Clinical Review

Management of pregnancies with RhD alloimmunisation

BMJ 2005; 330 doi: http://dx.doi.org/10.1136/bmj.330.7502.1255 (Published 26 May 2005) Cite this as: BMJ 2005;330:1255
  1. Sailesh Kumar, consultant in fetal medicine ([email protected])1,
  2. Fiona Regan, consultant haematologist1
  1. 1Centre for Fetal Care and Department of Haematology, Hammersmith Hospitals NHS Trust, Queen Charlotte's Hospital, Imperial College London, London W12 0HS
  1. Correspondence to: S Kumar
  • Accepted 13 April 2005

Introduction

Pregnancies complicated by red cell alloimmunisation may result in fetal anaemia secondary to transplacental passage of maternal immunoglobulin G, which causes progressive fetal haemolysis. In severe cases the anaemic fetus develops ascites, subcutaneous oedema, and pleural and pericardial effusions (hydrops fetalis) and dies in the womb. Many different antibodies (anti-D, anti-Kell, anti-c, anti-E, etc) can cause haemolytic disease of the fetus and newborn. This review covers the management of pregnancies affected with RhD alloimmunisation. The principles of management are similar regardless of the type of antibody involved, although care needs to be taken with pregnancies complicated by Kell alloimmunisation, where antibody concentrations do not always correlate with disease severity.

We searched PubMed for up to date references on current advances in the treatment of RhD alloimmunisation. In addition, we used guidelines on antenatal care and prophylaxis from the websites of the National Institute for Clinical Excellence (NICE, http://www.nice.org.uk/) and the Royal College of Obstetricians and Gynaecologists (http://www.rcog.org.uk/).

Hydrops fetalis was first described in 1609 by a French midwife, Louise Borgeois,1 after the birth of twins one of whom was oedematous and the other deeply jaundiced; both died soon after the birth. However, it was not until 1940 that Landsteiner and Weiner, using rhesus monkeys, discovered the RhD antigen.2

Pathophysiology

The RhD polypeptide is an integral membrane protein expressed exclusively on erythrocytes. Some 16% of white people are RhD negative because of deletion of the gene. During pregnancy, small volumes of fetal red cells continually get into the mother's circulation. This trafficking of red cells increases as gestation progresses. Bowman et al showed at least 0.01 ml of fetal cells in 3%, 12%, and 46% of women in each trimester.3 In most women, this load of RhD antigen on fetal erythrocytes and erythrocyte precursors does not stimulate the …

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