Rh Incompatibility
Preterm
Theoretically, no direct connection exists
between the fetal
and maternal circulation, so no fetal blood
cells should
enter the maternal circulation. In
actuality, occasional pla-cental villi break
and a drop or two of fetal blood does
enter
the maternal circulation. If the mother’s
blood type is Rh
(D) negative and the fetal blood type is Rh
positive (con-tains the D antigen), the
introduction of fetal blood causes
sensitization to occur, and the woman
begins to form anti-bodies against the D
antigen. Few antibodies form this
way, however. Most form in the woman’s
bloodstream in
the first 72 hours after birth because
there is an active ex-change of fetal–
maternal blood as placental villi loosen
and
the placenta is delivered. After this
sensitization, in a sec-ond pregnancy
there will be a high level of antibody D cir-
culating in the woman’s bloodstream,
which will then act
to destroy the fetal red blood cells early in
the pregnancy if
the new fetus is Rh positive. By the end of
pregnancy, a
fetus can be severely compromised by the
action of these
antibodies crossing the placenta and
destroying red blood
cells. Some infants require intrauterine
transfusions to
combat red cell destruction.
labor may be induced
to remove the fetus from the destructive
maternal environ-ment. Administering
phenobarbital to women during their
last weeks of pregnancy has been tried to
reduce symptoms
in newborns as it speeds liver maturity so
that the infant
liver better converts indirect to direct
bilirubin. This, un-fortunately, also carries
the risk of fetal sedation (Thomas,
Muller, & Wilkinson, 2009).
ABO Incompatibility
In most instances of ABO incompatibility,
the maternal
blood type is O and the fetal blood type is
A; it may also
occur when the fetus has type B or AB
blood. A reaction in
an infant with type B blood is often the
most serious.
Hemolysis can become a problem with a
first pregnancy
in which there is an ABO incompatibility
as the antibodies
to A and B cell types are naturally
occurring antibodies or are
present from birth in individuals whose
red cells lack these
antigens. Unlike the antibodies formed
against the Rh D fac-tor, these antibodies
are of the large (IgM) class and do not
cross the placenta. An infant of an ABO
incompatibility,
therefore, is not born anemic, as is the
Rh-sensitized child.
Hemolysis of the blood begins with birth,
when blood and
antibodies are exchanged during the
mixing of maternal and
fetal blood as the placenta is loosened;
destruction of red cells
may continue for up to 2 weeks of age.
Interestingly, preterm
infants do not seem to be affected by ABO
incompatibility.
This may be because the receptor sites for
anti-A or anti-B
antibodies do not appear on red cells until
late in fetal life.
Even in the mature newborn, a direct
Coombs’ test may be
only weakly positive because of the few
anti-A or anti-B sites
present. The reticulocyte count (immature
or newly formed
red blood cells) is usually elevated as the
infant attempts to
replace destroyed cells.
Assessment
Rh incompatibility of the newborn can be
predicted by find-ing a rising anti-Rh titer
or a rising level of antibodies (indi-rect
Coombs’ test) in a woman during
pregnancy. It can be
confirmed by detecting antibodies on the
fetal erythrocytes
in cord blood (positive direct Coombs’
test) by percutaneous
umbilical blood sampling (see Chapter 9)
or at birth. The
mother in this situation will always have
Rh-negative blood
(dd), and the baby will be Rh positive
(DDor Dd).
With Rh incompatibility, an infant may not
appear pale
at birth despite the red cell destruction
that has occurred in
utero. This is because the accelerated
production of red cells
during the last few months in utero
compensates to some de-gree for the
destruction. The liver and spleen may be
en-larged from an attempt to destroy
damaged blood cells. If the
number of red cells has significantly
decreased, the blood in
the vascular circulation may be hypotonic
to interstitial fluid;
fluid will shift from the lower to higher
isotonic pressure by
the law of osmosis, causing extreme
edema. Finally, the se-vere anemia can
result in heart failure as the heart has to
beat
so fast to push the dilute blood forward.
Hydrops fetalisis
an old term for the appearance of a
severely involved infant
at birth. Hydrops refers to the edema, and
fetalis refers to the
lethal state.
Most infants do not appear jaundiced at
birth because the
maternal circulation has evacuated the
rising indirect biliru-bin level. With birth,
progressive jaundice, usually occurring
within the first 24 hours of life, will begin,
indicating in both
Rh and ABO incompatibility that a
hemolytic process is at
work. The jaundice occurs because as red hyperbilirubinemia that range from mild
blood cells are de-stroyed, indirect dysfunction to
bilirubin is released. Indirect bilirubin is
kernicterus (invasion of bilirubin into
fat
brain cells) can
soluble and cannot be excreted from the
occur. An infant needs to use glucose
body. Under normal
stores to maintain
circumstances, the liver enzyme
metabolism in the presence of anemia.
glucuronyl transferase con-verts indirect
This can cause a
bilirubin to direct bilirubin. Direct bilirubin
is progressive hypoglycemia, compounding
the initial prob-lem. A decrease in
water soluble and combines with bile for
hemoglobin during the first week of life
excretion from the
to a level less than that of cord blood is a
body with feces. In preterm infants or
later indication of
those with extreme he-molysis, the liver
cannot convert indirect to direct bilirubin, blood loss or hemolysis
so jaundice becomes extreme.

Pregnanediol, the breakdown product of

progesterone,

can interfere with the conjugation of

indirect bilirubin. This

is excreted in breast milk until the high

levels of progesterone

that were present during pregnancy are

decreased, usually 24

to 48 hours after birth. Breastfed babies,

therefore, may evi-dence more jaundice
than bottle-fed babies.

Normally, cord blood has an indirect

bilirubin level of 0

to 3 mg/100 mL. An increasing indirect

bilirubin level is

dangerous because if the level rises above

20 mg/dL in a

term infant or 12 mg/dL in a preterm

infant, brain damage

from bilirubin-induced neurologic

dysfunction (BIND) or

a wide spectrum of disorders caused by

increasingly severe