II.

NURSING CARE OF THE HIGH RISK PREGNANT CLIENT

High Risk Pregnancy- is one in which a concurrent disorder,

pregnancy-related complication or external
factors jeopardizes the health of the mother, the fetus or
both.
-is a condition in which some maternal factors or fetal factors
either psychosocial or physiologic is apt to result in the birth
of a high-risk infant or in some way the woman herself.
High Risk Infant – is one who is born with less ability or change
to survive or a greater chance to be left with a permanent
handicap, either psychological or physiological than the
average child.
When is the proper time
we start and end our
assessment of clients at
high risk?
-Assessment of clients at
risk begins with the 1 st

prenatal visit & continues

through puerperium.
 
When is the first
prenatal visit?
First pre-natal visit-1
week after the first
missed menstrual
period
What do you mean
by puerperium?
Puerperium – period of up to 6
weeks after childbirth during
which the size of the uterus
decreases to normal ( in other
book by Wong , 30 days after
birth)
why is it that we
must assess client
at risk?
 

-togive appropriate and timely

intervention hence prevent
morbidity and mortality among
mothers and infant .
Why is it that we must
assess from the
prenatal to
puerperium?
-to recognize & manage early the problem
hence there is a good perinatal outcomes
and perinatal morbidity may continue for
months or years. (postbirth maternal
complications usually are resolved with in 1
month of birth)
mortality- the incidence of death in the population in a given
period

morbidity – the state of being diseased

3 leading causes of maternal death attributed to pregnancy

( it may differ throughout the world)
1.Hypertensive disorder
2..Infection
3. hemorrhage
 
 
 
Factors that are strongly related to maternal death
1. age , younger than 20 & 35 years older
2. lack of prenatal care
3. low educational attainment
4. unmarried status
5. nonwhite race
 
leading causes of death in the neonatal period
1. congenital anomalies
2. disorder relating to short gestation & LBW
3. respiratory distress syndrome
4. effects of maternal complications
 Universal Risk Factors
( this could be the basis for assessing the high risk pregnancy)

1.Age
= 18 years old below or above 35 years old ( maternal
mortality is high)
=teenager ( LBW infant)
=adolescents (increase high risk for psychosocial & physical
complication- anemia, preeclampsia,prolonged labor,
contracted pelvis, cephalopelvic disproportion)
= advanced age ( placenta previa, LBW, abruption placenta,
hypertension, toxemia, uterine inertia, chromosomal
abnormalities, varicosities, hemorrhoid)
2.Parity – a term used to indicate the number of pregnancy a
woman has had that have each resulted in the birth of an
infant capable of survival. ( associated with age)

=first pregnancy (high risk)- incidence of preeclamia &

dystocia is higher
= risk increase in para..2,3,4,5.. especially if age 40 above
 
3.civil status/cultural group
( unwed mother, single parent, belong to cultural minority,
poverty)
= perinatal mortality is high
 
4.Nutritional state
= underweight/malnourish ( deliver early, pre eclampsia,
eclampsia, LBW, impaired NS
=adverse effect on fertility – embyonesis, fetal growth
= women below 20 lbs. – malnourish fetus
Increase 30 lbs. – diabetes mellitus, toxemia,
polyhydramios, H mole, multiple pregnancy

5.birth interval ( short birth interval (pregnancy after 3

months of previous pregnancy )
= increase frequency of LBW
= increase 4 years interval- hazardous
 
6.Antenatal care/prenatal care
=increase perinatal morbidity & mortality due to lack of knowledge,
complications cannot be detected, treated & prevented

7.Course of labor
= induced/precipitated/prolonged
Mother= ruptured uterus, hemorrhage, infection
Fetus = premature, infection, hypoxia, injury to CNS
 
8.Type of delivery
= operative delivery – risk complications to both ( baby develops
respiratory distress, NS abnormality)
=urgent operative measures ( offspring immature, severely distressed)
 
9.Anesthesia (poorly chosen)
Fetus= Apnea (temp.cessation of breathing) vascular collapse,
bradycardia(slowing of heart rate to less than 50bpm),
convulsions
Mother = hypotension, decrease uterine blood flow, infection,
faintness
 
10.Past pregnancy outcomes
= Hx 0f abortion (possibility of another)
= other pregnancy outcomes which incur greater risk in
subsequent pregnancies such as;
-2 previous premature labor, post maturity, still birth, congenital
anomaly, 2 excessively large infant, infant with genetic/familial
disorders, Hx with birth damage infant or special neonatal infant
care, ABO compatability, poor fetal malpresentation, multiple
pregnancy.
11. deviation from normal anatomy ( cervix, uterus, pelvis)
=abortion, premature, ectopic pregnancy, breech, transverse
lie, hemorrhage
 
12.Malignancy/myomas
= interfere with reproductive organ function & jeopardize
fetal well being
 
13.Pregnancy with pre-existing conditions
= risk for perinatal morbidity & mortality increases.
 
 
 
RISK FACTORS INCLUDES PSYCHOLOGICAL,SOCIODEMOGRAPHIC
/ENVIRONMENTAL ,PHYSIOLOGICAL
(factors that categorize a pregnancy as high risk) Page 348 by pillitteri
(MCHN)
 Pre-pregnancy
 Psychological sociodemographic
1.Hx of drug dependence including alcohol 1.occupation involving handling of
toxic substances
2.Hx of intimate partner abuse2.environmental contaminants at home
3.Hx of mental illness 3. isolated
4.Hx of poor coping mechanism 4. Lower economic level
5.Cognitivelly challenged 5. Poor access to transportation for care
6.Survivor of childhood sexual abuse 6. High altitude
7.poor housing
8. lack of support people
Physiological
1.Visual or hearing challenges
2.Pelvic inadequacy or misshape
3.Uterine incompetency, position or structure
4.Secondary major illness (heart disease, DM, kidney D., Hpn, chronic infaction such as
tuberculosis, hemopoetic or blood disorder, malignancy)
5.Poor gynecologic or obstetric Hx
6.Hx of child with congenital anomalies
7.Obesity
8.Pelvic inflammatory D.
9.Hx of inherited disorder
10.Small stature
11.Potential of blood incompatability
12.Younger than 18 years of age or older than 35 years old
13.Cigarette smoker (decreased birth weight)
14.Substance abuser ( teratogenic, cause metabolic disorder, alteration of CNS)
15.Drinks liquor ( fetal alcohol syndrome, fetal alcohol effects, learning disability,
hyperactivity)
Pregnancy
 
Psychological Sociodemographic
1.loss of support person1. Refusal or neglected prenatal care
2.illness of a family member 2. Exposure to environmental
teratogens
3.decrease self-esteem 3. Disruptive family accident
4.drug abuse (alcohol) 4. Decreased economic support
5. Conception less than 1 year after
last pregnancy within 12 months of the first pregnancy

6.cigarette smoking
7. poor acceptance of pregnancy
Physical
1.subject to trauma
2. fluid or electrolyte imbalance
3. intake of teratogen such as drug
4. multiple gestation
5.poor placental formation or position
6. gestational Dm
7. nutritional deficiency of iron, folic acid, or protein
8.Poor Weight Gain
9. PIH
10. Infection
11. Amniotic fluid Abnormality
12. Post Maturity 
Labor & Delivery
 
Phychological
1.severely frighten by labor & delivery
2. inability to participate due to anesthesia
3. separation of infant at birth
4. lack of preparation for labor
5.birth of infant who is disappointing in some
way
(ex. Sex, appearance, or congenital anomalies)
Physical
1. Hemorrhage 7. Cephalopelvic
2. Infection disproportion
3. Fluid & electrolyte imbalance 8. Internal fetal
4. Dystocia monitoring
5. Precipitous birth 9. Retained placenta

6. Laceration of cervix & vagina

 
Social
1.Lack of support person
2. inadequate home for infant care
3.unplanned cesarean birth
4.lack of access to continued health care
5.lack of access to emergency personnel or equipment
VULNERABLE GROUPS ARE PREGNANT WOMEN WITH;
 
1.Physiologic problems such as concurrent illness with
malnutrition
2. mothers who are too young, too old, pregnant too frequently
3.presence of physical deformity
4.psychological/mental illness/mental retardation
5.marginalized because of
a. poverty
b. unemployment
c.lack of education
d.exposure to teratogens due to occupation
e. victims of abuse or domestic violence, rape, incest
f. single or separated mother
LESSON 1
 ANEMIA
-Reduction in oxygen carrying capacity of the blood due
to reduced number of RBC, low concentration of Hgb or
both. ( in pregnancy plasma volume increase)

Routine Screening:
MCN (mean cell volume) “ most useful”prophylactic
Iron -“more appropriate in 3rd tri”
Ferritin ( total body iron stores)
=30ug(micrograms)/l in women
=90 ug/l first trimester
=30 2nd tri & 15 - 3rd tri
Types of Anemia
 
1. Fe deficiency Anemia- most common anemia of pregnancy
-complicating as 15%-25% of all pregnancy
-deficiency in iron store resulting from diet low in iron, heavy menstrual period or
unwise weight reducing programs.
-when the hemoglobin level is below 12mg.dl(hematocrit under 33%- iron
deficiency is suspected, confirmed by a corresponding low serum iron level and
increased iron-binding capacity
-fe is made available to the body by absorption from duodenum into the
bloodstream after it is ingested. In the bloodstream, it is bound to transferring for
transport to the liver, spleen and bone marrow. At these sites, it is incorporated
into hemoglobin or stored as ferritin.
-Characteristically a Microcytic (small red blood cells) & Hypochromic (less
hemoglobin than average red cell) anemia ,because when an adequate supply of
iron is ingested, fe is unavailable for incorporation into RBC. Both hematocrit &
hemoglobin will be reduced ( under 33% & 12mg.dl respectively)
 
Causes:S&S:

1.Due to blood loss/hemorrhage 1.pallor 4. dyspnea

2.Reduced absorption 2.fainting 5. tachycardia
3.Multiple pregnancy3.fatigue 6. palpitation
4.Chronic infection ( urinary tract)
 
Effects on fetus
1.Increase intrauterine hypoxia / growth retardation
2.Preterm birth ( less than 37 wks)
3.LBW (less than 2500 grams)
 
Risk: Hgb less than 10.4 g/dl
 
Effects on the mother
1.decrease pregnancy enjoyment
2. decrease resistance to infection
3. prone to postpartum hemorrhage
Management:
1.Eat Fe rich foods ( more on meat) & Food rich in fiber ( prevent constipation)
2.Oral Fe ( FeSO4 200mg; Fe gluconate 300mg)-take with meals & with Vit C (prevent
GI irritation & for easy absorption.

Note:
-women who develop this type of anemia will be prescribed therapeutic levels of
medication (120-180 mg elemental Fe/day)- usually in the form of Ferrous sulfate or
ferrous gluconate.
-Fe is best absorbed from acid medium.( with orange juice or vit. C supplement)
-when constipation & gastric irritation is experience because of Fe supplement
increase roughage in the diet and take it with food.
-if Fe deficiency is severe & woman has difficulty with oral iron supplement, IM iron
DEXTRAN can be prescribed.
 
2. Folic Acid-Deficiency Anemia
-anemia found towards end of pregnancy when fetus is growing rapidly
-is seen in 1%-5% of pregnancies
occurs most often in;
-multiple pregnancies (because of increased fetal demand)
-women with secondary hemolytic illness(rapid destruction & production of new
RBC)
-women who are taking hydantoin(anticonvulsant agent that interfers with folate
absorption)
-women who have been taking oral contraceptives.
 
-the anemia that develops is a MEGALOBLASTIC ANEMIA(enlarged red blood cells)
(-the mean corpuscular volume will be elevated in contrast to the lowered level
seen with Fe deficiency anemia.)
-S&S, Hgb 3.5 g/dl, decrease WBC &platelets, increase MCV, anorexia, sore tongue.
-the deficiency may take a number of weeks to develop so it often becomes
most apparent during the second trimester of pregnancy.
-Effects , neural tube defects, (CNS),early miscarriage , antipartum hemorrhage,
abruptio placenta,and premature labor
prevention/ management
1. oral supplement of folic acid, during pregnancy daily 600ug or 5
mg/day,
2.folacin-rich foods(green leafy veg., oranges, dried beans)

Folic acid or folacin ( one of B Vit.)

- necessary for the formation of RBC in the mother as well as
being associated with preventing neural tube defect in the fetus.
Causes:
1.Decrease dietary intake
2.Drugs interference with utilization ( anticonvulsant, alcohol)
3.Excessive demand & loss ( hemolytic anemia, multiple
pregnancy)
3.Sickle Cell Anemia
-is recessively inherited hemolytic anemia caused by an
abnormal amino acid in the beta chain of hemoglobin.

If the abnormal amino acid

-replaces the amino acid VALINE – sickle hemoglobin
-replaces the amino acid LYSINE – non-sickling hemoglobin

-An individual who is heterozygous(has only 1 gene in which

the abnormal substitution has occurred) - has the sickle
cell trait
-If homozygous – sickle cell disease
-with the disease, the majority of RBC are irregular or sickle shaped
so cannot carry as much hemoglobin as normally shaped RBC.
When oxygen tension becomes reduced , as happens at high
altitudes or blood becomes more viscid than usual (dehydration),
the cells tend to clump because of the irregular shaped. This
clumping can result in vessel blockage, with reduced blood flow to
organs. The cells then will hemolyze, reducing the number
available and causing severe anemia.

-approximately 1 in every 10 african has sickle cell trait., 1 in every

400 african American has the disease.

-sickle cell trait does not appear to influence the course of

pregnancy, prematurity, miscarriage or perinatal mortality rates
of these may be higher for woman with the homozygous disease.
sickle cell trait does not appear to influence the course of
pregnancy, prematurity, miscarriage or perinatal mortality
rates of these may be higher for woman with the homozygous
disease.
-at any time in life, sickle cell anemia is a threat to life if blood
vessels such as those of the liver, kidneys, heart, lungs, or
brain becomes blocked.
-in pregnancy, blockage to the placental circulation can directly
compromise the fetus, causing LBW and possibly fetal death.

ASSESSMENT: all African American women who have not been

previously tested should be screened for sickle cell anemia at
first pre-natal visit.
 
GESTATIONAL CONDITIONS
 
1.HYPEREMESIS GRAVIDARUM/PERNICIOUS VOMITING
-is nausea &vomiting of pregnancy that is prolonged past week
12 of pregnancy or is so severe that dehydration, ketonuria
and significant weight loss occur within the first 12 weeks of
pregnancy.
-occurs at an incidence of 1 in 200 -300 women
-cause is UNKNOWN but women with the disorder may have
increased thyroid function due to the thyroid stimulating
properties of human chorionic gonadotropin
-associated with HELICOBACTER PYLORI ( same bacteria that
causes ulcers)
 
S&S : decrease Urine output,Wt. loss,ketonuria, dry mucus membrane, poor
skin turgor, eleveated hemotocrit, decrease concentration of Na,K &
chloride,polyneuritis,
 
ASSESSMENT
1.hematocrit concentration.(Elevated hematocrit concentration/
hemoconcentration-(inability to retain fluid)
2. concentration of Na,K,&Chloride ( decrease- (low intake)
3.hypokalemic alkalosis (severe vomiting during the day or persisted for an
extended period)
4. polyneuritis (in some) (due to deficiency of B Vit.)
- disorder involving several of peripheral nerves, usually in symmetrical
distribution
5. wt. loss(severe)
6. ketonuria ( urine may test positive for ketones)( evidence that woman’s
body is breaking down stored fat & protein for cell growth.
EFFECTS (if left untreated)
1.IUGR ( because of dehydration & can no longer provide a fetus nutrients for
growth)
2.preterm birth
3. prolonged hospitalization/ home care(result to social isolation)
 
NOTE: try to determine exactly how much nausea & vomiting women are having
during pregnancy, ask woman to describe the events of the day before if she says
it was a typical day. How late into the day did nausea last? How many times did
she vomit, how much , what was the total amount of food she was able to eat.

THERAPEUTIC MANAGEMENT
1.Monitor I&O & do blood chemistry (prevent dehydration)
2.withheld Oral food & fluids ( usually)/ TPN (total parentheral Nutrition)
3.IVF (3000 ml Ringer’s lactate with added Vit.B) ( to increase hydration)
4.Antiemetic drug(to control vomiting) “METOCLOPRAMIDE”-(Reglan)
 
NOTE; if there is no vomiting after 24 hours of
oral restriction, small fluids may be begun &
woman may be discharged home, usually with
referral for home care. If she can continue to
take clear fluids, small quantities of dry toast,
crackers or cereal may be added every 2-3
hours then can gradually advanced to a soft
diet then to a normal diet. If vomiting returns
at any point enteral or TPN .
2. ECTOPIC PREGNANCY (second most frequent cause of bleeding during 1 st
tri of pregnancy)
-implantation outside the uterine cavity (on ovary, cervix & fallopian tube-
most common)
-Fallopian tube: ampullar 80%,isthmus 12%, interstitial or fimbrial 8%
-occurs more frequently in women who smoke compared to those who do
not

Causes: (obstructions)
1.Adhesion of the fallopian tube/tubal scarring (from previous infection-
chronic salpingitis or pelvic inflammatory disease)
2.Congenital malformations
3.Scars from tubal surgery
4.Uterine tumor pressing on the proximal end of the tube
5.Current use of IUD( it may slow the transport of the zygote)
 
Assessment/ S&S
1.Missed period/ amenorrhea
2.(+) for hCG
3.Sharp, stabbing pain in the lower abdominal quadrants& pelvic
pain( at time of rupture)
4. Scant vaginal spotting/bleeding
5.Rigid abdomen(from peritoneal irritation)
6. Leukocytosis ( not for infection but from trauma)- increase in
WBC”leukocytes” in the blood.
7.Decrease BP & PR increase ( signs of shock)
8.Cullen’s sign ( bluish tinge umbilicus)
9.Tender mass palpable on cul-de sac Douglas (vaginal exam)
10. Falling hCG or serum progesterone level (suggest that pregnancy has
ended)
11.No gestational sac on ultra sound
 NOTE: - the extent of the bleeding that occurs depends on the number &
size of ruptured vessels insterstitial portion(can cause severe peritoneal
bleeding)

-ampullar area (third distal, bld. Vessels are smaller- profuse hemorrhage is
less likely but continued bleeding in this area may result in large amount of
bld. Loss.)
-ruptured ectopic pregnancy is serious regardless of the site of implantation
- the amount of bleeding evident with ruptured ectopic pregnancy often
does not reveal the actual amount present because the products of
conception from the ruptured tube & the accompanying bld. May be
expelled into the pelvic cavity rather than the uterus.
-if internal bleeding progresses woman may experience
lightheadedness, rapid thready pulse, rapid respiration, & falling BP
(signs of shock)
 
 
THERAPEUTIC MANAGEMENT
 
a.If ectopic pregnancy is diagnosed through sonogram before the tube has raptured
-oral administration of methotrexate followed by leucovorin
Methotrexate- a folic acid antagonist chemotherapeutic agent, attacks and destroys
fast growing cells. Woman is treated until hCG titer is achieved
-hyterosalpingogram or sonogram is performed after chemotherapy(to assess
whether the tube is fully patent.
-Mifepristone(abortifacient)- causing sloughing of the tubal implantation site.
 
*advantage of these therapy: tube is left intact, with no surgical scarring that could
cause a second ectopic implantation.

b.If ectopic pregnancy rupture (emergency situation)

-the therapy is laparoscopy (examination of the abdominal structures –
laparoscope)- to ligate the bleeding vessels and to remove or repair the damage
in the fallopian tube.
NOTE: Abdominal pregnancy
-the products of conception are expelled into the pelvic cavity and implant on the
organ such as an intestine.
-the fetal outline is easily palpable because it is directly below the abdominal wall
not inside the uterus. Woman may experience painful fetal movements and
abdominal cramping
-sudden lower quadrant pain earlier in pregnancy
-sonogram or magnetic resonance imaging ( to reveal the fetus outside the uterus.)
-DANGER of this kind of pregnancy: the placenta will infiltrate and erode a major
bld. Vessel in the abdomen leading to hemorrhage. If in the intestine, it may
erode so deeply that it causes bowel perforation & peritonitis.
-Fetus: at high risk because there is no good uterine blood supply ( fetal deformity
or IUGR)
-survival rate: 60%, term infant be born by laparotomy(surgical incision into the
abdominal cavity) Placenta is often difficult to remove after birth if it is implanted
on the abdominal organ such as intestine. It may be left in place and allowed to
absorb spontaneously in 2-3 months.
•  
3.HYDATIDIFORM MOLE ( H- mole)/ GESTATIONAL
TROPHOBLASTIC DISEASE/ MOLAR PREGNANCY
( fist common cause of bleeding in second Tri. Of Preg.)

-a gestational anomaly of the placenta consisting of a

bunch of clear vesicles(that look like grapes). This
neoplasm is formed from the swelling of the chorionic
villi and is the result of a fertilized egg whose nucleus is
lost, and the nucleus of sperm duplicates, producing a
diploid number 46 xx. It grows & enlarge the uterus
very rapidly.
-is abnormal proliferation & generation of the trophiblastic
villi. As the cells generate, they become filled with fluid &
appear as clear fluid filled, grape sized vesicles. With this
condition the embryo fails to develop beyond a primitive
start. (associated with choriocarcinoma – rapidly
metastasizing malignancy)

-incidence , approximately 1 in every 1500 pregnancies

1. women from low socio-economic group ( decrease
protein intake)
2. under 18 & above 35 Y.O.
3. women of Asian heritage
4. recieving clomiphene citrate (clomid) – induced ovulation
 2 types of molar growth ( can be identified by chromosome analysis)
 
1. Complete /Classic H-mole
-all trophoblastic villi swell & become cystic
-absence of embryonic or fetal tissue, if an embryo forms, it dies early at
only 1-2 mm in size.
-no fetal blood present in the villi
-on chromosomal analysis, although the karyotype is normal (46XX or
46XY, this chromosome component was contributed only by the father or
an empty ovum was fertilized & the chromosome material was
duplicated.
-toxemia (early)illustration:
-HCG titer high
-Risk for malignancy is high
-large for date uterus
-contents expelled 10-16 weeks
2. Partial mole /incomplete H-mole
- some of the villi form normally
-presence of fetal or embryonic tissue(fetus with multiple
congenital defects, stunted, won’t survive)
-small for date uterus
-contents expelled 10-26 weeks
-HCG titer low, titers also return to normal faster after mole
evacuation
-risk for malignancy low
-syncytiotrophoblastic layer of villi is swoolen & misshapen
-rarely lead to choriocarcinoma
-macerated embryo of approximately 9 weeks gestation may
be present &fetal blood may be present in the villi.
-partial mole has 69 chromosomes (triploid formation in
which there are 3 chromosomes instead of two for every
pair, one set supplied by an ovum that apparently was
fertilized by two sperm or an ovum fertilized by one
sperm in which meiosis or reduction division did not
occur. This also occur if one set of 23 chromosomes was
supplied by one sperm & an ovum that did not undergo
reduction division supplied 46.

Illustration ( page 411 0f MCN by pillitteri)

 
 
 
Assessment/S&S
 
1.Uterus tends to expand faster than normal
Note: this Diagnostic is also similar with multiple pregnancy or a
miscalculated due date
2.No fetal heart sounds are heard (no viable fetus)/no fetal
growth(sonogram-typically a snowflakes patter3
3.Serum or Urine test of hCG for pregnancy will be strongly (+)
(normal=400,00IU level, Abnormal=1-2 Million)-because hCG is produced
by the trophoblast cells that are overgrowing, continue until after day
100 og pregnance when the level of hCG normally would begin to decline.
-this must be also characteristics of multiple pregnancy with more than
one placenta.
4. nausea and vomiting of early pregnancy(due to high level of hCG.)
5. symptoms of PIH (hpn,edema& proteinuria,)are present before week 20
of pregnancy(abt. 12 weeks)
6.vaginal bleeding( begin with vaginal spotting of dark-brown blood or as a
profuse fresh flow.
7. progress vaginal bleeding accompanied by discharge of fluid-filled vesicles.
(confirmed H-MOLE)
 
Diagnosis:
1.ultrasound
2.chest x-ray (lung metastasis)
3. amniocentesis ( no fluid)
4. hysteroscopy (via cervix)
 
Management
1.D&C ( to evacuate the mole)
2. Blood transfusion
3. Hysterectomy
4.Baseline pelvic exam
5.chest x-ray,
6. serum test for the beta subunit of hCG
-hCG analyzed every 2 weeks until levels are again
normal
-serum hCG levels assessed every 4 weeks for 6-12
months

NOTE; gradually declining hCG titer = no complication

Levels that plateau for 3 times orincrease=malignant
transformation has occurred
 
-woman should be instructed to use reliable contraceptive agent for 12
months (so that a positive pregnancy test resulting from a new pregnancy
will not be confused with the increasing levels and developing pregnancy.
 
-after 6 months, if hCG levels are still (-)= free of risk of a malignancy
developing
By 12 moths= could plan second pregnancy

-if malignancy occur, can be treated with methotrexate.

Dactinomycin is added if metastasis occurs.

Causes of mortality:
1.Hemorrhage
2.Infection
3. Metastasis with hemorrhage
4.PREMATURE CERVICAL DILATATION/ INCOMPETENT CERVIX
(second common cause of bleeding in second tri. Of preg.)
-cervix that dilates and causes birth of a fetus before term or cervix that dilates
prematurely & therefore cannot hold a fetus until term.
-occurs about 1% of women
-commonly occurs at approximately week 20 when fetus is still too immature to survive
- may be diagnosed by an early sonogram before symptoms occur but usually diagnose
only after the pregnancy is lost.

S&S
1. painless dilatation ( usually)NOTE: either 2 or 3 often the first
symptoms
2.show -pink stained vaginal discharge
3. increased pelvic pressure
4. rupture of the membranes & discharge of amniotic fluid
*uterine contraction begin and after short labor the fetus is born
Causes:
1.increased maternal age
2.congenital structural defects
3.trauma to the cervix (cone biopsy or repeated D&C’s)
 
cervical cerclage -done after the loss of one child due to premature cervical
dilatation.
-surgical operation to prevent loss of child due to premature cervical dilatation.
NOTE: as soon as sonogram confirms the that the fetus of a second pregnancy is
healthy, approximately weeks 12-14, PURSE-STRING SUTURE are placed in the
cervix by the vaginal route under regional anesthesia, this procedure is called
“McDonald or a Shirodkar procedure”- the suture serve to strengthen the
cervix & prevent it from dilating.
 
McDonald procedure-nylon sutures are placed horizontally and vertically across
the cervix and pulled tight to reduce the cervical canal to a few millimeters in
diameter.
Shirodkar technique – sterile tape is threaded in a purse-string manner
under the submucous layer of the cervix and sutured in placed to
achieve a closed cervix.

Sutures can be placed by transabdominal route even if routinely

through vaginal route.

-sutures through vaginal route,sutures are then removed at week 37-38

of pregnancy so the fetus can be born vaginally.
- When a trans abdominal approach is used the sutures may be left in
place and Cesarean birth is performed
 
-women who are discovered to have cervical dilatation but with
membranes intact at a prenatal visit may have emergent cerclage
sutures placed in the cervix even at that point as prophylaxis against
preterm birth.
after clerclage surgery, women remain on bed rest for a few days (slight or
modified trendelenburg position)- to decrease pressure on the new
sutures. Sexual relations can be resumed in most instances after this rest
periods.)
***********
5. ABORTION- termination of pregnancy by any means before the fetus is
sufficiently developed to survive, or before an age of viability

Viable fetus – weight 400-500 grams or at least 20-24 wks. AOG

 
Types of Abortion
1. SPONTANEOUS MISCARRIAGE/ ABORTION
( 1st most common cause of bleeding during the first trimester)
-pregnancy interruption due to natural causes
-early miscarriage=before week 16 of pregnancy
- late miscarriage =between 16-24
Causes:
1.abnormal fetal formation (due to either to a teratogenic factor or to a chromosomal
aberration.)
2. implantation abnormalities/poor implantation (inadequate endometrial formation or
inappropriate site of implantation.
3.corpus luteum fails to produce enough progesterone to maintain the desidua basalis.
(progesterone theraphy – if this cause is documented)
4.infection caused by rubella,syphilis,poliomyelitis,cytomegalovirus &toxoplasmosis-
readily crosses the placenta possibly causing death. &urinary tract infection

NOTE: with an infection, if fetus fails to grow, estrogen & progesterone production by
the placenta falls.
-This leads to endometrial sloughing. With this sloughing, prostaglandins are released
leading to uterine contraction & cervical dilatation along with the expulsion of the
pregnancy.
5.ingestion of teratogenic drug
Isotretinoin (accutane) –if taken in early pregnancy –lead to miscarriage or fetal
abnormality
Alcohol ingestion at the time of conception
TYPES OF ABORTION
1.SPONTANEOUS ABORTION
1.1 Threatened Abortion(50% continue pregnancy)
-mild cramping, vaginal spotting(bright red), cervix close
-avoid strenuous activity for 24-48 hours
-restrict coitus for 2 weeks after bleeding episodes(prevent infection &
avoid inducing further bleeding
1.2 Inevitable/Imminent Abortion
- with profuse bleeding, uterine contraction, cervical dilatation

A.complete-all products of conception expelled spontaneously, bleeding usually

slows within 2 hours then ceases within a few days after passage of the
products of conception.
B.Incomplete – part of the conceptus is expelled usually the fetus but membranes
or placenta is retained in the utero
-save tissue fragments passed
-Dilatation & Curettage done/vacuum extraction (D&E=evacuation)
1.3 Missed Abortion/early pregnancy failure
-fetus dies in the utero but not expelled(died 4-6 weeks before onset of
miscarrhage sx)
-painless vaginal bleeding
-undelivered = induction of labor to prevent hypofibrinogenemia &sepsis
By prostaglandin suppository or misoprostol(cytotec) to dilate the cervix
followed by oxytocin stimulation or administration of mifepristone.
= D&E if pregnancy is over 14 weeks

 
1.4 Habitual Abortion/Recurrent pregnancy loss
-3 or more consecutive spontaneous abortion
-possible causes: defective spermatozoa or ova, endocrine factors(lowered
levels of protein bound iodine-PBI,butanol-extractable iodine-BEI & globulin-
bound iodine-GBI, poor thyroid function or luteal phase defect), deviations of
the uterus (septate or bicornuate uterus), infection,autoimmune disorders
(those involving lupus anticoagulant &antiphospholipid antibodies.
2.INDUCED ABORTION- a procedure performed in controlled setting to
deliberately end a pregnancy
 
2.1 Therapeutic/medical/legal- done if life of a woman is in danger, if there
is chromosomal defect of Fetus
2.2 Illegal Abortion
 
Complications of abortion
1.Hemorrhage (more than 1 sanitary pad per hour)
2.Infection ( E.coli)- endometritis, parametritis, peritonitis, thrombophelitis,
septicemia)
-danger sign of infection; fever, abdominal pain or tenderness, foul vaginal
discharge)
-caution: wipe perineal area fro front back after voiding & defecating-E.coli,
not to use tampons
 
Septic abortion- an abortion that is complicated
by infection but can happen after spontaneous

miscarriage (frequently occur in women who

tried to self abort)
-fever, crampy abdominal pain uterus feels
tender to palpation
-left untreated can lead to toxic shock syndrome,
septicemia, kidney failure, death
 
Management of abortion
1.Bed rest
2.Emotional support
3.Sedation
4.D&C for Incomplete, Missed-surgical removal
5.Antibiotics
6.Blood transfusion
 
FIRST TRIMESTER THIRD TRIMESTER
1.Spontaneous abortion 1.Placenta Previa
2.Ectopic pregnancy -abrupt painless b.
-sharp stabbing pain -bright red
-scant V. bleeding 2.Abruptio Placenata
SECOND TIMESTER -sharp stabbing pain
1.H-MOLE -heavy bleeding
-dark brown V. spotting, profuse fresh flow
2.PREMATURE DILATATION OF CERVIX
-painless
-pink stained V. discharge
LESSON 2
6. PLACENTA PREVIA
(first common cause of bleeding in third tri.
Of preg.)
-placenta implanted in lower uterine segment,
low implantation of placenta
- 5 per 1000 pregnancies
-bleeding occurs when the lower uterine
segment begins to differentiate from the upper
segment late in pregnancy(approximately week
30) & cervix begins to dilate
-bleeding results from placenta’s inability to stretch to accommodate the
differing shape of the lower uterine segment of the cervix.
-the degree to which the placenta covers the internal os is generally estimated
in percentages: 100%, 75%,30%...
-incidence 5 in every 1,000 pregnancies
- an increase in congenital fetal anomalies if low implantation does not allow
optimal fetal nutrition or oxygenation.(placenta is loosened-fetal oxygen is
compromised)
-with placental loosening, preterm labor may begin, posing additional threat of
preterm birth.
-uterine desidua(maternal blood), places the mother at risk for hemorrhage.
 
S&S : abrupt, painless bleeding ( bright red) – may stop as abruptly as it began
or may slow after the initial hemorrhage but continue as continuous spotting.
Earlier bleeding – more serious
Types:
1.total placenta previa-implantation that totally
obstructs the cervical os
2.partial placenta previa – implantation occludes
a portion of the cervical os
3. marginal placenta previa –the placenta edge
approaches that of the cervical os
4. low lying placenta previa – implantation in the
lower rather than in the upper portion of the
uterus
-*all associated with possible life threatening hemorrhage during pregnancy & labor.
-* in low-lying placentas detected on early sonogram migrate upward to a non-cervical
position
-If this happen , avoid coitus, adequate bed rest, if any sign of vaginal bleeding –visit
health care provider.

Cause(unknown)

Factors:
1.Multiparity
2.advance maternal age
3.past cesarean births
4.past uterine curettage(multiple induced abortion)
5.multiple gestation(large placenta)
6. male fetus
7.abnormal uterine position or shape
8.defective vascularization – deciduas
 
Therapeutic management

Immediate care measure.

1.bed rest in a side lying position (ensure an adequate blood supply to woman &
fetus)

2.inspect the perineum for bleeding.

-assess the duration of pregnancy,time of bleeding began ,woman’s
estimation of the amount of blood(a cup-240 ml, tablespoon-15
ml),whether there is accompanying pain, color of the blood
(redder blood indicates the bleeding is fresher or is continuing)what
was done for the bleeding(if tampon is inserted to halt the bleeding
there may be hidden bleeding), whether there were prior episodes of
bleeding during the pregnancy, whether she had prior cervical surgery
for premature cervical dilatation)
*kleihauser-betke test(test strip procedures)-can be done to detect whether
the blood is fatal or maternal origin)
*never attempt a pelvic or rectal exam with painless bleeding late in preg.
(if placenta previa-it initiate hemorrhage-fetal to both)

3.obtain baseline VS (to determine whether symptoms of shock is present)-

continue to assess BP every 5-15 min.
4.intravenous therapy(use large gauge catheter
5.monitor urine output frequently(every hour- blood volume adequacy)
6. record fetal heart sounds &uterine contraction(external fetal monitor)
7. ready blood for replacement
8.vaginal birth(safest for infant- if previa is under 30% -transvaginal
sonogram)
CS( safest for both -if previa is over 30% & fetus is mature)
9.oxygen (in case of fetal distress-bradycardia,tachycardia, late decelaration)
 Continuing measures

1.Birth must be accomplished regardless of gestational

age(if labor has begun, bleeding is continuing or fetus
is being compromised)
2.watching(if bledding stopped, fetal heart sounds are
good quality, maternal VS are good & fetus is not 36
weeks of age.
3.Bedrest for close observation for 48 hours
4. Betamethasone (celestone)is given(steroid that
hastens fetal maturity if fetus is less than 34 weeks of
gestation) (page 414) “fetal maturity through lecithin-
spingomyelin ratio)
 
Hemorrhage is severe: deliver fetus despite fetal immaturity, blood transfusion, CS
 
Maternal complications: uterine atony(lacking their normal
elasticity),lacerations,infections, hemorrhage,placenta accrete(deep attachment
of the placenta to uterine myometrium)

Fetus complications:
premature, prolapsed cord, transplacental hemorrhage, hypoxia
 

Neonatal Complications: premature, asphyxia, hypovolemia, hyaline membrane

disease(respiratory disease syndrome

fetal mortality:due to prematurity or shock while maternal mortalityi s hemorrhage

& infection
Diagnosis:
1.Characteristic of bleeding( abrupt, painless
bleeding ( bright red)
2.Indirect careful abdominal exam(uterus-soft,
palpable,nontender, contractile/ fetus-
breech,shoulder)
3. Ultrasound
4. Amniography/placentography(radiography of
the pregnant uterus to determine the position
of the placenta.
7. ABRUPTIO PLACENTA/ PREMATURE SEPARATION OF
PLACENTA/ACCIDENTAL HEMORRHAGE/PLACENTAL
ABRUPTION, ABLATIO PLACENTA
- ( second cause of bleeding in third tri. of preg.)
-separation of a normally implanted placenta after 20 th week
of pregnancy or before birth of the fetus.
-most frequent cause of perinatal death
-separationgenerally occurs late in pregnancy, it may occur as
late as during the first or second stage of labor.
-primary cause is unknown
-premature separation of the placenta may also follow a
rapid decrease uterine volume, such as occurs with
sudden release of amniotic fluid.
Predisposing factors:
1.high parity
2.advanced maternal age
3.short umbilical cord
4.chronic hypertensive disease
5.PIH
6.direct trauma (automobile accident, intimate partner
abuse)
7.cocaine or cigarette use(vasoconstriction)
8. thrombophilitic conditions (autoimmune antibodies, CHON
C & factor V Leiden(common inherited thrombophilia)
 
Classification according to the Extent
1.Total/complete abruptio placenta (concealed hemorrhage)
2.Partial abruptio placenta ( concealed or apparent hemorrhage)
 
S&S
1.Sharp, stabbing pain (high in the uterine fundus)-as initial
separation occurs
2.Contraction accompanied by pain over & above pain of the
contraction(if labor begins with the separation.)
3.Tenderness is felt on uterine palpation(in some pain is not
evident until palpation)
4.Heavy bleeding usually accompanies premature separation
(although it may not readily apparent.)
5. External bleeding(if the placenta separates first at the edges
& blood escapes freely from the cervix)
-If the center of the placenta first, blood can be pool under the
placenta &hidden from view blood may infiltrate the uterine
musculature (couvelaire uterus or uteroplacental apoplexy),
forming a hard , board like uterus with no apparent or
minimally apparent bleeding present.
6.Signs of shock (because of the blood loss)
7.Uterus becomes tense & feels rigid to the touch
8. DIC (disseminated intravascular coagulation)syndrome can
occur. “acquired blood clotting disorder in which fibrinogen
levels falls to below effective limits”-2-4 g/l & 4-6 g/l during
pregnancy. (S&S-bruising or bleeding from intravenous site)
Therapeutic Management
 
1.IVF (fluid replacement)
2.Oxygen by mask(limit fetal hypoxia)
3.Monitor fetal heart sounds externally & record maternal
VS (every 5-15 min to establish baseline data)
4.Fibrinogen determination (up to the time of delivery)-IV
of fibrinogen or cryoprecipitate which contains fibrinogen
5. Lateral position( to prevent pressure on the vena cava)
6. Assess the degree of placental separation
 
 
O= no symptoms of separation are apparent from
maternal & fetal signs
=Dx that slight separation did occur is made after
birth
1=minimal separation but enough to cause vaginal
bleeding & changes in the maternal vital signs
2=moderate separation, there is evidence of fetal
distress, uterus is tense & painful on palpation.
3=extreme separation, without immediate
interventions, maternal shock & fetal death may
result
Management may vary: massive bleeding=blood transfusion, prompt delivery
Bleeding slow =depend on fetal status
 
*note: do not disturb injured placenta (don’t perform vaginal or pelvic exam or give
enema)
-If birth does not seem imminent CS is the method of choice
-If DIC developed, surgery may pose a grave risk because of the possibility of
hemorrhage during surgery & later from surgical incision.
-Fetal prognosis depends on the extent of the placental separation & degree of fetal
hypoxia
-Maternal prognosis depends on how promptly Tx is instituted.
 
Complications:
1.DIC (disseminated Intravascular Coagulation)
2.postpartum hemorrhage/massive hemorrhage(shock-circulatory collapse-death)
3.renal failure (from circulatory collapse)
4. post partum infection (more prone if bleeding happen before birth)
Diagnosis: S&s, ultrasound, MRI (unexplained 3 rd tri.
bleeding)

8. PREMATURE RUPTURE OF MEMBRANES

-rapture of fetal membranes with loss of amniotic fluid
during pregnancy before 37 weeks
-cause is unknown but associated with infection of the
membranes(chorioamnionitis)/vaginal
infection(neisseria gonorrhea, streptococcus B &
Chlamydia)
-occurs in 5%-10% of pregnancy
effect: preterm labor
Assessment /S&S
1.sudden gush of clear fluid from the vagina with continued minimal
leakage
-sterile vaginal speculum examination is done to observe for vaginal pooling
of fluid
-if fluid is tested with NITRAZINE PAPER, amniotic fluid causes an alkaline
reaction on the paper (appears blue) if urine –acidic remains yellow)
-fluid can be tested for ferning or typical appearance of a high-estrogen
fluid on microscopic examination(amniotic shows, urine does not)
-sonogram(to assess amniotic fluid index)

2. signs of infection( assess for WBC &C-reactive Protein)-increase

temp.uterine tenderness, odorous vaginal discharge) WBW – count of
more than 18.000-20,000 mm3 suggest infection

 
NOTE: avoid doing routine vaginal exam(risk for infection rises)
-If fetus is estimated to be mature &labor does not begin in 24H, labor
contractions are induced by intravenous administration of oxytocin.

Therapeutic Management:

1.bed rest & corticosteroid(to hasten fetal lung majority)- if labor does
not begin &fetus is near point of viability
2.prophylactic administration of spectrum antibiotics(reduce risk for
infection) – can delay onset of labor)
3. intravenous administration of penicillin or ampicillin (women (+) for
strepto.B)- reduce this infection in
the newborn.
4.resealed membranes through the use of a fibrin-based commercial
sealant
Complications:
1.fetal infection-(if rapture occurs in early pregnancy, it poses
a major threat to the fetus)
2.increased pressure on the umbilical cord (from loss of
amniotic fluid-inhibit fetal nutrient supply)
3. cord prolapsed(extension of the cord out of the uterine
cavity into the vagina-interfere fetal circulation)
-most apt to occur when fetal head is still too small to fit
cervix firmly
4.development of potter-like syndrome or distorted facial
features & pulmonary
hypoplasia(underdevelopment ) from pressure.
 
9. PREGNANCY INDUCED HYPERTENSION ( PIH)/
TOXEMIA)
-is a condition in which vasopasm occurs during
pregnancy in both small & large arteries.
-vasospasm may be caused by increased cardiac
output that injures the endometrial cells of the
arteries & the action of prostaglandin
(decreased prostaglandin & increased
thromboxane
-basic causes of PIH’s symptoms is VASOSPASM
-classic signs of hpn, protenuria, & edema (later)
-symptoms rarely occur before 20 weeks of pregnancy
-cause is unknown

Risk factor:
1.multiple pregnancy
2.primiparas younger than 20 or older than 40 years old
3. low socioeconomic background(poor nutrition)
4. five or more pregnancy
5.hydramious
6. underlying disease such as heart d., DM with vessel or renal
involvement/HPN
7.Rh incompatibility
8.Hx of H-mole
 2 categories of PIH
1.Pre-eclampsia
2.Eclampsia
 
Pathophysiologic Events
*normally blood vessels during pregnancy are resistant to
the effects of pressor substances scuh as angiotensin &
norepiniphrine, so BP remains normal in pregnancy.
*with PIH reduce responsiveness to blood pressure
changes appears to be lost.Vasoconstriction occurs &
BP increases dramatically.
 
 VASOSPASM
 
VASCULAR EFFECTS KIDNEY EFFECTS INSTERSTITIAL EFFECTS
 
Vasoconstriction decreased glomeruli filtration diffusion of fluid from
rate & increased permeability blood stream into
interstitial
Poor organ perfusion of glomeruli membranes fluid.
(heart is forced to pump
against rising peripheral resistance)
Kidney
Pancreas(ischemia-epigastric pain increased serum blood, urea edema
&elevated amylase-creatinine ratio) nitrogen, uric acid & creatinine
Placenta (fetal hypoxia-acidosis-
Perinatal death or decrease nutrients-IUGR)
Brain
Liver decreased urine output & proteinuria
 
Increased blood pressure
 
Classification of PIH

1.Gestational Hpn
-blood pressure 140/90 or systolic pressure elevated 30mmHg or diastolic
pressure elevatyed 15 mm Hg above pre pregnancy level.
-no proteinuria or edema
-blood pressure returns to normal after birth
- no drug therapy necessary (perinatal mortality is not increased)

2.Mild pre-eclampsia
- blood pressure 140/90 or systolic pressure elevated 30mmHg or
diastolic pressure elevated 15 mm Hg above pre pregnancy level.
-protenuria of 1-2+ on a random sample
-weight gain over 2 lb per wk. in second tri. & 1lb. per wk in third tri.
-mild edema in upper extremities or face
3. Severe pre-eclampsia
-blood pressure of 160/110
-proteinuria 3-4+ on a random sample & 5g on a 24H sample
-oliguria(500ml or less in 24 H or altered renal function test.
-elevated serum creatinine more than 1.2 mg/dl
-cerebral or visual disturbances(headache,blurred vision), pulmonary & cardiac
involvenment
-extensive peripheral edema
-hepatic dysfunction
-thrombocytopenia
-epigastric pain

4. eclampsia
-seizure or coma accompanied by signs & symptoms of pre-eclampsia
-usually happens late in pregnancy but can happen up to 48 hours after childbirth.
-temp. 39.4-40 C(from increased cerebral pressure)
-blurring of vision or severe headache(increased
cerebral edema)
-reflexes becomes hyperactive.
-vascular congestion of the liver or pancreas can
lead to epigastric pain &nausea
-urinary output may decrease abruptly to less
than 30ml/h. Eclampsia has actually occurred
however, only when a woman experiences
seizure
Eclampsia (precided by S&S of pre –eclampsia)
1.stage of invasion – roll eyes and stare flixedly
2.Stage of contraction –body rigid, generalized muscular contraction
3.stage of convulsion-jaws open & close, muscles contract/relax, blood
tinged from mouth, face congested & purple, eyes bloodshot
*convulsion alternate with coma
 
Management:
 
Pre-Eclampsia
1.Mild symptoms remain at home(rest, balanced diet with increase CHON,
left lateral position)
2.Proteinuria (hospitalize)
3.Severe –diazepam(sedative), hydralazine apresoline(antihypertensive),
MgSO4 (convulsion) Ca Gluconate (antidote for magnesium
intoxication)Refer-page431MCN Peli..
4.Fetal monitoring
5.Induction of labor (CS)
6.Monitor Deep tendon reflexes

Eclampsia
Stages of Tonic-clonic Seizures
1.tonic phase
2.clonic phase
3.postictal state (semicomatose &cannot be aroused
except by painful stimuli for 1-4 hours
 
Stages of Tonic-clonic Seizures
1.tonic phase(last approximately 20 seconds)
-maintain patent airway
-oxygen administration by face mask
-assess oxygen saturation via pulse oximeter
-apply an external fetal heart rate monitor(assess
the condition of fetus)
-turn woman on her left(allow secretion to drain
from her mouth)
 
2.clonic phase ( all musles of the body contract & relax repeatedly causing to
flail wildly, enhales & exhales irregularly as her thoracic muscles contract
& relax, lasts up to one min.)
-continue oxygen therapy
-magnesium sulfate or diazepam(valium) IV
 
3.postictal state (semicomatose &cannot be aroused except by painful
stimuli for 1-4 hours
-extreme close observation (can cause premature separation of placenta &
labor may begin,painful stimulus of contraction may initiate another
seizure.)
-keep woman from her side
-nothing to eat or drink by mouth
-assess fetal heart sounds & uterine contraction
-check for vaginal bleeding every 15 min.
 
FIRST TRIMESTER THIRD TRIMESTER
1.Spontaneous abortion 1.Placenta Previa
2.Ectopic pregnancy -abrupt painless b.
-sharp stabbing pain -bright red
-scant V. bleeding 2.Abruptio Placenta
SECOND TIMESTER -sharp stabbing pain
1.H-MOLE -heavy bleeding
-dark brown V. spotting, profuse fresh flow
2.PREMATURE DILATATION OF CERVIX
-painless
-pink stained V. discharge