Isoimmunization
causing a risk of brain damage.
 Also known as RH Sensitivity
 Refers to the condition in which
the pregnant woman is RH
negative but her fetus is RH
positive.
 If left untreated, isoimmunisation
can lead to haemolytic disease in
the neonate (erythroblastosis
fetalis).
*RH-
Pathophysiology:
 Subsequent pregnancy with an
RH positive fetus processes
increasing amounts of maternal
agglutinating antibodies to cross
the placental barrier, attach to an
RH positive celss in the fetus and
causes hemolysis and anemia.
 To compensate for this, the fetus
steps up the production of RBC’s
and erythroblasts (Immature
RBC’s) appear in fetal circulation.
 Extensive hemolysis results in the
release of large amounts of
unconjugated bilirubin, which the
liver can’t conjugate and excrete,
causing hyperbilirubenia and
haemolytic anemia.
Hemolytic-post pregnancy
Symptoms of hemolysis:
 In mild case, the newborn baby
becomes jaundiced during the
first 24 hours of life (due to
excess bilirubin in the blood) and
slightly anemic.
 In more severe cases, the level of
bilirubin in the blood may
increase to a dangerous level,
 The most severely affected
babies have marked anemia
while still in the uterus, become
very swollen; and are often
stillborn.
Diagnostic findings:
 Increased concentration (optical
densits) of bilirubin and RBC
breakdown products in the
amniotic fluid.
 An anti-D antibody titer of 1:16 or
greater.
 Radiologic studies possibly
showing edema.
 Hydrops fetalis, the halo
sign (edematous elevated
subcutaneous fat layers)
and the Buddha position
(legs are crossed)
Management:
 Monitoring the indirect coomb’s
test (measures the amount of
antibodies in the maternal blood.)
 Intrauterine infusion
 Emotional support to the parents
 Possibly early delivery of the
fetus.
 Administration of Rho (D)
immunoglobulin (RHIG) at 28
weeks gestation and within 72
hours following a delivery of RH
positive neonate to attain passive
antibody protection of future
pregnancies.
Nursing intervention:
 Assess all pregnant women for
possibility of RH incompatibility.
  Expect to administer Rho (D)
 Administer RhoGam as ordered
to RH negative wome at 28
weeks gestation and within 72
hours after delivery.
 Prepare the patient for planned
delivery usually 2-4 weeks before
term date depending on the
maternal history, serologic test
and amniocentesis.
 Provide emotional support.
 Is there a connection
between fetal blood and
maternal blood?
 Theoretically, there is NO
connection between fetal
blood and maternal blood
during pregnancy, so the
mother should not be
exposed to fetal blood.
 If it is well documented,
however, that’s an
occasional villus
ruptures, allowing a drop
or two of fetal blood to
enter the maternal
circulation.
*Villus rupture- rupture of the
capillaries, mixture of maternal and fetus
blood.
Other causes:
 Amniocentesis
 Percutaneous umbilical blood
sampling.
Immunoglobulin- a passive agent
prescribed to prevent sensitization.
 IM as ordered to all RH
negative women after
transfusion reactions,
ectopic pregnancy or
abortion, or during the
second or third trimester to
patients with abruption
placenta, placenta previa
or amniocentesis.
*Amniocentesis- extracting amniotic
fluid in the abdomen.
The Anemias:
 The sickle cell anemia
 Folic-acid deficiency anemia
 Iron deficiency anemia
*Bilirubin- a neurotoxic in the blood.
*Sickle cell- from mother.
*Folic and Iron- developed
Sickle cell anemia
 A recessive inherited
haemolytic anemia in
which the RBC’s become
sickle shaped.
 Occurs primarily in 1/10
people of African and
Meditarrean decent.
 Women with sickle
cell trait seem to
experience an
increase incidence
of asymptomatic
bacteriuria, resulting
in an increased
incidence of
pyelonephritis.
 Majority of the RBC’s are
irregular or sickled shaped
so, it cannot carry as much
haemoglobin as normally
shaped RBC’s.
 When O2 tension
becomes reduced, as
happens in height attitudes
 or blood becomes more
viscid than usual
(dehydrated) the cell tends
to dump because of the
irregular shape.
 The clumping can result in
vessel blockage with
reduced blood flow to
organs > cell to hemolyze
> reducing the # of
available RBC’s > causing
a severe Anemia.
 At any time in life, SCA is
a threat to life if vital
blood vessles (lover,
kidneys, heart, lungs, or
brain) become blocked.
 In pregnancy, blockage to
the placental circulation
can directly compromise
the fetus, causing low birth
weight and possibly fetal
death.
Pathophysiology:
1. Sickle cell anemia results from
substitution of the amino acid
valine for glutamic acid in the
haemoglobin S gene encoding
Assessment findings:
the beta chain of haemoglobin.
2. Abnormal haemoglobin S, found
in the RBC’s of patients,
becomes insoluble during
hypoxia.
 These cells become rigid,
rough and elongated,
forming a crescent shape
or sickle shape.
 The sickling produces
hemolysis.
 The altered celss also pile
up in the capillaires and
smaller blood vessels,
making the blood more
viscous.
 Normal circulation is
impaired, causing pain,
tissue infarction and
swelling.
 Vascular obstruction in the
capillaries leads to
anemia.
 Each patient with sickle
cell anemia has a different
hypoxic threshold and
different factors that trigger
a sickle cell crisis.
 Illness, exposure to
cold, stress, acidotic
states or a
pathologic process
that causes water to
move out of the
sickle cells
precipitates a crisis
in most patients.
 The blockages then
cause anoxic
changes that lead to
further sickling and
obstruction.
 Anemia
 Fatigue
 Complaints of
burning and pain on
urination
 Pooling of blood in
lower extremities.
 Severe pain (if crisis
developed)
 Generally have no
symptoms
  Can pass the sickle
cell gene on their
children.
Diagnostic test findings:
 Positive family history
 Haemoglobin level of 6-8
mg/100ml or less
 Clean-catch urine specimen
positive for bacteria.
 Stained blood smear show sickle
celss
 Decreased RBC count and
erythrocyte sedimentation rate
 Increased bilirubin level (during a
crisis)
*120-150- normal RBC of women
*140-160- normal RBC of men
Management:
 Evaluation of blood studies,
including haemoglobin and
haematocrit levels.
 Folic acid supplements- keep the
new cells produced from being
megaloblastic.
 As a role: No iron
supplementation > cells
cannot incorporate iron in
the usual manner that
usual cells can do >
excessive iron build up will
result.
 Assess lower extremities for
varicosities or pooling of blood in
leg veins > red cell destruction.
 Prevention of thrombophlebitis
(inflammation of the veins)
 (+) Homan’s sign- pain in
the calf with dorsiflexion of
the foot.
 Blood transfusion therapy- to
replace sickle cell with normal
cell.
 Oxygen therapy
 Fluid therapy- lower viscosity/
keep plasma tension low
 An analgesic for relief of pain
during crisis.
 Avoidance of contributing factors,
such as dehydration, stress,
hypoxia, infection, acidosis and
sudden cooling.
Nursing intervention:
 Monitor the patients CBC daily.
 Asses the patients hydration
status- Monitor I and O, drink at
least 8 oz fluids per day.
 Monitor vital signs and fetal heart
rate pattern
 Monitor weight gain and assess
fundal height for changes
indicating adequate fetal growth
 Assess for signs for sickle cell
crisis and chronic complications;
give analgesics and IV fluids if
crisis develops.
 Obtain a clean catch urine
specimen for culture to assess for
possible bacteriuria.
 Assess lower extremeties for
venous poolong, encourage the
woman to avoid standing for long
periods of time and rest in a chair
with legs elevated or in a side-
lying position to promote venous
return to the heart.
 Prepare the patient for ultrasound
at 16 and 24 weeks and weekly
non stress tests.
 Watch for signs and symptoms of
infection.
  Provide comfort and emotional
support to the patient and her
family.
 Assist with measures to maintain
hydration during labor and
delivery.
Possible complication:
 Pregnant women experience an
increase incidence of PIH, UTI,
heart failure, pneumonia,
pulmonary infarction, crisis and
postpartum haemorrhage.
 Risk for intrauterine growth
retardation results in low birth
weight infants
 Perinatal fetal death may results
from spontaneous and
prematurity
Folic acid deficiency anemia
 A common, slowly
progressive megaloblastic
anemia (enlarged rbc’s)
 Folic acid, or folacin, is
one of the B vitamins
important for the normal
formation of rbc’s
 Folic acid plays a major
role in preventing neural
tube defects in the fetus.
 Most apparent during the
2nd trimester of pregnancy
Pathophysiology
Folic acid is found in most body tissues
where it acts as a coenzyme in
metabolic process.
 Although its body stores
and comparatively small,
this vitamin is plentiful in
most well-balanced diets.
 However, folic acids is
water-soluble and heat-
labile, and is easily
destroyed by cooking.
 About 20% of folic acid is
excreted unabsorbed.
 An insufficient intake
usually less than 50
mcg/day, generally results
in folic acid-deficiency
within 4 months.
 Seen in 1% to 5% of
pregnancies
 During pregnancy, folic
acid deficiency anemia
usually occurs in women
with multiple gestations-
believed to be the result of
the increased demand for
folic acid by the foetuses.
 It’s also seen in women
who have underlying
haemolytic illness- results
in rapid destruction and
production of RBC.
Certain drugs:
 Hydantoin (an anticonvulsant that
interfere with folate absorption)
 Hormonal contraceptives may
also a causative role.
Assessmemnt findings:
 Severe, progressive fatigue (the
hallmark of folic acid deficiency)
 Pallor or jaundice
 Shortness of breath
 Palpitations
 Diarrhea
 Nausea or anorexia
 Headaches, weakness or slight
madness
 Forgetfulness
  Irritableness
Diagnostic findings:
 Macrocytic RBC’s
 Decrease reticulocyte count
 Increase corpuscular volume
 Abnormal platelet count
 Decrease serum folate levels
(below 4 mg/ml)
Management:
1. folic acid complementation
 Pre pregnant: 400 ug/day
 Pregnant: 600 ug/ day
2. Diet high in folic acid
 Spinach, green leafy vegetable,
lover, kidney, asparagus, nuts,
orange juice, whole-grain cereals.
Nursing intervention:
 Strongly urge women expecting
to become pregnant to begin a
vitamin supplement (over the
counter) or be conscious about
eating folic-rich foods during this
time.
 Assist with planning a well-
balanced diet, including foods
high in folic acid and between-
meal snacks.
 Encourage the woman to eat a
rich of vitamin C at each meal to
enhance the absorption of folic
acid.
 Administer the folic acid,
supplement as ordered.
 If the patient has severe anemia
and requires hospitalization.
 Monitor pulse rate after.
 If tachycardia occurs, the
patient’s activity are too
strenuous.
 Monitor the patient’s CBC and
platelet count.
Possible complications:
1. Early spontaneous abortion
2. Premature rupture of the placenta.
3. Fetal neural tube defects (NTD)
Iron deficiency anemia
 A disorder of oxygen transport in
which haemoglobin synthesis is
deficient.
 Most common anemia during
pregnancy, affecting up to 25% of
all pregnancies.
 Associated with low fetal birth
weight and preterm birth.
 Iron-made available to the body
by absorption to the duodenum
into the bloodstream after it is
ingested.
 In the bloodstreams, it is bound to
transferrin for transport to the
liver, spleens and bone marrow.
At these sites, it is incorporated
into haemoglobin ferritin.
Pathophysiology:
 During pregnancy, the
development of iron deficiency
anemia is directly related to the
pregnancy, which result in the
maternal iron stores being used
for fetal RBC production.
 Many women enter pregnancy
with a deficit of rion stores,
resulting from diet low in iron
(inadequate intake), heavy
menstrual periods (blood loss), or
 unwise weight-reducing
programs.
 Iron-stores are apt to below in
women experiencing a short
period (under 2 years) between
pregnancies or those from low
socioeconomic communities.
 Iron deficiency anemia is
considered a microcytic (small
rbc) hypochromic (less
haemoglobin than average RBC)
anemia.
 When iron intake is
inadequate, it’s
unavailable for
incorporarion into RBC’s.
 As a result, cells aren’t as
large or as rich in
haemoglobin as they
normally are.
Gestational conditions
Hyperemesis gravidarum- severe and
unremitting nausea and vomiting that
persists after 1st trimester.
-Usually occurs with tha first pregnancy
and commonly affects pregnant women
with conditions that produce high levels
HCG such gestations thropoblastic.
Pathophysiology:
 Exact cause is unknown but it is
linked to trophoblastic activity,
gonadotropin production and
psychological factors.
 Various possible cause:
 Pancreatitis
 Biliary heart disease
 Decreased secretion of
free hydrochloric acid in
the stomach.
 Decreased gastric motility
 Drug toxicity
 Inflammatory obstructive
bowel disease
 Vitamin deficiency
(especially of B6)
 Psychological factors.
Assessment findings:
 Unremitting nausea and vomiting
(cardinal sign)
 Substantial weight loss
 Thirst
 Oliguria
 Electrolyte imbalance
 Dehydration
 Metabolic acidosis
Diagnostic findings:
 Decreased serums protein,
sodium and potassium levels
 Increased blood urea nitrogen
levels
 Elevated haemoglobin levels
 Elevated white blood cell count
 Ketomeria and right proteiruruia
Management:
 Restore fluid and electrolyte
balance with IV fluid therapy
 Administer antiemetic to control
vomiting
 Maintain adequate nutrition and
rest
 Progress to oral feedings as
tolerated
Nursing interventions:
 Administer IV fluids as ordered.
 Monitor intake and output, VS,
skin turgor and daily weight
serum electrolyte level, and urine
ketone levels.
  Suggest decreased liquid intake
at mealtime.
 Instruct the patient to remain
upright for 45 minutes after
eating.
 Suggest that the patient eat two
or three day crackers on
awakening.
 Provide reassurance and a calm,
restful atmosphere.
 Encourage the patient to discuss
her feelings.
 Help the patient develop affecting
coping strategies.
 Teach the patient measures to
conserve energy.
Possible complications
 Substantial weight loss
 Starvation, with the ketosis and
acetonuria
 Dehydration, with subsequent
fluid and electrolyte imbalances
(hypokalemia)
 Acid-base imbalances (acidosis
and alkalosis)
 Retinal, neurologic and renal
damage.
Gestational trophoblastic disease
 Abnormally of the placenta that
converts the chorionic villi into a
mass of clear resides.
 Also called molar pregnancy
Types of moles:
 Complete moles- there’s neither
an embryo nor an amniotic sac.
 Partial mole- there’s neither an
embryo (usually with multiple
abnormalities) nor amniotic sac.
Normal level of HCG:
 In most normal pregnancies with
HCG levels below 1,200 Miu/ml,
the HCG usually doubles every
48.72 hours and increased by at
least 60% every two days.
Cancer
 Gestations thropoblastic disease
is a major cause of second
trimester bleeding.
 Early detection is necessary
because it is associated with
choriocarcinoma, a fast growing,
and highly invasive malignancy.
Pathophysiology:
 Exact cause is unknown
 Poor maternal nutrition,
specifically an insufficient intake
of CHON and folic acid, defective
ovum, chromosomal
abnormalities, or hormonal
imbalances.
 With this disorder, the
throphoblastic villi cells rapidly
increase in size and fill with fluid.
 Disproportionate, enlargement of
the uterus; possible grapelike
clusters noted in vagina or pelvic
examination.
 Excessive nausea and vomiting
 Intermittent or continuous bright
red or brownish vaginal bleeding
by the 12th week of gestation.
Assessment findings:
 Passage of tissue resembling
grapelike cluster
 Symptoms of PIH before the 20th
week of gestation
 Absence of fetal heart tones
Diagnostic test findings:  Assess patient’s vital signs to
obtain a baseline.
 Radio immune assay of HCG
 Observe the patient for signs of
revels extremely elevated for
complications (hemorrhage,
early pregnancy.
uterine infection, vagfinal
 Histologic examination of
passage)
possible vesicles helps confirm
 Encourage patient and her family
diagnosis.
to express their feelings and offer
 Ultrasonography performed after
support.
the 3rd mount revealing grapelike
 Help the patient and her family
clusters.
develop effective coping
 Haemoglobin level, haematocrit,
strategies.
red blood cell count, prothombin
 Help obtain baseline information
time, partial thromboplastin time,
(pelvic examination, chest Xray,
fibronegon levels and hepatic and
serum HCG levels)
renal function finding are all
 Stress the need for regular
abnormal.
monitoring of HCG levels.
 White blood cells count and
 Instruct the patient to promptly
erythrocyte sedimentation rate
report any new signs and
increased.
symptoms and to use
Management: contraceptives to prevent
pregnancy for at least one year
 Increased abortion if a
after HCG levels return to normal.
spontaneous one doesn’t occur.
 Follow up care vital because of Gestational diabetes mellitus
increased risk of
 Metabolic disorder characterized
choriocarcinoma.
by hyperglycemia resulting from
 Weekly monitoring of HCG levels
lack of insulin effect or both.
until they remain normal for three
 An endocrine disorder in which
consecutive weeks
the pancreas cannot produce
 Periodic follow up for 1-2 years adequate insulin to regulate body
 Pelvic examinations and chest x- glucose levels.
rays at regular intervals.  A disorder of carbohydrate,
 Emotional support for the couple protein and fat metablosim.
who are grieving for the lost
pregnancy and unsure obstetric *70-120 mg/dl- normal glucose
and medical future. *Insulin (storage)  glucose 
 Avoidance of pregnancy until glucagon (release)
HCG levels are normal (may take
up to one year) Types of Diabetes mellitus:

Nursing interventions: 1. Type 1- an absolute insulin

insufficiency
2. Type 2- an insulin resistance with Risk factors:
ranging degree of insulin secretory
 Obesity
defects.
 Age over 25 years
3. Gestational diabetes- diabetes that  History of large babies (10 lbs or
emerges during pregnancy. more)’
 History of unexplained fetal or
Pathophysiology:
perinatal loss
 Factors that contribute to DM:  History of congenital anomalies in
 Hereditary previous pregnancy
 Obesity  Family history of diabetes (1
 Sedentary lifestyles close relative or 2 distant ones)
 Diet (high fat, low fat) Assessment findings:
 HPN
 Aging  Hyperglycemia
 Glycosuria (presence of glycogen
Gestational Diabetes mellitus
in urine
 Occurs when a woman not  Polyuria (leads to polydipsia)
previously diagnosed with  Polyphagia
diabetes shows glucose interlace  Increased incidence of cardinal
having pregnancy. infections
 This cause is unknown.  Polyhydramnios
 A phenomenon that is possible
caused by Diagnostic test:
 Hormone human placental  100g glucose load used at 24th to
lactogen (chorionic 28th weeks AOG
somatomamotropin)  If 1 hour glucose level is >180
Highblood glucose levels in mother mg/dl, a 3 hour glucose tolerance
test using 100g glucose load is
| scheduled.
Brings extra glucose to baby Oral glucose challenge test values
| (Fasting plasma glucose values) for
pregnancy
Cause baby to put on extra weight
Test type Prganancy
GDM glucose level
(mg/dl)
 Mother must increase insulin
Fasting 95
dosage beginning at 24th week of
1hour 180
pregnancy- to prevent
2hours 155
hypoglycaemia.
3hours 140
 Continue use of maternal glucose
of the fetus may lead to
hypoglycaemia to the mother.
  Two abnormal levels or a fasting
a glucose level >95 mg/dl
confirms diagnosis of GDM.
Managing GDM:
 Blood glucose level monitoring
(fasting blood sugar and 2 hour
postprandial)
 Target glucose levels for FBS
<100mg/dl and postprandial
<120mg/dl
 Carefully monitoring of diet,
exercise and insulin
administration and patient
education.
 Oral antidiabitic agents are
contraindicated during
pregnancy because of
their adverse effects on
the fetus and neonate;
may be used in 2nd or 3rd
trimester.
Nursing intervention:
 Monitor the woman’s status
carefully throughout the
pregnancy
 Review results of fingerstick
blood glucose monitoring
 Assist with arranging follow up
laboratory studies
 Encourage a consistent exercise
program, including the use of
snacks.
 Instruct in all aspects of diabetic
care management
 Assist with preparation for labor
 Closely assess the woman in the
postpartum period for changes in
blood glucose levels and insulin
requirements.
 Encourage to adhere to follow up
health maintenance visits to
obtain glucose testing to allow for
early detection of possible type2
diabetes.
 Urine culture each trimester-
detect asymptomatic UTI.
Possible complications:
 Patient with GDM is 30% to 40%
chance of developing DM 1 to 25
years.
 Ophthalmic examination
 Once during pregnancy for
GDM
 Each trimester for known
diabetic
 Background retinal changes
 Increased exudates, dot
haemorrhage, macular
edema
 Proliferative retinopathy
before pregnancy and
progress can lead to be
blindness.
 Laser therapy
 Incompetent cervix
 Also called premature
cervical dilation
 Refers to a painless
premature dilation of the
cervix
 It generally occurs in the
4th to 5th month of
glutation, most commonly
around the 20th week of
gestation.
Pathophysiology:
 This condition is associated with
congenital structural defects or
previous cervical trauma resulting
from surgery or delivery.
  It is also associated with  Prepare woman for cervical
increasing maternal age. cerclage under regional
anesthesia as indicated; monitor
Assessment:
maternal VS and FHR patterns
 History of repeated second closely.
trimester spontaneous abortions.  Instruct woman in signs and
 Cervical dilation in the absence of symptoms of labor with the need
contractions or pain. to notify healthcare provide if any
 Pink-stained vaginal discharge. occur.
 Increased pelvic pressure with
possible ruptured membranes
and release of amniotic fluid.
Diagnostic findings:
 Ultrasound revealing defect
 Nitrazine-test result indicates
rupture of membranes.
Management:
 Placement of cerclage in the
cervix-help keep the cervix closed
until termed the patient goes into
labor.
 McDonalds procedure- using
nylon sutures horizontally and
vertically to close of the cervix to
only a few months.
 Shirodkar procedure- using
sterile tape in a purse-striving
fashion to close off cervix entirely.
Management:
 Bed rest after surgery
 Removal of sutures at 37 to 39
weeks gestation
 Emotional support
Nursing intervention:
 Assess complaints of vaginal
drainage and investigate history
for previous cervical surgeries.