mechanisms.
Monitoring
Rectal bleeding
Amount and character of stools
Patient teaching
Be sure to cover:
importance of watching for and reporting bleeding
and other persistent symptoms.
Discharge planning
Refer the patient to a colorectal surgeon, if appro-
priate.
Proctitis
655
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Prostate cancer
Overview
Description
Proliferation of cancer cells that usually take the
Assessment
History
Symptoms rare in early stages
Later, urinary problems, such as difficulty initiating a
urinary stream, dribbling, and urine retention
form of adenocarcinomas and typically originate in

the posterior prostate gland
May progress to widespread bone metastasis and
death
Is the leading cause of cancer death in males
Physical findings
Pathophysiology
Test results
Slow-growing prostate cancer seldom causes signs
Laboratory
Elevated serum prostate-specific antigen (PSA) level
may indicate cancer with or without metastasis.
Imaging
Transrectal prostatic ultrasonography shows prostate
size and presence of abnormal growths.
Bone scan and excretory urography determine the
diseases extent.
Magnetic resonance imaging and computed tomography scan define the extent of the tumor.
Other
Standard screening test: digital rectal examination
and PSA test identify cancer (recommended yearly by
the American Cancer Society for males older than age
40).
and symptoms until its well advanced.

Typically, when a primary prostatic lesion spreads
beyond the prostate gland, it invades the prostatic
capsule and spreads along ejaculatory ducts in the
space between the seminal vesicles or perivesicular
fascia.
Endocrine factors may play a role, leading researchers to suspect that androgens speed tumor
growth.
Malignant prostatic tumors seldom result from the
benign hyperplastic enlargement that commonly develops around the prostatic urethra in older men.
Causes
In early stages: nonraised, firm, nodular mass with a
sharp edge
In advanced disease: edema of the scrotum or leg; a
hard lump in the prostate region
Unknown
Risk factors
Older than age 50
Family history
Heavy metal exposure (cadmium)
Exposure to androgens
High-fat diet
Treatment
General
Varies with cancer stage
Radiation therapy or internal beam radiation
Well-balanced diet
Incidence
Medications
Most common among Blacks; least common among
Hormonal therapy
Chemotherapy
Asians
Unaffected by socioeconomic status or fertility
Most common neoplasm in males older than age 50
Urinary problems
Complications
Spinal cord compression
Deep vein thrombosis
Pulmonary emboli
Myelophthisis
Death
Surgery
Prostatectomy
Orchiectomy
Radical prostatectomy
Transurethral resection of prostate
Cryosurgical ablation
Key outcomes
The patient will:
discuss the diseases impact on self and family
members
656
Prostate cancer
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Monitoring
Pain level
Wound site
Postoperative complications
Medication effects
Patient teaching
Be sure to cover:
perineal exercises that decrease incontinence
follow-up care
adverse effects.
Discharge planning
Refer the patient to appropriate resources and sup-
port services.
Prostate cancer
657
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Prostatitis
Overview
Description
Inflammation of the prostate gland
Occurs in acute, chronic, and several other forms
Acute prostatitis
Easily recognized and treated
Chronic prostatitis
Most common cause of recurrent urinary tract infection in males
More difficult to recognize than acute prostatitis
Other prostatitis forms
Granulomatous prostatitis (also called tuberculous
prostatitis)
Nonbacterial prostatitis
Prostatodynia (painful prostate)
Pathophysiology
Infectious organism spreads to the prostate gland by
the hematogenous route, an ascending urethral infection, invasion of rectal bacteria via lymphatic vessels, or reflux of infected bladder urine into prostate
ducts.
Inflammation results.
Causes
Bacterial prostatitis: Escherichia coli (80% of cas-
es); Klebsiella, Enterobacter, Proteus, Pseudomonas, Serratia, Streptococcus, Staphylococcus,

and diphtheroids (20% of cases)
Chronic prostatitis: bacterial invasion from urethra
Granulomatous prostatitis: miliary spread of Mycobacterium tuberculosis
Nonbacterial prostatitis: Mycoplasma, Ureaplasma,
Chlamydia, or Trichomonas vaginalis, or a virus
Prostatodynia: unknown
Complications
Prostatic abscess
Acute urinary retention
Pyelonephritis
Epididymitis
Assessment
History
Sudden fever, chills
Lower back pain
Perineal fullness
Arthralgia, myalgia
Urinary urgency and frequency
Dysuria, nocturia
Transient erectile dysfunction
Chronic bacterial prostatitis

May be asymptomatic
Usually causes same urinary symptoms as the acute
form, but to a lesser degree
Hemospermia
Persistent urethral discharge
Painful ejaculation
Dysuria
Mild perineal or lower back pain
Frequent nocturia
Prostatodynia
Perineal, lower back, or pelvic pain
Physical findings
Cloudy urine
Distended bladder
Prostatic tenderness, induration, swelling, firmness,
and warmth
Crepitation (if prostatic calculi present)
Chronic bacterial prostatitis

Stony, hard induration of the prostate
Risk factors
Test results
Invasive urethral procedures

Infrequent or excessive sexual intercourse
Laboratory
Urine culture identifies infectious organism.
In nonbacterial prostatitis: inflammatory cells are
found in smears of prostatic secretion.
In prostatodynia: urine cultures are negative and
theres an absence of inflammatory cells in smears of
prostatic secretions.
In granulomatous prostatitis: prostate tissue biopsy
shows M. tuberculosis.
Urodynamic evaluation reveals detrusor hyperreflexia
and pelvic floor myalgia (from chronic spasms).
Incidence
Chronic prostatitis
Affects up to 35% of males older than age 50
Seen in 5 of every 1,000 outpatient visits
Bacterial prostatitis
Urinary frequency and urgency
Fever
658
Prostatitis
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Treatment
Patient teaching
General
After surgery
Avoidance of lifting, strenuous exercise, and long automobile rides
No sexual activity for several weeks after discharge
Be sure to cover:
adverse effects
importance of increased fluid intake
benefits of regular sexual activity (with chronic prostatitis)
prescribed activity limits
importance of getting immediate medical attention
for fever, inability to void, or bloody urine.
Medications
Discharge planning
Analgesics
Antipyretics
Refer the patient to counseling or support group as
Sitz baths
Regular, protected sexual intercourse
Prostatic massage
Increased oral fluids
Bed rest until the condition improves
needed.
Acute prostatitis
Systemic antibiotic therapy
Chronic prostatitis
Oral antibiotics
Granulomatous prostatitis
Antitubercular drug combinations
Oral antibiotics
Anticholinergics
Prostatodynia
Muscle relaxants
Alpha-adrenergic blockers
Surgery
Transurethral resection of the prostate or total
prostatectomy, if drug therapy unsuccessful
Key outcomes
The patient will:
demonstrate skill in managing urinary elimination
problems
express his feelings about potential or actual changes
in sexual function
use available counseling, referrals, or support
groups.
Ensure bed rest and adequate hydration.
Give sitz baths.
Avoid rectal examinations.
Monitoring
After surgery
Intake and output
Catheter function and drainage
Signs of infection
Pain control
Prostatitis
659
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Pseudomembranous
enterocolitis
Overview
Description
Acute inflammation and necrosis of the small and
large intestines
Usually affects the mucosa but may extend into the
submucosa and, rarely, into other layers

Marked by severe diarrhea
Can be fatal in 1 to 7 days from severe dehydration
or from toxicity, peritonitis, or perforation
Peritonitis
Toxic megacolon
Assessment
History
Current or recent antibiotic treatment
Sudden onset of copious, watery, or bloody diarrhea
Cramping abdominal pain
Low-grade fever
Nausea
Vomiting
Physical findings
Abdominal tenderness
Pathophysiology
Test results
Pseudomembranous enterocolitis is associated with
Laboratory
Hypoalbuminemia occurs due to poor protein
absorption.
Stool culture identifies C. difficile.
Imaging
Abdominal X-ray reveals mucosal edema.
Computed tomography scan may show distention as
well as diffuse and focal thickening of the colon wall.
Rectal biopsy through sigmoidoscopy confirms
pseudomembranous enterocolitis.
Endoscopy reveals characteristic pseudomembranes.
antibiotic use.
Normal intestinal flora balance is altered, and overgrowth of certain organisms occurs.
Necrotic mucosa is replaced by a pseudomembrane
filled with staphylococci, leukocytes, mucus, fibrin,
and inflammatory cells.
Causes
Unknown
Possible role of Clostridium difficile
Risk factors
Antibiotic therapy
Recent abdominal surgery
Cancer chemotherapy
Compromised immune system
Advanced age
Bone-marrow transplantation
Intestinal ischemia
Uremia
Burns
Incidence
Most common in nursing home and hospital patients
Affects 6 of every 100,000 people treated with antibi-
otics
Treatment
General
Discontinuation of offending antibiotics
Avoidance of opioids and antidiarrheals
Supportive treatment
I.V. fluids (if the condition is severe)
Nothing by mouth until bowel recovery occurs (if the
condition is severe)
Bed rest until recovery begins
Enteric precautions
Medications
Oral metronidazole or oral vancomycin

Watery, green, foul-smelling diarrhea

Up to 30 stools per day
Surgery
Complications
Severe dehydration
Electrolyte imbalance
Hemorrhage
Hypotension
Hypovolemia
Sepsis
Shock
Colonic perforation
660
Pseudomembranous enterocolitis
Diverting ileostomy or bowel resection (with perfora-
tion or toxic megacolon)

Early subtotal colectomy
Key outcomes
The patient will:
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regain normal bowel function
regain normal laboratory values.
Administer prescribed drugs and I.V. fluids.
Keep the patient as comfortable as possible.
Maintain precautions to prevent the infection from
spreading to other patients.
Monitoring
Vital signs
Skin integrity
Bowel function
Electrolytes
Patient teaching
Be sure to cover:
adverse effects
signs and symptoms of a recurrence
importance of cautioning future prescribers (if the
disorder was antibiotic-related).
Discharge planning
Refer the patient to home care services as indicated.
Pseudomembranous enterocolitis
661
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Psoriasis
Overview
Description
Pruritus and burning

Arthritic symptoms such as morning joint stiffness
Remissions and exacerbations
Physical findings
Erythematous, well-demarcated papules and plaques
as they migrate from the basal membrane to the surface or stratum corneum.
As a result, the stratum corneum develops thick,
scaly plaques (the cardinal manifestation of psoriasis).
covered with silver scales, typically appearing on the

scalp, chest, elbows, knees, back, and buttocks
In mild psoriasis: plaques scattered over a small skin
area
In moderate psoriasis: plaques more numerous and
larger (up to several centimeters in diameter)
In severe psoriasis: plaques covering at least half the
body
Friable or adherent scales
Fine bleeding points or Auspitz sign after attempts to
remove scales
Thin, erythematous guttate lesions, alone or with
plaques, and with few scales (see Identifying types
of psoriasis)
Small indentations or pits, and yellow or brown discoloration of fingernails or toenails
In severe cases, separation of nail from nail bed
Causes
Test results
Genetic predisposition
Possible autoimmune process
Physical trauma
Beta-hemolytic streptococci infection
Laboratory
Serum uric acid level is elevated.
In early-onset familial psoriasis: human leukocyte
antigens Cw6, B13, and Bw-57 are present.
Skin biopsy helps rule out other diseases.
Hereditary chronic skin disease marked by epider-
mal proliferation
Causes lesions of erythematous papules and plaques
covered with silvery scales (Lesions vary widely in

severity and distribution.)
Involves recurring remissions and exacerbations
Exacerbations unpredictable, but usually controllable
with therapy
Pathophysiology
Psoriatic skin cells have a shortened maturation time
Risk factors
Pregnancy
Endocrine changes
Cold weather
Emotional stress
Treatment
Incidence
Depends on the psoriasis type, extent, and effect on
Affects about 2% of the United States population

Can occur at any age
More common among whites
Two periods of onset: early (young adulthood) and
late (middle adulthood)
Silvery scales on red plaques
Pruritus
Knee-elbow-scalp distribution
Complications
Infection
Altered self-image
Social isolation
Depression
Assessment
History
Family history of psoriasis
Risk factors
662
Psoriasis
General
the patients quality of life
Lesion management
Lukewarm baths
Ultraviolet B light or natural sunlight
Medications
Topical corticosteroid creams and ointments
Antihistamines
Analgesics
Occlusive ointment bases
Urea or salicylic acid preparations
Coal tar preparations
Vitamin D analogs
Emollients
Kerolytic agents
Methotrexate for severe, unresponsive psoriasis
Potent retinoic acid derivative for resistant psoriasis
Cyclosporine for severe, widespread psoriasis
Immunomodulators (biologics), such as alefacept,
efalizumab, or etanercept for psoriatic arthritis or

failed treatment
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Identifying types of psoriasis

Psoriasis occurs in various forms, ranging from one or two localized plaques that seldom require long-term medical attention to widespread lesions and crippling arthritis.
Erythrodermic psoriasis
Psoriasis vulgaris
Erythrodermic psoriasis is marked by extensive flushing all

over the body, which may result in scaling. The rash may
develop rapidly, signaling new psoriasis or gradually in
chronic psoriasis. Sometimes the rash occurs as an adverse drug reaction.
Psoriasis vulgaris is the most common. It begins with red,

dotlike lesions that gradually enlarge and produce dry, silvery scales. The plaques usually appear symmetrically on
the knees, elbows, extremities, genitalia, scalp, and nails.
Guttate psoriasis
Pustular psoriasis features an eruption of local or extensive

small, raised, pus-filled plaques. Possible triggers include
emotional stress, sweating, infections, and adverse drug
reactions.
Guttate psoriasis typically affects children and young

adults. Erupting in drop-size plaques over the trunk, arms,
legs and, sometimes, the scalp, this rash generalizes in
several days. Its commonly associated with upper respiratory streptococcal infections.
Pustular psoriasis
Inverse psoriasis
Smooth, dry, bright red plaques characterize inverse psoriasis. Located in skin folds (armpits and groin, for example),
the plaques fissure easily.
Surgery
Surgical nail removal to treat severely disfigured or
damaged nails caused by psoriasis
likelihood of exacerbations and remissions

adverse effects
how to apply prescribed ointments, creams, and lo-
Key outcomes
The patient will:
exhibit improved or healed lesions
verbalize feelings about changed body image
demonstrate understanding of proper skin care
express an understanding of the condition and its
treatment.
tions
importance of avoiding scratching plaques
measures to relieve pruritus
importance of avoiding sun exposure
stress-reduction techniques
safety precautions
relationship between psoriasis and arthritis
Discharge planning
Refer the patient to the National Psoriasis Founda-
tion.

Apply topical medications using a downward motion.
Encourage the patient to verbalize his feelings.
Involve family members in the treatment regimen.
Monitoring
Lipid profile results
Liver function tests
Renal function
Blood pressure
Signs and symptoms of hepatic or bone marrow
toxicity
Patient teaching
Be sure to cover:
risk factors
incommunicability of psoriasis
Psoriasis
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Ptosis
Overview
Assessment
History
Description
History of causative factor

Family history
Trauma or ocular surgery
Drooping of the upper eyelid

May be congenital or acquired, unilateral or bilater-
Physical findings
al, constant or intermittent

If severe, usually responds to treatment; if slight, may
not require treatment
Also known as blepharoptosis
Pathophysiology
Ptosis is caused by dysfunction of one or both upper
eyelid levator muscles.
Causes
Congenital ptosis
Transmitted as an autosomal dominant trait
Results from a congenital anomaly in which the levator muscles of the eyelids fail to develop
Acquired ptosis
Advanced age (involutional ptosis, the most common
form, usually seen in older patients following
cataract surgery)
Mechanical factors that make the eyelid heavy
Myogenic factors
Neurogenic (paralytic) factors
Nutritional factors
Trauma
Ocular surgery
Abnormal eyelid
Drooping eyelid (see Recognizing ptosis)
Elevated eyebrow
Wrinkled forehead
Fixed, dilated pupil
Test results
Imaging
Digital subtraction angiography and magnetic resonance imaging (MRI) show aneurysm.
MRI reveals multiple sclerosis.
Glucose tolerance test detects diabetes.
Tensilon test detects myasthenia gravis (in acquired
ptosis with no history of trauma).
Other
Physical examination reveals upper lid retraction.
Examination with the Hertel exophthalmometer reveals the degree of proptosis.
Treatment
General
Incidence
Treatment of underlying cause

Special glasses with an attached suspended crutch on
Congenital ptosis: occurs at birth

Acquired ptosis: can occur at any age but mostly
Eye protection with potentially dangerous activities
affects adults
the frames to elevate the eyelid
Medications
Topical antibiotic ointment (after surgery)
An infant with congenital ptosis has a smooth, flat up-
Surgery
per eyelid, without the eyelid fold normally caused by

the pull of the levator muscle; associated weakness of
the superior rectus muscle isnt uncommon.
Ptosis due to oculomotor nerve damage produces a
fixed, dilated pupil; divergent strabismus; and slight
depression of the eyeball.
Resection of the weak levator muscles
Complications
Disturbed vision
Amblyopia
Infection (after surgery)
Psychosocial effects
Key outcomes
The patient will:
avoid injury
demonstrate improvement in eyelid function
express understanding of the disorder and its treatment.
Provide a safe environment.
Apply ointment to the sutures as prescribed.
Monitoring
Signs of bleeding (after surgery)
Visual acuity
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Ptosis
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Recognizing ptosis
A drooping upper eyelid typically apparent on visual
examination is the hallmark of ptosis. The disorder
may affect one or both eyelids.
Patient teaching
Be sure to cover:
the need to report postsurgery bleeding immediately
the need to prevent accidental trauma to the surgical
site until healing is complete.
Discharge planning
Refer the patient to a neurologist if myasthenia gravis
or multiple sclerosis is diagnosed.
Ptosis
665
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Pulmonary edema
Overview
Description
Accumulation of fluid in the extravascular spaces of
the lung
Common complication of cardiovascular disorders
May be chronic or acute
Can become fatal rapidly
Pathophysiology
Pulmonary edema results from either increased pul-
Orthopnea
Paroxysmal nocturnal dyspnea
Complications
Respiratory and metabolic acidosis
Cardiac or respiratory arrest
Death
Assessment
History
Predisposing factor
Persistent cough
Dyspnea on exertion
Paroxysmal nocturnal dyspnea
Orthopnea
monary capillary hydrostatic pressure or decreased

colloid osmotic pressure. Normally, the two pressures are in balance.
If pulmonary capillary hydrostatic pressure increases, the compromised left ventricle needs higher filling pressures to maintain adequate output; these
pressures are transmitted to the left atrium, pulmonary veins, and pulmonary capillary bed. Fluids
and solutes are then forced from the intravascular
compartment into the lung interstitium. With fluid
overloading the interstitium, some fluid floods peripheral alveoli and impairs gas exchange.
If colloid osmotic pressure decreases, the pulling
force that contains intravascular fluids is lost, and
nothing opposes the hydrostatic force. Fluid flows
freely into the interstitium and alveoli, causing pulmonary edema.
Physical findings
Causes
Laboratory
Arterial blood gas (ABG) analysis shows hypoxemia,
hypercapnia, or acidosis.
Imaging
Chest X-rays show diffuse haziness of the lung fields,
cardiomegaly, and pleural effusion.
Pulse oximetry may show decreased oxygen saturation.
Pulmonary artery catheterization may reveal increased pulmonary artery wedge pressures.
Electrocardiography may show valvular disease and
left ventricular hypokinesis or akinesis.
Left-sided heart failure

Diastolic dysfunction
Valvular heart disease
Arrhythmias
Fluid overload
Acute myocardial ischemia and infarction
Barbiturate or opiate poisoning
Impaired pulmonary lymphatic drainage
Inhalation of irritating gases, smoke inhalation
Left atrial myxoma
Pneumonia
Pulmonary veno-occlusive disease
Kidney disease
Altitude above 8,000 feet
Ascent to high altitudes without becoming acclimated
Incidence
More common in middle-aged and elderly people
Persistent cough
Dyspnea on exertion
666
Pulmonary edema
Restlessness and anxiety

Rapid, labored breathing
Intense, productive cough
Frothy, bloody sputum
Jugular vein distention
Sweaty, cold, clammy skin
Wheezing
Crackles
S3
Tachycardia
Hypotension
Thready pulse
Peripheral edema
Hepatomegaly
Test results
Treatment
General
Fluid overload reduction
Improved gas exchange and myocardial function
Correction of underlying disease
Sodium-restricted diet
Fluid restriction
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Medications
Supplemental oxygen
Diuretics
Antiarrhythmics
Morphine
ALERT
Be aware that morphine can further compromise
respirations in a patient with respiratory distress.
Keep resuscitation equipment at hand in case the
patient stops breathing.
adverse effects
fluid and sodium restrictions
daily weight
signs and symptoms of fluid overload
energy conservation strategies
avoidance of alcohol
Discharge planning
Refer the patient to a cardiac rehabilitation program,
if indicated
Preload-reducing agents, such as furosemide and
indicated.
nitroglycerin
Afterload-reducing agents, such as nitroprusside and
enalapril
Bronchodilators
Positive inotropic agents
Vasopressors
Surgery
Valve repair or replacement or myocardial revascu-
larization if appropriate to correct the underlying

cause
Key outcomes
The patient will:
maintain adequate cardiac output
verbalize decreased anxiety and fear
demonstrate adequate coping mechanisms.
Place the patient in high Fowlers position.
Restrict fluids and sodium intake.
Promote rest and relaxation.
Monitoring
Vital signs
Intake and output
Daily weight
Respiratory status
Complications
Heart rhythm
ABG values
Pulse oximetry values
Hemodynamic values
Patient teaching
Be sure to cover:
Pulmonary edema
667
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Pulmonary embolism
Overview
Description
Obstruction of the pulmonary arterial bed occurring
when a mass (such as a dislodged thrombus) lodges

in the main pulmonary artery or branch, partially or
completely obstructing it
Most thrombi originate in deep veins of the leg
Can be asymptomatic, but sometimes causes rapid
death from pulmonary infarction
Pathophysiology
Thrombus formation results from vascular wall dam-
age, venous stasis, or blood hypercoagulability.
Complications
Pulmonary infarction
Embolic extension
Hepatic congestion and necrosis
Pulmonary abscess
Shock
Massive atelectasis
Right-sided heart failure
Ventilation-perfusion mismatch
Death
Assessment
History
Predisposing factor
Shortness of breath for no apparent reason
Pleuritic pain or angina
Trauma, clot dissolution, sudden muscle spasm, in-
Physical findings
travascular pressure changes, or peripheral blood

flow changes can cause the thrombus to loosen or
fragmentize.
The thrombus (now an embolus) floats to the hearts
right side and enters the lung through the pulmonary
artery. There, the embolus may dissolve, continue to
fragmentize, or grow.
By occluding the pulmonary artery, the embolus prevents alveoli from producing enough surfactant to
maintain alveolar integrity. Alveoli collapse and atelectasis develop.
If the embolus enlarges, it may occlude most or all of
the pulmonary vessels and cause death.
Tachycardia
Low-grade fever
Weak, rapid pulse
Hypotension
Productive cough, possibly with blood-tinged sputum
Warmth, tenderness, and edema of the lower leg
Restlessness
Transient pleural friction rub
Crackles
S3 and S4 with increased intensity of the pulmonic
Causes
Test results
Deep vein thrombosis

Pelvic, renal, and hepatic vein thrombosis
Right heart thrombus
Upper extremity thrombosis
Atrial fibrillation
Valvular heart disease
Rarely, other types of emboli, such as bone, air, fat,
Laboratory
D-dimer level is elevated.
Imaging
Lung ventilation-perfusion scan shows a ventilationperfusion mismatch.
Pulmonary angiography shows a pulmonary vessel
filling defect or an abrupt vessel ending and reveals
the location and extent of pulmonary embolism.
Chest X-rays may show a small infiltrate or effusion.
Spiral chest computed tomography scan may show
central pulmonary emboli.
Electrocardiography may reveal right axis deviation
and right bundle-branch block; it also may show atrial fibrillation.
amniotic fluid, tumor cells, or a foreign body
Risk factors
Various disorders and treatments (see Whos at risk
for pulmonary embolism?)
Incidence
600,000 to 700,000 cases annually
More common with advancing age
Shortness of breath for no apparent reason
Tachycardia
Anxiety
Pleuritic or anginal pain
component of S2
With a large embolus: cyanosis, syncope, distended
neck veins
Treatment
General
Maintenance of adequate cardiovascular and pul-
monary function
Mechanical ventilation, if indicated
668
Pulmonary embolism
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Whos at risk for pulmonary embolism?

Many disorders and treatments heighten the risk of pulmonary embolism. At particular risk are surgical patients. The anesthetic used during surgery can injure lung vessels, and surgery or prolonged bed rest can promote venous stasis, which
compounds the risk.
Predisposing disorders
Lung disorders, especially chronic types

Cardiac disorders
Infection
Diabetes mellitus
History of thromboembolism, thrombophlebitis, or vascular insufficiency
Sickle cell disease
Autoimmune hemolytic anemia
Polycythemia
Osteomyelitis
Long-bone fracture
Manipulation or disconnection of central lines
Venous stasis
Prolonged bed rest or immobilization

Obesity
Older than age 40
Burns
Recent childbirth
Orthopedic casts
Venous injury
Surgery, particularly of the legs, pelvis, abdomen, or

thorax
Leg or pelvic fractures or injuries
I.V. drug abuse
I.V. therapy
Increased blood coagulability
Cancer
Use of high-estrogen hormonal contraceptives
Possible fluid restriction

Bed rest during the acute phase
Medications
Oxygen therapy
Thrombolytics
Anticoagulation
Corticosteroids (controversial)
Diuretics
Antiarrhythmics
Vasopressors (for hypotension)
Antibiotics (for septic embolus)
Surgery
Vena caval interruption
Vena caval filter placement
Pulmonary embolectomy
Key outcomes
The patient will:
verbalize feelings of increased comfort
Avoid I.M. injections.
Encourage active and passive range-of-motion exer-
cises, unless contraindicated.

Avoid massage of the lower legs.
Apply antiembolism stockings.
Provide adequate nutrition.
Assist with ambulation as soon as the patient is
stable.
Encourage the use of an incentive spirometer.
Monitoring
Vital signs
Intake and output
Respiratory status
Pulse oximetry
ABG values
Signs of deep vein thrombosis
Complications
Coagulation study results
Abnormal bleeding
Stools for occult blood
Patient teaching
Be sure to cover:
the disease, diagnosis, and treatment
adverse effects
ways to prevent deep vein thrombosis and pulmonary
embolism
signs and symptoms of abnormal bleeding
prevention of abnormal bleeding
how to monitor anticoagulant effects
dietary sources of vitamin K
Discharge planning
Refer the patient to a weight-management program, if
indicated.
Pulmonary embolism
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Pulmonary
hypertension
Overview
Description
Pulmonary condition exhibiting increased pressure
in the pulmonary artery

Occurs in a primary form (rare) and a secondary
form
In both forms, resting systolic pulmonary artery pressure (PAP) above 30 mm Hg and mean PAP above
20 mm Hg
Primary form also known as PPH
Pathophysiology
In PPH, the intimal lining of the pulmonary arteries
thickens for no apparent reason. This narrows the

artery and impairs distensibility, increasing vascular
resistance.
Secondary pulmonary hypertension occurs from hypoxemia caused by conditions involving alveolar hypoventilation, vascular obstruction, or left-to-right
shunting.
Causes
Primary pulmonary hypertension
Unknown
Possible hereditary factors
Possible altered autoimmune mechanisms
Associated with portal hypertension
Secondary pulmonary hypertension
Chronic obstructive pulmonary disease
Sarcoidosis
Diffuse interstitial pneumonia
Malignant metastasis
Scleroderma
Use of some diet drugs
Obesity
Sleep apnea
Hypoventilation syndromes
Kyphoscoliosis
Pulmonary embolism
Vasculitis
Left atrial myxoma
Congenital cardiac defects
Mitral stenosis
Living at a high altitude
Incidence
Primary pulmonary hypertension
Most common in females ages 20 to 40
More prevalent in people with collagen disease
670
Dyspnea on exertion
Weakness, fatigue
Syncope
Complications
Cor pulmonale
Heart failure
Cardiac arrest
Death
Assessment
History
Shortness of breath with exertion
Weakness, fatigue
Pain during breathing
Near-syncope
Physical findings
Ascites
Peripheral edema
Restlessness and agitation
Decreased diaphragmatic excursion
Apical impulse displaced beyond mid-clavicular line
Right ventricular lift
Reduced carotid pulse
Hepatomegaly
Tachycardia
Systolic ejection murmur
Widely split S2
S3 and S4
Hypotension
Tubular breath sounds
Test results
Laboratory
Imaging
Ventilation-perfusion lung scan may show a
ventilation-perfusion mismatch.
Pulmonary angiography may reveal filling defects in
the pulmonary vasculature.
Electrocardiography may reveal right-axis deviation.
Pulmonary artery catheterization shows increased
PAP, with systolic pressure above 30 mm Hg; increased pulmonary artery wedge pressure; decreased
cardiac output; and decreased cardiac index.
Pulmonary function tests may show decreased flow
rates and increased residual volume or reduced total
lung capacity.
Echocardiography may show valvular heart disease
or atrial myxoma.
Other
Lung biopsy may show tumor cells.
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Treatment
General
Low-sodium diet
Fluid restriction (in right-sided heart failure)
Bed rest during acute phase
frequent rest periods

signs and symptoms of right-sided heart failure
Discharge planning
indicated.
Medications
Oxygen therapy
Cardiac glycosides
Diuretics
Vasodilators such as treprostinil
Calcium channel blockers such as amlodipine
Bronchodilators
Beta-adrenergic blockers
Iloprost
Prostacyclin
Endothelin receptor antagonists such as bosentan
Anticoagulants
Surgery
Heart-lung transplantation, if indicated
Key outcomes
The patient will:
express an understanding of the disorder
Implement comfort measures.
Provide adequate rest periods.
Monitoring
Vital signs
Intake and output
Daily weight
Respiratory status
Signs and symptoms of right-sided heart failure
Heart rhythm
ABG values
Hemodynamic values
Patient teaching
Be sure to cover:
adverse effects
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Pulmonic insufficiency
Overview
Description
Heart condition in which blood ejected into the pul-
monary artery during systole flows back into the right

ventricle during diastole
Also called pulmonary regurgitation
Fatigue
Angina
Palpitations
Physical findings
Tachycardia
Crackles in the lungs
Hepatomegaly (right-sided failure)
Palpable right ventricular systolic pulsation at left
lower sternal border
Pathophysiology
S3 or S4 at left mid-to-lower sternal border

Hemoptysis
Pulmonic valve is incompetent.

Incompetency is caused by:
Test results
dilation of the pulmonic valve ring

acquired alteration of pulmonic cusp morphology
congenital absence or malformation.
Blood flows back into the right ventricle from the
pulmonary artery.
Fluid overload occurs in the ventricle.
Chronic backflow causes ventricular hypertrophy and
right-sided heart failure.
Causes
Infective endocarditis
Tetralogy of Fallot
Rheumatic heart disease
Carcinoid heart disease
Dilated cardiomyopathy
Incidence
Variable age of occurrence
Affects both males and females; frequency based on
specific cause
Dyspnea on exertion
Peripheral edema
Tachycardia
Fatigue
Imaging
Chest X-rays reveal cardiomegaly, right-sided heart
enlargement, and pulmonary hypertension.
Echocardiography shows right ventricular hypertrophy and dilation.
Electrocardiography may show incomplete right
bundle-branch block and right axis deviation.
Cardiac catheterization may determine underlying
etiology.
Treatment
General
Symptomatic treatment
Low-sodium diet
Medications
Diuretics
Inotropic agent
Angiotensin-converting enzyme inhibitors
Oxygen
Possible prophylactic antibiotics before and after
surgery or dental care to prevent endocarditis
Complications
Surgery
Heart failure
Pulmonary edema
Thromboembolism
Endocarditis
Arrhythmias
Annuloplasty or valvuloplasty to reconstruct or repair
Assessment
Key outcomes
History
Infective endocarditis
Tetralogy of Fallot
Orthopnea
Dyspnea
672
the valve
Valve replacement with a prosthetic valve
The patient will:
perform activities of daily living without weakness or
fatigue
maintain adequate ventilation.
Administer prescribed oxygen.
Watch for signs of heart failure or pulmonary edema.
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Monitoring
Vital signs and pulse oximetry
Cardiac rhythm
Pulmonary artery catheter readings
Intake and output
Adverse effects of drug therapy
Patient teaching
Be sure to cover:
adverse effects.
Discharge planning
Encourage follow-up care with a cardiologist.
673
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Pulmonic stenosis
Physical findings
Overview
Peripheral edema
Split S2
Systolic ejection click
Crackles in the lungs
Hepatomegaly (right-sided failure)
Palpable impulse from the right ventricle along the
left parasternal border
Description
Heart condition in which obstructed right ventricular
outflow causes right-ventricular hypertrophy, eventually resulting in right-sided heart failure

Also called pulmonary regurgitation
Pathophysiology
Dynamic or fixed obstruction affects blood flow from
the right ventricle to the pulmonary arteriole vasculature.

Chronic obstruction may result in right-sided heart
failure.
Causes
Congenital defect
Sinus of Valsalva aneurysm
Aortic graft aneurysm
Incidence
Test results
Imaging
Chest X-rays reveal prominence of the main, right, or
left pulmonary arteries.
Echocardiography shows thickening of the valves,
characteristic doming of nondysplastic valves, and
right ventricular hypertrophy.
Cardiac ultrasound reveals thickening of valves, characteristic doming of nondysplastic valves, and rightventricular hypertrophy.
Electrocardiography may show mild right axis
deviation.
Treatment
Affects females slightly more than males
General

Low-sodium diet
Avoidance of vigorous physical activity
Dyspnea on exertion
Peripheral edema
Cyanosis
Tachycardia
Fatigue
Complications
Heart failure
Pulmonary edema
Thromboembolism
Endocarditis
Arrhythmias
Assessment
History
Congenital defect
Sinus of Valsalva aneurysm
Aortic graft aneurysm
Orthopnea
Exertional dyspnea
Fatigue
Angina
Palpitations
Medications
Diuretics
Inotropic agents
Angiotensin-converting enzyme inhibitors
Oxygen
Possible prophylactic antibiotics before and after
surgery or dental care to prevent endocarditis
Surgery
Balloon valvoplasty
Pulmonary artery balloon angioplasty
Valvotomy
Key outcomes
The patient will:
perform activities of daily living without weakness or
fatigue
state understanding of disorder and treatment.
Administer prescribed oxygen.
Watch for signs of heart failure or pulmonary edema.
Encourage verbalization and provide support.
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Pulmonic stenosis
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Monitoring
Vital signs and pulse oximetry
Cardiac rhythm
Pulmonary artery catheter readings
Intake and output
Adverse effects of drug therapy
Patient teaching
Be sure to cover:
activity restrictions
adverse effects.
Discharge planning
Encourage follow-up care with a cardiologist.
Pulmonic stenosis
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Q
Q fever
Overview
Description
H Acute systemic disease that affects people exposed to
cattle, sheep, or goats
Assessment
History
H Exposure to cattle, sheep, or goats
H Headache
H Myalgia
H Chills, fever
H Rare human-to-human transmission; possible sexual
Physical findings
transmission
H Crackles (pneumonia)
H Hepatomegaly and jaundice (hepatitis)
H Heart murmur, signs of heart failure (endocarditis)
Pathophysiology
H Coxiella burnetii is excreted in urine, milk, and
Test results
feces of infected animals.

H Once ingested, it proliferates in macrophages (in the
acidic phagolysosome vacuole) and then gains access to the blood, producing a transient bacteremia.
H It may invade many organs, most commonly the
lungs and liver.
H Inflammation occurs, manifested by granulomas in
the liver, spleen, and bone marrow. These classic
doughnut granulomas disappear with convalescence.
Laboratory
H Patients with the acute form may have an elevated
white blood cell count, transient thrombocytopenia,
and elevated transaminases and alkaline phosphatase
levels.
H Cerebrospinal fluid evaluation reveals lymphocytosis,
elevated protein level, and normal glucose level.
H Complement fixation reveals antephase II antibody
titers of 40 or more (acute disease) and antephase I
antibody titers of 200 of more (chronic disease).
H Microimmunofluorescence reveals immunoglobulin
(Ig) G antephase II antibody titers of 200 or more
and IgM antephase II antibody titers of 50 or more
(acute). (The presence of antephase I antibodies indicates chronic Q fever; the presence of IgG antephase I antibody titers of 800 or more is highly predictive of endocarditis.)
Imaging
H Chest X-rays may show segmental or lobar opacities,
multiple round opacities, and pleural effusion.
H Echocardiography may show pericardial effusion
with pericarditis.
H Electrocardiography shows T-wave abnormalities
with myocarditis and pericarditis.
Causes
H Coxiella burnetii
Incidence
H Affects males more than females because males more
likely to be exposed to livestock

H Most commonly affects people ages 25 to 40
H Self-limiting, febrile illness with headache, myalgia,
chills
H May have symptoms of pneumonia, hepatitis, or en-
docarditis (chronic)
Complications
H Chronic fatigue syndrome
H Heart failure
H Endocarditis (see Treating Q fever endocarditis)
Treating Q fever endocarditis

Chronic Q fever endocarditis typically requires the use of
multiple drugs to treat effectively. Two different drug treatment protocols have been evaluated:
H doxycycline with quinolones, for at least 4 years
H doxycycline with hydroxychloroquine, for 112 to 3
years.
The second drug treatment protocol causes fewer relapses but requires routine eye examinations to detect
accumulation of chloroquine.
Some patients with C. burnetii endocarditis require
surgery to remove damaged valves.
676
Q fever
Treatment
General
H Symptomatic
H Diet as tolerated
Medications
H Antibiotics such as doxycycline
H Antimalarials such as hydroxychloroquine
Surgery
H Possible valve replacement
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Key outcomes
The patient will:
H express understanding of illness and treatment
regimen
H remain free from complications.
Monitoring
H Vital signs
H Cardiac status
Patient teaching
Be sure to cover:
H the importance of follow-up care and compliance
with long-term therapy
adverse effects.
Q fever
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Rabies
Overview
Description
H An acute central nervous system (CNS) infection usu-
ally transmitted by animal bite
H Incubation period varies but usually 1 to 3 months

H 70% of cases in the United States from raccoon,
skunk, fox, or bat bite; vaccinations have reduced

transmission from dogs
H Almost always fatal if symptoms occur, although
prompt treatment may prevent fatal CNS invasion
Pathophysiology
H The rabies virus is transmitted through the bite of an
infected animal that introduces the virus through the

skin or mucous membrane.
H The virus begins to replicate in the striated muscle
cells at the bite site.
H It then travels up the nerve to the CNS and replicates
in the brain.
H Finally, it moves through the nerves into other tissues, including the salivary glands.
Causes
H Bite from a rabid animal
H Occasionally transmitted by airborne droplets and in-
fected tissue transplants
Incidence
H Can affect anyone at any age
H Annually, an estimated 35,000 to 50,000 deaths
worldwide
First aid for animal bites

H Immediately wash the bite vigorously with soap and
water for at least 10 minutes to remove the animals
saliva.
H Flush the wound with an antiviral, followed by a clearwater rinse.
H Apply a sterile dressing.
H If possible, dont suture the wound, and dont immediately stop the bleeding (unless its massive) because
blood flow helps to clean the wound.
H Question the patient about the bite. Ask whether he
provoked the animal (if so, chances are it isnt rabid)
and whether he can identify it or its owner. (The animal
may be confined for observation.)
H Consult local health authorities for treatment information.
678
Rabies
H Progressive signs and symptoms
H After incubation period, local or radiating pain or
burning and coldness, pruritus, and tingling at the

bite site
H Slight fever (100 to 102 F [37.8 to 38.9 C])
H Malaise
H Nervousness that progresses into agitation and cranial nerve dysfunction, causing ocular palsies
H Hyperesthesia
H Photophobia
H Sensitivity to loud noise
H Pupillary dilation
H Tachycardia
H Shallow respirations
H Excessive salivation, lacrimation, and perspiration
H Hydrophobia, during which forceful, painful pharyngeal muscle spasms expel liquids from the mouth
and cause dehydration
H After about 3 days, gradual, generalized, flaccid
paralysis that ultimately leads to peripheral vascular
collapse, coma, and death
Complications
H Paralysis
H Coma
H Death
Assessment
History
H Animal bite
H Fever
H Malaise
Physical findings
H Burning at wound site
H Tachycardia
H Excessive salivation
H Shallow respirations
H Dilated pupils and photophobia
Test results
Laboratory
H Virus is isolated from the patients saliva or throat;
examination of blood shows fluorescent rabies antibody (FRA).
H White blood cell count is elevated with increased
polymorphonuclear and large mononuclear cells.
H Urinary glucose, acetone, and protein levels are elevated.
Other
H Animal should be confined and observed for 10 days
by a veterinarian. (If the animal appears rabid, it
should be killed and its brain tissues tested for FRA
and Negri bodies.)
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Treatment
General
H Immediate wound treatment (see First aid for ani-
mal bites)
Medications
H Tetanus-diphtheria prophylaxis, if needed
H Passive immunization with rabies immune globulin
and active immunization with human diploid cell vaccine as soon as possible (if not previously immunized)
H Vaccine booster (if already immunized)
Key outcomes
The patient will:
H express understanding of the treatment regimen
H express concerns regarding infection.
H When injecting the rabies vaccine, rotate injection
sites on the upper arm or thigh.

H Cooperate with public health authorities to determine
the animals vaccination status. If the animal is

proven rabid, help identify others at risk.
H Provide aggressive supportive care (even after onset
of coma).
Monitoring
H Injection site reactions
H Cardiac and pulmonary function
Patient teaching
Be sure to cover:
H the need for vaccination of household pets that may
be exposed to rabid wild animals
H importance of not touching wild animals, especially if
they appear ill or overly docile (a possible sign of rabies)
H prophylactic rabies vaccine for high-risk people,
such as farm workers, forest rangers, spelunkers
(cave explorers), and veterinarians.
Rabies
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Radiation exposure
Overview
Description
H Exposure to excessive radiation that causes tissue
damage
H Damage varies with amount of body area exposed,
length of exposure, dosage absorbed, distance from

the source, and presence of protective shielding
H Can result from cancer radiotherapy, working in a
radiation facility, or other exposure to radioactive
materials
Pathophysiology
H Ionization occurs in the molecules of living cells.
H Electrons are removed from atoms. Charged atoms
or ions form and react with other atoms to cause cell

damage.
H Rapidly dividing cells are the most susceptible to radiation damage. Highly differentiated cells are more
resistant to radiation.
Causes
H Exposure to radiation through inhalation, ingestion,
or direct contact
Risk factors
H Cancer treatment
H Employment in a radiation facility
Incidence
H Unknown
H Nausea
H Diarrhea
H General weakness
H Immunosuppression
H Infections
Complications
H Leukemia
H Thyroid cancer
H Fetal growth retardation or genetic defects in off-
spring (from exposure during childbearing years)

H Decreased fertility
H Shortened life span
H Anemia
H Malignant neoplasms
H Bone necrosis and fractures
680
Radiation exposure
Assessment
History
Acute hematopoietic radiation toxicity
H Bleeding from the skin, genitourinary tract, and GI
tract
H Nosebleeds
H Hemorrhage
GI radiation toxicity
H Intractable nausea, vomiting, and diarrhea
Cerebral radiation toxicity
H Nausea, vomiting, and diarrhea
H Lethargy
Cardiovascular radiation toxicity
H Hypotension, shock, and cardiac arrhythmias
Physical findings
Acute hematopoietic radiation toxicity
H Petechiae
H Pallor
H Weakness
H Oropharyngeal abscesses
GI radiation toxicity
H Mouth and throat ulcers and infection
H Circulatory collapse and death
Cerebral radiation toxicity
H Tremors
H Seizures
H Confusion
H Coma and death
Generalized radiation exposure
H Signs of hypothyroidism
H Cataracts
H Skin dryness, erythema, atrophy, and malignant
lesions
H Alopecia
H Brittle nails
Test results
Laboratory
H White blood cell, platelet, and lymphocyte counts are
decreased.
H Serum potassium and chloride levels are decreased.
Imaging
H X-rays may reveal bone necrosis.
H Bone marrow studies may show blood dyscrasia.
Other
H Geiger counter helps determine if radioactive material was ingested or inhaled and evaluates the amount
of radiation in open wounds.
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Treatment
Patient teaching
General
Be sure to cover:
H the injury process, diagnosis, and treatment
H effects of radiation exposure
H how to prevent a recurrence
H skin care
H wound care
H need for follow-up care.
H Management of life-threatening injuries

H Symptomatic and supportive treatment
H Based on the type and extent of radiation injury
H Activity as tolerated by clinical status
Medications
H Chelating agents
H Potassium iodide
H Aluminum phosphate gel
H Barium sulfate
Discharge planning
H If the patient was exposed to significant amounts of
radiation, provide a referral to genetic counseling

resources.
Key outcomes
The patient will:
H maintain an acceptable weight
H Implement appropriate respiratory and cardiac sup-
port measures.
H Administer prescribed I.V. fluids and electrolytes.
H For skin contamination, wash the patients body thor-
oughly with mild soap and water.

H Debride and irrigate open wounds, as ordered.
H For ingested radioactive material, perform gastric
lavage and whole-bowel irrigation, and administer

activated charcoal, as ordered.
H Dispose of contaminated clothing properly.
H Dispose of contaminated excrement and body fluids
according to facility policy.
Monitoring
H Intake and output
H Vital signs
H Signs and symptoms of hemorrhage
Radiation exposure
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Rape-trauma syndrome
Overview
Description
H Syndrome that occurs after rape (forced sexual inter-
course) or attempted rape and causes varying degrees of physical and psychological trauma
H Refers to the victims short- and long-term reactions
and the methods used to cope with trauma
H Carries a good prognosis if the victim receives physical and emotional support and counseling to help
deal with feelings
Pathophysiology
H Rape causes psychological and physiologic reactions.
H Early stage (short-term) and late stage (long-term)
reactions can occur.
Causes
H Late stage
Anxiety
Nightmares
Sleep disturbances
Flashbacks
Depression
Anger
Disinterest in sex
Anorgasmia
Suicidal ideation
H Rape or attempted rape
H Time the victim arrived at the facility
H Date and time of alleged rape
H Time the victim was examined
H Whether the victim was pregnant at the time of the attack
H Date of last menstrual period
H Details of obstetric and gynecologic history
H Victims statements (recorded in the first person, using quotation marks)
H Objective information provided by others
H Rape or attempted rape
Incidence
H Affects all ages (reported victims from ages 2 months
ALERT
Be aware that your assessment notes may be used
as evidence if the rapist goes to trial.
to 97 years)
H Most common in females ages 16 to 19 (about 8%
of American females experience rape or attempted

rape)
H Usually perpetrated by family member if victim a
child
H Signs of physical trauma, depending on length of the
Physical findings
H Sore throat
H Difficulty swallowing
H Vaginal pain
H Rectal pain
H Pain from other injuries incurred during the assault
H Early stage:
attack and whether additional physical violence occurred

H Tearfulness, crying
H Withdrawal
H Anxiousness
Complications
H Lasting psychiatric problems, such as depression,
guilt, anxiety, and suicidal ideation

H Sexually transmitted disease (STD)
H Unwanted pregnancy
Assessment
History
H Early stage
682
Disbelief
Panic
Severe anxiety
Anger
Self-blame
Humiliation
Depression
Reddened (sore) throat

Mouth irritation
Ecchymoses
Rectal pain and bleeding
Lacerations, contusions, and abrasions to vulva,
cervix, and vaginal walls
Lacerations and contusions in a male victim
Outward calm
Compliance
Glibness
Talkativeness
Test results
Laboratory
H STD screening tests may reveal positive results.
H Rapid plasma reagin card test may show positive for
syphilis.
H Urine pregnancy test may be positive 0 to 3 weeks after missed period.
H Serum human chorionic gonadotropin test becomes
positive 24 to 48 hours after implantation.
H Drug screen (if symptoms warrant) may be positive.
H Serum ethanol level (if symptoms warrant) may be
elevated.
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ALERT
If the rape occurred within 7 days, the following
specimens may be obtained for legal purposes:
blood; samples for deoxyribonucleic acid testing
(should be collected within 48 hours); hairs of a
different color than the victims or that are obviously out of place; fibers; soiled or torn material;
body fluids, such as blood or semen, that dont belong to the victim; and specimens from the cervical
canal, throat, or rectum.
Treatment
General
H Treatment of physical injuries
H Crisis intervention and counseling
H Follow-up gynecologic examination after 7 to
Monitoring
H Mental status
H Vital signs
H Signs and symptoms of shock
Patient teaching
Be sure to cover:
H verbal and written instructions regarding treatment
adverse effects.
Discharge planning
H Encourage the patient to get follow-up care.
14 days; for male patient, follow-up urologic

examination
H Emergency contraception such as the Copper-T
intrauterine device
H Activity based on injuries
Medications
H Tetanus prophylaxis
H STD prophylaxis
H Emergency contraceptive pills
Key outcomes
The patient will:
H express relief of pain
H report absence of or reduction in anxiety
H discuss feelings related to the rape and its effect on
self-esteem.
H Dont leave the patient alone unless requested.
H Place the patients clothing in paper, not plastic,
bags. Label each bag and its contents.

H Collect and label fingernail scrapings and foreign
material obtained by combing the patients pubic

hair.
H Label all specimens with the patients name, physicians name, and site from which the specimen was
obtained.
H Note the name of the person to whom specimens
were given.
H Report the rape if required by state law.
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Raynauds phenomenon
Overview
Description
H Primary arteriospastic disorder
H Causes episodic vasospasms in the small peripheral
arteries and arterioles in response to cold exposure

or stress
H Typically occurs in three phases
H Diagnosis requires exclusion of secondary causes
H More than half of patients have Raynauds disease
H Also called vasospastic arterial disease
Pathophysiology
H Blood flow to digits decreases in response to stress
or cold.
H Proposed explanations for decreased digital blood
flow include an antigen-antibody immune response

(most probable theory), intrinsic vascular wall hyperactivity to cold, ineffective basal heat production,
and increased vasomotor tone from sympathetic
stimulation or stress.
Causes
Primary causes
H Unknown
Secondary causes
H Collagen vascular disease
H Arterial occlusive disease
H Neurologic disorders
H Blood dyscrasias
H Trauma
H Drugs
H Pulmonary hypertension (see Causes of Raynauds
phenomenon)
Incidence
H More common in females, particularly between late
adolescence and age 40
H Occurs bilaterally
H Usually affects the hands or, less commonly, the feet;
rarely, the earlobes and tip of nose
Complications
H Ischemia
H Gangrene
H Amputation
Physical findings
H First stage marked pallor of affected skin areas
H Second stage cyanosis of affected skin areas
H Third stage red, warm skin
H Between attacks normal appearance of affected
areas (occasionally, coolness and excessive perspiration of these areas)

H In long-standing disease trophic changes, such as
sclerodactylia and ulcerations
Test results
H Arteriography and digital photoplethysmography may
aid diagnosis.
Treatment
General
H Smoking cessation
H Biofeedback therapy
H Avoidance of activities involving exposure to cold and
mechanical or chemical injury
Medications
H Phenoxybenzamine
H Nifedipine
H Reserpine
H Guanethidine combined with prazosin
Surgery
H Sympathectomy, if conservative treatment fails to pre-
vent ischemic ulcers
Key outcomes
The patient will:
H describe feelings of increased comfort and decreased
pain
H maintain adequate skin temperature in affected areas
H maintain adequate collateral circulation
H perform normal activities to the extent possible
H Evaluate the patients occupation and its effect on
symptom occurrence.
H Help the patient identify stress triggers and use effec-
tive coping strategies.

H Provide psychological support and reassurance.
Assessment
Monitoring
History
H Signs and symptoms of skin breakdown
H Altered skin color in response to cold or stress

H Numbness and tingling (second stage)
H Throbbing, burning, painful sensation (third stage)
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Causes of Raynauds phenomenon

In primary or idiopathic Raynauds phenomenon, more than half of patients have Raynauds disease. Raynauds phenomenon
may also occur secondary to the following diseases and conditions as well as with the use of certain drugs.
Collagen vascular disease
H Dermatomyositis
H Polymyositis
H Scleroderma
H Acute arterial occlusion

H Atherosclerosis of the extremities
H Thoracic outlet syndrome
H Thromboangiitis obliterans
Neurologic disorders

H Stroke
H Intervertebral disk disease
H Poliomyelitis
H Spinal cord tumors
H Syringomyelia
H Myeloproliferative disorders
H Waldenstrms disease
Trauma
H Cold injury
H Electric shock
H Hammering
H Keyboarding
H Piano playing
H Vibration injury
Drugs
H Beta-adrenergic blockers
H Bleomycin
H Cisplatin
H Ergot derivatives such as ergotamine
H Methysergide
H Vinblastine
Other
Blood dyscrasias
H Cold agglutinins
H Cryofibrinogenemia
Patient teaching
Be sure to cover:
H prevention of attacks (see Preventing a Raynauds
phenomenon attack)
H need to inspect skin frequently and to seek immediate care for evidence of skin breakdown or infection
Discharge planning
H Refer the patient to a smoking-cessation program or
a support group, as indicated.

Prevention
Preventing a Raynauds
phenomenon attack
A Raynauds phenomenon attack can be prevented by following these guidelines:
H Avoid exposure to cold.
H Dress warmly in cold weather, including wearing a hat
to reduce heat loss.
H Wear mittens, gloves, or oven mitts when handling
cold items in the kitchen.
H Use insulated drinking glasses.
H Wear mittens and socks to bed during cold weather.
H Warm up the car for a few minutes before driving during winter.
H Decrease air conditioner temperature during hot
weather.
H Avoid stress.
H Avoid cigarette smoking.
Raynauds phenomenon
685
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Reiters syndrome
H Skin lesions (keratoderma blennorrhagicum)

H Thick, opaque, brittle nails with keratic debris accu-
Overview
H Painless, transient ulcerations on the buccal mucosa,
mulation under nails
Description
H Self-limiting syndrome associated with polyarthritis,
urethritis, mucocutaneous lesions, and conjunctivitis

(or, less commonly, uveitis)
H Also called reactive arthritis
Pathophysiology
H Infection is thought to trigger an aberrant and hyper-
active immune response that causes inflammation in

involved target organs.
Causes
H Unknown
H Typically follows venereal or enteric infection, espe-
cially with Mycoplasma, Shigella, Campylobacter,

Salmonella, Yersinia, or Chlamydia
H May involve genetic susceptibility
Incidence
H Most common in males ages 20 to 40, especially
those positive for human immunodeficiency virus

H Rare in females and children
H Polyarthritis (dominant feature)
Complications
H Ankylosing spondylitis
H Persistent joint pain and swelling
H Anterior uveitis, glaucoma, blindness
H Prostatitis and hemorrhagic cystitis
H Cardiomyopathy, pericarditis
H Pulmonary edema
H Vertebral inflammation
H Foot deformity and chronic heel pain
palate, and tongue

H Patches of scaly skin on the palms, soles, scalp, or
trunk
Test results
Laboratory
H Human leukocyte antigen (HLA) test is positive for
HLA B27.
H White blood cell (WBC) count and erythrocyte sedimentation rate are elevated.
H Complete blood count and anemia panel show mild
anemia.
H Many WBCs (mostly polymorphonuclear leukocytes)
appear in urethral discharge and synovial fluid.
H Synovial fluid is grossly purulent with high complement and protein levels.
H Cultures of urethral discharge and synovial fluid are
used to rule out other possible causes of symptoms.
Imaging
H During the first few weeks of the syndrome, X-rays
are normal. Later they may show osteoporosis in inflamed areas. If inflammation persists, X-rays may
show small joint erosion, periosteal proliferation
(new bone formation) of involved joints, and calcaneal spurs.
Treatment
General
H Physical therapy
H Padded or supportive shoes
H During acute stages, weight-bearing restrictions or
complete bed rest
Medications
Assessment

H Cytotoxic agents such as azathioprine
H Corticosteroids
History
Surgery
H Initially, dysuria, hematuria, urinary urgency and fre-
H Surgical reconstruction of joints (if medical manage-
quency, and mucopurulent penile discharge with

swelling and reddening of the urethral meatus
H Possible suprapubic pain, fever, and anorexia with
weight loss
Physical findings
Key outcomes
H Small, painless ulcers on glans penis

H Asymmetrical and extremely variable polyarticular
The patient will:

pain
confines of the disease.
arthritis, usually in weight-bearing joints of the legs

and sometimes in the lower back or sacroiliac joints
H Warm, erythematous, painful joints
H Muscle wasting near affected joints
H Swollen, sausagelike appearance of fingers and toes
686
Reiters syndrome
ment doesnt prevent severe joint damage)
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H Provide a high-calorie, high-protein diet.
H Develop an exercise program with the physical
therapist.
H Maintain a nonjudgmental attitude.
Monitoring
H Complications
Patient teaching
Be sure to cover:
H importance of using condoms and avoiding multiple
sex partners (bacteria that leads to Reiters can be
passed from person to person but Reiters syndrome
cant be passed from person to person)
H how to avoid exposure to enteric pathogens (such as
via anal intercourse)
H importance of taking NSAIDs with meals or milk
H maintaining normal daily activities and moderate exercise
H good posture and body mechanics
H use of a firm mattress.
Discharge planning
H If the patient has severe or chronic joint impairment,
arrange for occupational counseling.
Reiters syndrome
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Relapsing fever
summer, when ticks and their hosts (chipmunks,

goats, and prairie dogs) are most active; occasional
cold-weather outbreaks in people such as campers
who sleep in tick-infested cabins
Overview
Description
H An acute infectious disease caused by Borrelia spiro-
chetes
H Transmitted to humans by lice or ticks and charac-
terized by relapses and remissions

H Primary Borrelia reservoirs in rodents and other
wild animals
H Secondary reservoir possible in people, requiring no
transmission by ordinary contagion and allowing

possible congenital infection and transmission by
contaminated blood
H Mortality rate for untreated louseborne relapsing
fever usually above 10%, possibly up to 50% in an
epidemic
H With treatment, excellent prognosis for both louseborne and tickborne relapsing fevers
H Also called tick, fowl-nest, cabin, or vagabond
fever or bilious typhoid
Pathophysiology
H Inoculation occurs when the victim crushes the
louse, causing its infected blood or body fluid to enter the victims bitten or abraded skin or mucous
membranes.
H Because tick bites are virtually painless and most Ornithodoros ticks feed at night but dont embed themselves in the victims skin, many people are bitten unknowingly.
Causes
H Bite from body louse (Pediculus humanus
corporis) that carries Borrelia spirochete, which

typically occurs in epidemics during wars, famines,
and mass migrations
H Cold weather and crowded living conditions, which
favor the spread of body lice
H Bite from tick that carries one of three species of
Borrelia most closely identified with tick carriers:
B. hermsii (associated with Ornithodoros hermsi),
B. turicatae (associated with O. turicata), or
B. parkeri (associated with O. parkeri)
Incidence
H Most common in indigent victims already suffering
from other infections and malnutrition

H Louseborne disease most common in North and Cen-
tral Africa, Europe, Asia, and South America; no cases in the United States since 1900
H Tickborne disease in the United States most prevalent
in Texas and other western states, usually during the
688
Relapsing fever
H Incubation period 5 to 15 days (average 7 days)

H Fever 105 F (40.5 C)
H Prostration
H Headache
H Severe myalgia
H Arthralgia
H Diarrhea
H Vomiting
H Coughing
H Eye or chest pain
Complications
H Nephritis
H Bronchitis
H Pneumonia
H Endocarditis
H Seizures
H Cranial nerve lesions
H Paralysis
H Coma
H Death
Assessment
History
H Recent travel to an epidemic or louse-infested area
H Recent exposure to tick-infested area
H Fever
H Headache
H Malaise
H Arthralgia
H Attacks that subside and recur
Physical findings
H Splenomegaly
H Hepatomegaly
H Lymphadenopathy
H Transient petechial rash over torso during febrile pe-
riods
Test results
Laboratory
H During febrile periods, spirochetes may appear in
blood smears using Wrights or Giemsa stain.
H In severe infection, spirochetes appear in urine and
cerebrospinal fluid.
H White blood cell (WBC) count may reach 25,000/l;
lymphocytes and erythrocyte sedimentation rate may
increase.
H Syphilis test may show a false-positive result.
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Treatment
General
Medications
H Antipyretics
H Doxycycline or erythromycin
Prevention
Preventing relapsing fever

Relapsing fever can be prevented by following these
guidelines:
H Practice proper hand-washing techniques.
H In tick-infested areas, wear clothing that covers as
much skin as possible and tuck pant legs into boots or
socks. Also, wear insect repellent containing DEET or
permethrin and cover clothing with it.
H Rodent proof buildings and remove nesting materials
from walls.
ALERT
Antibiotics shouldnt be given at the height of a severe febrile attack because they may cause JarischHerxheimer reaction, resulting in malaise, rigors,
leukopenia, flushing, fever, tachycardia, rising respiratory rate, and hypotension. This reaction,
which is caused by toxic by-products from massive
spirochete destruction, can mimic septic shock and
may prove fatal. Antibiotics should be postponed
until the fever subsides.
Key outcomes
The patient will:
H verbalize accurate information about the disease
H attain the highest degree of mobility possible.
H Give tepid sponge baths and antipyretics.
H Encourage fluid intake.
H Administer antibiotics carefully. Document and re-
port any hypersensitive reactions (rash, fever, anaphylaxis), especially a Jarisch-Herxheimer reaction.
H Report all cases of louseborne or tickborne relapsing
fever to the local public health department as required by law.
Monitoring
H Vital signs
Patient teaching
Be sure to cover:
H symptoms of relapsing fever in family members and
in others who may have been exposed to ticks or lice
along with the victim
H prevention techniques. (See Preventing relapsing
fever.)
Relapsing fever
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Renal calculi
H Pain of fluctuating intensity; may be excruciating at
its peak
Overview
H Nausea, vomiting
H Fever, chills
H Anuria (rare)
Description
Physical findings
H Formation of calculi (stones) anywhere in the uri-
H Hematuria
nary tract
H Most common in the renal pelvis or calyces
H Vary in size; may be single or multiple (see Variations in renal calculi)
H Necessitate hospitalization in roughly 1 of every
1,000 United States residents
Pathophysiology
H Calculi form when substances normally dissolved in
the urine, such as calcium, uric acid, struvite, or cystine.

H Large, rough calculi may occlude the opening to the
ureteropelvic junction.
H The frequency and force of peristaltic contractions
increase, causing pain.
Causes
Test results
Laboratory
H 24-hour urine collection shows calcium oxalate,
phosphorus, and uric acid excretion levels.
H Urinalysis shows increased urine specific gravity,
hematuria, crystals, casts, and pyuria.
Imaging
H Kidney-ureter-bladder (KUB) radiography reveals
most renal calculi.
H Excretory urography helps confirm the diagnosis and
determines calculi size and location.
H Kidney ultrasonography can detect obstructive
changes and radiolucent calculi not seen on KUB.
H Unknown
Treatment
Risk factors
General
H Dehydration
H Infection
H Urine pH changes
H Urinary tract obstruction
H Immobilization
H Metabolic factors
H Percutaneous ultrasonic lithotripsy

H Extracorporeal shock wave lithotripsy
H Vigorous hydration (more than 3 qt [3 L]/day)
H Dietary restrictions based on stone composition
Medications
H Analgesics
H Diuretics
H Methenamine mandelate
H Allopurinol (for uric acid calculi)
H Ascorbic acid
H Flank pain
H Nausea, vomiting
Surgery
Complications
H Parathyroidectomy for hyperparathyroidism

H Cystoscopy
H Renal parenchymal damage

H Renal cell necrosis
H Hydronephrosis
H Complete ureteral obstruction
Incidence
H Affect more males than females
H Rare in blacks and children
Assessment
History
H Classic renal colic pain severe pain that travels
from the costovertebral angle to the flank and then to

the suprapubic region and external genitalia
H With calculi in the renal pelvis and calyces relatively constant, dull pain
690
Renal calculi
Key outcomes
The patient will:
H identify risk factors that increase calculus formation
and modify lifestyle accordingly
H demonstrate the ability to manage urinary elimination problems.
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Variations in renal calculi

Renal calculi vary in size and type. Small calculi may remain in the renal pelvis or pass down the ureter. A staghorn calculus
(a cast of the calyceal and pelvic collecting system) may develop from a calculus that stays in the kidney.
Staghorn
calculus
Multiple
small calculi
H Provide I.V. fluids, as ordered; encourage fluids as
needed.
H Strain all urine and save solid material for analysis.
H Encourage ambulation to aid spontaneous calculus
passage.
Monitoring
H Intake and output
H Daily weight
H Pain control
H Catheter function and drainage
Patient teaching
Be sure to cover:
H prescribed diet and importance of compliance (see
Preventing renal calculi)
H drug therapy
H ways to prevent recurrences
H how to strain urine for calculi
H immediate return visit to hospital for fever, uncontrolled pain, or vomiting.
Discharge planning
H Patients who dont meet admission criteria should
arrange for a follow-up with a urologist in 2 to

3 days.
Prevention
Preventing renal calculi

Prevention of renal calculi, or kidney stones, requires
lifestyle and dietary changes as recommended by the
practitioner. The restrictions vary based on the chemical
composition of the calculi. Some recommendation may
include:
H Drink enough fluid, about 312 quartswater preferredto create 212 quarts of urine per day.
H Take calcium supplement with a meal onlyavoiding
dietary calcium isnt necessary.
H Reduce animal protein intake.
H Avoid chocolate, coffee, tea, and cola.
H Reduce salt intake.
H Avoid rhubarb, star fruit, beets, beet greens, collards,
okra, refried beans, spinach, Swiss chard, sweet potatoes, sesame seeds, almonds, and soy products.
Renal calculi
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Renal failure, acute

Overview
Description
H Sudden interruption of renal function resulting from
obstruction, reduced circulation, or renal parenchymal disease

H Classified as prerenal failure, intrarenal failure (also
called intrinsic or parenchymal failure), or postrenal failure
H Usually reversible with medical treatment
H If not treated, may progress to end-stage renal disease, uremia, and death
H Normally occurs in three distinct phases: oliguric,
diuretic, and recovery
Oliguric phase
H May last a few days or several weeks
H Urine output dropping below 400 ml/day
H Fluid volume excess, azotemia, and electrolyte imbalance occurring.
H Local mediators that are released, causing intrarenal
vasoconstriction
H Medullary hypoxia causing cellular swelling and adherence of neutrophils to capillaries and venules
H Hypoperfusion occurring
H Cellular injury and necrosis occurring
H Reperfusion that causes reactive oxygen species to
form, leading to further cellular injury
Diuretic phase
H Renal function recovered
H Urine output gradually increasing
H Glomerular filtration rate improving, although tubular transport systems remaining abnormal
Recovery phase
H May last 3 to 12 months, or longer
H The patient gradually returning to normal or near
normal renal function
Pathophysiology
Prerenal failure
H Prerenal failure is caused by impaired blood flow.
H Decrease in filtration pressure causes a decline in
glomerular filtration rate (GFR).
H Failure to restore blood volume or blood pressure
may cause acute tubular necrosis (ATN) or acute
cortical necrosis.
Intrarenal failure
H A severe episode of hypotension, commonly associated with hypovolemia, is commonly a significant contributing event.
H Cell swelling, injury, and necrosis a form of reperfusion injury that may also be caused by nephrotoxins results from ischemia-generated toxic oxygenfree radicals and anti-inflammatory mediators.
Postrenal failure
H Postrenal failure usually occurs with urinary tract obstruction that affects the kidneys bilaterally such as
prostatic hyperplasia.
692
Causes
Prerenal failure
H Hypovolemia
H Hemorrhagic blood loss
H Loss of plasma volume
H Water and electrolyte losses
H Hypotension or hypoperfusion
Intrarenal failure
H ATN
H Glomerulopathies
H Malignant hypertension
Postrenal failure
H Obstructive uropathies, usually bilateral
H Ureteral destruction
H Bladder neck obstruction
Incidence
H Seen in 5% of hospitalized patients
H Vary with renal failure phase
Complications
H Renal shutdown
H Acute pulmonary edema
H Hypertensive crisis
H Infection
Assessment
History
H Predisposing disorder
H Recent fever, chills, or central nervous system prob-
lem
H Recent GI problem
Physical findings
H Oliguria or anuria, depending on renal failure phase
H Tachycardia
H Bibasilar crackles
H Irritability, drowsiness, or confusion
H Bleeding abnormalities
H Dry, pruritic skin
H Uremic breath odor
Test results
Laboratory
H Blood urea nitrogen, serum creatinine, and potassium levels are elevated.
H Hematocrit, blood pH, bicarbonate, and hemoglobin
H Urine casts and cellular debris are present, and specific gravity is decreased.
H In glomerular disease, proteinuria and urine osmolality are close to serum osmolality level.
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H Urine sodium level is below 20 mEq/L, caused by
decreased perfusion in oliguria.

H Urine sodium level is above 40 mEq/L from an intrarenal problem in oliguria.
H Urine creatinine clearance is used to measure GFR
and estimate the number of remaining functioning
nephrons.
Imaging
Imaging tests that may show the cause of renal failure
include:
H kidney ultrasonography
H kidney-ureter-bladder radiography
H excretory urography renal scan
H retrograde pyelography
H computed tomography scan
H nephrotomography.
H Electrocardiography shows tall, peaked T waves; a
widening QRS complex; and disappearing P waves if
hyperkalemia is present.
Treatment
General
H Hemodialysis or peritoneal dialysis (if appropriate)
H High-calorie, low-protein, low-sodium, and low-
potassium diet
H Fluid restriction
Medications
H Supplemental vitamins
H Diuretics
H In hyperkalemia, hypertonic glucose-and-insulin in-
fusions, sodium bicarbonate, sodium polystyrene sulfonate
Preventing acute tubular necrosis

Acute tubular necrosis occurs mainly in elderly hospitalized patients. Contributing causes include aminoglycoside
therapy and exposure to industrial chemicals, heavy metals, and contrast media. Patients who have been exposed
must receive adequate hydration; monitor their urinary
output closely.
To prevent acute tubular necrosis, make sure every patient is well hydrated before surgery or after X-rays that
use a contrast medium. Administer mannitol, as ordered,
to a high-risk patient before and during these procedures.
Carefully monitor a patient receiving a blood transfusion,
and stop the transfusion immediately if signs of transfusion reaction (fever, rash, and chills) occur.
Monitoring
H Intake and output
H Daily weight
H Vital signs
H Effects of excess fluid volume
H Dialysis access site
Patient teaching
Be sure to cover:
adverse effects
H recommended fluid allowance
H compliance with diet and drug regimen
H daily weight and importance of immediately reporting changes of 3 lb (1.4 kg) or more
H signs and symptoms of edema and importance of
reporting them to the physician.
Surgery
Discharge planning
H Creation of vascular access for hemodialysis
H Encourage follow-up care with nephrologist.
Key outcomes
The patient will:
H verbalize risk factors for decreased tissue perfusion
and modify lifestyle appropriately
H demonstrate the ability to manage urinary elimination problems.
H Identify patients at risk for and take steps to prevent
ATN. (See Preventing acute tubular necrosis.)
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Renal failure, chronic

Overview
Description
H The end result of gradually progressive loss of renal
function
H Symptoms sparse until more than 75% of glomerular
filtration lost, worsening as renal function declines

H Fatal unless treated; to sustain life, may require
maintenance dialysis or kidney transplantation
Pathophysiology
H Nephron destruction eventually causes irreversible
renal damage.
H Disease may progress through the following stages:
reduced renal reserve, renal insufficiency, renal failure, and end-stage renal disease.
Causes
H Chronic glomerular disease
H Chronic infections such as chronic pyelonephritis
H Congenital anomalies such as polycystic kidney
disease
H Vascular diseases
H Obstructive processes such as calculi
H Collagen diseases such as systemic lupus erythema-
tosus
H Nephrotoxic agents
H Endocrine disease
Incidence
H Affects about 2 of every 100,000 people
H Can occur at all ages but more common in adults
H Affects more Blacks than Whites
H Fatigue
H Decreasing urine output
H Increasing edema
H Fluid overload
Complications
H Anemia
H Lipid disorders
H Platelet dysfunction
H Pulmonary edema
694
Assessment
History
H Predisposing factor
H Dry mouth
H Fatigue
H Nausea
H Hiccups
H Muscle cramps
H Fasciculations, twitching
H Infertility, decreased libido
H Amenorrhea
H Impotence
Physical findings
H Hypotension or hypertension
H Peripheral edema
H Bibasilar crackles
H Pleural friction rub
H Gum ulceration and bleeding
H Uremic fetor
H Abdominal pain on palpation
H Poor skin turgor
H Pale, yellowish bronze skin color
H Thin, brittle fingernails and dry, brittle hair
H Growth retardation (in children)
Test results
Laboratory
H Blood urea nitrogen, serum creatinine, sodium, and
potassium levels are elevated.
H Arterial blood gas (ABG) analysis shows decreased
arterial pH and bicarbonate levels.
H Hematocrit and hemoglobin level are low; red blood
cell (RBC) survival time decreases.
H Mild thrombocytopenia and platelet defects appear.
H Aldosterone secretion is increased.
H Hyperglycemia and hypertriglyceridemia occur.
H High-density lipoprotein levels are decreased.
H ABG analysis shows metabolic acidosis.
H Urine specific gravity is fixed at 1.010.
H Patient has proteinuria, glycosuria, and urinary
RBCs, leukocytes, casts, and crystals.
Imaging
H Kidney-ureter-bladder radiography, excretory urography, nephrotomography, renal scan, and renal
arteriography show reduced kidney size.
H Renal biopsy allows histologic identification of the
underlying disease process.
H EEG shows changes suggesting metabolic encephalopathy.
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Treatment
General
H Hemodialysis or peritoneal dialysis
H Low-protein (with peritoneal dialysis, high-protein),
high-calorie, low-sodium, low-phosphorus, and lowpotassium diet

H Fluid restriction
H fluid restrictions
H dialysis site care, as appropriate
H importance of wearing or carrying medical identifi-
cation.
Discharge planning
Medications
H Loop diuretics
H Cardiac glycosides
H Antihypertensives
H Antiemetics
H Iron and folate supplements
H Erythropoietin
H Antipruritics
H Supplementary vitamins and essential amino acids
Surgery
H Creation of vascular access for dialysis
H Possible kidney transplant
Key outcomes
The patient will:
H demonstrate the ability to manage urinary elimination problems
the disease.
H Perform meticulous skin care.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Signs and symptoms of fluid overload
Patient teaching
Be sure to cover:
H dietary changes
695
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Respiratory acidosis
Overview
Description
H Acid-base disturbance characterized by reduced alve-
olar ventilation, as shown by hypercapnia (partial

pressure of arterial carbon dioxide [PaCO2] above
45 mm Hg)
H Carries varying prognosis, depending on severity of
underlying disturbance and the patients general clinical condition
Pathophysiology
H Depressed ventilation causes compromised carbon
dioxide elimination.
H Carbon dioxide is then retained and combines with
water molecules increasing hydrogen ion concentration.
H Respiratory acidosis results.
Causes
H Central nervous system (CNS) trauma
H CNS-depressant drugs
H Chronic metabolic alkalosis
H Neuromuscular disease
H Parenchymal lung disease
H Asthma
H Severe acute respiratory distress syndrome
H Chronic bronchitis
H Large pneumothorax
H Extensive pneumonia
H Pulmonary edema
Incidence
H Headache
Complications
H Shock
H Cardiac arrest
Physical findings
H Diaphoresis
H Bounding pulses
H Rapid, shallow respirations
H Tachycardia
H Hypotension
H Papilledema
H Mental status changes
H Asterixis (tremor)
H Depressed deep tendon reflexes
Test results
Laboratory
H Arterial blood pH is below 7.35, and PaCO2 is above
45 mm Hg (hypercapnia)
Treatment
General
H Correction of the condition causing alveolar hypo-
ventilation
H Possible mechanical ventilation
H Possible dialysis
H I.V. fluid administration
H Possible need for parenteral nutrition
Medications
H Oxygen
H Bronchodilators
H Antibiotics
H Sodium bicarbonate
H Drug therapy for the underlying condition
Surgery
H Bronchoscopy
Key outcomes
The patient will:
H demonstrate effective coping strategies.
Assessment
H Administer prescribed drugs and oxygen.

H Provide adequate fluids.
H Perform tracheal suctioning, as needed.
History
Monitoring
H Predisposing factor
H Headache
H Vital signs
H Intake and output
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H Neurologic status
H Serum electrolyte values
H Mechanical ventilator settings
ALERT
Be aware that pulse oximetry, used to monitor oxygen saturation, wont reveal increasing carbon
dioxide levels.
Patient teaching
Be sure to cover:
H supplemental oxygen
H how to perform coughing and deep-breathing exercises
H signs and symptoms of acid-base imbalance and
Discharge planning
H Refer the patient for home oxygen therapy if
indicated.
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syndrome
Overview
Description
H Respiratory disorder that involves widespread alveo-
lar collapse
H Most common cause of neonatal death
H If mild, subsides slowly after about 3 days
H Also called RDS or hyaline membrane disease
Pathophysiology
H In neonates born before the 27th week of gestation,
immaturity of alveoli and capillary blood supply lead

to alveolar collapse from lack of surfactant (a lipoprotein normally present in alveoli and respiratory
bronchioles).
H Surfactant deficiency causes widespread atelectasis,
resulting in inadequate alveolar ventilation and
shunting of blood through collapsed lung areas.
H Hypoxia and acidosis result.
H Compensatory grunting occurs, producing positive
end-expiratory pressure (PEEP) that helps prevent
further alveolar collapse.
Causes
H Surfactant deficiency stemming from preterm birth
H Maternal history of diabetes or antepartum hemor-
rhage
Physical findings
H Intercostal, subcostal, or sternal retractions
H Nasal flaring
H Audible expiratory grunting
H Pallor
H Frothy sputum
H Low body temperature
H Diminished air entry and crackles
H Possible hypotension, peripheral edema, and oliguria
H Possible apnea, bradycardia, and cyanosis
Test results
Laboratory
H Partial pressure of arterial oxygen (PaO2) is decreased; partial pressure of arterial carbon dioxide
may be normal, decreased, or increased; and arterial
pH is decreased.
H Lecithin-sphingomyelin ratio shows prenatal lung
development and RDS risk.
Imaging
H Chest X-rays may show a fine reticulonodular pattern
and dark streaks, indicating air-filled, dilated bronchioles.
Treatment
General
H Aggressive management, assisted by mechanical ven-
27th gestational week; occurs in about 60% of those

born before the 28th week
H Most common in neonates of mothers with diabetes,
neonates delivered by cesarean birth, and neonates
delivered suddenly after antepartum hemorrhage
tilation with PEEP or continuous positive airway pressure (CPAP) administered by a tight-fitting face mask
or, when necessary, an endotracheal tube
H For a neonate who cant maintain adequate gas exchange, high-frequency oscillation ventilation
H Radiant warmer or Isolette
H Warm, humidified, oxygen-enriched gases given by
oxygen hood or mechanical ventilation
H Tube feedings or total parenteral nutrition
Medications
H Preterm birth
H Labored breathing within minutes to hours after birth
H I.V. fluids and sodium bicarbonate

H Pancuronium bromide
H Diuretics
H Surfactant replacement therapy
H Vitamin E
H Antenatal corticosteroids
Incidence
H Almost exclusively affects neonates born before the
Complications
H Respiratory insufficiency
H Shock
H Bronchopulmonary dysplasia
H Death
Assessment
History
H Preterm birth
H Cesarean birth
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Respiratory distress syndrome
Surgery
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Key outcomes
The patient will:
H maintain intact skin integrity.
The patients family will:
H identify factors that increase the risk of neonatal
injury.
ALERT
Watch for evidence of complications from oxygen
therapy: lung capillary damage, decreased mucus
flow, impaired ciliary functioning, and widespread
atelectasis. Also be alert for signs of patent ductus
arteriosus, heart failure, retinopathy, pulmonary
hypertension, necrotizing enterocolitis, and neurologic abnormalities.
Patient teaching
H Check the umbilical catheter for arterial or venous
hypotension, as appropriate.
H Suction, as necessary.
H Change the transcutaneous PaO2 monitor lead place-
ment site every 2 to 4 hours.
H Adjust PEEP or CPAP settings as indicated by arterial
blood gas (ABG) values.

H Implement measures to prevent infection.
H Provide mouth care every 2 hours.
H Encourage parents to participate in the infants care.
H Encourage parents to ask questions and to express
their fears and concerns.

H Advise parents that full recovery may take up to
12 months.
Be sure to cover (with the parents):

H explanations of respiratory equipment, alarm
sounds, and mechanical noise
H potential complications
Discharge planning
H Refer the parents to counselors and social worker, as
indicated.
H Refer the patient for follow-up care with a neonatal
ophthalmologist, as indicated.
ALERT
In a neonate on a mechanical ventilator, watch
carefully for signs of barotrauma and accidental
disconnection from the ventilator. Check ventilator
settings frequently. Be alert for signs of complications of PEEP or CPAP therapy, such as decreased
cardiac output, pneumothorax, and pneumomediastinum.
Monitoring
H Vital signs
H ABG values
H Intake and output
H Thrombosis
H Decreased peripheral circulation
H Pulse oximetry
H Daily weight
H Skin color
H Skin integrity
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Respiratory syncytial
virus infection
Overview
Description
H Virus thats the leading cause of lower respiratory
tract infection in infants and young children and upper respiratory infections in adults
H Suspected cause of fatal respiratory diseases in infants
H Can cause serious illness in immunocompromised
adults, institutionalized elderly people, and patients
with underlying cardiopulmonary disease
H Also known as RSV
Pathophysiology
H The virus attaches to cells, eventually resulting in
necrosis of the bronchiolar epithelium; in severe infection, peribronchiolar infiltrate of lymphocytes and
mononuclear cells occurs.
H Intra-alveolar thickening and filling of the alveolar
spaces with fluid results.
H Narrowing of the airway passages on expiration prevents air from leaving the lungs, causing progressive
overinflation.
Causes
H Respiratory syncytial virus, a subgroup of myxovirus-
es resembling paramyxovirus
H Sudden infant death syndrome

H Residual lung damage
Assessment
History
H Nasal congestion
H Coughing
H Wheezing
H Malaise
H Sore throat
H Earache
H Dyspnea
H Fever
Physical findings
H Nasal and pharyngeal inflammation
H Otitis media
H Severe respiratory distress (nasal flaring, retraction,
cyanosis, and tachypnea)

H Wheezes, rhonchi, and crackles
Test results
Laboratory
H Cultures of nasal and pharyngeal secretions show
respiratory syncytial virus.
H Serum respiratory syncytial virus antibody titers are
elevated.
H Arterial blood gas analysis shows hypoxemia and
respiratory acidosis.
H In dehydration, blood urea nitrogen levels are elevated.
H Transmitted from person to person by respiratory se-
cretions
H Probably spread to infants and young children by
school-age children, adolescents, and young adults

with mild reinfections
Incidence
H Almost exclusively affects infants and young children,
especially those in day care settings

H Highest among infants ages 1 to 6 months, peaking
between ages 2 and 3 months

H Annual epidemics during winter and spring
Treatment
General
H Respiratory support
H Adequate nutrition
H Avoidance of overhydration
Medications
H Ribavirin
H Bronchodilator such as albuterol
H Rhinorrhea, low-grade fever, and mild systemic
Surgery
symptoms accompanied by cough and wheezing

H Tachypnea, shortness of breath
H Cyanosis
H Apneic episodes
H Reinfection common; produces milder symptoms
than primary infection
Complications
H Pneumonia and progressive pneumonia
H Bronchiolitis
H Croup
H Otitis media
700
Respiratory syncytial virus infection
Key outcomes
The patient will:
H maintain a respiratory rate within 5 breaths/minute
of baseline
H express or indicate feelings of increased comfort
while maintaining adequate air exchange
H cough effectively
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H Institute contact isolation.
H Perform percussion, drainage, and suction when
necessary.
H Use a croup tent, as needed.
H Observe for signs and symptoms of dehydration, and
administer I.V. fluids accordingly.

H Promote bed rest.
H Offer diversional activities tailored to the patients
condition and age.
Monitoring
Patient teaching
H how the infection spreads
H preventive measures (RSV immune globulin)
H importance of a nonsmoking environment in the
home
H importance of keeping follow-up appointments.
Discharge planning
H Refer the patient to home care services, as necessary.
Respiratory syncytial virus infection
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Retinal detachment
Incidence
Overview
Description
H Painless vision loss

H Sensation of floaters or of looking through a veil,
H Partial or complete separation of the sensory retina
from the underlying pigment epithelium

H May be primary or secondary
H Commonly occurs spontaneously
H Usually involves only one eye; may occur in the other
eye later
H Rarely heals spontaneously; usually can be reattached successfully with surgery
H Carries varying prognosis depending on the retinal
area affected
Pathophysiology
H A hole or tear in the retina allows the liquid vitreous
to seep between the retinal layers.

H Liquid separates the sensory retinal layer from its
choroidal blood supply. (See Understanding retinal
detachment.)
Causes
H Intraocular inflammation
H Trauma
H Age-related degenerative changes
H Tumors
H Systemic disease
H Traction placed on the retina by vitreous bands or
membranes
H Hereditary factors, usually related to myopia
Special populations
In a child, retinal detachment can result from
retinopathy of prematurity, tumors (retinoblastomas), or trauma.
Risk factors
H Myopia
H Cataract surgery
H Trauma
H Affects twice as many males as females

H More common with increased age
curtain, or cobweb
Complications
H Severe vision impairment
H Blindness
Assessment
History
H Sensation of seeing floaters and flashes
H Painless vision loss, described as sensation of look-
ing through a veil, curtain, or cobweb (which may

obscure objects in a particular area of the visual
field)
Physical findings
H Visual field loss
Test results
Imaging
H Ocular ultrasonography may be used to examine the
retina if the lens is opaque and shows intraocular
and intraorbital pathology. It also commonly detects
retinal detachments, characteristically producing a
dense, sheetlike echo on a B-mode scan.
H Direct ophthalmoscopy shows folds or discoloration
in the usually transparent retina.
H Indirect ophthalmoscopy shows retinal tears.
Treatment
General
H Varies with location and severity of detachment
H Nothing by mouth before surgery
H Bed rest before surgery
H Restriction of eye movements before surgery by
patching affected eye

H Positioning of the patients head to allow gravity to
Understanding retinal detachment

Traumatic injury or degenerative changes cause retinal detachment by allowing the retinas sensory tissue layers to
separate from the retinal pigment epithelium. This permits
fluid from the vitreous, for example to seep into the
space between the retinal pigment epithelium and the rods
and cones of the tissue layers.
The pressure, which results from the fluid entering the
space, balloons the retina into the vitreous cavity away
from choroidal circulation. Separated from its blood supply, the retina cant function. Without prompt repair, the
detached retina can cause permanent vision loss.
702
Retinal detachment
pull the detached retina closer to the choroid
Medications
H Antiemetics
H Analgesics
H Mydriatics
H Cycloplegics
H Steroidal eyedrops
H Antibiotic eyedrops
Surgery
H Cryothermy
H Laser therapy
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H Scleral buckling (may be followed by vitreous
replacement with silicone, oil, air, or gas)

H Diathermy
Key outcomes
The patient will:
H avoid harm or injury
H express feelings and concerns
H regain the previous level of visual functioning.
H Prepare the patient for surgery.
H Administer prescribed antibiotics and cycloplegic or
mydriatic eyedrops.
H In macular involvement, maintain bed rest to prevent
further retinal detachment.

H Postoperatively, position the patient as directed.
H Discourage activities that increase intraocular
pressure.
H With retrobulbar injection, apply a protective eye
patch.
H Apply cold compresses.
H Avoid putting pressure on the eye.
H Provide encouragement and emotional support.
Monitoring
H Localized corneal edema and perilimbal congestion
after laser therapy

H Persistent pain
H Vital signs
H Visual acuity
Patient teaching
Be sure to cover:
H leg and deep-breathing exercises
H possible persistence of blurred vision for several
days after laser therapy
H importance of avoiding driving, bending, heavy lifting, and other activities that affect intraocular pressure for several days after surgery
H avoidance of activities that could cause eye trauma
H how to instill eyedrops
H importance of wearing sunglasses
H applying cold compresses
H signs and symptoms of increasing ocular pressure
and infection
H early symptoms of retinal detachment.
Retinal detachment
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Reyes syndrome
Overview
Description
H An acute childhood illness that causes fatty infiltra-
tion of the liver with concurrent hyperammonemia,

encephalopathy, and increased intracranial pressure
(ICP)
H Possible fatty infiltration of the kidneys, brain, and
myocardium
H Variable prognosis depending on the severity of central nervous system depression
Pathophysiology
H Damaged hepatic mitochondria disrupt the urea cy-
cle, which normally changes ammonia to urea for excretion from the body.
H This results in hyperammonemia, hypoglycemia, and
an increase in serum short-chain fatty acids, leading
to encephalopathy.
H Simultaneously, fatty infiltration is found in renal
tubular cells, neuronal tissue, and muscle tissue, including the heart.
Causes
H Viral infection
H Associated with aspirin use
Incidence
H Linked to aspirin use
H Usually increased during influenza outbreaks
Special populations
Reyes syndrome is most common in children ages
4 to 12, with peak incidence at age 6.
Assessment
History
H Viral infection
H Aspirin use
H Vomiting
Physical findings
H Increased blood pressure
H Tachycardia
H Lethargy
Test results
Laboratory
H Low or absent serum salicylate level rules out aspirin
overdose.
H Liver-function studies show aspartate aminotransferase and alanine aminotransferase levels elevated
to twice normal; bilirubin level is usually normal.
H Cerebrospinal fluid (CSF) analysis reveals a white
blood cell count of less than 10; with coma, CSF
pressure increases.
H Coagulation studies result in prolonged prothrombin
and partial thromboplastin times.
H Blood values show elevated serum ammonia levels;
normal or, in 15% of cases, low serum glucose levels; and increased serum fatty acid and lactate levels.
H Liver biopsy reveals fatty droplets uniformly distributed throughout cells.
Other
H History of a recent viral disorder with typical signs
and symptoms strongly suggests Reyes syndrome.
Treatment
H Dictated by stage of the syndrome (see Stages of
treatment for Reyes syndrome)
H Five-stage development, signs and symptoms varying
in severity with the degree of encephalopathy and

cerebral edema
H Possible atypical presentation for infants
H Brief recovery period after initial viral infection, during which child doesnt seem seriously ill
H A few days later, intractable vomiting, lethargy, rapidly changing mental status (mild to severe agitation,
confusion, irritability, delirium), hyperactive reflexes,
and rising blood pressure, respiratory rate, and
pulse rate
Complications

H Provide skin and mouth care.
H Perform or assist with ROM exercises.
H Increased ICP
H Coma
H Seizures
704
Reyes syndrome
Key outcomes
The patient will:
H remain hemodynamically stable.
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Stages of treatment for Reyes syndrome

Signs and symptoms
Treatment
Stage I
Vomiting, lethargy, hepatic dysfunction
Start baseline treatment:

To decrease intracranial pressure (ICP) and brain edema, administer
I.V. fluids at two-thirds of the maintenance dose. Also administer an
osmotic diuretic or furosemide.
To treat hypoprothrombinemia, administer vitamin K; if vitamin K
proves unsuccessful, administer fresh frozen plasma.
Monitor serum ammonia and blood glucose levels and plasma osmolality every 4 to 8 hours to check progress.
Stage II
Hyperventilation, delirium, hepatic
dysfunction, hyperactive reflexes
Continue baseline treatment.
Stage III
Coma, hyperventilation, decorticate
rigidity, hepatic dysfunction
Continue baseline and seizure treatment.

Monitor ICP with a subarachnoid screw or other invasive device.
Provide endotracheal intubation and mechanical ventilation to control
partial pressure of carbon dioxide. A paralyzing agent, such as pancuronium I.V. may help maintain ventilation.
Administer mannitol I.V. or glycerol by nasogastric tube.
Stage IV
Deepening coma; decerebrate rigidity;
large, fixed pupils; minimal hepatic
dysfunction
Continue baseline and supportive care.

If all previous measures fail, some pediatric centers use barbiturate
coma, decompressive craniotomy, hypothermia, or an exchange
transfusion.
Stage V
Seizures, loss of deep tendon reflexes,
flaccidity, respiratory arrest, ammonia
level greater than 300 mg/dl
Continue baseline and supportive care.
Monitoring
H Vital signs
H Intake and output
H ICP
Patient teaching
Be sure to cover:
H the disorder, diagnosis and treatment
H using a nonsalicylate analgesic and an antipyretic
such as acetaminophen for children.
Discharge planning
H Refer parents to the National Reyes Syndrome Foun-
dation for more information.

H Refer the patient to home care or rehabilitation ser-
vices, as needed.
Reyes syndrome
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Rhabdomyolysis
Overview
Description
H Breakdown of muscle tissue, causing myoglobinuria
H Usually follows major muscle trauma, especially a
muscle crush injury

H Good prognosis if contributing causes are stopped or
disease is checked before damage is irreversible
Pathophysiology
H Muscle trauma that compresses tissue causes ische-
mia and necrosis.

H The ensuing local edema further increases compart-
ment pressure and tamponade; pressure from severe

swelling causes blood vessels to collapse, leading to
tissue hypoxia, muscle infarction, neural damage in
the area of the fracture, and release of myoglobin
from the necrotic muscle fibers into the circulation.
H Excessive muscular activity associated with status
epilepticus, electroconvulsive therapy, or highvoltage electrical shock

H Alcohol use
H Recent soft tissue compression
H Seizure activity
Incidence
H Greater occurrence in males than females
H May occur at any age
H Tenderness, swelling, and muscle weakness caused
by muscle trauma and pressure

H Dark, reddish-brown urine from myoglobin
Complications
H Renal failure
H Amputation
Assessment
Causes
History
H Disorders that damage skeletal muscle
Risk factors
H Muscle trauma or breakdown

H Muscle pain
H Presence of any risk factors
H Traumatic injury
H Prescription and nonprescription drugs (see Drugs
Physical findings
that may cause rhabdomyolysis)

H Strenuous exertion such as long-distance running
H Infection, especially severe infection with necrosis
H Anesthetics that cause intraoperative rigidity
H Heat stroke
H Electrolyte disturbances
Drugs that may cause rhabdomyolysis

The use of these drugs may cause rhabdomyolysis:
H aminocaproic acid
H amphetamines
H amphotericin B
H anesthetic and paralytic agents
H antihistamines
H caffeine
H cocaine
H corticosteroids
H cyclic antidepressants
H fibric acid derivatives
H heroin
H neuroleptics
H phencyclidine
H propofol
H quinine
H salicylates
H selective serotonin-reuptake inhibitors
H statins
H theophylline.
706
Rhabdomyolysis
H Dark, reddish-brown urine

H Tense, tender muscle compartment (compartment
syndrome)
Test results
Laboratory
H Urine myoglobin level exceeds 0.5 mg/dl (evident
with only 200 g of muscle damage).
H Creatinine kinase level is elevated (0.5 to 0.95 mg/dl)
due to muscle damage.
H Serum potassium, phosphate, creatinine, and creatine levels are elevated.
H Hypocalcemia occurs in early stages, hypercalcemia
in later stages.
H Intracompartmental venous pressure measurements
(using a wick catheter, needle, or slit catheter inserted into the muscle) are elevated.
Imaging
H Computed tomography scan, magnetic resonance
imaging, and bone scintigraphy are used to detect
muscle necrosis.
Treatment
General
H For underlying disorder
H Prevention of renal failure
H Bed rest
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Medications
H Anti-inflammatory drugs
H Corticosteroids (in extreme cases)
H Analgesics
Surgery
H Immediate fasciotomy and debridement if compart-
ment venous pressure exceeds 25 mm Hg
Key outcomes
The patient will:
H maintain normal renal function
H verbalize understanding of the disorder and treatment.
H Administer prescribed I.V. fluids and drugs.
H Measure intake and output accurately.
H Promote comfort measures.
Monitoring
H Intake and output
H Urine myoglobins
H Renal studies
H Pain control
Patient teaching
Be sure to cover:
H the need for prolonged, low-intensity training as opposed to short bursts of intense exercise
Rhabdomyolysis
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Rheumatic fever and

rheumatic heart disease
Special populations
In children, mitral insufficiency is the major consequence of rheumatic heart disease.
Overview
Assessment
Description
History
H Systemic inflammatory disease of childhood that oc-
H Recent streptococcal infection

H Recent history of low-grade fever spiking to at least
curs 2 to 6 weeks after an inadequately treated upper

respiratory tract infection with group A beta-hemolytic streptococci
H Principally involves the heart, joints, central nervous
system, skin, and subcutaneous tissues
H In rheumatic heart disease, early acute phase that
may affect endocardium, myocardium, or pericardium, possibly followed later by chronic valvular disease
H Commonly recurs
Pathophysiology
H Rheumatic fever appears to be a hypersensitivity re-
action in which antibodies produced to combat

streptococci react and produce lesions at specific tissue sites.
H Antigens of group A streptococci bind to receptors in
the heart, muscle, brain, and synovial joints, causing
an autoimmune response.
H Because the antigens are similar to the bodys own
cells, antibodies may attack healthy body cells by
mistake.
Causes
H Group A beta-hemolytic streptococcal pharyngitis
H Familial tendency
Incidence
H In the United States, most common in northern states
H Worldwide, 15 to 20 million new cases each year
H Most common during cool, damp weather in winter
and early spring
H Fever
H Joint pain
H Rash and skin nodules
H Sydenhams chorea
H Nose bleeds
H Cardiac effects
Complications
H Destruction of mitral and aortic valves
H Severe pancarditis
H Pericardial effusion
H Heart failure
H Systemic emboli
708
Rheumatic fever and rheumatic heart disease
100.4 F (38 C) in late afternoon, along with unexplained epistaxis and abdominal pain
H Migratory joint pain (polyarthritis)
Physical findings
H Swelling, redness, and signs of effusion, most com-
monly in the knees, ankles, elbows, and hips

H With pericarditis: sharp, sudden pain that usually
starts over the sternum and radiates to the neck,

shoulders, back, and arms; increases with deep inspiration and decreases when the patient sits up and
leans forward
H With heart failure caused by severe rheumatic carditis: dyspnea, right upper quadrant pain, and a hacking, nonproductive cough
H Skin lesions, such as erythema marginatum, typically
on the trunk and extremities
H Subcutaneous nodules, 3 mm to 2 cm in diameter,
that are firm, movable, and nontender occurring
near tendons or bony prominences of joints, persisting for several days to weeks
H With left-sided heart failure: edema and tachypnea,
bibasilar crackles, and ventricular or atrial gallop
H Transient chorea up to 6 months after original streptococcal infection
H Heart murmurs and gallops
Test results
Laboratory
H During acute phase, white blood cell count and erythrocyte sedimentation rate are elevated.
H During inflammation, complete blood count shows
slight anemia.
H C-reactive protein test is positive, especially during
acute phase.
H In severe carditis, cardiac enzyme levels are increased.
H Antistreptolysin-O titer is elevated in 95% of patients
within 2 months of onset.
H Throat cultures show group A beta-hemolytic streptococci.
Imaging
H Chest X-rays show normal heart size (except with
myocarditis, heart failure, and pericardial effusion).
H Echocardiography helps evaluate valvular damage,
chamber size, and ventricular function and detects
pericardial effusion.
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H Electrocardiography reveals no diagnostic changes,
but 20% of patients show a prolonged PR interval.
H Cardiac catheterization evaluates valvular damage
and left ventricular function in severe cardiac dysfunction.
Treatment
General
H Dietary sodium restriction, if indicated
H Bed rest during acute phase
H Gradual activity increase, as tolerated
Medications
H Antibiotics such as penicillin
Surgery
H Commissurotomy, valvuloplasty, or heart valve
replacement
Patient teaching
Be sure to cover:
H the importance of resuming activities of daily living
slowly and scheduling frequent rest periods as instructed by the physician
H what to do if signs of an allergic reaction to penicillin
occur
H the importance of reporting early signs and symptoms of left-sided heart failure, such as dyspnea and
a hacking, nonproductive cough, and immediately
reporting signs of recurrent streptococcal infection
H keeping the child away from people with respiratory
tract infections
H transient nature of chorea
H compliance with prolonged antibiotic therapy and
follow-up care
H the possible need for prophylactic antibiotics before
any dental work or invasive procedures
Key outcomes
The patient will:
H avoid arrhythmias
fatigue
H express feelings about diminished capacity to perform usual roles.
H Find out if the patient has ever had a hypersensitivity
reaction to penicillin. Warn the parents (if appropriate) that such a reaction is possible.
H Administer prescribed antibiotics on time.
H Stress the importance of bed rest. Provide a bedside
commode.
H Position the patient upright.
H Provide analgesics and oxygen, as needed.
H Allow the patient to express feelings and concerns.
H Help the parents overcome any guilt feelings they
may have about their childs illness.
H Encourage the parents and child to vent their frustrations during the long recovery. If the child has severe
carditis, help them prepare for permanent changes
in the childs lifestyle.
Monitoring
H Vital signs
H Heart rhythm
H Heart and breath sounds
Rheumatic fever and rheumatic heart disease
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Overview
Description
H Chronic, systemic, symmetrical inflammatory disease
H Primarily attacking peripheral joints and surround-
ing muscles, tendons, ligaments, and blood vessels

H Marked by spontaneous remissions and unpre-
dictable exacerbations
H Potentially crippling
Pathophysiology
H Pain on inspiration
Physical findings
H Joint deformities and contractures
H Painful, red, swollen arms
H Foreshortened hands
H Boggy wrists
H Rheumatoid nodules
H Leg ulcers
H Eye redness
H Joints that are warm to the touch
H Positive Babinskis sign
H Cartilage damage resulting from inflammation trig-
Test results
gers further immune responses, including complement activation.

H Complement, in turn, attracts polymorphonuclear
leukocytes and stimulates release of inflammatory
mediators, which exacerbates joint destruction.
Laboratory
H Rheumatoid factor test is positive in 75% to 80% of
patients, as indicated by a titer of 1:160 or higher.
H Synovial fluid analysis shows increased volume and
turbidity but decreased viscosity and complement
(C3 and C4) levels, with white blood cell count possibly exceeding 10,000/l.
H Serum globulin levels are elevated.
H Complete blood count shows moderate anemia and
slight leukocytosis. (See Classifying rheumatoid
arthritis.)
Imaging
H In early stages, X-rays show bone demineralization
and soft-tissue swelling. Later, they help determine
the extent of cartilage and bone destruction, erosion,
subluxations, and deformities and show the characteristic pattern of these abnormalities.
H Magnetic resonance imaging, computed tomography
scan may provide information about damage extent.
Other
H Synovial tissue biopsy shows inflammation.
Causes
H Unknown
H Possible influence of infection (viral or bacterial),
hormonal factors, and lifestyle
Incidence
H Strikes three times as many females as males
H Can occur at any age; peak onset, ages 35 and 50
H Stiff, swollen joints
Complications
H Fibrous or bony ankylosis
H Soft-tissue contractures
H Joint deformities
H Sjgrens syndrome
H Osteoporosis
H Recurrent infections
H Hip joint necrosis
Assessment
History
H Insidious onset of nonspecific symptoms, including
fatigue, malaise, anorexia, persistent low-grade fever,

weight loss, and vague articular symptoms
H Later, more specific localized articular symptoms,
commonly in the fingers
H Bilateral and symmetrical symptoms, which may
extend to the wrists, elbows, knees, and ankles
H Stiff joints
H Stiff, weak, or painful muscles
H Numbness or tingling in the feet or weakness or loss
of sensation in the fingers
Treatment
General
H Adequate sleep (8 to 10 hours every night)
H Splinting
H Range-of-motion (ROM) exercises and carefully indi-
vidualized therapeutic exercises

H Moist heat application
H Frequent rest periods between activities
Medications
H Salicylates
naproxen, nabumetone, and indomethacin

H Gold salts such as auranofin
H Corticosteroids
H Cox-2 inhibitors such as celecoxib
H Disease-modifying antirheumatic drugs (DMARDS),
such as hydroxychloroquine and methotrexate

H Immunosuppressants, such as leflunomide, azathio-
prine, and penicilliamine
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H Tumor necrosis factor blockers (class of DMARDS),
such as etanercept and infliximab

H Interleukin-1 receptor antaognist such as anakinra
H Abatacept
H Rituximab
Surgery
H Metatarsal head and distal ulnar resectional arthro-
plasty; insertion of silastic prosthesis between metacarpophalangeal and proximal interphalangeal joints
H Arthrodesis (joint fusion)
H Synovectomy
H Osteotomy
H Repair of ruptured tendon
H In advanced disease, joint reconstruction or total
joint arthroplasty
Key outcomes
The patient will:
pain
H attain the highest degree of mobility possible
H verbalize feelings about limitations
H express an increased sense of well-being.
Classifying rheumatoid arthritis

A patient who meets four of seven American College of
Rheumatology criteria is classified as having rheumatoid
arthritis. She must experience the first four criteria for at
least 6 weeks, and a physician must observe the second
through fifth criteria.
H Morning stiffness in and around the joints that lasts for
1 hour before full improvement
H Arthritis in three or more joint areas, with at least three
joint areas (as observed by a physician) exhibiting
soft-tissue swelling or joint effusions, not just bony
overgrowth (the 14 possible areas involved include the
right and left proximal interphalangeal, metacarpophalangeal, wrist, elbow, knee, ankle, and metatarsophalangeal joints)
H Arthritis of hand joints, including the wrist, the metacarpophalangeal joint, or the proximal interphalangeal joint
H Arthritis that involves the same joint areas on both
sides of the body
H Subcutaneous rheumatoid nodules over bony prominences
H Demonstration of abnormal amounts of serum rheumatoid factor by any method that produces a positive
result in less than 5% of patients without rheumatoid
arthritis
H Radiographic changes, usually on posteroanterior hand
and wrist X-rays, must show erosions or unequivocal
bony decalcification localized in or most noticeable adjacent to the involved joints
H Administer prescribed analgesics; watch for adverse
reactions.
H Perform meticulous skin care.
H Supply adaptive devices, such as a zipper-pull, easyto-open beverage cartons, and lightweight cups.
After total knee or hip arthroplasty
H Administer prescribed blood replacement products,
antibiotics, and pain medication.
H Have the patient perform active dorsiflexion; immediately report inability to do so.
H Supervise isometric exercises every 2 hours.
H After total hip arthroplasty, check traction for pressure
areas; keep head of bed raised 30 to 45 degrees.
H Change or reinforce dressings, as needed.
H Have the patient turn, cough, and breathe deeply
every 2 hours.
H After total knee arthroplasty, keep the leg extended
and slightly elevated.
H After total hip arthroplasty, keep the hip in abduction. Watch for and immediately report inability to
rotate the hip or bear weight on it, increased pain, or
a leg that appears shorter.
H Assist patient in activities, keeping the weight on the
unaffected side.
Monitoring
H Joint mobility and pain level
H Skin integrity
H Vital signs and daily weight
H Sensory disturbances
H Serum electrolyte and hemoglobin level and hema-
tocrit
H Complications of corticosteroid therapy
Patient teaching
Be sure to cover:
H chronic nature of rheumatoid arthritis and possible
need for major lifestyle changes
H importance of a balanced diet and weight control
H sexual concerns.
If the patient requires total knee or hip arthroplasty,
be sure to cover:
H preoperative and surgical procedures
H postoperative exercises, with supervision
H deep-breathing and coughing exercises to perform
after surgery
H performing frequent ROM leg exercises after surgery
H use of a constant-passive-motion device after total
knee arthroplasty, or placement of an abduction pillow between the legs after total hip arthroplasty
H how to use a trapeze to move about in bed
Discharge planning
H Refer the patient for physical and occupational therapy.
H Refer the patient to the Arthritis Foundation.
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Rocky Mountain
spotted fever
Assessment
History
H Recent exposure to ticks or tick-infested areas, or a
Overview
Description
H Acute infectious, febrile, rash-producing illness asso-
ciated with outdoor activities

H Fatal in about 5% of patients
Pathophysiology
H Infecting organism multiplies in endothelial cells and
spreads via the bloodstream.

H Focal areas of infiltration lead to thrombosis and
leakage of red blood cells into surrounding tissue.
Causes
H Rickettsia rickettsii, transmitted by the wood tick
(Dermacentor andersoni) in the western United

States and by the dog tick (D. variabilis) in the eastern United States; enters humans or small animals
with the prolonged bite (4 to 6 hours) of an adult
tick
H Occasionally, inhalation or contact of abraded skin
with tick excreta or tissue juices
Incidence
H Endemic throughout the continental United States,
but most common in southeastern and south-central

regions
H Particularly prevalent in children ages 5 to 9
H Increased occurrence in spring and summer
H Fever, headache, mental confusion, and myalgia
H Macular papular rash on palms and soles in about
90% of patients
H Rash, evident in about 15% of patients on day 1 and
in nearly half of patients by day 3, starting at the

wrists, ankles, or forehead and spreading to the remainder of the extremities and trunk
H Within 2 days, rash seen over the entire body (including scalp, palms, and soles)
Complications
H Lobar pneumonia
H Otitis media
H Parotitis
H Renal failure
H Hepatic injury
H Enterocolitis
H Death
known tick bite

H Abrupt symptom onset, including persistent fever
(temperature of 102 to 104 F [38.9 to 40 C]);

generalized, excruciating headache; and aching in
bones, muscles, joints, and back
Physical findings
H Erythematous macules, 1 to 5 mm in diameter, be-
coming maculopapules that blanch with pressure

H Frank hemorrhage at the center of maculopapules,
creating petechia that dont blanch with pressure

H Bronchial cough
H Tachypnea
H Decreased urine output; dark urine
H Tachycardia
H Hypotension
H Hepatomegaly, splenomegaly
H Generalized pitting edema
Test results
Laboratory
H Serologic tests may be negative in initial stages.
H Indirect immunofluorescence assay has diagnostic
titer of 64 or greater, detectable between days 7 and
14 of the illness.
H Latex agglutination diagnostic titer is 128 or greater
1 week after onset.
H Platelet count, white blood cell (WBC) count, and
fibrinogen levels are decreased.
H Prothrombin time and partial thromboplastin time
are prolonged.
H Serum protein levels (especially albumin) are decreased.
H Hyponatremia and hypochloremia occur, related to
increased aldosterone excretion.
H Serum creatinine, blood urea nitrogen, and potassium levels are elevated.
H Hepatic function is abnormal.
H Cerebrospinal fluid analysis shows mild mononuclear pleocytosis with slightly elevated protein content.
H Immunohistologic examination of cutaneous biopsy
of a rash lesion shows R. rickettsii.
Treatment
General
H Careful tick removal
H Careful fluid administration
H Intubation and mechanical ventilation, if needed
H Hemodialysis, if needed
H Treatment of hemorrhage and thrombocytopenia, if
needed
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H Parenteral nutrition, if the patient cant receive oral
intake
Medications
H Doxycycline (drug of choice), tetracycline, or chlo-
ramphenicol (in pregnant females)

H Anticonvulsants
Key outcomes
The patient will:
H remain afebrile
H maintain normal WBC count and differential
H report increased comfort and decreased pain.
H Provide oxygen therapy and assisted ventilation for
pulmonary complications as ordered.

H Offer mentholated lotions if the rash itches.
H Turn the patient frequently.
H Encourage incentive spirometry and deep breathing.
H Plan care to promote adequate rest periods.
Monitoring
H Vital signs
H Neurologic status
Patient teaching
Be sure to cover:
H importance of reporting recurrent symptoms immediately
H importance of completing antibiotic course
H preventive strategies, including avoiding tick-infested
areas, whole-body inspection (including scalp) every
3 to 4 hours for attached ticks, protective clothing,
and insect repellent
H correct tick removal technique using tweezers or forceps and steady traction.
Discharge planning
H Refer the patient to an infectious disease specialist if
needed.
Rocky Mountain spotted fever
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Rosacea
Overview
Description
H Chronic adult skin disorder that affects the skin and
eyes
H Produces flushing and dilation of small blood vessels
in the face, especially the nose and cheeks
H May cause papules and pustules, but without the
characteristic comedones of acne vulgaris
H Usually spreads slowly; rarely subsides spontaneously
H Commonly more severe in males and usually associated with rhinophyma (dilated follicles and thickened, bulbous skin on the nose)
Pathophysiology
H Vascular reactivity leads to varying degrees of pap-
ules, pustules, and hyperplasia of the sebaceous

glands.
Causes
H Unknown
H Factors that cause flushing:
Drinking hot beverages

Using tobacco or alcohol
Eating spicy foods
Engaging in physical activity
Being exposed to extreme heat or cold or to
sunlight
Incidence
H Most common in white females ages 30 to 50
With ocular involvement

H Blepharitis
H Conjunctivitis
H Uveitis
H Keratitis
Assessment
History
H Facial flushing
H Gritty feeling in eyes
H Facial edema
H Predisposing or aggravating factors
H Complaints of burning or stinging of face
Physical findings
H Flushed areas on the cheeks, nose, forehead, and
chin, usually starting across the central oval of the

face (see Lupoid or granulomatous rosacea)
H Telangiectasia with pustules and papules
H Rhinophyma (thickened and disfigured noses) (in
severe rosacea)
H Dry skin appearance
H Facial edema
H Ocular rosacea:
Conjunctival infection
Chalazion
Episcleritis
Test results
H Rosacea is confirmed by observation of typical vascu-
lar and acneiform lesions without comedones.

H Skin biopsy may be done to rule out other diseases
such as lupus erythematosus.
H Flushed areas on cheeks, nose, forehead, and chin

H Ocular involvement (50% of cases)
Treatment
Complications
General
H Decreased self-esteem
H Rosacea fulminans
H Identification and avoidance of aggravating factors,
such as hot beverages, alcohol, and spicy foods

H Avoidance of physical activities involving sunlight or
exposure to extreme heat or cold
Lupoid or granulomatous rosacea

Firm yellow, brownish, or reddish cutaneous papules or
nodules characterize the variant form called lupoid or
granulomatous rosacea. The lesions are less inflammatory
that those of rosacea. Typically, the surrounding skin is
relatively normal looking, but sometimes its red and
thickened diffusely. Usually, the lesions are monomorphic
in each patient, affecting the cheeks and periorificial areas.
Other signs or symptoms of rosacea arent needed to
make the diagnosis of this form of rosacea. Diascopy with
a glass spatula reveals the lupoid character of the infiltrations. Lupoid or granulomatous rosacea may scar the
skin.
714
Rosacea
H Facial massage
Medications
H Topical azelaic acid
H Topical sodium sulfacetamide
H Topical metronidazole
H Oral doxycycline (for ocular involvement)
H Corticosteroids
H Isotretinoin for severe cases
Surgery
H Electrosurgery
H Laser therapy
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Key outcomes
The patient will:
H demonstrate an appropriate skin care regimen
H report feelings of improved self-image.
H Encourage patient to express feelings.
H Assist with identification of triggers.
Monitoring
H Complications
Patient teaching
Prevention
Preventing rosacea flare-up

Rosacea flare-ups may be prevented by following these
guidelines:
H Practice proper hand-washing techniques.
H Stay cool in hot weather by staying in air conditioned
areas, drinking cold beverages, and avoiding overexertion.
H Avoid cold wind on face by wearing a scarf or face
mask in cold weather.
H Use moisturizer in cold weather to protect against drying.
H Practice stress-management techniques.
H Avoid foods that trigger flare-ups, such as spicy foods,
hot beverages, and alcohol.
H Avoid heavy exertion during exercise, exercise in wellventilated areas, and exercise in short intervals. Also
apply a cold compress to face during exercise.
H Wash face gently and pat dry. Allow to air dry before
using creams and lotions.
H Avoid hot tubs, hot baths, and saunas.
H Avoid skin care products that burn or sting and use
products labeled fragrance free.
H Use a noncomedogenic, high-factor sunscreen when
exposed to sunlight and wind.
Be sure to cover:
H aggravating factors
H prevention of rosacea flare-ups (see Preventing
rosacea flare-up)
H stress-reduction techniques
H meticulous hand washing and personal hygiene
H ways to prevent infection
Rosacea
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Roseola infantum
Assessment
History
Overview
H Abruptly increasing, unexplainable fever that peaks
Description
H Common acute, benign, presumably viral illness
characterized by fever with subsequent rash (see

Incubation and duration of common rashproducing infections)
H Also known as exanthema subitum or sixth disease
Pathophysiology
between 103 and 105 F (39.4 and 40.5 C) for

3 to 5 days and then drops suddenly
H Anorexia
H Irritability
H Listlessness
H Cough
Physical findings
H When temperature drops abruptly, maculopapular,
H Human herpesvirus (HHV) type 6B, which causes the
nonpruritic rash appears that blanches with pressure
disorder, is similar to cytomegalovirus.

H HHV-6 shows persistent and intermittent or chronic
shedding in the normal population, resulting in the
unusually early infection of children.
H HHV-6 is thought to be latent in salivary glands and
blood.
H Profuse rash on the trunk, arms, and neck; mild rash
Causes
H Usually, roseola infantum is diagnosed from clinical
H HHV-6B
H May be transmitted by saliva and possibly by genital
secretions
Incidence
H Affects infants and young children, typically from age
6 months to 3 years
H Occurs year-round, but most common in spring and
fall
on the face and legs; fades within 24 hours

H Nagayama spots (red papules on soft palate and
uvula)
H Periorbital edema
Test results
observation.
Laboratory
H Causative organism is present in saliva.
H HHV-6 is isolated in peripheral blood.
H Complete blood count shows leukopenia and relative
lymphocytosis as temperature increases.
H Immunofluorescence or enzyme immunoassays may
show seroconversion during the convalescent phase.
Treatment
H Incubation period of 10 to 15 days
H High fever with rash appearing after the fever breaks
Complications
H Encephalopathy
H Thrombocytopenic purpura
H Febrile seizures
H Meningitis
H Hepatitis
General
H Supportive and symptomatic
H Rest until fever subsides
Medications
H Antipyretics
H Anticonvulsants
Incubation and duration of common
rash-producing infections
Key outcomes
Infection
Incubation
(days)
Duration
(days)
Roseola
5 to 15
3 to 6
The patient will:

H regain a normal body temperature
H maintain adequate nutritional intake
H exhibit improved or healed lesions or wounds.
Varicella
10 to 14
7 to 14
Rubeola
13 to 17
Rubella
14 to 21
716
Roseola infantum
H Give tepid sponge baths and prescribed antipyretics.

H Provide emotional support to parents.
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Monitoring
H Neurologic status
Patient teaching
Be sure to cover:
H methods to reduce fever:
tepid sponge baths
dressing the child in lightweight clothing
keeping a comfortable room temperature
use of antipyretics
H importance of adequate fluid intake
H no need for isolation
H reassurance that brief febrile seizures wont cause
brain damage and will stop as the fever subsides
Roseola infantum
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Rotavirus
Overview
Assessment
History
H Fever, nausea, and vomiting followed by diarrhea
Description
Physical findings
H Self-limiting intestinal illness that causes mild to se-
H Diarrhea
H Signs of dehydration, such as:
vere diarrhea in children

H Causes hospitalization of about 55,000 children each
year in the United States and kills more than 600,000
children worldwide
Pathophysiology
H Rotavirus invades and damages the cells of the in-
testinal mucosa.
H Damage decreases viable absorptive surface, causing
an imbalance of secretion and absorption that results

in diarrhea.
Tachycardia
Hypotension
Dry mucous membranes
Concentrated urine
Poor tear production
Poor skin turgor
Oliguria
Sunken eyeballs
Sunken anterior fontanel
H Rectal excoriation
Causes
Test results
H Infection with rotavirus, a member of the Reoviridae
Laboratory
H Rapid antigen detection shows rotavirus in stool.
family
H Transmitted primarily by the fecal-oral route through
ingestion of contaminated water or food or through
contact with contaminated surfaces (see Spreading
rotavirus infection)
Incidence
H Highest among infants and young children; affects
most children in the United States by age 2

H Winter seasonal pattern in the United States and
other temperate climate countries, with annual

epidemics from November to April
Treatment
General
H Skin care
Medications
H None (antibiotics and antimotility drugs contraindi-
cated)
H Vomiting and watery diarrhea for 3 to 8 days

H Fever
H Abdominal pain
Complications
Key outcomes
H Severe dehydration and shock

H Skin breakdown
H Worsening of other conditions such as cystic fibrosis
The patient will:

H maintain adequate nutritional status
H verbalize or demonstrate increased energy.
Spreading rotavirus infection

Rotavirus infection is contagious. Rotavirus particles pass
in the stool of infected persons before and after they have
symptoms of the illness. A child can catch a rotavirus infection if he puts his fingers in his mouth after touching
something that has been contaminated by the stool of an
infected person. Usually this happens when the child forgets to wash his hands often enough, especially before
eating and after using the toilet. Because of the widespread nature of rotavirus and the fact that almost 100%
of children get rotavirus illness, total prevention of the
spread of rotavirus is nearly impossible.
718
Rotavirus
H Institute enteric precautions.
H Enforce strict hand washing and careful cleaning of
all equipment, including toys.

H Implement measures to ensure adequate hydration.
H Clean the patients perineum thoroughly to prevent
skin breakdown.
H Be aware that breast-fed infants can continue to
breast-feed without restrictions. Bottle-fed infants

can use lactose-free soybean formulas.
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Monitoring
H Intake and output (including stools)
H Skin integrity
Patient teaching
H instructions on diaper changing and thorough
cleaning of the perineum and all affected surfaces
H the importance of notifying the physician of
increased diarrhea or signs of dehydration
H oral vaccine available for infants only.
Rotavirus
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Rubella
Overview
Description
H Acute, mildly contagious viral disease that causes a
H Rash covering the trunk and body; begins to fade in
the opposite order in which it appeared by the end of

day 2
H Rash subsiding on the face; on the trunk may be confluent and hard to distinguish from scarlet fever rash
H Rash disappearing on day 3
distinctive maculopapular rash (resembling measles

or scarlet fever) and lymphadenopathy
H Self-limiting with an excellent prognosis, except for
congenital rubella, which can have disastrous consequences
H Transmitted through contact with blood, urine,
stools, or nasopharyngeal secretions of an infected
person; can also be transmitted transplacentally
H Communicable from about 10 days before until
5 days after rash appears
H Also called German measles
Complications
Pathophysiology
Assessment
H A ribonucleic acid virus enters the bloodstream, usu-
ally through the respiratory route.
H Arthritis
H Postinfectious encephalitis
H Thrombocytopenic purpura
H Congenital rubella
In fetal infection (rare after 20th week

of gestation)
H Intrauterine death
H Spontaneous abortion
H Congenital malformations of major organ systems
History
H The incubation period lasts 14 to 21 days, with a
H Inadequate immunization, exposure to a person with
duration of 3 days.
H The rash is thought to result from virus dissemination to the skin.
rubella infection within the previous 2 to 3 weeks, or

recent travel to an endemic area without reimmunization
H In a child, absence of prodromal symptoms
H In an adolescent or adult, headache, malaise,
anorexia, coryza, sore throat, and cough preceding
rash onset
H Polyarthralgias and polyarthritis (in some adults)
Causes
H Rubella virus (a togavirus) spread by direct contact
or contaminated airborne respiratory droplets
Incidence
H Occurs worldwide
H Most common among children ages 5 to 9, adoles-
cents, and young adults

H Epidemics seen in institutions, colleges, and military
populations
H Flourishes during spring, with limited outbreaks in
schools and workplaces
Giving the rubella vaccine

Know how to manage rubella immunization before giving
the vaccine. First, ask about allergies, especially to
neomycin. If the person has this allergy or has had a reaction to any immunization in the past, check with the physician before giving the vaccine.
If the person is a female of childbearing age, ask if shes
pregnant. If she is or thinks she may be, dont give the
vaccine.
Give the vaccine at least 3 months after any administration of immune globulin or blood. These substances may
have antibodies that could neutralize the vaccine.
Dont vaccinate an immunocompromised person, a person with immunodeficiency disease, or a person receiving
immunosuppressant, radiation, or corticosteroid therapy.
Instead, administer immune serum globulin, as ordered,
to prevent or reduce infection.
720
Rubella
Physical findings
H Rash accompanied by low-grade fever (99
to 101 F
[37.2 to 38.3 C]) that may reach 104 F (40 C)
H Exanthematous, maculopapular, mildly pruritic rash;
typically beginning on the face, and spreading rapidly, covering the trunk and limbs within hours
H Small, red, petechial macules on the soft palate
(Forschheimer spots) preceding or accompanying
the rash
H Coryza
H Conjunctivitis
H Suboccipital, postauricular, and postcervical lymph
node enlargement
Test results
H Usually, the diagnosis is made from clinical observa-
tion.
Laboratory
H Cultures of throat, blood, urine, and cerebrospinal
fluid isolate the rubella virus; convalescent serum
shows a fourfold increase in antibody titers.
H Enzyme-linked immunosorbent assay for immunoglobulin (Ig) M antibodies reveals rubella-specific
IgM antibody.
H In congenital rubella, rubella-specific IgM antibody
is present in umbilical cord blood.
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Treatment
General
H Isolation precautions
H Rest until fever subsides
H Skin care
Medications
H Antipyretics
H Analgesics
Key outcomes
The patient will:
H exhibit improvement or healing of lesions or wounds
H express or demonstrate feelings of increased comfort
and decreased pain.
H Institute isolation precautions until 5 days after the
rash disappears. Keep an infant with congenital

rubella in isolation for 3 months, until three throat
cultures are negative.
H Keep the patients skin clean and dry.
H Ensure that the patient receives care only from nonpregnant hospital workers who arent at risk for
rubella. As ordered, administer immune globulin to
nonimmunized people who visit the patient. (See
Giving the rubella vaccine.)
H Report confirmed rubella cases to local public health
officials.
H Refer the patient to an infectious disease specialist if
congenital rubella is confirmed.
H Provide parents of an infant with congenital rubella
with support, counseling, and referrals, as needed.
Monitoring
H Vital signs
H Skin for signs of exanthem
H Auditory impairment in congenital rubella
Patient teaching
H ways to reduce fever
H devastating effects of rubella on an unborn neonate
H importance of people with rubella avoiding pregnant
females
H avoidance of aspirin in a child receiving rubella
vaccine.
Rubella
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Rubeola
Overview
Description
H Acute, highly contagious infection causing a charac-
teristic rash
H In the United States, a usually excellent prognosis
H Can be severe or fatal in patients with impaired cell-
mediated immunity
H Mortality highest in children younger than age 2 and
in adults
H Also called measles or morbilli
Pathophysiology
H Virus invades the respiratory epithelium and spreads
via the bloodstream to the reticuloendothelial system,

infecting all types of white blood cells.
H Viremia and viruria develop, leading to infection of
the entire respiratory tract, which spreads to the integumentary system.
H In measles encephalitis, focal hemorrhage, congestion, and perivascular demyelination occur.
Causes
H Rubeola virus
H Spread by direct contact or by contaminated air-
borne respiratory droplets, with portal of entry in the

upper respiratory tract
Incidence
H Affects mostly preschool children
H In temperate zones, most commonly seen in late win-
ter and early spring
H Fever, Kopliks spots, and characteristic red, blotchy,
rash that begins on the face and becomes generalized

H Peak communicability from 1 to 2 days before symp-
tom onset until 4 days after the rash appears
Complications
H Coryza
H Hoarseness
H Hacking cough
Physical findings
H Temperature peaking at 103
to 105 F (39.4 C to
40.5 C)
H Periorbital edema
H Conjunctivitis
H Kopliks spots (tiny, bluish gray specks, surrounded
by red halo) on oral mucosa opposite the molars,
which may bleed
H Pruritic rash starting as faint macules behind the ears
and on the neck and cheeks, becoming papular and
erythematous, and rapidly spreading over the face,
neck, eyelids, arms, chest, back, abdomen, and
thighs
H Fading of rash when it reaches the feet 2 to 3 days
later, occurring in the same sequence it appeared,
leaving brown discoloration that disappears in 7 to
10 days
H Severe cough
H Rhinorrhea
H Lymphadenopathy
Test results
Laboratory
H The measles virus appears in blood, nasopharyngeal
secretions, and urine during the febrile period.
H Serum antibodies appear within 3 days after rash onset and reach peak titers 2 to 4 weeks later.
Treatment
General
H Respiratory isolation precautions
H Use of vaporizer
H Warm environment
H Rest until symptoms improve
H Skin care

H Autoimmune reaction
H Bronchitis
H Otitis media
H Pneumonia
H Encephalitis
Medications
Assessment
The patient will:

H remain free from complications related to oral mucous membrane trauma.
The patients family will:
H communicate an understanding of the patients special dietary needs.
History
H Inadequate immunization and exposure to someone
with measles in the past 14 days

H Photophobia
H Malaise
H Anorexia
722
Rubeola
H Antipyretics
Key outcomes
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H Institute respiratory isolation measures for 4 days af-
ter rash onset.

H Encourage bed rest during the acute period.
H If photophobia occurs, darken the room or provide
sunglasses.
H To prevent disease spread, administer measles
vaccine, as ordered and needed.

H Report measles cases to local health authorities.
Monitoring
H Vital signs
H Skin for signs of exanthem
H Eyes for conjunctivitis
H Mental status
H Signs and symptoms of pneumonia
H Ears for otitis media
Patient teaching
H supportive measures, isolation, bed rest, and increased fluids
H instructions on cleaning a vaporizer (if used) and the
importance of changing the water every 8 hours
H early signs and symptoms of complications that
should be reported.
Rubeola
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Saint Louis encephalitis

Overview
Description
H Acute inflammatory disease of short duration that in-
volves the brain, spinal cord, and meninges following

the bite of an infected mosquito (mosquitoes infective for life)
H Usually asymptomatic, but severe infection may have
acute onset
H Incubation period of 4 to 21 days
H No person-to-person transmission
H No chronic infection or reports of relapsing infection
H Also known as SEV, SLEV, mosquito-borne
encephalitis, arbovirus, and viral encephalitis
Pathophysiology
H The virus is found in common birds, such as spar-
rows, finches, blue jays, robins, and doves.

H Culex mosquitoes feed on these birds, contract the
virus, and then pass it on to human hosts through a

bite.
H A primary viremia follows reproduction of the virus
at the site of inoculation.
H In subclinical disease, the pathogen is cleared by the
liver, spleen, and lymph nodes before invasion of the
central nervous system.
H Secondary viremia occurs with continued viral replication, which overwhelms the liver, spleen, and
lymph nodes.
H The virus then invades the central nervous system, including the brain and spinal cord.
Causes
H Transmitted by the bite of an infected mosquito
H Laboratory-acquired infections possible through in-
fected blood, cerebrospinal fluid (CSF), urine, and

exudates
Risk factors
H Human immunodeficiency virus infection
H Age older than 70 (tenfold increased risk of clinical
illness)
H Travel to endemic areas
H Participation in outdoor activities
H Outdoor occupations
Incidence
H Occurs in North, South, and Central America and the
Caribbean; major health problem in the United Sates

H Highest incidence in late summer or early fall
H Higher incidence in males, probably because of
more outdoor exposure
724
H Symptoms usually mild
H In severe infections
Acute onset of headache

High fever
Nausea
Myalgia
Malaise
Meningeal signs of stupor
Coma
Seizures (especially in infants)
Spastic paralysis
Death
H In children, possible urinary tract symptoms
Complications
H Acute encephalitis
H Movement disorders and motor deficits
H Seizures and coma
H Death
ALERT
Patients with atherosclerosis, heart disease, and
hypertension have an increased risk of death from
this infection.
Assessment
History
H Exposure to infected insect
H Onset of encephalitis characterized by:
Malaise
Fever
Cough and sore throat, followed by common
symptoms of headache, nausea, vomiting, confusion, disorientation, irritability, tremors, and possible seizures
Physical findings
H Temperature elevation
H Normal neurologic examination
H 5% of patients present in a deep coma
H Cranial nerve palsies in about 25% of patients
H Possibly ataxia
H Possibly seizures (infrequent, but more common in
children)
Test results
Laboratory
H One of the following will be present: A fourfold increase in the antivirus antibody titer between the
acute and the convalescent periods; virus isolation
from tissue, blood, or CSF; or specific immunoglobulin M antibody.
H Pyuria or proteinuria occurs.
H Sodium level is decreased.
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H CSF pressure is normal to mildly elevated, blood glu-
cose level is normal, and protein level is normal to

mildly elevated; CSF white blood cell count usually is
less than 200/l..
Treatment
General
H Supportive
H Management of seizures or neurologic symptoms
H Diet as tolerated
H Bed rest
Medications
H Antipyretics
H Analgesics
Prevention
Preventing mosquito bites

Mosquito bites may be prevented by following these
guidelines:
H Stay indoors between dusk and dark.
H Wear long pants and long-sleeved shirts when outside.
H Wear socks and tuck pants legs into socks.
H Choose light-colored clothing.
H Spray exposed skin with insect repellent.
H Avoid areas of standing water where mosquitoes congregate.
H Eliminate standing water around home to prevent
breeding, such as:
unclogging gutters
removing old tires
emptying wading pools or change water frequently
changing bird bath water frequently
checking flower pots for pooling water and drain.
H Use an electronic bug zapper.
H Change outdoor lights to yellow bug lights.
Key outcomes
The patient will:
H remain safe from falls caused by ataxia or seizures
H accept comfort measures
H maintain adequate nutrition and fluid intake.
H Encourage nutritional intake.
H Encourage fluids and lying flat after lumbar punc-
ture.
H Assist with ambulation, as needed.
H Frequently reposition the unconscious patient.
H Encourage range-of-motion (ROM) exercises (pas-
sive ROM exercises if the patient is unconscious).
Monitoring
H Vital signs
H Skin breakdown
H Seizure activity
H Complications of lumbar puncture, if performed
Patient teaching
Be sure to cover:
H mosquito bite prevention. (See Preventing mosquito
bites.)
Discharge planning
H Encourage follow-up appointments, as needed.
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Salmonella infection
Overview
Description
H One of the most common intestinal infections in the
United States
and those already weakened by other infections, especially human immunodeficiency virus infection
Complications
H Dehydration
H Hypovolemic shock
H Abscess formation
H Sepsis
H Toxic megacolon
H Occurs as enterocolitis, bacteremia, localized infec-
tion, typhoid fever, or paratyphoid fever

H Nontyphoid forms, usually mild to moderate illness
with low mortality

H Typhoid fever most severe form; usually lasts from
1 to 4 weeks and confers lifelong immunity, although
patient may become a carrier
Pathophysiology
H Invasion occurs across the small intestinal mucosa,
altering the plasma membrane and entering the lamina propria.

H Invasion activates cell-signaling pathways, which alter
electrolyte transport, and may cause diarrhea.
H Some salmonella produce a molecule that increases
electrolyte and fluid secretion.
Causes
H Gram-negative bacilli of the genus Salmonella
(member of the Enterobacteriaceae family)

Typhoid fever: S. typhi
Enterocolitis: S. enteritidis
Bacteremia: S. choleresis
H Nontyphoidal infection usually, ingestion of contaminated water or food or inadequately processed
food, especially eggs, chicken, turkey, and duck
H Contact with infected person or animal
H Ingestion of contaminated dry milk, chocolate bars,
or pharmaceuticals of animal origin
Special populations
Salmonella infection in children younger than age
5 is usually from fecal-oral spread.
H Typhoid fever usually, drinking water contaminat-
ed by excretions of a carrier
Incidence
H Increasing in the United States due to travel to en-
demic areas, especially the borders of Mexico
Assessment
History
H With enterocolitis, possible report of contaminated
food eaten 6 to 48 hours before onset of symptoms

H With bacteremia, patient usually reveals immuno-
compromised condition, especially acquired immunodeficiency syndrome

H With typhoid fever, possible ingestion of contaminated food or water, typically 1 to 2 weeks before symptoms develop
Physical findings
H Fever
H Abdominal pain
H With enterocolitis, severe diarrhea
H With typhoidal infection, headache, increasing fever,
and constipation
Test results
Laboratory
H Blood culture in typhoid or paratyphoid fever and
bacteremia shows causative organism in most cases.
H Stool culture in typhoid or paratyphoid fever and enterocolitis shows causative organism.
H Other culture specimens (urine, bone marrow, pus,
and vomitus) show causative organism.
H Presence of S. typhi in stools 1 or more years after
treatment indicates that the patient is a carrier
(about 3% of patients).
H Widals test, an agglutination reaction against somatic
and flagellar antigens, suggests typhoid fever with a
fourfold increase in titer.
H Complete blood count (CBC) shows transient leukocytosis during the first week of typhoidal salmonella
infection.
H CBC shows leukopenia during the third week of typhoidal salmonella infection.
H CBC shows leukocytosis with local infection.
H Lifelong immunity after initial attack of typhoid fever,
but patient may become a carrier

H Paratyphoid fever rare in the United States
Treatment
General
H Nontyphoidal forms usually, mild to moderate ill-
H Possible hospitalization for severe diarrhea
H Fluid and electrolyte replacement
H High-calorie fluids
ness, with low mortality

H Enterocolitis and bacteremia especially common
(and more virulent) among infants, elderly people,
726
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Medications
H Antimicrobials
H Antidiarrheals
ALERT
Dont give antipyretics. They may mask fever and
lead to hypothermia. Instead, promote heat loss by
applying tepid, wet towels to the patients groin
and axillae.
Surgery
H Surgical drainage of localized abscesses
Key outcomes
The patient will:
H regain and maintain fluid and electrolyte balance
H return to a normal elimination pattern
H conserve energy while carrying out daily activities
H report adequate pain relief
Prevention
Preventing recurrence of
salmonella infection
To prevent salmonella infection from recurring, follow
these teaching guidelines:
H Explain the causes of salmonella infection.
H Show the patient how to wash his hands by wetting
them under running water, lathering with soap and
scrubbing, rinsing under running water with his fingers
pointing down, and drying with a clean towel or paper
towel.
H Tell the patient to wash his hands after using the bathroom and before eating.
H Tell him to cook foods thoroughly especially eggs
and chicken and to refrigerate them at once.
H Teach him how to avoid cross-contaminating foods by
cleaning preparation surfaces with hot, soapy water
and drying them thoroughly after use; cleaning surfaces between foods when preparing more than one
food; and washing his hands before and after handling
each food.
H Tell the patient with a positive stool culture to avoid
handling food and to use a separate bathroom or clean
the bathroom after each use.
H Tell the patient to report dehydration, bleeding, or recurrence of signs of salmonella infection.
H Follow enteric precautions until three consecutive
Discharge planning
stool cultures are negative the first one 48 hours

after antibiotic treatment ends, followed by two more
at 24-hour intervals.
H Watch closely for signs of bowel perforation.
H Maintain adequate I.V. fluid and electrolyte therapy,
as ordered.
H Provide good skin and mouth care.
H Apply mild heat to relieve abdominal cramps.
H Report salmonella cases to public health officials.
H Arrange for follow-up with an infectious disease
specialist or a gastroenterologist as needed.
Monitoring
H Vital signs
H Daily weight
Patient teaching
Be sure to cover:
H the need for close contacts to obtain a medical examination and treatment if cultures are positive
H how to prevent salmonella infections (see Preventing recurrence of salmonella infection)
H the need to be vaccinated (for those at high risk for
contracting typhoid fever, such as laboratory workers
and travelers)
H the importance of proper hand washing
H the need to avoid preparing food or pouring water
for others until salmonella infection is eliminated.
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Sarcoidosis
Overview
Description
H A multisystemic, granulomatous disorder that char-
acteristically produces lymphadenopathy, pulmonary

infiltration, and skeletal, liver, eye, or skin lesions
H May be acute (usually resolves within 2 years) or
chronic
H Chronic, progressive sarcoidosis (uncommon) associated with pulmonary fibrosis and progressive pulmonary disability
Pathophysiology
H An excessive inflammatory process begins in the alve-
oli, bronchioles, and blood vessels of the lungs.

H Monocyte-macrophages accumulate in the target tis-
sue where they induce the inflammatory process.

H CD4+ T-lymphocytes and sensitized immune cells
form a ring around the inflamed area.

H Fibroblasts, mast cells, collagen fibers, and proteo-
glycans encase the inflammatory and immune cells,

causing granuloma formation.
Causes
H Possible causes:
Hypersensitivity response to atypical mycobacteria,

fungi, and pine pollen
Chemicals
T-cell abnormalities
Lymphokine production abnormalities
Incidence
H Most common in people ages 20 to 40
H In the United States, predominant occurrence among
blacks
H Affects twice as many females as males
H Incidence slightly higher in families, suggesting
Assessment
History
H Pain in the wrists, ankles, and elbows
H General fatigue and malaise
H Unexplained weight loss
H Breathlessness and dyspnea
H Nonproductive cough
H Substernal pain
Physical findings
H Erythema nodosum
H Punched out lesions on the fingers and toes
H Cranial or peripheral nerve palsies
H Extensive nasal mucosal lesions
H Anterior uveitis
H Glaucoma and blindness occasionally in advanced
disease
H Bilateral hilar and paratracheal lymphadenopathy
H Splenomegaly
H Arrhythmias
Test results
Laboratory
H Arterial blood gas (ABG) analysis shows a decreased
partial pressure of arterial oxygen and increased carbon dioxide levels.
Imaging
H Chest X-rays show bilateral hilar and right paratracheal adenopathy, with or without diffuse interstitial
infiltrates.
H Kveim-Siltzbach skin test shows granuloma development at the injection site in 2 to 4 weeks when positive.
H Lymph node, skin, or lung biopsy shows noncaseating granulomas with negative cultures for mycobacteria and fungi.
H Pulmonary function tests show decreased total lung
capacity and compliance and reduced diffusing capacity.
genetic predisposition
H Pain in the wrists, ankles, and elbows
H Malaise
H Unexplained weight loss
H Shortness of breath on exertion
H Substernal pain
Complications
H Cor pulmonale
Treatment
General
H None needed for asymptomatic sarcoidosis
H Protection from sunlight
H Low-calcium diet for hypercalcemia
H Reduced-sodium, high-calorie diet
H Adequate fluids
Medications
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Key outcomes
Discharge planning
H Refer a patient with failing vision to community sup-
port and resource groups such as the American

Foundation for the Blind, if necessary.
The patient will:

H express an understanding of the illness
the illness
H Administer supplemental oxygen.
H Provide a nutritious, high-calorie diet.
H Provide a low-calcium diet for hypercalcemia.
H Include the patient in care decisions whenever
possible.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Sputum production
H ABG results
H Cardiac rhythm
ALERT
Because corticosteroids may induce or worsen diabetes mellitus, test the patients blood by fingersticks for glucose and acetone at least every
12 hours at the beginning of corticosteroid therapy.
Also, watch for other adverse effects, such as fluid
retention, electrolyte imbalance (especially hypokalemia), moon face, hypertension, and personality changes.
Patient teaching
Be sure to cover:
H steroid therapy
H the need for regular follow-up examinations
jewelry
H infection prevention.
Sarcoidosis
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Scabies
Overview
Description
H Transmissible skin infestation with Sarcoptes scabiei
var. hominis (itch mite)

H Characterized by burrows, severe pruritus, and exco-
riations
Pathophysiology
H Mites burrow into the skin on contact, progressing
2 to 3 mm per day.
H Females live about 4 to 6 weeks and lay about 40 to
50 eggs, which hatch in 3 to 4 days.

H Pruritus occurs only after sensitization to the mite
develops. With initial infestation, sensitization requires several weeks. With reinfestation, sensitization
develops within 24 hours.
H Dead mites, eggs, larvae, and their excrement trigger
an inflammatory eruption of the skin in infested
areas.
Causes
H Occurs worldwide
H Can be endemic
H Burrows
H Severe pruritus
H Excoriations
Complications
H Abscess formation
H Septicemia
Assessment
History
H Predisposing factors
H May be asymptomatic initially
H Intense pruritus being more severe at night
Physical findings
H Characteristic gray-brown, threadlike burrows (0.5
to 1 cm long) with tiny papule or vesicle at one end

H Common sites: flexor surfaces of wrists, elbows, axil-
lary folds, waistline, nipples in females, and genitalia
H Direct (skin to skin) contact or contact with contam-
inated articles for up to 48 hours (see Scabies:

Cause and effect)
Risk factors
H Overcrowded living conditions
H Poor hygiene
H Day-care or institutional settings
Incidence
H Common in children and young adults
H Common in elderly and debilitated patients
Scabies: Cause and effect

Infestation with Sarcoptes scabiei the itch mite
causes scabies. This mite (shown enlarged below) has a
hard shell and measures a microscopic 0.1 mm.
Special populations
In infants, the burrows may appear on the head
and neck.
H Papules, vesicles, crusting, abscess formation, and
cellulites with secondary infection
Test results
Laboratory
H Wound culture demonstrates secondary bacterial infection.
H Mineral oil burrow-scraping reveals mites, nits, or
eggs, and feces or scybala.
H Punch biopsy may help confirm the diagnosis.
Other
H Resolution of infestation with therapeutic trial of a
pediculicide confirms the diagnosis.
Treatment
General
H Bathing with soap and water
Medications
H Topical scabicides
H Topical 6% to 10% sulfur solution
H Systemic antibiotics
H Antipruritics
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ALERT
Avoid the use of topical steroids, which may potentiate the infection.
Special populations
When treating infants, include the head in treatment.
Prevention
Preventing scabies transmission

and recurrence
Scabies transmission and recurrence may be prevented
by following these guidelines:
H Avoid sharing towels, linen, and clothing.
H Wash all infested items with hot, soapy water and dry
on high heat in the dryer.
H Place items you cant wash in a plastic bag and leave
for 1 week. Mites die within 48 to 72 hours away from
the human body.
H Practice good personal hygiene.
Key outcomes
The patient will:
H exhibit resolution of infestation
H report relief of pruritus
H demonstrate understanding of proper skin care
regimen.
H prevention of transmission and recurrence (see Pre-
venting scabies transmission and recurrence)

H proper application of the prescribed scabicide.
H Trim patients fingernails short.
H Isolate the patient until treatment is completed.
H Practice meticulous hand washing.
H Sterilize blood pressure cuffs in a gas autoclave
before using on other patients.

H Decontaminate linens, towels, clothing, and personal
articles.
H Disinfect the patients room after discharge.
H If the patient is a child, notify his school of the infes-
tation.
H Observe wound and skin precautions for 24 hours
after treatment with a scabicide.
Monitoring
H Complications
H Neurologic status
ALERT
Prolonged use of scabicides may lead to excessive
central nervous system stimulation and seizures.
Patient teaching
Be sure to cover:
H identification of characteristic lesions
H modes of transmission
H mite resistance to scabicides
H assessment of close personal contacts for infestation
H successful treatment for infestation with good hygiene and scabicides
Scabies
731
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Scarlet fever
H Malaise
H Likely high temperature (100 to 103 F [37.8 to
Overview
H Characteristic rash 12 to 48 hours after onset of fever
39.4 C])
Description
H A hypersensitivity reaction that usually follows strep-
tococcal pharyngitis
H May follow other streptococcal infections, such as
wound infections, urosepsis, and puerperal sepsis
H Also known as scarlatina
Pathophysiology
H After infection, an erythrogenic toxin is produced,
resulting in a hypersensitivity reaction.

H Replication site is the tonsils and pharynx.
H Inflammatory reaction occurs.
Causes
H Group A beta-hemolytic streptococci transmitted by
direct contact with infected person or droplet

spread; indirectly by contact with contaminated articles or ingestion of contaminated food
Incidence
Physical findings
H Inflamed and heavily coated tongue, progressing to
strawberry-like tongue
H Tongue that peels and becomes beefy red, returning
to normal by the end of the second week

H Red and edematous uvula, tonsils, and posterior
oropharynx, with mucopurulent exudate

H Fine, erythematous rash, appears first on the upper
chest and back, spreading to the neck, abdomen,

legs, and arms
H Rash resembling sunburn with goose bumps; blanches with pressure
H Flushed face; circumoral pallor
H Tachycardia
Test results
Laboratory
H Pharyngeal culture is positive for group A betahemolytic streptococci.
H Complete blood count reveals increased white blood
cell count and eosinophilia during the second week.
H Most common in children ages 3 to 15; peak inci-
dence ages 4 to 8
H Infection rate increased in overcrowded situations
H Males and females affected equally
H Incubation period typically lasting 2 to 4 days, may
last 1 to 7 days
H High fever
H Pharyngitis
H Rash
Complications
H Severe disseminated toxic illness
H Septicemia
H Liver damage
H Otitis media
H Peritonsillar and retropharyngeal abscess
H Sinusitus
H Glomerulonephritis
H Meningitis
H Brain abscess
Assessment
History
H Possible contact with person with a sore throat
H Sore throat
H Headache
H Chills
H Anorexia
H Abdominal pain
732
Scarlet fever
Treatment
General
H Appropriate skin care
Medications
H Antibiotics, such as penicillin and erythromycin
H Antipyretics
Key outcomes
The patient will:
H have moist, pink mucous membranes without lesions
H chew and swallow without discomfort
H have no signs or symptoms of infection
H express feelings of increased comfort or absence of
pain at rest.
H Implement respiratory secretion precautions for
24 hours after starting antibiotic therapy.

H Offer frequent oral fluids and oral hygiene.
H Provide skin care to relieve discomfort from the
rash.
H Provide warm liquids or cold foods to ease sore
throat pain.
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H Use a cool mist humidifier to keep the air moist and
prevent the throat from getting too dry and more

sore.
Monitoring
H Complications
H Body temperature
H Rash
Patient teaching
Be sure to cover:
H the need to take oral antibiotics for the prescribed
length of time to prevent serious complications
H proper disposal of purulent discharge
H follow-up care
H prevention of scarlet fever and strep throat by washing hands and avoiding others with the disease.
Scarlet fever
733
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Schistosomiasis
Incidence
Overview
H Uncommon in the United States

H Most prevalent in children and adolescents
H Initially, a transient, pruritic rash at the site of cer-
Description
H A slowly progressive disease caused by blood flukes
of the class Trematoda

H Three major types: Schistosoma mansoni and S.
japonicum that infect intestinal tract; S. haematobium that infects urinary tract (see Types of schistosomes)
H Degree of infection determines intensity of illness
H Also known as bilharziasis
Pathophysiology
H Larvae penetrate the skin or mucous membranes and
eventually work their way to the livers venous portal

circulation. They mature in 1 to 3 months and migrate to other parts of the body.
H The female cercariae (the final larval stage) lay spiny
eggs in blood vessels surrounding the large intestine
or bladder.
H After penetrating the mucosa of these organs, the
eggs are excreted in feces or urine.
H If the eggs hatch in fresh water, the first-stage larvae
(miracidia) penetrate freshwater snails, which act as
passive intermediate hosts. Cercariae produced in
snails escape into water and begin a new life cycle.
cariae penetration, along with fever, myalgia, and

cough
H Later, hepatomegaly, splenomegaly, and lymphadenopathy
Complications
H Portal hypertension
H Heart failure
H Ascites
H Hematemesis from ruptured esophageal varices
H Renal failure
H Flaccid paralysis
H Seizures
H Skin abscesses
Assessment
History
H Recent travel to endemic areas
H Fever
H Myalgia
H Cough
Causes
Physical findings
H Contamination with Schistosoma larvae transmitted
H Rash at site of contamination

H Hepatomegaly
H Splenomegaly
H Lymphadenopathy
by bathing, swimming, wading, or working in water
Types of schistosomes
Species and
incidence
Signs and
symptoms
Schistosoma mansoni
Western hemisphere,
particularly Puerto Rico,
Lesser Antilles, Brazil,
and Venezuela; also Nile
delta, Sudan, and central
Africa
Irregular fever, malaise,

weakness, abdominal distress, weight loss, diarrhea,
ascites, hepatosplenomegaly,
portal hypertension, fistulas,
and intestinal stricture
Schistosoma japonicum
Affects males more than
females; particularly
prevalent among farmers
in Japan, China, and the
Philippines.
Irregular fever, malaise,

weakness, abdominal distress, weight loss, diarrhea,
ascites, hepatosplenomegaly,
portal hypertension, fistulas,
and intestinal stricture
Schistosoma
haematobium
Africa, Cyprus, Greece,
and India
Terminal hematuria, dysuria,

uretal colic; with secondary
infection colicky pain, intermittent flank pain, vague
GI complaints, and complete
renal failure
734
Schistosomiasis
Test results
Laboratory
H Ova appear in the urine or stool.
H White blood cell count shows eosinophilia.
H Mucosal lesion biopsy confirms infection.
Treatment
General
H Supportive
H Fluid replacement
H Diet as tolerated
Medications
H Praziquantel
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Key outcomes
The patient will:
H express an understanding of the disorder and
treatment.
Schistosomal dermatitis
Schistosomal dermatitis, also known as swimmers itch or
clam diggers itch, affects those who bathe in and camp
along freshwater lakes in the eastern and western United
States. Its caused by schistosomal cercariae that are harbored by migratory birds and penetrate the skin, causing
a pruritus papular rash. Initially mild, the reaction grows
more severe with repeated exposure. Treatment consists
of 5% copper sulfate solution as an antipruritic and 2%
methylene blue as an antibacterial agent.
H Encourage fluid intake.

H Provide support.
H Encourage activity.
Monitoring
H Vital signs
H Comfort level
Patient teaching
Be sure to cover:
H avoiding possibly contaminated water or, if the patient must enter the water, the need to wear protective clothing and dry off thoroughly after leaving the
water. (See Schistosomal dermatitis.)
Discharge planning
H Before discharge, tell the patient to schedule a
follow-up visit between 3 and 6 months after treatment. (If this checkup reveals any living eggs, treatment may be resumed.)
Schistosomiasis
735
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Schizophrenia
Overview
Special populations
The onset of schizophrenia usually occurs during
late adolescence.
Description
H Disturbances in thought content and form, percep-
H Change in emotional expression

H Inappropriate behavior
H Inaccurate interpretation of events
H Ineffective communication
tion, affect, language, social activity, sense of self, volition, interpersonal relationships, and psychomotor
behavior
H Five types recognized by the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition,
Text Revision (DSM-IV-TR): catatonic, paranoid,
disorganized, residual, and undifferentiated
H Insidious onset and poor outcome
H Can progress to social withdrawal, perceptual distortions, chronic delusions, and hallucinations
H Up to one-third of patients having only one psychotic
episode
H Some patients having no disability between periods of
exacerbation; others needing continuous institutional
care
H Worsening prognosis with each acute episode
Complications
H Suicide (about 10%)
H Impairment of health
H Impairment of social functioning
Assessment
History
H Possible long-standing psychiatric illness with repeat-
ed episodes
H Decreased social functioning
Pathophysiology
Physical findings
H A biochemical hypothesis holds that schizophrenia
H Decreased emotional expression

H Impaired concentration
results from excessive activity at dopaminergic

synapses.
H Other neurotransmitter alterations may also contribute to schizophrenic symptoms.
H Structural abnormalities of the intraventricular system, temporal lobe abnormalities, decreased volume
of the amygdala and hippocampus of the limbic system, structural changes in prefrontal white matter,
and increased volume of the basal ganglia have been
found.
Causes
H May result from a combination of genetic, biological,
cultural, environmental, and psychological factors
Risk factors
H Familial history
H Gestational and birth complications
H Prenatal nutritional deficiencies
H In utero exposure to viruses or malnutrition
H Stressful environment
DSM-IV-TR criteria
Diagnosis depends on identifying two or more of the
following signs and symptoms for a significant portion
of time during a 1-month period (or only one symptom
if delusions are bizarre, hallucinations consist of a
voice issuing a running commentary, or hallucinations
consist of two or more voices conversing with each
other):
H delusions
H prominent hallucinations
H disorganized speech
H grossly disorganized or catatonic behavior
H negative symptoms (flat affect or inability to make
decisions or speak).
In addition, one or more major areas of functioning
(work, relationships, and self-care) are markedly below previous level, and the disturbance isnt due to a
substance, medical condition, or schizoaffective or
mood disorder.
Incidence
Treatment
H Affects about 1% of the United States population

H Close relatives of patients up to 50 times more likely
General
to develop schizophrenia; the closer the degree of

biological relatedness, the higher the risk
H Higher incidence among lower socioeconomic
groups
H Psychotherapy
H Social skills training
H Family therapy
H Vocational counseling
736
Schizophrenia
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Medications
H Antipsychotic drugs (neuroleptic drugs), such as
chlorpromazine and haloperidol

H Antidepressants
H Anxiolytics
H Atypical antipsychotics, such as clozapine and
risperidone
Key outcomes
The patient will:
H identify internal and external factors that trigger
delusional episodes
H identify and perform activities that decrease delusions
H participate with his family in care and prescribed
therapies
H demonstrate effective social interaction skills.
H Evaluate the patients ability to carry out activities of
daily living.
H Maintain a safe environment, minimizing stimuli.
H Adopt an accepting and consistent approach.
H Avoid promoting dependence.
H Reward positive behavior.
H Provide reality-based explanations for distorted body
images or hypochondriacal complaints.

H Set limits on inappropriate behavior.
H Offer simple and matter-of-fact explanations about
environmental safeguards, drugs, and policies.

H Build trust; be honest and dependable. Dont threat-
en, and dont promise what you cant fulfill.
Monitoring
H Suicidal ideation
H Homicidal ideation
H Effects of drug regimen
H Weight
Patient teaching
Be sure to cover:
adverse effects
H how family members can recognize an impending
relapse, and ways to manage symptoms.
Discharge planning
H Refer the patient to appropriate community re-
sources and support services.
Schizophrenia
737
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Scleroderma
Overview
Description
H Connective tissue disease characterized by inflamma-
tory, degenerative, and fibrotic changes in skin,

blood vessels, synovial membranes, skeletal muscles,
and internal organs; thickening of tissues
H May affect the visceral organs or remain localized to
the skin when the connective tissues of many organs,
including the heart, kidney, GI tract, and lungs, are
involved
H Cutaneous lesions usually on the face, hands, neck,
and upper chest
H Also known as systemic sclerosis
Pathophysiology
H The skin atrophies, and infiltrates containing CD4+
T cells surround the blood vessels; inflamed collagen

fibers become edematous, losing strength and elasticity.
H The dermis becomes tightly bound to the underlying
structures, resulting in atrophy of the affected dermal
appendages and destruction of the distal phalanges
by osteoporosis.
H As the disease progresses, atrophy can affect other
areas.
Causes
H Unknown
H Possible causes:
Systemic exposure to silica dust, polyvinyl chloride, or organic solvents

Anticancer agents such as bleomycin or nonopioid
analgesics such as pentazocine
Fibrosis due to an abnormal immune system response
Underlying vascular cause with tissue changes initiated by inconsistent perfusion
Asymptomatic or common viral infections
Incidence
H Rarely occurs in children or males younger than
age 35
H Affects females three to four times more commonly
than males, especially between ages 30 and 50

H Peak incidence from ages 50 to 60
H Skin thickening in face and fingers
Complications
H Related to thickening of tissues:
Slowly healing ulcerations on fingertips or toes

leading to gangrene
Decreased food intake and weight loss due to GI
symptoms
Arrhythmias and dyspnea
738
Scleroderma
Malignant hypertension
Respiratory failure
Renal failure
Esophageal or intestinal obstruction or perforation
H Raynauds phenomenon
Assessment
History
H Pain, stiffness, and swelling of fingers and joints (lat-
er symptoms)
H Frequent reflux, heartburn, dysphagia, and bloating
after meals due to GI dysfunction

H Diarrhea, constipation, and malodorous floating
stool
Physical findings
H Skin thickening, commonly limited to the distal ex-
tremities and face, but possibly involving internal organs

H CREST syndrome (a benign subtype of limited systemic sclerosis): calcinosis, Raynauds phenomenon,
esophageal dysfunction, sclerodactyly, and telangiectasia
H Patchy skin changes with a teardrop-like appearance
known as morphea (localized scleroderma)
H Band of thickened skin on the face or extremities
that severely damages underlying tissues, causing atrophy and deformity (linear scleroderma)
H Raynauds phenomenon (blanching, cyanosis, and
erythema of the fingers and toes); progressive phalangeal resorption that may shorten the fingers (early
symptoms)
H Taut, shiny skin over the entire hand and forearm
due to skin thickening
H Tight and inelastic facial skin, causing a masklike appearance and pinching of the mouth
H Thickened skin over proximal limbs and trunk (diffuse systemic sclerosis)
Test results
Laboratory
H Erythrocyte sedimentation rate is slightly elevated,
rheumatoid factor is positive in 25% to 35% of patients, and antinuclear antibody is positive.
H Urinalysis shows proteinuria, microscopic hematuria, and casts.
Imaging
H Hand X-rays show terminal phalangeal tuft resorption, subcutaneous calcification, and joint space narrowing and erosion.
H Chest X-rays show bilateral basilar pulmonary fibrosis.
H GI X-rays show distal esophageal hypomotility and
stricture, duodenal loop dilation, small-bowel malabsorption pattern, and large diverticula.
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H Pulmonary function studies show decreased diffusion
and vital capacity.
H Electrocardiography shows nonspecific abnormalities related to myocardial fibrosis and possible
arrhythmias.
H Skin biopsy shows changes consistent with disease
progression, such as marked thickening of the dermis and occlusive vessel changes.
Treatment
General
H Physical therapy
H Heat therapy
H Hemodialysis
H Lanolin emollients
H Soft, bland foods
H Possible enteral feedings
H Regular exercise, as tolerated
Medications
H Vasodilators
H Antihypertensives
H Antacids
H Histamine-2 receptor antagonist or proton pump in-
hibitor
H Broad-spectrum antibiotics
H Angiotensin-converting enzyme inhibitor
Surgery
H Digital sympathectomy or, rarely, cervical sympathet-
ic blockade
H Digital plaster cast
H Possible surgical debridement
H Kidney transplant
H Administer oxygen, as ordered, for pulmonary com-
plications.
Monitoring
H Intake and output
H Possible adverse reactions to prescribed drugs
H Daily weight
H End organ damage such as renal failure
H Skin integrity
H Renal function
H Electrocardiograms
H Pulmonary function
Patient teaching
Be sure to cover:
H how to assess skin for changes
H avoiding cold weather and cigarette smoking
H reporting abnormal bleeding or bruising and any
nonhealing abrasions
H the importance of staying as active as possible, with
frequent rest periods
H follow-up care
Discharge planning
H Refer the patient to physical therapy and occupation-
al therapy as needed.
needed.
H Refer the patient to the Scleroderma Foundation.
Key outcomes
The patient will:
pain
the confines of disease
H state feelings about limitations
H express an increased sense of well-being
H regain and maintain skin integrity.
H Avoid using fingersticks for blood tests.
H Provide heat therapy to relieve joint stiffness.
H Elevate the head of the bed to help relieve GI symp-
toms.
H Provide a soft, bland diet with frequent small meals.
Scleroderma
739
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Scoliosis
Overview
Description
H Fatigue
H Backache
H Dyspnea
H Change in appearance
H Kyphosis
H Lateral curvature of the spine thats apparent on
Complications
frontal projection, measures greater than 10 degrees,

and is associated with vertebral rotation
H Right thoracic curve most common
H Classified as nonstructural (flexible spinal curve,
with temporary straightening when patient leans sideways) or structural (fixed deformity)
H Debilitating back pain

H Severe deformity
H With thoracic curve exceeding 60 degrees, possible
Pathophysiology
H The vertebrae rotate, forming the convex part of the
curve.
reduced pulmonary function

H With thoracic curve exceeding 80 degrees, increased
risk of cor pulmonale in middle age
Assessment
H The rotation causes rib prominence along the tho-
History
racic spine and waistline asymmetry in the lumbar

spine.
H Severity of spinal deformity dictates physiological
impairment.
H Familial history
H Detected during community or school scoliosis
Causes
H Nonstructural scoliosis:
Leg-length discrepancies
Poor posture
Paraspinal inflammation
Acute disk disease
H Structural scoliosis: no known cause
H Neuromuscular scoliosis: may be caused by muscular dystrophy, polio, cerebral palsy, or spinal muscular atrophy
H Neurofibromatosis (Recklinghausens disease)
H Traumatic scoliosis: may result from vertebral fractures or disk disease
H Local inflammation and infection
Special populations
Degenerative scoliosis may develop in older patients with osteoporosis and degenerative joint
disease of the spine.
Risk factors
H Congenital or neuromuscular problem
Incidence
H Idiopathic
H Less than 1% of school-age children affected
H Seen at growth spurts between ages 10 and 13
H Affects females seven times more than males
H Infantile scoliosis: most common in boys ages 1 to 3
H Juvenile scoliosis: affects boys and girls ages 3 to 10
about equally
H Adolescent scoliosis: occurs after age 10 and during
adolescence
740
Scoliosis
screening
H Hemlines look uneven
H Pant legs appear unequal in length
H One hip higher than the other
H Backache, fatigue, and dyspnea
Physical findings
H Signs of scoliosis (see Testing for scoliosis)
Test results
Imaging
H Spinal X-ray studies confirm scoliosis and determine
the degree of curvature and flexibility of the spine;
they also determine skeletal maturity, predict remaining bone growth, and differentiate nonstructural
from structural scoliosis.
Other
H Bone growth studies may help determine skeletal
maturity.
Treatment
General
H Close observation
H Brace
H Spinal orthoses
H Functional strengthening program
H Gradually increased activity
H No vigorous sports
H Prescribed exercise regimen
H Swimming, but no diving
Surgery
H Posterior spinal fusion and internal stabilization
(rods and spinal hardware)
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Page 741
Testing for scoliosis

When assessing the patient for an abnormal spinal curve,
use this screening test for scoliosis. Have the patient remove
her shirt and stand as straight as she can with her back to
you. Instruct her to distribute her weight evenly on each
foot. While the patient does this, observe both sides of her
back from neck to buttocks. Look for these signs:
H uneven shoulder height and shoulder blade prominence
H unequal distance between the arms and the body
H asymmetrical waistline
H uneven hip height
H a sideways lean.
With the patients back still facing you, ask the patient to do
the forward-bend test. In this test, the patient places her
palms together and slowly bends forward, remembering to
keep her head down. As she complies, check for these signs:
H asymmetrical thoracic spine or prominent rib cage (rib
hump) on either side
H asymmetrical waistline.
Key outcomes
The patient will:
H experience feelings of increased comfort and decreased pain
H achieve the highest level of mobility possible
H demonstrate measures to prevent injury to self.
Rib hump
Asymmetrical
thoracic spine
Asymmetrical
waistline
Patient teaching
Be sure to cover:
H brace care
H skin care
H safe body mechanics
H cast care, if needed
H signs of cast syndrome
H relaxation techniques.
H Promote self-care while allowing adequate time.

H Encourage deep-breathing exercises.
H Promote active ROM arm exercises.
Monitoring
H Skin around the cast edge daily
H Sensation, movement, color, and pulses
H Intake and output
H Abdominal distention and bowel sounds
H Skin breakdown
ALERT
Watch for signs of cast syndrome (nausea, abdominal pressure, and vague abdominal pain), which
may result from hyperextension of the spine.
Scoliosis
741
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Septic arthritis
Overview
Description
H Inflammation of a synovial membrane
H Usually caused by bacteria
H Usually affects a single joint
H May have sudden onset
H Also known as infectious arthritis
Complications
H Osteomyelitis
H Loss of joint cartilage
H Ankylosis
H Fatal septicemia
Assessment
History
H Abrupt onset of intense pain in the affected joint
H Fever and chills
Pathophysiology
Physical findings
H Bacteria invade a joint, and inflammation of the syn-
H Affected joint kept in a flexed position

H Redness and edema over the affected joint
H Severely reduced range of motion (ROM)
H Warmth and extreme tenderness over the involved
ovial lining results.

H Organisms invade the joint cavity, and effusion and
pyogenesis follow.
H Eventual bone and cartilage destruction result.
Causes
H Bacteria spread from a primary site of infection
H Gram-positive cocci
H Streptococcus pyogenes
H Streptococcus pneumoniae
H Streptococcus viridans
H Gram-negative cocci
H Neisseria gonorrhoeae
H Haemophilus influenzae
H Gram-negative bacilli
H Escherichia coli
H Salmonella
H Pseudomonas
H Fungi or mycobacteria (rare cause)
Risk factors
H Concurrent bacterial infection
H Serious chronic illness
H Alcoholism
H Advanced age
H Immune system depression
H History of immunosuppressive therapy
H I.V. drug abuse
H Recent articular trauma
H Arthroscopy and joint surgery
H Intra-articular injections
H Local joint abnormalities
Incidence
joint
H Chills
Test results
Laboratory
H Synovial fluid analysis shows pus or watery, cloudy
fluid of decreased viscosity, typically with 50,000/l
or more white blood cells (WBCs) containing primarily neutrophils; also a low glucose level.
H Gram stain or culture of the fluid identifies the
causative organism.
H Countercurrent immunoelectrophoresis measures
bacterial antigens in body fluids and guides treatment.
H Positive blood cultures confirm the diagnosis even
with negative synovial culture.
H WBC count is elevated with many polymorphonuclear
cells.
H C-reactive protein level is elevated.
H Lactic assay distinguishes septic from nonseptic
arthritis.
Imaging
H X-rays may show distention of the joint capsule, narrowing of the joint space, and erosion of bone.
H Radioisotope joint scan may show infection or inflammation, especially in less accessible joints.
H Arthrocentesis allows collection of a synovial fluid
specimen for analysis.
H Biopsy of the synovial membrane confirms the diagnosis and identifies the causative organism.
H Gram-positive cocci more common in children age 2
and older and adults

H H. influenzae most common in children younger
than age 2
H Joint inflammation
H Severe pain
H Pseudoparalysis of affected area
H Warmth and erythema of affected area
742
Septic arthritis
Treatment
General
H Based on antimicrobial susceptibilities and the pa-
tients age
H Drainage by repeated closed-needle aspiration,
arthroscopy, or arthrotomy
H Exercise, as tolerated
H Joint immobilization
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Medications
H Analgesics
H Appropriate parenteral antibiotic for 3 to 4 weeks
Surgery
H Reconstructive surgery for severe joint damage
H Possible open surgical drainage
Key outcomes
The patient will:
pain
the disorder.
H Practice strict sterile technique.
H Check splints or traction regularly.
H Maintain proper alignment.
H Assist with ROM exercises.
H Allow adequate time for and promote self-care.
Monitoring
H Signs and symptoms of joint inflammation
H Vital signs and fever pattern
H Pain levels
H Response to pain medications
H Condition after joint aspiration
Patient teaching
Be sure to cover:
H the etiology of the disease
H the role of I.V. drug use
H the prevention of recurrence
H the exercise regimen
H rest periods
H home I.V. therapy, if required
H avoiding aggravating factors.
Discharge planning
H Refer the patient to drug counseling, if appropriate.
H Refer the patient to Alcoholics Anonymous, if appro-
priate.
Septic arthritis
743
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Severe acute respiratory

syndrome
Overview
Description
Complications
H Severe thrombocytopenia (low platelet count)
H Death
Assessment
History
H Contact with a person known to have SARS
H Travel to an endemic area
H Severe viral infection that may progress to pneu-
Physical findings
monia
H Believed to be less infectious than influenza
H Incubation period estimated to range from 2 to
7 days (average, 3 to 5 days)
H Not highly contagious when protective measures are
used
H Also known as SARS
H Rash
H High fever
H Diarrhea
H Respiratory distress in later stages
Pathophysiology
H Coronaviruses cause diseases in pigs, birds, and oth-
er animals.
H A theory suggests that a coronavirus may have mutat-
ed, allowing transmission to and infection of humans.
Causes
H A new type of coronavirus known as SARS-
associated coronavirus (SARS-CoV)
Risk factors
H Close contact with an infected person
H Contact with aerosolized (exhaled) droplets and
bodily secretions from an infected person

H Travel to endemic areas
Incidence
H More common in adults than children
H Outbreaks in China, Hong Kong, Toronto, Singapore,
Taiwan, and Vietnam, with many other countries reporting smaller numbers of cases
H Affects all races
H Fever greater than 100.4 F (38 C)
H Dry cough
H Shortness of breath or other respiratory difficulties
H Headache
H Muscle stiffness
H Loss of appetite
H Malaise
H Confusion
H Rash
H Diarrhea
H Sore throat
744
Severe acute respiratory syndrome
Test results
Laboratory
H SARS-specific polymerase chain reaction test detects
SARS-CoV ribonucleic acid.
H Antibodies to coronavirus are detected by enzymelinked immunosorbent assay.
H Sputum Grams stain and culture isolates coronavirus.
H Platelet count may be low.
Imaging
H Changes in chest X-rays indicate pneumonia (infiltrates).
Treatment
General
H Symptomatic treatment
H Isolation for hospitalized patients
H Strict respiratory and mucosal barrier precautions
H Quarantine of exposed people to prevent spread
H Diet as tolerated
H Global surveillance and reporting of suspected cases
to national health authorities
Medications
The following medications may be beneficial:
H Lopinavir-ritanavir with ribavirin
H Combination of steroids and antimicrobials
H Antipyretics
Key outcomes
The patient will:
H remain in isolation as recommended
H practice good hygiene to prevent further transmission
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Page 745
H maintain good nutritional status

H maintain a patent airway.
H Encourage adequate nutritional intake.
H Observe, record, and report nature of rash.
H Maintain proper isolation technique.
H Collect laboratory specimens, as needed.
Monitoring
H Vital signs
H Complications
Patient teaching
Prevention
Preventing transmission of SARS

Severe acute respiratory syndrome (SARS) transmission
may be prevented by following these guidelines:
H Wash hands frequently.
H Cover mouth and nose when coughing or sneezing.
H Avoid close personal contact with friends and family.
H Avoid going to work, school, or other public places until 10 days after fever and respiratory symptoms resolve.
H Wear a surgical mask when around other people or, if
the patient cant wear one, a mask should be worn by
those in contact with the patient.
H Avoid sharing silverware, towels, or bedding until they
have been washed in soap and hot water.
H Use disposable gloves and household disinfectant to
clean any surface that might have been exposed to the
patients body fluids.
Be sure to cover:
H prevention of transmission (see Preventing transmission of SARS)
H good nutrition, hydration, and rest during recovery
Discharge planning
H Refer the patient for follow-up, as needed.
Severe acute respiratory syndrome
745
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Severe combined
immunodeficiency
disease
Assessment
History
H Extreme susceptibility to infection within the first few
months after birth, but probably no sign of gramnegative infection until about age 6 months because
of protection by maternal immunoglobulin G
Physical findings
Overview
Description
H Disorder that involves deficient or absent cell-
mediated (T-cell) and humoral (B-cell) immunity

H Predisposes patient to infection from all classes of
microorganisms during infancy

H Also known as SCID
Pathophysiology
H Three types of SCID have been identified:
Reticular dysgenesis, the most severe type, in

which the hematopoietic stem cell fails to differentiate into lymphocytes and granulocytes
Swiss-type agammaglobulinemia, in which the
hematopoietic stem cell fails to differentiate into
lymphocytes alone
Enzyme deficiency, such as adenosine deaminase
deficiency, in which the buildup of toxic products
in the lymphoid tissue causes damage and subsequent dysfunction.
H Emaciated appearance and failure to thrive

H Assessment findings dependant on the type and site
of infection
H Signs of chronic otitis media and sepsis
H Signs of the usual childhood diseases such as chick-
enpox
Test results
H Defective humoral immunity is difficult to detect
before an infant reaches age 5 months.

Laboratory
H Tests show a severely diminished or absent T-cell
number and function.
Imaging
H A chest X-ray characteristically shows bilateral pulmonary infiltrates.
H Lymph node biopsy that shows an absence of lymphocytes can be used to confirm diagnosis.
Treatment
Causes
General
H Transmitted as autosomal recessive trait but may be
H Strict protective isolation (germ-free environment)

H Gene therapy (experimental)
X-linked
H Possible enzyme deficiency
H Failure of thymus or bursa equivalent to develop normally or possible defect in thymus and bone marrow
(responsible for T- and B-cell development)
Medications
H Immunoglobulin
H Antibiotic therapy as appropriate
Incidence
Surgery

H Occurs in 1 of every 100,000 to 500,000 births
H Histocompatible bone marrow transplantation

H Fetal thymus and liver transplantation
H Frequent infections in the first few months after birth
Complications
Key outcomes
H Without treatment, infection within 1 year of birth
The patient will:

H demonstrate age-appropriate skills and behaviors
H not experience chills, fever, and other signs of illness.
The parents will:
H establish eye, physical, and verbal contact with the
infant or child
H develop adequate coping mechanisms and support
systems.
causes death
H Pneumonia
H Oral ulcers
H Failure to thrive
H Dermatitis
746
Severe combined immunodeficiency disease
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H If infection develops, provide prompt and aggressive
drug therapy and supportive care, as ordered.

H Watch for adverse effects of any drugs given.
H Avoid vaccinations, and give only irradiated blood
products if a transfusion is ordered.
Special populations
Although SCID infants must remain in strict protective isolation, try to provide a stimulating atmosphere to promote growth and development.
H Encourage parents to visit their child often, to hold
him, and to bring him toys that can be easily sterilized.

H Maintain a normal day and night routine, and talk to
the child as much as possible.
H If parents cant visit, call them often to report on the
childs condition.
H Provide emotional support for the family.
Monitoring
H Skin integrity
H Complications
H Signs and symptoms of transplant rejection
Patient teaching
Be sure to cover:
H the proper technique for strict protective isolation
H the signs and symptoms of infection and the need to
notify a physician promptly
Discharge planning
H Encourage the parents to seek genetic counseling.
Severe combined immunodeficiency disease
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Shigellosis
Overview
Description
H An acute intestinal infection caused by the bacteria
Shigella, a short, nonmotile, gram-negative rod

H Can be classified into four groups:
Assessment
History
H Close contact with someone who has acute diarrhea
H Fever
H Diarrhea
H Tenesmus
Group A caused by S. dysenteriae: most common

in Central America; causes particularly severe infection and septicemia
Group B caused by S. flexneri together with Group
D: responsible for 90% of shigellosis cases
Group C caused by S. boydii: occurs internationally
Group D caused by S. sonnei
H Also known as bacillary dysentery
Physical findings
Pathophysiology
Laboratory
H Microscopic examination of stools reveals mucus,
red blood cells, and polymorphonuclear leukocytes.
H Direct immunofluorescence with specific antisera
may reveal Shigella.
H Sigmoidoscopy or proctoscopy may reveal typical superficial ulcerations.
H Highly contagious aerobic, nonmotile, glucose-
fermenting, gram-negative rods cause diarrhea after

ingestion of as few as 180 organisms.
H Rods invade the colonic epithelium and produce enterotoxin, which enhances virulence.
Causes
H Pus in stools
Test results
H Transmission of Shigella bacteria through the fecal-
oral route, by direct contact with contaminated objects, or through ingestion of contaminated food or
water
H Occasional transmission by housefly vector
Incidence
H Most common in children ages 1 to 4; many adults
acquire illness from children

H Endemic in North America, Europe, and the tropics;
in the United States, about 23,000 cases annually,

usually in children or elderly, debilitated, or malnourished people
H Commonly occurs among confined populations such
as those in mental institutions; also common in hospitals
H High fever (especially in children)
H Acute self-limiting diarrhea with tenesmus (ineffectu-
al straining at stool)
H Electrolyte imbalance and dehydration
Complications
H Electrolyte imbalance (especially hypokalemia)
H Shock
748
Shigellosis
Treatment
General
H Enteric precautions
H Low-residue diet
H Replacement of fluids and electrolytes with I.V. infu-
sions of normal saline solution (with electrolytes)
Medications
H Antibiotics (questionable value, but may be used)
ALERT
Antidiarrheals that slow intestinal motility are
contraindicated in shigellosis because they delay
fecal excretion of Shigella and prolong fever and
diarrhea.
ALERT
A vaccine to help prevent shigellosis is currently
under development.
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Key outcomes
The patient will:
H regain and maintain normal fluid and electrolyte
balance
H Maintain enteric precautions until microscopic bac-
teriologic studies confirm that the stool specimen is

negative.
Monitoring
H Vital signs
H Comfort level
H Intake and output
Patient teaching
Be sure to cover:
H prevention of infecting others, through proper hand
washing after using the toilet and before preparing
food.
Shigellosis
749
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Page 750
Assessment
Shock, cardiogenic
History
Overview
H Anginal pain
H Disorder, such as MI or cardiomyopathy, that severe-
ly decreases left ventricular function
Description
H A condition of diminished cardiac output that severe-
ly impairs tissue perfusion

H The most lethal form of shock
H Sometimes called pump failure
Pathophysiology
H Left ventricular dysfunction initiates a series of com-
pensatory mechanisms that attempt to increase cardiac output.

H As cardiac output decreases, aortic and carotid
baroreceptors activate sympathetic nervous responses.
H Responses increase heart rate, left ventricular filling
pressure, and peripheral resistance to flow to enhance venous return to the heart.
H This action initially stabilizes the patient but later
causes deterioration with increasing oxygen demands
on the already compromised myocardium.
H These events consist of a cycle of low cardiac output,
sympathetic compensation, myocardial ischemia, and
even lower cardiac output.
Causes
H Myocardial infarction (MI) (most common)
H Papillary muscle dysfunction
H End-stage cardiomyopathy
H Myocarditis
H Acute mitral or aortic insufficiency
H Ventricular septal defect
H Ventricular aneurysm
Incidence
H Typically affects patients in whom area of MI involves
40% or more of left ventricular muscle mass (a

group in which mortality may exceed 85%)
H Previous disorder that decreases left ventricular
function
Complications
H Multiple organ dysfunction
H Death
Physical findings
H Urine output less than 20 ml/hour
H Pale, cold, clammy skin
H Decreased sensorium
H Mean arterial pressure of less than 60 mm Hg in
adults
H Gallop rhythm, faint heart sounds and, possibly, a
holosystolic murmur
H Severe anxiety
H Decreased level of consciousness (LOC)
Test results
Laboratory
H Serum enzyme measurements show elevated levels of
creatine kinase, lactate dehydrogenase, aspartate
aminotransferase, and alanine aminotransferase.
H Troponin levels are elevated.
Imaging
H Cardiac catheterization and echocardiography may
reveal other conditions that can lead to pump dysfunction and failure, such as cardiac tamponade,
papillary muscle infarct or rupture, ventricular septal
rupture, pulmonary emboli, venous pooling, and hypovolemia.
H Pulmonary artery pressure monitoring reveals increased pulmonary artery pressure and pulmonary
artery wedge pressure, reflecting an increase in left
ventricular end-diastolic pressure (preload) and
heightened resistance to left ventricular emptying (afterload) caused by ineffective pumping and increased peripheral vascular resistance.
H Invasive arterial pressure monitoring shows systolic
arterial pressure less than 80 mm Hg caused by impaired ventricular ejection.
H Arterial blood gas (ABG) analysis may show metabolic and respiratory acidosis and hypoxia.
H Electrocardiography demonstrates possible evidence
of acute MI, ischemia, or ventricular aneurysm.
Treatment
General
H Intra-aortic balloon pump (IABP)
H Possible parenteral nutrition or tube feedings
H Bed rest
750
Shock, cardiogenic
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Page 751
Medications
H Vasopressors such as dopamine
H Inotropics such as milrinone
H Vasoconstrictors
H Analgesics; sedatives
H Osmotic diuretics
H Vasodilators such as nitroglycerin to treat cause
H Oxygen
Surgery
H Possible ventricular assist device
H Possible heart transplant
H Possible catheter-based procedure such as angio-
plasty to treat coronary artery occlusion
H Cardiac status
H Hemodynamics
H Intake and output
H LOC
Patient teaching
Be sure to cover:
H explanations and reassurance for patient and his
family
H the possibly fatal outcome.
Key outcomes
The patient will:
stability
H develop no complications of fluid volume excess
H express feelings and develop adequate coping mechanisms.
H Administer oxygen therapy.
H Follow IABP protocols and policies.
ALERT
When a patient is on an IABP, move him as little as
possible. Never place the patient in a sitting position higher than 45 degrees (including for chest
X-rays) because the balloon may tear through the
aorta and cause immediate death. Assess pedal
pulses and skin temperature and color. Check the
dressing on the insertion site frequently for bleeding, and change it according to facility protocol.
Also check the site for hematoma or signs of infection, and culture any drainage.
H Monitor the patient for cardiac arrhythmias.
H Plan your care to allow frequent rest periods, and
provide as much privacy as possible. Allow the patients family to visit and comfort him as much as
possible.
H Provide explanations and reassurance for the patient
and his family as appropriate.
H Prepare the patient and his family for a possibly fatal
outcome, and help them find effective coping strategies.
Monitoring
H ABG levels (acid-base balance) and pulse oximetry
H Complete blood count and electrolyte levels
H Vital signs and peripheral pulses
Shock, cardiogenic
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Shock, hypovolemic
Overview
Description
H Reduced intravascular blood volume causing circula-
tory dysfunction and inadequate tissue perfusion resulting from loss of blood, plasma, or fluids
H Potentially life-threatening
Pathophysiology
Incidence
H Depends on cause
H Affects all ages
H More frequent and less tolerated in elderly patients
H Pallor, tachycardia, hypotension
H Cool skin
Complications
H Acute tubular necrosis and renal failure
H Multiple organ dysfunction
H When fluid is lost from the intravascular space,
venous return to the heart is reduced.

H This decreases ventricular filling, which leads to a
drop in stroke volume.

H Cardiac output falls, causing reduced perfusion to
tissues and organs.
H Tissue anoxia prompts a shift in cellular metabolism
from aerobic to anaerobic pathways.
H This produces an accumulation of lactic acid, resulting in metabolic acidosis.
Causes
Assessment
History
H Disorders or conditions that reduce blood volume,
such as GI hemorrhage, trauma, and severe diarrhea

and vomiting
H Patient with cardiac disease: possible anginal pain
due to decreased myocardial perfusion and oxygenation
H Acute blood loss (about one-fifth of total volume)

H Burns
H Peritonitis
H Acute pancreatitis
H Ascites
H Dehydration, as from excessive perspiration, severe
Physical findings
diarrhea, protracted vomiting, diabetes insipidus, diuresis, or inadequate fluid intake

H Diuretic abuse
(in chronic hypotension, mean pressure may fall below 50 mm Hg before signs of shock)
H Orthostatic vital signs and tilt test results consistent
with hypovolemic shock (see Checking for early hypovolemic shock)
H Pale, cool, clammy skin

H Decreased sensorium
H Urine output usually less than 20 ml/hour
H Mean arterial pressure less than 60 mm Hg in adults
Test results
Checking for early hypovolemic shock
Orthostatic vital signs and tilt test results can help in assessing for the possibility of impending hypovolemic
shock.
Orthostatic vital signs

Measure the patients blood pressure and pulse rate while
hes lying in a supine position, sitting, and standing. Wait
at least 1 minute between each position change. A systolic
blood pressure decrease of 10 mm Hg or more between
positions or a pulse rate increase of 10 beats/minute or
more is a sign of volume depletion and impending hypovolemic shock.
Tilt test
With the patient lying in a supine position, raise his legs
above heart level. If his blood pressure increases significantly, the test is positive, indicating volume depletion and
impending hypovolemic shock.
752
Shock, hypovolemic
Laboratory
H Hematocrit is low, and hemoglobin levels and red
blood cell and platelet counts are decreased.
H Serum potassium, sodium, lactate dehydrogenase,
creatinine, and blood urea nitrogen levels are elevated.
H Urine specific gravity (greater than 1.020) and urine
osmolality are increased.
H The pH and partial pressure of arterial oxygen are
decreased, and partial pressure of arterial carbon
dioxide is increased.
H Aspiration of gastric contents through a nasogastric
tube identifies internal bleeding.
H Occult blood tests are positive.
H Coagulation studies show coagulopathy due to disseminated intravascular coagulation.
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Imaging
H X-rays (chest or abdominal) help to identify internal
bleeding sites.
H Gastroscopy helps identify internal bleeding sites.
H Invasive hemodynamic monitoring shows reduced
central venous pressure, right atrial pressure, pulmonary artery pressure, pulmonary artery wedge
pressure, and cardiac output.
H Coagulation studies for signs of impending coagu-
Treatment
Be sure to cover:
H all procedures and their purpose
H the risks associated with blood transfusions
H the purpose of all equipment such as mechanical
ventilation
General
H In severe cases, an intra-aortic balloon pump, ven-
tricular assist device, or pneumatic antishock garment

H Bleeding control by direct application of pressure
and related measures
H Bed rest
H Fluid replacement
H Blood infusion
lopathy
H Complete blood count and electrolyte measurements
H Intake and output
H Hemodynamics
Patient teaching
Medications
H Positive inotropes
H Possibly diuretics
Surgery
H Possibly, to correct underlying problem
Key outcomes
The patient will:
H express feelings and develop adequate coping mechanisms
H regain adequate fluid volume.
H Check for a patent airway and adequate circulation.
If blood pressure and heart rate are absent, start cardiopulmonary resuscitation.
H Obtain type and crossmatch, as ordered.
H Administer prescribed I.V. solutions or blood
products.
Monitoring
H Cardiac rhythm
Shock, hypovolemic
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Assessment
Shock, septic
History
Overview
H Previous invasive tests or treatments, surgery, or
H Disorder or treatment that can cause immunosup-
pression
Description
H Low systemic vascular resistance and an elevated car-
diac output (initially)

H Probably a response to infections that release mi-
crobes or an immune mediator
Pathophysiology
H Initially, the bodys defenses activate chemical media-
tors in response to the invading organisms.

H The release of these mediators results in low sys-
temic vascular resistance and increased cardiac

output.
H Blood flow is unevenly distributed in the microcirculation, and plasma leaking from capillaries causes
functional hypovolemia.
H Diffuse increase in capillary permeability occurs.
H Eventually, cardiac output decreases, and poor tissue
perfusion and hypotension cause multisystem dysfunction syndrome and death.
Causes
H Any pathogenic organism
H Gram-negative bacteria, such as Escherichia coli,
Klebsiella pneumoniae, Serratia, Enterobacter, and

Pseudomonas, most common causes (up to 70% of
cases)
Incidence
H Possible in any person with impaired immunity
Special populations
Neonates and elderly people are at greatest risk for
septic shock.
H About two-thirds of cases in hospitalized patients
(most have underlying diseases)
H Hyperdynamic or warm phase
H Hypodynamic or cold phase
Complications
H Renal failure
H Heart failure
H GI ulcers
H Abnormal liver function
H Death
754
Shock, septic
trauma
H Fever and chills (although 20% of patients possibly
hypothermic)
Physical findings
Hyperdynamic or warm phase
H Peripheral vasodilation
H Skin possibly pink and flushed or warm and dry
H Altered level of consciousness (LOC) reflected in agitation, anxiety, irritability, and shortened attention
span
H Respirations rapid and shallow
H Urine output below normal
H Rapid, full, bounding pulse
H Blood pressure normal or slightly elevated
Hypodynamic or cold phase
H Peripheral vasoconstriction and inadequate tissue
perfusion
H Pale skin and possible cyanosis
H Decreased LOC; possible obtundation and coma
H Respirations possibly rapid and shallow
H Urine output possibly less than 25 ml/hour or absent
H Rapid, weak, thready pulse
H Irregular pulse if arrhythmias present
H Cold, clammy skin
H Hypotension
H Crackles or rhonchi if pulmonary congestion present
Test results
Laboratory
H Blood cultures are positive for the causative organism.
H Complete blood count shows the presence or absence of anemia and leukopenia, severe or absent
neutropenia, and usually the presence of thrombocytopenia.
H Blood urea nitrogen and creatinine levels are increased, and creatinine clearance is decreased.
are abnormal.
H Serum lactate dehydrogenase levels are elevated, with
metabolic acidosis.
H Urine studies show increased specific gravity (more
than 1.02), increased osmolality, and decreased
sodium levels.
H Arterial blood gas (ABG) analysis demonstrates increased blood pH and partial pressure of arterial
oxygen and decreased partial pressure of arterial
carbon dioxide with respiratory alkalosis in early
stages.
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H Invasive hemodynamic monitoring shows:
increased cardiac output and decreased systemic
vascular resistance in warm phase
decreased cardiac output and increased systemic
vascular resistance in cold phase.

Treatment
H ABG levels and pulse oximetry

H Intake and output
H Hemodynamics
H Cardiac rhythm
H Heart and breath sounds
General
H Removal of I.V., intra-arterial, or urinary drainage
catheters as infection source whenever possible
family.
H Document the occurrence of a nosocomial infection,
and report it to the infection-control practitioner.
Monitoring
H In patients immunosuppressed from drug therapy,
drugs discontinued or reduced, if possible

H Mechanical ventilation if respiratory failure occurs
H Fluid volume replacement
H Bed rest
Medications
H Antimicrobial
H Granulocyte transfusions
H Colloid or crystalloid infusions
H Oxygen
H Diuretics
H Vasopressors
H Antipyretics
Patient teaching
Be sure to cover:
H all procedures and their purpose (to ease the patients anxiety)
H risks associated with blood transfusions
H all equipment and its purpose
H possible complications.
Key outcomes
The patient will:
H express feelings and develop adequate coping mechanisms
H Remove any I.V., intra-arterial, or urinary drainage
catheters, and send them to the laboratory to culture

for the presence of the causative organism.
H Administer prescribed I.V. fluids and blood products.
ALERT
A progressive drop in blood pressure accompanied
by a thready pulse generally signals inadequate
cardiac output from reduced intravascular volume.
Notify the physician immediately and increase the
infusion rate.
H Notify the physician if urine output is less than
30 ml/hour.
Shock, septic
755
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Silicosis
Overview
Description
Complications
H Cor pulmonale
H Cardiac or respiratory failure
H Pulmonary tuberculosis
H Lung infection
H Pneumothorax
H Progressive pneumonoconiosis disease characterized
by nodular lesions, commonly leading to fibrosis

H Classified according to severity of pulmonary disease
and rapidity of onset and progression

H Usually a simple, asymptomatic illness
H Considered an industrial disease
H Prognosis good unless complications occur
Pathophysiology
Assessment
History
H Long-term exposure to silica dust
H Dry cough, especially in the morning
H Small particles of mineral dust are inhaled and de-
Physical findings
posited in the respiratory bronchioles, alveolar

ducts, and alveoli.
H The surface of these particles generates silicon-based
radicals that lead to the production of hydroxy, hydrogen peroxide, and other oxygen radicals that
damage cell membranes and inactivate essential cell
proteins.
H Alveolar macrophages ingest the particles, become
activated, and release cytokines, such as tumor
necrosis factor and others that attract other inflammatory cells.
H The inflammation damages resident cells and the
extracellular matrix.
H Fibroblasts are stimulated to produce collagen,
resulting in fibrosis.
H Decreased chest expansion

H Tachypnea
H Lethargy
H Decreased mentation
H Areas of increased and decreased resonance
H Medium crackles, wheezing
Causes
Test results
H Silica dust due to:
Laboratory
H Arterial blood gas analysis shows:
normal partial pressure of oxygen in simple silicosis (may be significantly decreased in late stages
or complicated disease)
normal partial pressure of carbon dioxide in early
stages of the disease. (Hyperventilation may cause
it to decrease; partial pressure of carbon dioxide
may increase if restrictive lung disease develops.)
Imaging
H Chest X-rays in simple silicosis show small, discrete,
nodular lesions distributed throughout both lung
fields, although they typically concentrate in the upper lobes.
H Lung nodes may appear enlarged and show eggshell
calcification.
H Chest X-rays in complicated silicosis show one or
more conglomerate masses of dense tissue.
H Pulmonary function tests show:
reduced forced vital capacity (FVC) in complicated
silicosis
reduced forced expiratory volume in 1 second
(FEV1) with obstructive disease
reduced FEV1 with a normal or high ratio of FEV1
to FVC in complicated silicosis
manufacture of ceramics (flint) and building materials (sandstone)

mixed form in construction materials (cement)
powder form (silica flour), in paints, porcelain,
scouring soaps, and wood fillers
mining of gold, lead, zinc, and iron
Incidence
H Highest incidence in those who work around silica
dust, such as foundry workers, boiler scalers, and

stone cutters
H Acute silicosis possible after 1 to 3 years in sand
blasters, tunnel workers, and others exposed to high
concentrations of respirable silica
H Accelerated silicosis possible in those exposed to
lower concentrations of free silica, usually after
about 10 years of exposure
H More common in those ages 40 to 75
H Dry cough, especially in the morning
756
Silicosis
ALERT
Assess patient for the presence of an intensified
ventricular gallop on inspiration, which is a hallmark of cor pulmonale.
H Hemoptysis
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Page 757
reduced diffusing capacity for carbon monoxide

when fibrosis destroys alveolar walls and obliterates pulmonary capillaries or when it thickens the
alveocapillary membrane.
Treatment
H Changes in mentation
H Sputum production
H Breath sounds
Patient teaching
H Bronchodilators
H Oxygen
H Antibiotics
H Anti-inflammatory drugs
Be sure to cover:
H when to notify a physician
H the need to avoid crowds and people with known
infections
H home oxygen therapy, if needed
H transtracheal catheter care, if needed
H the need to consume a high-calorie, high-protein diet
H adequate hydration
H the risk of tuberculosis
H energy conservation techniques.
Surgery
Discharge planning
H Possible lung transplantation
H Whole lung lavage
H Refer the patient for influenza and pneumococcus
H Refer the patient for tuberculosis testing, if indicated.
General
H Relief of respiratory symptoms
H Management of hypoxia and cor pulmonale
H Prevention of respiratory tract infections
H Steam inhalation and chest physiotherapy
H Regular exercise program, as tolerated
Medications
immunizations, as needed.
indicated.
Key outcomes
The patient will:
H use energy conservation techniques
H Administer prescribed drugs and oxygen
H Provide a high-calorie, high-protein diet.
H Provide small, frequent meals.
H Ensure adequate hydration.
H Encourage daily exercise as tolerated.
H Provide diversional activities as appropriate.
H Help with adjustment to the lifestyle changes associ-
ated with a chronic illness.

H Include the patient and family in care decisions
whenever possible.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Complications
Silicosis
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Sinusitis
Overview
Description
H Inflammation of the paranasal sinuses
H Usually follows upper respiratory infections
H May be acute, subacute, chronic, allergic, or hyper-
plastic
H In hyperplastic sinusitis, a combination of purulent
acute sinusitis and allergic sinusitis or rhinitis

H For all types, prognosis good
Pathophysiology
H Impairment in drainage of sinuses and retention of
secretions result in inflammation.
Causes
H Bacterial infections (common)
H Viral infections
H Fungal infections (uncommon)
H Any condition that interferes with sinus drainage and
ventilation
H Swimming in contaminated conditions
H Immunocompromised states
H Diabetes
H Blood dyscrasias
H Allergic rhinitis
H Orofacial trauma
H Endotracheal intubation
Risk factors
H Anatomic abnormalities
H Viral upper respiratory infection
H Allergies
H Overuse of topical decongestants
H Asthma
Assessment
History
H Nasal congestion
H Nasal discharge, clear turning purulent
H Sore throat
H Localized headache
H Generalized malaise; fatigue
H Pain specific to the affected sinus (see Locating the
paranasal sinuses)
H Vague facial discomfort
Physical findings
H Edematous nasal mucosa
H Low-grade fever
H Edema over sinuses
H Enlarged turbinates
H Mucosal lining thickening
H Mucosal polyps (hyperplastic sinusitis)
H Pain and pressure over affected sinus areas with pal-
pation
Test results
Laboratory
H Culture and sensitivity testing of purulent nasal
drainage shows the causative bacterial organism.
Imaging
H Sinus X-rays show cloudiness in affected sinus, airfluid levels, or thickened mucosal lining.
H Ultrasonography and computed tomography scan
show recurrent or chronic sinusitis, unresolved sinusitis.
H Transillumination of sinuses may be diminished.
H Sinus endoscopy shows purulent nasal drainage,
nasal edema, and obstruction of ostia.
Incidence
Treatment
H Affects 16% of population annually

H Affects all ages
General
H Nasal congestion
H Purulent nasal discharge
H Facial pain specific to affected sinus
H Fever
Complications
H Meningitis
H Cavernous and sinus thrombosis
H Bacteremia or septicemia
H Brain abscess
H Osteomyelitis
H Mucocele
H Orbital cellulitis or abscess
758
Sinusitis
H Depends on type of sinusitis

H Indirect drainage of ethmoid and sphenoid sinuses
H Steam inhalation
H Local heat applications
H Adequate rest periods
Medications
H Antibiotics
H Analgesics
H Vasoconstrictors
H Nasal corticosteroids
H Antihistamines
Surgery
H Antral puncture to remove purulent material
H Sinus irrigation
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Page 759
Key outcomes
The patient will:
H exhibit an adequate breathing pattern
H develop no complications.
Locating the paranasal sinuses

The location of a patients sinusitis pain indicates the affected sinus. For example, an infected maxillary sinus can
cause tooth pain. (Note: The sphenoid sinus, which lies
under the eye and above the soft palate, isnt depicted
here.)
H Elevate the head of the bed no more than 30 degrees.
H Encourage expression of concerns.
H Encourage use of a humidifier.
Frontal
sinuses
Ethmoid
sinuses
Maxillary
sinuses
ALERT
Watch for and report vomiting, chills, fever, edema
of the forehead or eyelids, blurred or double vision,
and personality changes.
After surgery
H Apply ice compresses over the nose and iced saline
gauze over the eyes for 24 hours.
H Frequently change the mustache dressing or
drip pad.
H Provide meticulous and frequent mouth care.
H importance of medical follow-up

H avoidance of bending and stooping during the acute
Monitoring
Discharge planning
H Complications
H Pain control
H Nasal discharge
H Refer the patient to a smoking-cessation program.
phase
H avoidance of contact with an infected person.
After surgery
H Excessive drainage or bleeding
H Consistency, amount, and color of drainage
H Vital signs
Patient teaching
Be sure to cover:
H cautions against driving a motor vehicle or consuming alcohol while taking antihistamines or analgesics
H the need to complete the full course of prescribed
antibiotics
H the need to leave nasal packing in place for 12 to
24 hours after surgery
H the need to breathe through the mouth and refrain
from blowing the nose and sneezing
H the need to refrain from smoking for at least 2 or
3 days after surgery
H signs and symptoms of complications
Sinusitis
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Sjgrens syndrome
H Possible epistaxis, hoarseness, chronic nonproduc-
Description
tive cough, recurrent otitis media, and frequent respiratory tract infections
H Possible dyspareunia
H Generalized itching, fatigue, recurrent low-grade
fever, and arthralgia or myalgia
H Connective tissue disease: the most common autoim-
Physical findings
mune disorder after rheumatoid arthritis

H May be primary disorder or associated with other inflammatory connective tissue disorders
H Mouth ulcers, dental caries and, possibly, enlarged
Overview
Pathophysiology
H Lymphocytic infiltration of exocrine glands causes
tissue damage resulting in xerostomia and dry eyes.

H Immunologic activation occurs.
Causes
H Unknown
H Possible genetic and environmental factors
H Immunologic activation
Incidence
H Affects more females (about 90%) than males
H Mean age of occurrence: 50
H Dry eyes and mouth
Complications
H Corneal ulceration or perforation
H Epistaxis
H Deafness
H Otitis media
H Splenomegaly
H Renal tubular necrosis
Assessment
History
H Xerophthalmia or xerostomia
H Gritty, sandy eye along with redness, burning, photo-
sensitivity, eye fatigue, itching, and mucoid discharge

H Difficulty swallowing and talking; an abnormal taste
or smell sensation (or both); thirst; ulcers of the

tongue, mouth, and lips (especially at the corners of
the mouth); and severe dental caries
Diagnosing Sjgrens syndrome
salivary glands
H Palpable purpura
H Palpable lymph node enlargement
H Dry, sticky, erythematous oral mucosa
Test results
Laboratory
H Erythrocyte sedimentation rate is elevated in more
than 90% of patients.
H Complete blood count shows mild anemia and
leukopenia in about 30% of patients.
H Serum protein electrophoresis shows hypergammaglobulinemia in about 50% of patients.
H Typically, 75% to 90% of patients test positive for
rheumatoid factor, and between 50% and 80% of patients test positive for antinuclear antibodies.
H For a diagnosis of Sjgrens syndrome, symptoms
must meet specific criteria. (See Diagnosing Sjgrens syndrome.)
H Tests supporting the diagnosis include measuring eye
involvement with the Schirmers test and a slit-lamp
examination with rose bengal dye.
H Labial salivary gland biopsy (to detect lymphoid foci)
is the only specific diagnostic technique.
H Salivary gland involvement may be evaluated by measuring the volume of parotid saliva, by secretory
sialography, and by salivary scintigraphy.
H Salivary gland biopsy results typically show lymphocytic infiltration in Sjgrens syndrome; lower lip
biopsy findings show salivary gland infiltration by
lymphocytes.
Treatment
General
H Meticulous oral hygiene
H Humidifier
H Unscented skin lotions
H Frequent dental care
H Avoidance of sugar, tobacco, alcohol, and spicy, salty,
or highly acidic foods

For a diagnosis of Sjgrens syndrome, the patient must
have the following:
H keratoconjunctivitis sicca
H diminished salivary gland flow
H a positive salivary gland biopsy, showing mononuclear
cell infiltration
H the presence of autoantibodies in a serum sample, indicating a systemic autoimmune process.
760
Sjgrens syndrome
H Increased oral fluid intake for mouth dryness
Medications
H Pilocarpine and cevimeline
H Preservative-free artificial tears and sustained-release
cellulose capsules
H Artificial salivas
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H Glucocorticoids or other immunosuppressive agents
for extraglandular manifestations such as systemic

vasculitis
H Saline nasal sprays
H Vaginal lubricants
H Antifungal agents
H Ophthalmic lubricants
Key outcomes
The patient will:
H have pink, moist oral mucosa
H demonstrate thorough oral hygiene practices
H acknowledge problems in sexual function.
H Instill artificial tears as often as every 30 minutes to
prevent eye damage, and instill an eye ointment at

bedtime.
H Provide plenty of fluids, especially water, for the patient to drink, and sugarless chewing gum or candy.
Monitoring
H Extraglandular manifestations
H Complications
Patient teaching
Be sure to cover:
H the instillation of eye drops and ointments
H the need to wear sunglasses to protect the eyes
H the need to keep the face clean and to avoid rubbing
the eyes
H avoidance of saliva-decreasing drugs, such as atropine derivatives, antihistamines, anticholinergics,
and antidepressants
H meticulous oral hygiene and regular dental visits
H high-calorie, protein-rich liquid supplements to
prevent malnutrition if mouth lesions make eating
painful
H the need to consume a nutritious diet
H avoidance of sugar, tobacco, alcohol, and spicy, salty,
or highly acidic foods
H the need to humidify the home and work environments
H use of normal saline solution, in drop or spray form,
to relieve nasal dryness
H avoidance of prolonged hot showers and baths and
the use of moisturizing lotions on dry skin. (Suggest
use of a water-soluble gel such as a vaginal lubricant.)
Sjgrens syndrome
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Skull fracture
Overview
Description
H Break in the integrity of the skull bone
H May be simple (closed) or compound (open)
H May displace bone fragments
H May be linear (common hairline break, without dis-
placement of structures), comminuted (splintering

or crushing the bone into several fragments), or depressed (a fracture that pushes the bone toward the
brain)
ALERT
Because possible damage to the brain is the first
concern, rather than the fracture itself, a skull
fracture is considered a neurosurgical condition.
H Classified according to location, such as cranial vault
fracture and basilar fractures
ALERT
Because of the danger of grave cranial complications and meningitis, basilar fractures are usually
far more serious than vault fractures.
Pathophysiology
H Trauma to the head causes a fracture at certain
anatomic sites, such as:

parietal bone
squama of temporal bone
foramen magnum
petrous temporal ridge
inner parts of the sphenoid wings at the skull base
middle cranial fossa
cribriform plate
roof of orbits in the anterior cranial fossa
bony areas between the mastoid and dural sinuses
in the posterior cranial fossa.
Causes
H Head trauma
Incidence
deep tendon reflexes, and altered pupillary and motor response

In sphenoidal fracture
H Blindness
In temporal fracture
H Unilateral deafness or facial paralysis
In basilar fracture
H Hemorrhage from the nose, pharynx, or ears
H Blood under the periorbital skin (raccoon eyes) and
conjunctiva
H Battles sign (supramastoid ecchymosis)
H Cerebrospinal fluid (CSF) or brain tissue leakage
from the nose or ears
Complications
H Epilepsy
H Hydrocephalus
H Organic brain syndrome
H Headaches, giddiness, fatigability, neuroses, and be-
havior disorders
Assessment
History
H Head trauma
H Headache
Physical findings
H Decreased pulse and respirations
H Scalp wound
H Bleeding in the periorbital area, nose, pharynx, ears,
or under the conjunctivae

H CSF leakage from the nose or ears; halo sign on pil-
lowcase (a blood-tinged spot surrounded by a lighter

ring)
Test results
Laboratory
H Reagent strips turn blue if CSF is present.
Imaging
imaging show fracture, intracranial hemorrhage
from ruptured blood vessels, and swelling.
Treatment
H Simple linear fracture most common, especially in
General
children younger than age 5

H May occur at any age
H Depends on type and severity of fracture

H Supportive
H Cleaning and debridement of wounds
H Diet as tolerated; nothing by mouth if surgery is nec-
H Persistent, localized headache

H Scalp wounds abrasions, contusions, lacerations,
H Limited activity
or avulsions
H Signs of brain injury agitation and irritability, loss
of consciousness, labored respirations, abnormal
762
Skull fracture
essary
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Medications
H Mild analgesics
H Dexamethasone (basilar and vault fractures)
ALERT
Dont give the patient opioids or sedatives because
they may depress respirations, increase carbon
dioxide levels, lead to increased intracranial pressure, and mask changes in neurologic status.
Surgery
H Craniotomy to elevate or remove fragments that have
been driven into the brain and to extract foreign bodies and necrotic tissue, thereby reducing the risk of
infection and further brain damage (severe injury)
Key outcomes
The patient will:
H remain neurologically and hemodynamically stable
H relate fears and feelings related to traumatic event.
ALERT
Nasal airways are contraindicated in patients with
possible basilar skull fractures. Intubation may be
necessary.
H Suction through the mouth, not the nose, to prevent
the introduction of bacteria.

H Position the patient with a head injury for proper se-
cretion drainage. Elevate the head of the bed 30 degrees if intracerebral injury is suspected.
H Apply appropriate dressings; control bleeding as necessary.
Monitoring
H Vital signs
H Neurologic status
H Comfort level
Patient teaching
Be sure to cover:
H preoperative and postoperative care, if appropriate
H need to watch closely for changes in mental status,
LOC, or respirations
H use of mild analgesics as opposed to opioids
H wound care.
Skull fracture
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Sleep apnea
Overview
Alcohol or sedative intake before bedtime

Smoking
H Central
Neurologic conditions affecting respiratory center
Heart disease
Description
Incidence
H Breathing that stops or gets very shallow during sleep

H Pause typically lasts 10 to 20 seconds or more
H Can occur 20 to 30 times or more per hour
H Most common type: obstructive (insufficient air flow
H Predominantly middle-age males

H 90% of cases, obstructive; 10%, central
into the lungs)

H Rare type: central
H Blood oxygen levels that drop
H Breaths that resume with a loud snort or gasping
sound
H Repetitive apneas that produce sleep disruption,
leading to excessive daytime sleepiness

H Usually chronic
Pathophysiology
H Obstructive
Nasopharynx or oropharynx briefly narrows or

collapses during inspiration.
This occurs because throat muscles and tongue
relax more than normal, tonsils and adenoids are
large, anatomic abnormalities create smaller airway, or excess weight makes it harder to keep the
throat area open.
H Central
Theres no breathing effort for brief periods.
Malfunction of respiratory control center in brain
doesnt send correct signals to respiratory muscles.
Causes
H Upper airway narrowing possibly caused by:
Obesity
Enlarged tonsils or uvula
Low soft palate
Redundant tissue in soft palate or tonsillar pillars
Large or posteriorly located tongue
Craniofacial abnormalities
Alcohol or sedative use before bedtime
H Central form: primarily caused by heart disease,
sleeping at high altitudes, and neurologic conditions,
such as stroke and brain tumors
Risk factors
H Obstructive
Obesity
Male gender
Postmenopausal female
Older than age 40
Nasal obstruction (such as polyps, rhinitis, or deviated septum)
Anatomic narrowing (such as tonsillar hypertrophy, macroglossia, craniofacial abnormalities)
Hypothyroidism
Neurologic syndromes (such as muscular dystrophy, cerebral palsy)
764
Sleep apnea
H Obstructive
Excessive daytime sleepiness

Loud snoring
Snort or gasp that arouses patient from sleep
H Central
Typically no snoring
Difficulty staying asleep
Abrupt awakenings accompanied by shortness of
breath
Daytime sleepiness
Complications
H Increases risk of hypertension, stroke, myocardial
infarction, diabetes, and cardiovascular disease

H Work-related and driving accidents due to sleepiness
Assessment
History
H One or more risk factors for either type
H Witnessed apneic episodes at night
H Progression of daytime sleepiness from mild (occur-
ring during quiet activities) to severe (occurring during dynamic activities, such as work or driving)
H Complaints of poor concentration, memory problems, irritability, and mood changes
H Morning headaches
Physical findings
H Most patients have a normal physical examination
H May have hypertension, obesity, or appear sleepy
H Possible findings with obstructive type:
Narrowing of the lateral airway wall

Tonsillar hypertrophy
Long or thick uvula
High, arched hard palate
Soft palate edema
Macroglossia
Deviated nasal septum
Poor nasal airflow
Short neck with large circumference
H Central type may cause cardiac and neurologic symptoms
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Test results
Laboratory
H Thyroid studies, such as triiodothyronine, thyroidstimulating hormone, or free thyroxine rule out hypothyroidism.
H Elevated hematocrit shows polycythemia, which can
occur in nocturnal hypoxemia.
H Arterial blood gas analysis evaluates daytime hypercapnia.
Imaging
H Head measurements and neck X-rays are used as
aids during surgical treatments.
H Polysomnogram, or PSG, records brain activity, eye
movement, muscle activity, breathing, and heart rate;
how much air moves in and out of the lungs during
sleep; and percentage of oxygen in the blood.
H Multiple sleep latency testing provides an objective
measurement of daytime sleepiness.
Other
H Apnea-hypopnea index determines severity and is defined as the total number of apneas and hypopneas
divided by the total sleep time.
Mild: apnea-hypopnea index 5 to 15
Moderate: apnea-hypopnea index 15 to 30
Severe: apnea-hypopnea index greater than 30
Treatment
General
H Continuous positive airway pressure, also known as
CPAP, most effective treatment

H Bilevel positive airway pressure, also known as Bi-
PAP, (boosts the weak breathing pattern of central

sleep apnea; can be set to automatically deliver a
breath if the patient hasnt taken a breath after a certain number of seconds)
H Adaptive servo-ventilation, also known as ASV, for
central sleep apnea; (monitors the patients normal
breathing patterns and stores the information in a
built-in computer; then, as needed, uses pressure to
regulate the breathing to the patients normal pattern)
H Treatment for associated medical problems
H Supplemental oxygen
H Weight loss
H Modification of activities or habits
Key outcomes
The patient will:
H regulate sleep patterns
H demonstrate effective breathing pattern while sleeping.
H Place the patient in semi-Fowlers position for sleep.
H Maintain pulse oximetry while patient sleeps.
H Administer oxygen via appropriate method, as or-
dered.
Monitoring
H Breathing pattern
H Pulse oximetry (during sleep)
H Sleep patterns
Patient teaching
Be sure to cover:
H the use of CPAP, BiPAP, or ASV if indicated
H positioning for sleep for optimum oxygenation
H diet modification for weight control (if appropriate)
H avoidance of driving or operating equipment when
drowsy
H avoidance of alcohol intake
H necessity of follow-up appointments.
Discharge planning
H Refer the patient for home respiratory supplies and
support.
Medications
H Generally not effective in treating this disorder
Surgery
H Surgical correction of the upper airway may be indi-
cated, depending on the cause of the apnea

H Experimental treatments, such as the Pillar proce-
dure, that involves placement of three tiny polyester

rods in the soft palate; recommended for some people with mild to moderate obstructive sleep apnea
Sleep apnea
765
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H In temperate zones, incidence highest during winter

H In tropics, incidence highest during hot, dry months
Smallpox
Overview
Complications
Description
H Acute, highly contagious infectious disease caused by
the poxvirus variola

H Associated with tremendous morbidity and mortality
H Two related viruses:
Variola major (classic smallpox), with a case

mortality of 20% to 50%
Variola minor (alastrim), a clinically milder form
with mortality less than 1%
H Eliminated worldwide in 1980 (World Health Organization declaration) as a result of a global vaccination
and eradication program; routine smallpox vaccination stopped; variola virus, preserved in two research
laboratories, remains unlikely but potential source of
infection; humans were sole reservoir of infection;
no carrier state
H Potential for use in bioterrorism and biological warfare; classified as category-A biological disease,
transmitted human to human with no known treatment
H Also known as variola
Pathophysiology
H Poxviruses are characterized by a large double-
stranded deoxyribonucleic acid (DNA) genome and a

brick-shaped morphology.
H Poxviruses are the only DNA viruses that replicate in
cytoplasm.
H The virus is spread through direct contact or inhalation of respiratory droplets.
H The incubation period is 7 to 19 days. Illness onset is
in 10 to 14 days, with onset of the characteristic rash
in 2 to 4 days. Fever and macular rash appear after
an average incubation period of 12 days, with a progression to typical vesicular and pustular lesions over
1 or 2 weeks.
H Its most contagious during the first week of illness
(before the eruptive period) and during the time between lesion development and scab disappearance.
H Fever
H Maculopapular rash
H Secondary bacterial infections

H Encephalitis
H Death
Assessment
History
H Influenza-type symptoms
H High fever, chills
H Rash
H Malaise
H Headache, backache
H Abdominal pain
H Nausea, vomiting
Physical findings
H After average incubation period of 12 days:
Fever
Macular rash
Progression to typical vesicular and pustular lesions, and then crusted scabs
Centrifugal distribution to rash; starts on the face
and extremities; moves to the trunk
Test results
Laboratory
H Culture of aspirate from vesicles and pustules shows
presence of variola.
H Electron microscopy of vesicular scrapings shows
presence of variola.
Treatment
General
H Poxvirus variolae
H Home treatment if possible to reduce spread

H No current treatment other than supportive
H Strict isolation
H Diet as tolerated
H I.V. fluids
Incidence
Medications
H Last known case in the United States reported in
H Cidofovir possibly given within 1 to 2 days of expo-
1949
H Last case of endemic smallpox reported in Africa in
1977
H Affected people of all ages
H Smallpox vaccine given within 4 days of exposure

H Antibiotics for secondary infection
H Antipruritics
Causes
766
Smallpox
sure
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H Antihistamines
H Analgesics
Key outcomes
The patient will:
H maintain adequate nutrition
H verbalize feelings of fear and anxiety
H Report any case of smallpox to the appropriate pub-
lic health office.

H Institute strict exposure precautions, including isola-
tion and airborne, contact, and standard precautions.

H Autoclave all laundry and hospital waste before laundering or incinerating.
H Encourage verbalization of fears and concerns.
H Provide a well-balanced diet.
H Assist in the development of effective coping mechanisms.
Monitoring
H Vital signs
H Intake and output
H Complications
H Signs and symptoms of secondary bacterial infection
Patient teaching
Be sure to cover:
H isolation precautions
H hydration
H skin lesion care.
Discharge planning
H Refer those in direct contact with an infected person
for pre-exposure and postexposure vaccination if

more than 3 years have passed since last vaccination.
Smallpox
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Spinal injury
Physical findings
Overview
H Limited movement and activities that cause pain

H Surface wounds
H Pain location
H Loss of sensation below the level of injury
H Deformity
H Level of injury and any spinal cord damage located
by neurologic assessment
Description
H Fractures, contusions, or compressions of the spine
H Most common sites: C5, C6, C7, T12, and L1 verte-
brae
Pathophysiology
H Injury causes microscopic hemorrhages.
H All of the gray matter is filled with blood.
H Necrosis results.
H Edema causes spinal cord compression.
H Blood supply is further decreased.
H Long-term scarring and meningeal thickening occur.
H Nerves are blocked or tangled.
H Sensory and motor deficits occur.
Causes
Serious injury
H Fall
H Diving into shallow water
H Gunshot and related wound
Less serious injury
H Improper lifting of heavy object
H Minor fall
H Neoplastic lesion
H Osteoporosis
Incidence
H Based on severity and location of injury:
Muscle spasm or back pain (worsens with movement)

Mild paresthesia to quadriplegia
Shock
Loss of motor function, muscle flaccidity
Bladder and bowel atony
Loss of perspiration below the level of the injury
Respiratory impairment
Complications
H Paralysis
H Death
H Autonomic dysreflexia
H Spinal shock
H Neurogenic shock
Assessment
History
H Muscle spasm
H Back or neck pain
H In cervical fractures, point tenderness
768
Spinal injury
Test results
Imaging
H Spinal X-rays, myelography, computed tomography
scan, and magnetic resonance imaging can indicate
the location of the fracture and the site of the compression.
Treatment
General
H Stabilization of spine and prevention of cord damage
H Hemodynamic support
H Application of a hard cervical collar
H Wound care (if appropriate)
H Chemotherapy and radiation for neoplastic lesion
H Aspiration precautions
H Skeletal traction with skull tongs
H Bed rest on a firm surface
H Rotation bed with cervical traction (if appropriate)
H Splinting: thoracic lumbar sacral orthotics
Medications
H Corticosteroids
H Analgesics
H Muscle relaxants
H Chemotherapy for neoplastic lesion
Surgery
H Decompression of spinal cord
H Stabilization of spinal column
Key outcomes
The patient will:
pain
H develop effective coping mechanisms
H attain the highest degree of mobility
H show no signs of aspiration.
H Apply a hard cervical collar.
H Immobilize the patient.
H Comfort and reassure the patient.
H Provide wound care, if appropriate.
H Provide diversionary activities.
H Provide proper skin care.
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Monitoring
H Neurologic changes
H Changes in skin sensation and loss of muscle
strength
H Skin integrity
H Pain control
Patient teaching
Be sure to cover:
H traction methods used
H exercises to maintain physical mobility
adverse effects
H the prescribed home care regimen
H the importance of follow-up examinations.
Discharge planning
H Refer the patient to the appropriate rehabilitation
center.
Spinal injury
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Sprains and strains
Incidence
Overview
H More common in athletes (occurs in 80% of ath-
letes)
Description
H Sprain complete or incomplete tear in supporting
ligaments surrounding a joint

H Strain acute or chronic injury to a muscle or
tendinous attachment
H Classified as mild, moderate, or severe (see Classify-
ing sprains and strains)
Pathophysiology
Sprain
H A ligament tear causes bleeding.
H A hematoma forms.
H Inflammatory exudates follow.
H Granulation tissue develops.
H Collagen forms.
H Swelling or stretching of nerves or vessels occurs.
H Persistent laxity and chronic joint instability result.
Strain
H Strains result from the same process as sprains.
H New tendon or muscle eventually becomes strong
enough to withstand normal muscle strain.
Sprain
H Localized pain
H Swelling and warmth
H Progressive loss of motion
H Ecchymosis
Strain
H Pain
H Inflammation
H Erythema
H Ecchymosis
H Elevated skin temperature
Complications
Sprain
H Avulsion fracture
Strain
H Complete rupture of muscle tendon unit
Assessment
Causes
History
H Fall
H Trauma
H Excessive or new exercise
H Sports injury
H Physical activity
H Similar past injury
H Systemic disease with high risk factors
H Local pain that worsens during joint movement
H Loss of mobility
H Sharp, transient pain and rapid swelling
H Stiffness, soreness, and generalized tenderness
Risk factors
H Participation in sports
Classifying sprains and strains

The guide below will help you classify the severity of
sprains and strains.
Sprains
H Grade 1 (mild): minor or partial ligament tear with normal joint stability and function
H Grade 2 (moderate): partial tear with mild joint laxity
and some function loss
H Grade 3 (severe): complete tear or incomplete separation of ligament from bone, causing total joint laxity
and function loss
Strains
H Grade 1 (mild): microscopic muscle or tendon tear (or

both) with no loss of strength
H Grade 2 (moderate): incomplete tear with bleeding into
muscle tissue and some loss of strength
H Grade 3 (severe): complete rupture, usually resulting
from separation of muscle from muscle, muscle from
tendon, or tendon from bone (usually stems from sudden, violent movement or direct injury)
770
Sprains and strains
Physical findings
H Ecchymosis
H Swelling
H Point tenderness
Test results
Imaging
H X-ray results are used to rule out fractures and confirm damage to ligaments.
Treatment
General
H RICE rest, ice, compression (wrapping in an elas-
tic bandage), and elevation to affected area

H Rehabilitation or exercise program
H Nothing by mouth if surgery scheduled
H Limited activity and weight bearing to injured area,
based on extent of injury

H Elevation of affected joint above the level of the heart
for 48 to 72 hours
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Medications
H Vitamin C supplements
H Analgesics
H Cox-2 inhibitors
Surgery
H Based on extent of injury
Key outcomes
The patient will:
H attain the highest possible level of mobility
pain
H identify factors that increase the potential for injury.
H Apply ice intermittently.
H Apply an elastic bandage or air cast.
H Elevate the extremity.
Monitoring
H Edema
H Pain control
H Complications
H Adverse effects of drugs
H ROM
Patient teaching
Be sure to cover:
H how to apply ice intermittently for the first 12 to
48 hours
H how to reapply elastic bandage or air cast
H crutch-gait training
H avoidance of further injury to the joint
adverse effects.
Sprains and strains
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Spurious polycythemia
Overview
Description
H Blood disorder characterized by increased hemat-
ocrit and a normal or low red blood cell (RBC) total

mass
H Results from diminished plasma volume and subsequent hemoconcentration
H Also known as relative polycythemia, stress erythrocytosis, stress polycythemia, benign polycythemia, Gaisbcks disease, or pseudopolycythemia
Pathophysiology
H Conditions that promote severe fluid loss decrease
plasma volume and lead to hemoconcentration.

H Nervous stress causes hemoconcentration by an un-
known mechanism. This form of erythrocytosis

(chronically elevated hematocrit) is particularly
common in the middle-aged male whos a chronic
smoker and has a type A personality (tense, hard driving, and anxious).
H In many patients, an increased hematocrit merely reflects a normally high RBC mass and low plasma volume. This is particularly common in patients who
dont smoke, arent obese, and have no history of hypertension.
Causes
Assessment
History
H Headaches
H Dizziness
H Cardiac or pulmonary disease
H Fatigue
H Diaphoresis
H Dyspnea
H Claudication
Physical findings
H Ruddy appearance
H Short neck
H Slight hypertension
H Hypoventilation when recumbent
Test results
Laboratory
H Hemoglobin level and hematocrit are increased.
H RBC count is increased.
H RBC mass is normal or decreased
H Arterial oxygen saturation is normal.
H Bone marrow is normal.
H Plasma volume is decreased or normal.
H Hyperlipidemia may be present.
H Uricosuria may be present.
Treatment
H Dehydration
H Hemoconcentration from stress
H High-normal RBC mass and low-normal plasma
General
volume
H Hypertension
H Thromboembolic disease
H Elevated serum cholesterol and uric acid
H Familial tendency
H Pregnancy
H Cessation of dietary diuretics such as caffeine

H Low-cholesterol, low-fat diet
H Adequate exercise
Incidence
H Appropriate fluids and electrolytes to correct dehy-
dration
Medications
H Antidiarrheals, if needed
H Usually affects middle-aged people

Key outcomes
H Headaches or dizziness
H Ruddy appearance
H Slight hypertension
H Tendency to hyperventilate when recumbent
H Cardiac or pulmonary disease
The patient will:

Complications
H Thromboemboli

H Encourage activity.
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H Provide dietary counseling if appropriate.
Monitoring
H Intake and output
H Blood studies
Patient teaching
Be sure to cover:
H changing the patients work habits, if appropriate
H the need for proper relaxation
H importance of proper hydration
H recognizing and reporting of signs and symptoms of
increasing polycythemia and thromboembolism.
Discharge planning
necessary.
H Emphasize the need for follow-up examinations every
3 to 4 months after leaving the hospital.
773
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Squamous cell
carcinoma
Overview
Description
H Invasive tumor arising from keratinizing epidermal
cells
Pathophysiology
H Transformation from a premalignant lesion to squa-
mous cell carcinoma may begin with induration and

inflammation of an existing lesion.
H When squamous cell carcinoma arises from normal
skin, the nodule grows slowly on a firm, indurated
base. If untreated, this nodule eventually ulcerates
and invades underlying tissues. (See Squamous cell
carcinoma nodule.)
Causes
H Unknown
H Actinic damage from solar ultraviolet radiation
H Ionizing radiation
H Chemical carcinogens
H Burns, scars
H Ulcerations
Risk factors
H Overexposure to the suns ultraviolet rays
H Radiation therapy
H Ingestion of herbicides containing arsenic
H Chronic skin irritation and inflammation
H Exposure to local carcinogens (such as tar and oil)
H Hereditary diseases (such as xeroderma pigmento-
H Presence of premalignant lesions (such as actinic
keratosis or Bowens disease)

H Rarely, develops on site of smallpox vaccination, pso-
riasis, or chronic discoid hippus erythematosus
Incidence
H Most common in fair-skinned, light-eyed, and light-
haired people
H Risk greatly increased by outdoor employment and
residence in sunny, warm climate
H Chronic skin ulceration
Complications
H Lymph node involvement
H Visceral metastasis
Assessment
History
H Areas of chronic ulceration, especially on
sun-damaged skin
H Pain, malaise, anorexia, fatigue, and weakness
Physical findings
H Lesions on the face, ears, or dorsa of the hands and
forearms, and on other sun-damaged skin areas (lesions possibly scaly and keratotic with raised, irregular borders; in late disease, lesions growing outward
or exophytic and friable and tending toward chronic
crusting)
Test results
H Excisional biopsy allows a definitive diagnosis.
sum and albinism)
Treatment
Squamous cell carcinoma nodule
An ulcerated nodule with an indurated base and a raised,
irregular border is a typical lesion in squamous cell carcinoma.
General
H Determined by size, shape, location, and invasiveness
of tumor and condition of underlying tissue

H Radiation therapy for older or debilitated patients
Medications
H Chemotherapy
H Topical corticosteroids
Surgery
H Wide surgical excision, curettage, and electrodesic-
cation
H Cryosurgery
H Mohs micrographic surgery
774
Squamous cell carcinoma
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Key outcomes
The patient will:
H experience feelings of increased energy
H Encourage verbalization and provide emotional sup-
port.
H Provide periods of rest between procedures if the
patient fatigues easily.

H Provide small, frequent meals and a high-protein,
high-calorie diet.
Monitoring
H Wound site
H Adverse effects of radiation therapy, such as nausea,
vomiting, hair loss, malaise, and diarrhea

H Pain control
Patient teaching
Be sure to cover:
adverse effects
H information about skin examination
H the importance of follow-up skin surveillance
H avoidance of excessive sun exposure to prevent recurrence; the need to use strong sunscreen.
Discharge planning
Squamous cell carcinoma
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Stomatitis
Incidence
Overview
Acute herpetic stomatitis

H Common in children ages 1 to 3
Aphthous stomatitis
H Common in young girls and female adolescents
Description
H Inflammation of oral mucosa; may extend to the buc-
H Painful gums
H Ulcers on gum papillae
cal mucosa, lips, palate, and tongue

H Common infection occurring alone or as part of systemic disease
H Two main types: acute herpetic stomatitis and aphthous stomatitis
H Usually heals spontaneously, without scarring, in 10
to 14 days
Pathophysiology
H Stomatitis is an inflammatory reaction that may cause
loss of the oral epithelium as a protective barrier.
Causes
H Herpes simplex virus
Aphthous stomatitis
H Unknown (autoimmune and psychosomatic causes
under investigation)
Risk factors
H Smoking
H Poor oral hygiene
H Stress
H Poor nutrition
H Chemotherapy
H Immunosuppression
Looking at aphthous stomatitis

In aphthous stomatitis, numerous small, round vesicles
appear. They soon break and leave shallow ulcers with red
areolae.
Complications
H Dysphagia
H Sepsis (in immunocompromised patient)
H Ocular or central nervous system involvement (her-
petic stomatitis)
Assessment
History
H Burning mouth pain
H Malaise
H Lethargy
H Anorexia
H Irritability
H Fever
H Extreme tenderness of the oral mucosa
Physical findings
Herpetic stomatitis
H Bleeding and swollen gums
H Papulovesicular ulcers in the mouth and throat
H Submaxillary lymphadenitis
Aphthous stomatitis
H Slight swelling of the mucous membrane
H Single or multiple shallow ulcers with whitish centers
and red borders, about 2 to 5 mm in diameter (see
Looking at aphthous stomatitis)
Test results
Laboratory
H Smear of ulcer exudate identifies the causative organism in Vincents angina (painful pseudomembranous
ulceration of gums, oral mucous membranes, pharynx, and tonsils).
H Viral cultures performed on fluid and herpetic vesicles in acute herpetic stomatitis identify the virus.
Treatment
General
H Symptom relief
H Nonantiseptic warm-water mouth rinses
H Ice
H Soft-bristled toothbrush
H Smoking cessation
H Soft, pureed, or liquid diet, as tolerated; avoidance of
salty, spicy foods

776
Stomatitis
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Medications
H I.V. fluids (severe cases)

H Topical anesthetic solutions
H Acyclovir
Aphthous stomatitis
H Topical anesthetic coating agent
Key outcomes
The patient will:
H show improvement or complete healing of lesions or
wounds
pain
H demonstrate good oral hygiene practices.
H Advise using a sponge instead of a toothbrush for
brushing teeth.
H Suggest rinsing with hydrogen peroxide or normal
saline mouthwash.
H Develop a meal plan based on soft, liquid, or pureed
foods.
H Offer iced drinks.
Monitoring
H Lesion state
H Complications
Patient teaching
Be sure to cover:
H the infection and expected course
H the importance of good oral hygiene
H the proper application of topical drugs
H recommended dietary changes
H (with aphthous stomatitis) the need to avoid such
precipitating factors as stress and fatigue.
Discharge planning
appropriate.
Stomatitis
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Streptococcus
pneumoniae infection,
drug-resistant
Overview
Incidence
H 3% to 35% of pneumococcal illness due to drug-
resistant strains
H DRSP possibly causing:
Bacteremia
Meningitis
Otitis media
Peritonitis
Pneumonia
Sinusitis
Description
Complications
H Infections caused by Streptococcus pneumoniae
H Colonized people not commonly detected or treated

H Treatment failures, prolonged hospitalization, recur-
among leading causes of illness and death among

young, elderly, and debilitated people
H Also known as DRSP
H Seven serotypes (6A, 6B, 9V, 14, 19A, 19F, and 23F)
accounting for most DRSP
H Vaccine available for the 23 most common serotypes
H Commonly resistant to penicillin; also resistant to
erythromycin, co-trimoxazole, vancomycin, tetracycline, chloramphenicol, and ofloxacin
H In pneumonias caused by resistant strains, death rate
twice as high as in those sensitive to antibiotics
Pathophysiology
H DRSP can affect people by colonization or infection.
H People who carry S. pneumoniae as part of their
normal flora but remain asymptomatic may unknowingly spread the infection.
H Disease results when bacteria multiply locally (otitis
media), multiply after aspiration (pneumonia), or
invade a sterile site (central nervous system or
blood).
Causes
H Abuse of antimicrobial agents
H Increasing prevalence of strains resistant to multiple
drug classes
Risk factors
H Contact with infected respiratory droplets or direct
or indirect contact with objects freshly soiled with

respiratory discharge
H Populations at risk:
Elderly people
Children age 2 and older
Blacks
Native Americans
People with autoimmune disorders
Nursing home residents
Child-care workers
Special populations
The Advisory Committee on Immunization Practices recommends the S. pneumoniae vaccine be
given to people age 2 and older with certain medical conditions and to all people age 65 and older.
778
rent disease, and increased cost

H Death in 14% of adults with invasive disease
H Neurologic sequelae after meningitis
H Hearing impairment from recurrent otitis media
H Developmental delay in children with recurrent otitis
media
Assessment
History
H Member of high-risk population
H Recent exposure to respiratory secretions of infected
person
H Recent antimicrobial use
Physical findings
In meningitis
H Fever
H Stiff neck
H Drowsiness
H Rash
H Seizures
H Increased white blood cells in cerebrospinal fluid
(CSF)
In otitis media
H High fever (101.3 F [38.5 C])
H Irritability
H Possibly effusion
H Bulging tympanic membrane thats red, opaque,
white, yellow, or purple and immobile on pneumatic
otoscope
In pneumonia
H Fluid-filled tissue and lobes
H Shaking chills
H Cough
H Rust- or green-colored mucus
H High fever
H Diaphoresis
H Elevated pulse and respirations
H Bluish lips and nailbeds
H Confusion or delirium
Streptococcus pneumoniae infection, drug-resistant
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Test results
Discharge planning
Laboratory
H Bacteria are isolated from a fluid sample (blood, CSF,
sputum, respiratory drops, ear).
Imaging
H Chest X-rays display pneumonia.
H Lumbar puncture is performed for suspected meningitis.
H Refer the patient for follow-up, as needed.

H Recommend to the patient that close contacts receive
the S. pneumoniae vaccine.
Treatment
General
H Supportive, symptomatic care
H Diet as tolerated
Medications
H Analgesics
H Antibiotics (type depending on resistance patterns in
community)
H Vancomycin (meningitis)
Key outcomes
The patient will:
H report resolution of symptoms
H have adequate oxygen levels
H have normal laboratory values.
H Provide rest periods as needed.
Monitoring
H Seizures
H Vital signs
H Intake and output
H Complications after lumbar puncture
Patient teaching
Be sure to cover:
H the importance of covering the mouth and nose when
sneezing or coughing
H regular hand washing
H taking the entire prescription of antibiotic for any
infection
H never giving a prescribed antibiotic to anyone else
H importance of reporting a change in symptoms to the
physician.
Streptococcus pneumoniae infection, drug-resistant
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Stroke
Overview
Description
H Sudden impairment of blood circulation to the brain
H Third most common cause of death in the United
States
H Affects 500,000 people each year, causing death in
half
H Most common cause of neurologic disability
H About 50% of stroke survivors permanently disabled
H Recurrences possible within weeks, months, or years
H Also known as cerebrovascular accident or brain
attack
Pathophysiology
H The oxygen supply to the brain is interrupted or di-
minished.
H In thrombotic or embolic stroke, neurons die from
lack of oxygen.
H In hemorrhagic stroke, impaired cerebral perfusion
causes infarction.
Causes
Cerebral thrombosis
H Most common cause of stroke
H Obstruction of a blood vessel in the extracerebral
vessels
H Site possibly intracerebral
Cerebral embolism
H Second most common cause of stroke
H History of rheumatic heart disease
H Endocarditis
H Posttraumatic valvular disease
H Post open-heart surgery
Cerebral hemorrhage
H Third most common cause of stroke
H Chronic hypertension
H Cerebral aneurysms
H Arteriovenous malformation
Risk factors
H History of transient ischemic attack
H Heart disease
H Smoking
H Familial history of cerebrovascular disease
H Obesity
H Alcohol use
H High red blood cell count
H Diabetes mellitus
H Gout
H High serum triglyceride levels
780
Stroke
H Use of hormonal contraceptives in conjunction with
smoking and hypertension

H Elevated cholesterol and triglyceride levels
Incidence
H Mostly affects older adults but can strike at any age
H Affects Blacks and Hispanics more commonly than
other groups
H Sudden unilateral weakness or numbness in limb
H Sudden speech difficulties
H Sudden vision disturbances
H Sudden ataxia, gait disturbance
H Sudden altered level of consciousness (LOC)
H Sudden severe headache
Complications
H Unstable blood pressure from loss of vasomotor con-
trol
H Fluid and electrolyte imbalances
H Malnutrition
H Infections
H Altered LOC
H Aspiration
H Contractures
H Skin breakdown
H Pulmonary emboli
H Depression
Assessment
History
H Varying clinical features, depending on:
artery affected
severity of damage
extent of collateral circulation
H One or more risk factors present
H Sudden onset of hemiparesis or hemiplegia
H Gradual onset of dizziness, mental disturbances, or
seizures
H Loss of consciousness or sudden aphasia
Physical findings
H With stroke in left hemisphere, signs and symptoms
on right side
H With stroke in right hemisphere, signs and symptoms
on left side
H With stroke that causes cranial nerve damage, signs
and symptoms on same side

H Change in LOC
H With conscious patient, anxiety along with communi-
cation and mobility difficulties

H Urinary incontinence
H Hemiparesis or hemiplegia on one side of the body
H Decreased deep tendon reflexes
H Hemianopsia on the affected side of the body
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H With left-sided hemiplegia, problems with visuospa-
tial relations
H Sensory losses
Test results
Laboratory
H Laboratory tests including anticardiolipin antibodies, antiphospholipid, factor V (Leiden) mutation,
antithrombin III, protein S, and protein C may
show increased thrombotic risk.
Imaging
H Magnetic resonance imaging and magnetic resonance angiography allow for evaluation of the location and size of the lesion.
H Cerebral angiography details the disruption of cerebral circulation and is the test of choice for examining the entire cerebral blood flow.
H Computed tomography scan detects structural abnormalities.
H Positron-emission tomography provides data on
cerebral metabolism and on cerebral blood flow
changes.
Other
H Transcranial Doppler studies evaluate the velocity of
blood flow.
H Carotid Doppler measures flow through the carotid
arteries.
H Two-dimensional echocardiogram evaluates the heart
for dysfunction.
H Cerebral blood flow studies measure blood flow to
the brain.
H Electrocardiography evaluates electrical activity in an
area of cortical infarction.
Treatment
General
H Careful blood pressure management
H Pureed dysphagia diet or tube feedings, if indicated
H Physical, speech, and occupational rehabilitation
H Helping patient adapt to specific deficits
Medications
H Tissue plasminogen activator when the cause isnt he-
morrhagic (emergency care within 3 hours of onset)

H Anticonvulsants
H Stool softeners
H Anticoagulants or antiplatelets
H Analgesics
H Antidepressants
H Lipid-lowering agents
H Antihypertensives
Surgery
H Craniotomy
H Endarterectomy
H Extracranial-intracranial bypass
H Ventricular shunts
Prevention
Preventing stroke
Risk of stroke may be reduced by following these guidelines:
H Stop smoking through a smoking-cessation program.
H Maintain ideal body weight.
H Control diabetes and hypertension.
H Follow a low-cholesterol, low-sodium diet.
H Take prescribed medications as ordered, especially anticoagulants or platelet aggregation inhibitors.
H Perform physical exercise regularly.
H Avoid prolonged bedrest.
H Minimize stress.
H Seek prompt treatment if experiencing signs and
symptoms of stroke.
Key outcomes
The patient will:
H achieve maximal independence
H maintain joint mobility and range of motion.
H Maintain a patent airway and oxygenation.
H Offer the urinal or bedpan every 2 hours.
H Insert an indwelling urinary catheter, if necessary.
H Ensure adequate nutrition.
H Provide careful mouth and eye care.
H Follow the physical therapy program.
H Establish and maintain patient communication.
H Protect the patient from injury and complications.
H Position to prevent aspiration and contractures.
Monitoring
H Neurologic, GI, and respiratory status
H Vital signs
H Fluid, electrolyte, and nutritional intake
H Development of deep vein thrombosis and pul-
monary embolus
Patient teaching
Be sure to cover:
H the dietary regimens
H stroke prevention. (See Preventing stroke.)
Discharge planning
H Refer the patient to home care services, outpatient
services, and speech and occupational rehabilitation

programs as needed.
Stroke
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Strongyloidiasis
Overview
Description
H A parasitic intestinal infection caused by the helminth
Strongyloides stercoralis
H Doesnt confer immunity; in people with autoimmune
disorders, possibly overwhelming disseminated infection

H Because threadworms reproductive cycle may continue in untreated host for up to 45 years, autoinfection highly probable
H Most patients recover, but death resulting from debilitating protein loss possible
H Also called threadworm infection
Pathophysiology
H Larvae develop from noninfective rhabdoid larvae in
human feces.
H The filariform larvae penetrate the human skin, usu-
ally at the feet, and then migrate by way of the lymphatic system to the bloodstream and the lungs.
H Once they enter into pulmonary circulation, the filariform larvae break through the alveoli and migrate
upward to the pharynx, where they are swallowed.
H Larvae then lodge in the small intestine, where they
deposit eggs that mature into noninfectious rhabdoid
larvae.
H These larvae migrate into the large intestine and are
excreted in feces, starting the cycle again.
H In autoinfection, rhabdoid larvae mature in the intestine to become infective filariform larvae.
Causes
H Contact with soil that contains infective S. stercoralis
filariform larvae
Incidence
Assessment
History
H Institutionalization
H Autoimmune susceptibility
H Cough
H Abdominal pain and diarrhea
H Recent travel to endemic area
Physical findings
H Erythematous, pruritic rash at entrance site
H Normal or hyperactive bowel sounds
H Crackles
Test results
Laboratory
H S. stercoralis larvae can be observed in a fresh stool
specimen (2 hours after excretion, look like hookworm larvae).
H Eosinophils and larvae may appear in sputum, with
marked eosinophilia in disseminated strongyloidiasis
(pulmonary phase).
H Hemoglobin level is decreased.
H In white blood cell count with differential, eosinophil
count is 450 to 700/l.
Imaging
H Chest X-rays show alveolar or interstitial infiltrates or
pulmonary effusions (pulmonary phase).
Treatment
General
H High-protein diet
H I.V. fluids
H Blood transfusion
Medications
H Thiabendazole
H Endemic to the tropics and subtropics

H Universal susceptibility
Key outcomes
H Erythematous maculopapular rash at the site of pene-
The patient will:

H maintain normal fluid and electrolyte balance
pain.
tration producing swelling and pruritus

H Pulmonary signs including minor hemorrhage, pneumonitis, and pneumonia
H Intestinal infection producing frequent, watery, and
bloody diarrhea, accompanied by intermittent abdominal pain
Complications
H Malnutrition
H Anemia
H Perforated intestine
H Septicemia
782
Strongyloidiasis
H Encourage high-protein diet.
H Wear gloves when handling bedpans or giving per-
ineal care, and dispose of feces promptly.

H In pulmonary infection, reposition the patient fre-
quently, encourage coughing and deep breathing,

and administer oxygen, as ordered.
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Monitoring
H Intake and output
H Amount and character of stools
Patient teaching
Be sure to cover:
H the possibility that thiabendazole may cause mild
nausea, vomiting, drowsiness, and giddiness
H proper hand-washing technique, stressing the importance of washing hands before eating and after defecating
H the need to wear shoes when in endemic areas.
Discharge planning
H Check the patients family and close contacts for
signs of infection.
H Emphasize the need for follow-up stool examination,
continuing for several weeks after treatment.
Strongyloidiasis
783
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Subarachnoid
hemorrhage
Overview
Description
H Bleeding into subarachnoid space
Subarachnoid space located between the pia mater

and the arachnoid layer of the meninges that surround the brain and spinal cord; normally filled
with clear, colorless cerebrospinal fluid (CSF) and
a network of arteries and veins
Blood also entering the CSF pathways
H Two types
Traumatic: more common
Spontaneous (nontraumatic)
Pathophysiology
H Bleeding occurs into the subarachnoid space.
H Blood spreads through the CSF, across the surface of
the brain, collecting and clotting in the ventricles,

cisterns, and foramen.
H Intracranial pressure (ICP) increases due to the
pressure exerted within a closed system.
H Perfusion distal to the rupture is decreased as well as
cerebral perfusion.
H Veins are compressed and venous outflow is reduced.
H Vasospasm occurs from irritation of the meninges,
further decreasing perfusion.
H Subacute or chronic hydrocephalus and brain infarctions can result.
Causes
H Head trauma
H Rupture of intracranial saccular aneurysm
H Intracranial arteriovenous malformation (AVM)
H Hypertension
H Rarely, tumors and blood dyscrasias
H Arterial dissection
H Extension from intracerebral hemorrhage
H Iatrogenic during surgery or intervention
H Meningitis
Risk factors
H Congenital weakness in arterial wall
H Degenerative weakening in the arterial wall from ath-
erosclerosis
H Cerebral aneurysms (associated with genetic abnor-
malities, such as polycystic kidney disease and fibromuscular dysplasia)

H Hypertension
H Pregnancy
H Smoking
H Drug and alcohol abuse
784
Subarachnoid hemorrhage
Incidence
H About 30,000 people a year in the United States have
a nontraumatic subarachnoid hemorrhage

H Predominant between ages 40 and 70
H More common in females then in males
H Ruptured saccular aneurysms: account for about
80% of nontraumatic cases

H AVMs: account for about 10% of cases
H Estimated 23% to 39% occurring due to severe head
injury
H Vary with location, duration and amount of va-
sospasm, and the degree of increased ICP

H Typically, change in level of consciousness occurring
H Sudden onset of severe headache
H Neck pain and nuchal rigidity
H Photophobia
H Seizures
H Possible prodromal headaches caused by minor
blood leakage, also called sentinel headaches: occur in 30% to 50% of cases with aneurysm as the
cause; may occur a few hours to a few months before
the rupture
Complications
H Rebleeding
H Hyponatremia
H Severe neurologic damage
H Paralysis
H Coma
H Death
Assessment
History
H Traumatic head injury
H Headaches
H Recent onset of seizures
H Symptoms of meningeal irritation
H Photophobia and visual changes
Physical findings
All or none of these findings may be present:
H Global or focal neurologic abnormalities
H Symptoms of cranial nerve compression
H Vision loss
H Motor deficits
H Retinal hemorrhage
H Papilledema
H Mild-to-moderate blood pressure elevation
H Tachycardia
H Weakness, paralysis, or numbness on one side of
body
H Difficulty speaking
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Test results
Laboratory
H Complete blood count may show decreased hemoglobin level and hematocrit.
may be increased.
H Blood typing and crossmatching is done for possible
transfusion.
Imaging
H Computed tomography (CT) scan, initially without
contrast, establishes diagnosis.
H Cerebral angiography assesses vascular anatomy and
bleeding site also assists in surgical planning.
H Magnetic resonance imaging is done if other testing
is negative.
H Lumbar puncture, only if contrast CT scan shows
negative results and there are no signs of increased
ICP; may detect blood in CSF; contraindicated with
increased ICP because brain stem herniation may result.
H Electrocardiography detects myocardial ischemia
caused by the increased circulation of catecholamines.
H Radiosurgery possibly used to treat small, deep AVMs

H Endovascular obliteration of aneurysms
Key outcomes
The patient will:
H express relief from or decrease in pain
H achieve optimum functioning
H demonstrate improvement in orientation
H maintain optimal gas exchange and ventilation
H maintain adequate cerebral perfusion
H verbalize decrease in or relief from nausea
H remain free from injury.
H Provide supplemental oxygen and mechanical venti-
lation, as needed.
H Evaluate fluid and electrolyte status.
H Avoid overhydration with I.V. fluids to prevent in-
creases in intracranial pressure.

H Turn patient often, one movement at a time, and use
Treatment
General
H Establishing and maintaining airway, breathing, and
antiembolism stockings.
H Institute measures to prevent skin breakdown.
H Institute seizure precautions, as indicated.
H Prepare the patient for surgery, as appropriate.
circulation as necessary; providing supplemental

oxygen
H Directed at preventing complications, including rebleeding, hydrocephalus, and cerebral vasospasm
H Vasospasm treated with generous volume expansion
and hypertension to promote cerebral perfusion, after aneurysm obliterated
H Providing a darkened, quiet, private room to minimize stimuli
H Elevating the head of the bed 30 degrees to facilitate
intracranial venous drainage
H Vigorous rehabilitation program
Monitoring
Medications
Be sure to cover:
H importance of preventing Valsalvas maneuver
(straining at stool, coughing)
H medication regimen
H tests, neurologic examinations, treatments, and procedures
H avoidance of unnecessary physical activity for patients receiving conservative treatment
H need to report adverse reactions to prescribed medications
H need to report signs of rebleeding
H Analgesics to reduce pain

H Calcium channel blockers, such as nimodipine for
21 days to prevent vasospasm and to enhance collateral blood flow

H Osmotic agent, such as mannitol, or loop diuretic
such as furosemide to reduce ICP
H Antihypertensive agents and vasopressors (possibly
indicated)
H Possibly, antiemetics for nausea or vomiting and
stool softeners to prevent constipation and straining
to defecate
Surgery
H Neurologic status (hourly)

H Signs of increased ICP
H Cerebral perfusion pressure
H Signs of decreased level of consciousness
H Vital signs
H Respiratory and cardiac status
H Seizure activity
H Laboratory test results
Patient teaching
H Hydrocephalus: cerebral spinal fluid drainage or
Discharge planning
permanent shunting procedures

H AVMs and certain aneurysms: possibly obliterated
with embolization; cranial surgery possibly necessary
H Refer the patient to physical therapy, occupational
therapy, and speech therapy as appropriate.

H Refer the patient to social services as appropriate.
Subarachnoid hemorrhage
785
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Subdural hematoma
Overview
Description
H Meningeal hemorrhage resulting from accumulation
of blood in subdural space

H May be acute (less than 72 hours old), subacute (3
to 20 days old), or chronic (older than 20 days)
H May be unilateral or bilateral
Pathophysiology
Acute
H Blunt impact to the skull may cause a tear in connecting veins (rarely, arteries) in the cerebral cortex.
Chronic
H Chronic subdural hematoma begins as a separation
in the dura-arachnoid interface, which is then filled
by cerebrospinal fluid (CSF).
H Dural border cells proliferate around this CSF collection to produce a neomembrane.
H Fragile new vessels grow into the membrane and
hemorrhage.
Causes
H Head trauma
Risk factors
H Dilated, nonreactive pupil ipsilateral to the
hematoma
H Hemiparesis contralateral to the hematoma
Complications
H Coma
H Death
Assessment
History
H Head trauma
H Headache
H Change in level of consciousness (LOC)
Physical findings
H Dilated, nonreactive pupil ipsilateral to the
hematoma
H Hemiparesis contralateral to the hematoma
H Balance problems
H Altered LOC
Test results
Laboratory
H CSF is yellow with relatively low protein (chronic
subdural hematoma).
H Coagulation studies may be abnormal.
Imaging
H Computed tomography scan, X-rays, and arteriography reveal mass and altered blood flow in the area.
Acute
H Anticoagulant therapy
H Age
Chronic
H Alcoholism
H Epilepsy
H Coagulopathy
H Arachnoid cysts
H Anticoagulant therapy (including aspirin)
H Cardiovascular disease (hypertension, arteriosclerosis)
H Thrombocytopenia
H Diabetes
Treatment
Incidence
H Vitamin K, fresh frozen plasma, platelets, or clotting
H Acute type: occurs in 5% to 25% of patients with
severe head injuries.

Most common in people older than age 40
H Chronic type: most common in people older than
age 50
H Both types occurring more commonly in males than
in females
H Headache
H Deteriorating mental status
786
Subdural hematoma
General
H Supportive treatment
H Wound care
H Fresh frozen plasma (to correct coagulation)
H Diet based on extent of injury
H Nothing by mouth if surgery necessary
H Bed rest initially, then activity as tolerated
H Flat bed after evacuation of hematoma
Medications
products (if coagulation studies are abnormal)
H Analgesics (after extent of injury is determined)
H Osmotic diuretics
H Anticonvulsants
H Prophylactic antibiotics (with surgery)
Surgery
H Burr holes
H Craniotomy
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Key outcomes
The patient will:
H remain neurologically stable
pain
H express an understanding of the disorder and treatment regimen.
Monitoring
H Vital signs
H Neurologic status
H Wound healing
H Seizure activity
Patient teaching
Be sure to cover:
H the disorder, diagnosis, anad treatment
H importance of reporting changes in neurologic status
H avoiding aspirin as a pain treatment
H observing for CSF drainage and signs of infection.
Discharge planning
H Refer the patient to physical therapy, occupational
therapy, and speech therapy, as appropriate.

H Refer the patient to social services, as appropriate.
Subdural hematoma
787
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Substance abuse and

dependence
Overview
Description
H Use of a legal or an illegal substance that causes
physical, mental, emotional, or social harm, such as

opioids, stimulants, depressants, antianxiety agents,
and hallucinogens
H Number one health problem in the United States
Pathophysiology
H Tolerance develops when a drug is administered
long-term (such as an opioid for a cancer patient),

with cross-tolerance developing.
H Withdrawal occurs with abrupt discontinuation or
administration of an antagonist due to rebound noradrenergic activity in the central nervous system
(CNS).
Causes
H Combination of low self-esteem, peer pressure, inad-
equate coping skills, and curiosity

H May follow the use of prescribed drugs to relieve
H Hepatitis
H Cirrhosis
H Vasculitis
H Septicemia
H Thrombophlebitis
H Pulmonary emboli
H Gangrene
H Malnutrition and GI disturbances
H Respiratory infections
H Musculoskeletal dysfunction
H Trauma
H Depression and increased risk of suicide
H Psychosis
H Toxic or allergic reactions
H Impaired social and occupational functioning
Assessment
History
H Abdominal pain, nausea, or vomiting
H Painful injury or chronic illness
H Feigned illnesses
H Overdose
H High tolerance to potentially addictive drugs
H Amenorrhea
H Suggestive behavior patterns or the presence of
known risk factors
physical pain
H Mood swings, anxiety, impaired memory, sleep dis-
Risk factors
turbances, flashbacks, slurred speech, depression,

and thought disorders
H Male gender
H History of depression
H History of other substance abuse disorders
H Familial history
H Peer pressure
Incidence
H Experimentation common beginning in adolescence
and preadolescence
H Affects more than 18 million United States residents
who use alcohol and 5 million who use illicit drugs
(fewer than one-fourth treated)
Physical findings
H Lacrimation (with opiate withdrawal)
H Nystagmus (with CNS depressants and phencyclidine
intoxication)
H Drooping eyelids (with opiate or CNS depressant
use)
H Constricted pupils (with opiate use or withdrawal)
H Dilated pupils (with hallucinogens or ampheta-
mines)
H Rhinorrhea (with opiate withdrawal or cocaine
abuse)
H Inflammation, atrophy, or perforation of the nasal
mucosa (with drug sniffing)

H Sweating (with opiates or CNS stimulants or drug
withdrawal)
H Nutritional deficiency
H Mood swings, anxiety, impaired memory, sleep dis-
H Sensation of bugs crawling on the skin (with alcohol
turbances, flashbacks, slurred speech, depression,

and thought disorders
H Physical signs of substance abuse (based on substance)
H Withdrawal signs when substance not used
H Excoriated skin
H Needle marks or tracks
H Cellulitis or abscesses
H Thrombophlebitis
H Fascial infection
H Bilateral crackles and rhonchi (with smoking and in-
Complications
H Cardiac and respiratory arrest
H Subacute bacterial endocarditis
788
Substance abuse and dependence
withdrawal)
haling drugs or by opiate overdose)

H Cardiopulmonary signs of overdose (respiratory de-
pression and hypotension)

H Acute-onset hypertension
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H Hemorrhoids
H Tremors, hyperreflexia, hyporeflexia, and seizures
H Uncooperative, disruptive, or violent behavior
DSM-IV-TR criteria
H Diagnosis is confirmed with at least three of the fol-
lowing criteria (some symptoms must have persisted

for at least 1 month or have occurred repeatedly over
a longer time):
substance usually taken in larger amounts or for a
longer time than the patient intended
persistent desire or one or more unsuccessful efforts to cut down or control substance use
excessive time devoted to activities necessary to
obtain the substance
frequent intoxication or withdrawal symptoms
when expected to fulfill major obligations at work,
school, or home or when substance use is physically hazardous
impaired social, occupational, or recreational activities
continued substance use despite the recognition of
a persistent or recurrent social, psychological, or
physical problem thats caused or exacerbated by
the use of the substance
marked tolerance
characteristic withdrawal symptoms
substance commonly taken to relieve or avoid
withdrawal symptoms.
Test results
Laboratory
H Serum or urine drug screen reveals the substance.
H Serum protein electrophoresis shows elevated serum
globulin levels.
H Serum glucose measurement shows hypoglycemia.
H Complete blood count (CBC) shows leukocytosis.
H Liver function is abnormal.
H CBC shows elevated mean corpuscular hemoglobin
levels.
H Uric acid levels are elevated.
H Blood urea nitrogen levels are decreased.
Medications
H Detoxification with the same drug or a pharmacolog-
ically similar drug

H Sedatives
H Anticholinergics
H Antidiarrheal agents
H Antianxiety drugs
H Anticonvulsants
H Nutritional and vitamin supplements
Key outcomes
The patient will:
H express his feelings related to self-esteem
process
H engage in social interactions with others
H participate with his family to identify and use support
systems.
H Maintain a quiet, safe environment.
H Set limits for dealing with demanding, manipulative
behavior.
Monitoring
H Vital signs
H Suicide ideation
H Visitors
H Nutrition
H Effects of pharmacologic therapy
Patient teaching
Treatment
Be sure to cover:
H detoxification and rehabilitation, as appropriate
H measures for preventing human immunodeficiency
virus infection and hepatitis
H measures for safer sex and birth control.
General
Discharge planning
H Symptomatic treatment based on the drug ingested

H Fluid replacement therapy
H Symptomatic treatment for complications
H Gastric lavage, induced emesis, activated charcoal in-
H Recommend participation in a drug-oriented
self-help group.
stillation, forced diuresis and, possibly, hemoperfusion or hemodialysis

H Detoxification (inpatient or outpatient)
H Psychotherapy
H Exercise
H Relaxation techniques
H Rehabilitation
H Monitored activity for safety
Substance abuse and dependence
789
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Sudden infant death

syndrome
Overview
Description
H Sudden death of an infant younger than age 1 year
without identifiable cause

H Also known as SIDS and crib death
Pathophysiology
Hypotheses
H The infant may have damage to the respiratory control center in the brain from chronic hypoxemia.
H The infant may not respond to increasing carbon
dioxide levels. During an episode of apnea, carbon
dioxide levels increase, but the child isnt stimulated
to breathe. As apnea continues, high levels of carbon
dioxide further suppress the ventilatory effort until
the infant stops breathing.
H The infant may have periods of sleep apnea and eventually die during one of these episodes.
Causes
H Possibly viral
H Hypoxia theory
H Apnea theory
H Possible Clostridium botulinum toxin
H Possibly associated with diphtheria, tetanus, and per-
tussis vaccines
Incidence
H About 7,000 SIDS deaths annually in United States
H 2 in every 1,000 live births; about 60% male
Special populations
SIDS occurs mostly between ages 1 and 4 months.
Incidence declines rapidly between ages 4 and
12 months.
H Increased incidence in nonbreast-fed infants
H Occurs most commonly in fall and winter
H Slightly higher incidence in:
Preterm neonates
Inuit neonates
Disadvantaged black neonates
Neonates of mothers younger than age 20
Neonates of multiple births
H Apnea
790
Sudden infant death syndrome
Complications
H Always fatal
Assessment
History
H Occasionally, respiratory tract infection
H Possible abnormal hepatic or pancreatic function
H Previous near-miss respiratory event in 60% of cases
H With infant wedged in a crib corner or with blankets
wrapped around head, suffocation ruled out by autopsy as the cause of death
H With frothy, blood-tinged sputum found around infants mouth or on crib sheets revealing a patent airway, aspiration of vomitus ruled out by autopsy as
cause of death
H No crying or signs of disturbed sleep by infant
Physical findings
H Postmortem examination possibly showing:
Changes indicating chronic hypoxia, hypoxemia,

and large airway obstruction
Bruising; possible fractured ribs
Blood in the infants mouth, nose, or ears
Mottled complexion; extremely cyanotic lips and
fingertips
Pooled blood in legs and feet
Diaper possibly wet and full of stool
Test results
H Autopsy may show:
small or normal adrenal glands
enlarged thymus
petechiae over the visceral surfaces of the pleura,
within the thymus, and in the epicardium
well-preserved lymphoid structures
signs of chronic hypoxemia
increased pulmonary artery smooth muscle
edematous, congestive, and fully expanded lungs
liquid blood in the heart
stomach curd inside the trachea.
Treatment
General
H Emotional support for the family
H Prevention for any surviving infant found apneic and
any sibling with apnea; assessment with home apnea

monitor until the at-risk infant passes age of vulnerability
Key outcomes
The family will:
H use available support systems to assist in coping
H share feelings about the event
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H identify feelings of hopelessness regarding the cur-
rent situation
H use effective coping strategies to ease spiritual dis-
comfort.
H Ensure that both parents are present when the childs
death is confirmed.
H Stay calm and allow the parents to express their feel-
ings.
H Reassure the parents that they arent to blame.
H Allow the parents to see the infant in a private room
and to express their grief. Stay in the room with

them, if appropriate.
H Offer to call clergy, friends, or relatives.
H Return the infants belongings to the parents.
H Ensure that the parents receive the autopsy report
promptly.
Monitoring
H Parents reactions and coping mechanisms
Patient teaching
Be sure to cover:
H the need for an autopsy to confirm the diagnosis
H basic facts about SIDS
H information to help parents cope with pregnancy and
the first year of a new infants life, if they decide to
have another child.
Discharge planning
H Refer the parents and family to community and
health care facility support services.

H Refer the parents to a local SIDS parents group.
H Advise the parents to contact the SIDS hot line
(1-800-221-SIDS).
H Refer the parents to cardiopulmonary resuscitation
classes, if appropriate.
H Refer the family to a home health nurse for contin-
ued support, if indicated.
Sudden infant death syndrome
791
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Syndrome of
inappropriate
antidiuretic hormone
H Cerebrovascular disease
H Cancer
H Pulmonary disease
H Recent head injury
H Anorexia, nausea, vomiting
H Weight gain
H Lethargy, headaches, emotional and behavioral
changes
Physical findings
Overview
Description
H Disease of the posterior pituitary marked by exces-
sive release of antidiuretic hormone (ADH) (vasopressin)

H Potentially life-threatening
H Prognosis depends on underlying disorder and response to treatment
H Also known as SIADH
Pathophysiology
H Tachycardia
H Disorientation
H Seizures and coma
H Sluggish deep tendon reflexes
H Muscle weakness
Test results
Laboratory
H Serum osmolality levels are less than 280 mOsm/kg.
H Serum sodium levels are less than 123 mEq/L.
H Urine sodium levels are greater than 20 mEq/L without diuretics.
H Renal function tests are normal.
H Excessive ADH secretion occurs in the absence of
normal physiologic stimuli for its release.

H Excessive water reabsorption from the distal convo-
luted tubule and collecting ducts results in hyponatremia and normal to slightly increased extracellular
fluid volume. (See Understanding SIADH.)
Causes
H Oat cell carcinoma of the lung
H Neoplastic diseases
H Central nervous system disorders
H Pulmonary disorders
H Drugs
H Miscellaneous conditions, such as myxedema and
psychosis
Incidence
Treatment
General
H Based primarily on symptoms
H Correction of the underlying cause
H Restricted water intake (500 to 1,000 ml/day)
H High-sodium, high-protein diet or urea supplements
to enhance water excretion

Medications
H Demeclocycline or lithium for long-term treatment
H Loop diuretics if fluid overload, history of heart fail-
ure, or resistance to treatment

H 3% sodium chloride solution if serum sodium level
H Common cause of hospital-acquired hyponatremia
less than 120 or if the patient seizing
Surgery
H Increased water retention

H Fluid and electrolyte imbalance
H Hyponatremia
H To treat underlying cause such as cancer
Complications
H Water intoxication
H Cerebral edema
H Severe hyponatremia
H Heart failure
H Seizures
H Coma
H Death
Assessment
History
H Possible clue to the cause
792
Key outcomes
The patient will:
H remain alert and oriented to the environment
H verbalize understanding of the disorder and treatment regimen
H maintain adequate fluid balance.
H Restrict fluids.
H Provide comfort measures for thirst.
H Reduce unnecessary environmental stimuli.
H Orient as needed.
Syndrome of inappropriate antidiuretic hormone
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Understanding SIADH
The events that produce the syndrome of inappropriate antidiuretic hormone (SIADH) secretion are depicted in this
flowchart.
Excessive antidiuretic hormone secretion
Increased renal tubule permeability
Increased water retention and expanded extracellular fluid volume
Reduced plasma
osmolality
Dilutional
hyponatremia
Diminished
aldosterone secretion
Elevated glomerular
filtration rate
Decreased sodium
reabsorption in
proximal tubule
Intracellular
fluid shift
Increased sodium
excretion
Cerebral edema
Hyponatremia
Patient teaching

H Institute seizure precautions as needed.
Be sure to cover:
H fluid restriction
H methods to decrease discomfort from thirst
H self-monitoring techniques for fluid retention such as
daily weight
H signs and symptoms that require immediate medical
intervention.
Monitoring
H Intake and output
H Vital signs
H Daily weight
H Serum electrolytes, especially sodium
H Breath sounds
H Heart sounds
H Neurologic checks
H Changes in level of consciousness
ALERT
Watch closely for signs and symptoms of heart failure, which may occur due to fluid overload.
Syndrome of inappropriate antidiuretic hormone
793
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Syphilis
Overview
Description
H Chronic, infectious, sexually transmitted disease
H Untreated, progresses in four stages: primary, sec-
ondary, latent, and late (formerly called tertiary)
Pathophysiology
H The infecting organism penetrates intact mucous
membranes or abrasions in the skin, entering lymphatics and blood.

H Systemic infection and systemic foci precede primary
lesion development at the site of inoculation.
H Organ involvement occurs from dissemination.
Causes
H The spirochete Treponema pallidum
H Transmission primarily through sexual contact dur-
ing the primary, secondary, and early latent stages of

infection
H Prenatal transmission possible
H Transmission by way of fresh blood transfusion
(rare)
Incidence
H In the United States, incidence highest in urban pop-
ulations, especially in people between ages 15 and

39, drug users, and those infected with human immunodeficiency virus (HIV)
H About 34,000 cases, in primary and secondary
stages, reported in the United States annually
Complications
H Irreversible neurologic disease
H Irreversible organ damage
H Membranous glomerulonephritis
H With fetal infection:
Spontaneous abortion
Stillbirth
Low birth weight
Deafness
Assessment
History
H Unprotected sexual contact with an infected person
Physical findings
Primary syphilis
H One or more chancres (small, fluid-filled lesions) on
the genitalia; others on the anus, fingers, lips,
tongue, nipples, tonsils, or eyelids
H In female patient, possible chancres on cervix or
vaginal wall
H Unilateral or bilateral adenopathy
794
Syphilis
Secondary syphilis
H Headache, malaise
H Nausea, vomiting
H Anorexia, weight loss
H Sore throat, slight fever
H Symmetrical mucocutaneous lesions
H Rash possibly macular, papular, pustular, or nodular
H Lesions uniform, well defined, and generalized
H Macules typically erupting between rolls of fat on the
trunk and proximally on the arms, palms, soles, face,
and scalp
H In warm, moist body areas, lesions enlarged and
eroding, producing highly contagious, pink or grayish white lesions (condylomata lata)
H Alopecia
H Brittle and pitted nails
H Generalized lymphadenopathy
Latent syphilis
H Physical signs and symptoms absent except for possible recurrence of mucocutaneous lesions that resemble those of secondary syphilis
Late syphilis
H Findings that vary with the involved organ
H Three subtypes:
Neurosyphilis affecting meningovascular tissues:
headache, vertigo, insomnia, hemiplegia, seizures,
and psychological difficulties; if parenchymal tissue affected: paresis, alteration in intellect, paranoia, illusions, and hallucinations; in addition, Argyll Robertson pupil (a small, irregular pupil
thats nonreactive to light but accommodates for
vision), ataxia, slurred speech, trophic joint
changes, positive Rombergs sign, and a facial
tremor
Late benign: gummas (lesions that develop between 1 and 10 years after infection and may be a
chronic, superficial nodule or a deep, granulomatous lesion thats solitary, asymmetrical, painless,
indurated, and large or small) visible on the skin
and mucocutaneous tissues; commonly affect
bones and can develop in any organ
Cardiovascular: decreased cardiac output that may
cause decreased urine output and decreased sensorium related to hypoxia, pulmonary congestion
Test results
Laboratory
H Dark-field microscopy identifies T. pallidum from lesion exudate to provide an immediate syphilis diagnosis. (See Identifying syphilis by dark-field microscopy.)
H Non-treponemal serologic tests include the Venereal
Disease Research Laboratory (VDRL) slide test, the
rapid plasma reagin (RPR) test, and the automated
reagin test, detecting nonspecific antibodies.
H Treponemal serologic studies include the fluorescent
treponemal antibody absorption test, the T. pallidum
hemagglutination assay, and the microhemagglutination assay, detecting the specific antitreponemal antibody and confirming positive screening results.
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H Cerebrospinal fluid examination identifies neu-
rosyphilis when the total protein level is above

40 mg/dl, the VDRL slide test is reactive, and the
white blood cell count exceeds 5 mononuclear
cells/l.
Identifying syphilis by dark-field

microscopy
The presence of spiral-shaped bacteria (Treponema pallidum) on dark-field examination confirms the diagnosis
of syphilis.
Treatment
General
H Immediate examination of all sexual contacts
H Avoidance of pregnancy until a good response to
therapy is demonstrated
H Hospitalization for symptomatic late syphilis
H No sexual activity until cured
Medications
H Antibiotics (penicillin being the treatment of choice)
Key outcomes
H risks to the fetus if the patient is contemplating preg-
nancy
The patient will:

H voice feelings about changes in sexual activity
body image
H report feelings of increased comfort.
H following safer sex practices.
H Consult a social worker to determine home care

H Promote rest and adequate nutrition.
H In secondary syphilis, keep lesions clean and dry;
Discharge planning
H As needed, obtain a physical or occupational therapy
consultation.
H Refer the patient for contact tracing.
H Refer the patient to a specialist if congenital syphilis
is suspected.
needs.
dispose of contaminated materials properly.

H Report all syphilis cases to the appropriate health au-
thorities.
Monitoring
H Neurologic status
H Complications
H Compliance with treatment
Patient teaching
Be sure to cover:
H the importance of completing the prescribed course
of therapy even after symptoms subside
H the importance of informing, testing, and treating
sexual partners
H the need to refrain from sexual activity until treatment is completed and follow-up VDRL/RPR test results are normal
H information for patient and sexual partners about
HIV infection
Syphilis
795
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Systemic lupus
erythematosus
Assessment
History
H Onset acute or insidious; no characteristic clinical
Overview
Description
H A chronic inflammatory autoimmune disorder that
affects connective tissues

H Two forms: discoid lupus erythematosus (DLE) and
systemic lupus erythematosus (SLE)

H Only the skin affected by DLE
Pathophysiology
H The body produces antibodies, such as antinuclear
antibodies (ANAs), against its own cells.

H The formed antigen-antibody complexes suppress the
bodys normal immunity and damage tissues.

H Patients with SLE produce antibodies against many
different tissue components, such as red blood cells

(RBCs), neutrophils, platelets, lymphocytes, and almost any organ or tissue in the body.
Causes
H Unknown
H Predisposing factors:
Stress
Streptococcal or viral infections
Exposure to sunlight or ultraviolet (UV) light
Injury
Surgery
Exhaustion
Emotional upsets
Immunization, pregnancy
Abnormal estrogen metabolism
Incidence
H Affects females eight times more commonly than
males (15 times more common during childbearing

years)
H Occurs worldwide; most prevalent among Asians and
Blacks
H Recurrent seasonal remissions and exacerbations,
especially during spring and summer
Complications
H Pleurisy
H Pleural effusions
H Pericarditis, myocarditis, endocarditis
H Coronary atherosclerosis
H Renal failure
H Seizures and mental dysfunction
796
pattern
H Possible fever, anorexia, weight loss, malaise, fatigue,
abdominal pain, nausea, vomiting, diarrhea, constipation, rash, and polyarthralgia

H Possible drug history with one of 25 drugs that can
cause SLE-like reaction
H Irregular menstruation or amenorrhea, particularly
during flare-ups
H Chest pain and dyspnea
H Emotional instability, psychosis, organic brain syndrome, headaches, irritability, and depression
H Oliguria, urinary frequency, dysuria, and bladder
spasms
Physical findings
H Joint involvement that resembles rheumatoid arthritis
H Raynauds phenomenon
H Skin eruptions provoked or aggravated by sunlight or
UV light
H Tachycardia, central cyanosis, and hypotension
H Altered level of consciousness, weakness of the ex-
tremities, and speech disturbances

H Skin lesions
H Butterfly rash over nose and cheeks
H Patchy alopecia (common)
H Vasculitis
H Lymph node enlargement (diffuse or local and non-
tender)
Test results
Laboratory
H Complete blood count with differential shows anemia
and a reduced white blood cell (WBC) count, decreased platelet count, and elevated erythrocyte sedimentation rate; serum electrophoresis shows hypergammaglobulinemia.
H ANA, anti-deoxyribonucleic acid, and lupus erythematosus cell test findings are positive in most patients with active SLE, but these are only slightly useful in diagnosing the disease. (ANA test is sensitive
but not specific for SLE.)
H Urine studies show RBCs, WBCs, urine casts, sediment, and significant protein loss (more than 3.5 g
in 24 hours).
H Blood studies demonstrate decreased serum complement (C3 and C4) levels, indicating active disease.
(Leukopenia, mild thrombocytopenia, and anemia
are also seen during active disease.)
H C-reactive protein level is increased during flare-ups.
H Rheumatoid factor is positive in 30% to 40% of patients.
Imaging
H Chest X-rays may disclose pleurisy or lupus pneumonitis.
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H Central nervous system (CNS) involvement may account for abnormal EEG results in about 70% of patients, but brain scans and magnetic resonance imaging may be normal in patients with SLE despite CNS
disease.
H Electrocardiography may show a conduction defect
with cardiac involvement or pericarditis.
H Renal biopsy shows progression of SLE and the extent of renal involvement.
H Skin biopsy shows immunoglobulin and complement
deposition in the dermal-epidermal junction in 90%
of patients.
Treatment
General
H Use of sunscreen with sun protection factor of at
least 15
H No dietary restrictions unless renal failure occurs
H Regular exercise program
Medications
H Topical corticosteroid creams
H Fluorinated steroids
H Antimalarials
H Corticosteroids
H Cytotoxic drugs
H Antihypertensives
H Immunosuppressants, such as azathioprine and
cyclophosphamide
Surgery
H Possible joint replacement
Key outcomes
The patient will:
pain
H maintain fluid balance.
H Institute seizure precautions if you suspect CNS in-
volvement.
H Warm and protect the patients hands and feet if she
has Raynauds phenomenon.

H Support the patients self-image.
Monitoring
H Signs and symptoms of organ involvement
H Urine, stools, and GI secretions for blood
H Scalp for hair loss and skin and mucous membranes
for petechiae, bleeding, ulceration, pallor, and

bruising
H Complications
H Joint mobility
H Seizure activity
Patient teaching
Be sure to cover:
H ROM exercises and body alignment and postural
techniques
H ways to avoid infection, such as avoiding crowds and
people with known infections
H the need to notify the physician if fever, cough, or
rash occurs or if chest, abdominal, muscle, or joint
pain worsens
H the importance of eating a balanced diet
H the importance of good skin care
H the benefits of exercise
H the importance of keeping regular follow-up appointments and contacting the physician if flare-ups occur
H the need to wear protective clothing and use a sunscreen
H how to perform meticulous mouth care.
Discharge planning
H Arrange for a physical therapy and occupational ther-
apy consultation if musculoskeletal involvement compromises mobility.

H Refer the patient to a rheumatology specialist if she
becomes pregnant.
H Provide a balanced diet.
H Provide bland, cool foods if the patient has a sore
mouth.
H Provide a mouth rinse of normal saline solution after
meals to assist healing of oral lesions.

H Apply heat packs to relieve joint pain and stiffness.
H Encourage regular exercise to maintain full ROM.
H Explain the expected benefit of prescribed drugs, and
watch for adverse effects.
797
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Taeniasis
H Particularly prevalent among institutionalized mental-
Overview
Description
H A parasitic infestation by Taenia saginata (beef tape-
worm), T. solium (pork tapeworm), Diphyllobothrium latum (fish tapeworm), or Hymenolepis nana
(dwarf tapeworm)
H Although usually a chronic, benign intestinal disease,
dangerous systemic and central nervous system
(CNS) symptoms possible if T. solium larvae invade
the brain or striated muscle of vital organs
H Also called tapeworm disease and cestodiasis
Pathophysiology
H Gastric acid activates larvae, allowing them to ma-
ture, after ingestion of undercooked, bacteriainfested beef or pork.

H Mature tapeworms fasten to the intestinal wall and
produce ova that are passed in the feces.
H A single tapeworm produces an average of 50,000
eggs per day and may live 25 years.
Causes
T. saginata
H Uncooked or undercooked beef
T. solium
H Uncooked or undercooked pork
D. latum
H Uncooked or undercooked freshwater fish, such as
pike, trout, salmon, and turbot
H. nana
H No intermediate host
H Person-to-person transmission via ova passed in
stool
ly retarded children and in underdeveloped countries
T. saginata
H Crawling sensation in the perianal area caused by
worm segments that have passed rectally
T. solium
H Seizures
H Headaches
D. latum
H Anemia
H. nana
H Dependent on patients nutritional status and number
of parasites
H Commonly no symptoms with mild infestation
H With severe infestation, anorexia, diarrhea, restlessness, dizziness, and apathy
Complications
H Appendicitis
H Obstruction of bile ducts and pancreatic duct
Assessment
History
H Ingestion of raw or undercooked beef or pork
H Occasionally, worm segments exiting through the
anus and appearing on bed clothes

H Increased hunger
H Weight loss
H Nausea
H Abdominal pain (usually in the morning) relieved by
eating
H Pruritus ani
Risk factors
Physical findings
H Handling or eating contaminated food

H Poor hygiene
H Inadequate hand-washing facilities
H Weight loss
H Intraocular larvae
Incidence
T. saginata
H Worldwide, but most prevalent in Europe and East
Africa
T. solium
H Incidence highest in Mexico and Latin America
H Lowest incidence among Muslims and Jews
D. latum
H Most prevalent in Finland, parts of Russia, Japan,
Alaska, Australia, the Great Lakes region of the United States, Switzerland, Chile, and Argentina
H. nana
H Most common tapeworm in humans
798
Taeniasis
Test results
Laboratory
H Tapeworm ova or body segments are seen in feces
(may require multiple specimens).
Treatment
General
H Diet as tolerated
Medications
H Anthelmintics
H High-dose glucocorticosteroids
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ALERT
During treatment for T. solium, other health-related
measures, such as laxative use and induced vomiting, are contraindicated because of the danger of
autoinfection and systemic disease.
Surgery
H Possible if complications develop
Key outcomes
The patient will:
H express understanding of illness
H regain or maintain optimal weight.
H Dispose of the patients excretions carefully. Wear
gloves when giving personal care and handling fecal

excretions, bedpans, and bed linens; wash your
hands thoroughly and instruct the patient to do the
same.
H Tell the patient not to consume anything after midnight on the day niclosamide therapy begins because
the drug must be taken on an empty stomach. After
administering the drug, document passage of strobilae.
Monitoring
H Stool specimens
H Daily weight
Patient teaching
Be sure to cover:
H expected response to treatment
H preventing reinfection by washing hands thoroughly
and cooking meat and fish thoroughly.
Discharge planning
H After drug treatment, all types of tapeworm infesta-
tion require a follow-up laboratory examination of

stool specimens during the next 3 to 5 weeks to
check for any remaining ova or worm segments.
H Persistent infestation typically requires a second
course of medication.
Taeniasis
799
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Tay-Sachs disease
Overview
Description
H Lipid storage disease that results from a congenital
enzyme deficiency
H Leads to progressive mental and motor deterioration
H Always fatal, usually before age 5
H Rare form occurs in patients between ages 20 and 30
H No known cure
Pathophysiology
H In this autosomal recessive disorder, the enzyme hex-
osaminidase A is absent or deficient.

H Without hexosaminidase A, lipid pigments (ganglio-
side GM2) accumulate and progressively destroy and

demyelinate central nervous system cells.
H The juvenile form typically appears between ages 2
and 5 as a progressive deterioration of psychomotor
skills and gait.
Causes
H Autosomal recessive disorder
Incidence
H Affects fewer than 100 infants born yearly in the Unit-
ed States
H About 100 times more common (about 1 in 3,600
live births) in those with Ashkenazic Jewish ancestry

than in the general population
H About 1 in 30 Ashkenazi Jews, French Canadians, and
American Cajuns heterozygous carriers of gene for
this disorder
H Progressive mental and motor deterioration
H Blindness
H Deafness
H Inability to swallow
H Cherry-red spot on the retina
Complications
H Recurrent bronchopneumonia
H Dementia
H Blindness
H Seizures
H Paralysis
H Death, usually before age 5
800
Tay-Sachs disease
Assessment
History
H Familial history of Tay-Sachs disease
H Normal appearance at birth (but with possible exag-
gerated Moros reflex)

H Onset of clinical signs and symptoms between ages 5
and 6 months
H Progressive deterioration
H Blindness
H Dementia
Physical findings
H In 3- to 6-month-old infant:
Apathetic appearance
Augmented response to loud sounds
Progressive weakness of the neck, trunk, arm, and
leg muscles that prevents child from sitting up or
lifting head
Difficulty turning over
Inability to grasp objects
Progressive vision loss
H By age 18 months:
Possible seizures
Generalized paralysis
Spasticity
Blindness
Holding eyes wide open and rolling eyeballs
Pupils always dilated
Decerebrate rigidity
Complete vegetative state
Head circumference possibly showing enlargement
Pupils nonreactive to light
Ophthalmoscopic examination possibly showing
optic nerve atrophy and a distinctive cherry-red
spot on the retina
H In a child who survives bouts of recurrent bronchopneumonia: possible ataxia and progressive motor
retardation between ages 2 and 8 years
Test results
Laboratory
H Serum analysis shows deficient hexosaminidase A.
H Amniocentesis or chorionic villus sampling allows
prenatal diagnosis of hexosaminidase A deficiency.
Treatment
General
H Supportive care
H Suctioning
H Postural drainage to remove secretions
H Meticulous skin care
H Tube feedings with nutritional supplements
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H Active and passive range-of-motion exercises
Medications
H Mild laxatives
H Anticonvulsants
Key outcomes
The patient (or family, if appropriate) will:
H express understanding of the disease process and
treatment regimen
H seek outside sources to assist with coping and adjusting to the patients situation.
H Help the patients family deal with progressive illness
and death.
H Prevent skin breakdown.
H Provide adequate nutrition.
H Implement seizure precautions.
H Stress the importance of amniocentesis in future
pregnancies.
Monitoring
H Vital signs
H Intake and output
H Neurologic status
Patient teaching
Be sure to cover:
H how to perform suctioning when needed
H how to perform postural drainage
H how to give tube feedings
H need for proper skin care to prevent breakdown.
Discharge planning
H Refer the parents for genetic counseling.
H Refer the parents to the National Tay-Sachs and Allied
Diseases Association.
H Refer the parents for psychological counseling if in-
dicated.
H Refer the siblings for screening to determine whether
theyre carriers.
H If the siblings are adult carriers, refer them for ge-
netic counseling; stress that the disease isnt transmitted to offspring unless both parents are carriers.
Tay-Sachs disease
801
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Temporomandibular
joint disease
Overview
Description
H Pain, stiffness, and tenderness in jaw muscles, face,
or neck
H Headache
H Earache
H Painful clicking or popping over the TMJ
H Limitation of mandibular movement or locking of jaw
H Malalignment of upper and lower teeth
H Disorder of the temporomandibular joint (TMJ),
Complications
which connects the jaw to the skull

H Includes several conditions that cause tenderness
and pain in the TMJ, including:
Muscle tension and spasm
Psychological stress
Degenerative joint disease
Internal joint derangement
H Secondary degenerative joint disease

H Chronic TMJ dislocation
H Loss of joint range of motion
H Depression
H Chronic pain syndromes
Pathophysiology
Assessment
H Lower jaw has rounded ends called condyles that
History
glide in and out of the joint socket with movement of

the jaw.
H Surfaces of the condyles and socket of the temporal
bone are covered with cartilage and separated by a
small disk, which absorbs shock and keeps the
movement smooth.
H Displacement of the disc causes pressure on and
stretching of sensory nerves, especially the trigeminal
nerve, causing pain.
H Popping or clicking occurs when the disk snaps into
place with jaw movement.
H Chronic malposition of the disc and persistent wear
on the cartilage lining causes further damage.
H Complaints of jaw pain

H Jaw injury
H Recent dental treatments
Causes
H Synovitis
H Disc derangement
H Hypermobile TMJ
H Bruxism
H Muscle spasm
H Trauma
H Poorly fitting dentures
H Poor posture of the head, neck and shoulders
H Hereditary conditions affecting the structures of the
Physical findings
H Pain or tenderness without jaw movement; worsens
with jaw movement

H Limited jaw opening
H Facial muscle spasm
H Unilateral facial swelling
H Clicking or popping in the TMJ
H Tenderness to palpation
H Crepitus over joint
H Excessive wear patterns on teeth
Test results
Imaging
H Videoarthrography shows abnormal jaw motion.
H Panoramic dental X-rays show abnormal wear.
H Computed tomography scan shows altered bone
structure.
H Magnetic resonance imaging aids in treatment options.
joint
Risk factors
H Chronic oral habits, such as clenching or grinding
the teeth
H Osteoarthritis and rheumatoid arthritis
H Dental malocclusion
H Fibrositis
H Psychosocial stress
Treatment
General
H Jaw rest
H Heat therapy
H Correction of malocclusion with orthodontic appli-
ance
Incidence
H Stress reduction
H Behavior modification to eliminate tension-relieving
H Estimated that over 10 million Americans affected

H Soft diet to reduce chewing
802
Temporomandibular joint disease
oral habits
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Medications
H Anti-inflammatories
H Muscle relaxants
H Analgesics
H Botulinum toxin
Surgery
H Possibly, a procedure to correct disc displacement or
replace a damaged disc
Key outcomes
The patient will:
H experience relief or decrease in pain
H verbalize an understanding of the condition
H express understanding of measures for relief of
symptoms
H comply with the treatment plan.
H Help identify the underlying cause.
H Help the patient identify risk factors.
H Assist the patient with the proper use of malocclusion
orthodontic appliances.
H Help the patient identify triggers for stress.
H Refer the patient to a behavior-modification program
for stress.
H Incorporate stress-reduction techniques.
H Encourage the patient to frequently rest the jaw.
H Apply heat to affected area.
Monitoring
H Compliance with therapeutic plan
Patient teaching
Be sure to cover:
H use of orthodontic appliances
H stress management
H avoidance of clenching or grinding teeth
H diagnostic studies
H consumption of a soft diet to reduce chewing
H avoidance of wide yawning.
Temporomandibular joint disease
803
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Tendinitis and bursitis

Overview
Description
Tendinitis
H Inflammation affecting the tendons and tendonmuscle attachments
Shoulder rotator cuff
Hip
Achilles tendon
Hamstring
Elbow
Bursitis
H Painful inflammation of one or more bursae
Subdeltoid
Subacromial
Olecranon
Trochanteric
Calcaneal
Prepatellar
H May be septic, calcific, acute, or chronic
Pathophysiology
Tendinitis
H Inflammation causes localized pain around the
affected area.
H Joint movement is restricted.
H Swelling results from fluid accumulation.
H Calcium deposits form in and around the tendon.
H Further swelling and immobility result.
Bursitis
H Bursae sacs hold lubricating synovial fluid.
H Inflammation causes gradual pain and limits joint
motion.
Causes
Tendinitis
H Trauma (such as a strain during sports activity)
H Musculoskeletal disorders (rheumatic diseases and
congenital defects)
H Postural malalignment
H Abnormal body development
H Hypermobility in calcific tendinitis
Bursitis
H Recurring trauma from an inflammatory joint disease
H Common stressors:
Repetitive kneeling
Jogging in worn-out shoes on hard asphalt surfaces
Prolonged sitting with crossed legs on hard surfaces
H Septic bursitis: wound infection or bacterial invasion
(see Anatomy of tendons and bursae)
804
Incidence
H More common in elderly people
H Common in those performing activities that over-
stress a tendon or repeatedly stress a joint
H Localized pain
H Interrupted sleep
H Limited movement
H Crepitus over involved area
H Swelling over involved area
Complications
H Scar tissue with subsequent disability
Assessment
History
Tendinitis
H Traumatic injury or strain from athletic activity
H Concurrent musculoskeletal disorder
H Palpable tenderness over the affected site
H Referred tenderness in the related segment
H Shoulder:
Localized pain; most severe at night
Pain usually interfering with sleep
Pain aggravated by heat
H Elbow: pain when grasping objects or twisting the
elbow
H Hamstring: pain in the posterolateral aspect of the
knee
H Foot: pain over the Achilles tendon and on dorsiflexion
Bursitis
H Unusual strain or injury 2 to 3 days before pain
began
H Pain that develops suddenly or gradually
H Pain that may limit movement
H Work or leisure activity that may involve repetitive
action
Physical findings
Tendinitis
H Shoulder: restricted shoulder movement (especially
abduction)
H Elbow: tenderness over the lateral epicondyle
H Hamstring: palpable tenderness when knee flexed at
a 90-degree angle
H Foot: crepitus when the patient moves his foot
Bursitis
H Tenderness over the affected site
H Swelling with severe bursitis
Test results
Laboratory
H Various serum and urine test results rule out other
disorders.
Imaging
H X-rays in tendinitis may show bony fragments, osteophyte sclerosis, or calcium deposits.
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Anatomy of tendons and bursae

Tendons, like stiff rubber bands, hold the muscles in place and enable them to move the bones. Bursae are located at friction
points around joints and between tendons, cartilage, or bone. Bursae keep these body parts lubricated so they move freely.
SHOULDER JOINT
Clavicle
Acromioclavicular joint
Subacromial bursa
Humerus
Subscapularis muscle
Biceps tendons
H X-rays in calcific bursitis may show calcium deposits
in the joint.
H Arthrography is usually normal in tendinitis with minor irregularities on the tendon under the surface.
H Arthrocentesis may identify causative microorganisms and other causes of inflammation.
H Apply cold or heat therapies, as ordered.

H Promote self-care.
H Administer drug therapy.
H Encourage use of active ROM exercises.
Treatment
General
H Cold, heat, or ultrasound applications
H Resting the affected joint
Medications
H Local anesthetics
H Corticosteroids
H Oral anti-inflammatories
H Short-term analgesics
Key outcomes
The patient will:
H have increased comfort and decreased pain
H express understanding of the treatment regimen and
disease process.
Monitoring
H Severity and pattern of pain
H ROM
Patient teaching
Be sure to cover:
H how to minimize GI distress caused by NSAIDs
adverse effects
H activities that promote rest and relaxation
H strengthening exercises
H the prescribed exercise regimen
H need for proper sports equipment, shoes, and playing surfaces
H use of cushioned shoes
H application of cold packs
H proper body mechanics.
Discharge planning
H Refer the patient to a weight-management program,
as appropriate.
805
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Testicular cancer
H Metastasis
H Ureteral obstruction
Overview
Assessment
Description
History
H Proliferation of cancerous cells in the testicles

H Most originating from germinal cells and about 40%
H Previous injury to the scrotum

H Viral infection (such as mumps)
H Use of DES or other estrogen-progestin drugs by the
becoming seminomas
H Prognosis dependent on cancer cell type and stage
(with treatment, a more than 5-year survival rate)
Pathophysiology
H Testicular cancer spreads through the lymphatic sys-
tem to the iliac, para-aortic, and mediastinal nodes.

H Metastasis affect the lungs, liver, viscera, and bone.
Causes
Risk factors
H Cryptorchidism (see Cryptorchidism and testicular
cancer)
H Mumps orchitis
H Inguinal hernia in childhood
H Maternal use of diethylstilbestrol (DES) or other
estrogen-progestin combinations during pregnancy
Incidence
H Most common in males ages 20 to 40
H Rare in nonwhite males
H Accounts for less than 1% of all male cancer deaths
H Rare in children
H Fullness of testes
H Lump in testes
Complications
H Back or abdominal pain from retroperitoneal
adenopathy
Cryptorchidism and testicular cancer

In males with cryptorchidism (the failure of a testicle to
descend into the scrotum), testicular tumors are about 50
times more common than in males with normal anatomic
structure. A simple surgical procedure, called orchiopexy,
can bring the testicle to its normal position in the scrotum
and reduce the testicular cancer risk. Nevertheless, testicular tumors occur more commonly in a surgically descended testicle than in a naturally descended one.
What happens in orchiopexy

In orchiopexy, the surgeon incises the groin area and separates the testicle and its blood supply from surrounding
abdominal structures. Then he creates a tunnel into the
scrotum to accommodate the descent of the testicle.
Reducing the risk further

After orchiopexy, urge the patient to examine his testicles
monthly to detect a tumor at its earliest stage.
806
Testicular cancer
patients mother during pregnancy

H Feeling of heaviness or a dragging sensation in the
scrotum
H Weight loss (late sign)
H Fatigue and weakness (late sign)
Physical findings
H Enlarged testes
H Gynecomastia
H Lethargic, thin, and pallid appearance (later stages)
H Palpable firm, smooth testicular mass
H Enlarged lymph nodes in surrounding areas
Test results
Laboratory
H Elevated levels of the proteins (tumor markers)
human chorionic gonadotropin (HCG) and alphafetoprotein (AFP) suggest testicular cancer and
can differentiate a seminoma from a nonseminoma.
H Elevated HCG and AFP levels indicate a nonseminoma.
H Elevated HCG and normal AFP levels indicate a seminoma.
H Biopsy confirms the diagnosis and can be used to
stage the disease.
H Scrotal ultrasound shows the tumor.
Treatment
General
H Varies with tumor cell type and stage
H Radiation therapy
H Autologous bone marrow transplantation for patients
nonresponsive to standard therapy

Medications
H Chemotherapy
H Hormonal therapy
Surgery
H Orchiectomy and retroperitoneal node dissection
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Key outcomes
The patient will:
H express positive feelings about himself
H report feeling less tension or pain
H voice understanding of treatment
H express feelings and perceptions about change in
sexual performance.
H Apply an ice pack to the scrotum.
Monitoring
H Wound site
H Vital signs
H Pain control
Patient teaching
Be sure to cover:
H reassurance that infertility and impotence usually
dont follow unilateral orchiectomy
H sperm-banking procedures before the patient begins
treatment, especially if infertility and impotence may
result from surgery
H testicular self-examination.
Discharge planning
H Refer the patient to available resource and support
services.
Testicular cancer
807
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Testicular torsion
Incidence
Overview
H Occurs in 1 in 4,000 males younger than age 25
H Most common between ages 12 and 18, but may oc-
cur at any age
Description
H An abnormal twisting of the spermatic cord caused
by rotation of a testis or the mesorchium (a fold in

the area between the testis and epididymis)
H Causes strangulation and eventual infarction of the
testis if untreated
H 90% of cases unilateral
Pathophysiology
H Normally, the tunica vaginalis envelops the testis and
attaches to the epididymis and spermatic cord.

H In intravaginal torsion (the most common type of testicular torsion in adolescents), testicular twisting
may result from an abnormality of the tunica, in
which the testis is abnormally positioned, or from a
narrowing of the mesentery support.
H In extravaginal torsion (most common in neonates),
loose attachment of the tunica vaginalis to the scrotal
lining causes spermatic cord rotation above the
testis. A sudden forceful contraction of the cremaster
muscle may precipitate this condition. (See Extravaginal torsion.)
Causes
H Congenital anomaly
H Trauma
H Sexual activity
H Undescended testicle
H Exercise
Extravaginal torsion
In extravaginal torsion, rotation of the spermatic cord
above the testis causes strangulation and, eventually,
infarction of the testis.
H Excruciating pain in the affected testis or iliac fossa
Complications
H Loss of testicle
H Infarction of testicle
H Infection
H Infertility
Assessment
History
H Previous episodes of intermittent testicular pain that
resolved spontaneously
H Sudden scrotal pain
H Abdominal pain
H Fever
Physical findings
H Scrotal swelling
H Painful testicle
H Horizontal lie of the testicle
H Scrotal erythema
H Ipsilateral loss of the cremasteric reflex
Test results
H Doppler ultrasonography helps distinguish testicular
torsion from strangulated hernia, undescended
testes, or epididymitis.
Treatment
General
H Manual detorsion
H Nothing by mouth before surgery; diet as tolerated
after surgery
H Activity as tolerated after surgery
Spermatic
cord rotation
Medications
H Analgesics
Surgery
H Immediate surgical repair by orchiopexy (fixation of
Mesorchium
Testis
808
Testicular torsion
a viable testis to the scrotum) or orchiectomy (excision of a nonviable testis); as with ovarian torsion in
the female, preservation of the organ preferred
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Key outcomes
The patient will:
H develop no complications.
H Promote the patients comfort before and after
surgery.
H After surgery, administer drugs for pain.
H Apply an ice bag with a cover to reduce edema.
H Protect the wound from contamination.
Monitoring
H Voiding
H Scrotal swelling
H Pain control
Patient teaching
Be sure to cover:
H wound care.
Testicular torsion
809
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Tetanus
Overview
Description
H An acute exotoxin-mediated infection
H Usually systemic, but possibly localized
H Up to 60% fatal in unimmunized patients
H Also known as lockjaw
Pathophysiology
H After the organism enters the body, local infection
and tissue necrosis result.

H Toxins enter the bloodstream and lymphatics, eventually spreading to central nervous system tissue.
H The incubation period is 3 to 21 days.
Causes
H Anaerobic, spore-forming, gram-positive bacillus
H Rhabdomyolysis
H Death
Assessment
History
H Inadequate immunization
H Recent wound or burn
H Pain or paresthesia at the site of injury
H Complaints of difficulty chewing or swallowing food,
drooling
Physical findings
H Spasm and increased muscle tone near the wound
(local infection)
H Irregular heartbeat and tachycardia
H Marked muscle hypertonicity
H Profuse sweating, low-grade fever
H Painful, involuntary muscle contractions
H Rigid neck and facial muscles, resulting in lockjaw
Clostridium tetani
H Transmission through puncture wounds, burns, or
minor wounds contaminated by soil, dust, or animal
excreta containing C. tetani
(trismus) and a grotesque, grinning expression (risus sardonicus)

H Rigid somatic muscles causing arched-back rigidity
(opisthotonos)
H Intermittent tonic seizures
Risk factors
Test results
H Participating in outdoor sports or occupations

H Exposure to animal feces
H Gardening
Laboratory
H Blood cultures and tetanus antibody tests are negative.
H Wound culture is positive in one-third of patients.
H Cerebrospinal fluid (CSF) pressure is increased.
H Lumbar puncture (spinal tap) may show elevated CSF
pressure.
Incidence
H Occurs worldwide, but more prevalent in agricultural
regions and developing countries that lack mass immunization programs

H One of the most common causes of neonatal deaths
in developing countries
H In the United States, about 110 cases each year, all
in patients not immunized or whose immunization
expired
H About 75% of cases between April and September
H Usually, a normal body temperature or a slight fever
in the early stages; fever possibly increasing as the

disease progresses
H Despite pronounced neuromuscular symptoms, normal cerebral and sensory function
Complications
H Pneumonia
H Heart failure
H Fractures
810
Tetanus
Treatment
General
H Airway maintenance
H Enteral or parenteral feeding
H Bed rest until recovery
Medications
H Tetanus immune globulin
H Tetanus antitoxin
H Tetanus toxoid immunization
H Muscle relaxants
H Neuromuscular blockers
H Antibiotics
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Key outcomes
The patient will:
pain
H have a patent airway and adequate ventilation
H show no signs of neurologic compromise.
H Debride and clean the injury site.
H Check the immunization history.
H Maintain an adequate airway and ventilation.
H Keep emergency airway equipment on standby.
H Administer I.V. therapy as prescribed.
H Minimize stimulation.
H Perform range-of-motion exercises.
Monitoring
H Injury site
H Complications
H Deep tendon reflexes
H Muscle tone
Patient teaching
Be sure to cover:
H the importance of getting a booster dose of tetanus
toxoid every 10 years
H the need for tetanus prophylaxis in case of a skin
injury or burn
H the need to avoid external stimulation (evokes
muscle spasms) and to keep the room dark and
quiet.
Tetanus
811
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Tetralogy of Fallot
Overview
Description
H A combination of four cardiac defects: ventricular
septal defect (VSD); right ventricular outflow tract

obstruction (pulmonary stenosis); right ventricular
hypertrophy; and dextroposition of the aorta, with
overriding of the VSD
Assessment
History
H Blue spells
H Diminished exercise tolerance
H Increasing dyspnea on exertion
H Eating difficulties
Physical findings
H Blood shunts right to left through the VSD, permitting
H Clubbing
H Cyanosis
H Loud systolic heart murmur (best heard along the
unoxygenated blood to mix with oxygenated blood,

resulting in cyanosis.
H Condition sometimes coexists with other congenital
heart defects, such as patent ductus arteriosus or
atrial septal defect.
left sternal border), which may diminish or obscure

the pulmonic component of S2
H Cardiac thrill at the left sternal border and an obvious right ventricular impulse
H Prominent inferior sternum
Causes
Test results
H Unknown
H Associated with fetal alcohol syndrome and thalido-
Laboratory
H Arterial oxygen saturation is diminished.
H Polycythemia is present. (Hematocrit may be more
than 60%.)
Imaging
H Chest X-rays may demonstrate decreased pulmonary
vascular marking, depending on the severity of the
pulmonary obstruction, and a boot-shaped cardiac
silhouette.
H Echocardiography identifies septal overriding of the
aorta, the VSD, and pulmonary stenosis, and detects
the hypertrophied walls of the right ventricle.
H Electrocardiography shows right ventricular hypertrophy, right axis deviation and, possibly, right atrial
hypertrophy.
H Cardiac catheterization confirms the diagnosis by
showing pulmonary stenosis, the VSD, and the overriding aorta and ruling out other cyanotic heart
defects.
Pathophysiology
mide use during pregnancy
Risk factors
H Maternal viral illness during pregnancy
H Poor prenatal nutrition
H Maternal age older than 40
H History of tetralogy of Fallot in parent
H Down syndrome
Incidence
H Accounts for about 10% of all congenital heart
diseases
H Cyanosis
H Blue spells, which are characterized by dyspnea;
deep, sighing respirations; bradycardia; fainting;

seizures; and loss of consciousness
H Children squat following exertion (increases blood
flow to lungs)
Treatment
Complications
General
H Cerebral abscesses
H Pulmonary thrombosis
H Venous thrombosis
H Cerebral embolism
H In females with tetralogy of Fallot living to childbear-
H Prevention and treatment of complications

H During cyanotic spells, knee-chest position and ad-
ing age, increased risk of spontaneous abortion, premature births, and low birth weight
812
Tetralogy of Fallot
ministration of oxygen and morphine to improve

oxygenation
Medications
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Surgery
H Palliative surgery: performed on infants with poten-
tially fatal hypoxic spells (The goal of surgery is to

enhance blood flow to the lungs to reduce hypoxia;
this is commonly accomplished by joining the subclavian artery to the pulmonary artery [BlalockTaussig procedure].)
H Complete corrective surgery: relieves pulmonary
stenosis and closes the VSD, directing left ventricular
outflow to the aorta
Key outcomes
The patient and family will:
H foster improved cardiac blood flow
H express understanding of condition and treatment.
H Explain the disorder and its treatment to the patients
parents. Inform them that their child will set his own
exercise limits and will know when to rest.
Monitoring
H Vital signs
H Blue spells
H Oxygenation levels
H Intake and output
Patient teaching
Be sure to cover:
H how to recognize serious hypoxic spells, which can
cause dramatically increased cyanosis; deep, sighing
respirations; and loss of consciousness
H preventing infective endocarditis and other infections, and keeping the child away from people with
infections
H following good dental hygiene, and watching for ear,
nose, and throat infections and dental caries, all of
which require immediate treatment
adverse effects.
Discharge planning
H Refer the patient and family to support and social
services.
H Refer parents to genetic counseling as needed.
Tetralogy of Fallot
813
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Thalassemia
Overview
Description
H A group of genetic disorders characterized by defec-
tive synthesis in one or more of the polypeptide

chains needed for hemoglobin production
H Most commonly occurring as a result of reduced or
absent production of alpha or beta chains
H Affects hemoglobin production and impairs red
blood cell (RBC) synthesis
Pathophysiology
In beta-thalassemia
H The fundamental defect is the uncoupling of alphaand beta-chain synthesis.
H Beta-chain production is depressed moderately in
beta-thalassemia minor and severely in betathalassemia major (also called Cooleys anemia).
H Depression of beta-chain synthesis results in erythrocytes with reduced hemoglobin and accumulations of
free-alpha chains.
H The free-alpha chains are unstable and easily precipitate in the cell; most erythroblasts that contain precipitates are destroyed by mononuclear phagocytes
in the marrow, resulting in ineffective erythropoiesis
and anemia.
H Some precipitate-carrying cells mature and enter the
bloodstream but are destroyed prematurely in the
spleen, resulting in mild hemolytic anemia.
In alpha-thalassemia
H Four forms exist:
Alpha trait (the carrier trait), in which a single
alpha-chain-forming gene is defective
Alpha-thalassemia minor, in which two genes are
defective
Hemoglobin H disease, in which three genes are
defective
Alpha-thalassemia major, in which all four alphachain-forming genes are defective; death is inevitable because alpha chains are absent and
oxygen cant be released to the tissues
Causes
H Inherited autosomal recessive disorder
Incidence
H Second most common cause of microcytic anemia
H Alpha-thalassemia more common in Blacks and
Asians
H Beta-thalassemia more common in Mediterranean
populations
H Anemia
Complications
H Iron overload from RBC transfusions
H Liver failure
H Heart failure
H Death
Assessment
Skull changes in thalassemia major
This illustration of an X-ray shows a characteristic skull
abnormality in thalassemia major: diploetic fibers extending from internal lamina and resembling hair standing on
end.
History
H Severity of anemia and symptoms range from mild to
severe:
Fatigue
Shortness of breath
Headache
Angina
Physical findings
H Pallor or bronze appearance
H Splenomegaly
H Hepatomegaly
H Tachycardia
H Systolic murmur (in moderate or severe anemia)
Test results
Laboratory
H Complete blood count shows decreased hemoglobin,
hematocrit, and mean corpuscular volume.
H Serum iron level is normal or increased.
H Serum ferritin level is normal or increased.
H Total iron-binding capacity is normal.
814
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H Reticulocyte count is normal or increased.

H Hemoglobin electrophoresis shows decreased alpha-
or beta-hemoglobulin chains.
Imaging
H In thalassemia major, X-rays of the skull and long
bones show thinning and widening of the marrow
space because of overactive bone marrow. Long
bones may show areas of osteoporosis. The phalanges may also be deformed (rectangular or biconvex). The bones of the skull and vertebrae may appear granular. (See Skull changes in thalassemia
major.)
Patient teaching
Be sure to cover:
H the importance of good nutrition
H signs and symptoms of iron overload
H follow-up care
H with the parents of a young patient, various options
for healthy physical and creative outlets. Such a child
must avoid strenuous athletic activity. Reassure the
parents that the child may be allowed to participate
in less stressful activities.
Treatment
Discharge planning
General
H Refer the patient to a hematologist.

H Refer the patient for genetic counseling.
H No treatment for mild or moderate forms

H Iron supplements contraindicated in all forms
H Avoidance of iron-rich foods
H Avoidance of strenuous activities
Medications
H Transfusions of packed RBCs
H Chelation therapy, such as desferal and exjade
Surgery
H Splenectomy
H Bone marrow transplantation
Key outcomes
The patient will:
H develop no arrhythmias
the extent possible.
H Administer blood transfusions, and watch for adverse
reactions.
H Provide an adequate diet, and encourage oral fluid
intake.
H Provide emotional support to help the patient and
family cope with the chronic nature of the illness and

the need for lifelong transfusions.
Monitoring
H Transfusion reaction
H Signs and symptoms of iron overload
H Complications
H Anemia symptom severity
Thalassemia
815
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Thrombocytopenia
Physical findings
Overview
H In adults, blood-filled bullae in the mouth
H Petechiae and ecchymoses, along with slow, continu-
ous bleeding from any injuries or wounds
Description
H A deficient number of circulating platelets
H The most common cause of hemorrhagic disorders
Pathophysiology
H Lack of platelets can cause inadequate hemostasis.
H Four mechanisms are responsible: decreased platelet
production, decreased platelet survival, pooling of

blood in the spleen, and intravascular dilation of circulating platelets.
H Megakaryocytes are giant cells in bone marrow that
produce the marrow. Platelet production decreases
when the number of megakaryocytes is reduced or
when platelet production becomes dysfunctional.
Test results
Laboratory
H Platelet count is diminished to less than 100,000/l
in adults.
H Prothrombin and partial thromboplastin times are
normal.
H In severe thrombocytopenia, a bone marrow study
shows the number, size, and cytoplasmic maturity of
the megakaryocytes (bone marrow cells that release
mature platelets); study may show ineffective platelet
production as the cause of thrombocytopenia and be
used to rule out a malignant disease process.
Causes
Treatment
H May be congenital or acquired

H Decreased or defective platelet production in the
General
bone marrow
H Increased platelet destruction outside the marrow
caused by an underlying disorder (such as cirrhosis
of the liver, disseminated intravascular coagulation,
or severe infection)
H Sequestration (hypersplenism, hypothermia) or
platelet loss
H Transient occurrence after a viral infection (such as
Epstein-Barr virus) or infectious mononucleosis
Incidence
H Acquired form more common
H Removal of the offending agents in drug-induced
thrombocytopenia
H Rest periods between activities
H During active bleeding, strict bed rest
Medications
H Platelet transfusions
H Corticosteroids
H Immune globulin
H Immunosuppressants, such as cyclophosphamide
and azathioprine
Surgery
H Sudden onset of petechiae or ecchymoses on skin

H Bleeding into any mucous membrane
H Splenectomy
Complications
In severe thrombocytopenia
H Hemorrhage
H Death
Key outcomes
Assessment
History
H Sudden onset of petechiae and ecchymoses or bleed-
ing into mucous membranes (GI, urinary, vaginal, or

respiratory)
H Malaise, fatigue, and general weakness (with or without accompanying blood loss)
H In acquired thrombocytopenia, possible use of one
or several offending drugs
H Menorrhagia
The patient will:

H incur no injury
H experience no fever, chills, or other signs or symptoms of illness
H demonstrate use of protective measures, energy conservation, a balanced diet, and adequate rest
H Provide rest periods between activities.
H Provide a stool softener if necessary.
H Protect all areas of ecchymosis and petechiae from
further injury.
H Take precautions against bleeding; protect the patient
from trauma.
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H Avoid invasive procedures.

H During active bleeding, maintain strict bed rest; keep
the head of the bed elevated.
Monitoring
H Daily platelet count
H Bleeding
H Ecchymoses and petechiae
H Occult blood in stool, urine, and emesis
H During corticosteroid therapy, fluid and electrolyte
balance and signs and symptoms of infection, pathologic fractures, and mood changes
Patient teaching
Be sure to cover:
H how to recognize and report signs of intracranial
bleeding and other signs of bleeding
H avoidance of straining with stools and coughing, both
of which can lead to increased intracranial pressure
H the function of platelets
H in severe thrombocytopenia, an understanding that
even minor bumps or scrapes may result in bleeding
H how to control local bleeding
H if thrombocytopenia is drug-induced, the importance
of avoiding the offending drug
H if the patient must receive long-term corticosteroid
therapy, the need to watch for and report cushingoid
symptoms and to discontinue corticosteroids gradually
H avoidance of aspirin in any form as well as other
drugs that impair coagulation
H if the patient experiences frequent nosebleeds, using
a humidifier at night
H how to examine the skin for ecchymoses and petechiae
H how to test stools for occult blood
jewelry.
Thrombocytopenia
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Causes
Thrombophlebitis
H Inflammation due to a blood clot
Risk factors
Overview
Description
H Development of a thrombus that may cause vessel oc-
clusion or embolization
H An acute condition characterized by inflammation
and thrombus formation
H May be idiopathic
H Prolonged bed rest
H Trauma
H Surgery
H Pregnancy and childbirth
H Hormonal contraceptives or replacement therapy
such as estrogens
H May occur in deep or superficial veins (see Major
venous pathways of the leg)

H Typically occurs at the valve cusps because venous
stasis encourages accumulation and adherence of

platelet and fibrin
Pathophysiology
H Alteration in epithelial lining causes platelet aggrega-
tion and fibrin entrapment of red blood cells, white

blood cells, and additional platelets.
H The thrombus initiates a chemical inflammatory
process in the vessel epithelium that leads to fibrosis,
which may occlude the vessel lumen or embolize.
Major venous pathways of the leg

Thrombophlebitis can occur in any leg vein. It most commonly occurs at valve sites.
H Neoplasms
H Fracture of the spine, pelvis, femur, or tibia
H Venous stasis
H Venulitis
H Family history of clotting disorder
H Smoking
H Obesity
Incidence
H Increasing with the use of subclavian vein catheters
H Risk for developing deep vein thrombophlebitis dra-
matically increased after age 40
H Tenderness, erythema, and warmth over affected area
H Swelling of affected leg
Complications
H Chronic venous insufficiency
Inferior vena cava

Common iliac
Assessment
External iliac
Common femoral
History
Internal iliac
H Possible tenderness, aching, or severe pain in the af-
fected leg or arm; fever, chills, and malaise
Greater saphenous
Physical findings
Popliteal
H Redness, swelling, and tenderness of the affected leg
Lesser saphenous
or arm
Communicating
(perforator)
Posterior tibial
Anterior tibial
818
Thrombophlebitis
H Asymptomatic in up to 50% of patients with deep vein
thrombophlebitis
Deep femoral
Superficial femoral
H Possible positive Homans sign

H Positive cuff sign
H Possible warm feeling in affected leg or arm
H Lymphadenitis in case of extensive vein involvement
Test results
H Doppler ultrasonography shows reduced blood flow
to a specific area and any obstruction to venous flow,
particularly in iliofemoral deep vein thrombophlebitis.
H Plethysmography shows decreased circulation distal
to the affected area and is more sensitive than ultrasonography in detecting deep vein thrombophlebitis.
H Phlebography confirms the diagnosis and shows filling defects and diverted blood flow.
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Treatment
Patient teaching
General
Be sure to cover:
H the importance of follow-up blood studies to monitor
anticoagulant therapy
H how to give injections (if the patient is being discharged on subcutaneous anticoagulation therapy)
H the need to avoid prolonged sitting or standing to
help prevent a recurrence
H proper application and use of antiembolism stockings
H the importance of adequate hydration
H use of an electric razor and avoidance of products
that contain aspirin.
H Application of warm, moist compresses to the affect-
ed area
H Antiembolism stockings
H Bed rest, with elevation of the affected extremity
Medications
H Anticoagulants
H Thrombolytics
H Analgesics
Surgery
H Simple ligation to vein plication, or clipping
H Embolectomy
H Caval interruption with transvenous placement of a
vena cava filter
Key outcomes
The patient will:
pain
H develop no signs or symptoms of infection.
H Enforce bed rest and elevate the patients affected
arm or leg, but avoid compressing the popliteal

space.
H Apply warm compresses or a covered aquathermia
pad.
H Mark, measure, and record the circumference of the
affected arm or leg daily, and compare this measurement with that of the other arm or leg.
H Administer prescribed anticoagulants.
H Perform or encourage range-of-motion exercises.
H Use pneumatic compression devices.
Monitoring
H Vital signs
H Partial thromboplastin time for patient on heparin
therapy
H Prothrombin time for patient on warfarin
H Signs and symptoms of heparin-induced thrombocy-
topenia
H Signs and symptoms of pulmonary embolism
Thrombophlebitis
819
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Thyroid cancer
Overview
Description
H Proliferation of cancer cells in the thyroid gland
H The most common endocrine malignancy
H Papillary carcinomas: nearly 70% of all cases
H Medullary cancer: may be associated with pheochro-
mocytoma; curable when detected before it causes

symptoms
Pathophysiology
H Papillary cancer is usually multifocal and bilateral. It
metastasizes slowly into regional nodes of the neck,

mediastinum, lungs, and other distant organs. Its the
least virulent form of thyroid cancer.
H Follicular cancer is less common but is more likely
to recur and metastasize to the regional lymph nodes
and spread through blood vessels into the bones, liver, and lungs.
H Medullary (solid) carcinoma originates in the parafollicular cells derived from the last branchial pouch
and contains amyloid and calcium deposits. It can
produce calcitonin, histaminase, corticotropin (producing Cushings syndrome), and prostaglandin E2
and F3 (producing diarrhea). Untreated medullary
cancer grows rapidly, commonly metastasizing to
bones, liver, and kidneys.
H Anaplastic carcinoma (giant and spindly cell cancer)
resists radiation and is almost never curable by resection. This cancer metastasizes rapidly, causing
death by invading the trachea and compressing adjacent structures.
Causes
H Previous exposure to radiation treatment in the neck
area
H Prolonged secretion of thyroid-stimulating hormone
(radiation or heredity)
Risk factors
H Familial predisposition (possibly inherited as an au-
tosomal dominant trait)

H Chronic goiter
Incidence
H 1.2 to 2.6 per 100,000 cases in males
H 2.0 to 3.8 per 100,000 cases in females
H Nearly two times the number of cases in Iceland and
Hawaii compared to Canada and the U.S. mainland

H Particularly common among Chinese males and Fil-
ipino females
H Rare in children
H Painless nodule; hard nodule in an enlarged thyroid
gland
820
Thyroid cancer
H Palpable lymph nodes with an enlarged thyroid

H Hoarseness
H Dysphagia
Complications
H Dysphagia
H Stridor
H Hormone alterations
Assessment
History
H Sensitivity to cold and mental apathy (hypothy-
roidism)
H Sensitivity to heat, restlessness, and overactivity
(hyperthyroidism)
H Diarrhea
H Dysphagia
H Anorexia
H Irritability
H Ear pain
Physical findings
H Hard, painless nodule in an enlarged thyroid gland
or palpable lymph nodes with thyroid enlargement

H Hoarseness and vocal stridor
H Disfiguring thyroid mass
H Bruits
Test results
Laboratory
H Calcitonin assay identifies silent medullary carcinoma. Measuring calcitonin level in a resting state and
during calcium infusion (15 mg/kg over 4 hours)
shows an elevated fasting calcitonin level and an abnormal response to calcium stimulation a higher
release of calcitonin from the node than from the
rest of the gland indicating medullary cancer.
Imaging
H Thyroid scan differentiates functional nodes, which
are rarely malignant, from hypofunctional nodes,
which are commonly malignant.
H Ultrasonography shows changes in the size of thyroid
nodules after thyroxine suppression therapy and is
used to guide fine-needle aspiration and to detect recurrent disease.
H Magnetic resonance imaging and computed tomography scans provide a basis for treatment planning because they show the extent of disease in the thyroid
and surrounding structures.
H Fine-needle aspiration biopsy differentiates benign
from malignant thyroid nodules.
H Histologic analysis stages the disease and thereby
guides treatment plans.
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Treatment
General
H treatments and home care

adverse effects.
H Radioisotope (131I) therapy with external radiation
Discharge planning
(sometimes postoperatively in lieu of radical neck

excision) or alone (for metastasis)
H Soft diet with small frequent meals (if dysphagia
occurs)
services.
Medications
H Suppressive thyroid hormone therapy
H Chemotherapy
Surgery
H Total or subtotal thyroidectomy with modified node
dissection (bilateral or homolateral) on the side of

the primary cancer (for papillary or follicular cancer)
H Total thyroidectomy and radical neck excision (for
medullary or anaplastic cancer)
Key outcomes
The patient will:
H maintain current weight without further loss
H not aspirate
pain.
Before surgery
H Prepare the patient for scheduled surgery.
H Establish a way to communicate postoperatively.
After surgery
H Keep the patient in semi-Fowlers position, with adequate neck support.
H Keep a tracheotomy set and oxygen equipment nearby in case of respiratory obstruction.
Monitoring
H Vital signs
H Wound site
H Pain control
H Serum calcium levels (if the parathyroid glands were
removed)
Patient teaching
Be sure to cover:
H (before surgery) the operation and postoperative
procedures and positioning
Thyroid cancer
821
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Thyroiditis
Tracheal or esophageal compression, necrosis,

and hemorrhage
Overview
Assessment
Description
History
H Several disorders that involve inflammation of the
H Recent viral or bacterial infection

H Disorder, such as systemic lupus erythematosus,
thyroid gland
H Autoimmune (Hashimotos) thyroiditis: the most
common chronic inflammatory disease of the thyroid
gland
H Postpartum thyroiditis: a form of autoimmune thyroiditis that occurs within 1 year of delivery
H Subacute thyroiditis: a transient inflammation of the
thyroid gland thats probably viral in origin
H Riedels thyroiditis: a rare condition with unknown
etiology possibly a variant of Hashimotos thyroiditis
H Supportive thyroiditis: an uncommon bacterial or
fungal infection of the thyroid thats potentially very
serious
H Silent thyroiditis: a transient hyperthyroid condition
characterized by a small painless goiter and may be
autoimmune in origin
Pathophysiology
H The inflammatory process has varying effects on thy-
roid hormone levels (may be low, normal, or high).

Also, lymphocytes and leukocytes may infiltrate thyroid tissue.
H Hashimotos thyroiditis is thought to result from lymphocytic infiltration of the thyroid gland and formation of antibodies to thyroid antigens in the blood.
H Riedels thyroiditis causes intense fibrosis of the thyroid and surrounding structures.
Causes
H Mumps
H Influenza, coxsackievirus, or adenovirus infections
H Tuberculosis
H Syphilis
H Actinomycosis
H Sarcoidosis and amyloidosis
Incidence
H Autoimmune thyroiditis most common in middle-age
females; most common cause of sporadic goiter in

children
H Signs and symptoms of hyperthyroidism or hypothy-
roidism
Complications
H Depending on type of inflammation:
Non-Hodgkins lymphoma of the thyroid gland

Permanent hypothyroid or hyperthyroid condition
Abscess formation and rupture
822
Thyroiditis
rheumatoid arthritis, pernicious anemia, or Graves

disease
H Gradual onset of hypothyroid-like symptoms
H Occasionally, symptoms of hyperthyroidism
H Local pain or pain referred to the lower jaw, ear, or
occiput
H Dysphagia
H Dyspnea
H Asthenia, malaise
Physical findings
H Enlargement of the thyroid gland (goiter)
H Reddened skin over the thyroid gland
H Indurated neck tissues
H Small, firm, and finely nodular thyroid gland with a
characteristic bandlike depression circling the gland

H A small lymph node in the midline above the isthmus
H Nodularity
H Swelling and warmth of the overlying skin
H Woody, hard enlargement that feels anchored to
surrounding structures
H Stridor
Test results
Laboratory
H In autoimmune processes, serum thyroglobulin and
microsomal antibody levels are increased.
HASHIMOTOS THYROIDITIS
H Thyroid-stimulating hormone (TSH) level is in-
creased.
H Triiodothyronine and thyroxine levels are normal or
decreased.
H Antimicrosomal and antithyroglobulin antibodies are
increased.
SUBACUTE THYROIDITIS
H Thyroid hormone levels may be elevated, suppressed,
or normal depending on the phase of the disorder.

H Protein-bound iodine levels are increased.
H TSH levels are decreased in the thyrotoxic phase, fail-
ing to respond to thyrotropin-releasing hormone; in

the hypothyroid phase, TSH levels are increased.
H Radioactive iodine (131I) uptake is decreased.
H Erythrocyte sedimentation rate, white blood cell
count, and hepatic enzyme levels are increased.
H Thyroid antibody levels are transiently low.
H Thyroglobin levels are increased.
RIEDELS THYROIDITIS
H 131I uptake is normal or decreased.
H Antimicrosomal antibody levels are increased.
Imaging
H Thyroid scan may show isolated areas of function or
total failure to visualize the gland.
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H Fine-needle thyroid gland biopsy offers histologic
confirmation.
Monitoring
Treatment
H Vital signs
H Intake and output
H Daily weight
H Signs and symptoms of hyperthyroidism or hypothy-
General
H Neck circumference
H Varies with the type of thyroiditis

Medications
H Thyroid hormone
H Analgesics
H Anti-inflammatories
H Corticosteroids
H Antibiotics
roidism
Patient teaching
Be sure to cover:
adverse effects
H signs and symptoms of respiratory distress
H signs and symptoms of hyperthyroidism and hypothyroidism
H long-term hormone replacement therapy after
thyroidectomy
H the importance of wearing or carrying medical
identification.
Key outcomes
Discharge planning
The patient will:

H consume adequate calories daily
Surgery
H Partial thyroidectomy
additional counseling if indicated.
H Elevate the head of the bed 90 degrees during meal-
times and for 30 minutes afterward.

H Keep suction equipment readily available.
H Consult a dietitian.
H Help develop effective coping strategies.
ALERT
After thyroidectomy, watch for signs of tetany secondary to accidental parathyroid injury during
surgery. Keep 10% calcium gluconate available for
I.V. use if needed. Check dressings frequently for
excessive bleeding. Watch for signs of airway obstruction, such as difficulty talking or increased
swallowing, and keep tracheotomy equipment
handy.
Thyroiditis
823
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Page 824
Tobacco abuse
Overview
Description
H Addiction to nicotine, the drug in tobacco
H Effects on the brain similar to heroin, morphine, and
cocaine
H Includes cigarettes, cigars, pipe tobacco, snuff, and
chewing tobacco
H Results in withdrawal symptoms when a person tries
to stop using tobacco
H Harmful effects of tobacco products dose-dependent
Pathophysiology
H Rapid absorption of nicotine through the lungs of
H Female smokers: generally have earlier menopause
H Important events given up because of restrictions of
tobacco use
H Continued tobacco use despite negative conse-
quences
H Cravings of tobacco
H Large amounts of time spent using tobacco
H Tolerance to nicotine effects
H Withdrawal symptoms: increased anger, hostility, and
aggression; disturbed emotional equilibrium following stress; impairment across a wide range of psychomotor and cognitive functions such as difficulty
with concentration
Complications
H Cardiovascular diseases: coronary artery disease, pe-
ripheral vascular disease, and stroke
cigarette smokers; bolus of nicotine reaches the

brain within 10 to 16 seconds.
H Equally fast absorption through the oral mucosa of
cigar, pipe, and smokeless tobacco users.
H In the brain, nicotine activates nicotinic acetylcholine
receptors, leading to the release of dopamine and a
discharge of epinephrine from the adrenal cortex.
H Stimulation of the central nervous system and endocrine glands causes a sudden release of glucose,
followed by depression and fatigue; leads the user to
seek more nicotine.
H Cancers of the head and neck, lung, and GI tract

H Chronic lung disease
H Hypertension
H Oral cancer
H Oral leukoplakia
H Nicotine palatinus stomatitis
H Smokeless tobacco keratosis
H Gingivitis
H Periodontitis
H Sinusitis
Causes
Assessment
H Physiologic and psychological dependence

H Pervasive media messages about tobacco use
H Minimization of risks of smoking
H Perception that smoking helps with relaxation
H Other drug or alcohol use
H Mental illnesses, such as depression or anxiety
Risk factors
H Addictive personality
H A friend who was a substance abuser
H Family members who smoke or with other addictions
H In adolescents, average to below average school per-
formance and divorce or family conflict
Incidence
H 25% to 33% of adult males and females smoking
H Numbers expected to diminish to 15% to 20% over
the next 30 years
History
H Use of tobacco products
H Inability to successfully stop using tobacco
Physical findings
H Increased pulse rate
H Cough
Test results
Imaging
H Chest X-ray shows chronic changes related to smoking.
Other
H Nicotine dependence assessment tool, such as the
Nicotine Dependence Syndrome Scale, shows the
level of addiction.
H Rates in adolescents showing a gradual increase
since 1987
H About 5 million smokers in the United States: be-
tween ages 12 and 17; more than 500,000: between

ages 8 and 11
H During the past 40 years: cigarette smoking caused
an estimated 12 million deaths, including 4.1 million
deaths from cancer, 5.5 million deaths from cardiovascular diseases, 2.1 million deaths from respiratory diseases, and 94,000 infant deaths related to
mothers smoking during pregnancy
824
Tobacco abuse
Treatment
General
H Motivation to stop using tobacco
H Behavioral counseling
H Skills training to overcome high-risk situations
H Psychological support
H Alternative rewards and reinforcers
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Page 825
Medications
H Nicotine replacement therapy in the form of nicotine
gum, lozenges, patches, nasal sprays, and inhalers

H Antidepressants
H Bupropion (Zyban)
H Clonidine (Catapres)
H Nortriptyline (Pamelor)
Key outcomes
The patient will:
H express a desire to stop abusing tobacco
H identify risks associated with tobacco abuse
H demonstrate improved physical health and function
H verbalize an improved sense of well-being and mental health
H develop a plan to stop abusing tobacco.
H Assess the patients attitude toward tobacco abuse.
H Be supportive and remain nonjudgmental.
H Advise the patient about health risks and effective
cessation methods.
H Assist the patient in developing a plan to quit.
H Suggest motivational strategies for quitting.
H Help the patient identify ways to avoid weight gain af-
ter stopping smoking.

groups.
H Arrange for follow-up care.
Monitoring
H Prescribed medications and possible adverse effects
H Vital signs
H Psychological and emotional response
Patient teaching
Be sure to cover:
H the risks of second-hand smoke
H withdrawal symptoms and ways to reduce their effects
H strategies to improve chance of successful quitting
H where to obtain support.
Tobacco abuse
825
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Tonsillitis
Overview
Description
H Headache
H Pain, commonly referred to the ears
H Constant urge to swallow
H Constricted feeling in the back of the throat
Physical findings
H Inflammation of the tonsils

H Typical viral infection: mild and of limited duration
H Fever
H Swollen, tender submandibular lymph nodes
H Generalized inflammation of pharyngeal wall
H Swollen tonsils projecting from between the pillars
Pathophysiology
H Purulent drainage with application of pressure to
H The inflammatory response to cell damage by viruses
or bacteria results in hyperemia and fluid exudation.
of the fauces and exuding white or yellow follicles

tonsillar pillars
H Uvula possibly edematous and inflamed
Causes
Test results
H Bacterial infection (group A beta-hemolytic strepto-
Laboratory
H Throat culture reveals the infecting organism.
H Serum white blood cell count usually reveals leukocytosis.
cocci)
H Viral infection
Risk factors
H Close contact with others in school or child care
facility
Incidence
Special populations
Commonly affects children between ages 5 and 10
H Tonsils tending to hypertrophy during childhood and
atrophy after puberty
Treatment
General
H Symptom relief
H Rest periods as needed
Medications
H Aspirin or acetaminophen
H Antibiotics
Surgery
H Sore throat
H Enlarged tonsils
H Possible tonsillectomy
Complications
H Chronic upper airway obstruction

H Sleep disturbance, sleep apnea
H Cor pulmonale
H Failure to thrive
H Eating or swallowing disorders
H Speech abnormalities
H Febrile seizures
H Otitis media
H Cardiac valvular disease
H Peritonsillar abscesses
H Bacterial endocarditis
H Cervical lymph node abscesses
Assessment
History
H Mild to severe sore throat
H Young child possibly stops eating
H Muscle and joint pain
H Chills
H Malaise
826
Tonsillitis
Key outcomes
The patient will:
H show no signs of aspiration
H maintain effective breathing pattern
H have balanced intake and output.
H Encourage oral fluids.
H Offer a child ice cream and flavored drinks and ices.
H Encourage gargling to soothe the throat and remove
debris from tonsillar crypts.

After surgery
H Watch for signs of airway obstruction or bleeding,
such as difficulty talking or increased swallowing.
H Prevent aspiration by side positioning.
H Keep suction equipment readily available.
H Provide water after gag reflex returns.
H Later, encourage nonirritating oral fluids.
H Avoid milk products and salty or irritating foods.
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H Provide analgesics for pain relief.

H Encourage deep-breathing exercises.
Monitoring
H Hydration status
H Effect of pain medication
Before surgery
After surgery
H Vital signs
ALERT
Immediately report excessive bleeding, increased
pulse rate, or decreasing blood pressure.
ALERT
The greatest risk of bleeding is 7 to 10 days after
surgery.
Patient teaching
Be sure to cover:
H the importance of completing the entire course of
antibiotics
H avoidance of irritants
H the need for soft foods for about 3 weeks after
surgery to decrease risk of rebleeding
adverse effects
H the possibility of throat discomfort and some bleeding after surgery
H expectation of a white scab to form in the throat 5 to
10 days after surgery
H the need to report bleeding, ear discomfort, or a
fever that lasts 3 days or more.
Tonsillitis
827
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H Half of all cases in settings other than menstruation

H Affects both sexes and all ages
Toxic shock syndrome
Overview
H Menstruation (the most common setting for TSS)

H Bacteremia (in about 60% of patients)
Description
Complications
H An inflammatory response syndrome linked to bacte-
H Septic abortion
H Musculoskeletal and respiratory infections
H Staphylococcal bacteremia
H Renal and myocardial dysfunction
H Desquamation of the skin
H Peripheral gangrene
H Muscle weakness
H Neuropsychiatric dysfunction
H In the early convalescent period: fever, hypotension,
rash, multiorgan dysfunction, and desquamation
rial infections
H An acute and life-threatening condition
H Also called TSS
Pathophysiology
H Toxic exoproteins are produced by infecting organ-
isms.
H TSST-1 is the most common toxin; staphylococcal
enterotoxin B is the second most common.

H For illness to develop, the patient must be infected
with a toxigenic strain of Staphylococcus aureus and

lack antibodies to that strain.
Causes
H Penicillin-resistant S. aureus
Risk factors
H Tampon use
H Varicella infection
H Streptococcal pharyngitis
Incidence
H Affects 1 in 100,000
H Primarily affects young people
Guidelines for diagnosing toxic shock

syndrome
Toxic shock syndrome is typically diagnosed based on the
following criteria.
H Fever 102 F (38.9 C) or higher
H Diffuse macular erythrodermal rash (sunburn rash)
H Hypotension (systolic blood pressure 90 mm Hg or
less in adults or below the 5th percentile for age)
H Involvement of at least three organ systems:
GI (vomiting, diarrhea)
Muscular (myalgias or liver function test at least
twice normal upper limit)
Mucous membrane hyperemia (conjunctiva, vagina,
oropharyngeal)
Renal (blood urea nitrogen or creatinine level at least
twice normal upper limit, or pyuria)
Hepatic (total serum bilirubin or aminotransferase
level twice normal level)
Hematologic (thrombocytopenia)
Central nervous system (disorientation or change in
level of consciousness)
H Desquamation, especially of palms and soles, 1 or 2
weeks after onset of illness
H Other conditions ruled out
828
Assessment
History
H Possible recent streptococcal infection
H Possible tampon use or menstruation
H Intense myalgia, headache
H Sore throat
H Dizziness
Physical findings
H Fever (104 F [40 C] or higher)
H Pharyngeal infection, strawberry tongue
H Hypotension
H Altered mental status
H Macular erythroderma (generalized or local)
H Peripheral edema
H Vaginal hyperemia, purulent vaginal discharge
Test results
Laboratory
H Isolation of S. aureus from vaginal discharge or infection site supports the diagnosis. (See Guidelines
for diagnosing toxic shock syndrome.)
H Blood urea nitrogen examination shows azotemia.
H Urinalysis shows pyuria.
H Serum albumin levels reveal hypoalbuminemia.
H Serum calcium levels reveal hypocalcemia.
H Serum phosphorus levels reveal hypophosphatemia.
H Complete blood count shows leukocytosis or
leukopenia.
H Platelet count shows thrombocytopenia.
H Serum creatinine level is increased.
Treatment
General
H Aggressive fluid resuscitation
H Correction of electrolyte imbalances
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H Supportive treatment such as possible ventilatory
support
H Identification and decontamination of toxin produc-
tion site
H Bed rest until acute phase resolved
Medications
H Antibiotics
H Inotropics
H Vasopressors
H I.V. immunoglobulin
Prevention
Preventing TSS
Toxic shock syndrome (TSS) may be prevented by following these guidelines:
H Wash your hands before inserting a tampon.
H Change tampons every 4 to 8 hours.
H Use the lowest absorbency tampon necessary for your
menstrual flow.
H Alternate between tampons and sanitary napkins.
H Dont use tampons if you have had TSS because of the
risk of recurrence.
Surgery
H Examination and irrigation of recent surgical wounds
Key outcomes
The patient will:
H attain and maintain hemodynamic stability
H remain afebrile
H Assess fluid balance and replace fluids I.V., as
needed.
H Reorient as needed.
H Use appropriate safety measures to prevent injury.
H Use standard precautions for any vaginal discharge
and lesion drainage.
Monitoring
H Neurologic status
H Vital signs
H Pulmonary status
H Complications
Patient teaching
Be sure to cover:
H TSS prevention. (See Preventing TSS.)
829
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Toxoplasmosis
H Chemotherapy
H Steroid use
H Pregnancy
Overview
Incidence
Description
H Up to 70% of people in United States infected

H Occurs worldwide; less common in cold or hot, arid
H One of the most common parasitic infectious dis-
eases
H Usually causes localized infection
H May produce significant generalized infection, especially in an immunodeficient patient
H Once infected, organism carried for life and acute infection can reactivate
H Congenital type characterized by lesions in the central nervous system (CNS); may result in stillbirth or
serious birth defects
Pathophysiology
H After ingestion, parasites are released from latent
cysts by the digestive process; they then invade the GI

tract and multiply.
H Parasites disseminate to various organs, especially
lymphatic tissue, skeletal muscle, myocardium, retina, placenta, and the CNS (most commonly).
H The parasite infects host cells, replicates, and then
invades adjoining cells, resulting in cell death and focal necrosis surrounded by an acute inflammatory
response.
Causes
H The protozoan Toxoplasma gondii, which exists in
trophozoite forms in the acute stages of infection and

in cystic forms (tissue cysts and oocysts) in latent
stages
H Transmitted by ingestion of tissue cysts in raw or undercooked meat or by fecal-oral contamination from
infected cats
H Congenital toxoplasmosis from transplacental transmission
Risk factors
H Human immunodeficiency virus and acquired
immunodeficiency syndrome
H Immunosuppression
climates and at high elevations
H Fever
H Rash
H Constitutional symptoms
Complications
H Seizure disorder
H Vision loss (see Ocular toxoplasmosis)
H Deafness
H Generalized infection
H Stillbirth
H Congenital toxoplasmosis
H Death
Assessment
History
H Possible immunocompromised state, exposure to cat
feces, or ingestion of poorly cooked meat

H Malaise
H Fatigue
H Myalgia
H Headache
H Sore throat
H Vomiting
Physical findings
H Fever (if generalized, possibly 106 F [41.1 C])
H Cough
H Dyspnea
H Cyanosis
H Coarse crackles
H Delirium, seizures
H Diffuse maculopapular rash (except on the palms,
soles, and scalp)
Ocular toxoplasmosis
Ocular toxoplasmosis (active chorioretinitis) is characterized by focal necrotizing retinitis. It accounts for about
25% of all cases of granulomatous uveitis. Although usually the result of a congenital infection, it may not appear
until adolescence or young adulthood, when infection is
reactivated.
Symptoms include blurred vision, scotoma, pain, photophobia, and impairment or loss of central vision. Vision
improves as inflammation subsides but usually without
recovery of lost visual acuity. Ocular toxoplasmosis may
subside after treatment with prednisone.
830
Toxoplasmosis
H In an infant with congenital toxoplasmosis:
Hydrocephalus or microcephalus
Jaundice, purpura, rash
Strabismus, blindness
Epilepsy, mental retardation
Lymphadenopathy, splenomegaly, and hepatomegaly
Test results
Laboratory
H Specimens (such as bronchoalveolar lavage material
from immunocompromised patients or lymph node
biopsy) contain parasites.
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H Intraperitoneal inoculation with blood or other body
fluids into mice or tissue cultures shows isolation of

parasites.
H Polymerase chain reaction detects parasites genetic
material (especially in detecting congenital infections
in utero).
Treatment
General
H No treatment in otherwise healthy patient who isnt
pregnant
H Seizure precautions
Medications
H Pyrimethamine plus sulfadiazine with leucovorin
Key outcomes
Prevention
Preventing toxoplasmosis
Toxoplasmosis may be prevented by following these
guidelines:
H Wash your hands after working with soil or uncooked
meat.
H Cook meat thoroughly before eating.
H Freeze uncooked meat if not using promptly.
H Protect childrens play areas from cat and dog feces.
H Cover childrens sandboxes.
H Keep flies away from food because flies transport
oocysts.
H Pregnant women should avoid cleaning and handling
cat litter boxes or wear gloves.
H ways to prevent the spread of toxoplasmosis. (See
Preventing toxoplasmosis.)
Discharge planning
H Refer the patient for follow-up with a neurologist or
infectious disease specialist if needed.
The patient will:

H have an adequate fluid volume
H report an increased energy level
baseline.
H Give tepid sponge baths to reduce fever.
H Provide chest physiotherapy, and administer oxygen,
as needed. Assist ventilations if needed.

ALERT
Dont palpate the patients abdomen vigorously;
this could lead to a ruptured spleen. For the same
reason, discourage vigorous activity.
H Report all cases of toxoplasmosis to the local public
health department.
Monitoring
H Neurologic status
H Complications
Patient teaching
Be sure to cover:
H necessary drugs, including the need for frequent
blood tests
H the importance of regularly scheduled follow-up care
Toxoplasmosis
831
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Genitourinary abnormalities
Intestinal atresia
Tracheoesophageal
fistula and
esophageal atresia
Overview
Description
H Tracheoesophageal fistula: a developmental anomaly
characterized by an abnormal connection between

the trachea and the esophagus; usually accompanies
esophageal atresia, in which the esophagus is closed
off at some point
H Malformations have numerous anatomic variations,
most commonly, esophageal atresia with fistula to
the distal segment
H Two of the most serious surgical emergencies in
neonates; requires immediate diagnosis and
correction
Pathophysiology
H Tracheoesophageal fistula and esophageal atresia re-
sult from failure of the embryonic esophagus and trachea to develop and separate correctly.
H Respiratory system development begins at about day
26 of gestation.
H Abnormal development of the septum during this
time can lead to tracheoesophageal fistula.
H The most common abnormality is type C tracheoesophageal fistula with esophageal atresia, in which
the upper section of the esophagus terminates in a
blind pouch, and the lower section ascends from the
stomach and connects with the trachea by a short
fistulous tract.
H In type A atresia, both esophageal segments are blind
pouches, and neither is connected to the airway.
H In types B and D, the upper portion of the esophagus opens into the trachea; infants with this anomaly
may experience life-threatening aspiration of saliva
or food.
H In type E (or H-type) tracheoesophageal fistula without atresia, the fistula may occur anywhere between
the level of the cricoid cartilage and the midesophagus but is usually higher in the trachea than in the
esophagus. Such a fistula may be as small as a pinpoint.
Causes
H Congenital anomalies
Risk factors
H Commonly found in infants with other anomalies,
such as:
Congenital heart disease
Imperforate anus
832
Incidence
H Esophageal atresia in about 1 of 4,000 live births;
about one-third of these neonates born prematurely
Tracheoesophageal fistula
H Type B (proximal fistula) and Type D (fistula to both
segments): immediate aspiration of saliva into the
airway and bacterial pneumonitis
H Type E (or H-type): suspected with repeated episodes
of pneumonitis, pulmonary infection, and abdominal
infection; choking followed by cyanosis
Esophageal atresia
H Type A: normal swallowing, excessive drooling, possible respiratory distress
H Type C: seemingly normal swallowing followed shortly afterward by coughing, struggling, cyanosis, lack of
breathing
Complications
H Aspiration of secretions into the lungs leading to res-
piratory distress, pneumonia, or cessation of breathing

H Death if untreated
After surgery
H Abnormal esophageal motility
H Recurrent fistulas
H Pneumothorax
Assessment
History
H Coughing and choking after eating
Physical findings
H Drooling
Test results
Imaging
H Chest X-rays demonstrate the position of the catheter
and can also show a dilated, air-filled upper esophageal pouch, pneumonia in the right upper lobe, or
bilateral pneumonitis. Both pneumonia and pneumonitis suggest aspiration.
H Abdominal X-rays show gas in the bowel in a distal
fistula (type C) but none in a proximal fistula (type
B) or in atresia without fistula (type A).
H Cinefluorography allows visualization on a fluoroscopic screen. After a size 10 or 12 French catheter
is passed through the patients nostril into the esophagus, a small amount of contrast medium is instilled
to define the tip of the upper pouch and to differentiate between overflow aspiration from a blind end
(atresia) and aspiration from passage of liquids
through a tracheoesophageal fistula.
Tracheoesophageal fistula and esophageal atresia
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Other
H A size 6 or 8 French catheter passed through the
nose meets an obstruction (esophageal atresia)
about 4 to 5 (10 to 12.5 cm) distal to the nostrils.
Aspirate of gastric contents is less acidic than normal.
H Administer antibiotics and parenteral fluids.

H Maintain gastrostomy tube feedings.
H Offer the parents support and guidance in dealing
with their infants acute illness. Encourage them to

participate in care and to hold and touch the infant
as much as possible to facilitate bonding.
Monitoring
Treatment
H Intake and output
General
After surgery
H Chest tubes
H I.V. fluids
H Supine position with the head low to facilitate
drainage or with the head elevated to prevent aspiration

H After surgery: placement of a suction catheter in the
upper esophageal pouch to control secretions and
prevent aspiration
Medications
H Antibiotics for superimposed infection
Surgery
Tracheoesophageal fistula and esophageal atresia require surgical correction and are usually surgical emergencies. The type and timing of the surgical procedure
depend on the nature of the anomaly, the patients general condition, and the presence of coexisting congenital defects.
H In premature neonates (nearly 33% of infants with
this anomaly) who are poor surgical risks: correction of combined tracheoesophageal fistula and
esophageal atresia done in two stages: first, gastrostomy (for gastric decompression, prevention of reflux, and feeding) and closure of the fistula; then, 1
to 2 months later, anastomosis of the esophagus
H Correction of esophageal atresia alone requiring
anastomosis of the proximal and distal esophageal
segments in one or two stages; end-to-end anastomosis commonly producing postoperative stricture;
end-to-side anastomosis less likely to do so
H If the esophageal ends widely separated: treatment
possibly including a colonic interposition (grafting a
piece of the colon) or elongation of the proximal
segment of the esophagus by bougienage
Patient teaching
Be sure to cover:
H feeding procedures
H recognizing and reporting complications
H proper positioning.
Discharge planning
H Instruct the parents that X-rays are required about 10
days after surgery, and again 1 and 3 months later, to

evaluate the effectiveness of surgical repair.
Key outcomes
The patient will:
H develop no respiratory complications
H remain hemodynamically stable.
The parents or family will:
H Administer oxygen as needed.
H Perform pulmonary physiotherapy and suctioning, as
needed.
H Provide a humid environment.
Tracheoesophageal fistula and esophageal atresia
833
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Transient ischemic
attack
Overview
Description
H Sudden onset of focal and transient neurologic deficit
due to brain ischemia

H Vascular (occlusive) in origin
H Rapid in onset; typically reaching maximum effect in
less than 5 minutes
H Headaches
H Confusion
H Vertigo
H Ataxia
H Facial paresis
H Nausea or vomiting
Complications
H Stroke
H Seizure
H Bleeding as a result of anticoagulants
H Trauma (if patient experiences a sudden fall)
H Variable duration; usually lasting 2 to 15 minutes;
Assessment
possibly lasting as long as 24 hours

H Also known as TIA
History
Pathophysiology
H Cerebral blood flow is temporarily reduced or
stopped.
H This affects neuronal function in cortical, subcorti-
cal, and nuclear regions of the central nervous system.
Causes
H Carotid and vertebral artery atherosclerosis
H Hypertension
H Embolism
H Arterial dissection
H Arteritis
H Mitral valve disease
H Acute anterior myocardial infarction
H Congestive cardiomyopathy
H Hypercoagulable states
H Sympathomimetic drugs such as cocaine
Risk factors
H Hypertension
H Cardiac disease
H Smoking
H Diabetes
H Obesity
H Family history
H Pregnancy and parturition
Incidence
H From 83 to 200 cases per 100,000
H Significantly higher in Blacks than in Whites
H Affects males at higher rates than females
H Uncommon in people younger than age 60
H Vision changes
H Hemiplegia
H Hemianesthesia
H Aphasia
834
Transient ischemic attack
H Include family members, coworkers, witnesses, and
emergency medical services personnel in questioning, if possible

H Reports of changes in behavior, speech, gait, memory, movement, and vision
H Symptoms lasting only several minutes
H Recent surgery
H Previous strokes
H Use of illicit drugs
H Complete medication regimen
H May have vague complaints of feeling short of breath;
possibly preceded by palpitations or slight chest
pain; followed by inability to speak properly and facial droop
H History of arteritis
Physical findings
H Low-grade fever
H Decreased peripheral pulses compared to the apical
pulse
H Carotid bruit
H Possibly poor language and memory skills
H Unequal pupil reaction to direct and consensual light
exposure
H Diminished cranial nerve response
H Decreased somatic motor strength
H Forehead wrinkling asymmetry
H Incomplete eyelid closure
H Asymmetrical mouth retraction
H Swallowing difficulty
H Lateral tongue movement
H Weak shoulder shrugging
H Visual field deficits
Test results
Laboratory
H Partial thromboplastin time may be decreased.
H Antiphospholipid antibodies are elevated.
H Platelet count may be elevated.
H Cholesterol levels are elevated.
H Elevated D-dimer shows hypercoagulability.
H Drug screens show illicit drug use.
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Imaging
H Duplex carotid ultrasonography shows narrowed arteries.
H Angiography shows cerebral or carotid artery stenosis.
H Transthoracic echocardiogram shows thrombus or
structural defect.
H Computed tomography scan of head identifies cause
of TIA.
H Brain magnetic resonance imaging identifies cause of
TIA.
H Magnetic resonance angiography of the brain or
blood vessels shows cause of TIA.
H Electrocardiography identifies underlying arrhythmia.
H Ophthalmoscopic examination shows retinal cholesterol emboli.
Treatment
General
H Maintaining patent airway and providing supplemen-
tal oxygen
Medications
H Aspirin or other antithrombotic therapy, such as
clopidogrel and dipyridamole

H Statins
H Anticoagulants
H Assess motor function.

H Maintain a safe environment.
H Assess the impact of TIAs on all systems and func-
tions of the body.

H Assess the impact of TIAs on psychosocial issues,
body image, and self-esteem.

H If swallowing ability is impaired, avoid giving thin liq-
uids.
Monitoring
H Vital signs
H Adverse reaction to medication
H Coagulation studies
H Neurologic status
Patient teaching
Be sure to cover:
H medication administration, dosage, and possible adverse effects, and the need to report them
H antiplatelet therapy, if indicated
H control of risk factors (see Preventing TIAs)
H dietary modification
H measures to maintain a safe environment
H importance of reporting a change in neurologic status.
Surgery
H Carotid endarterectomy
Key outcomes
The patient will:
H verbalize understanding of the condition, diagnostic
studies, treatment, and risk factors
H demonstrate effective ways to cope with sensory limitations
H achieve the maximum visual ability possible
H maintain optimum cerebral tissue perfusion
H remain free from injury and falls
H remain free from peripheral neurovascular impairment.
H Evaluate using a stroke scale such as National Insti-
tutes of Health Stroke Scale.

H Assess level of consciousness, mental status, and cog-
nition.
H Assess speech, facial symmetry, and sensory function.
H If speech is affected, provide alternative methods for
communication.
Prevention
Preventing TIAs
Transient ischemic attack (TIA) risk factors may be reduced by following these guidelines:
H Stop smoking.
H Avoid cholesterol and fat.
H Eat fruits and vegetables that contain potassium, folate
and antioxidants, which may protect against TIA.
H Avoid salt if you have hypertension.
H Exercise regularly.
H Drink alcohol moderately or not at all.
H Maintain a healthy weight.
H Manage diabetes and hypertension.
H Dont use cocaine or other illicit drugs that will increase your risk of TIA.
H Assess pupil reaction to light.
Transient ischemic attack
835
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Transposition of the
great arteries
Complications
Overview
H Heart failure
H Eisenmengers syndrome (irreversible and progres-
Description
H Congenital heart defect in which the great arteries
are reversed: aorta arising from right ventricle and

pulmonary artery from left ventricle, producing two
noncommunicating circulatory systems (pulmonary
and systemic)
H Commonly coexists with other congenital heart defects, such as ventricular septal defect (VSD), VSD
with pulmonary stenosis (PS), atrial septal defect
(ASD), and patent ductus arteriosus (PDA)
Pathophysiology
H In transposition, oxygenated blood returning to the
left side of the heart is carried back to the lungs by a

transposed pulmonary artery; unoxygenated blood
returning to the right side of the heart is carried to
the systemic circulation by a transposed aorta.
H Communication between the pulmonary and systemic
circulations is necessary for survival. In infants with
isolated transposition, blood mixes only at the patent
foramen ovale and at the patent ductus arteriosus,
resulting in slight mixing of unoxygenated systemic
blood and oxygenated pulmonary blood.
H In infants with concurrent cardiac defects, greater
mixing of blood occurs.
Causes
H Faulty embryonic development
Risk factors
H Maternal rubella or other viral illness during preg-
nancy
H Parent with transposition of the great arteries or oth-
er congenital heart defect

H Poor prenatal nutrition
H Prenatal alcohol exposure
H Maternal age older than 40
H Maternal diabetes
Incidence
H Accounts for about 5% of all congenital heart defects
H Affects males two to three times more than females
H Within the first few hours after birth, neonates with
transposition of the great arteries generally show

cyanosis and tachypnea, which worsen with crying.
H After several days or weeks, such neonates usually
develop signs of heart failure (gallop rhythm, tachycardia, dyspnea, hepatomegaly, and cardiomegaly).
S2 is louder than normal because the anteriorly
transposed aorta is directly behind the sternum; in
836
Transposition of the great arteries
many cases, however, no murmur can be heard during the first few days of life.
sive pulmonary vascular obstructive disease)
Assessment
History
H Diminished exercise tolerance
H Fatigability
H Coughing
Physical findings
H Cyanosis
H Clubbing of nailbeds
H Pronounced murmurs if ASD, VSD, PDA, or PS
present
Test results
Laboratory
H Arterial blood gas (ABG) values indicate hypoxia and
secondary metabolic acidosis.
Imaging
H Chest X-rays are normal in the first days of life. Within days to weeks, right atrial and right ventricular enlargement characteristically cause the heart to appear oblong. X-rays also show increased pulmonary
vascular markings, except when pulmonary stenosis
coexists.
H Echocardiography demonstrates the reversed position of the aorta and pulmonary artery and records
echoes from both semilunar valves simultaneously,
due to aortic valve displacement. It also detects other
cardiac defects.
H Electrocardiography typically reveals right axis deviation and right ventricular hypertrophy; it may be normal in a neonate.
H Cardiac catheterization reveals decreased oxygen saturation in left ventricular blood and aortic blood; increased right atrial, right ventricular, and pulmonary
artery oxygen saturation; and right ventricular systolic pressure equal to systemic pressure. Dye injection reveals the transposed vessels and the presence
of any other cardiac defects.
Treatment
General
H Atrial balloon septostomy (Rashkind procedure)
during cardiac catheterization

H Increased caloric density before correction; no di-
etary restrictions after correction

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Medications
Discharge planning
H Inotropic agents
H Loop diuretics
H Prostaglandin E1
services as needed.
Surgery
One of three surgical procedures can correct transposition, depending on the defects physiology:
H Mustard procedure: replaces the atrial septum with a
Dacron or pericardial partition that allows systemic
venous blood to be channeled to the pulmonary
artery, which carries the blood to the lungs for oxygenation and oxygenated blood returning to the heart
to be channeled from the pulmonary veins into the
aorta
H Senning procedure: accomplishes the same result using the atrial septum to create partitions to redirect
blood flow
H Arterial switch, or Jatene procedure: transposed arteries surgically anastomosed to the correct ventricle;
for this procedure to be successful, the left ventricle
must be used to pump at systemic pressure, as it
does in neonates or in children with a left ventricular
outflow obstruction or large VSD; surgery also correcting other heart defects
Key outcomes
The patient will:
H improve oxygenation
H have no signs of heart failure.
H Give digoxin and I.V. fluids, being careful to avoid
fluid overload.
H After Mustard or Senning procedures, watch for signs
of baffle obstruction such as marked facial edema.
Monitoring
H Vital signs
H ABG values
H Intake and output
Patient teaching
H how to recognize signs of heart failure and digoxin
toxicity (poor feeding and vomiting)
H the importance of regular checkups to monitor cardiovascular status
H protecting the infant from infection and giving antibiotics.
Transposition of the great arteries
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Trichinosis
Overview
Description
H An infection caused by larvae of the intestinal round-
worm Trichinella spiralis

H May produce multiple symptoms, such as respiratory,
central nervous system (CNS), cardiovascular complications and, rarely, death

H Also known as trichiniasis or trichinellosis
Pathophysiology
H T. spiralis cysts are found primarily in swine, less
commonly in dogs, cats, bears, foxes, wolves, and

marine animals. These cysts result from the animals
ingestion of similarly contaminated flesh. In swine,
such infection results from eating table scraps or raw
garbage.
H After gastric juices free the worm from the cyst capsule, it reaches sexual maturity in a few days.
H The female roundworm burrows into the intestinal
mucosa and reproduces.
H Larvae are then transported through the lymphatic
system and the bloodstream. They become embedded as cysts in striated muscle, especially in the diaphragm, chest, arms, and legs.
H Human-to-human transmission doesnt take place.
Causes
H Ingestion of uncooked or undercooked meat that
contains T. spiralis cysts
Risk factors
H Residing in a rural area
H Eating wild or noncommercial meats
H Improper food preparation
Incidence
H Occurs worldwide, especially in populations that eat
pork or bear meat

H Usually mild and seldom produces symptoms; when
symptoms occur, vary with the stage and degree of

infection
Stage 1 (invasion)
H Occurs 1 week after ingestion
H Release of larvae and reproduction of adult T. spiralis causing:
Anorexia
Nausea
Vomiting
Diarrhea
Abdominal pain
Cramps
838
Trichinosis
Stage 2 (dissemination)
H Occurs 7 to 10 days after ingestion
H Penetrates the intestinal mucosa and begins to migrate to striated muscle
H Signs and symptoms:
Edema, especially of the eyelids or face
Muscle pain, particularly in limbs
Occasionally, itching and burning skin, sweating,
skin lesions, a temperature of 102 to 104 F
(38.9 to 40 C), and delirium
In severe respiratory, cardiovascular, or CNS infections, palpitations and lethargy
Stage 3 (encystment)
H Occurs during convalescence, generally 1 week later
H Invades muscle fiber and becomes encysted
Complications
H Meningitis
H Subcortical infarcts
H Encephalitis
H Myocarditis with heart failure
H Nephritis
H Sinusitis
H Pneumonia
Assessment
History
H Ingestion of raw or improperly cooked pork or pork
products
H Myalgia
H Diarrhea
H Constipation
H Anorexia
H Nausea
Physical findings
H Diffuse weakness
H Hoarseness
H Cough
H Macular or petechial rash
H Periorbital edema
Test results
Laboratory
H Stools contain mature worms and larvae during the
invasion stage.
H Diagnosis is confirmed by elevated acute and convalescent antibody titers (determined by flocculation
tests 3 to 4 weeks after infection).
H Aspartate aminotransferase, alanine aminotransferase, creatine kinase, and lactate dehydrogenase
levels are increased during the acute stages, and
eosinophil count is increased (up to 15,000/l).
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H Cerebrospinal fluid lymphocyte level (to 300/l)
is normal or increased, and protein levels are increased, indicating CNS involvement.
H Skeletal muscle biopsies can show encysted larvae 10
days after ingestion; if available, analyses of contaminated meat also show larvae.
H Skin testing may show a positive histamine-like reactivity 15 minutes after intradermal injection of the
antigen (within 17 to 20 days after ingestion); however, such a result may remain positive for up to 5
years after exposure.
H for travelers to foreign countries or poor areas of the
United States, the importance of avoiding pork consumption; swine in these areas are commonly fed
raw garbage.
Treatment
General
H Supportive care as indicated
H Diet as tolerated
H Initially, bed rest with increased activity as tolerated
Medications
H Antipyretics
H Anthelmintics, such as albendazole and mebendazole
H Glucocorticoids
H Analgesics
Key outcomes
The patient will:
H express an understanding of the disorder and its
treatment
H Reduce fever with alcohol rubs, tepid baths, hypo-
thermia blankets, or antipyretics.

H Relieve muscle pain with analgesics, enforced bed
rest, and proper body alignment.

H Frequently reposition the patient, and gently massage
bony prominences to prevent pressure ulcers.

H Report all cases of trichinosis to local public health
authorities.
Monitoring
H Vital signs
Patient teaching
Be sure to cover:
H proper cooking (cooking to an internal temperature
of 150 F) and storing methods for all meat from
carnivores
Trichinosis
839
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Trichomoniasis
Overview
Description
H A protozoal infection of the lower genitourinary tract
H May be acute or chronic in females
H Risk of recurrence minimized when sexual partners
treated concurrently
Pathophysiology
H Trichomonas vaginalis a tetraflagellated, motile
protozoan causes trichomoniasis in females by infecting the vagina, the urethra and, possibly, the endocervix, bladder, Bartholins glands, or Skenes
glands; in males, it infects the lower urethra and,
possibly, the prostate gland, seminal vesicles, or epididymis.
H T. vaginalis grows best when the vaginal mucosa is
more alkaline than normal (pH about 5.5 to 5.8).
Causes
H Usually transmitted by sexual intercourse; less com-
monly, by contaminated douche equipment or moist

washcloths
Risk factors
H Factors that raise the vaginal pH, such as the follow-
ing:
Use of hormonal contraceptives
Pregnancy
Bacterial overgrowth
Exudative cervical or vaginal lesions
Frequent douching, which disturbs lactobacilli that
normally live in the vagina and maintain acidity
Incidence
H Affects about 15% of sexually active females and 10%
of sexually active males
H About 70% of females and most males asymptomatic
H In females: gray or greenish yellow and possibly pro-
fuse and frothy, malodorous vaginal discharge

H In males: mild to severe transient urethritis, possibly
with dysuria and urinary frequency
Complications
Assessment
History
H Severe itching
H Dyspareunia
H Dysuria
H Urinary frequency
H Postcoital spotting, menorrhagia, or dysmenorrhea
Physical findings
H Vaginal erythema, edema, and frank excoriation
H Frothy, malodorous, greenish yellow vaginal dis-
charge
H Rarely, a thin, gray pseudomembrane over the vagina
Test results
Laboratory
H Direct microscopic examination of vaginal or seminal discharge is decisive when it reveals T. vaginalis,
a motile, pear-shaped organism. Examination of
clear urine specimens may also reveal T. vaginalis.
Other
H Cervical examination demonstrates punctate cervical
hemorrhages, giving the cervix a strawberry appearance thats almost pathognomonic for this disorder.
Treatment
General
H Abstinence from sexual intercourse until cured
H Sitz baths to help relieve symptoms
Medications
H Single 2-g dose of oral metronidazole given to both
sex partners
Key outcomes
The patient will:
pain
H express understanding of the condition and treatment
H discuss the impact of the disorder on self and significant others.
H With pregnant women: preterm or low-birth-weight
infant
H Prostatitis
H Epididymitis
H Urethral stricture disease
H Infertility
H Instruct the patient to avoid using tampons.

H Practice standard precautions.
Monitoring
840
Trichomoniasis
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Patient teaching
Be sure to cover:
H the need to refer sex partners for treatment
H the need to avoid alcohol while taking metronidazole
because alcohol may provoke a disulfiram-type reaction (confusion, headache, cramps, vomiting, and
seizures)
H the possibility that metronidazole may turn urine
dark brown
H the need to avoid over-the-counter douches and vaginal sprays because they can alter vaginal pH
H the benefits of wearing loose-fitting, cotton underwear, which reduce the risk of genitourinary bacterial growth by allowing ventilation; bacteria flourish in
a warm, dark, moist environment
H prevention of a sexually transmitted disease by using
a condom.
Trichomoniasis
841
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Tricuspid insufficiency
Assessment
History
Overview
Description
H Heart condition in which the tricuspid valve doesnt
function properly
H Also called tricuspid regurgitation
H Occurrence of one of listed causes

H Orthopnea, dyspnea
H Fatigue
H Angina
H Palpitations
Physical findings
Pathophysiology
H Tachycardia
H Hepatomegaly (right-sided failure)
H S3
H Diminished peripheral pulses
H Ascites
H Peripheral edema
H Pansystolic murmur (see Identifying the murmur
H The tricuspid valve is incompetent.

H Blood flows back into the right atrium.
H Fluid overload occurs in the atrium.
H Congestive failure occurs, and impedance to the
pulmonary vasculature may result in hypoxemia,

cyanosis, and polycythemia.
Causes
H Endocarditis
H Epsteins anomaly
H Prolapse
H Papillary muscle dysfunction
H Trauma
H Connective tissue disease
of tricuspid insufficiency)
Test results
Imaging
H Chest X-rays show right atrial and ventricular enlargement.
H Echocardiography shows right ventricular dilation
and prolapse or flailing of the tricuspid leaflets.
H Electrocardiography shows right atrial hypertrophy,
right or left ventricular hypertrophy, atrial fibrillation, and incomplete right bundle-branch block.
H Right-sided heart catheterization shows high atrial
pressure, tricuspid insufficiency, and decreased or
normal output.
Incidence
H Usually occurs in childhood
H Peripheral edema
H Tachycardia
H Fatigue
Treatment
Complications
General
H Heart failure
H Pulmonary edema
H Thromboembolism
H Endocarditis
H Arrhythmias
H Underlying cause
H Low-sodium diet
H Fluid restriction
Medications
Identifying the murmur of tricuspid
insufficiency
A high-pitched, blowing pansystolic murmur in the tricuspid area characterizes tricuspid insufficiency.
SYSTOLE
S1
DIASTOLE
S2
SYSTOLE
S1
S2
H Diuretics
H Cardiac glycoside
H Anticoagulants
H Oxygen
H Prophylactic antibiotics in some patients before and
after surgery or dental care to prevent endocarditis
Surgery
H Annuloplasty or valvuloplasty to reconstruct or repair
the valve
H Valve replacement with a prosthetic valve
842
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Key outcomes
The patient will:
H carry out activities of daily living without weakness
or fatigue
H Keep patients legs elevated to improve venous return
to the heart.
Monitoring
H Cardiac rhythm
H Intake and output
Patient teaching
Be sure to cover:
H dietary restrictions and medications
H signs and symptoms that should be reported
H the importance of consistent follow-up care
H the need to elevate his legs when sitting.
843
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Tricuspid stenosis
Assessment
History
Overview
Description
H Heart condition in which the tricuspid valve improp-
erly functions, allowing backflow of blood into the

right atrium and causing right atrial enlargement
Pathophysiology
H Orthopnea
H Dyspnea
H Fatigue
H Angina
H Palpitations
Physical findings
H Diastolic murmur (see Identifying the murmur of
H Alterations in the structure of the tricuspid valve
tricuspid stenosis)
cause incompetence of the valve.

H Restriction of blood flow into the right ventricle and,
subsequently, to the pulmonary vasculature occurs.
H Obstructed venous return results in hepatic enlargement, decreased pulmonary blood flow, peripheral
edema, and right atrial enlargement.
H Split S1
H Hepatomegaly (with right-sided failure)
H Ascites
Test results
Imaging
H Chest X-ray reveals cardiomegaly.
H Echocardiography shows structure of the valves.
H Electrocardiography may show atrial fibrillation.
Causes
H Mitral and aortic valve disorders
H Endomyocardial fibrosis
H Tricuspid atresia
Treatment
General
Incidence
H Affects females slightly more commonly than males
H Peripheral edema
H Fatigue
H Ascites
H Underlying cause
H Low-sodium diet
H Fluid restriction
Medications
H Diuretics
H Inotropic agent
H Oxygen
H Antibiotics before and after dental procedures or
Complications
H Heart failure
H Pulmonary edema
H Thromboembolism
H Endocarditis
H Arrhythmias
surgery in some patients or if infection present
Surgery
H Balloon valvoplasty
H Pulmonary artery balloon angioplasty
H Valvotomy
Identifying the murmur of tricuspid

stenosis
A low, rumbling crescendo-decrescendo murmur in the

tricuspid area characterizes tricuspid stenosis.
Key outcomes
SYSTOLE
S1
DIASTOLE
S2
SYSTOLE
S1
S2
The patient will:

fatigue
844
Tricuspid stenosis
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H When sitting in a chair, elevate legs to improve
venous return to the heart.

H Elevate the head of the bed.
H Keep the patient on a low-sodium diet.
H If the patient has surgery, watch for hypotension,
arrhythmias, and thrombus formation.
Monitoring
H Cardiac rhythm
H Intake and output
Patient teaching
Be sure to cover:
adverse effects
H signs and symptoms that should be reported
H avoidance of triggers.
Discharge planning
H Refer the patient to support services as needed.
Tricuspid stenosis
845
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Trigeminal neuralgia
Incidence
Overview
Description
H Sudden onset of severe, throbbing pain

H Contortion of affected side of the face
H Painful disorder of the 5th cranial (trigeminal) nerve

H Right side of face affected more commonly than left
H Can subside spontaneously
H Remissions last from several months to years
H Also known as tic douloureux
Pathophysiology
H The trigeminal nerve has multiple branches. This
nerve affects chewing movements and sensations of

the face, scalp, and teeth. (See Trigeminal nerve
function and distribution.)
H A trigger zone is stimulated, and interaction or
short-circuiting of touch and pain fibers occurs.
H Paroxysmal attacks of excruciating facial pain result.
Causes
H Afferent reflex phenomenon
H Compression of the nerve root by:
Posterior fossa tumors

Middle fossa tumors
Vascular lesions
H Multiple sclerosis
H Herpes zoster
H Stroke
Trigeminal nerve function and

distribution
Function
H Motor: chewing movements

H Sensory: sensations of face, scalp, and teeth (mouth
and nasal chamber)
Distribution
I ophthalmic
II maxillary
III mandibular
H Affects people older than age 40

H Affects more females than males
Complications
H Excessive weight loss
H Depression
H Social isolation
Assessment
History
H Searing or burning facial pain occurring in lightning-
like jabs
Lasts from 1 to 15 minutes (usually 1 or 2 minutes)
Localized in an area innervated by the trigeminal
nerve
Initiated by a light touch to a hypersensitive area
H Attacks possibly following:
Draft of air
Exposure to heat or cold
Eating, smiling, and talking
Drinking hot or cold beverages
A pain-free period
Physical findings
H Favoring (splinting) of affected area
H Affected side of the face unwashed and unshaven
H Patient never touches affected area
H No impairment of sensory or motor function
Test results
Imaging
H Skull X-rays, computed tomography scan, and magnetic resonance imaging results rule out sinus or
tooth infections and tumors.
Treatment
I
General
H No activity restrictions
Medications
H Anticonvulsants, such as carbamazepine, gabapentin,
II
and phenytoin
H Antidepressants such as nortriptyline
H Baclofen
III
Surgery
H Microvascular decompression
H Radiosurgery with stereotactic technique
H Partial sensory rhizotomy to sever the nerve
846
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H Percutaneous balloon compression of the trigeminal
nerve
H Alcohol or glycerol injection
Other
H Radiation therapy
H Acupuncture
H Biofeedback
H Electrical stimulation of nerves
Key outcomes
The patient will:
pain
the disorder
H consume required caloric intake daily
fatigue
H perform routine roles.
H Provide nutritional management.
H After microsurgery, provide postcraniotomy care.
Monitoring
H Characteristics of each attack
H Precipitating factors of each attack
H Postoperatively, neurologic function and vital signs
Patient teaching
Be sure to cover:
H preoperative teaching if indicated
adverse effects
H nutritional management
H avoidance of triggers.
847
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Trisomy 13 syndrome
Overview
Description
H Third most common multiple malformation syn-
Complications
H Congenital heart defects (common), especially hy-
poplastic left heart, ventricular septal defect, patent

ductus arteriosus, or dextroposition, which may significantly contribute to the cause of death
H Musculoskeletal abnormalities
H Microphthalmia, cataracts, and other eye abnormalities
drome
H In most affected infants, full trisomy 13 at birth;
rarely, mosaic partial trisomy 13 syndrome (with

varying phenotypes) or translocation types
H Brain and facial abnormalities as well as major cardiac, GI, and limb malformations typical
H Full trisomy 13 syndrome fatal
H Also known as Pataus syndrome
Pathophysiology
Assessment
History
H Failure to thrive
H Seizures
H Apnea
H Feeding difficulties
H About 75% of all cases result from chromosomal
Physical findings
nondisjunction.
H About 20% of cases result from chromosomal
translocation, involving a rearrangement of chromosomes 13 and 14.
H About 5% of cases are estimated to be mosaics; the
clinical effects in these cases may be less severe.
H Sloping forehead with wide sutures and fontanel

H Scalp defect at the vertex
H Bilateral cleft lip with associated cleft palate
H Flat, broad nose
H Low-set ears and inner ear abnormalities
H Polydactyl hands and feet
H Club feet
H Omphaloceles
H Neural tube defects
H Cystic hygroma
H Genital abnormalities
Causes
H Chromosomal abnormality
Risk factors
H Advanced maternal age (mean maternal age
about 31)
Incidence
H Many trisomic zygotes spontaneously aborted (50%
to 70% die within 1 month after birth and 85% by the

first year)
H Only isolated cases of survival beyond 5 years in full
trisomy 13 patients; in all survivors, profound mental
retardation
H Estimated to affect 1 in 4,000 to 10,000 neonates
H Microcephaly
H Varying degrees of holoprosencephaly
H Sloping forehead with wide sutures and fontanel
H Scalp defect at the vertex
H Bilateral cleft lip with associated cleft palate
H Flat, broad nose
H Low-set ears and inner ear abnormalities
H Polydactyl hands and feet
H Club feet
H Omphaloceles
H Neural tube defects
H Cystic hygroma
H Genital abnormalities
H Cystic kidneys
H Hydronephrosis
848
Trisomy 13 syndrome
Test results
Laboratory
H Karyotype, done either prenatally or on peripheral
blood lymphocytes or skin fibroblasts in a neonate or
an aborted fetus, is diagnostic.
H Results are abnormal (but not diagnostic) in
multiple-marker maternal serum screening tests involving different combinations of alpha-fetoprotein,
human chorionic gonadotropin (HCG) or free betaHCG in some laboratories, and unconjugated estriol.
Imaging
H Ultrasonography usually reveals multiple abnormalities in the fetus.
Treatment
General
H Supportive care
Key outcomes
The patient will:
H appear comfortable.
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H Maintain the infants fluid balance.
H Position the infant comfortably.
H Allow adequate time for the parents to bond with and
hold their child.

H Provide emotional support to the family.
Monitoring
H Intake and output
H Safety
H Growth
Patient teaching
Be sure to cover:
H activities that can be carried out with the child
H safety factors.
Discharge planning
H Refer the parents of an affected infant for genetic
counseling to explore the cause of the disorder and

to discuss the risk of recurrence in future pregnancies.
H Refer the parents to a social worker or grief counselor for additional support if needed.
H Refer the parents to the Support Organization for
Trisomy 18, 13, and Related Disorders (S.O.F.T.)
national support program to allow them to interact
with other parents of infants with trisomy 18 and
trisomy 13.
Trisomy 13 syndrome
849
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Trisomy 18 syndrome
Overview
Description
Complications
H Congenital heart defects, such as ventricular septal
defect, tetralogy of Fallot, transposition of the great

vessels, and coarctation of the aorta (in 80% to 90%
of patients), which may be the cause of death in
many cases
H Other congenital anomalies, such as diaphragmatic
hernia, various renal defects, omphalocele, neural
tube defects, genital and perineal abnormalities (including imperforate anus), and oligohydramnios
H Second most common multiple malformation syn-
drome
H In most affected infants, full trisomy 18, involving an
extra (third) copy of chromosome 18 in each cell;

partial trisomy 18 (with varying phenotypes) and
translocation types also reported
H Intrauterine growth retardation, congenital heart defects, microcephaly, and other malformations in most
infants with this disorder
H Full trisomy 18 syndrome generally fatal or extremely
poor prognosis (30% to 50% of infants die within the
first 2 months and 90% die within the first year; most
surviving patients are profoundly mentally retarded.)
H Also known as Edwards syndrome
Pathophysiology
H Most cases of trisomy 18 result from spontaneous
meitotic nondisjunction, effecting an extra copy of

chromosome 18 in each cell.
Causes
H Chromosomal abnormality
Risk factors
H Typically increases with maternal age (mean mater-
nal age 3212)
Incidence
H Incidence ranges from 1 in 3,000 to 8,000 neonates;
three to four females affected for every male
Assessment
History
H Growth retardation, which begins in utero and re-
mains significant after birth
Physical findings
H Short, narrow nose with upturned nares
H Unilateral or bilateral cleft lip and palate
H Low-set, slightly pointed ears
H Short neck
H Conspicuous clenched hand with overlapping fingers
(commonly seen on ultrasound)

H Cystic hygroma
H Choroid plexus cysts (also seen in some normal in-
fants)
Test results
Laboratory
H Karyotype, done either prenatally or on peripheral
blood lymphocytes or skin fibroblasts in a neonate or
an aborted fetus, is diagnostic.
H Results are abnormal (but not diagnostic) in
multiple-marker maternal serum screening tests involving different combinations of alpha-fetoprotein,
human chorionic gonadotropin, and unconjugated
estriol.
Imaging
H Ultrasonography commonly reveals variable abnormalities in the fetus.
H Growth retardation, which begins in utero and re-
mains significant after birth

H Initial hypotonia that may soon give way to hyper-
tonia
H Microcephaly and dolichocephaly
H Micrognathia
H Short, narrow nose with upturned nares
H Unilateral or bilateral cleft lip and palate
H Low-set, slightly pointed ears
H Short neck
H Conspicuous clenched hand with overlapping fingers
(commonly seen on ultrasound)
H Cystic hygroma
H Choroid plexus cysts (also seen in some normal infants)
850
Trisomy 18 syndrome
Treatment
General
H Emotional support for the family
H Nutrition maintenance using gavage feedings
Key outcomes
The patient will:
H appear comfortable.
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H Allow adequate time for the parents to bond with and
hold their child.

H Provide emotional support to the family.
Monitoring
H Intake and output
H Growth
Patient teaching
Be sure to cover:
H home care and feeding techniques.
Discharge planning
H Refer the parents of a child affected with trisomy 18
syndrome for genetic counseling to explore the cause

of the disorder and discuss the risk of recurrence in
a future pregnancy.
H Refer the parents to a social worker or grief counselor for additional support if needed.
H Refer the parents to the Support Organization for
Trisomy 18, 13, and Related Disorders (S.O.F.T.)
national support program to allow them to interact
with other parents of infants with trisomy 18 and trisomy 13.
Trisomy 18 syndrome
851
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Tuberculosis
Overview

H Low-grade fever
H Night sweats
Description
Complications
H Acute or chronic lung infection characterized by pul-
H Massive pulmonary tissue damage

H Bronchopleural fistulas
H Pneumothorax
H Pleural effusion
H Pneumonia
H Infection of other body organs by small mycobacteri-
monary infiltrates and the formation of granulomas

with caseation, fibrosis, and cavitation
H Prognosis excellent with proper treatment and compliance
H Also known as TB
Pathophysiology
H Multiplication of the bacillus Mycobacterium tuber-
culosis causes an inflammatory process where deposited.

H A cell-mediated immune response follows, usually
containing the infection within 4 to 6 weeks.
H The T-cell response results in the formation of granulomas around the bacilli, making them dormant. This
confers immunity to subsequent infection.
H Bacilli within granulomas may remain viable for
many years, resulting in a positive purified protein
derivative or other skin test for TB.
H Active disease develops in 5% to 15% of those
infected.
H Transmission occurs when an infected person
coughs or sneezes.
Causes
H Exposure to M. tuberculosis
H Sometimes, exposure to other strains of mycobac-
teria
Risk factors
H Close contact with newly diagnosed TB patient
H History of prior TB exposure
H Multiple sexual partners
H Recent immigration from Africa, Asia, Mexico, or
South America
H Gastrectomy
H History of silicosis, diabetes, malnutrition, cancer,
Hodgkins disease, or leukemia

H Drug and alcohol abuse
H Residence in nursing home, mental health facility, or
prison
H Immunosuppression and use of corticosteroids
H Homelessness
Incidence
H Overall decrease in TB but greater among high-risk
populations
H Four times as common in nonwhites as in whites
H Higher incidence in Black and Hispanic males
between ages 25 and 44

H Highest incidence in people who live in crowded,
poorly ventilated, unsanitary conditions
852
Tuberculosis
al foci
H Liver disease involvement secondary to drug therapy
Assessment
History
In primary infection
H May be asymptomatic after a 4- to 8-week incubation
period
H Low-grade fever
H Night sweats
In reactivated infection
H Chest pain
H Productive cough for blood, or mucopurulent or
blood-tinged sputum
H Low-grade fever
Physical findings
H Dullness over the affected area
H Crepitant crackles
H Bronchial breath sounds
H Wheezes
H Whispered pectoriloquy
Test results
Laboratory
H Tuberculin skin test is positive in both active and inactive TB.
H Stains and cultures of sputum, cerebrospinal fluid,
urine, abscess drainage, or pleural fluid show
heat-sensitive, nonmotile, aerobic, acid-fast bacilli.
Imaging
H Chest X-rays show nodular lesions, patchy infiltrates,
cavity formation, scar tissue, and calcium deposits.
imaging shows presence and extent of lung damage.
H Bronchoscopy specimens show heat-sensitive, nonmotile, aerobic, acid-fast bacilli in specimens.
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Treatment
General
H After 2 to 4 weeks, when disease is no longer infec-
tious, resumption of normal activities while continuing to take medication

H Well-balanced, high-calorie diet
H Rest, initially; activity as tolerated
Medications
H Antitubercular therapy for at least 6 months with dai-
ly oral doses of the following:

Isoniazid
Rifampin
Pyrazinamide
Ethambutol, added in some cases
H Second-line drugs include the following:
Capreomycin
Streptomycin
Aminosalicylic acid (para-aminosalicylic acid)
Pyrazinamide
Cycloserine
Surgery
H For some complications
Key outcomes
The patient will:
H identify measures to prevent or reduce fatigue
H comply with treatment regimen.
Prevention
Preventing tuberculosis
The spread of tuberculosis (TB) can be prevented by following these guidelines:
H Hospitalized patients should follow respiratory and
standard precautions.
H A discharged patient should wear a mask around others until hes no longer contagious.
H Tell all health care providers, including dentists and optometrists about TB diagnosis so they can use infection control precautions.
H Cough and sneeze into a tissue and dispose of properly.
H Practice thorough hand washing with hot soapy water
after handling secretions.
H Wash eating utensils separately in hot, soapy water.
Patient teaching
Be sure to cover:
H need for isolation
H regular follow-up examinations
H signs and symptoms of recurring TB
H possible decreased hormonal contraceptive effectiveness while taking rifampin
H need for a high-calorie, high-protein, balanced diet
H TB prevention. (See Preventing tuberculosis.)
Discharge planning
H Refer anyone exposed to an infected patient for test-
ing and follow-up.
H Refer the patient to a support group such as the

H Isolate the patient in a quiet, properly ventilated
H Refer the patient to a smoking-cessation program
room, and maintain TB precautions.
American Lung Association.

if indicated.
H Provide diversional activities.

H Properly dispose of secretions.
H Provide well-balanced, high-calorie foods.
H Provide small, frequent meals.
H Consult with a dietitian if oral supplements are
needed.
H Include the patient in care decisions.
Monitoring
H Vital signs
H Intake and output
H Daily weight
H Complications
H Adverse reactions
H Visual acuity if taking ethambutol
H Liver and kidney function tests
Tuberculosis
853
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Tularemia
Overview
Description
H Francisella tularensis organism, a gram-negative
pleomorphic bacterium, causing disease in humans

and animals
H As few as 10 organisms able to cause disease
H Incubation period 3 to 4 days
H Six forms:
Ulceroglandular form
Glandular form
Oculoglandular form
Oropharyngeal form
Pneumonic form
Septicemic form
Pathophysiology
H The organism gains access to the host by skin or mu-
cous membrane inoculation, inhalation, or ingestion.

H After inoculation a papule (that eventually evolves
into an ulcer) and high fever develop.
Causes
H Bites of ticks and deerflies
H Eating or drinking contaminated food or water
H Contact with the blood of an infected animal, espe-
cially rabbits
H Breathing in the bacteria F. tularensis
Risk factors
H Participating in hunting and trapping
H Gardening
H Participating in outdoor sports or occupations
Incidence
H About 200 cases in humans annually
H Occurs more commonly in the south-central and
western United States
H Ulcer and fever
Complications
H Pneumonia
H Lung abscess
H Rhabdomyolysis
H Meningitis
H Pericarditis
H Osteomyelitis
Assessment
History
H Tick bite
H Exposure to contaminated food or water
H Exposure to contaminated blood
H Abrupt onset of fever, chills, headache, and malaise
H Contact with an infected carcass
Physical findings
Ulceroglandular
H Ulcers at the site of inoculation
H Swollen regional lymph nodes
Glandular
H Swollen regional lymph nodes
Oculoglandular
H Painful
H Red eye
H Purulent exudates
H Swollen submandibular, preauricular, or cervical
lymph nodes
Oropharyngeal
H Sore throat
H Abdominal pain
H Nausea
H Vomiting
H Diarrhea
H Occasionally, GI bleeding
Pneumonic
H Dry cough
H Dyspnea
Septicemic
H Fever, chills, myalgia, malaise, and weight loss
H Absence of ulcer
Test results
Laboratory
H White blood cell count is normal or elevated.
H Blood or sputum cultures are positive for F. tularensis.
H Serology is positive for antibodies to tularemia.
Imaging
H Chest X-ray shows pneumonia.
Treatment
General
H Proper skin care
Medications
H Antibiotics, such as streptomycin, gentamicin, and
tetracycline
H Antipyretics
854
Tularemia
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Key outcomes
The patient will:
H regain normal temperature
H regain or maintain normal fluid balance.
H Replace lost fluids through diet or I.V. fluids.
Monitoring
H Intake and output
H Vital signs
Patient teaching
Be sure to cover:
H medication administratiion, dosage, and possible
adverse effects
H preventive measures, such as using insect repellent
containing DEET on skin, or treating clothing with
repellent containing permethrin.
Tularemia
855
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Ulcerative colitis
Overview
Description
H Episodic inflammatory chronic disease causing ul-
cerations of the mucosa in the colon
H Condition beginning in the rectum and sigmoid colon
and possibly extending upward into the entire colon
H Rarely affecting the small intestine, except for the ter-
H Erythema nodosum on the face and arms
H Pyoderma gangrenosum on the legs and ankles
H Uveitis
H Pericholangitis, sclerosing cholangitis
H Cirrhosis
H Cholangiocarcinoma
H Ankylosing spondylitis
H Strictures
H Pseudopolyps, stenosis, and perforated colon leading
to peritonitis and toxemia

H Arthritis
minal ileum
H Produces congestion, edema (leading to mucosal
friability), and ulcerations

H Range of severity from mild, localized disorder to
fulminant disease causing many complications
Pathophysiology
H The disorder primarily involves the mucosa and the
submucosa of the bowel.

H Crypt abscesses and mucosal ulceration may occur.
H The mucosa typically appears granular and friable.
H The colon becomes a rigid, foreshortened tube.
H In severe ulcerative colitis, areas of hyperplastic
growth occur, with swollen mucosa surrounded by

inflamed mucosa with shallow ulcers.
H Submucosa and the circular and longitudinal muscles may be involved.
Causes
H Cause unknown
H May be related to an abnormal immune response in
the GI tract, possibly associated with genetic factors
Risk factors
H Stress (may increase severity of an attack)
H Family history
H Jewish ancestry
Incidence
H Primarily young adults, especially females
H More prevalent among Jews and higher socioeco-
nomic groups
H About 1 in 1,000 persons affected
H Onset of symptoms commonly peaking between ages
15 and 30 and again between ages 50 and 70
H Crampy lower abdominal pain
H Recurrent bloody diarrhea
Complications
H Perineal sepsis
H Anal fissure, anal fistula
H Perirectal abscess
H Perforation of the colon
H Hemorrhage, anemia
H Toxic megacolon
H Cancer
856
Ulcerative colitis
Assessment
History
H Remission and exacerbation of symptoms
H Mild cramping and lower abdominal pain
H Recurrent bloody diarrhea as often as 10 to 25 times
daily
H Nocturnal diarrhea
Physical findings
H Liquid stools with visible pus, mucus, and blood
H Possible abdominal distention
H Perianal irritation, hemorrhoids, and fissures
H Jaundice
H Joint pain
Test results
Laboratory
H Stool specimen analysis reveals blood, pus, and mucus, but no pathogenic organisms.
H Other supportive laboratory tests show decreased
serum levels of potassium, magnesium, hemoglobin,
and albumin as well as leukocytosis and increased
prothrombin time; an elevated erythrocyte sedimentation rate correlates with the severity of the attack.
Imaging
H Barium enema discloses the extent of disease and
complications, such as strictures and carcinoma.
This study isnt performed in a patient with active
signs and symptoms.
H Sigmoidoscopy confirms rectal involvement in most
cases by showing increased mucosal friability, decreased mucosal detail, and thick inflammatory exudates, edema, and erosions.
H Colonoscopy may be used to determine the extent of
the disease and to evaluate the areas of stricture and
pseudopolyps. This test isnt performed when the patient has active signs and symptoms.
H Biopsy, performed during colonoscopy, helps to confirm the diagnosis.
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Treatment
Patient teaching
General
Be sure to cover:
H prescribed dietary changes
H need to avoid GI stimulants, such as caffeine, alcohol, and smoking
adverse effects
H after a proctocolectomy and ileostomy, stoma care
H after a pouch ileostomy, procedures to insert the
catheter and care for the stoma
H the need for regular physical examinations because
of the increased risk of colorectal cancer.
H I.V. fluid replacement

H Blood transfusions (if needed)
H Nothing by mouth (if severe)
H Parenteral nutrition (with severe disease)
H Supplemental feedings
H Rest periods during exacerbations
Medications
H Corticotropin and adrenal corticosteroids
H Sulfasalazine
H Mesalamine
H Antispasmodics and antidiarrheals
H Fiber supplements
H Immune modifiers, such as azathioprine, 6-MP and
methotrexate
H Antibiotics
Surgery
Discharge planning
H Refer the patient to a smoking-cessation program if
indicated.
H Refer the patient to an enterostomal therapist if
appropriate.
H Treatment of last resort

H Proctocolectomy with ileostomy
H Pouch ileostomy
H Ileoanal reservoir with loop ileostomy
H Colectomy
Key outcomes
The patient will:
pain
H have normal fluid volume
H have intact skin
H exhibit no evidence of infection
H avoid or have only minimal complications
H Provide diet therapy.
H Administer blood transfusions.
H Schedule care to allow for frequent rest periods.
Monitoring
H Hemoglobin level and hematocrit
H Complications
After surgery
H Vital signs
H Wound site
H Pain level
H Bowel function
H Skin integrity
Ulcerative colitis
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Urinary tract infection,

lower
Incidence
Overview
Description
H Bacterial infection of the lower urinary tract system
H Two forms:
Cystitis (infection of the bladder)

Urethritis (infection of the urethra)
H Usually a ready response to treatment
H Possible recurring and resistant bacterial flare-ups
during therapy
H Also known as lower UTI
H Nearly 10 times more common in females than in
males (except elderly males), probably because

natural anatomic features facilitate infection
H Affects 10% to 20% of all females at least once
H Dysuria
H Cloudy, foul-smelling urine
H Mild fever
Complications
H Damage to the urinary tract lining
H Infection of adjacent organs and structures
H Kidney infections and damage
Special populations
Special populations
In adult males and children, lower UTIs are typically associated with anatomic or physiologic abnormalities and require close evaluation.
Pathophysiology
Elderly people and young children have the greatest

risk for kidney damage because they may lack the
typical symptoms, thereby delaying diagnosis.
Assessment
H Local defense mechanisms in the bladder break
History
down.
H Bacteria invade the bladder mucosa and multiply.
H Bacteria cant be readily eliminated by normal urination.
H The pathogens resistance to prescribed antimicrobial therapy usually causes bacterial flare-up during
treatment.
H Recurrent lower UTIs result from reinfection by the
same organism or a new pathogen.

H Bladder cramps or spasms
H Pruritus
H Feeling of warmth during urination
H Nocturia or dysuria
H Urethral discharge (in males)
H Lower back or flank pain
H Malaise and chills
Causes
Physical findings
H Ascending infection by a single gram-negative, en-
teric bacterium, such as Escherichia coli, Klebsiella,

Proteus, Enterobacter, Pseudomonas, and Serratia
H Simultaneous infection with multiple pathogens
H Pain or tenderness over the bladder

H Hematuria
H Fever
H Cloudy, foul-smelling urine
Risk factors
Test results
H Natural anatomical variations

H Inadequate fluid consumption
H Trauma or invasive procedures
H Urinary catheter
H Urinary tract obstructions
H Vesicourethral reflux
H Urinary stasis
H Diabetes
H Bowel incontinence
H Immobility
H Sexual intercourse (females)
Laboratory
H Microscopic urinalysis shows red blood cell and
white blood cell counts greater than 10 per highpower field, suggesting lower UTI.
H Urinalysis shows bacterial count of more than
100,000/ml, confirming UTI.
H Sensitivity testing determines appropriate antimicrobial drug.
H If the patient history and physical examination warrant, a blood test or a stained smear of urethral discharge rules out sexually transmitted disease.
Imaging
H Voiding cystourethrography or excretory urography
may demonstrate congenital anomalies, predisposing
the patient to recurrent UTIs.
858
Urinary tract infection, lower
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Treatment
General
H Increased fruit juice intake, especially cranberry
Medications
H Antimicrobials
Surgery
H In case of recurrent infections from infected renal
Prevention
Preventing UTIs
Urinary tract infections (UTIs) can be prevented by following these guidelines:
H Practice proper cleaning after toileting by wiping from
front to back.
H Empty your bladder after intercourse and drink a full
glass of water.
H Drink plenty of water each day.
H Urinate when you feel the urge, dont hold it in.
H Avoid irritating feminine products with deodorants,
such as douches and powders.
calculi, chronic prostatitis, or structural abnormalities
Key outcomes
The patient will:
H identify risk factors that worsen the condition, and
modify her lifestyle accordingly
H demonstrate skill in managing the urinary elimination problem
H complete the prescribed course of treatment.
H Collect all urine specimens appropriately.
H Encourage oral fluid intake unless contraindicated.
H Apply warm compresses to lower abdomen for com-
fort as needed.
Monitoring
H Intake and output
H Urine characteristics
H Voiding patterns
H Vital signs
H Adverse effects of antimicrobial therapy
Patient teaching
Be sure to cover:
H completing the prescribed course of antibiotic
therapy
adverse effects
H prevention. (See Preventing UTIs.)
Urinary tract infection, lower
859
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Urticaria
and angioedema
Assessment
History
H Drug history, including nonprescription prepara-
tions, such as vitamins, aspirin, and antacids
Overview
H Reported commonly troublesome foods and environ-
Description
H Exposure to physical factors, such as cold, sunlight,
mental factors
H Common allergic reactions

H Occur separately or simultaneously
H Urticaria: may be acute (present less than 6 weeks)
H Adverse reaction to iodinated contrast media used
or chronic (present at least 6 weeks)

H Also known as hives
Physical findings
Pathophysiology
exercise, and trauma (dermatographism)

for diagnostic radiologic studies
H Distinct, raised, evanescent dermal wheals surround-
ed by a reddened flare
H Urticaria is an episodic, rapidly occurring, usually
H Nonpitting swelling of deep subcutaneous tissue on
self-limiting skin reaction. It involves only the superficial portion of the dermis, which erupts with local
wheals surrounded by an erythematous flare.
H Angioedema involves additional skin layers and produces deeper, larger wheals (usually on the hands,
feet, lips, genitalia, and eyelids). It causes diffuse
swelling of loose subcutaneous tissue and may affect
the upper respiratory and GI tracts.
H Several mechanisms and disorders may provoke urticaria and angioedema. They include immunoglobulin (Ig) E-induced release of mediators from cutaneous mast cells and binding of IgG or IgM to
antigen, resulting in complement activation.
the eyelids, lips, genitalia, and mucous membranes

that doesnt itch but may burn and tingle
H Respiratory stridor and hoarseness
H Anxiety, gasping for breath, and difficulty speaking
H Abdominal colic with or without nausea and vomiting
H Signs of anaphylaxis: hypotension, respiratory distress, stridor
Causes
H Unknown
H Drug allergy
H Food allergy
H Insect bite
H Occupational skin exposure
H Inhalant allergens (animal dander, cosmetics)
H Viral infection
H Hormones
H Thyroid abnormality
H Rheumatological disease
H Cholinergic trigger (heat, exercise, stress)
Incidence
H Affect about 20% of general population at some time
H More common after adolescence, with highest inci-
dence in the 30s
Test results
Laboratory
H Decreased serum levels of C1, C2, and C4 inhibitors
H Diagnosis can be confirmed through careful skin
testing with the suspected offending substance to see
if a local wheal and flare result.
Treatment
General
H Emergency measures if signs of anaphylaxis
H Limited contact with triggering factors
H Desensitization to the triggering antigen
H Avoidance of food allergens
Medications
H Antihistamines
H Systemic glucocorticoids
H Affect females more commonly than males
Key outcomes
H Raised, red wheals

H Diffuse edema
H Pruritus
The patient will:

pain
H avoid or have only minimal complications
H correlate precipitating factors with appropriate skin
care regimen.
Complications
H Skin abrasion and secondary infection
H Laryngeal edema
H Severe abdominal colic
860
Urticaria and angioedema
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H Reduce or minimize environmental exposure to
offending allergens and irritants, such as wool

and harsh detergents.
H If food is a suspected cause, gradually eliminate
foods from the diet, and watch for improvement.
Monitoring
H Vital signs, with attention to respiratory status
H Skin, for signs of secondary infection caused by
scratching
Patient teaching
Be sure to cover:
H how to identify the cause by keeping a diary to
record exposure to suspected offending substances
and signs and symptoms that appear after exposure
H how to monitor nutritional status and food replacements for nutrients lost by excluding allergyprovoking foods and beverages
H the need to keep fingernails short to avoid abrading
the skin when scratching
H signs and symptoms that indicate a skin infection
H use of an epinephrine emergency kit if anaphylaxis
occurs
H use of medical identification jewelry.
Urticaria and angioedema
861
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Uterine bleeding,
dysfunctional
Overview
Description
H Abnormal endometrial bleeding without recognizable
organic lesions
H Metrorrhagia (episodes of vaginal bleeding between
menses)
H Hypermenorrhea (heavy or prolonged menses,
longer than 8 days, also incorrectly termed menorrhagia)

H Chronic polymenorrhea (menstrual cycle less than
18 days) or oligomenorrhea (infrequent menses)
H Fatigue from anemia
H Oligomenorrhea and infertility from anovulation
H The indication for almost 25% of gynecologic surgi-
Complications
cal procedures
H Prognosis varies with cause, but good prognosis with
correction of hormonal imbalance or structural
abnormality
H Also known as DUB
H Iron deficiency anemia (blood loss of more than
Pathophysiology
H Irregular bleeding is associated with hormonal im-
balance and anovulation (failure of ovulation to occur).

H When progesterone secretion is absent but estrogen
secretion continues, the endometrium proliferates
and becomes hypervascular.
H When ovulation doesnt occur, the endometrium is
randomly broken down, and exposed vascular channels cause prolonged and excessive bleeding.
H In most cases of abnormal uterine bleeding, the endometrium shows no pathologic changes; however,
in chronic unopposed estrogen stimulation (as from
a hormone-producing ovarian tumor), the endometrium may show hyperplastic or malignant
changes.
Causes
1.6 L over a short time)

H Hemorrhagic shock
H Right-sided heart failure (rare)
H Endometrial adenocarcinoma from chronic estrogen
stimulation
Assessment
History
H Abnormal uterine bleeding
H Fatigue
H Infertility
H Bleeding in response to a brief course of proges-
terone
H Absence of body temperature changes during ovula-
tory cycle
Physical findings
H Pallor
H Signs of underlying disorder
H Pelvic examination revealing uterine abnormality
H Usually an imbalance in the hormonal-endometrial
Test results
relationship involving persistent and unopposed

stimulation of the endometrium by estrogen
H Disorders causing sustained high estrogen levels:
Obesity (because enzymes present in peripheral
adipose tissue convert the androgen androstenedione to estrogen precursors)
Immaturity of the hypothalamic-pituitary-ovarian
mechanism (postpubertal teenagers)
Anovulation (females in their late 30s or early
40s)
H Trauma (foreign object insertion or direct trauma)
H Endometriosis
H Coagulopathy, such as thrombocytopenia or leukemia
(rare)
H Drug-induced coagulopathy
Laboratory
H Hemoglobin levels and hematocrit determine the
need for blood transfusion or iron supplementation.
H Serum progesterone levels are decreased.
H Dilatation and curettage (D&C) or office endometrial
biopsy rules out endometrial hyperplasia and cancer
in females older than age 35.
Incidence
H About 10% of females with normal ovulatory cycles
H More episodes of abnormal bleeding among black
females, possibly secondary to a higher incidence

of leiomyomas and higher levels of estrogen
H Most common in puberty and perimenopause
862
Uterine bleeding, dysfunctional
Treatment
General
H Monitoring of bleeding episodes
H Emotional support
H Balanced diet
Medications
H High-dose estrogen-progestogen combination thera-
py (hormonal contraceptives); maintenance therapy

with lower dose combination hormonal contraceptives
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H Progestogen therapy
H I.V. estrogen followed by progesterone or combina-
tion hormonal contraceptives if the patient is young

(more likely to be anovulatory) and severely anemic
(if oral drug therapy is ineffective)
H Iron supplementation or transfusions of packed cells
or whole blood
Surgery
H Endometrial biopsy to rule out endometrial adeno-
carcinoma (patients age 35 and older)

H D&C (short-lived treatment and not clinically useful,
but an important diagnostic tool) with hysteroscopy

as an adjunct
Key outcomes
The patient will:
H have normal menstrual cycles
H express understanding of the disorder and its treatment.
H Tell the patient to record the dates of the bleeding
and the number of pads she saturates per day. Instruct the patient not to use tampons.
H Offer reassurance and support.
H Suggest to the patient that she minimize blood flow
by avoiding strenuous activity and by lying down with
her feet elevated.
Monitoring
H Vital signs
H Amount of bleeding
H Hemoglobin levels
Patient teaching
Be sure to cover:
H the importance of following the prescribed hormonal
therapy
H the purpose and procedures of D&C or endometrial
biopsy procedure if ordered
H the need for regular checkups to assess the effectiveness of treatment
H the importance of reporting abnormal bleeding immediately to help rule out major hemorrhagic disorders such as those that occur in abnormal pregnancy
H having a Papanicolaou test and a pelvic examination
annually.
Uterine bleeding, dysfunctional
863
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Uterine cancer
Overview
Description
H Proliferation of cancer cells in the endometrium
H Most common gynecologic cancer
H Also known as endometrial cancer
Pathophysiology
H Uterine cancer is usually adenocarcinoma.
H Metastasis occurs late (usually from the endometri-
um to the cervix, ovaries, fallopian tubes, and other

peritoneal structures). It may spread to distant organs, such as the lungs and the brain, by way of the
blood or the lymphatic system; lymph node involvement can also occur.
H Less common uterine tumors include adenoacanthoma, endometrial stromal sarcoma, lymphosarcoma, mixed mesodermal tumors (including carcinosarcoma), and leiomyosarcoma.
Causes
Risk factors
H Low fertility index and anovulation
H History of infertility or failure of ovulation
H Abnormal uterine bleeding
H Obesity
H Hypertension
H Diabetes
H Nulliparity
H Familial tendency
H History of uterine polyps or endometrial hyperplasia
H Prolonged estrogen therapy with exposure unop-
posed by progesterone
Assessment
History
H Spotting and protracted, heavy menses (in younger
patient)
H In postmenopausal woman, possible bleeding begin-
ning 12 or more months after menses stopped

H Vaginal discharge, initially watery, then increasingly
blood streaked
Physical findings
H Palpable enlarged uterus (advanced disease)
Test results
H Endometrial, cervical, or endocervical biopsy confirms the presence of cancer cells.
H Fractional dilatation and curettage are used to identify the problem when the disease is suspected but the
endometrial biopsy result is negative.
H Multiple cervical biopsies and endocervical curettage
pinpoint cervical involvement.
H Papanicolaou test result may be normal or show
abnormal cells.
Other
H Schillers test involves staining the cervix and vagina
with an iodine solution that turns healthy tissues
brown. (Cancerous tissues resist the stain.)
Treatment
General
H Radiation therapy
H Tamoxifen therapy
Medications
Incidence
H Hormonal therapy such as progestin

H Chemotherapy
H Most common in postmenopausal females between
ages 60 and 70 (uncommon between ages 30 and 40

and rare before age 30)
H Most premenopausal patients having history of
anovulatory menstrual cycles or other hormonal
imbalances
H Annually about 33,000 new cases reported; about
5,500 eventually fatal
H Abnormal vaginal bleeding
H Lower abdominal bleeding
Complications
H Anemia
H Ascites
H Increasing pain
H Hemorrhage
864
Uterine cancer
Surgery
H Total abdominal hysterectomy, bilateral salpingo-
oophorectomy or, possibly, omentectomy with or

without pelvic or para-aortic lymphadenectomy
H Total pelvic exenteration
Key outcomes
The patient will:
H report feeling increased comfort and decreased pain
H (with partner) express feelings and perceptions
about change in sexual performance
H experience no signs or symptoms of infection.
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H Encourage the patient to breathe deeply and cough.
Monitoring
After surgery
H Wound site and drainage system
H Vital signs
H Pain control
Internal radiation therapy
H Safety precautions (time, distance, and shielding)
H Movement (limited while source is in place)
H Vital signs
H Complications from radiation therapy, such as skin
reaction, vaginal bleeding, abdominal discomfort,
and dehydration
Patient teaching
Be sure to cover:
H (if the patient is premenopausal) that removal of her
ovaries will induce menopause
H safety measures involved in internal radiation therapy
adverse effects
H importance of follow-up examinations with a gynecologist.
Discharge planning
services.
Uterine cancer
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Uterine leiomyomas
Overview
Description
H Most common benign uterine tumors in females
H Tumors composed of smooth muscle that usually oc-
cur in the uterine corpus, although they may appear

on the cervix or on the round or broad ligament
H Malignant (leiomyosarcoma) in less than 0.1% of
patients
H Also known as myomas, fibromyomas, or fibroids
Pathophysiology
H Malposition of the fetus

H Anemia secondary to excessive bleeding
H Bladder compression
H Infection (if tumor protrudes out of the vaginal
opening)
H Secondary infertility (rare)
H Bowel obstruction
Assessment
History
H Abnormal menstrual bleeding
H Urinary frequency, urgency, or incontinence
H Abdominal cramping during menstruation
H Classified according to location, tumors may be lo-
Physical findings
cated within the uterine wall (intramural) or protrude into the endometrial cavity (submucous) or
from the serosal surface of the uterus (subserous).
H Size varies greatly.
H Tumors are usually firm and surrounded by a pseudocapsule composed of compressed but otherwise
normal uterine myometrium.
H The uterine cavity may become larger, increasing the
endometrial surface area. This can cause increased
uterine bleeding.
H Pelvic pressure
Causes
H
Unknown, but some factors implicated as regulators

of leiomyoma growth include the following:
Several growth factors including epidermal growth
factor
Steroid hormones, including estrogen and progesterone (typically arise after menarche and regress
after menopause, implicating estrogen as a promoter of leiomyoma growth)
Risk factors
H Females of reproductive age
H Family member with uterine leiomyomas
Incidence
H May affect three times as many Blacks as Whites; true
incidence in either population unknown

H May occur at any age, but most common in females
older than age 30
Test results
Laboratory
H Blood studies show anemia caused by abnormal
bleeding (may support diagnosis).
Imaging
H Ultrasonography allows accurate assessment of the
dimension, number, and location of tumors.
H Magnetic resonance imaging reveals calcified
fibroids.
H Hysterosalpingography detects myomas.
Other
H Patient history reveals evidence.
H Bimanual examination shows enlarged, firm, nontender, and irregularly contoured uterus (also seen
with adenomyosis and other pelvic abnormalities).
H Endometrial biopsy rules out endometrial cancer
in patients older than age 35 with abnormal uterine
bleeding.
H Laparoscopy corroborates other testing.
Treatment
General
H Blood transfusions
Medications
H Abnormal bleeding, typically menorrhagia with dis-
H Gonadotropin-releasing hormone agonists to rapidly
rupted submucosal vessels (most common symptom)

H Pain only associated with torsion of a pedunculated
(stemmed) subserous tumor or leiomyomas undergoing degeneration
H Pelvic pressure and impingement on adjacent viscera
(indications for treatment, depending on severity)
resulting in mild hydronephrosis
Complications
H Recurrent spontaneous abortion
H Preterm labor
866
Uterine leiomyomas
suppress pituitary gonadotropin release

Surgery
H Abdominal, laparoscopic, or hysteroscopic myomec-
tomy
H Myolysis
H Uterine artery embolization (radiologic procedure)
to block uterine arteries using small pieces of

polyvinyl chloride
H Hysterectomy
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Key outcomes
The patient will:
H relate understanding of the disorder and treatment
and state feelings
H return to normal menstrual periods.
H Reassure the patient that she wont experience pre-
mature menopause if her ovaries are left intact.

H In a patient with severe anemia from excessive bleed-
ing, give iron supplements and blood transfusions.

H Encourage the patient to verbalize her feelings and
concerns related to the disease process and its effects on her lifestyle.
Monitoring
H Comfort level
H Amount of bleeding
Patient teaching
Be sure to cover:
H the importance of reporting abnormal bleeding or
pelvic pain immediately
H the importance of regular gynecologic examinations.
Uterine leiomyomas
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Vaginal cancer
Overview
Description
H Proliferation of cancer cells in the vagina

H Rarest gynecologic cancer
H Usually appears as squamous cell carcinoma, but
occasionally as melanoma, sarcoma, or adenocarcinoma
Pathophysiology
H Because the vagina is a thin-walled structure with
rich lymphatic drainage, vaginal cancer varies in

severity, depending on its exact location and effect on
lymphatic drainage.
H It may progress from an intraepithelial tumor to an
invasive cancer.
H The upper third of the vagina is the most common
site of vaginal cancer.
Causes
Risk factors
H Advanced age (most likely risk factor) combined
with the following:

Trauma
Chronic pessary use
Use of chemical carcinogens (such as those in
some sprays and douches)
Use of diethylstilbestrol (DES) by the patients
mother during pregnancy
Previous cancer of the endometrium, vulva, or
cervix
History of human papilloma virus
Incidence
H Usually occurs in females in their early to middle 50s
H Rarely, rhabdomyosarcoma in children
H Bloody vaginal drainage
H Urine retention
Complications
H Metastasis possibly affecting the cervix, uterus, and
rectum
Assessment
History
H Bloody vaginal discharge
H Irregular or postmenopausal bleeding
H Urine retention or urinary frequency (if the lesion is
close to the neck of the bladder)
868
Vaginal cancer
Physical findings
H Ulcerated lesion in any area of the vagina
Test results
Laboratory
H Papanicolaou test shows abnormal cells.
H Biopsy identifies cancerous cells. Biopsy of the cervix
and vulva may also be performed to rule out these
areas as primary cancer sites.
H Colposcopy is used to locate lesions that may have
been missed during the pelvic examination.
Other
H Lugols solution painted on the suspected area helps
to identify malignant areas by staining glycogencontaining normal tissue. (Abnormal tissue resists
staining.)
Treatment
General
H Radiation therapy (preferred treatment for all stages
of vaginal cancer)
H Limited activity with internal radiation therapy
Medications
H Topical chemotherapy with fluorouracil and laser
surgery
Surgery
H May be recommended when tumor is so extensive
that vaginas close proximity to the bladder and rectum allows only minimal tissue margins around resected vaginal tissue
Key outcomes
The patient will:
H experience feelings of increased comfort and decreased pain
H express feelings and perceptions about change in
sexual performance (with partner)
H exhibit no signs or symptoms of infection.
Monitoring
H Vaginal discharge
Internal radiation therapy

H Safety measures (time, distance, and shielding)
H Limited movement
H Complications caused by radiation therapy
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Patient teaching
Be sure to cover:
H safety measures (for internal radiation therapy)
H importance of regular gynecologic check-ups
H potential adverse reactions to chemotherapy and
ways to manage them
H signs and symptoms of infection and the need to report them to a physician immediately
H ways to avoid infection.
Discharge planning
H Refer the patient (and family) to American Cancer
Society for resources and support services.
Vaginal cancer
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Vancomycin
intermediate-resistant
Complications
Overview
History
Description
H Staphylococci infection that has decreased suscepti-
bility to vancomycin
H Common in chronically ill patients; most likely devel-
oping in health care setting

H Patient with methicillin-resistant Staphylococcus au-
reus (MRSA) normally most reliably and effectively

treated with vancomycin; MRSA with decreased susceptibility to vancomycin possibly a sign that vancomycin-resistant strains are emerging
H Also called VISA, VRSA (more severe form) and glycopeptide intermediate-resistant Staphylococcus
aureus
Pathophysiology
H Genes encode resistance and are carried on plasmids
that transfer themselves from cell to cell.

H Resistance is mediated by enzymes that substitute a
different molecule for the terminal amino acid so

that vancomycin cant bind.
Causes
H Colonized patient: more than 10 times as likely to be-
come infected with the organism as uncolonized patient such as through a breach in the immune system
H VISA that enters a health care facility through an infected or colonized patient or a colonized health care
worker
H Spread during direct contact between the patient and
caregiver or patient and patient; possibly being
spread through patient contact with a contaminated
surface such as an overbed table
Risk factors
H Diabetes
H Kidney disease
H Previous MRSA infection
H Recent hospitalization
H Recent antimicrobial therapy
Incidence
H First discovered in mid-1996
H Incidence rare, about 16 cases reported in the Unit-
ed States
H Noted in patients receiving multiple courses of van-
comycin for MSRA infections
H Causative organism possibly living for weeks on such
surfaces as patient gowns, bed linens, and handrails
H Sepsis
H Multisystem organ involvement
H Death in the immunocompromised patient
Assessment
H Possible breach in the immune system, surgery, or
condition predisposing the patient to the infection

H Multiple antibiotic use
Physical findings
H The carrier patient commonly asymptomatic but pos-
sibly exhibiting signs and symptoms related to the

primary diagnosis
H The patient possibly exhibiting cardiac, respiratory,
or other major symptoms
Test results
Laboratory
H Culture shows staphylococci with decreased susceptibility to vancomycin after 24-hour incubation.
Treatment
General
H With an infection, possibly no treatment (Stop all an-
tibiotics and simply wait for normal bacteria to repopulate and replace the strain.)
H Colonized patient in contact isolation until culturenegative or discharged
H Antimicrobial drugs (VISA isolates not susceptible to
vancomycin generally are susceptible to other
drugs.)
Medications
H Antimicrobials
Key outcomes
The patient will:
H remain afebrile

H Institute contact isolation precautions.
H Ensure judicious and careful use of antibiotics. En-
courage physicians to limit the use of antibiotics.
H No specific symptoms; cultures found incidentally
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H Use infection-control practices, such as wearing
gloves before and after contact with infectious body

tissues and proper hand washing, to reduce the
spread of VISA.
Monitoring
H Vital signs
H Complications
Patient teaching
Be sure to cover:
adverse effects
H how to prevent the spread of VISA. (See Preventing
the transmission of VISA.)
Prevention
Preventing the transmission

of VISA
The transmission of vancomycin-intermediate resistant
Staphylococcus aureus (VISA) can be prevented by following these guidelines:
H Practice proper hand-washing techniques using soap
and water.
H Avoid contact with open wounds or contaminated
dressings.
H Dispose of contaminated articles, including items used
for dressing change and protective equipment, properly.
H Family and friends should wear protective equipment
when visiting a patient with VISA.
Vancomycin intermediate-resistant Staphylococcus aureus
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Vancomycin-resistant
enterococcus
Assessment
History
H Possible breach in the immune system, surgery, or
condition predisposing the patient to the infection
Overview
H Multiple antibiotic use
Description
Physical findings
H Mutation of a common bacterium

H Easily spread by direct person-to-person contact
H Also called VRE
H Carrier commonly asymptomatic
Pathophysiology
Test results
Laboratory
H VRE is isolated from stool or a rectal swab.
H Genes encode resistance and are carried on plasmids
that transfer themselves from cell to cell.

H Resistance is mediated by enzymes that substitute a
different molecule for the terminal amino acid so

that vancomycin cant bind.
Causes
H Enters health care facility through infected or colo-
nized patient or colonized health care worker

H Spread through direct contact between patient and
caregiver, between patients, or through contact with
contaminated surfaces
Risk factors
H Immunocompromised condition
H Advanced age
H Indwelling catheter
H Major surgery
H Open wounds
H History of taking vancomycin or a third-generation
cephalosporin
H History of enterococcal bacteremia, commonly
linked to endocarditis
H Organ transplantation
H Prolonged or repeated hospital admissions
H Exposure to contaminated equipment or a VREpositive patient.
Incidence
H Reported in facilities in more than 40 states
H Rates as high as 14% in oncology units
Treatment
General
H With an infection, possibly no treatment
H Colonized patient placed in contact isolation until
culture-negative or discharged
Medications
H Antimicrobials (VRE isolates not susceptible to van-
comycin generally susceptible to other antimicrobial

drugs)
Key outcomes
The patient will:
H remain afebrile
H have adequate fluid volume.

H Institute contact isolation precautions.
H Ensure judicious and careful use of antibiotics. En-
courage physicians to limit the use of antibiotics.

H Use infection-control practices, such as wearing
gloves and proper hand-washing techniques, to reduce the spread of VRE.
Monitoring
H No specific signs and symptoms

H May be found incidentally when culture results show
H Vital signs
H Complications
the organism
Complications
H Sepsis
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Prevention
Preventing the spread of

VRE at home
The transmission of VRE can be prevented by following
these guidelines:
H Wash hands with soap and water after physical contact
with the patient and before leaving the home.
H Use towels only once when drying hands after contact.
H Wear disposable gloves if you expect to come in contact with the patients body fluids and wash hands after
removing the gloves.
H Change linens routinely and whenever they become
soiled.
H Clean the patients environment routinely and when it
becomes soiled with body fluids with a household disinfectant or a mixture of 14 cup of bleach and 1 qt of
water.
H Tell physicians and other health care personnel caring
for the patient that the patient is infected with an organism resistant to multiple drugs.
Patient teaching
Be sure to cover:
H the disorder, diagnosis, and treatment (see Preventing the spread of VRE at home)
H the need for family and friends to wear personal protective equipment when visiting the patient
H how to dispose of protective equipment
adverse effects.
Discharge planning
services.
Vancomycin-resistant enterococcus
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Varicella
Complications
Overview
H Reyes syndrome
H Pneumonia
H Myocarditis
H Bleeding disorders
H Arthritis
H Nephritis
H Hepatitis
H Acute myositis
H Congenital varicella-caused hypoplastic deformity,
H With scratching due to severe pruritus: infection,
scarring, impetigo, furuncles, and cellulitis
Description
H An acute, highly contagious viral infection
H The same virus that causes chickenpox, thought to
become latent until the sixth decade of life or later,

causing herpes zoster (shingles)
H Transmission through direct contact (primarily with
respiratory secretions, less commonly with skin lesions) and indirect contact (airborne)
H Commonly known as chickenpox
Pathophysiology
H Localized replication of the virus occurs (probably in
the nasopharynx), leading to seeding of the reticuloendothelial system and development of viremia.
H Diffuse and scattered skin lesions result with vesicles
involving the corium and dermis with degenerative
changes (ballooning) and infection of localized
blood vessels.
H Necrosis and epidermal hemorrhage result; vesicles
eventually rupture and release fluid or are reabsorbed.
H Incubation period lasts 13 to 17 days.
H Infection is communicable from 48 hours before lesions erupt until after vesicles are crusted over.
limb scarring, retarded growth, and central nervous

system and eye problems
Assessment
History
H Recent exposure to someone with chickenpox
H Malaise
H Headache
H Anorexia
Physical findings
H Temperature 101 to 103 F (38.3 to 39.4 C)
H Crops of small, erythematous macules on the trunk
or scalp
H Macules progressing to papules and then clear vesi-
H Lack of immunization
cles on an erythematous base (so-called dewdrops

on rose petals)
H Vesicles becoming cloudy and breaking easily; then
scabs forming
H Rash that spreads to face and, rarely, to extremities
H Rash containing a combination of red papules, vesicles, and scabs in various stages
H Ulcers on mucous membranes of the mouth, conjunctivae, and genitalia
Incidence
Test results
H Most common in children ages 5 to 9, but can occur
Laboratory
H Virus can be isolated from vesicular fluid within the
first 3 to 4 days of the rash.
H Giemsa stain distinguishes the varicella-zoster virus
from the vaccinia-variola virus.
H Serum samples contain antibodies 7 days after onset
of symptoms.
H Serologic testing differentiates rickettsial pox from
varicella.
Causes
H Varicella-zoster herpesvirus
Risk factors
H Close contact with others at home, school, or child
care facility
at any age
H Congenital varicella possibly in infants whose mothers had acute infections in first or early second
trimester
H Neonatal infection rare, probably because of transient maternal immunity
H Occurs worldwide; endemic in large cities with outbreaks occurring sporadically
H Equally affects all races and both sexes
H Seasonal distribution varies; in temperate areas, incidence higher during late winter and spring
Treatment
General
H Malaise
H Crops of macules progressing to vesicles
H Pruritus
H Strict isolation until all vesicles have crusted over; for
874
Varicella
congenital chickenpox, no isolation

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Medications
H Antipruritics
H Antibiotics
H Analgesic and antipyretic
H Acyclovir
H Varicella-zoster immune globulin
Key outcomes
The patient will:
H report or demonstrate an increased energy level
H interact with family and peers to decrease feelings of
isolation
H express or demonstrate increased comfort.
H Observe an immunocompromised patient for mani-
festations of complications, such as pneumonitis and

meningitis, and report them immediately.
H Provide skin care comfort measures (calamine lotion, cornstarch, sponge baths, or showers).
H Administer varicella-zoster immune globulin if ordered to lessen the severity of the disease.
H Institute strict isolation measures until all skin lesions have crusted.
H Prevent exposure to pregnant women.
Monitoring
H Complications
H Skin integrity
Patient teaching
Be sure to cover:
adverse effects
H how to correctly apply topical antipruritic medications
H the importance of good hygiene and keeping the
childs fingernails trimmed
H the need for the child to avoid scratching the lesions
H the parents need to watch for and immediately report signs of complications (severe skin pain and
burning that may indicate a serious secondary infection and require prompt medical attention)
H the need for parents to refrain from giving the child
aspirin because of its association with Reyes syndrome
H signs and symptoms of Reyes syndrome and the need
to immediately report them to a physician.
Varicella
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Varicocele
Overview
Description
H A mass of dilated and tortuous varicose veins in the
spermatic cord
H Commonly described as a bag of worms (see Tak-
ing a close look at a varicocele)
Pathophysiology
Incidence
H Present in 30% of all males diagnosed with infertility
H Occurs in the left spermatic cord 95% of the time
H Highest in males between ages 15 and 25
H Asymptomatic
H Feeling of heaviness on the affected side
H Testicular pain and tenderness on palpation
Complications
H Infertility
H Hydrocele
H Because of a valvular disorder in the spermatic vein,
blood pools in the pampiniform venous plexus.

H One function of the pampiniform plexus is to keep
the testes slightly cooler than body temperature,

which is the optimal temperature for sperm production.
H Incomplete blood flow through the testes thus interferes with spermatogenesis.
H Testicular atrophy may also occur because of the reduced blood flow.
Causes
H Incompetent or congenitally absent valves in the
spermatic veins
H Tumor or thrombus obstructing the inferior vena
cava (unilateral left-sided varicocele)
Assessment
History
H Infertility
H Feeling of heaviness on affected side
Physical findings
H Palpation of bag of worms when patient upright
H Drained, cant be felt when patient recumbent
H Testicular tenderness
Test results
Other
H Physical examination confirms varicocele.
Treatment
Taking a close look at a varicocele
Varicocele, an abnormal dilation of the veins of the spermatic cord, is asymptomatic, but its important to identify
and correct this condition in adolescent boys because it
causes infertility.
General
H Scrotal support to relieve discomfort
Surgery
H Surgical repair or removal involving ligation of the
spermatic cord at the internal inguinal ring (if infertility is an issue)
Key outcomes
The patient will:
H express understanding of the disorder and its treatment
H express feelings regarding effect on fertility
H Promote the patients comfort before and after
surgery.
H After surgery, administer prescribed drugs.
H Apply an ice bag with a cover to reduce edema.
H Protect the wound from contamination.
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H Allow the patient to perform as many normal daily
activities as possible.
Monitoring
H Intake and output
H Comfort level
H Wound healing
Patient teaching
Be sure to cover:
H wound care.
From Pillitte
Philadelphia
Varicocele
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Varicose veins
Overview
Description
H Dilated, tortuous veins, engorged with blood result-
ing from improper venous valve function

H Primary varicose veins originating in superficial veins
(the saphenous veins and branches)

H Secondary varicose veins occurring in deep and
perforating veins
Pathophysiology
Assessment
History
H Feeling of heaviness in the legs that worsens in the
evening and in warm weather

H Leg cramps at night
H Diffuse, dull, aching leg pain after prolonged stand-
ing or walking
H Aching legs during menses
H Fatigue
H Exercise possibly relieving symptoms because venous
return improves
H A weakened valve allows backflow of blood to the
Physical findings
previous valve in a vein.

H If the valve cant hold the pooling blood, it becomes
incompetent, allowing even more blood to flow backward.
H As the volume of venous blood builds, pressure in
the vein increases and the vein becomes distended.
H As the vein stretches, it loses elasticity, enlarges, and
becomes tortuous.
H Hydrostatic pressure increases, plasma is forced
out into surrounding tissue, and edema results.
H Dilated, purplish, ropelike veins, especially in the
Causes
H Congenital weakness of the valves or venous wall
H Pregnancy
H Tight clothing
H Occupations that necessitate standing for an extend-
ed period
H Trauma
Risk factors
H Polonged standing or time on feet
H Obesity
H Heavy lifting
H Pregnancy
Incidence
H Common in middle adulthood
H Primary varicose veins: Family tendency, affect both
legs, twice as common in females as males
calf
H Orthostatic edema and stasis of the calves and ankles
H Nodules along affected veins and valve incompetence
H In chronic condition, venous stasis ulcers, which
must be differentiated from arterial and diabetic

ulcerations
Test results
Imaging
H Ascending and descending venography demonstrate
venous occlusion and patterns of collateral flow.
H Photoplethysmography, a noninvasive test, characterizes venous blood flow by showing changes in the
skins circulation.
H Doppler ultrasonography quickly and accurately
shows the presence or absence of venous backflow
in deep or superficial veins.
H Venous outflow and reflux plethysmography can be
used to detect deep venous occlusion.
Treatment
General
H Wearing elastic stockings
H Avoiding tight clothing
H For moderate varicose veins: wearing antiembolism
stockings or elastic bandages
H Secondary varicose veins: usually in only one leg
H For severe varicose veins: custom-fitted, surgical-
H Avoidance of prolonged standing

H Routine exercise
H Elevation of the legs
H Dilated, purple, ropelike veins

H Edema of calves and ankles
H Venous stasis ulcers
Complications
H Venous insufficiency
H Venous stasis ulcers
weight stockings with graduated pressure
Medications
H Sclerotherapy
Surgery
H Stripping and ligation
H Laser surgery
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H Catheter-assisted procedures
H Phlebectomy
H Endoscopic vein surgery
Key outcomes
The patient will:
H maintain adequate distal and collateral circulation
pain
H carry out activities of daily living without excess
fatigue or discomfort.
Prevention
Preventing varicose veins

Individuals with risk factors for varicose veins may prevent them by following these guidelines:
H Rest your legs and elevate them periodically if standing
is prolonged.
H Wear supportive stockings.
H Avoid wearing high heels and panty leg girdles.
H Drink 2 to 3 qt (2 to 3 L) of fluid per day.
H Eat plenty of fiber and avoid salt to decrease swelling
caused by fluid retention and constipation.
H Avoid crossing your legs when sitting.
H Exercise regularly
H Maintain a healthy weight.
H After stripping and ligation or after injection of a
sclerosing agent, administer analgesics as ordered

to relieve pain.
H Frequently check circulation in toes and observe
elastic bandages for bleeding. When ordered, rewrap
bandages at least once per shift, wrapping from toe
to thigh, with the leg elevated. (See Preventing varicose veins.)
Monitoring
ALERT
Watch for signs and symptoms of complications,
such as sensory loss in the leg, calf pain, and fever.
H Skin integrity
H Pain control
Patient teaching
Be sure to cover:
H the need to avoid wearing constrictive clothing
H elevating the legs above heart level when possible
and avoiding prolonged standing or sitting
H how to put on the elastic, antiembolism, or compression stockings before getting out of bed in the morning (or lying with the legs raised for 1 minute before
putting on the stockings)
H how to avoid injury to the lower legs, ankles, and feet
and the need to observe for altered skin integrity of
those areas and to report any problems to the physician as soon as possible.
Varicose veins
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Vascular retinopathies
Overview
Central retinal vein occlusion

H Reduced visual acuity, allowing perception of only
hand movement and light within 3 to 4 months after
occlusion
Diabetic retinopathy
Description
NONPROLIFERATIVE DIABETIC RETINOPATHY

H Changes in the lining of the retinal blood vessels that
H Noninflammatory retinal disorders that result from
cause the vessels to leak plasma or fatty substances,

which decrease or block blood flow (nonperfusion)
within the retina
H Microaneurysms and small hemorrhages
H Significant loss of central visual acuity (necessary for
reading and driving)
H Diminished night vision
interference with the blood supply to the eyes

H Five distinct types: central retinal artery occlusion,
central retinal vein occlusion, diabetic retinopathy,
hypertensive retinopathy, and sickle cell retinopathy
Pathophysiology
H When one of the arteries maintaining blood circula-
tion in the retina becomes obstructed, the diminished blood flow causes visual deficits.
Causes
Central retinal artery occlusion
H Idiopathic
H Embolism
H Atherosclerosis
H Infection
H Conditions that retard blood flow, such as carotid
occlusion and heart valve vegetations
H External compression of the retinal vein
H Trauma
H Diabetes
H Thrombosis
H Granulomatous diseases
H Generalized and localized infections
H Glaucoma
H Atherosclerosis
H Juvenile or adult diabetes
Hypertensive retinopathy
H Prolonged hypertensive disease
Sickle cell retinopathy
H Impaired ability of the sickled cell to pass through
the microvasculature, producing vasocclusion
Incidence
H Most prevalent in elderly patients
H About 75% of patients with juvenile diabetes developing retinopathy within 20 years of onset of diabetes
H In adults with diabetes, incidence increasing with the
duration of diabetes; 80% of patients who have had
diabetes for 20 to 25 years developing retinopathy, a
leading cause of acquired adult blindness
H Occurs in 1% to 6% of sickle-cell patients
PROLIFERATIVE DIABETIC RETINOPATHY

H Fragile new blood vessels on the disk and elsewhere
in the fundus (neovascularization)

H Based on the location of retinopathy, mild visual disturbances such as blurred vision resulting from
retinopathy located near the macula
H Optic disc changes
H Macular changes
Complications
H Permanent vision loss
H Secondary glaucoma
PROLIFERATIVE DIABETIC RETINOPATHY
H Vitreous hemorrhage with corresponding sudden
vision loss
H Macular distortion
H Blindness
H Mild, prolonged disease
H Visual defects
H Optic nerve neovascularization
H Sickling crisis
H Optic nerve and macular infarction
Assessment
History
H Changes in visual acuity
H Causative factors
Physical findings
H Abnormal opthalmic examination
Test results

H Sudden, painless, unilateral loss of vision (partial or
complete)
H Appropriate diagnostic tests depend on the type of
880
vascular retinopathy. (See Diagnostic tests for vascular retinopathies.)
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Treatment
Diagnostic tests for vascular

retinopathies
General
H Immediate ocular massage
H Anterior chamber paracentesis
Medications
H Heparin (if the cause of the occlusion is the heart)

General
H Laser photocoagulation
Medications
H Aspirin
General
H Careful control of blood glucose levels
H Eye examinations 3 to 4 times per year; annually for
children with diabetes
H Laser photocoagulation (proliferative diabetic
retinopathy)
H Diabetic diet
H Regular exercise
Medications
H Antidiabetic drugs or insulin as appropriate
Surgery
H Vitrectomy for vitreous hemorrhage to restore vision
General
H Control of blood pressure with appropriate drugs
H Low-sodium, low-cholesterol diet
H Regular exercise

General
H Treatment of disease
Surgery
H Laser retinal photocoagulation
H Retinal cryotherapy
H Vitrectomy or membranectomy
H Ophthalmoscopy (direct or indirect): shows blockage

of retinal arterioles during transient attack.
H Retinal examination: within 2 hours of onset, shows
clumps or segmentation in artery; later, milky white
retina around disk caused by swelling and necrosis of
ganglion cells caused by reduced blood supply; also
shows cherry-red spot in macula that subsides after
several weeks.
H Color Doppler tests: evaluates carotid occlusion with
no need for arteriography.
H Ophthalmoscopy (direct or indirect): shows flameshaped hemorrhages, retinal vein engorgement, white
patches among hemorrhages, edema around the disk.
H Color Doppler tests: confirm or rule out occlusion of
blood vessels.
H Indirect ophthalmoscopic examination: shows retinal

changes, such as microaneurysms (earliest change),
retinal hemorrhages and edema, venous dilation and
beading, lipid exudates, fibrous bands in the vitreous,
and growth of new blood vessels. Infarcts of the nerve
fiber layer are observed.
H Fluorescein angiography: shows leakage of flourescein
from weak-walled vessels and lights up microaneurysms, differentiating them from true hemorrhages.
H Ophthalmoscopy (direct or indirect): in early stages,

shows hard, shiny deposits; flame-shaped hemorrhages; silver wire appearance of narrowed arterioles;
and nicking of veins where arteries cross them (arteriovenous nicking). In late stages, shows cotton wool
patches, lipid exudates, retinal edema, papilledema
caused by ischemia and capillary insufficiency, hemorrhages, and microaneurysms in both eyes.
H Ocular examination and dilated retinal evaluation:

shows staged ocular symptoms.
Stage 1: peripheral retinal arteriolar occlusion
Stage 2: peripheral arteriovenous anastamoses
Stage 3: neovascular fronds known as seafans
Stage 4: vitreous hemorrhage and tearing of neovascular membranes
Stage 5: severe vitreous traction and retinal detachment
Key outcomes
The patient will:
H regain visual function
H express understanding of condition and its treatment.
Monitoring
Patient teaching
H Vital signs
H Visual acuity
H Arrange for immediate ophthalmologic evaluation
when a patient complains of sudden, unilateral loss

of vision.
H Encourage a patient with diabetes to comply with the
prescribed regimen.
Be sure to cover:
H complying with therapy for underlying condition
H obtaining recommended follow-up care.
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Vasculitis
Overview
Description
H Autoimmune condition that includes a broad spec-
trum of disorders characterized by blood vessel inflammation and necrosis

H Clinical effects dependent on the vessels involved and
reflective of tissue ischemia caused by blood flow obstruction
Pathophysiology
H The process is initiated by excessive circulating anti-
gen, which triggers the formation of soluble antigenantibody complexes. The reticuloendothelial system
cant effectively clear these complexes, which are deposited in blood vessel walls.
H Increased vascular permeability (associated with the
release of vasoactive amines by platelets and basophils) enhances this deposition. The deposited complexes activate the complement cascade and result in
chemotaxis of neutrophils, which release lysosomal
enzymes.
H Vessel damage and necrosis result.
Causes
H Several theories:
Follows serious infectious disease and may be related to high doses of antibiotics
Formation of autoantibodies directed at the bodys
own cellular and extracellular proteins, which can
lead to the activation of inflammatory cells or cytotoxicity
Cell-mediated (T-cell) immune response
In atopic individuals, exposure to allergens
Assessment
History
H Varied findings, depending on blood vessels involved
Polyarteritis nodosa
H Fever
H Weight loss
H Malaise
H Headache
H Abdominal pain
H Myalgias
Physical findings
Polyarteritis nodosa (depends on body
system)
H Hypertension (renal)
H Arthritic changes (musculoskeletal)
H Rash, purpura, nodules, and cutaneous infarcts
(skin)
H Altered mental status and seizures (central nervous
system)
H Respiratory distress, peripheral edema, hepatomegaly, peripheral vasoconstriction (cardiovascular)
Test results
H Not all vasculitis disorders can be diagnosed definitively through specific tests. The most useful general
diagnostic procedure is biopsy of the affected vessel.
Treatment
General
H Avoidance of antigenic drugs
H Avoidance of antigenic foods
H Avoidance of offending environmental substances
Risk factors
Medications
H Hepatitis B or C
H Sjgrens syndrome
H Other immune system disorders
H Drug allergy
H Corticosteroids
H Antihypertensives
H Analgesics
H Immunosuppressive agents
H Antineoplastics
Incidence
H Can affect a person at any age (except mucocuta-
neous lymph node syndrome, which affects only children)
H Based on affected blood vessel
Complications
H Renal failure, renal hypertension, glomerulitis
H Fibrous scarring of the lung tissue
H Stroke
H GI bleeding, intestinal obstruction
H Myocardial infarction and pericarditis
H Rupture of mesenteric aneurysms
882
Vasculitis
Key outcomes
The patient will:
pain
H demonstrate adequate ventilation
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H Assess for dry nasal mucosa. Instill nose drops to lu-
bricate the mucosa and minimize crusting; irrigate

nasal passages with warm normal saline solution.
H Keep the patient well hydrated (about 3 qt [3 L] of
fluid daily).
H Make sure that a patient with decreased visual acuity
has a safe environment.
H Regulate environmental temperature to prevent additional vasoconstriction caused by cold temperatures.
Monitoring
H Vital signs and neurologic status
H Signs and symptoms of organ involvement
H Laboratory values
H GI disturbances and renal function tests
H Intake and output
H Daily weight
Patient teaching
Be sure to cover:
adverse effects
H watch for signs of bleeding and report adverse effects
to the physician
H the importance of wearing warm clothes and gloves
when going outside in cold weather.
Discharge planning
H Refer the patient to a smoking-cessation program if
appropriate.
Vasculitis
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Ventricular septal defect

Overview
Description
H Heart condition in which an opening in the septum
between the ventricles allows blood to shunt between

the left and right ventricles
H Most common congenital heart disorder
H Also known as VSD
Pathophysiology
H The ventricular septum fails to close completely by
the 8th week of gestation, as it would normally.
Assessment
History
H Dyspnea
H Cyanosis
H Slow weight gain
H Feeding difficulties
H Rapid grunting respirations
Physical findings
H Prominent anterior chest wall
H Clubbing
H Cyanosis
H With a large VSD, audible murmurs (at least a grade
Risk factors
3 pansystolic), loudest at the fourth intercostal

space, usually with a thrill; pulmonic component of
S2 loud and widely split
H With fixed pulmonary hypertension, diastolic murmur possibly audible on auscultation, systolic murmur becoming quieter, and S2 greatly accentuated
H Displacement of the point of maximal impulse to the
left
H Typical murmur associated with a VSD, blowing or
rumbling and varying in frequency
H In the neonate, moderately loud early systolic murmur along the lower left sternal border, possibly becoming louder and longer about the second or third
day after birth
H In infants, murmur possibly loudest near the base of
the heart, which may suggest pulmonary stenosis
H In small VSD, functional murmur or characteristic
loud, harsh systolic murmur
H Fetal alcohol syndrome

H Coexists with additional birth defects, especially
Test results
H VSDs are located in the membranous or muscular
portion of the ventricular septum and vary in size.

H Some defects close spontaneously; in other defects,
the entire septum is absent, creating a single ventricle.

H VSD isnt readily apparent at birth because right and
left ventricular pressures are approximately equal, so
blood doesnt shunt through the defect.
H As the pulmonary vasculature gradually relaxes, between 4 and 8 weeks after birth, right ventricular
pressure decreases, allowing blood to shunt from the
left to the right ventricle.
Causes
H Congenital
Down syndrome and other autosomal trisomies, renal anomalies, and cardiac defects, such as patent
ductus arteriosus and coarctation of the aorta
Incidence
H Affects 2% to 7% of live births
H Slightly more common in females
H Clinical features of VSD varying with the size of the
defect, the effect of the shunting on the pulmonary

vasculature, and the infants age
H A small VSD possibly closing spontaneously without
ever causing symptoms
H Large VSD shunts eventually causing biventricular
heart failure and cyanosis
Complications
H Heart failure
H Pneumonia
884
Imaging
H Chest X-rays are normal in small defects; in large
VSDs, they show cardiomegaly, left atrial and left ventricular enlargement, and prominent pulmonary vascular markings.
H Echocardiography may detect a large VSD and its location in the septum, estimate the size of a left-toright shunt, suggest pulmonary hypertension, and
identify associated lesions and complications.
H Electrocardiogram is normal in children with small
VSDs; in large VSDs, it shows left and right ventricular hypertrophy, suggesting pulmonary hypertension.
H Cardiac catheterization determines the size and exact
location of the VSD, calculates the degree of shunting
by comparing the blood oxygen saturation in each
ventricle, determines the extent of pulmonary hypertension, and detects associated defects.
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Treatment
General
H If the child has other defects and will benefit from
delaying surgery, pulmonary artery banding to normalize pressures and flow distal to the band and prevent pulmonary vascular disease
H Low-sodium diet
H Fluid restriction
H watching for signs of heart failure, such as poor
feeding, sweating, and heavy breathing

adverse effects
H letting the child engage in normal activities
H the importance of prophylactic antibiotics before
and after surgery.
Discharge planning
services.
Medications
H Digoxin
H Diuretics
H Antibiotics
After surgery
H Analgesics
H Antibiotics
H Vasopressors
Surgery
H For small defects, simple suture closure
H For moderate to large defects, insertion of a patch
graft using cardiopulmonary bypass

H Mesh patch or plug placement during cardiac
catheterization (investigational)
Key outcomes
The patient will:
H Adminster prescribed drugs.
Monitoring
H Vital signs
H Intake and output
After surgery
H Hemodynamics
H Cardiac rhythm
H Oxygenation
Patient teaching
Be sure to cover:
H preventing complications until the child is scheduled
for surgery or the defect closes
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Vesicoureteral reflux
Overview
Description
Complications
H Renal impairment
H UTIs
Assessment
H A genitourinary condition in which urine flows from
History
the bladder back into the ureters and eventually into

the renal pelvis or the parenchyma
H Because the bladder empties poorly, possible urinary
tract infection (UTI), which may lead to acute or
chronic pyelonephritis with renal damage
H Urinary frequency and urgency

H Burning on urination
Pathophysiology
H Incompetence of the ureterovesical junction and
shortening of intravesical ureteral musculature allow

backflow of urine into the ureter when the bladder
contracts during voiding.
Causes
H Congenital anomalies of the ureters or bladder
H Inadequate detrusor muscle buttress in the bladder,
stemming from congenital paraureteral bladder diverticulum

H Acquired diverticulum (from outlet obstruction)
H Flaccid neurogenic bladder
H High intravesical pressure from outlet obstruction
H Cystitis
H Sometimes unknown
Incidence
Special populations
Most common during infancy in boys and during
early childhood (ages 3 to 7) in girls
H Primary vesicoureteral reflux resulting from congeni-
tal anomalies most prevalent in females and rare in

blacks
H Also shown in up to 25% of asymptomatic siblings
of children with diagnosed primary vesicoureteral
reflux
H Signs and symptoms of UTI
H Dark, concentrated urine
H With upper urinary tract involvement: high fever,
chills, flank pain, vomiting, and malaise
ALERT
In children, fever, nonspecific abdominal pain, and
diarrhea may be the only clinical effects. Rarely,
children with minimal symptoms remain undiagnosed until puberty or later, when they begin to exhibit clear signs of renal impairment (anemia, hypertension, and lethargy).
886
Physical findings
H In infants, hematuria or strong-smelling urine
H Hard, thickened bladder (hard mass deep in the
pelvis) if posterior urethral valves are causing an

obstruction in male infants
Test results
Laboratory
H Clean-catch urinalysis shows a bacterial count
greater than 100,000/l.
H Microscopic examination may reveal white blood
cells, red blood cells, and an increased urine pH in
the presence of infection. Specific gravity less than
1.010 demonstrates inability to concentrate urine.
H Elevated creatinine levels (more than 1.2 mg/dl) and
elevated blood urea nitrogen levels (more than
18 mg/dl) indicate advanced renal dysfunction.
H Cystoscopy, with instillation of a solution containing
methylene blue or indigo carmine dye, may confirm
the diagnosis.
H Excretory urography may show dilated lower ureter,
ureter visible for its entire length, hydronephrosis,
calyceal distortion, and renal scarring.
H Voiding cystourethrography (either fluoroscopic or
radionuclide) identifies and determines the degree of
reflux and shows when reflux occurs. It may also
pinpoint the causative anomaly.
H Nuclear cystography and renal ultrasound may detect
reflux.
Other
H Catheterization of the bladder after the patient voids
determines the amount of residual urine.
Treatment
General
Medications
H Antibiotics
Surgery
H Vesicoureteral reimplantation (if UTI recurs despite
adequate prophylactic antibiotic therapy)

H Bladder outlet obstruction in neurogenic bladder re-
quiring surgery only if renal dysfunction present
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Key outcomes
The patient will:
H return to normal urinary function
H develop no complications of the disorder.
H Encourage one of the parents to stay with the patient
during all procedures.

H Explain the procedures to the parents and to the
child, if hes old enough to understand.

H Make sure catheters are patent and draining well.
Maintain sterile technique during catheter care.
Monitoring
H Intake and output
H Comfort level
H Vital signs
Patient teaching
Be sure to cover:
H utilizing the vesicoureteral reflux to double void
(void once and then try to void again in a few
minutes)
H voiding every 2 to 3 hours whether or not the urge
exists
H recognizing and reporting recurring signs of UTI
(painful, frequent, burning urination; foul-smelling
urine)
H the importance of completing the prescribed therapy
or maintaining low-dose antibiotic prophylaxis.
Discharge planning
H After surgery, close medical follow-up is necessary
even if symptoms havent recurred.
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Vitamin A deficiency
Overview
Description
H Deficiency of vitamin A in the body possibly resulting
in night blindness, decreased color adjustment, keratinization of epithelial tissue, and poor bone growth
H With therapy, excellent chance of reversing symptoms
of night blindness and milder conjunctival changes;
with corneal damage, emergency treatment necessary
Pathophysiology
H A fat-soluble vitamin absorbed in the GI tract, vitamin
A maintains epithelial tissue and retinal function.

H Healthy adults have adequate vitamin A reserves to
last up to 1 year; children typically dont.
Causes
H Inadequate dietary intake of foods high in vitamin A
H Night blindness (nyctalopia)
H Dry, scaly skin
H Follicular hyperkeratosis
H Shrinking and hardening of the mucous membranes
H Failure to thrive and apathy
H Corneal changes, which can lead to ulceration and
rapid destruction of the cornea (severe deficiency)
Complications
H Blindness
H Infections of the eyes and the respiratory or geni-
tourinary tract
Assessment
History
H Night blindness (nyctalopia)
H Failure to thrive
H Apathy
(liver, kidney, butter, milk, cream, cheese, and fortified margarine) or carotene, a precursor of vitamin
A found in dark green, leafy vegetables, and yellow or
orange fruits and vegetables
H Malabsorption caused by:
Celiac disease
Sprue
Obstructive jaundice
Cystic fibrosis
Giardiasis
Habitual use of mineral oil as a laxative
H Massive urinary excretion caused by:
Cancer
Tuberculosis
Pneumonia
Nephritis
H Decreased storage and transport of vitamin A from
hepatic disease
Physical findings
Incidence
General
H Affects more than 80,000 people annually world-
H Increased dietary intake of vitamin A

H Cream-based or petroleum-based products for dry
wide mostly children in underdeveloped countries

H Rare in the United States, although many disadvantaged children have substandard levels of vitamin A
Foods that contain vitamin A

The following foods contain significant amounts of
vitamin A.
H Butternut squash
H Cantaloupe
H Carrots
H Dandelion
H Kale
H Mangoes
H Red peppers
H Sweet potatoes
888
H Dry, scaly skin

H Follicular hyperkeratosis
H Conjunctival changes
H Shrinking and hardening of the mucous membranes
Test results
Laboratory
H Carotene levels below 40 mcg/dl suggest vitamin A
deficiency, but vary with seasonal ingestion of fruits
and vegetables.
H Serum levels of vitamin A below 20 mcg/dl are diagnostic.
Other
H Dietary history and typical ocular lesions suggest vitamin A deficiency.
Treatment
skin
H Control of underlying condition
Medications
H Vitamin A replacement
H Bile salts with biliary obstruction
H Pancreatin with pancreatic insufficiency
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Key outcomes
The patient will:
H improve vitamin levels
H express understanding of dietary changes needed to
improve nutritional status
H express understanding of diet high in vitamin A.
H Administer prescribed oral vitamin A supplements
with or after meals or parenterally.

H Provide information on foods high in vitamin A. (See
Foods that contain vitamin A.)
Monitoring
H Signs of hypercarotenemia (orange coloration of the
skin and eyes)

H Signs of hypervitaminosis A (children):
Rash
Hair loss
Anorexia
Transient hydrocephalus
Vomiting
H Signs of hypervitaminosis A (adults):
Bone pain
Hepatosplenomegaly
Diplopia
Irritability
Patient teaching
Be sure to cover:
H signs of hypercarotenemia and hypervitaminosis
H dietary counseling on foods high in vitamin A.
Discharge planning
H Refer the patient for nutritional counseling and, if
necessary, to an appropriate community agency.
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Vitamin B deficiency
Overview
Pyridoxine deficiency
H Rare
Cobalamin deficiency
H Most common in people older than age 40
Description
H Deficiency of vitamin B in the body

H Most common deficiencies: thiamine (B1), riboflavin
Thiamine deficiency
H Polyneuritis
H Wernickes encephalopathy
H Korsakoffs psychosis
H Palpitations
H Tachycardia
H Dyspnea
H Constipation and indigestion
Riboflavin deficiency
H Cheilosis (cracking of the lips and corners of the
mouth)
H Sore throat
H Glossitis
H Dermatitis
H Eye disturbances
Niacin deficiency
H Fatigue
H Anorexia
H Muscle weakness
H Headache
H Indigestion
H Mild skin eruptions
H Weight loss
H Dermatitis
H Dermatitis
H Occasional cheilosis or glossitis unresponsive to
riboflavin therapy
H Abdominal pain
H Vomiting
H Ataxia
H Seizures
H Pernicious anemia, anorexia, weight loss, abdominal
discomfort, constipation, diarrhea, and glossitis
H Ataxia, spasticity, and hyperreflexia
(B2), niacin (B3), pyridoxine (B6), cobalamin (B12)
Pathophysiology
H Vitamin B complex is a group of water-soluble vita-
mins essential to normal metabolism, cell growth,

and blood formation. (See Recommended daily
allowance of B-complex vitamins.)
Causes
Thiamine deficiency
H Malabsorption
H Inadequate dietary intake of vitamin B1
H Diet deficient in milk, meat, fish, green leafy vegetables, and legumes
Niacin deficiency
H Corn as a dominant staple food
H Carcinoid syndrome
H Hartnup disease
H Destruction of pyridoxine in infant formulas by autoclaving
H Pyridoxine antagonists, such as isoniazid and penicillamine
H Absence of intrinsic factor in gastric secretions
H Absence of receptor sites after ileal resection
H Malabsorption syndromes associated with sprue, intestinal worm infestation, regional ileitis, and gluten
enteropathy
H Diet low in animal protein
H Pernicious anemia
H Medication
Risk factors
H Prolonged diarrhea
H Exposure of milk to sunlight
H Treatment of legumes with baking soda
Incidence
Thiamine deficiency
H Most common nutrient deficiency in the United States
Niacin deficiency
H Usually affects adults
Complications
H Cardiomegaly
H Beriberi
H Pellagra
ALERT
Because of a triad of symptoms, pellagra is sometimes called a 3-D syndrome dementia, dermatitis, and diarrhea. If not reversed by therapeutic doses of niacin, pellagra can be fatal.
H Central nervous system disturbances
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Recommended daily allowance of B-complex vitamins

Vitamin
Men
(23 to 50)
Women
(23 to 50)
Infants
Children
(1 to 10)
B1*
1.4 mg
1.4 mg
0.4 mg
0.7 to 12 mg
B2*
1.6 mg
1.6 mg
0.5 mg
0.8 to 1.4 mg
Niacin*
18 mg
18 mg
5 to 8 mg
9 to 16 mg
B6
2.2 mg
2.2 mg
0.4 mg
0.9 to 1.6 mg
B12
3 mcg
3 mcg
0.3 mcg
2 to 3 mcg
*requirements per 1,000 kilocalories of dietary intake
Assessment
History
Thiamine deficiency
H Palpitations
H Dyspnea
H Constipation and indigestion
H Burning, itching, light sensitivity, and tearing of the
eyes
H Neuropathy
H Signs of mild anemia
Niacin deficiency
H Backache
H Sore mouth, tongue, and lips
H Confusion, disorientation, and neuritis may become severe enough to induce hallucinations and
paranoia
H Fatigue
H Distal limb numbness
H Depression
H Pernicious anemia
H Anorexia
H Weight loss
H Constipation, diarrhea
H Glossitis
Physical findings
Thiamine deficiency
H Tachycardia
H Ataxia, nystagmus, and ophthalmoplegia
H Seborrheic dermatitis in the nasolabial folds, scrotum, and vulva and, possibly, generalized dermatitis
involving the arms, legs, and trunk
Niacin deficiency
H Dark, scaly dermatitis, especially on exposed parts of
the body, that makes the patient appear to be severely
sunburned
H Red mouth, tongue, and lips
H Weakness
H Confusion
H Glossitis
H Seborrheic dermatitis
H Ataxia, spasticity, and hyperreflexia
Test results
Laboratory
THIAMINE DEFICIENCY
H 24-hour urine collection (commonly measured as
micrograms per deciliter [mcg/dl]) shows the following age-related deficiency levels.
Special populations
Ages 1 to 3, less than 120 mcg/dl

Adults, less than 27 mcg/dl
H In pregnant females, the 24-hour urine collection
results show:
less than 23 mcg/dl (second trimester)
less than 21 mcg/dl (third trimester).
RIBOFLAVIN DEFICIENCY
H 24-hour urine collection (measured as micrograms
per gram [mcg/g]of creatinine) shows the following

age-related deficiency levels.
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Special populations
Ages 1 to 3, less than 150 mcg/g

Adults, less than 27 mcg/g
results show:
less than 39 mcg/g (second trimester)
less than 30 mcg/g (third trimester).
NIACIN DEFICIENCY
H Deficiency is measured by N-methyl nicotinamide in
a 24-hour urine collection as micrograms per gram

(mcg/g) of creatinine.
H Adult deficiency levels are less than 0.5 mcg/g.
results show:
less than 0.5 mcg/g (first trimester)
less than 0.6 mcg/g (second trimester)
less than 0.8 mcg/g (third trimester).
PYRIDOXINE DEFICIENCY
H Xanthurenic acid is more than 50 mg/day in 24-hour
urine collection after administration of 10 g of

L-tryptophan.
H Serum and red blood cell transaminases levels are
decreased.
H Pyridoxic acid excretion in urine is reduced.
COBALAMIN DEFICIENCY
H Cobalamin serum levels are less than 150 pg/ml.
H Schilling test measures absorption of radioactive
cobalamin with and without intrinsic factor.

H Gastric analysis and hemoglobin studies uncover
causation.
Treatment
Thiamine deficiency
General
H High-protein diet, with adequate calorie intake and
thiamine rich foods (pork, peas, wheat bran, oatmeal, and liver)
Medications
H B-complex vitamins
H Thiamine supplements or thiamine hydrochloride as
part of a B-complex concentrate (with alcoholic
beriberi)
General
H Diet high in riboflavin foods (meats; enriched flour;
milk and dairy products; green, leafy vegetables;
eggs; and cereal)
Medications
H Supplemental riboflavin
Niacin deficiency
General
H Dietary enrichment (meats, fish, peanuts, brewers
yeast, enriched breads, and cereals rich in niacin;
milk and eggs, in tryptophan)
Medications
H Supplemental B-complex vitamins
H Niacinamide
General
H Symptomatic
H Dietary adjustments
H Increased carbohydrate intake before vigorous exercise
Medications
H Prophylactic pyridoxine therapy in infants and in
children with seizure disorder
H Supplemental B-complex vitamins
General
H Blood transfusion if severe
H Diet high in folate
Medications
H Parenteral cyanocobalamin in patients with reduced
gastric secretion of hydrochloric acid, lack of intrinsic factor, some malabsorption syndromes, or ileum
resections
H Folate
Key outcomes
The patient will:
H express understanding of dietary adjustments needed
to improve nutritional status.
H Administer prescribed supplements.
H Explain all tests and procedures.
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Monitoring
H Adverse effects from large doses of niacinamide, in
patients with niacin deficiency

H Dietary intake
Patient teaching
Be sure to cover:
H keeping an accurate dietary history
H that prognosis is good with treatment
H importance of adhering strictly to their prescribed
treatment for the rest of their lives
H dietary adjustments.
Discharge planning
H Refer the patient to appropriate assistance agencies if
his diet is inadequate due to adverse socioeconomic

conditions.
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Vitamin C deficiency
weaned from breast milk to cows milk without a vitamin C supplement

H Also known as scurvy
Overview
Pathophysiology
Description
H Deficiency of vitamin C in the body
H Historically common among sailors and others de-
prived of fresh fruits and vegetables for long periods;

uncommon today in the United States, except in alcoholics, people on restricted-residue diets, and infants
H Deficiency of vitamin C can lead to scurvy or inade-
quate production of collagen, an extracellular substance that binds the cells of the teeth, bones, and
capillaries.
H Because the body cant store this water-soluble vitamin in large amounts, the supply needs to be replenished daily.
Causes
Scurvys effect on gums and legs
In adults, scurvy causes swollen or bleeding gums and
loose teeth.
H Diet lacking foods rich in vitamin C, such as citrus
fruits, tomatoes, cabbage, broccoli, spinach, and

berries
H Destruction of vitamin C in foods by overexposure to
air or by overcooking
H Excessive ingestion of vitamin C during pregnancy,
which causes the neonate to require large amounts
of the vitamin after birth
H Marginal intake of vitamin C during periods of physiologic stress
Risk factors
H Hyperthyroidism
H Cancer
H Smoking
H Hemodialysis
H Alcoholism
H Economic hardship
Incidence
It also causes follicular hyperkeratosis, usually on the
legs.
H Rare in the United States

H Can affect males and females
H Petechiae
H Ecchymoses
H Follicular hyperkeratosis (especially on the buttocks
and legs)
H Signs of anemia
H Anorexia
H Limb and joint pain (especially in the knees)
H Swollen or bleeding gums (see Scurvys effect on
gums and legs)

H Loose teeth
H Insomnia
H Poor wound healing
H Ocular hemorrhages in the bulbar conjunctivae
H Beading, fractures of the costochondral junctions of
the ribs or epiphysis

H Psychological disturbances, such as irritability, de-
pression, hysteria, and hypochondriasis
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Complications
H Sudden death
Assessment
History
H Anorexia
H Limb and joint pain (especially in the knees)
H Insomnia
H Irritability
H Depression
H Hysteria
H Hypochondriasis
H Fatigue
Physical findings
H Pallor
H Petechiae
H Ecchymoses
H Follicular hyperkeratosis (especially on the buttocks
and legs)
H Swollen or bleeding gums
H Loose teeth
H Ocular hemorrhages in the bulbar conjunctivae
H Beading, fractures of the costochondral junctions of
the ribs or epiphysis
Test results
Laboratory
H Serum ascorbic acid levels are less than 0.2 mg/dl.
H White blood cell ascorbic acid levels are less than
30 mg/dl.
Other
H Dietary history revealing an inadequate intake of
ascorbic acid suggests vitamin C deficiency.
Foods that contain vitamin C

vitamin C.
H Kiwi
H Blackberries
H Lemons
H Broccoli
H Oranges
H Brussels sprouts
H Papaya
H Cantaloupe
H Strawberries
H Green and red peppers
H Peas
H Guava
H Tomatoes
H Kale
H Avoid moving the patient unnecessarily to avoid irri-
tating painful joints and muscles.

H Encourage the patient to consume foods high in vita-
min C. (See Foods that contain vitamin C.)
Monitoring
H Dietary intake
Patient teaching
Be sure to cover:
H the importance of supplemental ascorbic acid
H good dietary sources of vitamin C
H not taking too much vitamin C because excessive
doses of ascorbic acid may cause nausea, diarrhea,
and renal calculi formation and may also interfere
with anticoagulant therapy.
Treatment
General
H Diet high in foods rich in vitamin C
Medications
H Vitamin C supplements
Key outcomes
The patient will:
H Adminster prescribed ascorbic acid orally or by slow
I.V. infusion.
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Vitamin D deficiency
Incidence
Overview
H Occasionally appears in breast-fed infants not receiv-
H Once a common childhood disease, now rare in the
United States
Description
H Deficiency of vitamin D in the body
H Also known as rickets
Pathophysiology
H Deficiency of vitamin D causes failure of normal
bone calcification, which results in rickets in infants

and young children and osteomalacia in adults.
H With treatment, the prognosis is good; however, in
rickets, bone deformities usually persist, while in
osteomalacia, such deformities may disappear.
Causes
H Inadequate dietary intake of preformed vitamin D
H Malabsorption of vitamin D
H Too little exposure to sunlight
H Vitamin D-resistant rickets (refractory rickets, famil-
ial hypophosphatemia) from an inherited impairment of renal tubular reabsorption of phosphate

(from vitamin D insensitivity)
H Hepatic or renal disease
H Malfunctioning parathyroid gland (decreased secretion of parathyroid hormone), which contributes to
calcium deficiency (normally, absorption of calcium
and phosphorus through the intestine controlled by
vitamin D) and interferes with activation of vitamin D
in the kidneys
Recognizing bowlegs
This infant with rickets shows characteristic bowing of the
legs.
ing vitamin D supplementation and in infants receiving a formula with a nonfortified milk base
H May also occur in overcrowded, urban areas where
smog limits sunlight penetration
H Highest incidence in black children who, because of
their skin color, absorb less sunlight (solar ultraviolet rays irradiate 7-dehydrocholesterol, a precursor
of vitamin D, to form calciferol)
H Profuse sweating
H Restlessness
H Irritability
H Numerous bone malformations
Complications
H Spontaneous fractures
H Abnormal gait
H Short stature
Assessment
History
H Spontaneous multiple fractures
H Pain in the legs and lower back
Physical findings
H Bowlegs (see Recognizing bowlegs)
H Knock-knees
H Enlargement of wrists and ankles
H Pigeon breast
H Delayed closing of the fontanels
H Softening of the skull
H Bulging of the forehead
Test results
Laboratory
H Plasma calcium serum levels are less than 7.5 mg/dl.
H Serum inorganic phosphorus levels are less than
3 mg/dl.
H Serum citrate levels are less than 2.5 mg/dl.
H Alkaline phosphatase levels are less than 4 Bodansky
units/dl.
Imaging
H X-rays show characteristic bone deformities and abnormalities such as Loosers zones (pseudofractures).
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Treatment
General
H Sunlight exposure
Medications
H For osteomalacia and rickets (except when caused
by malabsorption), massive oral doses of vitamin D

or cod liver oil
H For rickets refractory to vitamin D or in rickets accompanied by hepatic or renal disease, 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, or a
synthetic analogue of active vitamin D
Key outcomes
The patient will:
H Obtain a dietary history to assess the patients current
vitamin D intake.
H Administer supplementary aqueous preparations of
vitamin D for chronic fat malabsorption, hydroxylated cholecalciferol for refractory rickets, and supplemental vitamin D for breast-fed infants.
Monitoring
H Dietary intake
H Comfort level
Patient teaching
Be sure to cover:
H watching for signs of vitamin D toxicity (headache,
nausea, constipation and, after prolonged use, renal
calculi).
Discharge planning
H If deficiency is due to socioeconomic conditions, re-
fer the patient to an appropriate community agency.
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Vitamin E deficiency
Overview
Description
Infants
H Edema
H Skin lesions
Adults
H Deficiency of vitamin E in the body
Complications
Pathophysiology
H Disorders of reproduction
H Abnormalities of muscle, liver, bone marrow, and
H Vitamin E (tocopherol) appears to act primarily as
brain function
an antioxidant, preventing intracellular oxidation of

polyunsaturated fatty acids and other lipids.
H Deficiency of vitamin E usually manifests as hemolytic
anemia in low-birth-weight or premature neonates.
With treatment, prognosis is good.
H Hemolysis of RBC
H Skeletal muscle dystrophy
Causes
History
H In infants, usually results from consuming formulas
high in polyunsaturated fatty acids that are fortified

with iron but not vitamin E (Such formulas increase
the need for vitamin E because the iron supplement
catalyzes the oxidation of red blood cell [RBC]
lipids.)
H Conditions associated with fat malabsorption
Incidence
H Uncommon in adults but possible in people whose
diets are high in polyunsaturated fatty acids, which

increase vitamin E requirements, and in people with
vitamin E malabsorption, which impairs RBC survival
Foods that contain vitamin E

vitamin E.
H Almonds
H Almond oil
H Asparagus
H Avocadoes
H Canola oil
H Corn
H Corn oil
H Cottonseed oil
H Hazelnuts
H Kiwi
H Mangoes
H Nuts
H Olives
H Safflower oil
H Soybeans
H Soybean oil
H Sunflower seeds
H Wheat germ
H Wheat germ oil
898
Assessment
Physical findings
H Edema
H Skin lesions
Test results
Laboratory
H Serum alpha-tocopherol levels are below 0.5 mg/dl
in adults and below 0.2 mg/dl in infants.
H Creatinuria, increased creatine kinase levels, hemolytic anemia, and an elevated platelet count support
the diagnosis.
Other
H Dietary and medical histories suggest vitamin E deficiency.
Treatment
General
H Diet high in foods rich in vitamin E, such as vegetable
oils, whole grains, dark green leafy vegetables, nuts,

and legumes
Medications
H Vitamin E supplementation
Key outcomes
The patient will:
H Encourage patient to consume foods high in vitamin
E. (See Foods that contain vitamin E.)
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Monitoring
H Dietary intake
Patient teaching
Be sure to cover:
H preventing deficiency by providing vitamin E supplements for low-birth-weight infants receiving formulas
not fortified with vitamin E and for adults with vitamin E malabsorption
H dietary changes
H that food manufacturers fortify many products
with vitamins and minerals (Read the nutrition facts
panel of food labels to find out if a food contains
vitamin E.)
H that most adults in the United States get enough vitamin E from their normal diets to meet current recommendations. (Caution those on low-fat diets that
low-fat intake can substantially decrease vitamin E
intake if appropriate food choices arent made.)
Discharge planning
H If vitamin E deficiency is related to socioeconomic
conditions, refer the patient to appropriate community agencies.
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Vitamin K deficiency
Overview
Incidence
H Vitamin K deficiency is common among neonates in
the first few days postpartum due to poor placental

transfer of vitamin K and inadequate production of
vitamin K-producing intestinal flora.
Description
H Deficiency of vitamin K in the body
H Abnormal bleeding tendency
Pathophysiology
Complications
H Vitamin K is an element necessary for formation of
H Bleeding
prothrombin and other clotting factors in the liver;

deficiency produces abnormal bleeding.
H If the deficiency is corrected, the prognosis is excellent.
H Vitamin K is found in specific foods and is also made
by the bacteria that line the GI tract.
Assessment
History
H Prolonged or easy bleeding
Causes
Physical findings
H Prolonged use of drugs, such as the anticoagulant
H Ecchymosis
H Petechiae
dicumarol and antibiotics that destroy normal intestinal bacteria

H Obstruction of the bile duct or bile fistula
H Malabsorption of vitamin K due to sprue, pellagra,
bowel resection, ileitis, or ulcerative colitis
H Chronic hepatic disease
H Cystic fibrosis
Test results
Laboratory
H Prothrombin time (PT) 25% longer than the normal
range of 10 to 20 seconds confirms the diagnosis of
vitamin K deficiency after other causes of prolonged
PT (such as anticoagulant therapy or hepatic disease) have been ruled out.
Foods that contain vitamin K
Treatment

vitamin K.
General
Breads, cereals, rice, and pasta
H Diet rich in foods high in vitamin K, such as green
H Oats
H Wheat bran
H Whole wheat flour
Fruits
H Avocados
Vegetables
H Broccoli
H Cabbage
H Cauliflower
H Endive
H Kale
H Lentils (dry)
H Lettuce (iceberg)
H Soybeans
H Spinach
H Swiss chard
H Turnip greens
H Watercress
Organ meats
H Beef liver
H Chicken liver
H Pork liver
Fats, oils, sugars

H Corn oil
H Soybean oil
leafy vegetables, cereals, soybeans, and other vegetables. (See Foods that contain vitamin K.)
Medications
H Vitamin K
Key outcomes
The patient will:
H show less tendency to bleed easily
H show improved laboratory values.
H Encourage the patient to consume foods high in vita-
min K.
H Administer vitamin K to neonates and patients with fat
malabsorption or with prolonged diarrhea caused by

colitis, ileitis, or long-term antibiotic therapy.
Monitoring
H PT
H Signs of bleeding
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Patient teaching
Be sure to cover:
H warning against self-medication with or overuse of
antibiotics, which destroy the intestinal bacteria necessary to generate significant amounts of vitamin K
H dietary counseling
H warning the patient to take safety precautions because vitamin K deficiency can cause an increased
risk of bruising and bleeding.
901
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Vitiligo
Overview
H About 50% of cases beginning between ages 10 and
30
H No racial predilection
H Males and females about equally affected (Females
tend to seek treatment more than males.)
Description
H Hypopigmentation condition of the skin

H May cause a serious cosmetic problem
H Concurrent risk of other diseases, especially thyroid
H Loss of pigment
H Locally increased sunburn
Pathophysiology
H Extreme photosensitivity in depigmented areas

H Hypersensitivity reactions to therapeutic agents and
H Destruction of melanocytes and circulating antibod-
ies results in hypopigmented areas.
Causes
H Unknown; may have both genetic and environmental
components
Risk factors
H In about 30% of patients, first-degree relative with
the same disorder

Stressful physical or psychological events

Chemical agents, such as phenols and catechols
H Associated concurrent diseases:
Thyroid dysfunction
Pernicious anemia
Addisons disease
Aseptic meningitis
Diabetes mellitus
Complications
to dyes or cosmetics used to camouflage lesions
Assessment
History
H Familial history of vitiligo
Physical findings
H Depigmented or stark-white skin patches; almost im-
perceptible on fair-skinned whites

H Patches usually bilaterally symmetrical, with distinct
Incidence
borders that may be raised and hyperpigmented (see

Recognizing vitiligo)
H Patches most likely over bony prominences, around
orifices, within body folds, and at sites of traumatic
injury
H Hair within lesions also possibly white
H Prematurely gray hair
H Ocular pigment changes
H Affects about 1% of U.S. population

H Onset at any age
Test results
Recognizing vitiligo
This illustration shows characteristic depigmented skin
patches in vitiligo. These patches are usually bilaterally
symmetrical, with distinct borders.
H Woods light examination in a darkened room shows
vitiliginous patches in fair-skinned patients.
H Skin biopsy result confirms the diagnosis.
Treatment
General
H Sunscreens
H Cosmetics and skin dyes as cover-ups
Medications
H Repigmentation compounds, such as topical corti-
costeroids or calcipotriene
H Depigmentation creams
H Oral psoralen photochemical therapy
Surgery
H Skin grafting
H Tattooing (micropigmentation)
Other
H Narrow-band ultraviolent B therapy
902
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Key outcomes
The patient will:
H verbalize understanding of the disorder and treatment
H verbalize feelings about changed body image
H Encourage expression of feelings about appearance.
H Reinforce treatment goals.
Monitoring
H Complications
Patient teaching
Be sure to cover:
H that exposure to sunlight also darkens normal skin in
patients undergoing repigmentation therapy
H the use of sunscreen, sunglasses, and protective
clothing
H that results of depigmentation are permanent
H adverse effects of sunlight.
Discharge planning
H Refer the patient to the National Vitiligo Foundation.
Vitiligo
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Volvulus
Overview
Description
H Twisting of the intestine at least 180 degrees on itself
H Marked by sudden onset of severe abdominal pain
H Results in blood vessel compression
H Causes obstruction both proximal and distal to the
twisted loop
H Occurs in a bowel segment long enough to twist,
most commonly the sigmoid colon (small bowel a
common site in children)
H Other common sites: the stomach and cecum
Pathophysiology
H The colon twists on its mesentery.
H A closed loop obstruction occurs, affecting venous
drainage and arterial inflow.

H Cecal volvulus is a congenital defect in the peri-
toneum with inadequate fixation of the cecum. (See

What happens in volvulus.)
Risk factors
H Straining at stool
H Pregnancy
H Intestinal malignancy
H Hernia
H High-bulk diet
H History of previous attacks
H Use of chronic neuropsychotropic drugs
H Chronic constipation and laxative abuse
Incidence
H Varies worldwide in cases of volvulus of the large
bowel
H Accounts for 1% to 5% of all large-bowel obstruc-
tions in advanced Western populations

H Most common sites: sigmoid colon (80%), cecum
(15%), transverse colon (3%), and splenic flexure

(2%)
H Common in regions of Africa, Southern Asia, and
South America
H About 50% of large-bowel obstructions caused by
volvulus occurring in the volvulus belt of Africa
and the Middle East
Causes
H Anomaly of bowel rotation in utero

H Ingested foreign body
H Adhesions
H Meconium ileus (in patients with cystic fibrosis)
H Severe abdominal pain and distention

H Vomiting
H Constipation
What happens in volvulus

Although volvulus may occur anywhere in a bowel segment long enough to twist, the most common site, as this illustration
depicts, is the sigmoid colon, causing edema within the closed loop and obstruction at its proximal and distal ends.
NORMAL BOWEL SEGMENT
Sigmoid colon
VOLVULUS
Edematous intestine
Counterclockwise
twist
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Volvulus
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Complications
H Strangulation of the twisted bowel loop
H Bowel ischemia and infarction
H Bowel perforation
Assessment
History
H Severe abdominal pain
H Bilious vomiting
H Constipation
Physical findings
H Palpable abdominal mass
Test results
Laboratory
H White blood cell count, in strangulation, is greater
than 15,000/ml; in bowel infarction, its greater than
20,000/ml.
Imaging
H Abdominal X-rays may show multiple distended bowel loops and a large bowel without gas. In midgut
volvulus, abdominal X-rays may be normal.
H Barium enema, in cecal volvulus, shows barium filling the colon distal to the affected section of cecum;
in sigmoid volvulus, barium may twist to a point and,
in adults, take on an ace of spades configuration.
H regain normal bowel function

H express an understanding of the disorder and treat-
ment regimen.
H Adminster prescribed drugs.
H Adminster prescribed I.V. fluids.
Monitoring
H Pain control
H Bowel function
H Vital signs
H Wound site
Patient teaching
Be sure to cover:
H preoperative teaching
adverse effects
H the signs and symptoms of infection
H the importance of follow-up care.
Discharge planning
Treatment
General
H For adults with sigmoid volvulus, nonsurgical treat-
ment: proctoscopy to check for infarction and reduction by careful insertion of a flexible sigmoidoscope
to deflate the bowel
H I.V. therapy
H Nothing by mouth until condition resolves
H Bed rest until condition resolves
Medications
H Antibiotics
H Analgesics
Surgery
H For children with midgut volvulus
H Detorsion (untwisting)
H Resection and anastomosis
Key outcomes
The patient will:
pain
Volvulus
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von Willebrands
disease
Overview
Description
H Hereditary bleeding disorder characterized by pro-
longed bleeding time, moderate deficiency of clotting

factor VIII (antihemophilic factor), and impaired
platelet function
H Also known as angiohemophilia, pseudohemophilia, and vascular hemophilia
Test results
Laboratory
H Bleeding time is prolonged to more than 6 minutes.
H Partial thromboplastin time is slightly prolonged to
more than 45 seconds.
H Factor VIII-related antigen levels are absent or reduced, and factor VIII activity level is low.
H In vitro platelet aggregation is defective using the ristocetin coagulation factor assay test.
H Platelet count and clot retraction are normal.
H Urinalysis is positive for blood cells.
H Stool sample is heme-positive.
Treatment
Pathophysiology
General
H Mild to moderate deficiency of factor VIII and defec-
H Depends on the symptoms and underlying type of
tive platelet adhesion prolong coagulation time.

H This disease results from a deficiency of von Willebrands factor (factor VIIIVWF), which appears to occupy the factor VIII molecule and may be necessary
for the production of factor VIII and proper platelet
function.
H Defective platelet function is characterized by decreased agglutination and adhesion at the bleeding
site, reduced platelet retention when filtered through
a column of packed glass beads, and diminished
ristocetin-induced platelet aggregation.
Causes
H Inherited as an autosomal dominant trait
H Acquired form identified in patients with cancer and
immune disorders
Incidence
H Affects males and females; tends to be more common
in males
H Bleeding from the skin or mucosal surfaces
H In females, excessive uterine bleeding
Complications
H Hemorrhage
Assessment
History
H Possible familial history of the disease
H Easy bruising and frequent bleeding from the nose or
gums (petechiae rare)

H Menorrhagia
H Hemorrhage after a laceration or surgery
H Possible episodes of GI bleeding
Physical findings
H Bruises
H Abnormal bleeding
H Rash
906
von Willebrands disease
disease
H Decreasing bleeding time by local measures and re-
placing factor VIII and, consequently, factor VIIIVWF
H Avoidance of aspirin
H Alternation of activities and rest periods (if patient is
fatigued after a bleeding episode)
Medications
H Cryoprecipitate (cryoprecipitated antihemophilic fac-
tor)
H Vasopressin analogue such as desmopressin
H Factor VIII concentrates
Key outcomes
The patient will:
H experience hemodynamic stability
H have palpable peripheral pulses
H incur no injury
H exhibit adequate coping skills.
H Provide emotional support as necessary.
H During a bleeding episode, elevate the area if possi-
ble, and apply cold compresses and gentle pressure

to the bleeding site. (Pressure is usually the only
treatment necessary.)
H Adminster prescribed drugs or transfusions.
H Prevent potential injury by using an electric razor,
keeping the room free from clutter, and providing a
cushioned sitting and sleeping surface (such as a
convoluted foam mattress).
Monitoring
H Signs and symptoms of decreased tissue perfusion
H Vital signs
H Frequently, for bleeding from the skin, mucous mem-
branes, and wounds
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H After surgery, bleeding time or other clotting proce-
dure for 24 to 48 hours and for signs of new bleeding

H Adverse reactions to blood products
Patient teaching
Be sure to cover:
H the need to notify a physician after even minor trauma and before all surgery, including dental procedures, to determine whether replacement of blood
components is necessary
H warnings against using aspirin and other drugs that
impair platelet function (how to recognize overthe-counter medications that contain aspirin)
H special precautions to prevent bleeding episodes
H the importance of wearing or carrying medical identification
H measures to control bleeding and how to prevent
bleeding, unnecessary trauma, and complications.
Discharge planning
H Refer parents of an affected child for genetic coun-
seling.
von Willebrands disease
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Vulvovaginitis
Overview
Description
H Inflammation of the vulva (vulvitis) and vagina
(vaginitis)
H Prognosis good with treatment
Pathophysiology
H Because of the proximity of the vulva and vagina, in-
flammation of one usually precipitates inflammation

of the other.
Causes
Vaginitis
H Protozoan infection (Trichomonas vaginalis)
H Fungal infection (Candida albicans)
H Bacterial infection (bacterial vaginosis)
H Venereal infection (Neisseria gonorrhoeae)
H Viral infection with venereal warts or herpes simplex
virus Type 2
Vulvitis
H Parasitic infection (Phthirus pubis, crab louse)
H Traumatic injury
H Chemical irritations
H Allergic reactions, such as to douches or toilet paper
H Retention of a foreign body such as a tampon
Risk factors
H Pregnancy
H Diabetes mellitus
H Systemic broad-spectrum antibiotics
H Vaginal mucosa and vulval atrophy in menopausal
women
Incidence
H Occurs at any age
H Affects most females at some time
H Vaginal itching in most cases
H Vaginal discharge in many cases
Complications
H Inflammation of the perineum
H Skin breakdown
H Dyspareunia
H Dysuria
908
Vulvovaginitis
Assessment
History
Trichomonal vaginitis
H Vaginal irritation and itching
H Urinary symptoms, such as burning and frequency
Candidal vaginitis
H Intense vaginal itching
H Thick, white, cottage cheese-like discharge
Bacterial vaginosis
H Fishy-smelling discharge
Gonorrhea
H Dysuria
Acute vulvitis
H Vulvar burning, pruritus
H Severe dysuria
H Dyspareunia
Physical findings
Trichomonal vaginitis
H Thin, bubbly, green-tinged, and malodorous vaginal
discharge
Candidal vaginitis
H Thick, white, cottage cheese-like discharge
H Red, edematous mucous membranes with white
flecks on vaginal wall
Bacterial vaginosis
H Gray, foul, fishy-smelling discharge
Gonorrhea
H Profuse and purulent discharge
Acute vulvitis
H Vulvar edema and erythema
Herpesvirus infection
H Ulceration or vesicle formation on the perineum (active phase)
H Severe edema that may involve entire perineum
(chronic infection)
Test results
Laboratory
H Wet slide preparation and microscopic examination
of vaginal exudates are used in obtaining various test
results:
Vaginitis diagnosis requires identification of the infectious organism.
In trichomonal infections, the presence of motile,
flagellated trichomonads confirms the diagnosis.
In monilial vaginitis, 10% potassium hydroxide is
added to the slide; diagnosis requires identification of C. albicans fungus.
In bacterial vaginosis, saline wet mount shows the
presence of clue cells, giving it a stippled appearance.
Gonorrhea requires a culture of vaginal exudate to
H Diagnosis of vulvitis or a suspected sexually transmitted disease (STD) may require a complete blood
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count, urinalysis, cytology screening, biopsy of

chronic lesions to rule out cancer, and culture of
exudate from acute lesions.
H proper application of vaginal ointments and supposi-
tories
H the need for meticulous hand washing before and af-
ter drug administration
Treatment
General
H Cold compresses or cool sitz baths to relieve pruritus
H Warm compresses for severe inflammation
H Avoidance of drying soaps
H Loose clothing to promote air circulation
H For chronic vulvitis, changing problematic environ-
H preventing skin breakdown and secondary infections

H good hygiene practices
H wearing all-cotton, white underpants and avoiding
tight-fitting pants and panty hose

H abstaining from alcoholic beverages with metronida-
zole therapy
H that metronidazole therapy may turn the urine dark
brown.
mental factors
Medications
H Antibacterials
H Antiprotozoal agents
H Antipruritics
H Topical estrogen ointments
H Antivirals
Key outcomes
The patient will:
H express concerns about self-concept, self-esteem,
and body image
H use available counseling or a support group.
H Encourage expression of feelings.
H Report cases of STDs to the public health authorities.
Monitoring
H Vaginal discharge
H Signs and symptoms of secondary infection
Patient teaching
Be sure to cover:
H the correlation between sexual contact and spread of
vaginal infections
H using condoms to prevent or decrease the spread of
sexually transmitted infections
H notifying sexual partners of the need for treatment
H abstaining from sexual intercourse until the infection
resolves
H completing prescribed drugs, even if symptoms subside
Vulvovaginitis
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W
Warts
Overview
Description
H Common, benign, skin growths

H Prognosis varies, some disappearing readily with
treatment, others necessitating more vigorous and

prolonged treatment
H Also known as verrucae
Pathophysiology
H Warts are small harmless tumors of the skin caused
by a virus.
H Most are well-defined.
H Mode of transmission is probably through direct
contact, but autoinoculation is possible.
Plantar
H Slightly elevated or flat
H Occur singly or in large clusters (mosaic warts), primarily at pressure points of the feet
Digitate
H Fingerlike, horny projection arising from a peashaped base
H On scalp or near hairline
Condyloma acuminatum (moist wart)
H Usually small, pink to red, moist, and soft
H Single or in large cauliflower-like clusters on the
penis, scrotum, vulva, or anus
H May be transmitted through sexual contact; not
always venereal in origin
Complications
H Scarring
H Recurrence of wart
H Formation of keloid
H Warts are categorized by location and appearance.
Causes
H Infection with the human papillomavirus, a group of
ether-resistant, deoxyribonucleic acid-containing papovaviruses
Risk factors
H Breaks in skin
H Nail biting
Incidence
H Highest in children and young adults, but may occur
at any age
H Clinical manifestations dependent on the type of wart
and its location.

Common (verruca vulgaris)
H Rough, elevated, rounded surface
H Appears most commonly on limbs, particularly hands
and fingers
H Most prevalent in children and young adults
Filiform
H Single, thin, threadlike projection
H Commonly occurs around the face and neck
Periungual
H Rough, irregularly shaped, elevated surface
H Occurs around edges of fingernails and toenails
H When severe, may extend under the nail and lift it off
the nail bed, causing pain
Flat (juvenile)
H Multiple groupings of up to several hundred slightly
raised lesions with smooth, flat, or slightly rounded
tops
H Common on the face, neck, chest, knees, dorsa of
hands, wrists, and flexor surfaces of the forearms
H Usually in children but can affect adults
H Distribution usually linear because spreading possible from scratching or shaving
910
Warts
Assessment
History
H Based on type and location
H Contact with someone having warts
Physical findings
H Small, hard, flat-to-raised lump or lesion on the skin
H Small, flat lesion on forehead, cheeks, arms, or legs
H Rough, round, painful lesion on sole
H Rough growth around fingernails or toenails
Test results
H Recurrent anal warts require sigmoidoscopy to rule
out internal involvement, which may necessitate
surgery.
H Skin biopsy may confirm diagnosis in some cases.
Other
H Visual examination usually confirms the diagnosis.
Treatment
General
H Cryotherapy
Medications
H Acid therapy (primary or adjunctive)
H 25% podophyllin in compound benzoin tincture (for
venereal warts)
H Imiquimod cream
H Bleomycin injection
Surgery
H Electrodesiccation and curettage (see Removing
warts by electrosurgery)
H Carbon dioxide laser therapy
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Removing warts by electrosurgery

1. Injection of 1% to 2% lidocaine under and around the
wart, avoiding the wart itself
2. Electrodesiccation of the wart
3. Removal of the wart tissue with a curette and

curved scissors
4. Light desiccation of the area to control bleeding and

prevent recurrence
Key outcomes
The patient will:
H express feelings about change in body image
H exhibit improved or healed lesions.
H During acid or podophyllin therapy, protect the sur-
rounding area with petroleum jelly or sodium bicarbonate (baking soda).
H Bleeding
H Lesion healing
Patient teaching
Be sure to cover:
H that conscientious adherence to prescribed therapy
is essential
H that the patients sex partner may also need treatment
H need to avoid direct contact with warts.
Monitoring
Warts
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West Nile encephalitis

Overview
Description
H An infectious disease, part of a family of vector-borne
diseases that also includes malaria, yellow fever, and

Lyme disease
H Mortality rate from 3% to 15%; higher in elderly
population
H Ticks infected with the virus found in Africa and Asia
only; role of ticks in transmission and maintenance
of the virus uncertain
H Also called West Nile virus
Pathophysiology
H Virus has an incubation period of 5 to 15 days after
exposure.
H Mosquitoes become infected by feeding on birds
contaminated with the virus.
Assessment
History
H Headache
H Myalgia
H Neck stiffness
H Possible recent exposure to bodies of water, dead
birds, or recent mosquito bites

H Decreased appetite
H Nausea
H Vomiting
H Diarrhea
Physical findings
H Fever
H Rash
H Swollen lymph glands
H Stupor and disorientation
H Stiff neck
H The virus is transmitted to a human by the bite of an
Test results
infected mosquito (mostly the Culex species).

H Disease primarily causes inflammation or encephalitis of the brain.
Laboratory
H White blood cell (WBC) count is normal or increased.
H Enzyme-linked immunosorbent assay (ELISA), the
MAC-ELISA, allows a rapid and definitive diagnosis.
H Accurate diagnosis is possible only when serum or
cerebrospinal fluid specimens are obtained while the
patient is still hospitalized with acute illness and they
show an elevated WBC count and protein levels.
Imaging
H Magnetic resonance imaging may show inflammation.
Causes
H A flavivirus commonly found in humans, birds, and
other vertebrates in Africa, West Asia, and the Middle

East
Risk factors
H Recent chemotherapy
H Recent organ transplantation
H Pregnancy
H Advanced age
H Breast-feeding
Incidence
H In temperate areas, occurs mainly in late summer or
early fall
H In milder climates, can occur year-round
H Risk greater in areas with active cases
H Greatest risk in those older than age 50 and those
with compromised immune systems
H Incubation period 5 to 15 days after exposure
H No symptoms in most patients bitten by infected mos-
quito; only 1 in 300 getting sick

H Fever
H Headache
H Myalgia
Complications
H Seizures
H Death
912
Treatment
General
H No specific treatment
H Respiratory support
Medications
H Antipyretics
Key outcomes
The patient will:
H have adequate cardiac output
H remain afebrile
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Prevention
H Maintain adequate hydration with I.V. fluids.

H Adminster prescribed medications.
H Provide respiratory support measures when needed.
H Follow standard precautions when handling blood or
Preventing West Nile

encephalitis
other body fluids.

H Report any suspected cases of West Nile encephalitis
to the state department of health.
Monitoring
H Neurologic status
H Vital signs
Patient teaching
Be sure to cover:
H the proper use of insect repellants, which can irritate
the eyes and mouth, and to avoid applying repellant
to the hands of children (shouldnt be applied to
children younger than age 3) (see Preventing West
Nile encephalitis)
H the expected course and outcomes of the illness
H the need to drink fluids to avoid dehydration
H how to stop mosquitoes from breeding by:
cleaning out birdbaths and wading pools at least
once per week
cleaning roof gutters and downspout screens
eliminating any standing water
not allowing water to collect in trash cans
turning over or removing containers in yards
where rainwater collects, such as toys and old
tires.
To reduce the risk of infection with West Nile encephalitis,

advise patients to follow these guidelines:
H Stay indoors at dawn and dusk and in early evening
when mosquitoes are biting.
H Wear long-sleeved shirts and long pants when outdoors.
H Apply insect repellent sparingly to exposed skin. Effective repellents contain 20% to 30% DEET (N,N-diethyltoluamide). DEET in high concentrations (greater than
30%) can cause adverse effects, particularly in children, and should be avoided; adults should apply repellent on children with no more than 10% DEET.
H Dont place repellent under clothing.
H Dont apply repellent over cuts, wounds, sunburn, or
irritated skin.
H Wash repellent off daily and reapply as needed.
Discharge planning
H Refer the patient to an infectious disease specialist.
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X-linked
infantile hypogammaglobulinemia
Overview
Description
H A congenital disorder in which all five immunoglobu-
lins (Ig) IgM, IgG, IgA, IgD, and IgE and circulating B cells absent or deficient but T cells intact
H Good prognosis with early treatment, except in infants developing polio or persistent viral infection;
usually causing some permanent damage, especially
in the neurologic or respiratory system
H Also called Brutons agammaglobulinemia or XLA
Pathophysiology
H B cells and B-cell precursors may be present in the
bone marrow and peripheral blood, but a mutation

in the B-cell protein tyrosine kinase causes failure of
the B cells to mature and to secrete immunoglobulin.
H Abnormal dental caries

H Polyarthritis resembling rheumatoid arthritis
Physical findings
H Retarded growth
H Lymphadenopathy and splenomegaly usually absent,
despite recurrent infections
Test results
Laboratory
H Immunoelectrophoresis confirms decreased levels or
a total absence of IgM, IgA, and IgG in the serum;
however, diagnosis by this method usually isnt possible until the infant is age 9 months.
H Antigenic stimulation confirms an inability to produce specific antibodies, although cellular immunity
remains intact.
Treatment
General
H Prevention or control of infections
H Fresh frozen plasma
Causes
Medications
H Congenital
H Immune globulin
H Antibiotics
Incidence
H Affects males almost exclusively
H Occurs in 1 in 50,000 to 100,000 births
Key outcomes
H Asymptomatic until age 6 months, when transplacen-
tal maternal immunoglobulins that provided immunity have been depleted

H Recurrent infections such as bacterial otitis media
The patient will:

H demonstrate an understanding of the disorder
H prevent infections by limiting exposure
H report signs and symptoms of infection promptly.
Complications
H Hepatitis
H Enteroviral infections
H Poliovirus
H Maintain adequate nutrition and hydration.

H Perform chest physiotherapy if required.
Assessment
H Vital signs
H Intake and output
History
H Recurrent infections:
914
Otitis media
Pneumonia
Dermatitis
Bronchitis
Meningitis
Conjunctivitis
X-linked infantile hypogammaglobulinemia
Monitoring
Patient teaching
Be sure to cover:
H recognizing early signs of infection and reporting
them promptly
H cleaning cuts and scrapes immediately
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H avoiding crowds and people who have active infec-
tions
H how to meet nutritional and fluid needs during acute
infection.
Discharge planning
H Suggest genetic counseling if parents have questions
about the vulnerability of future offspring.
X-linked infantile hypogammaglobulinemia
915
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Zinc deficiency
Overview
H Dysgeusia (unpleasant taste)

H Hyposmia (decreased odor acuity)
H Dysosmia (unpleasant odor in nasopharynx)
H Severe iron deficiency anemia
H Bone deformities
Description
Complications
H Insufficient amounts of zinc, an essential trace ele-
H Hypogonadism
H Dwarfism
H Hyperpigmentation
ment thats a vital component of many enzymes and

present in the bones, teeth, hair, skin, testes, liver,
and muscles
H Good prognosis with correction of the deficiency
Pathophysiology
Assessment
H Zinc deficiency causes impairment of synthesis of de-
History
oxyribonucleic acid, ribonucleic acid and, ultimately,

protein, and alters normal blood concentrations of
vitamin A by mobilizing it from the liver.
H About 90% of zinc stores are in bone and skeletal
muscle.
H Weight loss
H Poor appetite
H Short stature
H Mental lethargy
H Diarrhea
H Intercurrent infections
Causes
H Excessive intake of foods (containing iron, calcium,
vitamin D, and the fiber and phytates in cereals) that

bind zinc to form insoluble chelates that prevent its
absorption
H Blood loss from parasitism
H Low dietary intake of foods containing zinc
Risk factors
H Alcohol consumption
H Corticosteroids
H Celiac disease
Incidence
H Most common in people from underdeveloped coun-
tries, especially in the Middle East

H Children most susceptible to this deficiency during
periods of rapid growth
H Sparse hair growth
H Soft, misshapen nails
H Anorexia
H Hypogeusesthesia (decreased taste acuity)
Physical findings
H Sparse hair growth
H Rough skin
H Striae
H White spots on fingernails
H Acne
Test results
Laboratory
H Fasting serum zinc levels are below 70 mcg/dl.
Treatment
General
H Correction of the underlying cause
H Diet high in zinc
Medications
H Zinc supplementation
Key outcomes
Foods that contain zinc

The following foods contain significant amounts of zinc.
H Beans
H Dairy products
H Fortified breakfast cereals
H Nuts
H Oysters
H Poultry
H Red meat
H Seafood
H Whole grains
916
Zinc deficiency
The patient will:

H express understanding of dietary needs
H improve zinc levels
H experience improved skin condition.
H Provide information about dietary sources of zinc.
(See Foods that contain zinc.)
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Monitoring
Patient teaching
Be sure to cover:
H taking zinc supplements with milk or meals to prevent gastric distress and vomiting
H following a balanced diet that includes foods high
in zinc
H correct use of calcium and iron supplements.
Zinc deficiency
917
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Zollinger-Ellison
syndrome
H GI bleeding
H Steatorrhea
H Duodenal ulceration
Overview
H Metastatic disease
H Hemorrhage
H Perforation
H Obstruction
H Production of other substances, such as corti-
Description
H Rare disease characterized by:
Markedly elevated gastric acid secretion

Peptic ulcer disease
A gastrinoma or non-beta islet cell tumor of the
pancreas or duodenal wall that produces the hormone gastrin
H Gastrinomas, may be single or multiple, large or
small, and benign or malignant.
H More than two-thirds of gastrinomas malignant;
about one-third metastasized to the liver at the time
of diagnosis
H Causes numerous ulcers in unusual areas of the
stomach or intestine, more resistant to treatment
than other ulcers; ulcers commonly returning after
treatment
Pathophysiology
H Tumors that produce excess gastrin form in the pan-
creas, stomach, and duodenum.

H Hypergastrinemia causes hypertrophy of the gastric
mucosa, leading to increased numbers of parietal

cells and increased acid output.
H Gastrin also stimulates acid secretion, resulting in increased basal acid secretion.
H This leads to GI mucosal ulceration.
Causes
H Unknown
H May be hereditary or associated with some cancers
H May be associated with multiple endocrine neoplasia,
type I (MEN I); about 25% of people having gastrinomas have them as part of MEN I
Risk factors
H MEN I
H Family history of ulcer disease
Incidence
Complications
cotropin, with resulting Cushings syndrome

H Decrease in vitamin B12 levels possible due to med-
ication effects
Assessment
History
H Numerous ulcers resistant to treatment
H Presence of peptic ulcer disease without evidence of
bacterial etiology
H Signs and symptoms of disorder
H Anemia
Physical findings
H Weight loss
H Abdominal pain
H Hematemesis
Test results
Laboratory
H Gastrin secretion studies are elevated.
H Fasting serum gastrin level is elevated.
H Basal gastric acid output is elevated.
H Decreased gastric pH shows high acidity.
H Serum calcium, phosphorus, cortisol, and prolactin
levels rule out MEN I.
Imaging
H Computed tomography scans locate tumors.
H Magnetic resonance imaging locates tumors.
H Upper GI endoscopy shows ulcers.
H Endoscopic ultrasound locates tumors and allows a
biopsy to be obtained.
H Somatostatin receptor scintigraphy determines tumor
metastasis.
H Portal vein sampling
H Fewer than three out of every one million people in
the United States

H Average age at diagnosis: 50
H Slightly higher in males than in females
H Gnawing, burning abdominal pain
H Diarrhea
H Nausea
H Vomiting
H Weight loss
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Zollinger-Ellison syndrome
Treatment
General
H Blood transfusions, if necessary
H Surgical removal of tumors generally unsuccessful
because gastrinomas usually small, numerous, and

difficult to locate; regrowth common
Medications
H Proton pump inhibitors to suppress acid production
and promote healing
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H Histamine blockers to reduce the amount of hy-
drochloric acid released into the digestive tract

H Chemotherapy to treat malignant tumors
Surgery
H To stop hemorrhaging from bleeding ulcers, relieve
an obstruction, or close a perforation

H Sympathectomy of nerves that promote acid secretion
H Laparotomy to remove resectable tumors
Key outcomes
The patient will:
H maintain balanced fluid volume
H verbalize understanding of disorder and treatment
H return to normal bowel elimination
H maintain appropriate weight.
H Assist with dietary choices.
H Provide preoperative and postoperative care, as ap-
propriate.
Monitoring
H Intake and output
H Daily weight
H Pain control
H Wound healing (if surgery is performed)
Patient teaching
Be sure to cover:
H diet modifications
Zollinger-Ellison syndrome
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Less common diseases

Selected references
Web resources
Index
921
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Less common diseases

Names
Description
Treatment
Achilles tendon
contracture
Shortening of the Achilles tendon that results

in foot pain and strain with limited ankle dorsiflexion; may be due to a congenital abnormality, reaction to chronic poor posture, or a
paralytic condition
Conservative treatment includes raising the

inside heel of the shoe, lowering the heels
of shoes, stretching exercises, support
braces, casting, and analgesics.
Tenectomy may be performed for patients
with fixed footdrop.
Actinomycosis
(lumpy jaw)
Infection caused by gram-positive anaerobic

bacillus Actinomyces israelii, resulting in
painful swellings of granulomatous, suppurative lesions with abscesses commonly on the
head, neck, thorax, or abdomen
High-dose I.V. penicillin cycline is administered for 1 to 2 months, followed by oral

penicillin for 1 to 6 months.
Lesions are surgically excised and drained.
Adenovirus
infection
Acute, self-limiting febrile infection resulting

in inflammation of the respiratory or ocular
mucous membranes, or both; 35 serotypes
cause five major infections; transmitted by direct inoculation into the eye, oral-fecal route,
or inhalation of droplets; highly contagious
Bed rest, antipyretics, and analgesics may

be prescribed as needed.
Ocular infections may require corticosteroid
therapy and supervision by an ophthalmologist.
Hospitalization is required for infants with
pneumonia and in epidemic keratoconjunctivitis.
Alpha1-antitrypsin
deficiency
Autosomal recessive inherited disorder resulting in emphysema and liver dysfunction problems
Enzyme replacement therapy is given

weekly.
Smoking cessation and asthma control are
promoted to prevent infection and lung
problems.
Vaccination against hepatitis B is given prophylactically.
Liver and lung function are monitored.
Alports syndrome
Hereditary nephritis characterized by recurrent gross or microscopic hematuria; associated with deafness, eye defects, albuminuria,
and progressive azotemia
Antihypertensives are given for hypertension.

Hearing aids, learning sign language, and
corrective eyewear or surgical repair of
cataracts are employed.
Dialysis or kidney transplantation may be
required for end-stage renal failure.
American
trypanosomiasis
(Chagas disease)
Febrile parasitic illness prevalent in Central

and South America; cardiomyopathy may occur; megaesophagus and megacolon may develop many years later; can be severe in children
Nifurtimox or benznidazole is given during

the acute phase.
Supportive treatment is given for symptoms
caused by heart and intestinal complications during the chronic phase.
922 Less common diseases
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Names
Description
Treatment
Amyloidosis
A chronic disease resulting in the accumulation of an abnormal fibrillar scleroprotein,

which infiltrates body organs and soft tissues,
resulting in permanent and usually lifethreatening organ damage
Kidney transplantation is used for renal failure, although the new organ may also develop amyloidosis.
If the heart is affected, diuretics, digoxin,
antiarrhythmics, pacemakers, or heart
transplantation may be necessary.
In end-stage GI involvement, total parenteral nutrition is used as needed for malnutrition.
Anal stricture
(anal stenosis or
contracture)
Develops when the lumen of the anus decreases and stenosis prevents dilation of the
sphincter and defecation; can result from
scarring after surgery, inflammation, laxative
abuse, surgical trauma, or congenital abnormality
Conservative treatment includes laxatives,

suppositories, and enemas.
A dilator is used daily.
Anoplasty or excision of eschar is employed with lateral internal sphincterotomy.
Angiofibroma,
juvenile
Highly vascular nasopharyngeal tumor made

up of fibrous tissue with thin-walled blood
vessels that may grow to completely fill the
nasopharynx, nose, paranasal sinuses, and
the orbit
Surgery or cryosurgical techniques after

embolization decreases vascularization.
Barometer-makers
disease
(chronic mercury
poisoning)
Soreness of gums, loosening of teeth, hypersalivation, fetid breath, abdominal cramping

and diarrhea, weakness, peripheral neuropathy, ataxia, intention tremors, irritability and
depression, tachycardia, hypertension, reproductive failures, birth defects (especially developmental neurologic damage), and death
Chelation therapy with dimercaprol is initiated.

Neurologic toxicity generally isnt considered reversible.
Supportive therapy is given for chronic effects.
Berylliosis
A form of pneumoconiosis resulting from inhalation of beryllium or from its absorption

through the skin; characterized by systemic
granulomatous disorder with predominant
respiratory symptoms that can lead to respiratory failure, cor pulmonale, and death
Beryllium ulcer requires excision or curettage. Acute berylliosis requires corticosteroid therapy.
Hypoxia may require oxygen; respiratory
failure, mechanical ventilation. Other respiratory symptoms may be treated with bronchodilators and chest physiotherapy.
Chronic forms are treated with corticosteroids and immunosuppressants.
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Names
Description
Treatment
Blastocystis hominis
infection
(blastocystosis)
Parasitic infection resulting in watery or loose

stools, diarrhea, abdominal pain, anal itching,
weight loss, and flatus; conversely, no symptoms may be present
Drug therapy includes ketoconazole or itraconazole.

Amphotericin B is required for severe disease.
Provide nutritional support.
Monitor for fluid and electrolyte imbalances.
Bouillauds syndrome
(rheumatic endocarditis)
Manifests as a heart murmur of either mitral

or aortic insufficiency; pericarditis and heart
failure are seen in severe cases
Although no specific cure is available, a

course of penicillin should still be given to
eliminate group A streptococci.
Supportive therapy is provided to reduce
morbidity and mortality.
Budd-Chiari
syndrome
Hepatic vein obstruction that impairs blood

flow out of the liver, producing massive ascites and hepatomegaly; may be acute or
chronic
Surgery is performed to shunt hepatic

blood flow and remove obstruction.
If cause is congenital, transcardiac membranectomy or percutaneous stent placement is performed for patients with inferior
vena cava web.
Liver transplantation may be recommended
for patients with marked hepatocellular
dysfunction.
Cat-scratch fever
(cat-scratch disease)
Subacute self-limiting disease characterized

by a primary local lesion and regional lymphadenopathy; more common in children and
young adults in contact with cats (90% of
cases); disseminated form, bacillary angiomatosis, found in immunocompromised
people such as those infected with the human
immunodeficiency virus
Symptomatic treatment is given.

If patient is ill, ciprofloxacin, doxycycline,
co-trimoxazole, erythromycin, cefoxitin, cefotaxime, mezlocillin, aminoglycosides, or
antimycobacterials may be administered.
Celiac disease
(sprue, nontropical
sprue, gluten
intolerance)
Poor food absorption and gluten intolerance

from environmental and genetic factors; recurrent diarrhea, steatorrhea, abdominal distention, and anorexia, resulting in malnutrition; hematologic (anemia), musculoskeletal
(from vitamin D deficiency), neurologic, dermatologic, and endocrine systems affected
Gluten (wheat, rye, barley, and oat products, vegetable protein, malt, soy sauce,
grain vinegar) should be excluded from the
patients diet for life.
Supplements may be given to correct deficiencies.
Corticosteroids may be required.
Choriocarcinoma
Rapidly metastasizing malignant tumor of placental tissue that typically causes profuse
vaginal and intra-abdominal bleeding
Chemotherapy is initiated.
Uterine contents are evacuated.
A hysterectomy is rarely needed.
B-hCG levels are monitored to detect progressively decreasing levels.
Chronic
granulomatous
disease
An inherited disorder in which abnormal neutrophil metabolism impairs phagocytosis, resulting in increased susceptibility to low virulent or nonpathogenic organisms; infections
of the skin, lymph nodes, lungs, liver, and
bone occur
Antibiotics are used for early, aggressive

treatment.
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Names
Description
Treatment
Chronic
mucocutaneous
candidiasis
Inherited defect in cell-mediated (T-cell) immune responses leading to recurrent infections with Candida albicans and potential for
autoimmune-mediated endocrinopathies;
usually begins in early childhood with chronic
candidal infections; endocrinopathies include
hypoparathyroidism (and severe hypocalcemia), hypothyroidism, Addisons disease, diabetes, pernicious anemia; hepatitis
Topical or oral antifungal agents (miconazole, nystatin, fluconazole) control chronic

infection.
Therapy for endocrinopathy is organdirected, depending on the system affected.
Colorado tick fever

(mountain tick fever,
mountain fever,
American mountain
fever)
A benign infection from the bite of a wood

tick infected with Dermacentor andersoni
(Fever begins abruptly after a 3- to 6-day incubation; severe aching of the back, arms,
and legs; lethargy; headache with eye movement; photophobia; abdominal pain; nausea;
and vomiting.)
Remove the tick and keep it for identification.

Administer tetanus-diphtheria booster.
Monitor fluid and electrolyte balance.
Antipyretics are given to reduce fever.
Conversion disorder
(hysterical neurosis)
A disorder that allows a patient to resolve a

psychological conflict through the loss of a
specific physical function, such as paralysis
or blindness
Psychotherapy, family therapy, relaxation

therapy, behavioral therapy, or hypnosis
may be used alone or in combination.
Supportive therapy for affected body part is
used to prevent complications.
Cryptosporidiosis
Watery diarrhea, stomach cramps, upset

stomach, and slight fever caused by a onecelled parasite, Cryptosporidium parvum; life
threatening to those with weakened immune
systems and transplant recipients
Theres no cure, but paromomycin, atovaquone, nitazoxaine, and azithromycin

may reduce symptoms.
Reverse dehydration is used.
Immune status improves with antiviral
agents.
Cystinuria
Autosomal recessive disorder resulting from

an inborn error of amino acid transport in the
kidneys and intestine that allows excessive
urinary excretion of cystine and other dibasic
amino acids; resulting in recurrent cystine renal calculi
Theres no cure, but treatment can reduce

the risk of calculi formation.
Increase fluid intake to 3 L/day.
Sodium bicarbonate or sodium citrate help
alkalinize the urine.
Penicillamine is used to increase cystine
solubility.
Calculi are removed surgically or through
lithotripsy.
Prevent and treat urinary tract infections.
Depersonalization
disorder
Recurrent episodes of detachment in which

self-awareness is temporarily altered or lost
in the entire body or only in a limb; usually
caused by severe stress
Psychotherapy and reality-based coping

strategies may be helpful.
Dientamoeba fragilis
infection
Loose stools, diarrhea, and abdominal

cramping caused by contact with or ingestion
of stool, food, or water infected with the
parasite Dientamoeba fragilis
Infection can be prevented by prudent hand

washing.
Antimicrobial agents are available to treat
Dientamoeba fragilis.
Monitor for fluid and electrolyte imbalances.
DiGeorges syndrome
(congenital thymic
hypoplasia or
aplasia)
Fetal thymus fails to develop, leading to partial or total absence of T lymphocytes and
cell-mediated immunity; may be linked with
maternal alcoholism and fetal alcohol syndrome; increased susceptibility to infections;
hypoparathyroidism and cardiac anomalies
may also occur
Early development of life-threatening

hypocalcemia is treated immediately with
I.V. 10% calcium gluconate infusion.
Fetal thymic transplantation may be required to restore normal cell-mediated immunity.
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Names
Description
Treatment
Dissociative amnesia
Sudden inability to recall important personal

information that cant be explained by ordinary forgetfulness; usually caused by severe
psychological stress
Psychotherapy is necessary.
Hypnosis may be beneficial.
Antianxiety drugs may be ordered.
Dissociative fugue
Wandering or traveling while mentally blocking out a traumatic event; a different personality may be assumed and later cant recall
what happened; may be related to dissociative identity disorder, narcissistic personality
disorder, and sleepwalking
Psychotherapy is necessary.
Hypnosis may be beneficial.
Antianxiety drugs may be ordered.
Dissociative identity
disorder (multiple
personality disorder)
Existence of two or more distinct, fully integrated personalities in the same person;
cause unknown but some type of abuse may
have been experienced
Psychotherapy may be helpful.

Safety precautions may be needed.
Antipsychotic drugs may be ordered.
Duhrings disease
(dermatitis herpetiformis)
Chronic inflammatory disease marked by erythematous, papular, vesicular, bulbous, or

pustular lesions, with tendency toward grouping and associated with itching and burning;
usually symmetrical, with eruptions in elbows, knees, sacrum, buttocks, and occiput
Sulfa-based antibiotics are administered.

A strict gluten-free diet should be followed.
Epidermolysis
bullosa (EB)
Blisters occur in response to normally harmless heat and friction and may result in scarring with disfigurement; prognosis depends
on severity; may be inherited as an autosomal dominant or recessive disorder and
cause multiple complications because skin
and mucous membranes are affected
Avoid skin trauma. sun exposure, and high

environmental temperatures.
Severe forms may need constant medical
attention.
Supportive treatment includes protection of
the skin.
Diet therapy helps combat malnutrition and
promote healing.
Epstein-Barr virus
(mononucleosis)
Classic heterophil-positive infectious

mononucleosis, occasionally complicated by
neurologic diseases, such as encephalitis or
transverse myelitis
Generally, symptomatic treatment because

the disease has a benign course.
Fallopian tube cancer
Cancer that usually produces a palpable

mass, vague abdominal or pelvic complaints,
bloating, or pain in the early stages; over
time, excessive menstrual bleeding may occur; causes appear to be linked with nulliparity and infertility; more than half of the patients have never given birth
Total abdominal hysterectomy, bilateral

salpingo-oophorectomy, or omentectomy is
performed, followed by chemotherapy.
The patient receives external radiation for 5
to 6 weeks.
Fanconis syndrome
(de Toni-Fanconi
syndrome)
Hereditary renal disorder producing malfunctions of the proximal renal tubules, leading to
electrolyte losses and, eventually, retarded
growth and development and rickets
Symptomatic treatment may be given to

replace the patients specific deficiencies.
(Wilsons disease is treated with D-penicillamine; cystinosis is treated with cysteamine.)
Supportive therapy is given by replacing
electrolytes, normalizing pH, and giving dietary supplements.
Fever, relapsing
(tick, fowl-nest,
cabin, or vagabond
fever or bilious
typhoid)
An acute infectious disease caused by spirochetes of the genus Borrelia transmitted by

lice or ticks; presents with recurring high
fever, prostration, headache, severe myalgia,
arthralgia, diarrhea, vomiting, coughing, eye
or chest pain, splenomegaly, hepatomegaly,
lymphadenopathy, and macular rash
Tetracycline or erythromycin is given for

4 to 5 days, except during a severe febrile
attack because it may cause JarischHerxheimer reaction.
Symptomatic treatment is given; for example, parenteral fluids and electrolytes.
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Names
Description
Treatment
Gauchers disease
(glucosylceramide
storage disease,
GSDI)
Genetic enzyme deficiency that causes abnormal accumulation of glucocerebrosides in

reticuloendothelial cells; signs include hepatosplenomegaly and bone lesions
Long-term therapy includes I.V. replacement of the missing enzyme every 2 weeks.
Gene therapy is an experimental approach,
as well as N-butyldeoxynojirimycin
(OGT918) to inhibit production of glucocerebroside.
Gender identity
disorder (transsexualism)
Persistent feelings of gender discomfort and

dissatisfaction from a combination of predisposing factors (chromosomal anomaly, hormonal imbalance, impaired parent-child
bonding, and child-rearing practices)
The patient is referred for psychotherapy to

resolve conflict. Individual and family counseling is recommended.
Sex reassignment through surgery and hormonal therapy may be used.
Hallux valgus
Lateral deviation of the great toe at the

metatarsophalangeal joint, with medial enlargement of the first metatarsal head and
painful bunion formation; may be congenital
or familial, but is usually acquired from degenerative arthritis or prolonged pressure on
the foot, especially from narrow-toed, highheeled shoes
In the early stage, proper shoes and good

foot care such as felt pads to protect the
bunion, devices to separate the toes at
night, and a supportive pad and exercises
to strengthen the metatarsal arch may
eliminate the need for bunionectomy.
Surgery to realign the toe or bunionectomy
may be ordered.
Hand, foot, and

mouth disease
(HFMD)
Common disease of infants and children

characterized by fever, mouth sores, and a
rash with blisters on the hands and soles;
caused by coxsackievirus; highly contagious
Treatment is symptomatic only because

disease is self-limiting.
Acetaminophen and salt water mouth rinses (12 teaspoon salt to 1 glass warm water)
are used to provide soothing relief.
Herpangina
Acute infection caused by group A coxsackieviruses transmitted by the fecal-oral route,

resulting in sore throat, pain on swallowing,
headache, and fever that persist for 1 to 4
days and may cause seizures, anorexia, vomiting, malaise, diarrhea, and pain; grayish
white papulovesicles appear on the soft
palate
Symptomatic treatment emphasizes measures to prevent seizures (such as antipyretics and and tepid sponge baths), fluids
to prevent dehydration, and bed rest.
Provide topical anesthetics for the mouth
(benzocaine and xylocaine) as needed.
Provide a non-irritating diet.
Increase fluid intake.
Hydatidiform mole
Chorionic tumor of the placenta that occurs

early in pregnancy; may follow death of the
embryo and loss of fetal circulation, although
in many cases, there is no fetus
Uterus is evacuated by suction curettage or

abdominal hysterectomy.
Supportive treatment is given for postoperative hypovolemia and anemia.
Hypochondriasis
(Hypochondria)
The unrealistic misinterpretation of the severity and significance of physical signs or sensations as abnormal and preoccupation with
the fear of having a serious disease, which
persists despite medical reassurance to the
contrary; unlinked to cause, although stress
increases the risk; frequently develops in
people who have experienced an organic disease or have a relative who has experienced
one
The goal is to help the patient lead a productive life, despite distressing symptoms
and fears. Outpatient psychotherapy with
behavior modification is the first line of
treatment.
Symptoms must be evaluated to rule out
medical causes first.
Routine psychiatric appointments, regardless of new symptoms, help as part of psychotherapy.
Iodine deficiency
Insufficient iodine from inadequate intake or

thyroid dysfunction; complications range
from dental caries to cretinism
Iodine supplements (potassium iodide

[SSKI]) are administered to correct the deficiency.
Increase iodine intake with iodized table salt
and iodine-rich foods.
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Names
Description
Treatment
Lassa fever
Epidemic hemorrhagic fever caused by the

Lassa virus; transmitted to humans by contact with infected rodent urine, feces, and
saliva; fever persists for 2 to 3 weeks with
exudative pharyngitis, oral ulcers, lymphadenopathy and swelling of the face and neck,
purpura, conjunctivitis, and bradycardia;
shock and peripheral vascular collapse can
occur
Strict isolation is imposed for at least 3

weeks.
Drug therapy includes antiviral (I.V. ribavirin), I.V. colloids for shock, analgesics
for pain, and antipyretics for fever.
Immune plasma from patients who have recovered from Lassa fever is infused.
Leprosy
(Hansens disease)
Chronic, systemic infection with progressive

cutaneous lesions caused by Mycobacterium
leprae; attacks the peripheral nervous system
Drug regimen includes antimicrobial therapy with dapsone, rifampin, clofazimine, or

ethionamide.
Supportive care with aspirin, prednisone, or
thalidomide to control inflammation may be
used.
Leptospirosis
Infectious disease that causes meningitis, hepatitis, nephritis, or febrile disease; may be
mild (anicteric) or severe (icteric or Weils
disease)
Doxycycline or ampicillin is administered.

Supportive treatment of other symptoms is
provided.
Lichen planus
Benign, pruritic skin eruption producing scaling, purple papules with white lines or spots;
cause unknown
Relieve inflammation with topical steroids

and suppress immune response.
Antihistamines are used to reduce discomfort.
Viscous lidocaine is used for mouth lesions.
Corticosteroids may be injected into a lesion.
Topical retinoic (vitamin A) cream and other
anti-inflammatory or anti-pruritic ointments
or creams are used to reduce itching and
inflammation.
Ultraviolet light therapy may be used.
Maple syrup urine

disease
Enzyme defect in the metabolism of the

branched chain amino acids, resulting in
mental and physical retardation, reflex
changes, feeding difficulties, characteristic
odor of urine and perspiration, seizures, and
death; four clinical phenotypes: classic, intermediate, intermittent, and thiamine-responsive
Supportive treatment is provided.

Intake of protein is controlled.
Branched chain amino acids are eliminated
from the diet.
Peritoneal dialysis or hemodialysis is performed to reduce amino acid level.
One form is responsive to early initiation of
thiamine.
Marfan syndrome
Rare inherited, degenerative generalized disease of the connective tissue that causes ocular, skeletal, and cardiovascular anomalies
Treatment is aimed at relieving the symptoms such as surgical repair of aneurysms

and ocular deformities.
Preventive antibiotics are given before dental procedures.
Children shouldnt be involved in maximal
exercise programs because of concern of
aortic aneurysm.
Mastoiditis
Bacterial infection and inflammation of the air

cells of the mastoid antrum resulting in dull
ache and tenderness in the area of the mastoid process, low-grade fever, headache, and
thick, purulent drainage; meningitis, facial
paralysis, brain abscess, and suppurative
labyrinthitis may occur
Intense antibiotic therapy is administered

parenterally.
Myringotomy is performed if bone damage
is minimal.
Mastoidectomy is performed if the mastoid
is chronically inflamed.
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Names
Description
Treatment
Medullary sponge
kidney
Inherited disorder, possibly where collecting

ducts in renal pyramids dilate and cavities,
clefts, and cysts form, producing complications of calcium oxylate stones and infections
Supportive care focuses on preventing or

treating complications caused by stones
and infection. Includes increasing fluid intake and monitoring renal function.
Surgery may be required to remove stones
during acute obstruction. Nephrectomy is
required if serious, uncontrollable infection
or hemorrhage occur.
Monkeypox
Rare viral disease caused by the monkeypox

virus; occurs mainly in the rainforest areas of
central and western Africa; symptoms include
fever, headache, muscle aches, backache,
swollen lymph nodes, and exhaustion; a
papular rash develops within 1 to 3 days of
the onset of fever (In June 2003, monkeypox
was reported in prairie dogs and humans in
the United States.)
Theres no specific treatment for monkeypox.

Persons caring for infected individuals
should receive a smallpox vaccination.
Provide analgesics, antipyretics, and antihistamines as needed.
Multiple endocrine
neoplasia
A hereditary disorder in which two or more

endocrine glands develop hyperplasia, adenoma, or carcinoma concurrently or consecutively; symptoms depend on glands affected
Supportive treatment is dependent on the

affected glands.
Tumors are eradicated; subsequent treatment controls symptoms.
Neurofibromatosis
Group of inherited developmental disorders

of the nervous system, muscles, bones, and
skin that cause formation of multiple, pedunculated, soft tumors and caf-au-lait spots
Intracerebral or intraspinal tumors are removed and kyphoscoliosis is corrected.

Disfiguring or disabling growths are treated
with cosmetic surgery.
Annual eye examinations are strongly recommended.
Nocardiosis
Bacterial infection caused by gram-positive

species of the genus Nocardia and transmitted by inhalation; causes cough, mucopurulent sputum, high fever, chills, night sweats,
anorexia, malaise, and weight loss
Long-term antibiotic treatment with sulfonamides is given.

Abscesses are surgically drained and
necrotic tissue is excised.
Bed rest and supportive treatment are ordered.
Orbital cellulitis
Acute infection of the orbital tissues and eyelids that can spread to the cavernous sinus or
meninges; produces unilateral eyelid edema,
hyperemia, reddened eyelids, and matted
lashes
Hospitalization is required.
Appropriate antibiotics are given.
Supportive therapy includes administration
of fluids, application of warm moist compresses, and bed rest.
Surgical drainage may be necessary.
Parainfluenza
Group of respiratory illnesses caused by the

parainfluenza virus that affect the upper and
lower respiratory tracts; transmitted by direct
contact or inhalation of airborne droplets
Treatment regimen includes bed rest, antipyretics for fever, analgesics for pain, and
antitussives for cough.
Specific treatments are available for croup
and bronchiolitis.
Paroxysmal
nocturnal
hemoglobinuria
Red cell breakdown with release of hemoglobin in the urine, resulting in dark-colored
urine in the morning; symptoms include hemolytic anemia, thrombosis of large vessels,
and a deficiency of hematopoiesis resulting in
anemia (pancytopenia)
Symptomatic treatment with corticosteroids

is provided.
Androgen therapy is administered.
Oral iron supplements and folic acid are
given as needed.
Transfusions are administered to treat
severe anemia.
Thrombotic complications are treated.
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Names
Description
Treatment
Penile cancer
Malignant, ulcerative or papillary (wartlike,

nodular) lesions, which may become quite
large before spreading beyond the penis, potentially destroying the glans prepuce and invading the corpora; generally associated with
poor personal hygiene and phimosis in uncircumcised men, although the exact cause is
unknown
Depending on the stage of progression,

treatment includes surgical resection of the
primary tumor and, possibly, chemotherapy
(bleomycin) and radiation.
Invasive tumors require partial penectomy
(unless contraindicated because of the patients young age); tumors of the base of
the penile shaft require total penectomy and
inguinal node dissection.
Radiation therapy may improve treatment
effectiveness after resection of localized lesions without metastasis; it may also reduce the size of lymph nodes before nodal
resection.
Psychotherapy is recommended for related
emotional issues.
Pilonidal disease
Coccygeal cyst forms in the intergluteal cleft

on the posterior surface of the lower sacrum,
often becoming infected or developing a fistula; may be congenital or caused by irritation
from exercise, heat, perspiration, or constrictive clothing
Abscesses are incised and drained, protruding hairs are extracted, and sitz baths
are ordered.
Entire affected area is excised if infections
persist.
Polymyalgia
rheumatica
An inflammatory syndrome characterized by

significant stiffness and dull aching pain of
the proximal muscle groups, weight loss,
malaise, and fever; cause unknown, but it
predominantly involves whites, tends to run
in families, and is possibly associated with
HLA-DR4 antigens, all of which suggest a
possible genetic predisposition
Corticosteroids, such as prednisone or

prednisolone, are the treatment of choice to
help relieve discomfort and stiffness.
Puerperal infection
Inflammation of the birth canal during the

postpartum period or after abortion; caused
by streptococci, coagulase-negative staphylococci, Clostridium perfringens, Bacteroides
fragilis, and Escherichia coli
I.V. broad-spectrum antibiotics are ordered

to combat infection.
Supportive therapy includes analgesics, anticoagulants, antiemetics, bed rest, administration of I.V. fluids, and prevention of
thrombophlebitis (antiembolism stockings).
Rectal polyps
Mass lesions that result from unrestrained

cell growth in the upper epithelium and protrude into the intestinal lumen; varying in
appearance; include common polypoid adenomas, villous adenomas, polyposis syndromes, juvenile polyps, and focal polypoid
hyperplasia; predisposing factors include
heredity, age, infection, and diet
Specific treatment varies according to type

and size of the polyps and their location in
the colon.
Common polypoid adenomas less than
1 cm require polypectomy, frequently by
fulguration (destruction by high-frequency
electricity) during endoscopy. For common
polypoid adenomas over 4 cm and all invasive villous adenomas, treatment usually
consists of abdominoperineal resection or
low anterior resection. Transanal excision is
performed to remove an adenoma from the
rectum.
Depending on large-bowel involvement,
hereditary polyposis necessitate restorative
proctolectomy, ileoanal anastomosis with
temporary ileostomy.
Focal polypoid hyperplasia can be obliterated by a biopsy.
Increase fluid intake and provide stool softeners to reduce risk of constipation.
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Names
Description
Treatment
Rectal prolapse
Circumferential protrusion of one or more

layers of the rectum through the anus caused
by straining or conditions that affect the
pelvic floor or rectum; patient may also have
a feeling of rectal fullness, bloody diarrhea,
and pain
Treat the underlying cause and eliminate

predisposing factors (straining, coughing,
nutritional disorders).
Manual return of the rectal mucosa may be
necessary.
Surgical repair is performed in severe or
chronic cases.
Retinitis pigmentosa
Genetically induced progressive destruction

of the retinal rods resulting in visual field
constriction, cataracts, edema, atrophic maculopathy, and blindness
No cure exists.
Vitamin A supplementation may be given to
slow degeneration.
Advise the use of sunglasses to protect
from ultraviolet light.
Throat abscess
Either peritonsillar (quinsy) abscess that

forms in the connective tissue space between
the tonsil capsule and constrictor muscle of
the pharynx or retropharyngeal abscess that
forms between the posterior pharyngeal wall
and prevertebral fascia (Peritonsillar abscess
is a complication of acute tonsillitis, usually
after streptococcal or staphylococcal infection. Acute retropharyngeal abscess results
from infection in the retropharyngeal lymph
glands, which may follow an upper respiratory tract bacterial infection. Chronic retropharyngeal abscess may result from tuberculosis
of the cervical spine [Potts disease].)
For early-stage peritonsillar abscess, large

doses of a broad-spectrum antibiotic are
given.
For late-stage peritonsillar abscess with cellulitis of the tonsillar space, primary treatment is incision and drainage under a local
anesthetic, followed by antibiotic therapy
for 7 to 10 days.
For both stages of peritonsillar abscess,
tonsillectomy is recommended after several
episodes. It must be scheduled at least 1
month after acute infection.
Incision and drainage of abcesses.
Tinea versicolor
(pityriasis versicolor)
Chronic, superficial fungal (yeast) infection

producing a multicolored rash or macular or
raised scaly lesions, commonly on the upper
trunk and caused by Pityrosporum orbiculare
Treat with topical antifungals, such as

clotrimazole, ketoconazole, and miconalzole.
Over-the-counter dandruff shampoos applied to the skin for 10 minutes each day in
the shower may also eliminate it.
Toxocariasis
(ocular larva
migrans, visceral
larva migrans)
Infection caused by parasitic roundworms in

dogs and cats spread by the fecal-oral route
and resulting in eye infections that can cause
blindness or visceral (rare) symptoms with
swelling of body organs or central nervous
system
Infection is treated with mebendazole, albendazole, or diethylcarbamazine.

Preventive measures include treating animals and thorough hand washing.
Trachoma (granular
conjunctivitis,
Egyptian ophthalmia)
Infection by Chlamydia trachomatis that affects the eye but can also localize in the urethra; may cause permanent damage to the
cornea and conjunctiva
Topical or systemic antibiotic therapy with

erythromycin or doxycycline is given.
Surgical correction is necessary if severe
entropion occurs.
Uveitis (iritis)
Inflammation of one uveal tract producing

moderate to severe eye pain, severe ciliary injection, photophobia, tearing, a small nonreactive pupil, and blurred vision; results from
allergy, infection, chemicals, trauma, surgery,
or systemic diseases or may be idiopathic
Underlying cause is diagnosed and treated.

Topical cycloplegic and topical corticosteroids are given.
Steroid drops or ointment may be needed.
Oral systemic corticosteroids are given in
severe cases.
Vaginismus
Involuntary spastic constriction of the lower

vaginal muscles with pain on insertion of any
object into the vagina; cause may be physical
or psychological
Maladaptive muscle constriction is eliminated with dilators.

Education, counseling, and behavioral exercises are given.
Kegel exercises to improve voluntary control are ordered.
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Names
Description
Treatment
Whipples disease
(intestinal lipodystrophy, lipophagia
granulomatosis)
GI malabsorption disorder characterized by

chronic diarrhea and progressive wasting,
with skin pigmentation and polyarthralgia
Appropriate antibiotic therapy is initiated.

Supportive therapy with fluid and electrolyte replacement is provided.
Iron, folate, vitamin D, and magnesium
supplementation is administered.
Wilsons disease
(hepatolenticular
degeneration)
Rare, inherited metabolic disorder characterized by excessive copper retention in the

liver, brain, kidneys, and corneas; KayserFleischer rings of the eye are produced, and
deposits may lead to tissue necrosis and fibrosis.
Treatment with pyridoxine in conjunction

with penicillamine, a copper-chelating agent
that mobilizes copper from the tissues and
promotes its excretion in the urine, is lifelong.
Copper-containing foods should be avoided
as well as tap water (because of copper
pipes) and copper cooking utensils.
The patient and his family should receive
genetic counseling.
Wiskott-Aldrich
syndrome
(immunodeficiency
with eczema and
thrombocytopenia)
X-linked recessive inherited disease characterized by defective B- and T-cell functions

(increased susceptibility to infections) and
metabolic defects in platelet synthesis
(thrombocytopenia) (Male infants develop
early bleeding complications [bloody stools,
petechiae, and purpura] and by age 6 months
develop recurrent systemic infections; by age
1 year, eczema develops, leading to scratching and skin infections; high susceptibility to
neoplastic diseases, such as lymphoma and
leukemia, occurs. Average life span is 4
years.)
Bleeding is controlled with platelet transfusions.

Prophylactic or early aggressive therapy
with antibiotics is indicated for infections.
Topical steroids help control eczema symptoms.
Bone marrow transplantation may be effective in some patients.
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Page 933
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Web resources
Aetna Intelihealth
www.intelihealth.com
Alateen
www.al-anon.alateen.org
Alcoholics Anonymous
www.alcoholics-anonymous.org
Al-Anon
www.al-anon.org
ALS Association
www.alsa.org
American Academy of Allergy, Asthma, and Immunology
www.aaaai.org
American Academy of Dermatology
www.aad.org
American Academy of Neurology
www.aan.com
American Academy of Ophthalmology
www.aao.org
American Academy of Pediatrics
www.aap.org
American Association of Kidney Patients
www.aakp.org
American Burn Association
www.ameriburn.org
American Cancer Society
www.cancer.org
American College of Obstetricians and Gynecologists
www.acog.org
American Heart Association
www.americanheart.com
American Lung Association
www.lungusa.org
American Psychological Association Help Center
www.apahelpcenter.org
American Society for Reproductive Medicine
www.asrm.org
American Sudden Infant Death Syndrome Institute
www.sids.org
Arthritis Foundation
www.arthritis.org
Arthritis Society
www.arthritis.ca
Asthma and Allergy Foundation of America
www.aafa.org
Autism Society of America

www.autism-society.org
Center for AIDS Prevention Studies
www.caps.ucsf.edu
Centers for Disease Control and Prevention
www.cdc.gov
Centers for Disease Control and Prevention Injury Center
www.cdc.gov/ncipc
Centers for Disease Control and Prevention Sexually
Transmitted Diseases
www.cdc.gov/std
Dermatology Foundation
www.dermfnd.org
Digestive Disease National Coalition
www.ddnc.org
eMedicine
www.emedicine.com
EndocrineWeb.com
www.endocrineweb.com
Epilepsy.com
www.epilepsy.com
Hereditary Hemorrhagic Telangiectasia Foundation
www.hht.org
Huntingtons Disease Society of America
www.hdsa.org
Iron Disorders Institute
www.irondisorders.org
iVillage Total Health
www.totalhealth.ivillage.com
KidsHealth
www.kidshealth.org
Mayo Clinic
www.mayoclinic.com
Mental Health America
www.nmha.org
Myasthenia Gravis Foundation of America
www.myasthenia.org
NARAL Pro-Choice America (formerly the National
Abortion and Reproductive Rights Action League)
www.naral.org
Narcotics Anonymous
www.na.org
National Abortion Federation
www.prochoice.org
Web resources 935
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Page 936
National Association for Children of Alcoholics

www.nacoa.net
National Association of Anorexia Nervosa and Associated
Disorders
www.anad.org
National Asthma Education and Prevention Program
www.nhlbi.nih.gov/about/naepp
National Cancer Institute
www.cancer.gov
National Center for Infectious Disease
www.cdc.gov/ncidod
National Center for Learning Disabilities
www.ncld.org
National Cervical Cancer Coalition
www.nccc-online.org
National Council on Alcoholism and Drug Dependence
www.ncadd.org
National Down Syndrome Society
www.ndss.org
National Eye Institute
www.nei.nih.gov
National Fragile X Foundation
www.fragilex.org
National Health Information Center
www.health.gov/nhic
National Heart, Lung, and Blood Institute
www.nhlbi.nih.gov
National Institute for Occupational Safety and Health
www.cdc.gov/niosh
National Institute of Allergy and Infectious Diseases
www3.niaid.nih.gov
National Institute of Arthritis and Musculoskeletal and
Skin Diseases
www.niams.nih.gov
National Institute of Diabetes and Digestive and Kidney
Diseases
www2.niddk.nih.gov
National Institute of Neurological Disorders and Stroke
www.ninds.nih.gov
National Lung Health Education Program
www.nlhep.org
National Multiple Sclerosis Society
www.nationalmssociety.org
National Organization for Rare Disorders
www.rarediseases.org
National Right to Life
www.nrlc.org
National Womens Health Information Center
www.4woman.gov
Nephrology Channel
www.nephrologychannel.com
Overeaters Anonymous
www.oa.org
Sickle Cell Disease Association of America
www.sicklecelldisease.org
U.S. Food and Drug Administration
www.fda.gov
936 Web resources
9400_INDEX.qxd
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Index
A
Abdominal aortic aneurysm, 58-59
endovascular grafting for, 59i
Abdominal obesity, 519
ABO incompatibility, 276-277
Abortion, spontaneous, 2-3
Abruptio placentae, 4-5
degrees of separation in, 5i
Acceleration-deceleration injuries, 6-7
cervical collar for, 7i
Achilles tendon contracture, 922t
Acidosis
metabolic, 394
respiratory, 696-697
Acne vulgaris, 8-9
Acquired immunodeficiency syndrome, 10-11
Acromegaly, 408
Actinomycosis, 922t
Acute infective tubulointerstitial nephritis, 14-15
Acute leukemia, 482-483
Acute poststreptococcal glomerulonephritis, 12-13,
316-317
Acute pyelonephritis, 14-15
Acute respiratory distress syndrome, 16-17
Acute respiratory failure, 18-19
Acute tubular necrosis, 20-21, 693
Addisons anemia, 52-53
Addisons disease, 22-23
Adenovirus infection, 922t
Adrenal (addisonian) crisis, 22-23
Adrenal hypofunction, 22-23
Adrenogenital syndrome, 24-25
Adult chorea, 380-381
Adult respiratory distress syndrome, 16-17
Age-related macular degeneration, 26-27
central vision in, 26i
Airway crisis in epiglottiditis, 270
Alcoholism, 28-29
Allens test, 139i
Allergic purpura, 30-31

lesions of, 30i
Allergic rhinitis, 32-33
Alopecia, 34-35
cancer drugs causing, 35t
Alpha1-antitrypsin deficiency, 922t
Alports syndrome, 922t
Alzheimers disease, 36-37
Amebiasis (amebic dysentery), 38-39
Amenorrhea, 40-41
American mountain fever, 925t
American trypanosomiasis, 922t
Amnesia, dissociative, 926t
Amyloidosis, 923t
Amyotrophic lateral sclerosis, 42-43
modifying home for, 43
Anal stricture, 923t
Anaphylaxis, 44-45
Anemia
aplastic, 46-47
folic acid deficiency, 48-49
iron deficiency, 50-51
pernicious, 52-53
sickle cell, 54-55
sideroblastic, 56-57, 57i
Anencephaly, 550
Aneurysm
abdominal aortic, 58-59, 59i
femoral and popliteal, 60-61
intracranial, 62-63
thoracic aortic, 64-65
ventricular, 66-67
Angioedema, 860-861
Angiofibroma, juvenile, 923t
Angiohemophilia, 906-907
Animal bites, first aid for, 678
Anion gap, 394
Ankylosing spondylitis, 68-69
Anorexia nervosa, 70-71
i refers to an illustration; t refers to a table.
Index 937
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Anthrax, 72-73
Anthropometric arm measurements, 557i
Antimalarial drugs, 508, 509
Anxiety disorder, generalized, 304-305
Aorta, coarctation of, 190-191, 191i
Aortic aneurysm
abdominal, 58-59, 59i
thoracic, 64-65
Aortic insufficiency, 74-75
murmur of, 75i
Aortic stenosis, 76-77
murmur of, 77i
muscular, 151t, 152-153, 152i
Aphthous stomatitis, 776-777
lesions of, 776i
Aplastic anemia, 46-47
Apnea, sleep, 764-765
Appalachian Mountain disease, 372-373
Appendicitis, 78-79
Arbovirus, 724-725
Arterial occlusive disease, 80-81
Arteries of leg, 61i
Arteriovenous malformations, 82-83
Arthritis
juvenile rheumatoid, 454-455
osteo-, 564-565, 565i
reactive, 686-687
rheumatoid, 710-711
septic, 742-743
Asbestosis, 84-85
Ascariasis, 86-87
Aspergillosis, 88-89
Asphyxia, 90-91
Aspiration pneumonia, 626
Asthma, 92-93
Atelectasis, 94-95
Atopic dermatitis, 96-97
signs of, 97i
Atopy, factors contributing to, 96
Atrial fibrillation, 98-99
recognizing, 98i
Atrial septal defect, 100-101
Attention deficit hyperactivity disorder, 102-103
Autistic disorder, 104-105
Autotransfusion for chest wounds, 351i
Avian influenza, 106-107
B
Bacillary dysentery, 748-749
Bangs disease, 136-137
Barometer-makers disease, 923t
Basal cell carcinoma, 108-109
identifying, 108i
938 Index
Beckers muscular dystrophy, 536

Bedsores, 652-653, 653i
Bee sting, 446-447
Bells palsy, 110-111
facial paralysis in, 110i
Benign polycythemia, 772-773
Benign prostatic hyperplasia, 112-113
Berylliosis, 923t
Bilharziasis, 734-735, 734t
Bilious typhoid, 688-689, 926t
Bipolar disorder, 114-115
Bites
animal, first aid for, 678
insect, 446-447
mosquito, preventing, 725, 913
Black widow spider bite, 446-447
Bladder, neurogenic, 552-553, 553t
Bladder cancer, 116-117
Blastocystis hominis infection (blastocystosis), 924t
Blastomycosis, 118-119
European, 216-217
Blepharitis, 120-121
Blepharoptosis, 664-665, 665i
Blood transfusion reaction, 122-123
Body lice, 596, 597i
Body mass index measurement, 556
Bone tumors, primary malignant, 124-125
types of, 125t
Bordetella pertussis, 608i
Botulism, 126-127
Bouchards nodes, 565i
Bouillauds syndrome, 924t
Bowlegs, 896i
Brain attack, 780-781
Brain tumor, 128-129
Breast cancer, 130-131
sources and sites of, 131i
Brittle bone disease, 566-567
Bronchiectasis, 132-133
Bronchitis, chronic, 134-135
pathophysiology of, 135i
Brown recluse spider bite, 446-447
Brucellosis, 136-137
Brutons agammaglobulinemia, 914-915
Bubonic plague, 618-619
carrier of, 619i
Budd-Chiari syndrome, 924t
Buergers disease, 138-139
Allens test for, 139i
Bulimia nervosa, 140-141
Bullous impetigo, 438
Burns, 142-143
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Bursae, 805i
Bursitis, 804-805
C
Cabin fever, 688-689, 926t
Calculi
gallbladder, 176-177
renal, 690-691, 691i
Campylobacteriosis, 144-145
Cancer. See also Tumors; specific type.
basal cell, 108-109, 108i
bladder, 116-117
breast, 130-131, 131i, 584
cervical, 168-169
colorectal, 194-195
esophageal, 278-279
fallopian tube, 926t
gastric, 296-297
laryngeal, 470-471
liver, 490-491
lung, 494-495
oral and pharyngeal, 560-561
ovarian, 580-581
pancreatic, 586-587
penile, 930t
prostatic, 656-657
renal, 462-463, 462i
squamous cell, 774-775, 774i
testicular, 806-807
thyroid, 820-821
uterine, 864-865
vaginal, 868-869
Cancer drugs causing alopecia, 35t
Candidiasis, 146-147
chronic mucocutaneous, 925t
oropharyngeal, 146i
Carbunculosis, 288-289
hair follicles in, 288i
Cardiac tamponade, 148-149
Cardiogenic shock, 750-751
Cardiomyopathies
assessment findings in, 151t
dilated, 150-151, 150i
hypertrophic, 152-153, 152i
restrictive, 154-155, 154i
Carpal tunnel, 156i
Carpal tunnel syndrome, 156-157
Cataract, 158-159
removal methods for, 159i
Cat-scratch fever, 924t
Causalgia, 198-199, 199t
Celiac disease, 160-161, 506, 924t
Page 939
Cellulitis, 162-163
orbital, 929t
synergistic necrotizing, 546-547
Central Mississippi Valley disease, 372-373
Central retinal artery or vein occlusion, 880-881
Cerebral contusion, 164-165
intracranial pressure in, 165i
Cerebral palsy, 166-167
Cerebrovascular accident. See Stroke.
Cervical cancer, 168-169
preventing, 168
testing for, 169
Cervical collar, applying, 7i
Cestodiasis, 798-799
Chagas disease, 922t
Chalazion, 170-171
eye patch for, 171i
recognizing, 170i
Chancroid, 172-173
lesion in, 172i
Chest wounds, autotransfusion for, 351i
Chickenpox, 716t, 874-875
Chlamydial infections, 174-175, 175i
Chlamydia trachomatis, 175i
Chloride, dietary sources of, 418
Chloroquine, 508, 509
Cholangitis, 176
Cholecystitis, 176-177
Choledocholithiasis, 176
Cholelithiasis, 176-177
Cholera, 178-179
Chondrosarcoma, 125t
Chordoma, 125t
Chorea, Huntingtons, 380-381
Choriocarcinoma, 924t
Choriomeningitis, lymphocytic, 500-501
Chorioretinitis, active, 830
Chromaffin tumor, 612-613
Chronic bronchitis, 134-135, 135i
Chronic dermatitis, 230t
Chronic fatigue and immune dysfunction syndrome,
180-181
Chronic granulomatous disease, 924t
Chronic leukemia
granulocytic (myelogenous), 484-485
lymphocytic, 486-487
Chronic mucocutaneous candidiasis, 925t
Chronic progressive chorea, 380-381
Chvosteks sign, 417i
Cirrhosis, 182-183
Clam diggers itch, 735
Cleft lip and cleft palate, 184-185
types of, 185i
Index 939
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Clostridium difficile infection, 186-187

Clostridium perfringens, 294i
Clubfoot, 188-189
recognizing, 188i
Coarctation of aorta, 190-191
recognizing, 191i
Cobalamin. See Vitamin B12.
Coccidioidomycosis, 192-193
Cold, common, 196-197, 197i
Colitis
spastic or mucous, 452-453
ulcerative, 856-857
Colorado tick fever, 925t
Colorectal cancer, 194-195
Common cold, 196-197
Complete abortion, 3
Complex regional pain syndrome, 198-199
stages of, 199t
Concussion, 200-201
Condylomata acuminata, 308-309, 308i
Congenital (aganglionic) megacolon, 370-371
Congestive cardiomyopathy, 150-151, 150i, 151t
Conjunctival papillae, 202i
Conjunctivitis, 202-203
granular, 931t
papillae in, 202i
Conns syndrome, 388
Constrictive pericarditis, 604
Consumption coagulopathy, 242-243
Contact dermatitis, 230t
Contact precautions, 144
Conversion disorder, 925t
Corneal abrasion, 204-205
eye irrigation for, 205i
Coronary artery disease, 206-207
Cor pulmonale, 208-209, 342
Corticotropin deficiency, 430, 431
Coxa plana, 478-479
Crab lice, 596, 597i
Creutzfeldt-Jakob disease, 210-211
variant, 210
Crib death, 790-791
Crohns disease, 212-213
Croup, 214-215
upper airway in, 215i
Cryptococcosis, 216-217
Cryptorchidism, 218-219
testicular cancer and, 806
varieties of, 218i
Cryptosporidiosis, 925t
Cushings syndrome, 220-221
940 Index
Cyclothymic disorder, 114, 115

Cystic fibrosis, 222-223
Cystinuria, 925t
Cysts
ovarian, 582-583, 582i, 636-637
renal, 634-635
Cytomegalovirus infection, 224-225
D
Dacryocystitis, 226-227
Da Nang lung, 16-17
Dark-field microscopy for syphilis, 795i
Darlings disease, 372-373
Decubitus ulcers. See Pressure ulcers.
Defibrination syndrome, 242-243
Depersonalization disorder, 925t
Depression, major, 504-505
Dermal gangrene, acute, 546-547
Dermatitis, 228-229
atopic, 96-97, 97i
schistosomal, 735
types of, 230-231t
Dermatitis herpetiformis, 926t
de Toni-Fanconi syndrome, 926t
Developmental dysplasia of hip, 232-233
degrees of, 232i
signs of, 233
Diabetes insipidus, 234-235
Diabetes mellitus, 236-237
Diabetic retinopathy, 880-881
Dientamoeba fragilis infection, 925t
DiGeorges syndrome, 925t
Dilated cardiomyopathy, 150-151
Diphtheria, 238-239
Discoid lupus erythematosus, 496, 796
Dislocations, 240-241
elbow, 240i
hip, 232i
Disseminated intravascular coagulation, 242-243
Dissociative amnesia, 926t
Dissociative fugue, 926t
Dissociative identity disorder, 926t
Diverticular disease, 244-245
Down syndrome, 246-247
Droplet precautions, 238
Drowning, near, 544-545
Drugs
causing alopecia, 35t
causing gynecomastia, 332
causing hypercalcemia, 392
causing hyperchloremia, 394
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Drugs (continued)
causing hyperkalemia, 396
causing hypermagnesemia, 400
causing hypernatremia, 402
causing hyperphosphatemia, 406
causing hypochloremia, 418
causing hypokalemia, 420
causing hypomagnesemia, 422
causing hyponatremia, 424
causing hypophosphatemia, 428
aggravating porphyria, 645
causing rhabdomyolysis, 706
3-D syndrome, 890
Duchennes muscular dystrophy, 536
Duhrings disease, 926t
Duodenal ulcer, 600-601
Dysentery
amebic, 38-39
bacillary, 748-749
Dysfunctional uterine bleeding, 862-863
Dysmenorrhea, 248-249
Dysmetabolic syndrome, 518-519
E
Ear, hardening of, 578-579
Eardrum, perforated, 576, 602-603
Ebola virus infection, 250-251
Eclampsia, 310-311
Ecthyma versus impetigo, 439
Ectopic pregnancy, 252-253
implantation sites of, 252i
Eczema, immunodeficiency with, 932t
Edwards syndrome, 850-851
Egyptian ophthalmia, 931t
Elbow dislocation, 240i
Electric shock, 254-255
Electrosurgery for warts, 911i
Emphysema, 256-257
Empyema, 620-621
Encephalitis, 258-259
St. Louis, 724-725
West Nile, 912-913
Encephalocele, 550
Encephalopathy, hepatic, 352-353, 492
Endocarditis, 260-261
degenerative changes in, 261i
Q fever, treating, 676
rheumatic, 924t
Endolymphatic hydrops, 514-515
Endometrial cancer, 864-865
Endometriosis, 262-263
Endovascular grafting for abdominal aortic aneurysm, 59i
Enterobacteriaceae infections, 264-265

Enterococcus, vancomycin-resistant, 872-873
Enterocolitis, pseudomembranous, 660-661
Epidermolysis bullosa, 926t
Epididymitis, 266-267
Epidural hematoma, 268-269
Epiglottiditis, 270-271
airway crisis in, 270
Haemophilus influenzae, 334
Epilepsy, 272-273
Epstein-Barr virus, 926t
chronic, 180-181
Erbs muscular dystrophy, 536
Erectile dysfunction, 274-275
Erythema, 640-641
Erythroblastosis fetalis, 276-277
Rh isoimmunization in, 276i
Erythrodermic psoriasis, 663
Escherichia coli infection, 264-265
Esophageal atresia, 832-833
Esophageal cancer, 278-279
European blastomycosis, 216-217
Ewings sarcoma, 124, 125t
Exanthema subitum, 716-717, 716t
Exfoliative dermatitis, 230t
Exophthalmos, 280-281
detecting unilateral, 281i
recognizing, 280i
External otitis, 574-575
Extracapsular cataract extraction, 159i
Extravaginal torsion, 808i
Eye examination with slit lamp, 460
Eye irrigation, 205i
Eye patch, applying, 171i
F
Facial paralysis in Bells palsy, 110i
Failure to thrive, 282-283
Fallopian tube cancer, 926t
Fanconis syndrome, 926t
Fasciitis, necrotizing, 546-547
Femoral aneurysm, 60-61
Femoral hernia, 445i
Fibrocystic breast disease, 284-285
Fibroids, uterine, 866-867
Fibromyalgia syndrome, 286-287
tender points in, 287i
Fibromyomas, uterine, 866-867
Fibrosarcoma, 125t
Fire ant sting, 446-447
Flesh-eating bacteria, 546-547
Flu. See Influenza.
Folic acid, foods high in, 49t
Index 941
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Folic acid deficiency anemia, 48-49

Follicular cysts, 582i, 583
Follicular hyperkeratosis, 894i
Folliculitis, 288-289
Food poisoning, Vibrio parahaemolyticus, 178
Fowl-nest fever, 688-689, 926t
Fractures
hip, 368-369
skull, 762-763
Fragile X syndrome, 290-291
Frostbite, 292-293
Fugue, dissociative, 926t
Furunculosis, 288-289
G
Gaisbcks disease, 772-773
Gallstone ileus, 176
Gallstones, 176-177
Gangrene
gas, 294-295, 294i
hemolytic streptococcal, 546-547
Gas gangrene, 294-295
Gastric cancer, 296-297
Gastric ulcer, 600-601
Gastritis, 298-299
Gastroenteritis, 300-301
Gastroesophageal reflux disease, 302-303
Gauchers disease, 927t
Gender identity disorder, 927t
Generalized anxiety disorder, 304-305
Generalized salivary gland disease, 224-225
Genital herpes, 306-307
cycle in, 306i, 365i
primary, 364
Genital warts, 308-309
recognizing, 308i
German measles, 716t, 720-721
Gestational hypertension, 310-311
Giant cell tumor, malignant, 125t
Giardiasis, 312-313
Gigantism, 408
Gilchrists disease, 118-119
Glaucoma, 314-315
optic disk changes in, 314i
Glomerulonephritis, 316-317
acute poststreptococcal, 12-13
Glucosylceramide storage disease, 927t
Gluten intolerance, 160-161, 506, 924t
Glycopeptide intermediate-resistant Staphylococcus
aureus, 870-871
942 Index
Goiter, 318-319
simple, 318
toxic diffuse, 414-415
Gonadotropin deficiency, 320-321, 430-431
Gonorrhea, 322-323
Goodpastures syndrome, 316, 324-325
Gout, 326-327
tophi in, 327i
Graft rejection syndrome, 328-329
Granular conjunctivitis, 931t
Granulomatous disease, chronic, 924t
Granulomatous rosacea, 714
Graves disease, 414-415
Grawitzs tumor, 462-463, 462i
Grippe. See Influenza.
Ground itch, 376-377
Growth hormone excess, 408-409
Guillain-Barr syndrome, 330-331
Guttate psoriasis, 663
Gynecomastia, 332-333
H
Habitual abortion, 3
Haemophilus influenzae infection, 334-335
Hair follicles, bacterial infection of, 288i
Hair loss, 34-35, 35t
Hallux valgus, 927t
Hand, foot, and mouth disease, 927t
Hansens disease, 928t
Hantavirus pulmonary syndrome, 336-337
Sin Nombre virus in, 336i
Hashimotos thyroiditis, 822
Headache, 338-339
Head lice, 596, 597i
Hearing loss, 340-341
Heart attack, 540-541
Heartburn, 302-303
Heart failure, 342-343
right-sided, 208-209, 208i
Heat syndrome, 344-345
Heberdens nodes, 565i
HELLP syndrome, 310
Hematoma
epidural, 268-269
subdural, 786-787
Hemoglobinuria, paroxysmal nocturnal, 929t
Hemolytic disease of newborn, 276-277, 276i
Hemolytic streptococcal gangrene, 546-547
Hemophilia, 346-347
vascular, 906-907
Hemorrhoids, 348-349
types of, 348i
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Page 943
Hemothorax, 350-351
autotransfusion for, 351i
Hepatic encephalopathy, 352-353, 492
Hepatitis
nonviral, 354-355
viral, 356-357
Hepatolenticular degeneration, 932t
Hepatorenal syndrome, 492
Hereditary chorea, 380-381
Hereditary hemorrhagic telangiectasia, 358-359
lesions of, 358i
Hernias
hiatal, 360-361
identifying, 444
inguinal, 444-445
sites of, 445i
Herniated intervertebral disk, 362-363
Herpangina, 927t
Herpes simplex, 364-365
genital, 306-307, 306i, 365i
Herpes zoster, 366-367
lesions in, 366i
Herpetic stomatitis, acute, 776-777
Hiatal hernia, 360-361
Hip dysplasia, 232-233
degrees of, 232i
Hip fracture, 368-369
Hirschsprungs disease, 370-371
Histoplasmosis, 372-373
Hives, 860-861
Hodgkins disease, 374-375
Hookworm disease, 376-377
Human immunodeficiency virus, 10-11
Human papillomavirus, 378-379
Huntingtons disease, 380-381
Hyaline membrane disease, 698-699
Hydatidiform mole, 927t
Hydrocele, 382-383
Hydrocephalus, 384-385
Hydronephrosis, 386-387
Hyperaldosteronism, 388-389
Hyperbilirubinemia, unconjugated, 390-391
Hypercalcemia, 392-393
clinical effects of, 392t
Hyperchloremia, 394-395
Hyperkalemia, 396-397
false test results in, 397
Hyperlipoproteinemia, 398-399
Hypermagnesemia, 400-401
patellar reflex test for, 401i
Hypernatremia, 402-403
Hypernephroma, 462-463, 462i
Hyperparathyroidism, 404-405
Hyperphosphatemia, 406-407
Hyperpituitarism, 408-409
Hypersplenism, 410-411
Hypertension, 412-413
gestational, 310-311
pulmonary, 670-671
Hypertensive retinopathy, 880-881
Hyperthyroidism, 414-415
Hypertrophic cardiomyopathy, 152-153
Hypocalcemia, 416-417
signs of, 417i
Hypochloremia, 418-419
Hypochondriasis, 927t
Hypogammaglobulinemia, X-linked infantile, 914-915
Hypokalemia, 420-421
Hypomagnesemia, 422-423
Hyponatremia, 424-425
Hypoparathyroidism, 426-427
Hypophosphatemia, 428-429
Hypopituitarism, 430-431
Hypothermia, 432-433
Hypothyroidism, 434-435
Hypovolemic shock, 752-753
Hysterical neurosis, 925t
I
Idiopathic hypertrophic subaortic stenosis, 151t,
152-153, 152i
Idiopathic thrombocytopenic purpura, 436-437
Immunodeficiency with eczema and thrombocytopenia, 932t
Impetigo, 438-439
ecthyma versus, 439
recognizing, 438i
Impotence, 274-275
Incisional hernia, 445i
Incomplete abortion, 3
Inevitable abortion, 3
Infant botulism, 126
Infantile paralysis, 632-633
Infantile polyarteritis, 458-459
Infectious arthritis, 742-743
Infectious mononucleosis, 440-441
Index 943
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Influenza, 442-443
avian, 106-107
preventing spread of, 443
Inguinal hernia, 444-445
identifying, 444
site of, 445i
Insect bites and stings, 446-447
Insulin resistance syndrome, 518-519
Intervertebral disk, herniated, 362-363
Intestinal lipodystrophy, 932t
Intestinal obstruction, 448-449
Intestinal polyps, 642-643
Intracapsular cataract extraction, 159i
Intracranial aneurysm, 62-63
Intracranial pressure, increased, 165i
Intussusception, 450-451
bowel in, 450i
Inverse psoriasis, 663
Iodine deficiency, 927t
Iritis, 931t
Iron
absorption and storage of, 50
overdose of, 51
Iron deficiency anemia, 50-51
Irritable bowel syndrome, 452-453
J
Jarisch-Herxheimer reaction, 689
Jaundice, neonatal, 390-391
Juvenile rheumatoid arthritis, 454-455
K
Kanners autism, 104-105
Kaposis sarcoma, 456-457
Kawasaki syndrome, 458-459
Keratitis, 460-461
Kidney cancer, 462-463
unilateral, 462i
Kidney stones, 690-691, 691i
Klinefelter syndrome, 464-465
L
Labyrinthitis, 466-467
Lactase insufficiency, 468i, 506
Lactose intolerance, 468-469
Lambliasis, 312-313
Landouzy-Dejerine muscular dystrophy, 536
Laryngeal cancer, 470-471
Laryngitis, 214-215, 215i, 472-473
Laryngotracheobronchitis, 214-215, 215i
Lassa fever, 928t
Latex, products containing, 474
944 Index
Page 944
Latex allergy, 474-475

Laubensteins stages in Kaposis sarcoma, 456
Lead poisoning, 476-477
Left-sided heart failure, 342
Legg-Calv-Perthes disease, 478-479
Legionnaires disease, 480-481
Leiomyomas, uterine, 866-867
Leprosy, 928t
Leptospirosis, 928t
Leukemia
acute, 482-483
chronic granulocytic, 484-485
chronic lymphocytic, 486-487
Lice, 596-597
types of, 597i
Lichen planus, 928t
Lichen simplex chronicus, 230t
Lipophagia granulomatosis, 932t
Listeriosis, 488-489
Liver, functions of, 492
Liver cancer, 490-491
Liver failure, 492-493
Lockjaw, 810-811
Lou Gehrig disease, 42-43
Lower esophageal sphincter pressure, 303
Lumpy jaw, 922t
Lung cancer, 494-495
Lupoid rosacea, 714
Lupus erythematosus, 496-497
systemic, 497, 796-797
Lyme disease, 498-499
Lymphocytic choriomeningitis, 500-501
Lymphoma, non-Hodgkins (lymphosarcoma), 502-503
M
Macular degeneration, age-related, 26-27, 26i
Major depression, 504-505
Malabsorption, 506-507
Malaria, 508-509
Malignant giant cell tumor, 125t
Malignant hypertension, 412
Malignant lymphoma, 502-503
Malignant melanoma, 512-513
Malignant plasmacytoma, 530-531
Malta fever, 136-137
Mantle zone lymphoma, 502
Maple syrup urine disease, 928t
Marfan syndrome, 928t
Marginal zone lymphoma, 502
Marie-Strmpell disease, 68-69
Mastitis, 510-511
Mastoiditis, 928t
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Measles, 722-723
German, 720-721
incubation and duration of, 716t
Medullary sponge kidney, 929t
Megacolon, congenital, 370-371
Melanoma, malignant, 512-513
Mnires disease, 514-515
Meningitis, 516-517
lymphocytic, 500-501
Meningocele, 551i
Mercury poisoning, chronic, 923t
Mesothelioma, 84-85
Metabolic acidosis, 394
Metabolic syndrome, 518-519
Methicillin-resistant Staphylococcus aureus, 520-521
Midarm circumference, 557i
Migraine, 338-339
Miscarriage, 2-3
Missed abortion, 3
Mitral stenosis, 522-523
murmur of, 522i
Mitral valve insufficiency, 524-525
murmur of, 524i
Mitral valve prolapse, 526-527
Mongolism, 246-247
Moniliasis, 146-147, 146i
Monkeypox, 929t
Mononucleosis, infectious, 440-441, 926t
Morbilli, 716t, 722-723
Mosquito bites, preventing, 725, 913
Mosquito-borne encephalitis, 724-725
Motion sickness, 528-529
Mountain (tick) fever, 925t
Mucocutaneous lymph node syndrome, 458-459
Mucous colitis, 452-453
Multiple endocrine neoplasia, 929t
Multiple metabolic syndrome, 518-519
Multiple myeloma, 530-531
Multiple personality disorder, 926t
Multiple sclerosis, 532-533
Mumps, 534-535
parotid inflammation in, 535i
Murmurs
of aortic insufficiency, 75i
of aortic stenosis, 77i
of mitral insufficiency, 524i
of mitral stenosis, 522i
of tricuspid insufficiency, 842i
of tricuspid stenosis, 844i
Muscular aortic stenosis, 151t, 152-153, 152i
Muscular dystrophy, 536-537
Myalgic encephalomyelitis, 180-181
Myasthenia gravis, 538-539

Myelomatosis, 530-531
Myelomeningocele, 551i
Myocardial infarction, 540-541
Myocarditis, 542-543
Myomas, uterine, 866-867
Myxedema, 434
N
Near drowning, 544-545
Necrotizing fasciitis, 546-547
Neonatal jaundice, 390-391
Nephritis
acute infective tubulointerstitial, 14-15
acute tubulointerstitial, 20-21, 693
Nephrocarcinoma, 462-463, 462i
Nephrotic syndrome, 548-549
Neural tube defects, 550-551
spinal, 551i
Neurodermatitis, localized, 230t
Neurofibromatosis, 929t
Neurogenic bladder, 552-553
types of, 553t
Niacin, recommended daily allowance of, 891t
Niacin deficiency, 890-893
Nocardiosis, 554-555, 929t
Non-Hodgkins lymphoma, 502-503
Nucleus pulposus, herniated, 362-363
Nummular dermatitis, 231t
O
Obesity, 556-557
abdominal, 519
anthropometric measurements in, 557i
body mass index in, 556
Obsessive-compulsive disorder, 558-559
Ocular larva migrans, 931t
Ocular toxoplasmosis, 830
Ohio Valley disease, 372-373
Ophthalmic ointment, applying, 121
Optic disk in glaucoma, 314i
Oral cancer, 560-561
Orbital cellulitis, 929t
Orchiopexy, 806
Orchitis, 267
Orthostatic vital signs, 752
Ortolanis sign, 233
Osgood-Schlatter disease, 562-563
Osler-Weber-Rendu disease, 358-359, 358i
Osteitis deformans, 584-585
Osteoarthritis, 564-565
signs of, 565i
Osteoblastoma, 124-125, 125t
Index 945
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Page 946
Osteochondrosis, 562-563
Osteogenesis imperfecta, 566-567
Osteogenic sarcoma, 124, 125t
Osteomalacia, 568-569
Osteomyelitis, 570-571
Osteoporosis, 572-573
Osteosarcoma, 124-125, 125t
Otitis externa, 574-575
Otitis media, 576-577
Otosclerosis (otospongiosis), 578-579
Ovarian cancer, 580-581
Ovarian cysts, 582-583
follicular, 582i
multiple, 636-637
P
Pagets disease, 584-585
Pain syndrome, complex regional, 198-199, 199t
Pancreatic cancer, 586-587
Pancreatitis, 588-589
Panhypopituitarism, 430, 431
Panic disorder, 590-591
Paraesophageal hernia, 360
Parainfluenza, 929t
Paralysis, infantile, 632-633
Paranasal sinuses, 759i
Parkinsons disease, 592-593
Parosteal osteogenic sarcoma, 125t
Parotid inflammation, 535i
Parotitis, epidemic or infectious, 534-535
Paroxysmal nocturnal hemoglobinuria, 929t
Pataus syndrome, 848-849
Patellar reflex, testing, 401i
Patent ductus arteriosus, 594-595
Pediculosis, 596-597
types of, 597i
Pellagra, 890
Pelvic inflammatory disease, 598-599
Pelvic pain, causes of, 248
Penile cancer, 930t
Peptic ulcer, 600-601
Perforated eardrum, 576, 602-603
Pericarditis, 604-605
Peritonitis, 606-607
Pernicious anemia, 52-53
Pertussis, 608-609
pathogen in, 608i
Pharyngeal cancer, 560-561
Pharyngitis, 610-611
Pheochromocytoma, 612-613
Phosphorus, foods high in, 407
Pilonidal disease, 930t
Pituitary tumors, 614-615
946 Index
Pityriasis versicolor, 931t

Placental abruption, 4-5, 5i
Placenta previa, 616-617
types of, 617i
Plague, 618-619
carrier of, 619i
Plasma cell myeloma, 530-531
Pleural effusion, 620-621
Pleurisy (pleuritis), 622-623
Pneumocystis carinii pneumonia, 624-625
Pneumonia, 626-627
Pneumocystis carinii, 624-625
preventing, 627
Pneumothorax, 628-629
Poisoning, 630-631
lead, 476-477
mercury, 923t
preventing, 631
Poliomyelitis, 632-633
Polyarteritis, infantile, 458-459
Polyarteritis nodosa, 882
Polycystic kidney disease, 634-635
Polycystic ovary syndrome, 636-637
Polycythemia
secondary, 638-639
spurious, 772-773
Polycythemia (rubra) vera, 640-641
Polymyalgia rheumatica, 930t
Polyps
intestinal, 642-643
rectal, 930t
Popliteal aneurysm, 60-61
Porphyrias, 644-645
Poststreptococcal glomerulonephritis, 12-13, 316-317
Posttraumatic stress disorder, 646-647
Potassium, dietary sources of, 421
Precocious puberty, 648-649
Preeclampsia, 310-311
Pregnancy, ectopic, 252-253, 252i
Premenstrual syndrome, 650-651
Pressure ulcers, 652-653
stages of, 653i
Primaquine, 508, 509
Primary polycythemia, 640-641
Proctitis, 654-655
Prolactin deficiency, 430, 431
Prostate cancer, 656-657
Prostatic hyperplasia, benign, 112-113
Prostatitis, 658-659
Prostatodynia, 658, 659
Pruritus, essential, 230t
Pseudohemophilia, 906-907
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Page 947
Pseudomembranous enterocolitis, 660-661

Pseudopolycythemia, 772-773
Pseudoprecocious puberty, 648
Psoriasis, 662-663
Psoriasis vulgaris, 663
Ptosis, 664-665
recognizing, 665i
Puberty, precocious, 648-649
Pubic lice, 596, 597i
Puerperal infection, 930t
Pulmonary edema, 666-667
Pulmonary embolism, 668-669
Pulmonary hypertension, 670-671
Pulmonic insufficiency, 672-673
Pulmonic stenosis, 674-675
Pump failure, 750-751
Purpura
allergic, 30-31, 30i
idiopathic thrombocytopenic, 436-437
Purpuric lesions, 30i
Pustular psoriasis, 663
Pyelonephritis, acute, 14-15
Pyridoxine, recommended daily allowance of, 891t
Pyridoxine deficiency, 890-892
Pyrimethamine, 508, 509
Q
Q fever, 676-677
Quinine, 508, 509
R
Rabies, 678-679
Radiation exposure, 680-681
Rape-trauma syndrome, 682-683
Rash-producing infections, incubation and duration of, 716t
Raynauds phenomenon, 684-685
Reactive arthritis, 686-687
Reactive polycythemia, 638-639
Rectal polyps, 930t
Rectal prolapse, 931t
Reflex sympathetic dystrophy, 198-199, 199t
Reiters syndrome, 686-687
Relapsing fever, 688-689, 926t
Relative polycythemia, 772-773
Renal calculi, 690-691
preventing, 691
variations in, 691i
Renal carcinoma, 462-463, 462i
Renal failure
acute, 692-693
chronic, 694-695
Respiratory acidosis, 696-697

acute or adult, 16-17
neonatal, 698-699
Respiratory failure, acute, 18-19
Respiratory syncytial virus infection, 700-701
Restrictive cardiomyopathy, 154-155
Retinal detachment, 702-703
Retinitis pigmentosa, 931t
Retinopathies, vascular, 880-881
Reyes syndrome, 704-705
stages of treatment for, 705t
Rhabdomyolysis, 706-707
Rheumatic endocarditis, 924t
Rheumatic fever and rheumatic heart disease, 708-709
Rheumatoid arthritis, 710-711
classifying, 711
juvenile, 454-455
Rheumatoid spondylitis, 68-69
Rh incompatibility, 276-277
Rhinitis, allergic, 32-33
Rh isoimmunization, 276i
Rh system, 122
Riboflavin, recommended daily allowance of, 891t
Riboflavin deficiency, 890-892
Rickets, 568-569, 896-897
bowlegs in, 896i
Riedels thyroiditis, 822
Right-sided heart failure, 208-209, 208i, 342
Ringed sideroblast, 57i
Robin sequence, 184, 185
Rocky Mountain spotted fever, 712-713
Rosacea, 714-715
Roseola infantum, 716-717
Rotavirus, 718-719
Roundworm infection, 86-87
Rubella, 720-721
Rubella vaccine, giving, 720
Rubeola, 722-723
Ruptured disk, 362-363
Ruptures. See Hernias.
S
Salmonella infection, 726-727
San Joaquin Valley fever, 192-193
Sarcoidosis, 728-729
Scabies, 730-731
cause and effect of, 730i
preventing, 731
Index 947
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Scarlet fever (scarlatina), 732-733

Schistosomal dermatitis, 735
Schistosomes, 734t
Schistosomiasis, 734-735
Schizophrenia, 736-737
Scleroderma, 738-739
Scoliosis, 740-741
testing for, 741i
Scurvy, 894-895
gums and legs in, 894i
Seborrheic dermatitis, 231t
Seizure disorder, 272-273
Sensorimotor nerve degeneration, 331
Septic abortion, 3
Septic arthritis, 742-743
Septic shock, 754-755
Severe acute respiratory syndrome, 744-745
Severe combined immunodeficiency disease, 746-747
Shigellosis, 748-749
Shingles, 366-367, 366i
Shock
cardiogenic, 750-751
electric, 254-255
hypovolemic, 752-753
septic, 754-755
Shock lung, 16-17
Sickle cell anemia, 54-55
Sickle cell retinopathy, 880-881
Sideroblastic anemia, 56-57
ringed sideroblast in, 57i
Silicosis, 756-757
Sin Nombre virus, 336i
Sinuses, paranasal, 759i
Sinusitis, 758-759
Sixth disease, 716-717, 716t
Sjgrens syndrome, 760-761
Skull fracture, 762-763
Skull in thalassemia major, 814i
Sleep apnea, 764-765
Sliding hiatal hernia, 360
Slipped disk, 362-363
Slit-lamp examination of eye, 460
Smallpox, 766-767
Spastic colon or colitis, 452-453
Spider bite, 446-447
Spina bifida, 550
Spina bifida occulta, 550, 551i
Spinal cord defects, 550
types of, 551i
Spinal injury, 768-769
Splenomegalic polycythemia, 640-641
Splenomegaly, causes of, 410
Sprains, 770-771
948 Index
Sprue, celiac or nontropical, 160-161, 506, 924t

Spurious polycythemia, 772-773
Squamous cell carcinoma, 774-775
nodule in, 774i
St. Louis encephalitis, 724-725
methicillin-resistant, 520-521
vancomycin intermediate-resistant, 870-871
Stasis dermatitis, 231t
Steatorrhea, idiopathic, 160-161
Stiff lung, 16-17
Stings, insect, 446-447
Stomatitis, 776-777
aphthous, 776i
Strains, 770-771
Streptococcus pneumoniae infection, drug-resistant,
778-779
Stress erythrocytosis or polycythemia, 772-773
Stroke, 780-781
Strongyloidiasis, 782-783
Subarachnoid hemorrhage, 784-785
Subdural hematoma, 786-787
Subluxations, 240-241
hip, 232i
Substance abuse and dependence, 788-789
Sudden infant death syndrome, 790-791
Suicide prevention guidelines, 505
Suppurative fasciitis, 546-547
Swimmers ear, 574-575
Swimmers itch, 735
Syndrome of inappropriate antidiuretic hormone, 792-793
Syndrome X, 518-519
Synergistic necrotizing cellulitis, 546-547
Syphilis, 794-795
identifying, 795i
Systemic lupus erythematosus, 496, 497, 796-797
Systemic sclerosis, 738-739
T
Taeniasis (tapeworm disease), 798-799
Talipes, 188-189, 188i
Tay-Sachs disease, 800-801
Tears, drainage of, 226i
Telangiectasia, hereditary hemorrhagic, 358-359, 358i
Temporomandibular joint disease, 802-803
Tendinitis, 804-805
Tendons, 805i
Testicular cancer, 806-807
Testicular torsion, 808-809, 808i
Tetanus, 810-811
Tetralogy of Fallot, 812-813
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Thalassemia, 814-815
skull changes in, 814i
Thiamine, recommended daily allowance of, 891t
Thiamine deficiency, 890-892
Thoracic aortic aneurysm, 64-65
Threadworm infection, 782-783
Threatened abortion, 3
Throat abscess, 931t
Thromboangiitis obliterans, 138-139, 139i
Thrombocytopenia, 816-817
immunodeficiency with, 932t
Thrombocytopenic purpura, idiopathic, 436-437
Thrombophlebitis, 818-819
sites of, 818i
Thrush, 146i
Thymic hypoplasia or aplasia, congenital, 925t
Thyroid cancer, 820-821
Thyroiditis, 822-823
Thyroid-stimulating hormone deficiency, 430, 431
Thyrotoxicosis, 414-415
Tic douloureux, 846-847
Tick bite, 446-447
Tick fever, 688-689, 926t
Tilt test, 752
Tinea versicolor, 931t
Tobacco abuse, 824-825
Tonsillitis, 826-827
Tophi, gouty, 327i
Torulosis, 216-217
Toxic diffuse goiter, 414-415
Toxic shock syndrome, 828-829
Toxocariasis, 931t
Toxoplasmosis, 830-831
Tracheoesophageal fistula, 832-833
Trachoma, 931t
Transient ischemic attack, 834-835
Transposition of great arteries, 836-837
Transsexualism, 927t
Travelers diarrhea, preventing, 300
Trendelenburgs sign, 233
Triceps skinfold thickness, 557i
Trichinosis, 838-839
Trichomoniasis, 840-841
Tricuspid insufficiency, 842-843
murmur of, 842i
Tricuspid stenosis, 844-845
murmur of, 844i
Trigeminal nerve, 846i
Trigeminal neuralgia, 846-847
Trisomy 13 syndrome, 848-849
Trousseaus sign, 417i
Trypanosomiasis, American, 922t

Tuberculosis, 852-853
Tularemia, 854-855
Tumors. See also Cancer; specific type.
bone, 124-125, 125t
brain, 128-129
chromaffin, 612-613
pituitary, 614-615
renal, 462i
Turners syndrome, 464
Tympanic membrane rupture, 576, 602-603
Typhoid, bilious, 688-689, 926t
U
Ulcerative colitis, 856-857
Ulcers
peptic, 600-601
pressure, 652-653, 653i
Umbilical hernia, 445i
Uncinariasis, 376-377
Undulant fever, 136-137
Urinary tract, neuromuscular dysfunction of lower,
552-553, 553t
Urinary tract infection, lower, 858-859
Urticaria, 860-861
Uterine bleeding dysfunctional, 862-863
Uterine cancer, 864-865
Uterine leiomyomas, 866-867
Uveitis, 931t
V
Vagabond fever, 688-689, 926t
Vaginal cancer, 868-869
Vaginismus, 931t
Vaginitis, 908-909
Vagus nerve stimulation for epilepsy, 273
Valley fever, 192-193
Vancomycin intermediate-resistant Staphylococcus aureus,
870-871
Vancomycin-resistant enterococcus, 872-873
Vaquez-Osler disease, 640-641
Varicella, 874-875
Varicocele, 876-877
identifying, 876i
Varicose veins, 878-879
Variola, 766-767
Vascular hemophilia, 906-907
Vascular retinopathies, 880-881
diagnostic tests for, 881
Vasculitis, 882-883
Vasospastic arterial disease, 684-685
Venereal warts, 308-309, 308i
Index 949
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Page 950
Venous pathways of leg, 818i

Ventricular aneurysm, 66-67
Ventricular septal defect, 884-885
Verrucae. See Warts.
Vesicoureteral reflux, 886-887
Vestibular function, normal, 514
Vibrio parahaemolyticus food poisoning, 178
Viral encephalitis, 724-725
Viral hepatitis, 356-357
Viral pneumonia, 626
Visceral larva migrans, 931t
Vitamin A, foods containing, 888
Vitamin A deficiency, 888-889
Vitamin B complex, recommended daily allowance of, 891t
Vitamin B deficiency, 890-893
Vitamin B12
dietary sources of, 53
recommended daily allowance of, 891t
Vitamin B12 deficiency, 52-53, 890-892
Vitamin C, foods containing, 895
Vitamin C deficiency, 894-895
Vitamin D deficiency, 896-897, 896i
Vitamin E, foods containing, 898
Vitamin E deficiency, 898-899
Vitamin K, foods containing, 900
Vitamin K deficiency, 900-901
Vitiligo, 902-903
recognizing, 902i
Volvulus, 904-905
von Willebrands disease, 906-907
Vulvovaginitis, 908-909
W
Warts, 910-911
genital, 308-309, 308i
removing, 911i
Wasp sting, 446-447
West Nile encephalitis, 912-913
Wet or white lung, 16-17
Whiplash, 6-7, 7i
Whipples disease, 932t
Whooping cough, 608-609, 608i
Wilsons disease, 932t
Wiskott-Aldrich syndrome, 932t
X
X-linked infantile hypogammaglobulinemia, 914-915
Y
Yellow jacket sting, 446-447
Yuppie flu, 180-181
950 Index
Z
Zinc, foods containing, 916
Zinc deficiency, 916-917
Zollinger-Ellison syndrome, 506, 918-919

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9400 FM.

The clinical treatments described and recommended in

Diseases (in alphabetical order)

Less common diseases 922

Web resources 935

Kendra S. Seiler, RN, MSN

Elizabeth A. Archer, RN, EdD

LaDelle Smothers, RN, BSN, MS

Julie A. Calvery, RN, MS

Rita M. Wick, RN, BSN

Kim Cooper, RN, MSN

Lillian Craig, RN, MSN, FNP-C

Shelley Yerger Hawkins, APRN-BC, DSN, FNP, GNP,

Post Doctoral Fellow

Elizaveta House, RN, BSN

Angela R. Irvin, RN, MSN, ARNP, NP-C

Vanessa Kramasz, RN, MSN, FNP

H Also known as miscarriage

fore fetal viability (see Types of spontaneous abortion)

charge for several weeks before onset of cramps and

except in cases caused by an incompetent cervix

blood (severe bleeding)

with a negative indirect Coombs test

if remnants remain in the uterus

tient may expel uterine contents without knowing it.

Types of spontaneous abortion

H Disseminated intravascular coagulation (DIC)

H Premature separation of the placenta from the uter-

Mild abruptio placentae (marginal

H Spontaneous rupture of blood vessels at the placental

Mild abruptio placentae

bed may be due to lack of resiliency or to abnormal

H Blood loss evaluated and controlled

age 35, women with gestational hypertension, and

Degrees of placental separation in abruptio placentae

Internal bleeding between the placenta

In moderate separation, external hemorrhage occurs through the vagina.

External hemorrhage is also characteristic in severe separation.

H For severe placental separation with no signs of fetal

life, vaginal delivery unless contraindicated by uncontrolled hemorrhage or other complications

H Obtain blood samples for hemoglobin level and

hematocrit, coagulation studies, and type and crossmatching, as ordered.

The patient will:

H Refer the patient for professional counseling, if

H Neck muscle asymmetry

H Injury resulting from sharp hyperextension and flex-

ion of the neck that damages muscles, ligaments,

transmission of nerve impulses.

tact sports, until full recovery has been established

H Motor vehicle accident

H Absence of head restraint in automobile

injury: the late 40s

H Oral analgesics, such as acetaminophen, non-

steroidal anti-inflammatory drugs, and opioids

H Surgical stabilization possible in severe cervical

H Provide protection of the spine during all care.

after the accident

Applying a cervical collar

tiguous with a hair follicle (pilosebaceous follicle)

nodules) and noninflammatory (closed and open

the pilosebaceous unit.

terial and bacteria within the pilosebaceous follicle

Causes of acne flare-ups