MCN Dysfunction Nursing

High Risk Pregnancy

When there is an increase chance of morbidity or
mortality to the mother or her fetus or both.

High Risk Infant

Is one who is born with less ability or chance to
survive or a greater chance to be left with a
permanent handicap either psychosocial or
physiologic than the average child

Risk Factors:
1.Maternal Age Factor
a.Age > 35 yrs. old
i.Tendency to have:
1.Heavier babies
2.High perinatal mortality
3.High incidence of infants with down
syndrome
b.Adolescent pregnancy <18 yrs. old
i.Lack of perinatal care
1.Low socioeconomic background
2.Lack of motivation
3.Denial, pride
4.Ignorance, rebellion against
authority
ii.Malnutrition
 1.Anemia, vitamin deficiency,
excessive weight gain, toxemias,
prolonged labor, fetopelvic
disproportion, drug abuse, infections.

2.Social Problems
a.Failure to complete education or vocational
training
b.Dependence on other for support
c.Failure to establish stable family
d.High rate of marital failure
e.High incidence of repeated out-of-wedlock
pregnancies
3. Socioeconomic factors (financial)
a.Low income
i.Predisposed to low health status – OB
and neonatal complications
ii.2 balanced dietary intake
iii.Low birth weight
iv.Toxemia
v.Malnutrition, mental retardation
b.Use of elicit drugs
i.No prenatal
ii.Malnourished
iii.Drug addicted children
c.Smoke and alcohol drink
i.Low birth weight infants
ii.Higher rate of abortions and stillbirths
 4.OB factors
a.Previous difficult pregnancies, fetal loss,
premature
b.Diabetic, hypertension, anemia, cardiac,
renal, or respiratory disease
c.Evidence of vaginal bleeding
d.Rh negative, COPD
e.Exposed to teratogens, chemical,
environmental toxins, or radiation
f.Multiple pregnancy - close gap pregnancy – 2
months from last delivery

DANDER SIGNS THAT REQUIRE PROMPT REPORTING LEAKING OF AMNIOTIC

FLUID, VAGINAL BLEEDING, BLURRED VISION, RAPID WEIGHT GAIN,
ELEVATED BP. CONSTIPATION, BREAST TENDERNESS, NASAL STUFFINESS
ARE COMMON DISCOMFORTS ASSOCIATED WITH PREGNANCY.

Conditions: FIRST TRIMESTER

I.Bleeding
Occurs anytime
Never normal, no matter how slight
Frightening experience
Need to be assessed
Threatens both mother and fetus
Client needs reassurance – it is not because
of what she did to free her from guilt
DES (diethylstilbestrol)
i.Daughter – born with vaginal cancer
ii.Son – cystic testicular disease
 Table 39 – 1 Signs and Symptoms of Hemorrhagic
Shock

Assessment Significance
Increased pulse rate Heart attempting to
circulate decreased blood
volume
Decreased blood pressure Less peripheral resistance
because of decreased
blood volume
Increased respiratory Increased gas exchange
rate to better oxygenate
decreased red blood cell
volume
Cold, clammy skin Vasoconstriction occurs
to maintain blood volume
in central bloody core
Decreased urine output Inadequate blood is
entering kidney due to
decreased blood volume
Dizziness or decreased Inadequate blood is
level of consciousness reaching cerebrum due to
decreased blood volume
Decreased central venous Decreased blood is
pressure returning to heart due to
reduced blood volume
 Figure 39-1 The process of shock due to blood loss
(hypovolemia)
Blood Loss

Decreased intravascular volume

Decreased venous return, decrease cardiac output,

and lowered blood pressure

Body compensating by increasing heart rate to

circulate the decreased volume faster;
vasoconstriction of peripheral vessels) to save blood
for vital organs). Increased respiratory rate and a
feeling of apprehension at body changes also occur.

Cold, clammy skin decreased uterine perfusion. In

the face of continued blood loss, although the body
shifts fluid from interstitial spaces into intravascular
spaces, blood pressure will continue to fall

Reduced renal, uterine, and brain perfusion

Lethargy, coma, decreased renal output

Renal failure

Maternal and Fetal death

Emergency interventions for Bleeding in Pregnancy –

WITH UTERINE RUPTURE, THE CLIENT IS AT RISK FOR HYPOVOLEMIC

SHOCK. THEREFORE, THE PRIORITY IS TO PREVENT AND LIMIT
HYPOVOLEMIC SHOCK. IMMEDIATE STEPS SHOULD INCLUDE GIVING
OXYGEN, REPLACING LOST FLUIDS, PROVIDING DRUG THERAPY AS
NEEDED, EVALUATING FETAL RESPONSES AND PREPARING FOR
SUREGERY
-
Interventions
Alert health team of
emergency situation
Place woman flat in bed
on her side on bed rest
Begin IV fluid such as
lactated Ringers with an
18 – 19 gauge needle
Withhold oral fluid
Administer oxygen as
necessary at 2 – 4L/min
Monitor uterine and fetal
heart rate by external
monitor
Omit vaginal or rectal
examination
Order type and cross-
match of 2 units whole
Rationale
Provide maximum
coordination of care
Maintain optimal placental
and renal function
Replace intravascular fluid
volume; prepare IV line for
blood replacement
Anticipation of emergency
surgery
Provide adequate fetal
oxygenation despite
lowered circulating blood
volume
Assess whether labor is
present and fetal status;
use external system to
avoid cervical trauma
If a rectal or vaginal exam
is done with placenta
previa, the placenta may
be torn and hemorrhage
may occur
Prepare to restore
circulating maternal blood
blood volume
Measure intake and Assess renal function (will
output decrease with massive
circulating volume loss)
Assess vital signs (pulse, Assess maternal response
respirations and blood to blood loss
pressure) every 15
minutes
Assist with placement of Assess pressure of blood
central venous pressure returning to heart
catheter
Measure maternal blood Assess extent of
loss by weighing perineal continuing blood loss
pads; save any clots
passed
Set aside 5 ml of blood in Assess for possible blood
a clean test tube and coagulation problem
observe in 5 minutes for (disseminated
clot formation intravascular coagulation).
Suspect this if no clot
forms within time limit.
Maintain a positive Support mother-child
attitude toward fetal bonding
outcome
Support woman’s self- Problem solving is
esteem lessened by poor self-
esteem
Bleeding
Not directly related to pregnancy e.g. tumor,
polyps, erosions
Originating or as a consequence of pregnancy
oAbortion – loss of fetus before age of viability
<24 weeks of AOG
Induced
Therapeutic – medically indicated
Criminal – intentionally done
Septic – infected abortion; secondary
to infection

Spontaneous
Threatened
oPrior to end of 20th weeks of AOG
oOnly abortion can be save
oVaginal bleeding is slight
oAbdominal cramping is slight to
moderate
oCervix is closed
oComplete bed rest without
bathroom privileges
oDiet: normal diet high vitamins
and protein
Imminent (inevitable)
oCervix is opened
 oBleeding is moderate to profuse
oAbdominal pain is moderate to
severe
oNPO
oPossibility of neurogenic and
hypovolemic shock
Incomplete
oOne of the products of
conception has not been expelled
oCervix is opened
oSevere bleeding and pain
oPrepare for complete abortion –
D/C
Complete
Missed – cervix is closed; foul-
smelling discharge; fetus dies in utero
before 20 weeks AOG and retained
from 2 months or longer and will
undergo changes:
a.Fluffling
LES – gray scale
1.Thickening and
covering of fetal skull
and thorax
2.12 – 48 hours after
the death of the fetus –
amniotic fluid
b.Maceration – softening
 c.Mummification – leather-like
changes
d.Lithopedion formation – stoney
– material

Incidence of abortion increases in:

1.Age
2.Parity – gravida 6
3.History of previous pregnancy
4.10% of pregnancy end up in abortion – nature
way of eliminating undesirable mal-formed fetus

Therapeutic Abortion: According to US Supreme

court ruling (Jan. 22, 1973) Pregnancy may be
terminated as follows:
1.1st trimester abortion – decision is left to the
women and her physician
2.2nd trimester – state may not prohibit but may
regulate practice for woman’s health
3.Final trimester – state may choose to protect the
potential life of the fetus by prohibiting abortion
except when there is threat to the life or health of
the mother
4.Religious belief of the mother is always
respected.
Habitual Abortion
Repeated abortion (spontaneous of any type)
3 or more pregnancies at same age or pre-viable
stage

Causes of Recurrent or Habitual Abortion

1.Defective spermatozoa
2.Hormonal influence
3.Nutritional status
4.Deviation of uterus
5.Psychological factor – personality and stress
6.Blood incompatibility – ABO, Rh factor

Induced Abortion
Deliberately terminating pregnancy
Criminal, septic
Therapeutic, medical, and planned

Purposes:
1.When there is threat to mother’s life (heart disease)
2.Fetal malformation (chromosomal defects)
3.Psychological implication (rape)

Procedures Used to induce Abortion (Therapeutically)

I.Menstrual Extraction
Simplest type done on 4th – 6th weeks AOG
Uterine lining is suction – client bleeds as normal
menses
Oxytocin given orally
Follow-up check up and pregnancy test
 Complications:
oHemorrhage
2 pads/ hour
Clots
oInfection
Abdominal pain and tenderness
Fever over 100 OF
Endometritis

II.Dilatation and Vacuum Extraction

Paracervical block
Cervix is dilated with dilators
LAMINARIA – dried sterilized seaweeds – cervix
swells, after 24 hours becomes dilatable vacuum
extraction is inserted and evacuate uterus contents in
15 minutes
Antibiotics, oxytocin, MGH after 4 hours
Bleeding same as menses
Complications:
oHemorrhage
2 pads/ hour
Clots
oInfection
Abdominal pain and tenderness
Fever over 100 OF
Endometritis

III.Saline induction
“Salt poisoning Abortion” done on 14th – 16th weeks
of AOG then D and E is used
16th – 24th weeks of AOG Saline and prostaglandin
induction is used
Mechanisms:
 i.Saline interferes with progesterone functioning
causing endometrial sloughing
ii.Done through abdominal wall into uterus –
needle is inserted then 100 – 200 ml amniotic fluid
is aspirated and 20% hypertonic saline solution is
injected into uterus to replace aspirated fluid.
Then needle is removed 12 – 36 hours ff. injection
– labor contractions begin; supplemented by
oxytocin drip
Complications:
a.Hypernatremia - accidental injection of HSS to
blood vessels in the uterus
i.S/S: increase pulse, flushed face, severe
headache
ii.Mechanism:
1.To equalize osmotic pressure, fluid from
tissue transfer to blood vessel which then
leave the tissue dehydrated
b.Water intoxication
i.To large amount of oxytocin used, ADH effect
ii.Severe headache, confusion, drowsiness,
edema, decrease urinary output
iii.Rx: D/C oxytocin drip
c.Hemorrhage
d.Infection – D5W – to balance or restore fluid

IV.Prostaglandin Injection
Hormone which is abortive
Administration:
1.IV drip
i.½ - 1 hour after administration, labor will start
ii.No oxytocin needed
iii.S/E: nausea, vomiting, and diarrhea
iv.Dx: anticholinergic, and antidiarrheal
 v.CI: - HPN – vasoconstriction, Respiratory
disorder – bronchial constriction and
bronchospam
2.Vaginal suppository – given every 3-4 hours as
prn until labor starts
3.Oral – not recommended- causes severe nausea,
vomiting, shaky, chills, and increase temperature
V.Hysterotomy – done in AOG 16 – 18 weeks like CS

Ectopic pregnancy-
II. REFERS TO THE IMPLANTATION OF THE
PRODUCTS OF CONCEPTION IN A SITE OTHER THAN THE ENDOMETRIUM.
Extra-uterine
Does not occupy uterine proper

Types according to sites:

1.Tubal – most common frimbriae (1), ampullar (2)
60%, Isthmic (3), interstitial (4)
2.Ovarian – tubo-ovarian (5), ovarian (6)
3.Cervical – cervical (7)
4.abdominal/ peritoneal – rare (8)
Causes:
1.Adhesions in tubes – tubo-ovarian, fallopian tubes
2.Infection – chronic salphingitis, PID
3.Congenital malformations – infantile tubes
4.Scars of tubal surgery
5.uterine tumors pressing the tubes
6.endometriosis
7.tube spasms

S/S – ruptured
1.Spotting or bleeding – may or may not be present
2.Abdominal rigidity
3.Cullen’s sign – bluish discoloration around umbilicus
4.Shoulder pain – blood irritating the diaphragm
 5.Mass in Cul-de-Sac of Douglas (pouch) may be palpated
or bloody fluid maybe aspirated by CULDOCENTESIS
6.Excoriating pain at cervix when IE is done
7.Knifelike pain in either lower quadrant (affected site)
8.WBC – 15,000/uL>, RBC – decrease, ESR – Slightly
elevated
9.S/S of shock

S/S – early ectopic pregnancy

1.Amenorrhea or abnormal menses – spotting
2.Cul-de-Sac mass

S/S – Acute ruptue

1.Shock
2.Referred shoulder pain
3.Evidence of acute blood loss

S/S – chronic rupture

Occurs 50 % in tubal ectopic pregnancy
1.Slow-internal bleeding
2.Atypical or inconclusive symptoms as
a.Slight, dark, vaginal bleeding
b.Renal or pelvic pressure or fullness
c.Lower abdominal tenderness
d.Slight fever
e.Leukocytosis
f.Cullen’s sign
g.Decrease Hct and Hgb

Dx:
1.Utrasound – reveals site of Ectopic pregnancy
2.Culdocentesis – yields free blood that will not clot or is
already clotted
3.Laparoscopy – discloses extrauterine pregnancy
Treatment:
1.Culdotomy – release clotted blood and product of extra-
uterine pregnancy/ conception
2.Laparotomy – reveal correct diagnosis

Nursing Management
1. A priority nsg action: Monitor V/S, watch for signs of
shock (hypovopemic shock) by checking apical pulse.
2.Nursing care to bleeding clients
3.Observe nature of bleeding
4.Administration of narcotics or analgesic as ordered
5.Prepare clients for diagnosis and treatment
6.Provide post-op care

INCOMPETENT CERVIX - IS A CONDUCTION CHARACTERIZED BY

PAINFUL DILATION OF THE CERVIX WITHOUT UTERINE
CONTRACTIONS.

THIRD TRIMESTER BLEEDING

1.Placenta Previa- REFERS TO IMPLANTATION OF THE PLACENTA IN

THE LOWER UTERINE SEGMENT, CAUSINGPAINLESS BLEEDING IN THE THIRDS
TRIMESTER OF PREGNANCY
Implantation of the plancenta at the lower uterine
segment
30 % > than average placenta implanted at the
fundus – site and size related (surface area)
degree placenta covers the internal os is estimated
by 70 – 100%, 75 % etc.
2nd trimester – 45% of placenta are implanted at
lower uterine segment
this elongates and move upward but out of 150
pregnancy remains
Cause of bleeding:
differentiation of the upper and lower uterus segment late
in pregnancy (30 weeks of AOG) – the inability of the
placenta to stretch to accommodate this differing shape
results to bleeding

Classification
Based on the degree the internal os is covered by the
placenta

1.Complete or central or total

Internal or is covered entirely by the placenta and
blocking the baby
2.incomplete or partial
i.marginal
edge of the placenta approaches the internal os
ii.low-lying (low implantation)
is when the placenta is situated in the lower
uterine segment but away from the os
Causes:
1.Unknown
2.Can be attributed to the following conditions:
PREDISPOSING FACTORS:
a.Fibroid tumor in the uterus
b.Uterine scars from previous surgery os
c.Abnormal uterine position or shape
d.Multiparity – multiple gestation
e.Age – very young and very old

Ass/ P.E: (7 months AOG)

1.Uterine bright red bleeding – painless

2.Uterine tone
 Normal but relax completely between contractions
3.Pain
Painless non-tenderness uterus – may experience
labor contractions
4.Fetal position
Fundic height is greater – placenta hinders descent
of presenting parts
Leopolds maneuver reveals malposiition of fetus –
transverse or breech
5.Diagnostic tests
Ultrasound
i.Static imaging – diagnostic method of choice
Amniocentesis
i.Assess fetal lung maturity LS ratio 1:2
ii.If lung maturity is reached, CS delivery is done
No vaginal exam unless patient is place on double
prep procedure (prepared for vaginal or C/S delivery)
Laboratory tests – hemoglobin, hematocrit, Rh
factor, urinalysis

Major Problem:
Preterm delivery

Fetal Outcome:
Fetal distress or death occurs if placenta previa becomes
detached from deciduas basalis or if mother suffers shock

Nursing Care/ Management – predelivery – conservative

1.Keep NPO
2.maintain bedrest – head of bed elevated to 20 – 30 O
(semi-fowlers) – allow fetal body to act as tamponade
3.IV – large bore needle is started (LR vol. expander, blood
transfusion 2 units of WHB ready)
 4.delivery – if fetus reached maturity
a.if > 30% previa 0r complete – CS delivery-

b.if < 30 % previa – vaginal delivery – if delivery is not

attained within 6 hours – C/S is indicated

2. Abruptio Placenta
Ablatio placenta
>20 weks of AOG
is the premature separation of part or all of the
placenta from its site of implantation
can be an abnormal separation of a normally
implanted placenta. ,
Types:
1.Partial separation
a.Concealed
b.Apparent – marginal separation
2.Complete
Concealed
,
Problems:
Mother – shock – placenta separation
Infant – Perinatal death – hypoxia
Predisposing factors:

1.HPN
2.multiple gestation
3.multiparity
4.adv. Maternal age
5.DM
6.previous premature separation
7.hypotensive syndrome
8.rare – abdominal trauma 5%; short cord 1%
9.history of abortion; stillbirth; pre-natal hemorrhage;
premature labor,
 10. RENAL OR VASCULAR DISEASE AND ABDOMINAL TRAUMA MAY
PREDISPOSE A CLIENT TO ABRUPTIO PLACENTAE.

Degrees of Separation:

Grade Description
0 No symptoms were apparent from maternal or fetal
side; diagnosis of placental separation is made during
delivery; placenta shows recent adherent clots on
maternal surface
1 Minimal separation enough to cause vaginal bleeding
and changes in the maternal VS; no fetal distress or
hemorrhagic shock occurs
2 Moderate separation with evidence of fetal distress;
uterus is tense, painful on palpation
3 Extreme separation without immediate intervention;
maternal shock and fetal death will result

Fetal outcome:
15% perinatal death; also depends on the degree of
separation and fetal hypoxia

PE/Ass: symptoms vary with degrees of placental separation

1.Uterine Bleeding
Painful
Sharp stabbing pain high in uterus fundus
 Pain is felt on palpation not with contractions
Heavy dark red bleeding may or may not be apparent
In severe concealed bleeding, blood may infiltrate the
uterine musculature – COUVELAIRE uterus or
uteroplacental apoplexy – hard, boardlike uterus –
orange or bronze – uterus becomes tense and rigid to
touch
S/S of shock follows
In extensive bleeding, DIC syndrome occurs; the
woman’s reserve blood fibribogen may be used up in
her body’s attempt to accomplish effective clot
formation

2.Laboratory tests
Hemoglobin level, typing, cross-matching fibrinogen
level (DIC); tests for DIC – 5 ml blood to stand for 5
minutes; if clots formed – DIC negative; no clots – DIC
positive

Nursing Care/ Management

1.Admit to hospital
2.Give oxygen by mask (fetal anobia)
3.monitor FHT, VS and record
4.baseline fibrinogen determination
5.keep in lateral position – prevent pressure at vena cava;
further compromise fetal circulation
6.No IE, pelvic exam, enema
7.Depending on degree of separation if labor starts –
rupturing BOW may help speed delivery or administration
of oxytocin
Purpose of rupturing BOW
 a.Prevents development of couvelaire uterus,
prevents pooling of blood in the myometrium of
uterus
b.Prevents DIC
c.Speed up delivery
8. If delivery do not occur, C/S is the method of choice
9.Cause of maternal death
Massive hemorrhage which lead to shock; circulatory
collapse or renal failure
Infection

Post-Partum Bleeding
Normal delivery average blood loss: 300 – 350 ml
Post-partal hemorrhage: >500 ml within 24 hours period
Immediate: 1st 24 O bleeding
Late: occurring during the remaining days of the 6 weeks
puerperium

Reasons of Post Partum bleeding

1.Uterine Atony
2.lacerations
3.retained placental fragments
4.hematoma
5.D/C

Uterine Atony
Loss of uterine muscle tone; uterus fails to contract
completely; to seal off open uterus vessel after
delivery

Causes:
a.Conditions that distended the uterus beyond average
capacity
i.Multiple gestation
 ii.Hydramnios (AF > 2000 cc)
iii.Large baby (>9 lbs.)
iv.Presence of uterus myomas (fibroid tumor)
b.Conditions that leave the uterus too exhausted to
contract readily
i.Deep anesthesia/ analgesics
ii.Labor and oxytocin agent
iii.Maternal age over 30 years
iv.High parity
v.Dystocia
vi.2O illness as anemia
vii.endometritis
c.conditions with varied placental site or attachment
i.placenta previa
ii.placenta acreta
iii.placenta ablation

Ass:
1.Uterus suddenly relaxes
2.Occurs gradually – as lethal as sudden gush; following
delivery; post-partum period

Nursing Care/ Management:

A.Prevention
i.Inspect blood loss – blood seeps at back
ii.Palpate fundus
iii.Frequent assessment of lochial discharge/VS
iv.Empty bladder every 4 hours
B.Therapeutic
i.Massage uterus
ii.Apply cold (ice) compress
iii.Refer for administration of Methylergometrin Maleate

Management:
 1.Adminster oxytocin agent – S/E – Hypertension – BP
140 / 90 mmHg do not administer
2.Blood replacement - >500 ml needs BT; auto-transfusion
3.Bimanual massage
4.Prostaglandin Administration (IM/ IV)– strong uterus
contractions
5.Hysterectomy – removal of uterus last resort

Lacerations
Tearing at birth canal – expected consequence of
childbearing; more common in: primi, large babies >9
lbs, lithotomy used of instruments

Structures affected:
1.Cervical
2.Vaginal
3.Perineal

Classification of perineal tear

1st degree – vaginal mucosa, skin of perineum, fourchette

2nd degree - vagina, perineal skin, fascia, levator anterior
muscle and perineal body
3rd degree – entire perineum, external sphincter of rectum
4th degree – entire perineum, rectal sphincter and some
mucous membranes of rectum

Management:
1.Repair
2.pack
3.no enema/ suppositories/ rectal temperature
4.prevent constipation

Cervical lacerations R/O uterine atony

Retained Placental Fragments
placenta failed to be delivered entirely and fragments
or parts are left behind inside the uterus

Ass:
1.Bleeding depends on size of placental fragments
a.Large – immediate uterus does not contract
b.Small – 6th – 10th day post-partum – abrupt
discharge of blood clots
2.On examination, uterus not fully contracted
3.Doctor orders for serum HCG determination, U/S to
determine presence of placenta

Management:
1.Severe bleeding – Blood transfusion
2.D/C
3.placenta acreta – methotrexate – to destroy placental
tissues
4.advise patient to observe lochial discharge (alba, serosa,
rubra)

Abnormalities of Placenta:
Normal weight - 500 gms – 1/6 of fetal weight; diameter: 15 –
20 cm; thickness: 1.5 – 3 cm

Placenta is expectedly increase size in: ½ of fetal weight

1.DM
2.Erythroblastosis fetalis
3.Scars on septum – placenta spread to look for space to
implant (good BS)
A.Placenta Succenturiata
No fetal abnormality
Has one or more accessory lobes connected to
placenta by blood vessel
Small lobes maybe retained – maternal bleeding
B.Placenta circumvallata
Fetal side of placenta is covered to some extent
with chorion; no abnormality
C.Placenta marginata
The fold of chroion reaches just to the edge of the
placenta; no abnrmality
D.Battledore placenta
Cord is inserted marginally rather than centrally
Rare but with no known clinical significance
E.Velamentous insertion of the cord
Cord instead of entering the placenta centrally,
separates into small vessels the reaches the
placenta by spreading across a fold of amnion
Found in multiple pregnancies
Predispose to maternal hemorrhage
F.Placenta accreta
Deep attachment of placenta to uterus
myometrium
Management:
oManual extraction
oHysterectomy
omethotrexate
G.Vasa previa
Umbilical vessel of a velamentous cord insertion
cross the cervical os and delivers before fetus
H.Two vessel cord
Absence of one artery
Usually 2 arteries 1 vein
 Fetus congenital kidney and heart anomalies

Hematomas
Collection of blood with subcutaneous layer of perineum,
skin has no sign of trauma

Causes:
1.Injury to blood vessel – labor/ delivery
2.Rapid spontaneous deliveries – precipitate delivery
3.Perineal varicosities
4.Episiotomy repair site
5.Anesthesia infiltration

Ass:
Feeling of pressure between legs
Pain, discomfort, tenderness
Minor bleeding
Swelling/ bluish discoloration 1 –4 cm

Management:
1.Small - warm/ cold compress – ice pack absorb in 3 – 4
days
2.Large – incision and evacuation
3.Analgesia

Heart Disease in Pregnancy

Vulvular involvement e.g. Kawasaki disease

Expected in
30 – 50% increase volume/output Pregnancy

Innocent murmurs,
Heart Physiologic adjustment palpitations
 Heart becomes
Increase circulatory volume reached its peak overwhelmed
on 28 – 37 weeks AOG
Decrease vital organ
perfusion (uterus and
placenta

Decrease cardiac output (heart failure)

Rheumatic heart Improve management Skills e.g. Heart disease

disease Ultra Sound – research and corrected early
prevented and advance technology
treated

Team approach – heart specialist,

obstetrician, nurses

1. Initial visit to plan pregnancy

2. Pre-natal check up

Treatment and management of Heart Disease in Pregnancy

1.Promotion of Rest
LLRP to carry pregnancy to term about 36 weeks
AOG – increase fetal maturity
2.Promotion of healthy diet and Nutrition
 Enough to ensure normal weight gain during
pregnancy toe ensure healthy pregnancy and fetus
No additional cells to supply with nutrients and
oxygen – burden to the heart – excess weight gain
Iron supplement – prevent anemia
Sodium limitations with diuretics – before
pregnancy and to continue during pregnancy

3.Education about medication

1.Digitalis
Slows and strengthens myocardial
contraction
Crosses placenta but not teratogenic
2.Penicillin
Prevent bacterial invasion due to denuded
placenta and subacute bacterial endocarditis
Non-teratogenic
3.No over the counter drugs but exception to the rule.
NO DRUGS DURING PREGNANCY – client has to
continue heart medication.

4.Education in prevention of infection

1.Spreads more energy – increased cardiac output

5.Promote reduction of physiologic stress

1.Avoid worries on self and fetus “look at pregnancy
one day at a time”
6.Delivery
a.Position – semi-fowlers + oxygen inhalation }
facilitate effective breathing
Epidural/ caudal anesthesia + forcep delivery
(assisted) } effort free and pain free delivery
C/S not indicated:
Increase blood loss
 High risk for infection
Increase throboembolism formation
High risk of respiratory depression
(due to anesthesia)
b.Start penicillin if not given during pregnancy
c.IV line at KVO – for ER meds
7.Post-partum care
After delivery – blood supplying placenta goes back
to circulation

blood volume increase – 20-40% in just 5 minutes – heart to

make major rapid adjustments to increase blood volume

Intervention:
1.Prevent sudden distention of abdominal vein following
delivery of placenta. Applying pressure to woman’s
abdomen and gradually release it so blood theoretically
enters circulation slowly
2.Ambulate early – to prevent emboli formation
3.Wear elastic stocking (support) – increase venous return
to heart
4.Ergot compound given with caution – increase BP
5.Estrogen compound with caution - high risk to DVT or
thromboembolism, and decrease lactation
6.Needs for more reassurance on fetal outcome
Fear for fetus to have cardiac ailments –
acrocyanosis – expectedly normal
7.BF without difficulty but needs assistance – easily get
tired
8.Post partum exercises
i.abdominal exercise – needs doctor’s order
ii.perineal exercise – Kegel’s exercise to
strengthen pelvic floor
9.Stool softener – avoid straining
 10.Delay next pregnancy – to stabilize circulatory status
11.Follow – up care of heart disease
Use of antibiotics, anticoagulants – prone to bleeding,
high risk of congenital anomalies in infant
Anticoagulant – Heparin, Warfarin (Prothamine antidote)
a. do not cross placenta barrier if given pre-pregnancy
b. D/C before 2 weeks EDC to prevent infant to be born
with coagulation defect
c, Regional anesthesia should not be used – changes
of bleeding into spinal cord (mother)

Effects of heart disease on fetus:

1.Fetal growth – decrease birth weight
2.Fetal distress (acidotic) – immaturity
3.Delivery – lots deceleration (fetal monitor
4.neurologic – mental involvement – effects of placental
insufficiency

Assessment (Maternal)

1.History of heart disease (class)

2.Dyspnea – type
3.Edema – innocent edema – feet/ankles – 3rd trimester
expected
PIH – after 24th weeks AOG – serious/face fingers
Heart disease – failure + other S/S of heart disease
e.g. chest pain irregular pulse, orthopnea
4.Assess nail bed filling (less than 5 seconds)
a.Jugular venous distention
b.Liver size (right heart failure)
5.ECG – Chest X-ray

Obstetrical Analgesics of Heart disease classification

Class I and II normal pregnancy and delivery
Class III pregnancy if ok if abide with CBR
Class IV poor candidate, cardiac failure even at rest

Classification of Heart Diseases:

Class Description

I Client have no limitation of physical activity;

ordinary physical activity causes no discomfort,
no symptoms of heart insufficiency and no
anginal pain

II Slight limitations of physical activity; ordinary

physical activity causes excessive fatigue,
palpitations, dyspnea, or anginal pain

III Moderate to marked limitations of physical

activity; less than ordinary activity, client
experiences excessive fatigue, palpitations,
dyspnea or anginal pain

IV Unable to carry any physical activity without

experiencing discomfort; even at rest - experience
S/S of cardiac insufficiency and anginal pain

Pathophysiology of PIH
Peripheral arteriolar
Vasoconstriction Vasospasm

Decrease Blood Supply Hypertension

Decrease Oxygen Supply

TISSUE PERFUSSION TO VITAL ORGANS

 Kidney Liver/ Pancreas Eyes Uterus

Tissue Retina
Glomerolar Glomerolar Ischemia Muscle Placenta
degeneration Filtration tissue

Visual
Vascular tissue Changes
Increase Increase Blurring
Glomerolar Tubular of vision Ischemia
permeability absorption of
Sodium Epigastric
pain
Premature Premature
If with Labor Deterioration
hemorrhage
Albumin/ Water Nausea and Blindness
globulin Retention Vomiting
cross into
urine Fetal Abruptio
nutrients placenta
Increase
Edema Oliguria amylase/
crea ratio
Proteinuria
Fetal
Distress
Gen. Water
Fluid diffuse Retention
` from
circulatory Premature Delivery
system to ECS

Lungs Brain
Prematurity
Pulmonary Edema Cerebral Edema
(cyanosis) (Hypoxia)
Fetal Death

CHF Irritability

Maternal Convulsions
Death

Pregnancy Induced Hypertension

Main cause is unknown
3rd leading cause of maternal death in the US
“TOXEMIA” - poison

1.Hemorrhage
2.infection
3.researchers
pictured a toxin of some kind released by
the woman in response to the foreign protein
of the growing fetus which leads to the Triad
Symtptoms of PIH:
oHPN
oEdema
oProteinuria

EDEMA OF THE HANDS AND FACE IS A CLASSIC SIGN OF PIH. MANY

HEALTHY PREGNANT WOMAN EXPERIENCE FOOT AND ANKLE
EDEMA. A WEIGHT GAIN OF 2 LB OR MORE PER WEEK INDICATES A
PROBLEM. EARLY MORNING HEADACHE IS NOT A CLASSIC SIGN OF
PIH.
Predisposing Factors:

1.Primi and less than 18 and older than 35 years

2.Low socioeconomic – poor nutrition and low
CHON intake, low B6 (Pyridoxine)
3.Pregnancy >5x or more
4.Non-white
5.Multiple pregnancy
6.Hydramnios
7.Heart disease, DM renal involvement
8.Essential hypertension
9.Poor calcium intake
10.Parasitic invasion

Types of PIH

1.Gestational Hypertension
B/P 140/90 mmHg
30/15 mmHg – increase above pre-pregnancy level
No proteinuria, no edema
Woman may develop chronic hypertension later in
life
2.Mild Pre-eclampsia MAP2 higher 90 mmHg; MAP3 higher
105 mmHg
B/P 140/90mmHg
 Protein 1 – 2 + on RS (1 gm/L) – orthostatic
proteinuria – standing excrete CHON but not on bed
rest
Weight gain >2lbs/ week (2nd trimester); 1 lb./week
(3rd trimester)
Mild edema on face
3.Severe Pre-eclampsia
B/P 160/110 mmHg or higher
Protein 3-4 + on RS (5 gm/L)
Oliguria 500 ml or < every 24 hours
Cerebral or visual disturbances (headache/ blurred
vision)
Pulmonary edema; extensive peripheral edema –
pitting edema
Fetal mortality – 10%
Hepatic dysfunction
Thrombocytopenia

Description of Edema:

1+ Slightly idented
2+ Moderately idented
3+ Deeply idented
4+ Remain as a pit (pitting edema)
4.Eclampsia
Mark S/S of severe pre-eclampsia + convulsion
BP - > 160 over 90 mmhg
15% maternal mortality due to:
oCerebral hemorrhage
oCirculatory collapse
oRenal failure

Fetal prognosis poor – 25% mortality

 oHypoxia with acidosis

Management:

1.Bedrest
2.Monitor m aternal well-being
3.Monitor fetal well being
4.Ensure safety measure
5.Proper diet
6.Promote relaxation
7.Administer medications

Management:

Mild pre-eclampsia – if pregnancy <36 weeks LS ratio

decrease l:2; conservative bring fetus to term

1.Promote Bedrest
a.Sodium is excreted rapidly and recumbent than in
activity
Evacuation of sodium
Encouraging/ promoting sodium
b.Labor and delivery needs and spends more energy
(save caloric expenditure)
c.Always on left lateral recumbent position
Prevent uterus pressure on vena cava –
promote fetal circulation and prevent supine
hypotension syndrome
d.Patient confinement
Home; if non-compliant- hospitalization
2.Promote good nutrition
Increase protein diet with no salt restriction
 Decrease salt or no salt in diet may activate
angiotensin system and increase B/P
compounding the problem
3.Provide emotional support with bed rest
Do not take instructions seriously
Medicines not bed rest
Stop work
Assess to bring concerns to open work, family,
finances

Severe Pre-eclampsia- most important to include in the plan

of care is prevention of seizure.

1.Bed Rest
a.Admit to hospital
Private room – undisturbed
LLRP
No loud noises – triggers convulsion
Darkened room (no bright light)
No visitors – social visitors not support
people
2.Monitor maternal well-being
B/P every 4 hours
Blood studies – CBC, platelet, Hct, Hgb, Blood
Typing, fibrinogen
EENT – optic fundus S/S (1) arterial spasm, (2)
edema, (3) hemorrhage
Urine - >30 ml/hr, insertion FBC for accurate
recording, test for protein, maternal estriol
level
Weight – same time each day
3.Fetal well-being
FHT – external monitor (Doppler auscultation
every 4 hours)
 Oxygen administration – face masks
4.Safety
Side rails
Padded tongue blade

Diagnostic Tests for Hypertension

1.Roll Over or supine pressure test (SPT)

28th – 30th weeks of AOG
a. Lateral position – BP check
b.Roll to supine – BP check – repeat after 5 minutes
c.Diastole higher than 20 mmHg or more is significant
sign
1.Mean Arterial Pressure (MAP)
MAP = 1/3(S-D) + 80mmHg
MAP = 96.6 mmHg
MAP 2 = 90 mmHg
MAP 3 = 105 mmHg
oe.g. BP = 120/70 mmHg = 1/3 (120-70)+80
= 1/3(50)+80
= 16.6+80 = 96.66
2.Infusion angiotensin II
Results in increase BP (controversial)

Causes of Maternal Death: 15%

a.Aspiration pneumonia
b.Cardiac failure
c.Cerebral hemorrhage
d.Obstetrical bleeding secondary to ablation placenta

Causes of fetal death:

Intrauterine growth retardation
Perinatal death
Prematurity
Convulsions: (Grand Malconvulsion)

4 phases

1. Aura
Epigastric pain, sharp smell sight of bright light
Management:
1.Tongue blade placed in position promote
safety
2.Tonic
All body muscles contract back arch, arms/leg stiffen;
jaw closes abruptly (tongue maybe bitten); respiration
halted (last 20 seconds); cyanotic, cessation of
respiratory
Management:
a.Oxygen administration by mask
b.LLRP; place on side, allow secretion to drain
c.Fetal monitor
d.Insertion of tongue blade NOT RECOMMENDED
Broken teeth
Scraped gums
Bitten fingers (nurse)
Broken tongue blades
3. Clonic
Muscle relax, contract, ext. flail
Respiratory – inhale/ exhales irregularly; as thoracic
muscle relax and contract may aspirate saliva (place on
sides) forming at the mouth (mouth breathing)
incontinence of urine and feces
Ineffective brething – remain cyanotic; oxygen therapy for
fetus
Last up to 1 minute
4. Postictal
Semi-comatose, cannot be roused except with painful
stimuli
Last 1 –4 hours
Labor may begin – still unconscious; cannot report labor
contractions painful labor contractions initiate another
seizure
Monitor FHB
Check for vaginal bleeding every 15 minutes (abruption
placenta)
Anticipate delivery
Condition may stabilize in 12 –24 hours; prepare for
vaginal delivery (preferred method); induce labor. Why?
Fetus does not continue to grow after eclampsia
(convulsion) occurs. Fetal lung maturity appears to
advance rapidly due to (intrauterine stress) L/S ratio –
mature
C/S not best
Disadvantage:
oHazardous to fetus – sufficient strain
oMother not a good candidate for GA and surgery

How to induce labor:

1.Rupture the membrane (ROM)

2.oxytocin drip (OD)

Proper diet and nutrition

1.increase protein – replace protein loss (proteinuria)
2.moderate sodium – sodium restriction (4-6 grams/ 24
hours) . SALTY FOODS MAY INCREASE SODIUM CONCENTRATION,
RETENTION OF FLUIDS OCCUR THEREBY CAN CAUSE SHIFTING OF FLUIDS
FROM THE ICF TO VASCULAR COMPARTMENTS INCREASING BLOOD
PRESSURE, THUS SHOULD NOT BE INCLUDED IN THE DIET.
Medications: to prevent eclampsia

IV line – ER medication route; observe insertion site carefully

– infiltration triggers convulsions
Diastole – not lower than 80-90mmHg

I.Hypotensive drugs
a.Hydralazine (Apresoline)
Lowers BP by peripheral dilatation; DO NOT
interfere with placental perfusion
S/E – Tachycardia
Nursing Responsibility – (1) Check BP – pulse
before and after administration
b.Diazonide
Hyperstat
Cryptenamine
Unitensin
Produce rapid decrease in BP
Do not use for long term;
administration causes hyperglycemia

II. Cathartics
Magnesium sulfate
5 actions:
oHypotensive – dilating effect to blood vessels
oDiuretic – reduce edema by causing shift of fluids
from ECS into intestine
oCNS depressant (blocks peripheral neuromuscular
transmission)
Lower possibility of convulsions
DOSE below – 4 grams in 100 ml D5W
 Slow IV – 5 – 20 minutes duration effects 30 – 60
minutes
IV infusion – 1 – 2 grams/ hour piggy back
IM – 5 grams of a 50% saline every 4 hours
Deep IM – to reduce pain mix with procaine
oAnticonvulsant
oTocolytic
NB. Blood serum level to be monitored
Blood serum Level of Magnesium Sulfate

Blood Serum Level:Response 4 – 7 mg/ 100 m

Therapeutic level 8 – 10 mg/100 ml
Decrease patellar reflex/disappeared 10 – 12 mg/ 100 ml
Respiratory depression occurs 15 mg/ 100 ml and up
Cardiac conduction defects occur

Patellar Reflex Scoring

Score: Findings:

0 No response, hypoactive, abnormal

1+ Somewhat diminished response but not

abnormal

2+ Average response

3+ Brisker than average but nor abnormal

4+ +Hyperactive, very brisk – abnormal

ABSENCE OF PATELLAR REFLEXE IS AN INDICATOR OF

HYPERMAGNESEMIA, WHICH REQUIRES
ADMINISTRATION OF CALCIUM GLUCONATE.
III. Diuretics
Best in pre-eclampsia not in Eclampsia
Decrease absorption of sodium, thus lowering sodium in
plasma  Fluid shift back from ECS into circulation and
excreted thru urine  edema reduced, plasma already
lowered will be depleted further which result to:
oPoor placental perfusion
oStimulate release of renin; to increases permeability
of glomerular vessels; to increase protein urea
angiotensin = increase BP thus worsening conditions
IV. Sedatives
Barbiturates (Phenobarbital) PO, IM
Care should be taken not to depress baby diazepam
(Valium)

Nursing Care Management:

1.Assess patellar reflex

2.Assess urine output
3.Assess respiratory rate
4.Keep ready – 10 ml/ 10% of calcium gluconate (antidote
magnesium sulfate) 1 gram
5.Severe oliguria – IV infusion of Salt poor abdomen
(colloid saline will “call” fluid into IVS by osmotic pressure
– kidneys excrete extra fluid with Magnesium Sulfate
6.Watch for fetal depression – crosses placenta results to:
Late deceleration
Sonogram decrease fetal
movements
Decrease heart beat
7.Administer continued for 12-24 hours to prevent
eclampsia, dose then tapend D/C BF – should be delayed
until drug is discontinued.
 8.most important nsg assessment: EARLY SIGNS OF MAGNESIUM
TOXICITY THAT MAY LEAD TO RESPIRATORY ARREST ARE LOSS OF PATELLAR
REFLEXES (deep tendon reflex) AND DECREASED RESPIRATORY RATE (< 12/min).
SINCE MAGNESIUM SULFATE IS EXCRETED FROM THE BODY THROUGH THE
RENAL SYSTEM, HOURLY URINE OUTPUT SHOULD BE ASSESSED. ALTHOUGH
BP IS A STANDARD ASSESSMENT FOR MOST ANTEPARTUM CLIENTS, THERE IS
MINIMAL BP CHANGE, IF ANY ASSOCIATED WITH AMINISTRATION OF
MAGNESIUM SULFATE.

Diabetes Mellitus in Pregnancy

1921 – synthetic insulin was discovered

Before 1921 – without insulin

1.Women failed to survive to reach childbearing age
2.Infertile
3.DM causes spontaneous abortion

After 1921 – with insulin

1.Being women thru pregnancy with good control
2.care for newborn infant during 1st 24 hours after delivery
3.protect infant in utero from adverse effects of DM

S/S:
1.Polydypsia
Increase fluids to compensate fluids loss

2.polyuria
Decrease osmotic pressure, increase amount of
glucose in urine; decrease fluid absorption in kidney
3.polyphagia
Used up nutrients except glucose
4.Glucosuria
Kidney attempt to lower glucose level excrete large
quantities into urine
Physiologic Changes:

1.Increase insulin requirement in pregnancy

2.Hypoglycemia – 1st half of pregnancy; acidosis; coma –
last trimester
3.Decrease carbohydrate metabolism
4. Stress increase glucose tolerance
5.Increase estrogen level during predisposes DM in
pregnancy (gestational DM)

Assessments:

I.PE – History (large babies, unexplained fetal loss,

congenital anomalies, and family history of DM)

II.Laboratory exams and tests

i.Glucose screening
Blood
1.FBS – NV 80 –120 mg% (serum)
2.Glucose tolerance test (oral, IV)
One-hour-gtt
a.Fast 8 hours
b.FBS taken more than 90 mg/dL
c.50 grams glucose load
d. After 60 minutes – higher than 140
mg/dL glucose (NB: if result is positive,
patient is to undergo 3O drop three-
hour-gtt)
Three-hour-gtt
b.fast 8 hours
c.FBS taken – 105 mg/dL
d.100 grams glucose load
e.after 1 hour – more than 190 mg/dL
f.after 2 hours – more than 165 mg/dL
 g.after3 hours – more than 145mg/dL
3.HGT (Hemoglucotest)
Urine
a.Strips that measure only glucose –
preferred method e.g. Clinistik, Testope
i.Breastmilk (lactose) spills into
urine and cause positive reaction
b.Test on strips that measure all sugar
e.g. benedict’s test, clinitest

III.Opthalmic exams
i.DM retinopathy
1.Increase exudates
2.Hemorrhage
3.Edema

Pricilla White’s Classification of DM in Pregnancy (used to

predict pregnancy outcome)

Class Description

A hgt – only slightly abnormal; dietary regulation is minimal;

no insulin

B DM less than 10 years duration or DM begins at ages 20

or older no vascular involvement
C DM begin between 10 and 19 years or DM lasted from
10-19 years, there is minimal vascular involvement
D DM 30 years or more or DM begun before ages 10 years,
there is greater vascular involvement

D Subclasses

D1 under 10 years of onset

 D2 more than 20 years duration
D3 beginning retinopathy is present
D4 calcified vessels of legs are present
D5 Hypertension is present

E DM with calcification of pelvic arteries seen in X-rays

F DM with nephropathy
H DM with cardiomyopathy
R DM with active retinitis obliterans
T DM have had kidney transplant

Analysis

1.Class A high fetal survival

2.Class D and E – perinatal mortality is 20%
3.Class F and R – perinatal mortality is close to 100% (not
to be pregnant)
4.Class T – can complete pregnancy successfully

Management and Nursing Interventions:

1.Educate on diet during pregnancy

Good disease control
Diet regularly should be started as soon as DM is
diagnosed in pregnancy
Diet control is done to:
oMaintain an adequate glucose intake 80%
oprevent hypoglycemia during pregnancy due
to nausea and vomiting
o1800 – 2200 calories – 3 meals +3 snacks
evenly (less than 1800 calories cause
breakdown of fats =Acidosis)
ohypoglycemia at night – due to continuous
fetal use of glucose when woman is asleep;
 final snack of protein or complex carbohydrate
(slow digested)
oDaily nutrient proportion:
20% of protein – 1.3 – 1.7 gm/Kg BW or
125 grams of Protein
50% of carbohydrates – 200 – 500
grams/day
30% of fats – 70 –80 grams/day
oDecrease saturated fats and cholesterol and
increase amount of dietary fibers; high fibers
reduces postprandial hyperglycemia and
lowers insulin requirement
oSuitable weight gain – only 25 lbs.
Limit fetal size to facilitate vaginal
delivery

2.Educate on Exercise
a.Goals:
i.Reduce serum glucose
ii.Reduce insulin requirement
1.Exercise program should begin before pregnancy
and not during pregnancy
i.To avoid excessive glucose
fluctuations
ii.Exercise effect last – 12 hours
after exercise
2.Eat protein and carbohydrates complex before
exercise
3.Exercise program should be maintained
consistently e.g. best exercise – 30 minutes walking
once a day same time
3.Educate on insulin
a.Hospital admission only for insulin adjustments
b.Change of insulin done – change in metabolism
 i.Early pregnancy – less insulin – fetal
developing cells take more glucose
ii.Late pregnancy – more insulin
c.Oral hypoglycemics not used during pregnancy
because it crosses placental barrier and is potentially
teratogenics
d.Humulin Insulin – provokes lesser antibody
response than beef and pork
e.Insulin peaks – makes monitoring meaningful
f.Regular insulin – pre-breakfast 30 minutes to 1 hour
or after breakfast
g.Intermediate – given in the morning – lunch or late
in the afternoon; given in the afternoon peak reaches
at rest day before breakfast
h.Injection site – related – 5/8 inch needle – 90O insulin
syringe; arm absorb – than thigh

IDM – will result if DM in pregnancy is poorly controlled

Characteristics:

1.Typically longer and weighs more >9 lbs. (infantile

giants)
2.Greater to have congenital anomalies (cardiac defects)
3.Caudal regression syndrome or hypoplasia of L.E
4.cushingoid (fat and puffy)
5.Lethargic and limp – 1st few days of life
6.Large size is deceptive
7.polycythemia – to prevent: avoid clamping of cord early
to prevent RBC overload from placenta
8.Will show greater proportion of weight loss from extra
fluid accumulation – prevent accumulation

Complications:
1.Macrosomia – C/S
 2.Severe hypoglycemia
3.Hyperbilirubinemia
Due to inability of the liver to clear bilirubin from
system at this immature age
Normal value:
o<6 mg/dL Newborn 1st day
o<12 mg/dL 3-5 days
o0-1mg/dL adult
4.hypocalcemia
lowered blood calcium level due to change in
calcium or phosphorus metabolism (breastmilk)
Normal Value:
i.9 – 11 mEq/dL Newborn
ii.7-5 mg/dL Adult
Signs and symptoms: Latent tetany (Clinical
Manifestations)
a.Chvostek’s Sign
Ear tapped and facial muscle contract
unilaterally
a.Trousseau’s sign
Constricts arm 2-3 cm with tourniquet and
blanched and results to carpal spasms
a.Peroneal Sign
Fibular side of leg is tapped foot abducts
and dorsiflexes
a.Erb’s sign
Galvanic current is applied over peroneal
nerve, foot abducts and dorsiflexes

Post-partal Adjustments

1.Re-adjustment of insulin to non-pregnant requirement

a.Gestational DM, glucose normalizes after 24 hours
post delivery; BF- insulin does not pass to breast milk
 from bloodstream; hydramnios was present – watch
for hemorrhage
b.Use contraceptives:
i.Pill – high risk for hypertension – estrogen
ii.IUD - high risk for infection
1.plan for next pregnancy – disease must be
stabilized in good control

Tests for Placental function and fetal maturity

I. Amniocentesis
a.L/S ratio – NV 2:1; in DM 3:1 90% reliable lecithin/
spingomyelin – fetal lung maturity synthesis of
phosphatidylglycerol compound that stabilizes surfactant
is delayed in DM
b.Creatinine concentration – excreted in fetal urine;
assessfetal renal function and fetal muscle mass; Normal
Value >= 2 mg/dL = 36 weeks of AOG 60% reliable
c.Bilirubin levels – measures liver maturity; Increase level
– abnormal; decrease – normal
d.Cytologic findings – staining of cells with 0.1% nile blue;
nitrate – 20% fetal cells stained

Contraindicated – Amniocentesis
1.Abruptio placenta
2.Placenta previa
3.History of premature of labor
4.Inc cervix

Kleihaver-Boetke – test to determine whose blood stained of

the amniotic fluid; stains fetal blood/cells Pink

II. OCT – oxytocin challenge test

Use of temperature stress in a form of utrerud
contractions is applied to the fetus; FHB remain normal
 Normal Value: Negative

III. Estriol excretion studies


Normal Value: >12 mg/ 24O

Continuous rising estriol values indicate normal fetal
growth

IV. Non-Stress test (NST) 99% reliable

Normal Value: Reactive fetus (heart rate acceleration
associated with fetal movement)

V. Ultrasonography (OB echography)

Harmless, non-invasive, use of sound waves
Uses:
oDiagnosis of pregnancy
oAssess tumor, molar pregnancy
oDetermine fetal age
oMeasures fetal growth
oIdentify placental abnormality
oDetermine fetal position
o
Procedures:
oFluid – water 3-4 glasses one hour before study;
ASK NOT TO VOID – good transmission of waves
better visualization of uterus
oApply conduction paste cream – enhance
transmission and reception
oContraindicated: recent GI contrast studies – causes
distortion of reflected sound waves

Anemia and Pregnancy

Pseudoanemia
 Blood plasma volume expands during pregnancy
Limits oxygen exchange at the placental site because of
the reduced amount of oxygen present
Alteration in tissue perfusion (placenta)
o20% of pregnant women
oIncrease puerperal complications esp. infection
o90% - of all anemia – iron deficiency anemia
o10% - other anemias

Circulatory changes in pregnancy (Increase to)

plasma volume – 30%
RBC vol. – 20%
Hgb – 12 – 15%

Blood volume expected to drop (decrease)

30th – 40th weeks of AOG – due to fetal
consumption (circ.)

Anemia in Pregnancy defined:

1.First trimester
Decrease 11 gm/ dL – Hgb and 37% Hct
2.Second trimester
Decrease 10.5 gm/dL – Hgb and 35% Hct
3.Third trimester
Decrease 10 gm/dL – Hgb and 33% Hct
4.High in altitude
5,000 ft. above sea level
 14 gms/dL – anemia hemoconcentration

Common type of anemia:

I. Iron deficiency Anemia

Causes:
Poor diet
Unwise weight reduction program
Heavy menstrual period

Fetal Outcome:
a.Decrease birth weight
b.Prematurity

Rx: Iron supplement – FeSO4 0.3 gm TID or 1 gram OD

If constipated, take Colace

II. Folic Acid deficiency Anemia (Megaloblastic

anemia [enlarged RBC])
Causes:
Poor diet
Cooking in large volume of water
Malabsorption

Effects:
Early abortion
Abuptio placenta
 UTI

RX: Folic acid supplement – 150 ug OD; 5 mg OD

maintenance dose

III. Sickle cell anemia

Recessively inherited hemolytic anemia

Chances:
1 out of 12 black American has the sickle cell
trait which will predispose them to: polynephritis,
bacteriuria, UTI, hematuria

Occurrence:
First trimester: Nausea/ vomiting
Second trimester: pooling of blood in LE
Third trimester: infection, fever, dehydration

Assessment:
Diet: decrease water
Activity: prolong standing (Elevate legs, side lying
position)
Hgb: 6-8 mg/dL – hemolysis can occur if
hemoglobin falls to 5-6 mg/dL
Hyperbilirubinemia – no conjugation of bilirubin
since RBC are quickly destroyed-jaundiced sclera

Management:
 Oral contraception – C/I
No iron supplement
oCells cannot incorporate iron-binding to iron-
build-up

1.Prevent crisis – exchange transfusion

2.Crisis throughout pregnancy
3.Sickle cell crisis
a.control pain
b.oxygen administration
c.increase fluids
4.delivery – nerve block not GA; avoid tissue
anoxia
5.give folic acid – prevent new cells to be
megaloblastic
6.prevent infection

Alcohol in Pregnancy and the Newborn

(Ethanol) – substance

Ethanol crosses the placenta (teratogenic) => result

to:

I.FAS (fetal Alcohol syndrome)

Intake of 2 oz. Of alcohol/ day or increase
level of alcohol ingestion during pregnancy
Prominent nose and bird-like face
 Acetaldehyde
S/S: post partum manifestation
i.tremors
ii.fidgety
iii.irritable
iv.weak suck reflex
v.always awake or asleep
vi.distinct facial feature as short
palpebral fissures, hypoplastic upper lip
(thinned upper lip), thin vermillion, short
upturned noses and flattened nasal
bridges and epicanthic folds
vii.small eyes
viii.flattened maxilla
ix.hirsutism
long term effects:
a.mental retardation (pre-post natal)
b.growth retardation
c.central nervous system involvement
(behavior problem – hyperactive in school)
d.microcephaly
e.joint and cardiac anomalies
II.Neuroblastoma – a form of cancer
III.Withdrawal symptoms (syndrome)

Management:
Advice mother to quit alcohol or avoid alcohol
when pregnant
Reasons of taking alcohol:
1.Social
2.Therapeutic – ethanol has a tocolytic effect –
halt labor (stops prostaglandin production which is
responsible for progress of labor)

Smoking, Pregnancy and Newborn

Nicotine - >10cigarettes/ day

Harmful to fetus because:

1.Carbon monoxide entrapment by the placenta –
decrease blood flow => uterine hypoxia
2.Vasoconstriction of the uterine vessels –
decrease tissue perfusion
3.Constriction of uterine arteries

Effects:
I. Fetus
1.Premature rupture of the membranes
Vasoconstriction action of nicotine
Increase level of CO in blood stream
2.Small for gestation age (SGA)
3.Underweight (IUGR) –Intrauterine growth
absorption
Decrease supply of nutrient and oxygen
Smokers eat less
Nursing responsibilities:

1.Advice mother to quit smoking or < smoking less

10 cigarette/ day and none within 48O of delivery
2.Nutritional counseling – avoid junk foods,
nutritious food intake
3.Join non-smoking or stop smoking group.
4.Please No Smoking signs in areas of pregnant
mothers
5.Health care provider to serve as model
6.Quit smoking not only for fetus but for self

II. Mothers
1.Halitosis, stained teeth, lips and finger’s
2.Habit forming

Drug Dependence, Pregnancy and the Newborn

Drug abuse -overuse of one or more drugs

without medical prescription
Drug dependence -craving a particular drug for
psychological and physical
well-being (influenced)
Drug addiction -using habitually or compulsively
Drug tolerance -capacity to absorb a drug
continuously in large dose without
adverse effects
Use of amphetamines, narcotics,barbiturates and
alcohol-drug dependence

CARR – identified factors (3) why a woman becomes

involved deeply in drug
dependence
1.She is from a disrupted family background
Left home as early as adolescent
Few meaningful support people
Few skills or little education
2.She had negative sexual experiences
Victim of rape and incest
3.She has low self-esteem
Ease psychological pain
A sense of emptiness
Promote social interactions

Effects:
I. Maternal
PIH, phlebitis, sub-acute bacterial endocarditis,
Hepa B, HIV (shared infected needle)

II. Fetus
1.FOD – (fetal opiate dependence) with following
characteristics:
 Small for gestational age, fetal distress,
meconium aspiration, SIDS, withdrawal
symptoms
2.Physiologic – advantages
liver forced to mature; decreased
hyperbilirubinemia
fetal lung to mature; decrease SIDS
3.S/S of withdrawal symptoms
a.Sleep pattern disturbance
b.Abrasions on knees, elbows and nose
c.Others as: vomiting, high pitched cry,
sneezing, diarrhea, poor feeding, excessive
sweating, tachycardia

Management:
I. Mother
1.Enroll in a methadone maintenance program
during pregnancy
Supplied legally, readily available,
aseptically administered, monitored,
fetus assured of better nutrition
2.Reassurance
“Everything is doing well”; emotional
support
3.Anticipatory guidance throughout pregnancy
(no one to share their problems)

II. Infant
 1.preserve heat
2.isolate the infant
3.prepare for NGT insertion if with poor sucking
reflex
4.administer IVF for excessive vomiting and
diarrhea
5.give sedation – diazepam (valium)
6.high incidence of jaundice if not enrolled in
methodone program – skin care

Thyroid Disease, Pregnancy and the Newborn

Hypothyroidism Hyperthyroidism
 rare condition in young adult - common in
pregnancy than hypo.
- if untreated, woman is unable to - C/M:
conceive- unovulatory *rapid heart
rate
-C/M: *Exopthalmos
*history of
spontaneous
bortion

*easy
fatigability
*nervousness
 * obese, dry
skin (myxedema)
*palpitations
(tachycardia)
* cold intolerance *weight
loss
*if undiagnosed may
lead to:
>HPN of
pregnancy
>premature
labor
Management:
Thyroxine prep. Diagnostic
- To replace what is absent - radioactive
uptake of 131I subtype
during pregnancy, dose is increased

to sustain pregnancy
after delivery, dose is tapered back this
procedure should not be used
to pre-pregnant dose; if not then during
pregnancy because fetal
woman will develop hyperthyroidism thyroid
incorporate this dr
and
results to fetal
thyroid destruction
Effects to fetus: RX:
No known side effects to fetus if dose is -
thioamides (methimazole or
Monitored accordingly
propylthiouracil
* reduce thyroid
activity

Management: Effects:
1. Keep dose to the lowest; prevent omission
*teratogenic – enlarged thyroid and
or duplication [goiter]) in
the fetus
2. Should not Breastfeed as drug is excreted in *
obstruct airway and make
breast milk resuscitation
difficult in Newborn
Surgical Management: *potential
for bleeding during
- removal but preferably an interpregnancy
delivery
procedure

Tuberculosis, Pregnancy and the Newborn

Etiology:
Mycobacterium Tuberculosis – acid fast bacillus
Positive PPD-sensitized T lymphocytes

Mode of transmission:
Droplet

Effects to mother: Risks

I. Mother
Pre-partal:
a.Gravid uterus pushes diaphragm and lungs
to different shape may rupture calcified
lesions activating disease (PTB)
b.Pushing during labor; increase
intrapulmonary pressure
Post-partal:
c.Lungs suddenly returns to pre-pregnant
position and breaks open calcified lesion

II. Drugs – without apparent teratogenic effects

Management:
1.No pregnancy until PTB becomes inactive about
1-2 years
TB lesions never actually disappear but
only “closed off” and made inactive
2.Maintain adequate level of calcium during
pregnancy to ensure TB pockets “closed”
Calcium supplements must be given
Effects to infant:
Spread thru:
1.Placenta (circulation)
2.after birth (droplet)
a. Should have 3 concentrated negative
sputum for AFB
b. Holding and caring
c. No need to be isolated
d. Newborn with INH prophylaxis
a.Skin test with 3 months intervals
b.If mother is on INH and infant also on INH –
infant should not be breastfed causes
overdose (toxic effects)

Rh – ABO incompatibility

Incidence:
Rh negative mother
D- antigen
dd – genotype

Rh positive fetus
DD – genotype
Dd – genotype
 Rh positive father
DD – homozygous
Dd – heterozygous

DD – 100% of children Rh positive

Dd – 50% for trait

100% DD Dd 50%
Dd Dd

DD Dd
DD dd

Pathophysiology: D antigen (protein

factor) an Rh
positive has that Rh-

Rh positive fetus – mother’s body

invaded by a foreign antigen

Mother’s body reacts by forming

antibody

Rh factor (fetus) exist as a position of the RBC

in Rh invasion entire RBC must be destroyed
(hemolysis of fetal blood cells occur)
 Fetus becomes deficient of RBC (decrease oxygen
transposrt to fetus)

Causes Hemolytic disease of the Newborn or

Erythroblastosis fetalis

No connection between maternal and fetal blood during

pregnancy so mother is not exposed to fetal blood

Occasional villus rupture allowing a drop or two of fetal blood to

enter maternal circulation, which initiates antibody production

As the placenta separates following delivery of the newborn,

there is now an active exchange of fetal and maternal blood from
damage villi

Maternal antibodies are formed against Rh positive blood by an

Rh negative mother in the first 72 hours after delivery

Woman is advised that she should have no more than 3 children

As number of pregnancy increases, amount of antibodies formed

also increases; in many women, a lethal number of antibodies
would be present when 3rd pregnancy begins
Diagnostic:
1. Anti-D antibody titer test at 1 st ANC (32 or 38
weeks of AOG; 0-minimal l=8)
Titer increases or positive
1st pregnancy – Rh sensitization
oMonitor every 2 weeks throughout pregnancy
oMonitor fetal well-being every 2 weeks or
months by amniocentesis

2. Spectrophotometer
amniotic fluid reveal fluid density - extent of
involvement and bile level; if density remained low
(no fetal distress, Rh negative fetus)

Therapeutic management:
I. RhIg (RHO (D) immune globulin) RhoGAM

commercially prepared of passive antibodies against

Rh-factor

given to mother 72 hours after delivery of an Rh
positive child; mother forms no maternal antibody
RhIg – passive antibody protection (transient) 2
weeks – 2 months, the passive antibodies are
destroyed

Effects:
 1.Only those antibodies during pregnancy are left –
thus every pregnancy is like 1st pregnancy  lesser
antibodies  assuring safe intrauterine
environment to succeeding pregnancy
2.Newer techniques
RhIg given at 7 – 9 months AOG offers more
protection

RhIg – do not cross placenta in late pregnancy –
do not destroy RBC *antibodies are not the IgG
class – the only type that crosses placenta
RhIg – is ineffective to a woman who is already
sensitized to Rh factor

Reasons why currently Rh sensitization is still a

complication of pregnancy:

1.Childbearing began before RhIg was available - 

Rh antibody titer in blood
2.Woman do not receive RhIg injection following
abortions or ectopic pregnancy so antibody
formation begins; when to give RhIg injection – 32 –
39 weeks AOG no change in woman anti D fetus
a.Fetus Rh positive
II. Intrauterine Transfusion

Dangers of rising antibody titer in pregnancy:

1.Stillbirth
2.Died of neonatal heart failure (erythroblastosis fetalis)
3.Suffered brain damage
Motor and mental retardation from  bil. level
(Kernicterus)
Injection of red blood cells directly into a vessel in the
fetal cord using amniocentesis techniques using “O”
negative – 75 – 150 ml depending on fetal age
Risk:
1.Cord vessel laceration by needle
2.Uterus irritation by invasive procedure that labor begins
to reduce the possibility of the fetus receiving virus –
contaminated blood – the woman donates blood herself
woman restore blood volume promptly so no fetal or
maternal injury or hazard will result
Frequency:
once during pregnancy but can be injected every 2 weeks for 5-6
times
Delivery:
once fetal lung maturity is reached
Reassurance:
Day to day approach
III. Exchange transfusion:
To remove hemolyzed cells replace with healthy cells (after
delivery)
RhM– Incompatibility

Pregnancy
(Fetal blood) – Transfer of Rh
antigen into maternal circulation

F
 M

Transfer of Rh Antibodies into

fetal circulation

F
Note: Rh dd mother
Rh DD / Dd fetus
antibody Hemolysis of RBC in Fetal Blood
Erythroblastosis Fetalis (hemolytic
disease of the newborn)

During normal
Pregnancy  no
connection between
M - 1st pregnancy
maternal and fetal
- - Initiate maternal
blood
- antibody production
+ to Rh + blood of fetus
+ +
+
F
 M - M +
- - - +
- + -

Occ. Villi rupture

allowing a drop or
two of fetal blood to
maternal circulation
+ + (Desensitization)
+ + + + Rh0D or RHIG (Rhogam)
+ + 1.At 7 – 9 months
F F pregnancy
2.72 hours after
delivery  destroys the
antibodies formed in
maternal blood in 2
weeks to 2 months time
After delivery of fetus - transient only those
more antibodies formed antibodies during
against fetal blood in pregnancy are left (1st
maternal circulation pregnancy)

M -
- -
-
+ +

+
+ +
+
F

M -
- - 2nd pregnancy just like
+ 1st pregnancy,  fetal
- survival up to 3rd
+ pregnancy
+ +
+
F
Multiple Gestation

Gestation of 2 or more fetuses with considered as a condition

complicating pregnancy because the mother’s body must adjust
to the effects of more than one fetus

Incidence:
Frequent in non-whites
 in woman’s parity, age, inheritance
dizygote twins has a familial maternal pattern

Types:
I. Twin

Dizygotic Monozygotic
2 ovas 1 ova
2 spermatozoa 1 spermatozoa
2 placentas 1 placenta
2 amnion 2 chorion 2 amnions 1 chorion
2 umbilical cords 2 umbilical cords
Same or different sexes Same sex always
Familial maternal pattern

II. Multiple gestation pregnancy

3-4-5-6 etc
Assessment:
uterus size; rate faster than usual
ultrasound reveals multiple gestation
Alpha – fetoprotein levels – elevated
Quickening – flurries of action at different portion of the
abdomen rather than one persistent portion (foot area)
2 or more FHB one FHB when other twin’s back at woman’s
back
 appetite
discovered at delivery when uterus not empty backache and
fatigue

Effects to mother – susceptible to: PIH, Hydramios, placenta previa,

anemia
Fetus – prematurity
Management: Bring pregnancy to term

Hyperemesis gravidarum
pernicious vomiting – is nausea and vomiting of pregnancy that
is prolonged past 12 weeks of AOG .
  THE DESCRIPTION OF HYPEREMESIS GRAVIDARUM INCLUDES SEVERE
NAUSEA AND VOMITING, LEADING TO ELECTROLYTE, METABOLIC, AND
NUTRITIONAL IMBALANCE IN THE ABSENCE OF OTHER MEDICAL PROBLEMS.
HYPEREMESIS IS NOT A FORM OF ANEMIA.
 LOSS OF APPETITE MAY OCCUR SECONDARY TO THE NAUSEA AND
VOMITING OF HYPEREMESIS, WHICH, IF IT CONTINUES, CAN DEPLETE THE
NUTRIENTS TRANSPORTED TO THE FETUS. DIARRHEA DOES NOT OCCUR
WITH HYPEREMESIS.

S/S:
dehydration, ketonuria, and significant weight loss

Normal Pregnancy:
1.more severe in the morning; woman shuns breakfast
2.noon – nausea disappear – woman eats more
3.dinnertime – prepare lunch = adequate NUT maintained

History of prolonged vomiting past 12 weeks AOG

Assessment:
1. hematocrit or  hemoglobin – hemoconcentration –
dehydration
2. Na (136 – 145 mEq/L), K (*3.5 – 5 mEq/L),
Cl (90 – 110 mEq/L)
3.Polyneuritis – secondary to Vitamin B deficiency
4.weight loss and ketonuria – breakdown of fats and protein –
intrauterine fetal growth retardation

Management:
1.Admission prolonged hospitalization = social isolation

2.NPO – 1st 12 hours + 3L/LR + B complex

3.sedation – rest Phenobarbital
4.antiemetics (with fetal risk)
5.no visitors – til no more vomiting
 6.clear liquids
7.dry toast, crackers, or cereal every 2 – 3 hours
8.soft – astol
9.all above ineffective TPN

Pseudocyesis
false pregnancy

Assessment:
all S/S of pregnancy (Probable)
abdominal enlargement up to 7 – 8 mos. AOG
uterus empty on Ultrasound

Factors:
1.Wish Fulfillment
Woman’s desire to be pregnant = physiologic changes

2.Conflict Theory
Desire or fear of pregnancy = internal conflict leading to
physiologic changes
3.Depression Theory
Depression attributes the cause to create physiologic
changes

Management:
Psychologic counseling – to learn how to better handle
her needs or conflict

Precipitate labor/ delivery

Occurs when uterine contractions are so strong that the woman

delivers with only a few rapidly occurring contractions
 Labor that is completed in less than 3 hours
Likely to occur in multipara, following induction of labor or
amniotomy

Risks:
Fetus – sub-dural hemorrhages (sudden release of pressure on
the head)
Mother – lacerations of the birth canal, premature separation of
the placenta (strong sudden force)

Goal:
To bring the delivery in a controlled surroundings to prevent
risks to fetus and mother

Theories behind precipitate labor:

1.Uterine stretch theory
2.oxytocin theory
3.progesterone/prostaglandin theory
4.placental degeneration

Premature labor/ Delivery

or preterm labor
unknown cause
occurs in approximately 10% of all pregnancies
occurs before the end of 37 weeks AOG or before fetus
weigh 2500 gms.
Results in an immature infant, 2/3 neonatal death is due to
low birth weight

BIRTH BEYOND 40 WEEKS GESTATION IS CONSIDERED AS POST TERM.

BIRTH AT 38-40 WEEKS’ GESTATION IS CONSIDERED FULL TERM,
WHILE BIRTH FROM 20 WEEKS AND BEFORE THE BEGINNING OF THE
37 WEEKS IS CONSIDERED PRETERM. A SPONTANEOUS ABORTION
OCCURRED BEFORE 20WEEKS AOG.
Conditions resulting to premature labor:
1.Cervical surgery as cone biopsy
2.Chorioamnionitis
3.Hydramnios
4.Multiple gestation
5.Maternal age
6.Previous preterm labor
7.Polynephritis, UTI
8.Short inter-pregnancy period
9.Smoking
10.Strenuous or shift work
11.Uterine anomaly as tumor

Assessment:
1.More painless uterine contractions (30seconds duration, or
frequently as every 10 minutes for more than 1 hour)
2.More backaches
3.More vaginal discharges
4.Associated with UTI or chorioamnionitis

Managements:
1.Halt Labor when [Criteria]
Fetal membranes are intact [BOW]
Fetal heart sounds – good
No evidence of bleeding
Cervical dilatation not more than 3-4 cms
Effacement not more than 50%
(Note: all these criteria must be present)

Measures to halt labor: use of tocolytics:

1.Ethanol
(ethyl alcohol) administer IV
blocks the release of oxytocin by the pituitatry glands
thereby blocking or delaying labor pains
 stops production of prostaglandin stopping labor pain
(Note: new knowledge on the effects of alcohol on a growing fetus
nor made halting labor with the use of alcohol questionable thus use
of this method is no longer advised)

2.Beta – sympathomimetic drugs

Most frequently used beta receptor sites
Adipose tissue, heart, liver, pancreatic cells, GIT and
other smooth muscles as uterine muscles, bronchi, blood
vessels

Beta Adrenergic  myometrial cells  release of adremycyclase 

triggers conversion of adenosine triphosphate into  cyclic
adenosine  this substance is responsible for reducing the
intracellular concentration of calcium through protein binding 
with lowered IC calcium concentration, muscle contraction is
ineffective and uterine contractions stop thus labor is halted

e.g. Nifedifine – calcibloc/ adalat [calcium channel blocker]

Check vital signs every 4 hours
Antidote: propanolol [Inderal]

3.Ritodrine Hydrochloride [Yutopar]

Terbutaline (Brethine) – most used
Check pulse – should not be given if pulse exceeds 120
BPM
Also acts entirely on beta 2 receptor sites
Mild tachycardia and hypotensive effects

Beta 2 receptors relax, however bronchial and blood vessels relax

along with the uterine muscles  labor is halted but  hearty rate
increases to move blood effectively  hypocalcemia may occur from
a shift of K into the cells  blood glucose and plasma insulin
increase  pulmonary edema occurs  headache, nausea and
vomiting due to dilation of the blood vessels also manifests

(note: use with caution in patients with DM – increase BS overly

DM, thyroid dysfunction)
4.MgSO4
Effective to halt labor
Check for signs of toxicity
5.Other Measures
a.Bedrest – to take the pressure of the gravid uterus off the
cervix
b.Hydration – oral, hydration affects the secretion of ADH
and oxytocin by the pituitary gland – oxytocin causes
uterine contraction
c.Avoid psychologic stress
d.Administration of corticosteroid (betamethasone) to hurry
formation of fetal lung surfactant

Premature infant

An infant viable – born before the completion of 37 weeks AOG

(premature in age)
Weighs between 1500 – 2500 grams without regards to
gestational age (premature in weight

Etiology:
1.Unknown
2.Maternal factor
Chronic poor nutrition, DM, multiple births, drug
abuse, IUD in utero, chronic diseases – anemia, heart and
kidney diseases, infection, complication of pregnancy as
PIH and bleeding
3.fetal factor
chromosomal abnormality, anatomic abnormality, feto-
placental unit dysfunction
Characteristics:
I. General appearance
head disproportionately large
hair – lanugo, flaky
fingernails – soft
poor ear cartilage
skin – thin, capillaries visible
lack of subcutaneous fats
sole of feet – smooth (36 weeks AOG, 1/3 of foot is
creased; 38 weeks AOG 2/3 of foot is creased)
breast buds – 5mm (36 weeks AOG none 38 – 3 mm)
testis – undescended, scrotal rugae, very fine
labia minora – undeveloped
abdomen – relatively large
thorax – relatively small
muscle tone – poor
reflexes – weak
“OLD MAN FACIES”

II. Altered Physiology

immature poorly developed system

A. Respiratory system
respiratory distress – cyanosis
breathing labored irregular, period of apnea
abs. – cough reflex

B. Digestive system
malnutrition
stomach is small – vomiting
 fat absorption
C. Poor thermal stability
  subcutaneous fats – no heat storage and insulation limited
ability to shiver due to poor vasomotor control of blood flow to
skin
 sweat glands – cannot perspire under 32 weeks AOG
large skin area compared to body weight

D. Renal Function
 sodium excretion;  Potassium excretion (hyponatremia vs.
hyperkalemia)
 ability to concentrate urine (prone to dehydrate with vomiting
or diarrhea)
 ability to acidify urine (glomerular tubular imbalance 
accounts for sugar, protein, amino acids, and sodium presence in
urine)

E. Nervous system
center for function control poorly developed
slow response to stimulation
suck, swallow, gag, poor feeding and aspiration are problems

F. Infection
no active immunity, no passive immunity (IgM)
limited chemotaxis (reaction of cells to chemical stimuli)
decreased opsonization (prep. Of cells to phagocytosis)
limited phagocytosis (digestion of bacteria by cells)
decreased anti-inflammatory response (hypofunction of adrenal
glands)

G. Liver function
no ability to handle and conjugate bilirubin (NV: 1 – 12 mg/dl =
NB)
hypoglycemia – does not store or release sugar well
anemia – study  in hemoglobin and production of blood (NV:
hemoglobin NB 12 – 24 gms/dl)
 prone to hemorrhagic disease – does not store Vitamin K

H. Eyes
retinal atresia
RFP – retinal detachment
Note: if given oxygen beyond needed

I. Circulatory system
Anemia, polycythemia

Complication:
1. System problem – severity depends on gestational age
2. Major -  birth weight

Note: 1st 24 hours of life, most critical, nursing care depends on the
problem (physiologic)

Postmature pregnancy, delivery, infant

Post-gestational, post-mature
Pregnancy beyond normal AOG – (38 – 42 weeks)
Occurs approximately 10% of all pregnancy

Factors:
1.Faulty due date
E.g. women with long menstrual period or cycle 40 – 45 days –
delivery will be late about 12 – 17 days

2.True overdue due to

a.Salicylate ( dose) – for severe sinusitis, headache:
interferes with prostaglandin synthesis which is responsible
for the initiation of labor
 b.Myometrial quiescence or uterus do not respond to
normal labor stimulation

Risks:
1.Placenta is unable to adequately function due to  placental
perfusion
2.oligohydramnios <AF – lack of oxygen, fluids and nutrients
3.macrosomia – determine bi parietal diameter
4.meconeum aspiration

Nursing Care:
1.Predict true gestational age – fundic height
2.palpate gross fetal size
3.induce labor – prostaglandin gel, oxytocin drip – CS

Post-Mature Infant
Whose gestation age is 42 weeks or longer

May show signs of weight loss with placental insufficiency

Develop post-mature syndrome

Etiology:
1.Unknown in many instances
2.Maternal Factors
a.Primi and high parity at given age
b.Prolonged gestation in preceding pregnancies

Characteristics: (Seen in 44 weeks or more)

I. Physical Appearance
Reduced subcutaneous tissues
Loose skin turgor at buttocks and thighs
Long curved fingernails and toenails
 Amounts of vernix caseosa
Hypoglycemia-no adequate stores of glycogen
Abundant scalp hair
 Poor temperature regulation-Low levels of subcutaneous fat
Wrinkled macerated skin, pale, cracked – parchment- like skin
Alert appearance – 2-3 weeks old infant after delivery
Greenish-yellow stain on skin – fetal distress (meconium
aspiration)
Intrauterine malnutrition and hypoxia =  placental perfusion =
 oxygen and nutrients
Low levels of estrogen
One post-term to another post-term
Maternal weight loss and decrease uterine size

II. Complications:
Meconeum aspiration, hypo or hypercalcemia,
polycythemia(decreased oxygenation), pulmonary hemorrhage,
pneumonia, asphyxia neonatorum, pneumothorax

Note: severity of problems depends on length of gestation.

Nursing Care is the same with premature

Postpartum Complications
I.Infection
II.Psychosis

I. Endometritis
Inflammation of the lining of the uterus – endometrium,
often at the site of placental implantation
Incidence is higher after CS
An ascending infection

Assessment:
3rd or 4th day puerperium
Chills
Loss of appetite
 WBC: 20,000 – 30,000
General body malaise

Abdominal tenderness
“Boggy” uterus
Temperature over 38OC
Strong after pains
Lochia – dark brown, foul

Treatment: Antibiotics, oxytocin, analgesics

Nursing Management
1.Send specimen for lochial culture
2. oral fluids
3.good hand washing
4.fowler’s position – drain secretions
5.ambulate

Complication tubal scarring – infertility

II. Thrombophlebitis
inflammation of the blood vessels with formation of clots
Extension of endometrial infection

Precipitating factors
blood clotting abnormality-increased fibrinogen
dilated veins
pooling
stasis and clotting of blood in LE-prolonged in stirrups

Types:
a. Femoral
femoral, saphenous and popliteal 10th day postpartum
“milk leg” or phlegmasia alba dolens” (white, inflammation)
 Homan’s Sign (+)
4-6 weeks

b. Pelvic – ovarian, uterine, hypogastric veins 14th day puerperium,6

to 8 wks

Management:
1.total bed rest with cradle
2.Early ambulation
3.antibiotics
4.analgesics
5.anticoagulants – do not use heparin with aspirin
6.moist warm compresses
7.never rub or massage leg
8.assess bleeding sites – if Dicumarol is used –Check prothrombin
or clotting time before giving
9. Breast Feeding is temp. D/C but breast is continuously emptied

III. Peritonitis
inflammation of the peritoneal cavity
extension of endometritis
1/3 of all post partal deaths
spread thru lymphatic system
abcess formed in the Cul-de-Sac of Douglas – the lowest
point of the peritoneal cavity

Assessment:
as a surgical patient – S/S ASA rigid abdomen, abdominal pain,
high fever, rapid pulse, and vomiting
From Ft to uterus to abdomen

Management
1.NGT – if with paralytic ileus(intestinal paralysis)
2.IVF – TPN and meds
3.analgesics for pain relief
 4.antibiotics

Complications: Adhesions and scarring – infertility

IV. Mastitis
inflammation of the breast
7th post partum or when infant is a week or month old
pathologic organisms coming from infant’s nasal-oral
cavity(staphylococcal/streptococcal) enter cracked nipples
(tissues) milk good culture media
S/S: scanty BM, high fever, mastitis (unilateral)

Management:
A. To prevent fissures
1.Proper Breast feeding techniques
Not leaving baby too long at breast
Be certain baby sucks the areola not the nipple only
Release infants grasp at nipple 1st before removing infant
from breast
2.wash hands between handling perineal pads and breast
3.expose nipple to are at least a part of the day
4.use Vit. E or lanolin – based ointment or A and D cream to
soften the nipple daily
B. Broad spectrum antibiotics
C. Breastfeeding can be continued (other breast and keep other
breast empty to prevent bacterial growth
D. Manual expression of milk 2 – 3 days
E. Warm wet compresses
F. I and D for localized abscess
G. Assure client that this is not breast cancer a permanent disease;
she can still breastfeed after

V. Salphingitis
fallopian tubes are inflamed
portal of entry – uterine cavity, broad ligament
3 types:
1.Acute
 gonococci; both tubes can lead to local peritonitis
2.Chronic
Sequel gonococcal infection
Severe scarring of FT
Adhesions
Tubo-ovarian abscess may form
Cause sterility; tubal pregnancy
3.tuberculosis
PTB from TB of lungs
TB endometritis
Attack FT

Assessment:
1.Sudden abdomino-pelvic pain; tenderness, pressure
2. vaginal discharges
3.fever; malaise

Diagnostic:
I.Gram staining or secretions from endocervix or cul-de-sac
II.Ultrasound
III.Culdocentesis

Treatment and management:

Antibiotics – penicillin or tetracycline
Bedrest
Analgesics
IV therapy
Culdotomy
TAHBSO in complicated type
AntiTB therapy in Type 3

Postpartum Psychosis
 Also called Puerperal psychosis or postnatal psychosis.
Brief psychotic disorder
Radical hormonal change with neurotransmitter overactivity
Mother is unaware she is ill
Response of client to hormone shifts – estrogen/ progesterone
levels and change of rates

Post-partum Blues-or “baby blues”,emotionally labile, crying easily

for no apparent reason-5th to 10th day.Other symptoms include:
depression, let-down feeling, restlessness, insomnia

Etiology: unknown
Causes: emotional and psychologically overwhelmed of parental
responsibilities, fatigue after birth, mourn the passage of labor and
birth
Post-partum depression” mild to severe, :good days” or “bad days”,
more on the father

Assessment
Feeling of sadness; isolation
Short temper and irritability; hurts the baby
1.Postpartum “blues” – 1 – 2 days Management: Counseling
2.Postpartum depression – good support system
3.Postpartum psychosis – 1:500 presents C/S after delivery
2/3 – response to crisis in child bearing not a response to
physical aspect 1st 6 weeks after delivery
1/3 – had history of mental illness prior to pregnancy
Crisis, which will precipitate postpartum psychosis
1.Death in the family
2.loss of husband’s job
3.divorce
4.some major crisis

Management:
I. Psychiatric counseling
II. Do not leave woman alone; close watch!
Might harm self or her infant

Dystocia

Difficult labor(placenta, cord, membranes, and amniotic fluid)

Refers to any labor which does not advance normally

STAGES OF LABOR

1) Full Dilatational(preparatory, dilatational and deceleration

sequence)-12 TO 14 hrs primi,8 hrs multi
2) Full dilatational until fetus is expelled from birth canal(pelvic
or second stage)
3) Placenta is delivered

Factors:
a.Forces are inadequate
E.g. inertia – sluggishness of uterine contractions
b.Abnormal position of the passenger (infant)
c.Abnormal passageway (birth canal)

Inadequate forces

Uterine Contraction- interplay of contractile

hormones( ATP,estrogen and progesterone, electrolytes such as Na,
K and Ca, contractile proteins such as actin and myosin,
epinephrine and norepinephrine, oxytocin and prostaglandins

A. Uterine inertia (Dysfunctional labor)

Sluggishness of uterine contractions during labor

2 types:
According to time when it occurs
1.Primary uterine inertia
 Occurs at onset of labor or prolonged latent phase of
labor
Management: stimulate with not enemas, administer
oxytocin, encourage to walk

2.Secondary to uterine inertia

Occur later part of labor or prolonged active phase of
labor; fetus does not descend; cervix not dilated

Management:
maintain a serum glucose level e.g orange juice,IV glucose
Preventing fluid and electrolyte loss-ketones,SG,fluid
administration
Reduce psychosocial stress
Reduce pain-back rubs, change sheets
Maintain a side-lying position
Keeping the bladder empty

B. Abnormal Uterine Contractions

3 types:
According to strength

1.Hypertonic Uterine Contractions

Greater than normal tension
 15 mmHg resting tone
Very painful – not relieved by exercise
oAnoxic uterine muscles
oLack of relaxation
Management:
oFetal and uterine monitor every 15 min interval
oNo oxytocin
oRest and sedatives
oDarken room;  noise stimulation
 oProvide support to client
oAsk client to breath with contractions
2.Hypotonic uterine contractions
Tension is defective or inadequate to cause or accomplish
dilatation
Resting tone 10mmHg
uterine contractions not increasing 2 – 3/ 10 minutes
Causes:
1.Too early administration of analgesics before 3 – 4
cm
2.Bladder/ bowel distended
3.Overstretch uterus – multiple gestation
4.Large fetus
5.Hydramnios
Management:
1.Administer oxytocin - strength tone and
effectiveness
Disadvantage
a.Cause maternal exhaustion and
uterine exhaustion
b. post-partal hemorrhage
secondary to ineffective contractions
c.Prone to infection – over-dilation
of cervix
2.Administer antibiotics

3.Uncoordinated uterine contractions.

More than one contractions occur at the same time due to
myometrium acts independently from each other
Management: fetal and uterine external monitor applied
q15
Oxytocin to stimulate labor

Complication:
 Mother: exhaustion and dehydration
Fetus: injury and death

II. Abnormal in the Passenger (infant)

A. Congenital anomalies

1. Hydrocephalus – accumulation of CSF in brain ventricles

2. anencephalus – absence of the cranium or top portion of the
head,lack of firm cervical dilation
3. Condition causing abdominal (fetal) distention; overgrowth
of liver(hepatomegaly), ascetic cysts, cystic fibrosis(exocrine
glands produce excessive viscous glands secretions causing
problems in respiratory and gastrointestinal functions),
erythroblastosis fetalis (large immature RBCs compensating
for anemia producing edema in peritoneum,pericardium and
pleural spaces)
Risks:
Rupture of uterus
Difficult delivery
4. Excessive fetal size > 7 ½ kgm or 3, 400 grams
causes: large parents, DM, prolonged gestation, overeating,
multiparous
5. Mulitple Gestation-cord prolapsed,uterine
dysfunction,premature separation of placenta,abnormal fetal
presentation,overdistended uterus-prone to hemorrhage from
uterine atony

B. Abnormal fetal position/ Presentation

1.Persistent occiput posterior

2.Breech
3.Face
 4.Brow – fetal head is halfway between flexion and extension
between vertex and face
5.Transverse – long axis transversely lie across short axis of
uterus
6.Compound – more than one fetal parts presenting e.g. head
and hand; head and foot
7.Umbilical cord – cord lies in front of presenting part; ‘Vasa
Previa” – prolonged cord

Note: do not allow client to ambulate after rupture of BOW

Management:
A.Maneuvers
Internal podalic version-Direct manipulation of the baby
inside the uterine cavity to the breech position is called internal
podalic version

External podalic version-External cephalic version (ECV)

refers to a procedure by which an obstetrician or midwife
turns the baby from the breech to the cephalic position by
manipulating the baby through the maternal abdomen.

B.Trendelenburg position
Relieve pressure of presenting part to cord
C.Bed rest after rupture of BOW

C. Cephalopelvic disproportion – CPD-either Mother (contracted

pelvis) fetus abnormally (large vertex)

III. Abnormal Passageway (Birth Canal)

1.Dysfunction of preparatory phase of labor
2.dysfunction of dilatation phase of the labor
3.dysfunction in the pelvic phase (delivery) of the labor

a. Preparatory phase
 prolonged latent phase due to unequal, irregular contraction
20 hours – primi
14 hours – multi
Uterus in hypertonic state
Very painful and frightening
Fetal anoxia
Monitor contraction s and FHT
Administer IV to prevent dehydration
Administer morphine to relieve hypertonicity

b. Dilatation Phase
1.Prolonged active labor = 4 – 8 cm
a.Causes- fetal malposition and CPD
b.Multi – 1.5 cm /hour
c.Nulli – 1.2 cm /hour

2.protracted descent
a.multi – descent rate 2cm/hour
b.nulli – descent rate 1cm/hour
starts with good contractions then diminish
gradually and become infrequent and poor in quality

Assessment : anxiety, fear and apprehension or discouragement

Management:
amnionotomy (rupture of BOW)
oxytocin drip
keep client and kin informed of situation

Delivery Phase
Causes: CPD
prolonged deceleration
Characteristics:
oExtend beyond 3 hours (nulli); 1 hour (multi)
 oSecondary arrest of dilatation – no progress in dilatation of
cervix >2 hours
oArrest of descent –no descent occurred in one hour
oFailure of descent-does not begin
Management:
oNo oxytocin
oPlace in LLRP
oOxygen inhalation
oPrompt assisted delivery large forceps

Management for dystocia:

A. Preventive:
1.Maintain serum glucose level (e.g. juices, candies, IV – prevent
glucose used up)
2.Prevent F/E loss – prevent dehydration; prevent DVT in
Postpartum phase
3.Reduce stress
4.Give supportive measures; reduce pain, give praises, back rubs,
change soiled sheets
5.LLRP – give oxygen
6.Keep bladder empty

B. Curative Management Care:

1.Antibiotics
2.Sedative – stop abnormal contractions
3.Short acting barbiturates – to promote relax/ rest
4.Monitor FHB
5.NPO – prepare for Surgery – CS
6.Assist in delivery; vaginal or CS
7.Trial labor – in borderline or adequate pelvis

Conditions Complicating Dystocia

A.Precipitate delivery-only few rapidly occurring uterus
B.Pathologic Retraction Ring or Bandl’s ring
 Junction of upper and lower uterine segment
Sign that severe dysfunctional labor occurs
Forewarning of a uterine rupture
Grip fetus and placenta
Assessment:
1.Horizontal indentation across abdomen
2.Uncoordinated contractions early in labor
3.Dilation phase – caused by obstetrical manipulation and
administration of oxytocin

Pathophysiology:
Fetus is grasped by the ring and can’t advance or descent
If fetus is delivered, placenta can be held after delivery

Management:
1.Observe abdominal report immediately
2.administer IV morphine sulfate and amyl nitrate
3.C/S – or manual extraction of placenta if not attended leads to
Mother (uterine rupture and postpartum hemorrhage); fetus
(death)

C. Rupture of Uterus
Factors:
Strained uterus
Beyond its capacity
Previous C/S, repair or hysterotomy

Contributory:
Prolonged labor
Faulty presentation
Multiple gestation
Unwise use of oxytocin
Obstruction labor
Traumatic maneuvers using forceps
Assessment
1.Impending rupture suggested by pathologic retraction ring,
strong uterine contractions with cervical dilatation
Management:
Immediate CS
2.When uterus rupture
S/S: sudden severe pain during strong labor,
hemorrhage – uterus, vagina, intra-abdominal, Cullen’s
sign

D. Uterine Inversion
Turning of the uterus inside out
Fundus is formed thru the cervix, turned inside out
Assessment: protrude from vagina,sudden gush of blood,fundus no
longer palpable,sgins of blood loss,uterus is not contracted
Causes:
1.Attachment of placenta at fundus – sudden delivery of fetus
without support – fundus is pulled down
2.strong fundal push in an non-contracted state
3.attempts to deliver placenta before separation

Management:
Hysterectomy – due to severe hemorrhage

E. Amniotic Fluid Embolism

Solid particles from amniotic fluid enter maternal
circulation
Amniotic fluid is forced into circulation thru open maternal
sinuses
S/S as any embolism – fatal,woman sits up and grab chest
due to pain and inability to breathe

Management:
i.Supportive
ii.Oxygen administration
Abnormal Presentation and Delivery

I. Breech presentation/ extraction

Note: Majority of fetuses are in breech presentation early in

pregnancy  by week 38 AOG fetuses normally turn to cephalic
presentation

R – “retain most comfortable position”

Fetuses
Head is widest in single diameter; buttocks plus LE = take up
more space

Uterus
Fundus – largest part
97% of all pregnancies, fetuses turn so that the buttocks and LE
are in the fundus those who failed to turn are breech

Prevention:
woman to assume 15 minute knee-chest position for 3X a day
during pregnancy so breech presentation will be less likely to
occur

Classification:

1.Complete
Feet and legs are flexed on thigh; thighs flexed on abdomen
and buttocks; feet are presenting parts
2.Frank
 Legs are extended and lie against abdomen and chest; feet at
levels of shoulder; buttocks are the presenting parts

3.Footling
a.Double footling
Legs are unflexed and extended; presenting part - feet
b.Single footling
One leg is unflexed and extended; presenting part – one
of the feet
Risks:
1.High risk of anoxia
No molding (prolapsed cord, traumatic injury,
intracranial hemorrhage, fracture spine, arms)
2.Dysfunctional labor
Presenting part does not fit cervix
3.Early rupture of BOW
 risk of infection
4.meconeum aspiration  although meconeum leakage is not a
sign of fetal distress but expected from buttocks pressure

Assessment:
FHT – heard high in the abdomen
Leopold’s maneuver and vaginal examination (show breech
presentation
Ultrasound – to confirm

What to expect:
Parents
Examine baby more closely; frank breech-legs extended; footling
– one leg extended (1st 2-3 days of life)
Explain this to parents
Delivery by C/S

Etiology/Causes: Unknown
 1.Age of Gestation under 40 weeks
2.Abnormal in fetus – anencephaly, hydrocephalus, meningocele
3.Hydramios – free fetal movement
4.Pendulous abdomen – lax abdominal muscle
5.space-occupying mass in uterus e.g. midseptum – traps fetus in
position
6.multiple gestation – can’t turn to vertex position

Hazards/Risks:
1.Intracranial hemorrhage
2.cord compression
3.abruption placenta
4.Erb-Duchene paralysis (Erb’s palsy) – injury to the brachial
plexus
S/S: Loss of sensation at arm and paralysis
oAtrophy of deltoid and biceps and brachial muscles
II. Forceps Delivery

OB forceps – steel or metal instruments (2 blades left and right with

lock),used if the fetal head reaches the perineum
Maybe high forceps(non-engaged head) or mid-forceps(level of
ischial spines)
Maybe used with pudendal block

5 common types of OB forceps

1.Baxton
With hinge in the right blade used to rotate fetal head to
a more favorable position such as ROP/ROA
2.Kielland’s
With short handles and a marked cephalic curve use like
Baxton
3.Piper
Used to deliver the head in breech presentation
4.Simpson’s
 Used as outlet forcep
5.Tarnier’s
Axis traction forcep
Indications:
1.To shorten 2nd stage of labor
When woman is unable to push with contractions in
pelvic division of labor
i.After regional anesthesia
ii.Cessation of progress of labor
iii.Failure of fetal head to rotate

2.Fetal distress
Prolapsed cord
FHT 100 BPM or 160 bpm
Meconeum stain in cephalic presentation

Pre-requisites:
1.Pelvis should be adequate – no CPD
2.Fetal head must be deeply engaged (+3 - +4 station)
3.Cervix must be completely dilated and effaced
4.Accurate diagnosis position and station must be made – vertex
presentation
5.Membranes (BOW) must be ruptured
6.Some form of anesthesia must be used e.g. pudendal block – to
achieve pelvic relaxation and reduce pain
7.Rectum and bladder must be empty

Types of Forceps Application:

I. Low-forceps operation
Easy delivery; forceps are applied after the head has rendered
the perineal floor with sagittal suture in anterior-posterior of the
outlet – vertex at introitus

II. Mid forceps operation

 Forceps are applied before the criteria for low forceps are met
but after engagement has taken place – vertex at ischial spine

III. High forceps operation

Forceps are applied before engagement has taken place (only
used in modern OB – rarely done) – biparietal diameter above
ischial spine

Complications:
Maternal:
a.Lacerations – vagina, cervix = hemorrhage and infection
b.Rupture of uterus
c.Injury to bladder and rectum

Fetus:
a.Cephalhematoma
b.Brain damage
c.Skull fracture
d.Facial paralysis
e.Cord compression
f.Facial marks – temporary 24 – 48 hours only

Nursing Management:
1.prepare patient and explain
2.explain outcome ASAP especially on outcome of procedure e.g.
marks, bruising

III. Vacuum Extraction

used in place of forceps (duration – 30 minutes)
delivery of a fetus in vertex presentation with the use of a
cap suction device that is applied to fetal scalp for traction
e.g ventouse vacuum extrication

Complications:
1.Scalp ecchymoses – expected – posterior fontanelle
 2.cephalhematoma – prolonged used >30 minutes – damage to
scalp

Advantages over forceps:

1.Use of little anesthesia (fetus less depressed at birth)
2.fewer laceration (non-invasive)

Disadvantages:
1.Marked caput - >7 days after birth – assure mother
2.tentorial fear – from extreme pressure

Contraindicated if:
1.scalp blood sampling was done – bleeds
2.preterm – soft skull

Cesarean Section

History:
1879 – Sanger – 1st live C/S and uterus was saved
1800 – C/S done as post-mortem procedure
“caesus” latin of to cut
Julius Caesar – was believed to be delivered by cesarean birth
and name the procedure after him

Definition:
Surgical extraction of the fetus via the uterine incision through
the abdomen – trans-abdominal incision of the uterus

Indications:
CPD – most common
Uterine inertia
Previous C/S
Severe toxemia
Placental accident (eclampsia)
Fetal distress
 DM
OLD primi
Prolapsed cord
Post-term pregnancy
Failed forceps delivery

Types:
I. Low segment or low cervical
Method of choice; incision is made at the lower uterine segment
which is the thinnest and most passive portion

Advantages:
1.Minimal blood loss
2.easy to repair incision
3.lower incident of post-op infection
4.less activity
5.less possibility of uterine rupture
6. post-op adhesions – complication
7.allow vaginal delivery in the next pregnancy

Incision:”bikini” incision

Skin Uterus or skin and uterus (both)

II. Classical CS
Vertical incision. Recommended in the following cases:
1.Bladder or lower uterine segment is involved in extensive
adhesions resulting from previous surgery
2.Transverse lie
3.Anterior placenta previa
4.Active contractile portion of uterus
5.Unable to have subsequent vaginal delivery

Incision:
 Vertical incision of skin and uterus

III. Extra-peritoneal CS
Tissue around bladder is dissected providing access to lower
uterine segment without entering into peritoneal cavity

Advantages:
1.Prevent peritonitis
2.use of antibiotic and blood is reduced

IV. CS with hysterectomy (PORRO’S operation)

cesarean followed by the removal of the uterus

Indications:
1.Hemorrhage due to uterine atony
2.placenta previa and abruption placenta
3.placenta acreta
4.rupture of uterus, non-separable
5.gross multiple fibromyoma

Nursing Care:
A.Pre-op – secure consent
i.Carry out PE (assessment)
ii.Routine lab exams – typing/ cross-matching
iii.Monitor FHB
iv.Shave abdomen and perineum as directed
v.Insert FUC (retained). Keep away bladder from
operative site
vi.Start IV large bore needle
vii.Administer pre-op meds – Atropine sulfate – no
narcotics are given to prevent fetal respiratory depression
viii.Prepare oxytocic drug to be added to infusion following
delivery of infant
ix.Notify pedia department – resident – of surgery to
provide initial care and resuscitation of infant
 B.Post-op care: Surgical and OB care
i.Observe hemorrhage in both areas
1.perineum – pads and buttocks
2.abdominal dressing
3.V/S
ii.Ambulation
1.dangle after 12 hours
2.ambulate after 24 hours
3.deep breathing and coughing exercises, ROM of
extremities and neck
iii.Inspect uterus; massage with proper splinting; give
analgesics as ordered
iv.Administer oxytocin and analgesics
v.I and O
vi.BF – started after 24 hours after delivery

Hysterectomy
Surgical removal of the uterus

Indications:

1.Malignant and non-malignant growth on uterus, cervix, and

adnexa
2.life threatening (severe pelvic infection
3.control of uterine bleeding on hemorrhage
4.correction of problems associate with pelvic floor – relaxation;
rectocele and cystocele (Wertheim’s operation)
5.Treatment of endometriosis if conservative treatment failed

Qualifying considerations:
1.Woman’s age
2.woman’s desire to have children
 3.possible effectiveness of alt. Treatment
4.degree of dysfunction
Elective indications:

1.voluntary sterilization
2.prophylaxis when there is a strong or significant history of
uterine disease as CA

Types:
A.Abdominal – 70%
B.Vaginal

Abdominal Hysterectomy
Types:
1.Subtotal
Corpus (body) of uterus removed; cervical stump
remains
2.Total
Entire uterus and cervix are removed; tubes and ovaries
remain
3.TAHBSO
Entire uterus, tubes, and ovaries are removed

Vaginal hysterectomy (Spalding-Richardson’s operation)

1.Repair of pelvic relaxation; uterine displacement or prolapsed,
urinary stress incontinence cystocele and rectocele
2.high risk in patients who are very obese or those who can’t
withstand prolonged anesthesia

Advantages:
1.Less likelihood of paralytic ileus, post-op pains and intestinal
adhesions
2.Less chance of pulmonary complication and thrombophlebitis
3.Wound dehiscence possibility is less; shorter hospitalization
4.No abdominal scar
Disadvantages:
1.More limited surgical field and inability to examine intra-pelvic
and intra-abdominal organs condition
2.Increased risk of bleeding and postoperative infection

Psychosocial considerations:
1.Fears that cancer or VD be discovered
2.Conflict between medical diagnosis and religious beliefs
3.concerns about disturbed reproductive process
4.disappointments of not having any more children
5.fear of unable to fulfill role and needs of a woman
6.heightened depression and emotional sensitivity

NB – post – op care as abdominal surgery

Discharge Plans/ Health education post-op:

What to expect:
1.Produces surgical menopause (if adnexa were also removed)
2.hormonal replacement therapy (if TAHBSO is done)
3.“Tired feelings” 1st few days; depressed, nervousness
4.employment or job resumption on doctor’s diagnosis
5.follow-up check-up with gynecologist, report the following:
“Peace of mind”
a.temp >38 OC(100OF)
b.heavy vaginal bleeding
c.drainage
d.foul odor of discharge

What activities to engage in:

1.not to sit too long at one time as driving long distance – bleeding
and thrombophlebitis – delay driving after 3rd week post-op
2.Household activity – after 2 months back to “Normal self”
3.shower baths until post-op wounds healed
 4.resume sexual contact after 4-6 weeks; be cautious danger to
cause injuries to incision site and bleeding
Inflammatory conditions

I. Vulvitis
mucous membranes of the vulva
results from:
odirect irritation of vulvar tissues e.g. scratching
oextension of irritation from vagina

Etiology:
1.Skin disorders
2.infection
3.vulvar Krauposis (dryness and atrophy of vulva)
4.vulvar Leukoplakia (atopic disease of older woman)
5.vulvovaginitis
6.senile atrophy
7.pediculosis
8.DM
9.scabies
10.Cancer
11.allergens
12.urinary incontinence
13.poor perineal hygiene

Nursing Care:
1.Apply calamine lotion, hot compresses, sitz bath
2.Wear light, non-restrictive, well-washed, cotton underwear
3.avoid feminine hygiene sprays
4.apply hydrocortisone ointment or anesthetic sprays as ordered
5.keep vulva dry
6.proper application of perineal pad

For severe type

 7.heavy sedation
8.vulvectomy (radical surgical removal of the vulva)
II. Vaginitis
inflammation of the vagina – accompanied by vaginal
discharge (leukorrhea)  urethritis – due to proximity of
urethra to vagina
results from:
i.invasion of organsisms e.g. candida
ii.irritation – frequent coitus
iii.poor hygiene

S/S:
1.Leukorrheal discharges with itching, redness, burning, and
edema
2.Voiding and defecation aggravate the above symptoms

Pre-disposing factors/ Organisms:

1.Trichomoniasis vaginalis – protozoa – bubbly white leukorrheal
discharges
2.candida albicans – fungus – cheesy white discharge s common
in DM, prolonged used of antibiotics, steroids
3.Hemophilusvaginalis-Gardnerella vaginalis-gram positive,cause
of bacterial vaginosis
4.pediculosis pubis
5.contact allergens
6.excessive perspiration
7.poor hygiene

Treatment and care:

1.Enhance natural vaginal flora – lactic acid
2.stimulate growth of Doderleine bacillus-Doderlein's bacillus: A
species of gram-positive, rod-shaped bacteria isolated from the
intestinal tract of humans and animals, the human mouth, and
vagina. This organism produces the fermented product,
acidophilus milk.
 3.good wash after voiding and defecation
4.chemotherapy as ordered
III. Cervicitis
inflammation of the cervix

Predisposing factors:
1.Exposure to pathogens
2.douching
3.childbirth
4.trauma – coitus
5.surgical procedures

S/S: reddened, irritated areas around the cervical os – bleeds easily

Etiology: - Neisseria gonorrhea

- E. coli
- Streptococci and staphylococci

Management:

1.Cervical cautery
2.Cryotherapy – freezing with liquid nitrogen (7-8 weeks healing
time)
a.Inform woman on expected outcome
b.Minor vaginal bleeding with pelvic discomfort at short
period

IV. PID (Pelvic inflammatory disease)- all structures in the

pelvic cavity
Etiology:

Non-gonococcal infection e.g Chlamydia trachomatis

Gonococcal and mixed infection e.g. GC + E. coli, IUD TB,
streptococcus, and staphylococcus
S/S:
1.Abdominal pain, nausea, vomiting
2.Fever, malaise
3.leukocytosis
4.malodorous, purulent vaginal discharge

Goal of Care:

1.control the spread of infection within the client

2.control the spread of infection to others including nurse

Rx and care:

1.Place patient on semi-fowler’s position to facilitate drainage

2.avoid use of tampoons
3.support with proper nutrition
4.administer drugs – non GC (tetracycline); GC (penicillin G)
5.Control spread of infection
a. Handle pads with extreme precautions
b. Use of gloves or instrument
c. Proper disposal
d. Hand washing before and after patient’s contact
e. Proper disinfection of instruments, utensils, linens, etc.
f. Instruct patient how to prevent re-infection
6.use warm douches and heat compresses to abdomen as Rx
7.give moral support and understanding

Complications: (especially if untreated)

1. risk of spread to others
2.sterility
3.ectopic pregnancy
4.inflammatory masses
Menstrual disorders

Dysmenorrhea
painful menses

2 types:
1.Primary – unknown cause; emotional or psychologic factor
2.secondary – factors extrinsic to uterus as endometriosis, pelvic
infection

S/S Uterine Spasms:

pain colicky, cyclic and nagging dull ache at lower
abdominal to LE
severe chills, headache, diarrhea, nausea and vomiting and
syncope

Etiology:
I. Endocrine – release of prostaglandin
II. Anatomic – infantile uterus
III. Constitutional – chronic illness as anemia etc.
IV.Psychogenic – stress, tension, and anxiety

Treatment and care:

1.According to individual needs:
a.Proper psychological preparatory of girls for menarche
b.Good posture, exercise
2.psychotherapy and pharmacology
a.prostaglandin inhibitors – mefenamic acid
b.oral contraception
3.Psychological counseling
4.surgery – pre-sacral and ovarian neurectomy (cutting nerve
fibers)
II. Amenorrhea
absence of menses

2 types:
1.Primary – has not menstruated yet no menarche
a.Cause: embryonic maldevelopment – treated as to etiology
2.secondary – menses has begun but stops
a.Causes: normal pregnancy and lactation, menopause,
psychogenic (stress), hypothalamic distress, constitutional
(DM, TB, obesity)

III. Metrorrhagia
Bleeding between regular menstrual periods
Common in pill users
Assess for etiology as disease, tumors, etc

IV. Menorrhagia
Excessive bleeding during regular prior “Heavy Menses”
Causes: Endometrial distress, inflammatory disease, and
emotional stress
Management:
oAssess underlying cause
ocorrect hemoglobin deficiency with iron supplement and or
hormonal supplement

V.Oligomenorrhea

Markly diminish menstrual flow – nearing amenorrhea

VI. Polymenorrhea
Frequent menstruation occurring at intervals of <3 weeks
VII. PMS
Pre-menstrual syndrome
Clusters of symptoms that occur just before the menses
and disappear with menstrual flow
E.g. feeling of bloating and fullness of abdomen

4 classes:

1.PMS A
S/S anxiety, irritability, elevated estrogen,
decreased progesterone
RX:
oVit. B6 at 200 – 800 mg/day
oProgesterone therapy
oLimit intake of dairy products
o outdoor exercise
2.PMS B
S/S: water and salt retention = bloating, mastalgia,
weight gain,  aldosterone, B6, Mg, and 
prostaglandin
RX:
 i.Na intake
ii.Vit. E (600 u) reduce breast symptoms
iii. Methyxanthine as coffee, tea, choco, cola, and
nicotine
iv. refined sugar to 5 tbsp/ day
v. prostaglandin inhibitors

3.PMS C
S/S: Premenstrual craving for sweets,  appetite and
food binges, palpitations, fatigue, fainting spells,
headache, shakes, altered GTT,  prostaglandin, Vit.
B, Zinc, Vit. C and Mg
 Rx:
 refined sugar 5 tbsp/ day
 alcohol
 Na 3 grams/ day
 animal fat vegetable oil

4.PMS D
S/S: depression, withdrawn, insomnia, forgetfulness,
confusion, altered estrogen, and progesterone level
B6 and Mg
Rx: Therapy depends on serum evaluation

VIII. DUB

Dysfunctional uterine bleeding or abnormal uterine bleeding;

a significant deviation from client’s usual menstrual flow or
pattern
Normal menses cycle = 21 days
Lasts for: 7 days
Amount: <80 ml/ day

Causes:
1.Organic
2.Psychological

A. Organic
Anovulation
Assessment – history
Lab exams – coagulation studies, CBC, TSH
Rule out other diseases
Endometrial biopsy
Hysterosalpingography
Hysteroscopy, D and C with biopsy
 Rx:
i.Progentin
ii.Clomephine
iii.NSAIDs
iv.D and C
v.Ablation
vi.Hysterectomy if pregnancy is not anymore desired

Infertility and Sterility

Infertility
When pregnancy has not occurred after at least one
year of unprotected coitus

Types:
1.Primary – no previous conception has occurred
2.Secondary – there has been a previous viable pregnancy

Sterility
Some definite factors have been identified to prevent
conception

Male infertility
I. Causes:
1.Inadequate sperm count
NV: 20 – 50 mil/cc of seminal fluid
a.Chornic disease – persistent fever
b.Mumps orchitis
c.Exposure to x-ray
d.Excessive use of alcohol/ drugs
e.Endocrine imbalance
f. Vit. Intake as in Vit. E
g.Surgery on or near the testis
 h.Too frequent intercourse
2.Obstruction of sperm motility secondary to surgery
a.Adhesions, occlusion, congenital stricture of
spermatic ducts

3.changes in seminal fluids due to infection-UTI,STD

4.difficulty with ejaculation

a.anomalies of the penis e.g. hypospadias,
epispadias
b.debilitating diseases may result to impotence and
ejaculation
c.premature ejaculation – affects proper deposition
of sperms
d.psychological problems
e.use of pre-coital lubricants

II. Male fertility studies:

1.History and PE
2.Semen analysis
After 4 days of sexual abstinences, seminal fluid is
examined for numbers, appearance and motility
3.Lab Test
Urinalysis, CBC, blood typing
Testicular biopsy
KAHN and WASSERMANN test
Protein-bound iodine

4.Psychological assessment

III. Treatment:

1.Treat underlying causes as chronic diseases

2.In  sperm count >abstain 7-10 days at a time
3.In mumps orchitis > artificial insemination
Female infertility
A. Causes:
I. Anovulation
Most serious and most difficult to correct
Causes:
oPituitary or thyroid disturbance
oImmaturity or disease of ovaries e.g.
endometriosis
oChronic or excessive exposure to x-rays or
radioactive substances

II. Tests for ovulation

1.Basal Body temperature (BBT)
Progesterone causes body temperature to  a
day after ovulation
2.Spinnbarkheit test
 quantity and pH of cervical mucus during
ovulation; thin and watery, it can be stretched
to a distance of 10 – 13 cm
3.Fern test
levels of estrogen just before ovulation
mucus forms fern-like pattern when smeared
and dried or glass slide (arbonization) when
progesterone  no fern-like pattern
4.Uterine endometrial biopsy
5.culdoscopy
6.Laparoscopy
7.Hysteroscopy

B. Tubal Factors

I. Causes:
 1.Chronic salphingitis – PID, GC
2.ruptured AP – abdominal surgery with infection or
adhesion
3.congenital webbing or stricture

II. Test for tubal patency:

1.Rubin’s test – procedure
3rd day after menses, patient in lithotomy
position is given (100 mmHg) CO2 under
pressure instilled into cervix passes uterus
and fallopian tubes into pelvic cavity

if tubes are patent if another 200mmHg CO2

administation; no sound on auscultation; no
C/O of pain in one or both shoulders =
occlusion is present
both diagnositic and therapeutic test

2.Uterosalpingography

C. Uterine factors
I. Causes:
1.Tumors
Blocks tubes or limit space for implantation
e.g. leiomyomas
RX:
oMyomectomy
oCongenital deformity “infantile uterus”
oInadequate endometrium formation - 
estrogen and progesterone level
D. Cervical factors:
I. Causes:
1.Infection
2.tight cervical os
 II. Tests for cervical environment
1. Sims – Huhner test - procedure
ovulation time determination by BBT
couple do intercourse with ovulation without
pre-coital lubricant
after intercourse woman lies on her back for
30 minutes
no post-coital douches/ washing
within 2-8 hours doctors examine the cervical
mucus for ferning and spinnbarkheit and for
viable sperms including count

E. Vaginal Factor

I. Cause:
1.Infection
II. Test for vaginal environment
1.History of menstruation and PE
2.Lab tests
3.psycho assessment - R/O dyspareunia

III. Management:
1.Sodium bicarbonate douche for very acidic
environment
2.treat infection and other underlying cause
3.surgery for tumors
4.endocrine therapy e.g. clomid – HCG
Condition in the Female Reproductive System

I. Myomas
Circumscribed growth encapsulated
Other name: fibromyomas, fibroma, fibroids, leiomyomas
Benign tumors
Composed mainly of smooth muscles with some fibrous
connective tissue

Classifications (location):

1.Intramural
Uterine walls; surrounded by myometrium
Clinical manifestation:  uterus size, vaginal
bleeding between periods, and dysmenorrhea

2.subserous
Directly beneath (under) the serosa; penduculated;
to wander; to multiply and enlarge
Clinical manifestation: backache, constipation,
bladder problems

3.parasitic or wandering
pedunculated tumor attached to other tissues

4.intraligamentum
subserous tumor into the broad ligaments; implant
on pelvic ligament; displace uterus

5.submucous
 beneath the endometrium; they grow thin and
displace endometrium over their surface and
become the site of necrosis and infection

6.cervical
rare
7.sarcomatous (malignant)
rapidly enlarging and hemorrhagic
Clinical Manifestation: necrosis, ulceration, foul
smelling vaginal discharges

Secondary changes (degeneration)

1.Hyalinization
When tumor outgrows BS
Clinical manifestation: Mature or old myoma are
white containing soft gelatinous area of hyaline
change - asymptomatic
2.Cystic
Follows hyalinization; tumor liquefies
3.Calcification
Common in larger tumor
4.Fatty
Follow hyaline and cystic
5.infectious
appears with PID; common in pedunculated,
submucous tumors
6.carneous
red, associated with hemorrhage into tumor and
hemorrhage

Rx/ Management:
depend on symptoms, age, location, and size of
the tumor; onset of complication and desire to get
pregnant
 fibroid – D and C
small tumor – myomectomy (removal of tumor
without removal of the uterus)

large tumor – hysterectomy (removal of entire

utero)  tumor/ uterus hysteromyomectomy
radiation and chemotherapy

Nursing Care:
1.Full explanation – removal of uterus – menses,
pregnancy, sexual activity
2.Reassurance
3.surgery – pre and post op care

II. Endometriosis
chocolate cysts
abnormal growth of extra-uterine endometrial cells;
after in the cul-de-sac of the peritoneal cavity, uterine
ligaments and ovaries
excessive endometrial cells production plus reflex of
blood during menses

Incidence:
multi-parous
familial tendency

Clinical manifestation: based on location e.g lungs – S/S

grave and serious

1.uterine displacement – nodules at cul-de-Sac

2.dyspareunia – lesions at uterosacral ligaments and
posterior fornix of vagina
3.dysmenorrheal – incapacitating pain on defecation
4.infertility
5.“Chocolate cyst” in uterine surface
 6.abnormal uterine bleeding

Rx:
1.Estrogen/ progesterone – based oral contraception
2.Danazol – synthetic androgen – shrinks abnormal
tissues
3.laparotomy with excision by laser surgery
4.salpingo-oophorectomy
5.hysterectomy

III. Polyps
pedunculated tumors from the mucosa and
extending into the opening of a body cavity

Types:
1.Uterine
a.Hypermenorrhea
b.Metrorrhagia
c.DUB
2.Cervical
Bleeding following vaginal sexual activity and may
become infected

Rx:
Surgical excision – polypectomy

Nursing Care:
1.Secure Consent
2.Explain every procedure
3.follow up care and check up
4.surgery – pre – op and post – op care

IV. Ovarian Cysts

 are non-neoplastic tumors of the ovaries

Clinical manifestation:
may or may not be present = but is symptoms occur
i.pelvic pains – often one sided
ii.pressure in the lower abdomen
iii.backache and menstrual irregularities
Rx:
surgical excision of the cysts

Nursing care:
1.Explain procedure
2.observe for S/S of tumor growth
3.follow up care

V. Fistulas
Abnormal tube like passages within body tissues
Abnormal tortuous opening between two internal
hallow organs or between an internal hallow organ
and the exterior of the body/skin.

Types:
1.Ureterovaginal – between ureter and vagina
2.vesicovaginal – between urinary bladder and vagina
3.rectovaginal – between rectum and vagina

Causes:
1.Obstetrical injury
2.pelvic surgery (hysterectomy and vaginal reconstructive
surgery – common)
3.extension of carcinoma or complication of treatment
for CA
Clinical manifestation:
1.Trickling of urine into vagina

2.Fecal incontinence and flatus passed thru vagina and

malodorous
3.Irritation and excoriation of vulvar tissues

Diagnostic:
1.Methylene Blue test
Dye test
Dye is instilled into bladder
Dye in vagina – vesicovaginal fistula
None in ureteovaginal fistula
2.Indigo Carmine test
Injected IV
Appears in vagina is ureterovaginal fistula
3.IVP – for location of fistula
4.Cystoscopy
Determine numbers and locations of fistulas

Treament:
A. If to heal without surgery (rare)
1.maintain cleanliness - sitz bath; deodorant douches/
wash
2.use of perineal pads; plastic or rubber pants
3.prevent excoriations – use of bland creams dust of
cornstarch – sooths
4.use of feminine morale boosters as: attractive hairdo,
nail polish; perfumes new beaded jacket; latest fashion,
etc
B. Surgery
fistulotomy/ fistulectomy
diagnosed early – time of delivery to be repaired
immediately
 post-op heals 2 – 3 months for inflammation to
subside
maintain adequate nutrition,  vitamins, and
protein
administer chemotherapeutic agents
done in healthy tissues
post-menopausal – oral estrogen  for healthier
viable tissues
perineal hygiene

Post-op
Recto-vaginal:
1.limit bowel activity – clear liquids for few days and diet
resolve gradually
2.warm perineal irrigations, heat lamp treatments
3.bedrest

Vesicovaginal:
1.proper bladder drainage – FBC – I and O
2.Gentleness in administration of bladder and bowel
irrigations

Sexually Transmitted Diseases

I. Trichomoniasis

Etiology:
Trichomona Vaginalis – single cell protozoa (round
mobile structure)

S/S:
1.Frothy white to grayish green vaginal discharge
2.vaginal irritation, redness, and pinpoint petichiae
3.extreme vaginal itching
 4.dyspareunia
5. vaginal pH
6.males – asymptomatic

Diagnositic Test:
scrapping of vaginal discharge with drops of
Ringer’s Solution

Rx:
1.Metronidazole (Flagyl) single 2 gm dose p.o (given to
both woman and sex partner
Note: Should not be administered during 1st trimester of
pregnancy and must be used with caution for the
remaining of pregnancy (teratogenic); should not be taken
with alcohol = causes acute nausea and vomiting
2.Topical – povidone-iodine or vinegar douche only to
reduce symptoms until metronidazole can be used

Nursing Interventions:
1.Advise client to abstain from coitus; male sex partner
may use condom
2.Advise woman to use tampons to absorb discharges and
 comfort
3.Emphasize importance of perineal hygiene

II. Moniliasis
May affect skin, mucous membranes as in GIT,
mouth, vagina, anus, fingernails, and body folds –
groins, neck, axillae

Common in:
Obese people, perspires profusely, DM, Pregnancy,
using oral contraceptives pills, pseudopregnancy
 state, antibiotic and steroids users.

Etiology: Candida Albicans

S/S:
1.cheesy, white non-odorous vaginal discharge
2.vaginal and vulvar itching
3.red, beefy appearance of affected areas dyspareunia
4.causes thrush in newborn

Diagnostic:
scrapping of vaginal discharge with 3:4 gtts of 20%
(KOH) potassium hydroxide

Rx:
1.Rx 4 to 6 months
2. apply Gentium Violet 1% for relief of pruritus (stains
underwear permanently)
3. Nystatin (mycostatin) drug of choice –
4. male partner to be treated as well

Nursing Care:
1.Antibiotic by mouth should be stopped
2.rule out DM and treat properly
3.weight reduction for obese people
4.avoid coitus during infection or use condom during
treatment period

III. Herpes Genitalis

spreads by skin to skin contact and virus enters thru
a break in the skin or mucous membranes
highly contagious
incubation period – 3 – 14 days
Etiology:
Herpes Virus Hominis II
>HVH – 2 – genital virus (not airborn – not by fomites)
>HVH – 1 – non-genital forms – oral skin but it is possible
for each virus to cross infects
S/S:
1.Vesicular lesion on cervix, vagina, vulva, penis
2.systemic symptoms as headache, malaise,  grade fever
3.dysuria
4.pain in intense upon contact with clothing

Diagnostic:

1.History and clinical evaluation

2.isolation of virus in tissue culture (most accurate)
3.scrapping for pap smear or Tzanck smear

Rx:
Analgesics for pain – aspirin
 Anti-virals = Acyclovir (Zovirax) do not cure only alleviate
symptoms and reduce spread of virus

Nursing Care:
1.abstinences – condoms and spermicide less effective
2.keep lesion – clean and dry
3.culture virus during pregnancy to safeguard fetus – 50%
of newborn will be infected during delivery
4.when to abstain:
a.presence of fresh lesions
b.last 4 – 6 weeks of pregnancy if partner has HIV 1

IV. Syphilis

Etiology: Spirochette Treponema Pallidium

Transmission:
 Sexual contact/ congenital  moves thru skin and
mucous membrane and into the bloodstream and destroy
tissues in an organ in the body

Stages:
I. Incubation Period
Characteristics:
1.10 – 90 days – average 21 – days
2.no S/S or lesion
3.presence of etiology agent – blood is infective

II. Primary (early) syphilis

Characteristics:
1.Most infectious stage; lasting 1 – 6 weeks
2.S/S:
a.Chancre or primary sore painless ulcer appears 1 st
in site of entry of the organism (genitalia, anorectal,
lips, oral cavity, fingers)
b.Chancre erodes and heals 4 – 6 weeks leaves a scar
or none at all
c.Inguinal lymph nodes enlarges
d.Presence of indolent, painless ulceration in any part
of the body suspect

III. Secondary syphilis

Characteristics:
1.follows onset of chancre – 9 – 90 days
2.influenza like symptom and rashes ulcerations;
Condylomata – moist papules on cell site – highly
infectious
3.general patchy hair loss on scalp
4.acute iritis (inflammation of iris)
5.hoarseness, chronic sore throat
IV. Late Syphilis
Characteristics:
10 – 30 days
granulomata – lesions on skin, bones, liver, CVS (heart,
and CNS (brain)

Contact syphilis Chancre Condylomata

+ granulomata = RIP

Diagnostic:
Serologic test – VDRL
oNon-treponemal or Reagin Test – detect antibiotic
like substance
oTreponemal test – measure specific antibiotics to TP

Rx: Pen G benzathine – DOC

Nursing Care:
1.Isolation of infected materials
2.case follow-up
3.advise patient to refrain from sexual contact with
untreated previous partner

V. Gonorrhea
Etiology: Gonococcus Neisseria Gonorrea
Transmission: Sexual contact/ direct contact with discharge

S/S:

Women
1.Heavy green – purulent discharges, abnormal uterine
bleeding; abnormal menses
2.urinary frequency, pain and burning
3.ascending infection (PID)
Men
1.purulent discharge following painful urination, urethritis,
prostatitis, epididymitis (pain-burning)
2.pelvic pain and fever
Pharyngeal gonorrhea
1.Sore throat; maybe asymptomatic

Anorectal gonorrhea
1.anal-rectal burning, itching, and bleeding mucopurulent
discharge, painful defecation

Adult gonococcal conjunctivitis

1.Transmitted to eyes by fingers
Diagnostic:
1.gram stains smear, culture
2.direct fluorescent antibody test

Goal of care:
1.eradicate organism
2.educate patient about his condition
Treatment:
Tetracycline, Amoxicillin with Probenecid and
Penicillin with Probenecid
Nursing Care: Careful Hand washing

Fetal Outcome:
Opthalmia Neonatorum  Crede’s Prophylaxis –
used after delivery ( Terramycin Opthalmic Ointment
to both eyes )

Uterine displacements

Normal Uterus:
 Flexes anteriorly at 45O and movable; cervix points
downward and posterior
More inclined towards the bladder
25% of women – retroversion – still normal
to such number of women body lies back in the
posterior cul-de-sac and rectum; non-pathological
Types:
I. Upward displacement
Lifted forward; becomes on abdominal organ;
internal os is at level of upper border of symphysis
pubis and can’t be reached by examiner’s finger

S/S:
Asymptomatic but at times: backache during menses
and/ or prolonged standing
Secondary to amenorrhea, infertility, feeling of pelvic
pressure, dyspareunia (congestion and adhesion 
immobile uterus)

Treatment:
1. treat underlying cause
2.Insertion of vaginal pessary (infrequently used – irritates
and erodes cervical and vaginal mucosa)
Holds the uterus in normal position
Comes in different sizes and style

Nursing care: (Pessary)

1.Be sure it is properly in place
2.douche with weak vinegar solution 2x/ week – remove
vaginal debris
3.Pessary to be checked and removed ad cleansed every
3-4 months. Teach woman on how to do it by herself
4.make woman understand the needs for frequent check-
ups
Causes:
Vaginal/ paravaginal tumor
low cervical fibroid
tumor at Cul-de-Sac
collection of pus at pelvis

II. Lateral displacement

lateral deviation; tilting to one side

Causes:
unilateral tumor
fluid collection
pull to one side due to adhesions
Treatment:
treat underlying cause

III. Forward displacement

anterior; towards the front

Anteflexion – fundus bend forward

Anteversion – whole of uterus bend forward

IV. Backward displacement

posterior; towards the back

Retroposition (corrected by knee-chest position) or

retroversion – backward direction of whole uterus
Retroflexion – fundus bend forward

II.Downward
Or prolapse (protrusion of uterus to vagina) or descent or
procidentia (protrusion of uterus to or beyond introitus)

Causes:
Obstetrical trauma
 Multiple childbirths
Aging leads to overstretching of musculofascial support
Prolong standing
Straining
Coughing
Lifting heavy objects
Clinical manifestation:

1.Awareness of “something is coming down there”

2.dyspareunia
3.feeling of pressure, heaviness, backache
4.bladder/ bowel problems cystocele/ rectocele
5.stress incontinence

Management: Hysterectomy

Degrees of Uterus prolapse:

1st degree
Uterus descends at vaginal canal; cervix reaches but
does not go through the introitus

2nd degree
Body of uterus still in the vagina; cervix protrudes
through the introitus

3rd degree
Entire uterus and cervix protrude through the introitus;
vaginal canal is inverted (turned inside out)

Cystocele
Protrusion of urinary bladder through vaginal wall due to
weakened pelvic muscle
S/S:
Stress/ urinary incontinences; UTI
Management:
1.Kegel’s exercise – pubococcygeal muscle control 50 –
100 times/ day or BID
2.Anterior Colporrhapy or anterior repair (Care as in
Hysterectomy)

Rectocele
Protrusion of rectum

S/S: Constipation, heaviness, hemorrhoids

Management:
1.Posterior colporrhapy
Bowel preparation prior to surgery

Hormone Replacement Therapy

Also called: ERT, Estrogen replacement therapy, HRT,

Menopausal hormone therapy

Menopause is the time in a woman's life when her period stops.

It is a normal part of aging. In the years before and during
menopause, the levels of female hormones can go up and
down.

This can cause symptoms such as hot flashes and vaginal

dryness. Some women take hormone replacement therapy
(HRT) to relieve these symptoms.

HRT may also protect against osteoporosis.

However, HRT also has risks. It can increase your risk of

breast cancer, heart disease and stroke. Certain types of HRT
have a higher risk, and each woman's own risks can vary
depending upon her health history and lifestyle.
 You and your health care provider need to discuss the risks
and benefits for you. If you do decide to take HRT, it should
be the lowest dose that helps and for the shortest time
needed. Taking hormones should be re-evaluated every six
months.

What is Endometriosis?
Endometriosis is a
disease that affects
females in their
reproductive years.
It is a painful,
chronic disease that
affects more than 5
1/2 million women
and girls in the
USA, and millions
more worldwide.
The endometrium is
the tissue that lines
the inside of the uterus, which builds up and sheds each
month in the menstrual cycle. With Endometriosis this tissue
is found in locations outside of the uterus, and develops into
nodules, lesions, tumors, growths, or implants.
This misplaced tissue develops into growths or lesions which
respond to the menstrual cycle in the same way that the
tissue of the uterine lining does: each month the tissue
builds up, breaks down, and sheds. Menstrual blood flows
from the uterus and out of the body through the vagina, but
the blood and tissue shed from endometrial growths has no
way of leaving the body. This results in internal bleeding,
breakdown of the blood and tissue from the lesions, and
inflammation - and can cause pain, infertility, scar tissue
formation, adhesions, and bowel problems.

These endometrial growths are commonly found -

 in the abdomen
  on the ovaries,

 uterine tubes (called fallopian tubes in the past),

 and ligaments that support the uterus;

 the area between the vagina and rectum;

 the outer surface of the uterus;

 and the lining of the pelvic cavity.

 Other sites for these endometrial growths may include

the bladder, bowel, vagina, cervix, vulva, and in
abdominal surgical scars.

 Less commonly they are found in the lung, arm, thigh,

and other locations.

Infertility affects more than 40% of endometriosis

infected women, and is a common result with the
progression of the disease.
What are the most common Symptoms of
Endometriosis?
 Pain before and during periods

 Heavy or irregular bleeding

 Pain during and after sex

 Lower back pain

 Infertility

 Fatigue

 Painful urination during periods

 Painful bowel movements during periods

  Other Gastrointestinal upsets such as diarrhoea,
constipation, nausea.

In addition, many women with endometriosis suffer

from:

 Allergies
 Chemical sensitivities

 Frequent yeast infections

Some women also have the following problems:

 memory loss
 speech or vision problems

 numbness or tingling in their limbs

 bone & joint pain

 migraines and various other problems.

Conventionally, the diagnosis of endometriosis is considered

uncertain until proven by laparoscopy, a minor surgical
procedure done under anesthesia. A laparoscopy usually
shows the location, size, and extent of the growths.
What Causes Endometriosis?
The cause of endometriosis is unknown.

 The retrograde menstruation theory (transtubal

migration theory) suggests that during menstruation
some of the menstrual tissue backs up through the
fallopian tubes, implants in the abdomen, and grows.
Some experts believe that all women experience some
menstrual tissue backup and that an immune system
problem or a hormonal problem allows this tissue to
grow in the women who develop endometriosis.
  Another theory suggests that endometrial tissue is
distributed from the uterus to other parts of the body
through the lymph system or through the blood system.

 A genetic theory suggests that it may be carried in the

genes in certain families or that some families may have
predisposing factors to endometriosis.

 Surgical transplantation has also been cited in many

cases where endometriosis is found in abdominal scars,
although it has also been found in such scars when
accidental implantation seems unlikely.

 Another theory suggests that remnants of tissue from

when the woman was an embryo may later develop into
endometriosis, or that some adult tissues retain the
ability they had in the embryo stage to transform
reproductive tissue in certain circumstances.

 Research by the Endometriosis Association revealed a

startling link between dioxin (TCCD) exposure and the
development of endometriosis. Dioxin is a toxic
chemical byproduct of pesticide manufacturing,
bleached pulp and paper products, and medical and
municipal waste incineration. It is commonly found in
Tampons. The EA discovered a colony of rhesus
monkeys that had developed endometriosis after
exposure to dioxin. 79% of the monkeys exposed to
dioxin developed endometriosis, and, in addition, the
more dioxin exposure, the more severe the endo.

Is My Pain Due To Endometriosis?

Some women have pain all the time, while others may only
have pain before or during their period. Some women have
no symptoms, and the amount of pain is not necessarily
related to the extent or size of the growths.

As good as laparoscopic electrosurgical excision of

endometriosis is for temporary relief of pain, it will not treat
pain caused by other things. Pain due to endometriosis is
often described in very specific geographical or anatomical
terms and is associated with specific points of tenderness on
exam. These patients have the best results. If a patient
cannot describe her pain accurately, or if pelvic examination
does not reproduce the pain, excision of endometriosis may
not provide any pain relief at all.

Other causes of pelvic pain can include non-endometriotic

ovarian cysts, fibroid tumors, adhesions, adenomyosis, and
other unknown factors. For this reason, there is no way to
guarantee pain relief after endometriosis surgery.
Cysts:
The word "cyst" means a fluid-filled cavity, usually with a
lining. Cysts can occur in the normal monthly functioning of
the ovary. Two common types of "normal" cysts are follicular
cysts, which prepare the egg, and the corpus luteum cyst,
which forms after ovulation each month. Although these two
types of cysts are usually temporary, each may persist
longer than they should and can cause pain.

In practice we have found a dramatic rise in incidence of

ovarian cysts over the past few years. Almost three out of
every five woman that consult me today suffer from some
measure of ovarian cysts. This could be ascribed to the
massive exposure to hormones from our food, especially
meat (especially beef and chicken), from our drinking water
in the form of pseudo-estrogens, the same with beverages in
plastic bottles and also from the pseudo-estrogens contained
in the packings of cosmetics. Homoeopathy is one of the very
few disciplines that can successfully treat cysts by medicinal
means.

Cysts don't always have to be large to cause pain. Several

small cysts can occur within an ovary and cause pain by
stretching the ovary slightly. If scar tissue is on the ovary, a
cyst can expand and pull on the scar tissue and cause pain. A
medium-sized cyst can twist on its pedicle, and this can
cause pain. Other types of abnormal cysts include
endometriotic and dermoid cysts. Some patients can have
very large cysts and no pain at all.

When they cause pain, ovarian cysts usually cause pain off
on one side or the other, and the pain can radiate slightly
around the flank. A cyst which is bleeding or leaking some
irritative fluid can cause generalized pelvic and lower
abdominal pain which may seem to spread from the affected
side. Some women can have recurrent ovarian cysts after
spontaneous resolution of, or surgical removal of a cyst,
since each of some 200,000 oocytes (eggs) in each ovary at
birth is surrounded by a small follicle or potential cyst.

Fibroid tumors:
Fibroids (also called "leiomyoma") are accumulations of
smooth muscle which arise within the uterine muscular wall.
They expand in size somewhat concentrically, like a pearl
growing in an oyster. A large fibroid would be the size of a
grapefruit or larger. A small fibroid would be smaller than a
marble. They can cause uterine cramping between menstrual
flows and severe cramping and heavy bleeding with the flow,
unless they are hanging off the outside surface of the uterus,
in which case symptoms may be absent.

Fibroids sometimes cause difficulties with bowel or bladder

function since they can press against the bladder or bowel if
they get big enough. Low back pain can sometimes occur,
since the fibroid can press against the tailbone (sacrum) and
since the uterosacral ligaments can transmit uterine pain to
the sacrum as well. GnRh agonists can produce a dramatic,
but temporary reduction in the size of fibroids. Although
fibroids can be removed surgically, some fibroids that might
be too small to be seen or felt at surgery can remain in the
uterus to grow and cause problems later. Accounts of
successful treatment of fibroids with homoeopathy is too
numerous to mention here.

Adhesions (scar tissue):

Adhesions (also called scar tissue) stick things together.
They can be thin and wispy like wet tissue paper or dense
and thick like hardened glue. An adhesion goes from one
point in the pelvis to another point, although this distance
may be functionally non-existent, as when an ovary becomes
plastered to the side of the pelvis. Adhesions form after
injury to the peritoneum, whether by infection, surgery, or
chronic inflammation. The peritoneum is the Saran wrap-like
lining of the pelvic and abdominal cavities.
Occasionally, adhesions can form without apparent reason.
The tendency to form adhesions varies among patients,
which is not surprising since people are different. Why some
people form fewer adhesions than others with the same type
of surgery is not known. Some adhesions cause pain, others
do not. Some patients with extensive adhesions have no
pain, whereas one small, well-placed adhesion can kink a
loop of bowel and cause bowel obstruction.

When adhesions hurt, they hurt in the place they occur.

Patients sometimes use terms such as "pulling" or
"stretching" to describe adhesion pain. Adhesion pain would
not be expected to vary with the menstrual cycle unless
adhesions around an ovary get stretched by the slight
growth of a cyst. Many patients with endometriosis have
adhesions as well, and it is often not possible to determine
whether their pain is due to adhesions or endometriosis.

Falling Over of the Womb.

Anteversion. The womb sometimes falls over forward upon the bladder, towards the pubes.
This is called anteversion. The top is turned forward to the bladder; the mouth, back
towards the large bowel. (Fig. 141, b.)
Retroversion. When the womb falls over backward, between the rectum and the vagina, it
is said to be retroverted (d). This is just the opposite of being anteverted. In this
displacement, the mouth is turned forward, the top backward.
This displacement may occur suddenly or gradually. If the former, there is generally great
distress, and the organ should be immediately put back in its place; if the latter, the pain
will be less intense, and the replacement must be effected by pessaries, particularly with the
ring pessary, made of India rubber.
Anteflexion and Retroflexion. When these occur, the womb is doubled upon itself, the
mouth of the organ not being tilted up before or behind, but retaining its natural position.
These flexions are rep. resented by a, c, and e.
Besides these more common displacements of the womb, there are several slighter
deviations which it is scarcely necessary to describe. There is the obliquity of the womb,
which is simply a leaning of the organ backward or forward, or to one side.
There are still other more serious troubles, which are so very rare as not to require me to
dwell upon them, such as the inversion of the womb, or turning it wrong side out, like the
finger of a glove; and the hernia of the womb (hysterocele), which is like that of the bowel.

Pessaries. Much might be said about pessaries: they axe at times of the greatest assistance
in keeping a badly placed uterus in its proper position ; on the other hand, they are serious
hindrances to health. By their pressure they often cause inflammation of the ovaries and
tubes and light up afresh old, quiescent chronic inflammations. They often stretch unduly
the uterine ligaments and make a relaxed vagina. But it must be said that often, too, they
keep in place a simply misplaced womb with no trouble and little expense to the wearer,
thus avoiding long treatment and perhaps an operation. They should always fit accurately
and nicely and should never cause pain or make the wearer conscious that she wears such a
thing. The soft rubber variety, or at least those made of wire and covered with rubber, are
the least likely to cause trouble; but they need, on the other hand, more frequent inspection
and cleansing. The hard rubber are more easily kept clean, but are more dangerous.
Whenever a pessary is worn, it should be under the surveillance of the family doctor, lest
ulceration of the vagina and undue pressure on the internal parts ensue. Pessaries no doubt
are very useful in keeping in place a womb that has been replaced and in warding off an
operation otherwise indicated. They are of all shapes and designs, so that a description of
them seems superfluous here.

Displacements. The various displacements of the womb are such common occurrences
among womankind that they have always received considerable attention by the
gynecologist. They result from falls in young girls, from enlargement of the organ, from
weak uterine supports and poor health, from torn muscles of the vagina during labor, and
from new growths in the womb.
The symptoms of a misplaced womb are from nothing to an amazing amount of trouble.
Many a woman goes through life with a badly torn vaginal floor and retroflexed womb
without the slightest ill effect, while her neighbor suffer intensely from a much low degree
of displacement.

Operative Treatment. When for any reason a pessary cannot or ought not to be worn, and
there is much inconvenience from the misplacement, resort must be had to packing the
vagina and reducing the size of the womb, and allaying inflammation and pain before again
trying a pessary, or else some of the several operations must be performed. Of these latter
there are at the present day three principal methods in vogue, viz.:
Alexander's operation consists in cutting down on the little holes in. the lower abdomen,
near the pubic bones, called the hernial rings, through which in the male the cord and
vessels of the testes run, where hernia or rupture occurs, and through which in the female
the the round ligament of the womb runs. This ligament is a small round cord attached to
the anterior and top part of the uterus, acting as a stay. This ligament is dissected out and
pulled up taut on either side (there are two, one on each side of the womb) till the womb is
brought up into its normal position and there fastened. This operation is a very ingenious
one, and answers well in simple uncomplicated cases.
Ventral Fixation is a second method of fastening the womb in place, and consists in opening
the abdomen, lifting up the womb and fastening it to the under side of the abdominal wall.
This method is tolerably free from danger, like the preceding, but has the advantage of
parting adhesions which may bind down the uterus and prevent its rising, and of
permitting the operator to see and correct any existing disease of the tubes and ovaries
which so commonly accompany bad cases.
Vaginal Fixation is a third method, whereby the uterus is likewise fixed, but this time to the
vagina in front of the bladder. This last method is at present receiving considerable
attention; but it may be said that no one method is the best for all cases, the surgeon being
the best judge of the situation. These operations are safe and efficient, and forever do away
with pessaries and the existing disease. Women go on to term in labor quite generally after
these operations.

Absolute

 Hemodynamically significant heart disease

 Restrictive lung disease
 Incompetent cervix
 Multiple gestation at risk for premature labor
 Persistent second or third trimester bleeding
 Placenta previa after 26 weeks of gestation
 Premature labor during the current pregnancy
 Ruptured membranes
 Pre-eclampsia/pregnancy-induced hypertension
 Relative

 Severe anemia
 Unevaluated maternal cardiac arrhythmia
 Chronic bronchitis
 Poorly controlled type 1 diabetes

 Extreme morbid obesity

 Extreme underweight (BMI<12)
 History of extremely sedentary lifestyle
 Intrauterine growth restriction in current pregnancy
 Poorly controlled hypertension
 Orthopedic limitations
 Poorly controlled seizure disorder
 Poorly controlled hyperthyroidism
 Heavy smoker
 Third trimester breech presentation
 Multiple pregnancy (>twins)

Reason to terminate exercise

 Vaginal bleeding
 Dyspnea prior to exertion
 Dizziness or faintness
  Headache or visual disturbance
 Unexplained abdominal pain
 Muscle weakness
 Swelling of ankles, hands, or face
 Swelling, pain, and redness in the calf of one leg
 Preterm labor, persistent contractions (> 6-8/h)
 Decreased fetal movement
 Amniotic fluid leakage
 Elevated pulse or blood pressure persisting after exercise
 Fatigue, palpitations, chest pain
 Insufficient weight gain(<1.0kg/month during last two trimesters)

(ACOG, 2002; ACOG, 2003; Davies et al., 2003; Paisley, 2003)