Improvements in preventative and therapeutic fetal medicine, such as the better timing of delivery guided by Liley's charts, fetal blood transfusion and the wide-spread use of anti-D immunoglobulin, have had dramatic effects on morbidity and mortality due to HDFN. Advances in neonatal intensive care have further contributed to this reduction. This chapter reviews therapies which may be used to treat hydrops, anaemia and jaundice in affected neonates.

Features of haemolytic disease in the neonate

There are three main clinically significant conditions seen during the first 28 days after birth caused by maternal blood group alloantibodies transferred to the fetus. These are hydrops, jaundice and anaemia.

Hydrops

The most severely affected fetuses present with hydrops manifesting as generalized tissue oedema, pleural effusions and ascites. Although the pathogenesis of these features is not clear, presumably neonates born with hydrops suffer the end result of fetal heart failure due to both hypoxic myocardial dysfunction and increased intravascular fluid retention (Section 9.3.1). Fetal liver dysfunction may also contribute to the oedema because the extensive erythropoiesis causes disruption to the portal circulation and impaired albumin synthesis. Antenatal treatment is aimed at the correction of the anaemia by fetal blood transfusion (Section 10.3), but, when a neonate is born with hydrops, early neonatal death may result from the inability to resuscitate the severely hydropic and anaemic baby at delivery. Later postnatal death may result from other consequences of hydrops, such as pulmonary hypoplasia, the complications of prematurity or even complications of treatment such as exchange transfusion.