A
B O AND RHESUS ISOIMMUNIZATION.
GENERAL
CONSIDERATIONS
A fetus receives half
of its genetic components from its mother and half from its father, therefore,
the fetus may have different blood groups from those of its mother. Some blood
group may act as antigens in individual not possessing those blood groups. The
antigens reside on red blood cells. If enough fetal cell cross into the
maternal blood, a maternal antibodies
cross the placenta, they then can enter the fetal circulation and
destroy the fetal erythrocytes, causing hemolytic anemia. This leads to fetal
response to meet the challenge of enhanced blood cell breakdown. These changes
in the fetus and newborn are called erythroblastosis fetalis. Several blood
groups are capable of producing fetal risk, but those in the rh group have
caused the overwhelming majority of cases of erythroblastosis fetalis, so the
rh group is used as the example. The rh blood group is the most complex human
blood group. The rh antigens are grouped in 3 pairs: Dd, Cc, and Ee. The major
antigen in this group, rh (D), or rh factor, is of particular concern. A woman
who is lacking the rh factor (rh negative) may carry an rh positive fetus. If
fetal red blood cell is passing to the mother’ s circulation in sufficient
numbers, maternal antibodies to the rh positive antigen may develop and (fig 15..1 ). Hemolytic disease of the
newborn may occur, and severe disease may cause fetal death. In standard
resting when the father is rh positive, 2 possibilities exist; he is either
homozygous or heterozygous. Forty five percent of rh positive person are
homozygous for D and 55% are heterozygous. If the father is homozygous, all of
his children will be rh positive, if he is heterozygous, his children will have
a 50% chance of being rh positive. By
way of contrast, the rh negative individual is always homozygous.
INCIDENCE
Basque population
have the highest incidence of rh negativity (30-35% ). Caucasian population in
general have a higher incidence than other ethnic groups (15 16%). Blacks in
the united states
PATHOGENESIS
A
MATERNAL RH ISOIMMUNIZATION
Rh antigene are
lipoproteins that are comfined to the red cell membrane. Isoimmunization may
occur by 2 mechanisms> (1) following incompartiable blood transfusion or (2(
following fetomaternal hemorrhage beween a mother and an incompatible fetus.
Fetomaternal hemorrhage may occur during pregnancy or at deliverly. With no
apparent predisposing factors, fetal red
cell have been detected in maternal blood in 6.7% of woman during the first
trimester, 15.9% during the second trimester, and 28.9% during the thid
trimester. Predisposition to fetomaternal hemorrhage include spontaneous or
induced abortion amniocentesis chorinic
villus sampling abdominal trauma (eg, due to motor vehicle accident or
external version ), placentra previa, abruption placentrae, fetal death,
multiple pregnancy, manual removal of the placentra and cesarean setion.
Although the exact number of rh positive cell necessary to cause
isoimmunization of the rh negative pregnant woman is unknown, as little as 0.1
ml of rh positive cell can cause sensitization. Even with delivery, this amount
occur in less than half of cases. Fortunately, there are other mitigating
factor to rh isoimmunization. A very important fator tis that about 30% of rh negative persons never become sensitized
(nonresponders ) when gives rh positive blood . ABO incompatibility also
confers a protective effect (see incidence). The initial maternal immune
response to rh sensitization is low level of immunoglobulin (ig) m. within weeks to 6 months, igG antibodies become
detecrable. In contrast to igM, igG is capable of crossing the placenta and
destroying fetal rh positive cells.
B. OTHER BLOOD GROUP
ISOIMMUNIZATION
Of the other blood
group that may evoke an immunoglobulin capable of crossing the placenta (often
called atypical or irregular immunizing antibodies ) those that may cause
several fetal hemolysis (listed in decending order of occurrence ) are kell,
duffy, kidd, MNSs, and diego . p, Lutheran and xg groups may also cause fetal
hemolysis, but it usually is less severe.
Figure 15 1 a; rh
negative woman before pregnancy .
B pregnancy occurs.
The fetus is rh positive
C separation of the
placenta
D following delivery,
rh isoimmunization occur in the mother, and she develops antibodies (s) to the
rh positive antigen.
E the next pregnancy
with an rh positive fetus maternal antibodies
C. FETAL EFFECTS
Hemolytic disease of
the newborn occur when the maternal antibodies cross the placenta and destroy
the rh positive fetal red blood cells. The fetal anemia results, stimulating
extramedullary erythopoietic sites to produce high level of nucleated red cell
element immature erythrocytes are present in the fetal blood because of poor
maturation control to bilirubin; both of these substances, heme and bilirubin
are effectively removed by the placenta and metabolized by the mother. When
fetal red blood cell destruction far exceeds production and severe anemia
occurs, erythroblastosis fetails may result .
this is characterized by extramedullary hematopiesis, heart failure,
edema, ascites, and pericardial effusion. Tissue hypoxia and acidosis may
result. Normal hepatic architecture and afunction may be distrurbed by
extensive liver erythropoiesis, which may lead to decreased protein production,
portal hypertension and ascites.
D. NEONATAL EFFECTS
In the immediate
neonatal interval, the primary proble may relate to anemia and the sequelae
mentioned abovehowever, hyperbilirubinemia may also pose an immediate risk and
certainly pose a risk as futher red cell breakdown
ccur. The immature
(and often compromised )liver, with its low level of glucurony, transferase, is
unable to conjugate the large amount of bilirubin. This result in a high serum
bilirubin level, with resultant kernictterus (bilirubin deposition in the basal ganglia).
MANAGEMENT OF THE
UNSENSITIZED RH –NEGATIVE PREGNANCY
A. PERPREGNANCY
OR FIRST PRENATAL VISIT
On
the first prenatal visit, all pregnant woman should be screened for the ABO
blood group and the rh group, including Du. They should also undergo antibody
screening (indirect coombs’ test )unless the father of the baby is know to be rh negative, all rh
negative mother should receive prophylaxis according to the following protocol.
B. VISIT
AT 28 WEEKS
Antibody
screening is performed. If negative 300ug of rh immunoglobulin (RhlgG) is
given. If positive, the patient should be managed as rh sensitized.
C. VISIT
AT 35 WEEKS
Antibody
screening is repeated. If negative, the patient is merely observed. If
positive, the patient is managed as rh sensitized
D. POSTPARTUM
If
the infant is rh-positive or Du-positive 300ug of rhlgG is administered to the
mother (provide maternal antibody screening is negative ). Although RhlgG
should generally be given within 72hours after delivery, it has been show to be
effective in preventing isoimmunization if given up to 28 days after delivery.
If the antibody screen is positive, the patient is managed as if she will be rh
sensitized during the next pregnancy.
E. SPECIAL
FETOMATERNAL RISK STATES
Several
circumstance that may occur during
preganacy mandate administration of RhlgG to the unsensitized.
1. Abortion
–sensitization will occur in 2%of spontaneous abortion and 4-5% of induced
abortion. In the first trimester, because the small amount of fetal blood 50ug
of RhlgG apparently is sufficient to
prevent sensitization. However, because of the cost of RhlgG
has dropped, a full 300ug dose is usually given. The same dose is
recommerded for exposure after the threatened abortion is less well understood,
but many experts agree that RhlgG should also be given to these patients.
2. amniocentesis
chorionic villus sampling and cord blood sampling –if the placenta is treversed
by the needle, there is up to an 11%chance of sensitization. Therefore,
administration of 300ug of RhlgG is recommended when these procedures are
performed in the unsensitized patient.
3. anteparum
hemorrhage –in cases of placenta previa or abruption placentae, administration
of 300ug of RhlgG is recommeneded. If the pregnancy is carried more than
12weeks from the time of RhlgG
administration, a repeat prophylactic dose is recommended.
4. external
cephalic version – fetomaternal hemorrhage occur in 2-6%of patient who undergo
external cephalic version whether failed or successful therefore, these patient
should receive 300ug of RhlgG.
F. DELIVERY
WITH FETOMATERNAL HEMORRHAGE
Fetomaternal
hemorrhage so extensive that it cannot be managed with 300ug of RhlgG occur in only about 0.4% of patients. If the
sensitive screening test is positive for persistent antibody after RhlgG administrated by the kleihanuer-bethke test
and additional does of RhlgG given
according to the amount of ex
EVALUATION OF THE PREGNANCY WITH ISOIMMUNIZATION
Evaluation
of the pregnancy complicated by
isoimmunization is guided by 2factors: whether the patient has a history
of an affected fetus in a previous pregnant (ie fetus with sever anemia or
hydrops )and maternal antibody titers.
A. NO
HISTORY OF PREVIOUS FETUS AFFECTED BY RH ISOIMMUNIZATION
Once
the antibody screen is positive for isoimmunization, these patient should be followed by antibody
titer at intake, 20 week EGA, and then every 4 weeks. As long as antibody titer
remain below the critical titer (<1:32
in our laboratory, but each laboratory must establish its own norms) there is
no indication for further intervention. Once antibody titer reach 1:32 ammioncetesis should be
performed because a titer of 1:32
place the fetus at significant risk for demise before 37 weeks. An alternative
to serial ammiocentesis in patient with abnormal antibody titer or a history of
a prior affecter fetus is assessment of blood flow in the fetal middle cerebral
artery
(MCA)
by dopplex. Ultrasound is performed to idenitify the circle of willis, and
blood flow in the proximal third of the MCA can be estimated using Doppler.
High peak velocity blood flow in this area (>1.5 multiples of the median )
correlates well with sever fetal anemia. This test can be performed at 2-week
intervals in these patient, so more invasive diagnostic intervention can be
avoided until evidence of server anemia is observed.
B. HISTORY OF A PRIOR
AFFECTED BY RH ISOIMMUNIZATION
Anti body titers need
not be followed in these pregnancies because ammnicentesis is indicates by the
history of prior affected fetus. Ammnicentesis should be performed 4-8 weeks
earlier than the gestational age in the pervious pregnancy when rh associated
morbidity was first identified. Ammiocentesis, when determined to be necessary
should be performed under ultrasound guidance to minimize the risk of
transplacental hemorrhage. The ammiotic fluid is analyzed by spectrophotometry.
The opical density of the fluid is at a wavelength of 450 nm is plots on a
semilogarithmic scale versus gestational age. The ammiotic fluid concentration
of bilirubin in the unsensized patient
decrease as pregnancy pregreses thus the severity of fetal afficition
may be approximared and this information used as a guide for further studies
and treatment. . The alternatives of MCA
dopplex peavelopcity assessment. Is now more widely used. In addition to MCA
dopplex, ultrasound play an important role in evaluating the isoimmunized
patient for hydrop. Ultrasound can be used to evaluate fetal heart and amniotic
fluid index and to detect edema. Pericardial effusion, and ascites. Serial
ultrasound can document the progesion or reversal of disease.
MANAGEMENT OF THE
PRENANCY WITH ISIOMMIUNZATION
Management of these
patient is dictated by ammicentesis or MCA dopplex results (fig 15-2 ).
A. MILDLY
AFFECTED FETUS
The
fetus that falls in to zone 1 on the liley curve or has normal MCA dopplex
studies is considered to unaffected or mildly affected. Testing should be near
term and after the fetus has achieved pulmonary maturity.
B. MODERATELY
AFFECTED FETUS
The fetus that falls in to zone 2 or has MCA
dopplex studies nearing 1.5 multiples of the median (fig 15-2-) should be
tested more frequently, every 1-2 weeks. Delivery may be required prior to
term, and the fetus is delivered as soon as pulmonary maturity is reached. In
some cases, enhancement of pulmonary maturity by use of corticosteroids may be
necessary.
C. SEVERELY
AFFECTED FETUS
The
severely affected fetus falls in to zone on the liley curves has MCA dopplex
studies >1.5 multiples of the median, or has frank evidence of hydrops (eg,
ascites pleural or pericardial effusion, subcutaneous edema ) intervention
usually is needed to allow the fetus to reach a gestational age at which
delivery and neonatal risks are fewer than the risks of in utero therapy. If
the fetus is preterm, cordocentesis or percutaneous umbilical cord blood
sampling (PUBS ) is recommended at this
stage to directly assess the fetal hematocrit. Once severe anemia is performed
using o negative cytomegalovirus –negative, washed leukocyte- deplated ,
irradiates packed red cell. The intraperitoneal technique was used in years
past but has largely been replaced by intravascular fetal transfusion secondary
to its more predictable absorption. After transfusion, repeat transfusion or
delivery usually will be necessary as production of fetal blood markedly
decreases or ceases. Timing of these transfusion may be assisted by ultrasonic
determination of MCA dopplex studies. Delivery should take place when the fetus
has document pulmonary maturity.
ABO
HEMOLYTIC DISEASE
About hemolytic disease is much milder than the
isoimmiunzation evoked by rh and other antigens. The reason for this difference
is poorly understood because both igG and igM are produced antenatally.
Although 20-25% of pregnancies have potential maternal-infant ABO
incompatibility, a recognizable process in the neonate occurs in only 10% of
those cases. Those affected are almost always group A (especially A1) or B
infants of group O mothers. The neonatal direct comb’s test are also variable.
In rh isoimmunization, only 1-2% of cases occur in the first born infant,
whereas 40-50% of ABO incompatibilities occur in the first born infant. Serious
fetal sequelea (eg stillbirth, hydrops ) almost never occur, and sever fetal
anemia is rare. ABO hemolytic disease is primarily manifest following birth,
with early neonatal onset of jaundice (at<24 hours )and variable elevation
of the indirect bilirubin level. Management of ABO incompartibility (required
in 10% of cases). The infant may have hepatosplenomegaly. Exchange transfusion
is necessary in only 10% of cases, and the incidence oflate anemia is rare.
Sequelae such as kernicterus almost never occur.
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July 09, 2015
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