Page 432 - Essential Haematology

418 / Chapter 30 Pregnancy and neonatal haematology

1 Haemorrhage Fetomaternal, twin – twin, cord, HDN. Fetal platelets that possess a paternally inher-
internal, placenta. ited antigen (HPA - 1a in 80%; HPA - 5b in 15%)

2 Increased destruction Haemolysis (immune or that is not present on maternal platelets can sensi-
non - immune) or infection. tize the mother to make antibodies that cross the

3 Decreased production Congenital red cell aplasia, placenta, coat the platelets which are then destroyed
infection (e.g. parvovirus). Anti - Kell causes by the reticuloendothelial system and lead to serious
alloimmune anaemia of the fetus and newborn bleeding, including ICH. Alloimmune thrombocy-

with decreased erythropoiesis. topenia differs from HDN in that 50% of cases
occur in the first pregnancy. Its incidence is approxi-

Generally, anaemia at birth is usually secondary to
mately 1 in 1000 – 5000 births.
immune haemolysis or haemorrhage; non - immune

Thrombocytopenia can lead to serious, some-
causes of haemolysis appear within 24 hours.
times fatal, bleeding in utero or after birth. Treatment
Impaired red cell production is usually not apparent
is unsatisfactory. Severe postnatal cases may be
for at least 3 weeks. Haemolysis is often associated
treated with a platelet transfusion that is negative
with severe jaundice and the causes include HDN,
for the relevant antigen. Antenatal treatment
autoimmune haemolytic anaemia in the mother
may be either maternal intravenous immunoglobu-
and congenital disorders of the red cell membrane
lin or fetal transfusion with HPA - compatible
or metabolism.
platelets.
Red cell transfusion may be needed for sympto-
matic anaemia with Hb < 10.5 g/dL or a higher
threshold if there is severe cardiac or respiratory Coagulation
disease.
Standard tests need to be interpreted with caution

in the neonate. The APTT and PT are prolonged
Anaemia of p rematurity because of reduced levels of the vitamin K - dependent
factors II, VII, IX and X, and become normal at
Premature infants have a more marked fall in Hb around 6 months. The thrombin time (TT) is com-

after birth and this is termed physiological anaemia parable with adult values. Neonates have an
of prematurity . Features include a slowly falling increased risk of thrombosis. This is a result of

Hb, normal blood film and reticulocytopenia. It physiologically low levels of inhibitors of coagula-
can be minimized by ensuring adequate iron and tion and the use of indwelling vascular catheters.
folate replacement and limiting phlebotomy. Antithrombin and protein C levels are approxi-
Erythropoietin is used in some centres. mately 60% of normal for the first 3 months.

Homozygous protein C deficiency is associated

with fulminant purpura fulminans in early life.
Neonatal p olycythaemia
Therapeutic protein C concentrates are now avail-

This is defined as a venous haematocrit over 0.65 able. Homozygous antithrombin defi ciency usually

and can occur with twin – twin transfusion, intrau- presents later in childhood but arterial and venous
terine growth restriction and maternal hypertension thrombosis may also occur in the neonate.
or diabetes. If symptoms are present it should be
treated with partial exchange transfusion using a
crystalloid solution.
Haemolytic d isease of
the n ewborn
Fetomaternal a lloimmune
HDN is the result of red cell alloimmunization in
t hrombocytopenia
which IgG antibodies passage from the maternal
Fetomaternal alloimmune thrombocytopenia results circulation across the placenta into the circulation
from an immunological process similar to that of of the fetus where they react with fetal red cells and