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Hemolytic Disease 112702

Hemolytic disease can arise from Rh isoimmunization and ABO incompatibility, affecting about 10% of women during pregnancy. Rh incompatibility leads to the production of antibodies that can cause fetal anemia and other complications, while prevention includes careful prenatal screening and administration of RhoGAM. Management of affected newborns involves monitoring and treatment strategies such as phototherapy to address hyperbilirubinemia.
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0% found this document useful (0 votes)
12 views22 pages

Hemolytic Disease 112702

Hemolytic disease can arise from Rh isoimmunization and ABO incompatibility, affecting about 10% of women during pregnancy. Rh incompatibility leads to the production of antibodies that can cause fetal anemia and other complications, while prevention includes careful prenatal screening and administration of RhoGAM. Management of affected newborns involves monitoring and treatment strategies such as phototherapy to address hyperbilirubinemia.
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© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

HEMOLYTIC DISEASE

MIDTERM CONCEPT
INCIDENCE
•About 10 percent of women are at risk for Rh
isoimmunization, which can cause severe
hemolytic disease (anemia) and death of the
fetus or newborn
•The approximately incidence of Rh-related
neonatal morbidity is one in 1000 births.
(Moise, 1995)
ABO INCOMPATIBILITY
ABO incompatibility between mother and
fetus occurs when maternal blood type is O
and fetus is:
•Type A- most common
•Type B- most serious
•Type AB- rare
However, it is uncommon for maternal blood
to enter fetal circulation or the fetal blood to
enter maternal circulation during pregnancy
because the antibodies are the large IgM
type which cannot cross the placenta barrier.
During delivery, when the placenta
separates from the decidua, this barrier is
broken allowing some fetal blood to
enter the maternal blood vessels and
some maternal blood that contains
antibodies to enter the placenta and
infant’s blood stream.
RH INCOMPATIBILITY
1. Rh Factor
 the Rh factor is a distinct protein antigen that is found on the
covering of RBC. If this Rh factor protein is present on the cells, the
person is Rh positive. If there is no Rh factor protein, the person is
Rh negative.
Presence of the Rh factor makes the blood cells incompatible with
blood cells that do not have the Rh factor.
If Rh (+) blood enters an Rh (-) blood, the Rh (-) blood will produce
antibodies to destroy the Rh (+) blood.
About 85% of people are Rh (+) and 15% are Rh (-)
Rh factor are genetically determined
Rh (+) is dominant
RH INCOMPATIBILITY
2. Rh Sensitization/ Rh isoimmunization
 the exposure of Rh (-) blood to an Rh (+) blood and the resultant
production of antibodies by the immune system of the person having
an Rh (-) blood against Rh (+) blood.
Sensitization from a previous pregnancy (stimulating antibody formation by
the mother’s immune system)
Inadequate response to prophylaxis
Incompatible BT
Fetal blood and maternal blood are separated by placental barrier.
Sometimes, breaks in the placental barrier can occur during
pregnancy and cause a few RBCs from the fetus to leak across the
placenta and enter the mother’s circulation.
RH INCOMPATIBILITY
2. Rh Sensitization/ Rh isoimmunization
 antibodies do not disappear in maternal blood stream. If any of the
fetuses in subsequent pregnancies is Rh (+), the antibodies already
present in the maternal bloodstream will enter the fetal circulation via
the placenta, will attack and destroy the fetal RBC resulting to
fetal anemia.
As a compensatory mechanism, the fetal bone marrow will release
immature RBCs/ erythroblasts, into the fetal peripheral circulation,
causing erythroblastosis fetalis------IUFD
The destruction of the RBC results in massive production and
resultant accumulation of bilirubin as the immature fetal liver is
unable to clear them from the body, this lead to hyperbilirubinemia
and kernicterus.
RH INCOMPATIBILITY
3. Fetal Complications of Erythroblastosis Fetalis
 anemia
Spleenomegaly and hepatomegaly
Hyperbilirubinemia
Hydrops fetalis
Stillbirth
PREVENTION
Prenatal Screening
1. History: When the woman is Rh (-), the nurse elicit a
careful history of her:
Past pregnancies
Blood transfusion
Abortion
Invasive dx procedure during pregnancy (amniocentesis,
intrauterine percutaneous umbilical blood sampling / IPUB,
fetal scalp blood sampling and chorionic villus sampling.
PREVENTION
Prenatal Screening
2. Screening tests: Blood typing and Rh factor determination. If
the mother is Rh (-), the father’s blood type and Rh should be
determined. If the father is Rh positive:
 antibody titer is done by Coomb’s Test to find out if the
mother is sensitized.
Indirect Coomb’s Test: detects presence of antibodies in maternal
serum
Direct Coomb’s Test: detects presence of antibodies in fetal cord
blood
PREVENTION
if the antibody titer is negative
Maternal Rh antibody titers should be measured again at 16
to 20 wk and then, at 26 to 27 wk of pregnancy.
She should be given Rh immune globin IM or AKA anti-
Rho(D) gamma globulin (RhoGAM) at 28 wks and within 72
hours after delivery in order to destroy fetal cells that have
entered her circulation thereby preventing maternal
antibody production
PREVENTION
RhoGAM should be given to all Rh (-) women who:
Have delivered Rh (+) fetus
Have had untypeable pregnancies such as ectopic
pregnancies, still birth and abortion
Have received ABO compatible Rh positive blood
Have had invasive diagnostic procedure such as
amniocentesis
MANAGEMENT
1. Fetal Surveillance- done if the result of the mother’s antibody
titer test is positive
Amniocentesis q2 weeks beginning 26 wks: bilirubin level
Spectrophotometry- measures the concentration of bilirubin in the
amniotic fluid
Percutaneous umbilical blood sampling (PUBS)- may be done if the
result of spectrophotometry is (+) indicate severe hemolysis
Ultrasound- once diagnosis of Rh incompatibility is made, UTZ
evaluations may be done to assess for complications including
hydrops fetalis, polyhydramnios, and enlargement of the heart
MANAGEMENT
2. Intrauterine Blood Fetal Transfusion (IUFT)- intraperitoneal or
intravascular
Nursing interventions:
Prepare the mother
Monitor for s/sx of preterm labor
Counting and recording of fetal movement
Advised to immediately contact HCP if notices decreased fetal
movement, vaginal bleeding, PROM, or preterm labor
MANAGEMENT
3. Labor and Delivery: The goal of intrapartum management of Rh
(-) woman is to minimize opportunity for maternal-fetal bleeds.
Do not remove placenta manually to avoid squeezing fetal cells
into the maternal circulation
Clamp the cord immediately after birth
Ensure that a blood sample is drawn from the mother for
Kleihauer-Betke blood test shortly after birth to test for the
presence and quantity of fetal blood that entered maternal
circulation
MANAGEMENT
4. Postpartum Care: The goals of post partum management are to
prevent sensitization in the unsensitized woman and to quickly dx
and tx hemolytic disease in the new born
Immunize the mother with RhoGAM within 72 hours after delivery if the
Coombs test is negative
If the kleihauer-betke shows that larger quantity of fetal blood entered
the maternal circulation, repeated doses of RhoGAM are necessary
If the mother’s indirect Coombs’ test is (+), this means that mother has
already produced antibodies against Rh (+) blood. RhoGAM should no
longer be given to the mother. But the new born should be monitored for
signs of hemolytic disease and treated appropriately.
MANAGEMENT
5. Management of hemolytic disease in the newborn
A. Suspension of BF during the first 24hours to prevent
pregnanediol from interfering with the conjugation of indirect
bilirubin to direct bilirubin
B. Phototherapy: speeds up the maturation of the liver to enable
it to conjugate indirect to direct bilirubin more efficiently
C. Use single quarts halogen lamp or a bank of 4-8 cool white, day
bright, or special blue fluorescent lights positioned 12-30
inches above the infant
MANAGEMENT
5. Management of hemolytic disease in the newborn
D. Nursing interventions
Close eyes and cover with dressing
Expect the stool to be loose and bright green from excessive
bilirubin excretion
Provide good skin care because the stool is highly irritating to
the skin. Remove all traces of stool completely from skin
Expect the urine to be dark colored
MANAGEMENT
5. Management of hemolytic disease in the newborn
Assess DHN. Monitor I & O and skin turgor d/t insensible water
loss
Offer glucose water q2 to prevent DHN
Maintain body temperature
The infant should be removed from the isolette during feeding
and eye patches remove to allow interaction and visual
stimulation
Home phototherapy- exposure to early morning sunlight

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