Page 436 - Essential Haematology

422 / Chapter 30 Pregnancy and neonatal haematology

Clinical f eatures of HDN exchange. The donor blood should be less than 5

days old, CMV - negative, irradiated and Rh
1 Severe disease Intrauterine death from hydrops
D - negative and ABO compatible with the baby s
’
fetalis (Fig. 30.7 a).
’
and mother s serum. Phototherapy (exposure of the

2 Moderate disease The baby is born with anaemia
infant to bright light of appropriate wavelength)
and jaundice and may show pallor, tachycardia,
degrades bilirubin and reduces the likelihood of
oedema and hepatosplenomegaly. If the uncon-
kernicterus.
jugated bilirubin is not controlled and reaches
levels exceeding 250 μ mol/L, bile pigment depo-
sition in the basal ganglia may lead to kernicterus ABO h aemolytic d isease of the n ewborn
– central nervous system damage with general-
In 20% of births, a mother is ABO incompatible
ized spasticity and possible subsequent mental
with the fetus. Group A and group B mothers

deficiency, deafness and epilepsy. Th is problem
usually have only IgM ABO antibodies. Th e major-
becomes acute after birth as maternal clearance
ity of cases of ABO HDN are caused by ‘ immune ’
of fetal bilirubin ceases and conjugation of
IgG antibodies in group O mothers. Although 15%
bilirubin by the neonatal liver has not yet reached
of pregnancies in white people involve a group O
full activity.
mother with a group A or group B fetus, most

3 Mild disease Mild anaemia with or without
mothers do not produce IgG anti - A or anti - B and
jaundice.
very few babies have severe enough haemolytic
Investigations will reveal variable anaemia with a disease to require treatment. Exchange transfusions
high reticulocyte count; the baby is Rh D - positive, are needed in only 1 in 3000 infants. Th e mild
the direct antiglobulin test is positive and the serum course of ABO HDN is partly explained by the A
bilirubin raised. In moderate and severe cases, many and B antigens not being fully developed at birth
erythroblasts are seen in the blood film (Fig. 30.7 b) and by partial neutralization of maternal IgG anti-

and this is known as erythroblastosis fetalis . bodies by A and B antigens on other cells, in the
plasma and tissue fl uids.
In contrast to Rh HDN, ABO disease may be
Treatment
found in the first pregnancy and may or may not

Exchange transfusion may be necessary; the indica- affect subsequent pregnancies. The direct antiglobu-
’
tions for this include severe anaemia (Hb < 10 g/dL lin test on the infant s cells may be negative or only
at birth) and severe or rapidly rising hyperbilirubi- weakly positive. Examination of the blood fi lm
naemia. More than one exchange transfusion may shows autoagglutination and spherocytosis, poly-
be required and 500 mL is usually suffi cient for each chromasia and erythroblastosis.

SUMMARY ■ Pregnancy results in changes in the ■ Serum vitamin B 12 levels fall in pregnancy

but defi ciency is rare. Platelets counts also
haematological systems.
fall on average by 10%, but in some

■ There is a fall in haemoglobin because of
women this physiological fall may be
an increased plasma volume that is
severe or may be caused by immune
proportionally greater than a 25% increase

thrombocytopenia.

in red cell mass.
■ Pregnancy is a hypercoagulable state with

■ Iron defi ciency is frequent; folate defi ciency

is associated with maternal anaemia and

risk of thrombosis or disseminated
with neural tube defects (NTDs) in the
intravascular coagulation.
fetus. increased levels of coagulation factors and