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EXAM 4 PEDS STUDY GUIDE

CARDIAC
Cardiac Assessment
o Normal pediatric vital signs HR
o Newborn
100-180
o 1 wk-3 mo
100-220
o 2 mo- 2 yr
60-150
o 2-10 yr
70-110
o 10 yr-adult
55-90
Cardiovascular disease has 2 major groups
o Congenital heart disease (CHD)
Primarily anatomic abnormalities present at birth that result in
abnormal cardiac function
2 types
Heart failure (HF)
Hypoxemia
o Acquired cardiac disorders
Disease processes or abnormalities that occur after birth and can be
seen in normal heart or the presence of genital heart defects
Various factors:
Infection
Autoimmune responses
Environmental factors
Familial tendencies
History & physical exam
o HISTORY HISTORY HISTORY!!!!
o Inspection
Nutritional state- failure to thrive or poor weight gain is associated
with heart disease
Color- cyanosis common feature of CHD
Pallor associated with poor perfusion
Chest deformities- enlarged hears distorts chest configuration
Unusual pulsations- visible pulsations of the neck veins are seen
sometimes
Respiratory excursion- refers to ease or difficulty of respiration
Clubbing of fingers- associated with cyanosis
o Palpation and Percussion
Chest- maneuvers help discern heart size and other characteristics
Abdomen hepatomegaly or spenomegaly
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Peripheral pulses- rate, regularity, and amplitude
o Auscultation
Heart rate and rhythm- listen for fast heart rates, slow, and irregular
rhythms
Character of heart sounds- listen for distinct or muffled sounds,
murmurs, and additional heart sounds
o Diagnostic
Electrocardiogram
Nurse should assess the patient, not the monitor
Echocardiography
Most frequently used tests for detecting cardiac dysfunction
Involves use of ultra-high-frequency sound waves to produce
an image of hearts structure
Transducer placed directly on chest wall delivers repetitive
pulses of ultrasound and processes the returned signals

Cardiac Catheterization
Invasive diagnostic procedure in which a radiopaque catheter is inserted thru a
peripheral blood vessel into the heart
Catheter is guided thru the heart with aid of fluoroscopy
After tip of catheter is within a heart chamber, contrast material is injected, and
films are taken of the dilution and circulation of the material (angiography)
Types:
o Diagnostic catheterizations:
Used to diagnose congenital cardiac defects- particularly in
symptomatic infants & before surgical repair
Divided into right-sided catheterizations, in which cateheter is
introduced through a vein & threaded into right atrium
Left-sided catheterization- catheter is threaded thru an artery into
aorta and into the heart
o Interventional catheterizations:
Therapeutic catheterization
A balloon catheter or other device is used to alter the cardiac anatomy
Interventions:
Balloon atrioseptostomy
o Transposition of great arteries
o Some complex single-ventricle defects
Balloon dilation
o Valvular pulmonic stenosis
o Branch pulmonary artery stenosis
o Congenital valvular aoritic stenosis
o Rheumatic mitral stenosis
o Recurrent coarctations of aorta
o Congential mitral stenosis
Coil occlusion
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o PDA (<4mm(
Transcatheter device closure
o ASD
Amplatzer septal occluder
o ASD
VSD devices
o VSDs
Stent placement
o Pulmonary artery stenosis
o Coarctation of the aorta in adolescents
o Use to treat other lesions
RF ablation
o Some tachydysrthymias
o Electrophysiology studies
Catheters with tiny electrode that record the impulses of the heart
directly from conduction system are used to evaluate dysrthymias &
sometimes destroy accessory pathways that cause some
tachydsrthmias
Possible side effects:
o Acute hemorrhage from entry site
o Low-grade fever
o Nausea
o Vomiting
o Loss of pulse in catheterized extreme
o Transient dysrhythmias
Rare risks:
o Stroke
o Seiure
o Tamponade
o Death
Preprocedural care:
o Prepare child & fam for procedure
o Use developmentally appropriate materials
o Assess & mark pulses
o Basline O2 sats
o NPO for 4-6 hours before procedure
Postprocedural:
o Observe of the following for signs of complications:
Pulses
Temp & color of affected extremity
Vital signs- q 15 minutes
Blood pressure
Dressing
Fluid intake
Bloog glucose levels- for hypoglycemia
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Postpericardiotomy syndrome
o Symptoms:
Fever
Pericardial friction rub
Pericardial & pleural effusion
o Occurs immediate post op
o Also can occur later (day 7-21)
o Cause=unknown

CONGENTIAL HEART DISEASE (CHD)
Incidence:
o 5-8 per 1000 live births
o 2-3 are symptomatic in 1
st
year of life
o CHD=major cause of death in first year of life (after prematurity)
o Most common anomaly= ventricular septal defect
Causes:
o Chromosomal/genetic 10-12%
o Maternal/environmental 1-2%
Maternal drug use
Infants that have FAS- 5-% have CHD
Maternal illness
Rubella infection PDA & pulmonary branch stenosis
Cytomegalovirus, toxoplasmosis, other viral illness
Infants of diabetic mothers (IDMs)
o Multifactorial 8%%
Normal fetal circulation changes
o When newborn takes 1
st
breath, the fetal vascular system undergoes abrupt
changes
Umbilical vein & umbilical arteries
Before birth, umbilical vein delivers O2 and nutrients to a fetus
Foramen ovale
Closes as pressure in left atrium exceed pressure in right
atrium
Ductus arteriosus
Starts to close in presence of increased O2
o The following are NO LONGER NEEDED:
Foramen ovale
Shunts highly oxygenated blood from RA to LA & supplies
upper extremities and head
Ductus venosus
Fetal blood vessel connecting UV to IVC
Umbilical vessels
o WITH THE FIRST BREATH
Lungs expand causing dramatic fall in pulmonary vascular resistance
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Market increase in pulmonary blood flow (raising LA pressure above
that of IVC)
A progressive thinning of the walls of pulmonary arteries occurs
Blood pressure is now high in the aorta & the babys systemic
circulation is well established
The ductus arteriosus contstricts at birth, but there is often a small
shunt of blood from the aorta to the Left Pulmonary Artery for a few
days
This decreases with increases PO2 which stimulates
bradykinin release
Umbilical arteries constrict functionally, later become fibrous
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o History indicators of cardiac dysfunction
Symptoms may appear 4-12 weeks after birth
Failure to thrive, poor weight gain, activity intolerance
Developmental delays
Positive prenatal history
Positive family history of cardiac disease
o Physical indicators of cardiac dysfunction:
Poor feeding
Tachypnea, tachydardia
Diaphoresis
Crackles
Hepatomegaly
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Cyanosis
Murmur Sternal lift
Impaired myocardial function
Tachycardia
Fatigue
Weakness
Restlessness
Pale
Cool extremities
Decreased BP
Decreased output
Pulmonary congestion
Tachypnea
Dyspnea
Respiratory distress
Exercise intolerance
Cyanosis
Systemic venous congestion
Peripheral & periorbital edema
Weight gain
Hepatomegaly
Neck vein distention
Goals of management
o Support maximal growth & nutrition
o Reduce cardiac workload
o Prevent & treat congestive heart failure
o Maintain optimal cardiac output
o Provide palliative procedures to protect lungs from too much bloow flow, or
too little blood flow
o Correct the underlying defect
o Maintain fluid & electrolyte balance
o Prevent secondary complications (failure to thrive, cardiogenic shock,
infection, respiratory compromise, cardiac dysrthythmia, thromboembolism)
Diagnostic tests:
o H&P
o Chest x-ray
o Echocardiogram, EKG
o Labs:
ABGs
CNC
Electrolyte panel
Therapeutic & diagnostic cardiac catheterization
Therapeutic nursing management
o Avoid situations that increase cardiac demands (fever, pain, agitation)
o Avoid unnecessarily disturbing the infant
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o Monitor weights
o Small frequent feedings (increased calorie formula as needed)
o O2 as needed
o Administer pharmacologic agents as ordered; evaluate patient response to
treatment
o Portect from infection
o Accurate I&O
Pharmacology:
o Depends on defect & MOST IMPORTANTLY patients clinical condition
Digoxin
Diuretics
Prostaglandin
Keep PDA open
Indomethacin
Close PDA
Vasopressors
Vasodilators
Vaccinations as indicated
Complications:
o Heart failure
o Postpericardiotomy syndrome
Post-op period: fever, pericardial friction rub, pleural effusion
o Cerebral thrombosis
o Failure to thrive
o Death
Older Classifications of CHD
o Acyanotic
May become cyanotic
o Cyanotic
May be pink
May develop congestive heart failure
Newer classification of CHD
o Hemodynamic characteristics (blood flow patterns within the heart):
1. Increased pulmonary blood flow
2. Decreased pulmonary blood flow
3. Obstruction of blood flow out of the heart
4. Mixed blood flow

Increased Pulmonary Blood Flow Defects
Abnormal connection between the 2 side of the heart
o Either the septum or great vessels
Increase blood volume on RIGHT side of heart
Increased pulmonary blood flow
Decreased systemic blood flow
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Defects:
o Atrial Septal Defect (ASD)
Acyanotic
Hole between two atria
Allowing blood from
higher pressure left
atrium to follow into the
lower pressure right
atrium
Closes naturally, with
therapeutic catheterization of
surgery
Loud, harsh murmur
With fixed split second heart sound
Enlarged right side of heart
Increased oxygen saturiation in right atrium
Mild congestive heart failure
May be asymptomatc
Surgical patch closure
o Ventricular Septal Defect (VSD)
Acyanotic
Hole between right & left ventricles
Most common cardiac defect
Closes naturally or with surgical
correction
Loud, harsh murmur that begins at
about 4-8 weeks of age
O2 saturation is higher that normal in
right ventricle
Congestive heart failure
Failure to thrive
Dysrthymias
Small defects may be asymptomatic
o Atrioventricular canal defect
Combo of ASD & VSD
Acyanotic
Incomplete fusion of endocardium creating
a large central AV valve that allows blood
to flow between all four chambers of the
heart
Most common cardiac defect in children
with Down syndrome
Flow is determined by pulmonary and
systemic resistance
Surgical repair required
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CHF
Loud systolic murmur
Cyanosis increases with crying
Pulmonary vascular obstructive disease
Increased blood volume is pumped into the lungs, which may
eventually result in increased pulmonary vascular resistance
o Patent Ductus Arteriosus (PDA)
Acyanotic
Fetal vessel between the pulmonary
artery and the aorta that fails to
close
PDA is common in premature
infants
Closure occurs naturally, with
Indomethacin, therapeutic
catherization, or surgery
Machinery-like murmur
Patients at risk for BE and
pulmonary vascular obstructive
disease later in life from chronic excessive pulmonary blood flow
Tachycardia
Enlargement of left ventricle
Wide pulse pressure
Bounding pulses
Tachypnea

OBSTRUCTIVE DEFECTS
Blood exiting the heart meats an area of anatomic narrowing (stenosis) causing
obstruction to blood flow
The pressure in ventricle and in great artery before obstruction is increased, and the
pressure in the area beyond the obstruction is decreased
Location of narrowing is usually near the valve:
o Vavlular- at site of valve
o Subvalvular- narrowing in the ventricle below the valve (ventricular outflow
tract)
o Suprvalvular- narrowing in great artery above valve
There is a pressure load on the ventricle and decreased cardiac output
Clinically exhibit signs of HF
Defects:
o Coarctation of the Aorta
Acyanotic
Narrowing of the aorta due to a
constricting band
Increased blood pressure and
oxygen saturation in the upper
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extremities as compared with the lower extremities
Headaches
Vertigo
Nosebleeds
Absence of femoral pulses
High blood pressure
Leg pain
Decreased cardiac output
CHF
Surgical repair & reconstruction
is usually needed
Cool lower extremities
o Aortic Stenosis
Acyanotic
Narrowing of aortic valve
Causing resistance to
blood flow in left
ventricle, decreased
cardiac output, left
ventricular hypertrophy,
& pulmonary vascular congestion
Left ventricular enlargement
Systolic ejection murmur
Faint pulses, hypotension, tachycardia, poor feeding
Exercise intolerance, chest pain, and dizziness
Decreased cardiac output
Opened with balloon procedure or surgery
Risk for:
o BE, coronary insufficiency, & ventricular dysfunction
o Pulmonic Stenosis
Acyanotic
Narrowing of the pulmonary valve or pulmonary artery
Resistance to blood flow causes right ventricular hypertrophy &
decreased pulmonary blood flow
Right ventricular enlargement
Systolic ejection murmur
Exercise intolerance
CHF, cyanosis
Opened with balloon procedure or surgery

DECREASED PULMONARY BLOOD FLOW DEFECTS
Tetralogy of Fallot
o Cyanotic
o Four anamolies are present:
Pulmonary stenosis
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VSD
Dextroposition of aorta
Enlargement of the right ventricle
o Palliative shunt may be placed until child is
able to have the surgical corrective repair
o Systolic murmur
o Cyanosis
o Polycthemia
o Clot formation
o Severe dyspnea
o Squatting position
o Hypercyanotic spells (Tet Spells)
o Acidosis
o Clubbing of the fingers
o Growth retardation
o Failure to thrive
Tricuspid Atresia
o Cyanotic
o Tricuspid valve is completely closed
o Generally requires several complex
surgeries
o Incompatible with life if there is
inadequate pulmonary blood flow
o PGE infusion is used until an emergency
shunt procedure can be performed
o The Fontan procedure is the surgical
repair
o No blood flow from right atrium to right
ventricle
o Severe cyanosis within hours after birth (Increased as the PDA closes)
o CHF
o Failure to thrive

MIXED DEFECTS
Transposition of the great arteries or transposition of the great vessels
o Cyanotic
o Aorta arises from the right ventricle instead of the left, and the pulmonary
artery arises from the left instead of the right
o Incompatible with life if there is no
connection between right and left sides
o Emergency septostomy is performed to
create a connection between the right and
left sides
o The surgical repair is the atrial switch
procedure
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o Severe cyanosis hours to days after birth (as PDA closes)
o Various murmurs
o Presence of ASD and VSD
o CHF
Total anomalous pulmonary venous connection
o Cyanotic
o Total anomalous pulmonary venous
return
o Rare defect characterized by failure
of pulmonary veins to join the left
atrium; instead are connected with
the venous system
o Repaired surgically
o Cyanosis (inversely related to
amount to pulmonary blood flow)
o May initially be asymptomatic
o CHF, cardiac failure, death
Truncus Arteriousus
o Cyanotic
o Failure of normal separation in development of the pulmonary artery and
aorta, resulting in a single vessel that
overrides both ventricles; mixing
pulmonary & systemic circulations
o Repaired in first few months of life
(closing VSD and hemographs-
modified Rastelli procedure)
o CHF
o Cyanosis
o Poor growth
o Activity intolerance
o Murmur
o Brain abscess
o Bacterial endocarditis
Hypoplastic heart syndrome
o Left sided
Cyanotic
Left ventricle is NONFUNCTIONAL
Requires several complex surgeries
or cardiac transplantation for
survival
Right ventricular enlargement
Severe cyanosis
Severe decreases in cardiac output


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CHF IN CHILDREN
Impaired myocardial function
o Tachycardia
o Fatigue
o Weakness
o Restlessness
o Pale
o Cool extremities
o Decreased blood pressure
o Decreased urinary output
Pulmonary congestions
o Tachypnea
o Dyspnea
o Respiratory distress
o Exercise intolerance
o Cyanosis
Systemic venous congestions
o Peripheral & periorbital edema
o Weight gain
o Ascites
o Hepatomegaly
o Neck vein distention


ENDOCARDITIS
Bacterial endocarditis (BE) and subacute endocarditis (SBE) are now referred to as
infective endocarditis (IE)
Often a sequela of bacteremia in children with CHD or AHD
Most common causative agents:
o Streptococcus viridans or Staphylococcus aureus
o Fungal agents such as Candida albicans
Prophylaxis for 1 hour before procedures (IV) or may use PO in some cases
o Antibiotics
Clinical manifestations:
o Onset usually insidious
o Unexplained fever
o Anorexia
o Malaise
o Weight loss
o Characteristic findings caused by extracardiac emboli formation
Splinter hemorrhage (think black lines) under the nails
Osler nodes
Janeway lesions
Petechiae on oral mucous membranes
o May be present:
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Heart failure
Cardiac dysrthmias
New murmur

RHEMATIC FEVER (RF) & RHEMATIC HEART DISEASE (RHD)
Rheumatic Fever
o Inflammatory disease occurring after group A B-hemolytic stremptococcal
pharyngitis (GABHS)
o Infrequently seen in US
o Self-limiting
Affects joints, skin, brain, serous surfaces, & heart
Rheumatic heart disease
o Most common complication of RF
o Damage to valves as a result of RF
Clinical manifestations:
o Jones criteria (Presence of 2 major manifestations or one major
manifestation & two minor manifestations)
Carditis
Polyarthritis
Erythema Marginatum
Subcutaneous Nodes
Chorea (St. Vitus Dance, Sydenham Chorea)
Treatment
o Prevention of GABHS
o Tx of streptococcal tonsillitis and pharyngitis
Penicillin G IM once
Penicillin V by mouth for 10 days
Sulfa by mouth for 10 days
Erythromycin (if patient is allergic to the above agent) by mouth for
10 days
o Tx of recurrent RF
Same as above


KAWASAKI DISEASE (KD); Mucocutaneous lymph node syndrome
An acute systemic vasculitis of unkown cause
75% of cases, the child is younger than 5 years of age
3 phases:
o Acute phase
Sudden high fever, unresponsive to antipyretics & antibiotics
o Subacute phase
Lasts from end of fever thru end of all KD clinical signs
o Convalescent phase:
Clinical signs have resolved, but laboratory values have not returned
to normal
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Ends when normal values have returned (6-8 weeks)
Diagnostic criteria for Kawasaki disease
o Changes in extremities
In acute phase: edema, erythema of palms and soles
Subacute: periungual desquamation (peeling) of hands & fet
o Bilateral conjuctival injection (inflammation) without exudation
o Changes in the oral mucous membranes
o Polymorphous rash
o Cervical lymphadenopathy
Treatment of KD
o Acetylsalicyclic acid (ASA) 80-11 mg/kg/day for fever
o IV immunoglobulin (IVIG)
o Then 3-5 mg/kg/day antiplatelet

Hyperlipidemia
Identify kids at risk & treat early
Tx is lifestyle modifcation
o Restrict intake of cholesterol & fats
o Increase intake of whole grains, fruits, & veggies
o Exercies for 60 min a day 5 days a week
o Stop smoking and avoid second-hand smoke
If there is no response to diet changes & meds:
o Colestipol (Colestid)
o Cholestyramine (Questran)


Systemic Hypertension
Essential hypertension has no known cause
Secondary has an identifiable cause
Pediatric hypertension is generally secondary to structural abnormality or an
underlying pathologic condition
o Renal disease
o Cardiovascular disease
o Endocrine or neurologic disorders
Pharmacologic treatment:
o B-blockers
o Calcium channel blockers
o Angiotensin-converting enzyme (ACE) inhibitors
o Angiotensin receptor blockers
o Diuretics


MS

Immobilized patient
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Atrophy
Joint contracture
Major musculoskeletal consequences of immobilization are:
o Significant decrease in muscle size, strength, and endurance
o Bone demineralization leading to osteoporosis
o Contractures and decreased joint mobility
DVT


Developmental Dysplasia of the Hip (DDH)x
Wide range of abnormal development of the hip leading to hip instability
1 per 100 live births
80% are female
Lift hip affected most commonly
Caucasion children most often affected
Degrees of DDH
o Acetabular dysplasia
Acetabular rool shallow; mildest form
o Subluxation
Head of femur is partially displaced
Flattened socket; most common form
o Dislocation
Femoral head not in contact with acetabulum
Clinical manifestations of DDH
o Infant:
Shortened limb on affected side
Restricted abduction of hip on affected side
Unequal gluteal folds when infant prone
Positive Ortolani test
Positive Barlow test
o In older infant & child
Affected leg shorter than other
Telescoping or piston mobility of joint
Trandelenburg sign
Trandelenburg gait
Greater tochanter is prominent and appears above line from
anterosuperior iliac spine to tuberosity of ischium
Marked lordosis if bilateral dislocations
Waddling gait if bilateral disclocations
Sign of gluteus medius weakness or relative inhibition
Sign is elicited by asking patient to stand on involved leg
If sign is positive, the pelvis will drop on uninvolved side
Ortolani & Barlow tests
o Barlow test shows that hip has potential to dislocate
o Ortolani test confirms its dislocation
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o
o Never do at the same time; do one knee then the other
Diagnosis
o Newborn assessment tools most reliable in early infancy
o X-ray not reliable in infancy due to incomplete ossification of femoral head
o Ultrasound as adjunct to abnormal physical findings
Therapeutic management of DDH
o Importance of early intervention
o Newborn to age 6 months:
Palvik harness for abduction of hip
o Age 6-18 months:
Dislocation unrecognized until child begins to stand and walk; use
traction and cast immobilization (spica)
o Older child:
Operative reduction
Tenotomy (muscle contracture)
Osteotomy (rebuild acetabular roof)
Difficult after 4 years
Management: 0-6 months
o Splinting: Palvik harness
Worn continuously x 3-5 months until hip stable
Straps checked q 1-2 weeks for adjustment
o 95% effective if hips reducible at birth
o prevent adduction
o Nursing care of child in palvik harness
Newborn hip assessment
Management of reduction device
Teaching application/use of harness
o Removal, adjustment discouraged
Prevent skin breakdown
o Clothing, diaper under straps
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o Check for reddening under straps often
Management: 6-18 months
o Gradual reduction by traction x 3 weeks
o Closed/open reduction under anesthesia
o Hip spica cast x 3 months
Management: Older child
o Operative reduction
o Construction of acetabular roof
o Post-operative casting
o Successful reduction difficult after 4 years

TALIPES: Congenital Clubfoot
Includes multiple foot, ankle deformity and malposition, and soft tissue
contractures
Incidence: 1-2: 1000 live births
Male: female= 2:1
50% are bilateral
increase risk of hip dysplasia
Etiology
o Not well identified
o Strong family disposition
Q:10 if parent affected
o Possible arrested fetal development of skeletal & soft tissue (9-10 weeks
gestation)
o Associated with other syndrome (myelomeningocele)
o Idiopathic clubfoot most common form
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o
o Talipes varus: inversion, or bending inward
o Talipes valgus: eversion, or bending out
o Talipes equinus: plantar flexion with toes lower than the heel
o Talipes calcaneus: dorsiflexion with toes higher than the heel
o Talipes equinovarus: when the foot turns inward and downward; most
common form
Classification of clubfoot
o Mild or postural
May correct spontaneously or require passive exercise or serial
casting
o Tetralogic
Associated with other congenital anomalies
Usually requires surgical correction with high incidence or
recurrence
o Idiopathic
Bony abnormality almost always requiring surgical intervention
Treatment
o Started as a neonate
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o Serial casting of affected leg(s)
o Recasting frequent until maximum correction achieved (~8-12 weeks)
o X-Ray to evaluate efficacy of casting
o If casting unsuccessful, surgery @6-12 months & casting/brace after surgery


Metatasus Adductus
Most common
Treatment usually not needed
Due to abnormal intrauterine positioning
Associated with pigeon toed gait
Different from Talipes deformities because foot has full ROM

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Kyphosis
o Abnormally increased convex angulation of the curvature of the thoracic
spine
o Most common form is postural
o Can result from tuberculosis, arthritis, osteodystrophy, or compression
fracture
o PT w/ strengthening excercises
o Not associated with pain
Lordosis
o Accentuation of the cervical or lumbar curvature beyond physiologic limits
o May be idiopathic or secondary complication or trauma
o May occur with flexion contractures of hip, congenital dislocated hip
o In obese children, abdominal fat alters center of gravity, causing lordosis
o Treat cause ie excess weight and manage pain; associated with pain
Scoliosis
o Most common spinal deformity
o Complex spinal deformity in 3 planes:
Lateral curvature
Spinal rotation causing rib asymmetry
Thoracic kyphosis
o Congenital or develop during childhood
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Congenital associated w/ myelomeingocele
o Idiopathic scoliosis during growth spurt of early adolescence most common
form
o Early manifestations of Idiopathic scoliosis
Seldom apparent before preadolescent growth spurt
May be picked up in school screening
Uneven pants length
Rarely painful
Right curvature is usually scoliosis
Left curvature often associated with disorders and have a neurologic
component
o Diagnosis
Physical exam
Asymmetry of shoulder, hip height; flank, scapular shape when
standing
Asymmetry of ribs & flanks with bend at waist
Stand & twist to evaluate flexibility of curve
X-Ray of spine to measure curve magnitude
MRI if indications of other spinal abnormalities
Spinal curvature and treatment
o 10 degree normal postural variation
o 10-20 mild, no treatment if no progression
o 20-40- bracing
o >40 surgery
Bracing/exercise
o Bracing can slow or stop progression of curvature
o TLSO (thoracolumbarsacral orthosis)
Wear 16-23 hours per day; adjusted periodically
Milwaukee brace; Boston brace (less visible)
o Daily exercises to prevent atrophy of spinal and abdominal muscle
Operative management
o Curves >40, difficult sitting, breathing, pain require surgery
o Realignment and internal fixation with bony fusion or realigned spine
o Harrington rod system
Immobilized postoperatively
Post-Op Nursing care
o Pain management
Considerable pain 2-3 days post-op
o Neurologic dysfunction
Post-op paralysis a risk
o GI dysfunction
Paralytic ileus
o GU dysfunction
Urine retention & hypoperfusion possible
o Respiratory dysfunction
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Anesthesia & immobility atelectasis
o Immobility consequences
High potential for skin breakdown
Potential for phlebitis
Discharge education
o Recommended physical activity
o Pn meds & side effects
o Psychological adjustment to brace, altered body image
o Assess family, peer support
o Schooling
o National Scoliosis Foundation

Fractures
Bone structure in a child
o Ossification incomplete until 18-21 years
o Epiphyseal plate
Growth plate
o Periosteum
Vascular membrane
Critical for growth and healing of bone
Bone healing in children
o Generally faster in children due to thick vascular periosteum
o Healing of bone
Neonate: 2-3 weeks
Early childhood: 4 weeks
Later childhood: 5-8 weeks
Adolescence: 8-12 weeks
Adult: 10-16 weeks
o Remodeling
Fractures in infant & small child:
o Infancy:
Birth trauma
MVA
Child abuse (twisting, rough handling, pulling)
Periosteal bleeding not visible on x-ray for weeks after injury
o Small child:
Multiple fractures at varied stages of healing warrants investigation
for abuse
Causes:
o Breaking a fall- clavicle, forearm
o Auto vs peds- femoral neck or femur
Most commonly seen in 4-7 years old
Triad of auto vs peds injuries:
Femur fracture
Trunk trauma
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Head injury


Epiphyseal fractures
o Epiphyseal plate weakest point of long bones
o Normally heals quick and completely
o Risk of damage to growth plate
o Can be mistaken for dislocation
o Early identification critical to minimize growth problems & angular
deformities
Clinical course of fracture
o Muscles contract to splint broken bone
o Contusion or severe hemorrhage of surrounding soft tissue may occur
o Stable bone due to intact periosteum
o Neurovascular damage less common than in adults
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o
o 5 Ps of ischemia from vascular injury:
Pain
Pallor
Pulselessness
Paresthesia
Paralysis
o Slight rise in WBC due to inflammation & hgb decreases
Management
o Usually closed reduction & casting
o Femur, humerus fractures may require hospitalization and traction
o Internal fixation more quickly stabilizes injury (ORIF)
o Casting
Bone will grown in the direction in which stress is placed on it- Wolffs
law
Critical to check for skin injury prior to application of cast
Check for neurovascular compromise
TRACTION
o Primary goals of traction
To fatigue involved muscle and reduce muscle spasm
To realign distal and proximal bone ends to promote satisfactory bone
healing
To immobilize fracture until realignment has occurred and boen has
healed well enough to cast or splint
o Complications of fractures
Circulatory impairment
Nerve compression
Compartment syndrome
Epiphyseal damage
Non union or malunion of bone
Osteomyelitis
Pulmonary emboli


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Sprains & Strains
Sprain:
o Ligament stretched or torn by force created as joint twisted
Vessel, tendon, nerve damage common
Joint laxity best indicator of severity of sprain
Strain:
o Microscopic tear of tendon
Painful & swollen
Usually do not occur immediately but over time
Management of soft tissue injuries
o RICE
Rest
Ice (some controversy about icing)
Compression
Elevation
First 6-12 hours critical for treatment

Shin Splints
Extensive running pressure on tibia
Ligaments tear away from shaft of tibia
Painful but rarely serious


Nursemaids elbow
Most common dislocation in young children
Usually <5
Sudden jerk and pull of arm
Tx: pop back into place just like a shoulder

Osgood-Schlatter disease
Painful inflammatory disorder of proximal tibia at point of insertion of patellar
tendon
Repeated stress and overuse of quadriceps causes irregularities of growth
Presentation:
o Knee pain, inflammation at tibial tubercle
o Prominent tibial tubercle
o Pn exacerbated by activity, improved with rest
o Hip examination necessary to rule out hip abnormalities
o Knee x-ray findings variable
Treatment:
o Self-limiting
o When growth of proximal tibia ceases, pain disappears
o Rest, avoiding activity that contract quadriceps


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Osteogenesis Imperfecta (OI)
Group of heterogenous inherited disorders of connective tissue
Characterized by excessive fragility and bone defects
Defective periosteal bone formation and reduced cortical thickness of bones
Hyperextensibility of ligaments
Therapeutic management
o Primarily supportive care
o Drugs of limited benefit
o May rule out OI if multiple fractures occur
o Nursing care management:
Caution with handling to prevent fractures
Fam education
Occupational panning and genetic counseling

Legg-Calve-Perthes disease
Self-limiting, idiopathic, occurs in juveniles ages 3-12 , more cmmon in males 4-8 yo
Avascular necrosis of femoral head
10-15% of cases have bilateral hip involvement
Most have delayed bone age
Pathophysiology:
o Cause is unkown but involved disturbed circulation to the femoral head with
ischemic aseptic necrosis
Treatment goal:
o Keep head of femur in acetabulum
o Containment with various appliances/devices
o Rest, no weight bearing initially
o Surgery in some cases
o Home traction in some cases
Prognosis
o Self-limiting
o Outcome has wide variations due to multiple factors
Nursing care management:
o Identification of affected children & referral teaching care and management
o Compliance issues with child and family

OSTEOMYELITIS
Inflammation and infection of bony tissue
May be caused by exogenous or hematogenous sources
Signs and symptoms begin abruptly, resemble symptoms of arthritis and leukemia
Marked leukocytosis
Bone cultures obtained from biopsy or aspirate
Early x-rays may appear normal
Bone scans for diagnosis
Exogenous Osteomyelitis
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o Infectious agent invades bone following penetrating wound, open fracture,
contamination in surgery, or secondary from extension from abscess or burn
Hematogenous osteomyelitis
o Preexisting infection
o Source may be furuncles, skin infections, upper respiratory tract infection,
abscessed teeth, pyelonephritis
o Any organism can cause osteomyelitis
o Infective emboli travel to artiers in bone metaphysis, causing abscess
formation and bone destruction
Therapeutic management of osteomyeleitis
o May have subacute presentation with walled off abscess rather than
spreading infection
o Prompt, vigorous IV antibiotics for extended period (3-4 weeks or up to
several months)
o Monitor hematologic, renal, hepatic responses to treatment
Nursing care:
o COMPLETE bed rest & immobility of limb
o Pn management concerns
o Long-term IV access (for antibiotic administration)
o Nutritional considerations
o Long-term hospitilzation, therapy
o Psychosocial needs
Juvenile Idiopathic Arthritis (JIA)
AKA juvenile rheumatoid arthritis, juvenile chronic arthritis, or idiopathic arthritis
of childhood
Possible causes
Peak ages: 1-3 years and 8-10 years
Often undiagnosed
Actually a heterogenous group of diseases:
o Pauciarticular onset involves 4 or more joints
o Polyarticular onset- involves 5 or more joints
o Systemic onset- high fever, rash, hepatosplenomegaly, pericarditis, pleuritis,
lymphadenopathy)
Symptoms may burn out and become inactive
Chronic inflammation of synovium with joing effusion, destruction of cartilage, and
ankylosis of joints as disease progresses
Symptoms:
o Stiffness
o Swelling
o Loss of mobility in affected joints
o Warm to touch, usually without erythema
o Tender to touch in some cases
o Symptoms increase with stressors
o Growth retardation
Diagnostic evaluation of JIA
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o No definitive diagnostic tests
o Elevated sedimentation rate in some cases
o Antinuclear antibodies common, but not specific for JIA
o Leukocytosis during exacerbations
o Diagnosis based on criteria of American College of Rheumatology
Their diagnostic criteria:
Age of onset <16 years
1 or more affected joints
Duration of arthritis >6 weeks
Exclusion of other forms of arthritis
Therapeutic management:
o No cure
o Goals of therapy:
Preserve function
Prevent deformities
Relieve symptoms
o Iridocyclitis, uveitis:
Inflammation of iris & ciliary body
Unique to JIA
Requires opthalmologist
MEDS
o NSAIDs
o SSARDs
o Corticosteroids
o Cytotoxic agents
o Immunologic modulators
Management of JIA
o Therapy individualized to child
o Physical & occupational therapy
o Nutrition, exercise
o Splinting devices
o Pn management
o Prognosis
Systemic Lupus Erythematosus (SLE)
A chronic, multisystem, autoimmune disease of the CT and blood vessels characterized
by inflammation on potentially any body issue
Course and symptoms: unpredictable, mild to life threatening complications
o Clinical manifestations of systemic lupus erythematosus related to tissues
involved:
Constitutional- fever, fatigue, weight loss, anorexia
Cutaneous- erythematous butterfly rash over bridge of nose and
across cheeks, discoid rash, photosensitivity, mucocutaneous
ulceration, alopecia, periungual telangiectasias
Musculoskeletal- arthritis, arthralgia, myositis, myalgia, tenosynovitis
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Neurologic- headache, seizure, forgetfulness, behavior change, change
in school performance, psychosis, chorea, stroke, cranial and
peripheral neuropathy, pseudotumor cerebri
Pulmonary and cardiac- pleuritis, basilar pneumonitis, atelactasis,
pericarditis, myocarditis, endocarditis
Renal- Glomerulonephritis, nephritic syndrome, hypertension
GI- abdominal pain, NV, blood in stool, abdominal crisis, esophageal
dysfuntion, colitis
Hepatic, splenic, and nodal- hepatomegaly, splenomegaly,
lymphadenopathy
Hematologic- anemia, cytopenia
Ophthalmologic- cotton wool spots, papilledema, retinopathy
Vascular- Raynaud phenomenon, thrombophleitis, livedo reticularis
o Diagnostic Criteria for SLE:
1. Malar rash- fixed malar erythema
2. Discoid rash- patchy erythematous lesions
3. Photosensitivity- pain with sun exposure
4. Oronasal ulcers- painless ulcers in mouth or nose
5. Arthritis- swelling, tenderness, or effusion in two or more peripheral
joints (nonerosive)
6. Serositis- pleuritis, pericarditis
7. Renal disorder- proteinuria, casts
8. Neuro disorder- psychosis, seizures
9. Hematologic disorder- hemolytic anemia, thrombocytopenia,
leucopenia, lymphopenia
10. Immunologic disorder- anti double stranded DNA, anti Sm,
antiphospholipid antibodiesl lupus anticoagulant; false positive
syphilis test (rapid plasma reagin [RPR])
11. Antinuclear antibodies
Neonatal lupus: another form of lupus, which occurs when maternal auto antibodies
cross the placenta and cause transient lupus like symptoms in a newborn, with
potential complications of heart block
Therapeutic management
o Ensure childs health by balancing meds necessary to avoid exacerbation and
complications while preventing or minimizing treatment associated
morbidity.
o MEDS
Corticosteroids-to control inflammation administered in doses
sufficient to control and then taper to lowest suppressive dose
Antimalarial (rash and arthritis)
NSAIDS (relieve muscle and joint inflammation)
Immunosuppressive agents
such as cyclophosphamide- renal and CNS disease
mycophenolate, azathioprine, and methotrexate-effective, may
be used to control SLE and allow steroids to be reduced
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Antihypertensives, aspirin, antibiotics, may be needed to treat or
avoid complications
General supportive care: sufficient nutrition, sleep and rest, exercise.
o Limit exposure to sun and ultraviolet B (UVB) light is limited bc of
association with SLE exacerbation
Sunscreens, wearing sun resistant clothes, and altering outdoor
activities; must be provided with great sensitivity to ensure
compliance while minimizing the associated feeling of being different
from peers
Nursing Care Management
o Principal nursing goal: help child and fam positively adjust to disease and
therapy
o Learn S/S of exacerbation
o Key issues:
Therapy compliance, body-image problems associated with rash, hair
loss, and steroid therapy; school attendance; vocational activities,
social relationships; sexual activity; and pregnancy.
Maintain reg med supervision, seek attention quickly when ill, or
before elective surgical procedures, such as dental extraction, bc of
potential needs for increasd steroids or prophylactic antibiotics
o Carry ID for disease and steroid dependence