Objective To identify the reasons behind failures to prevent the development of Rhesus (D) haemolytic disease of the newborn. Design Retrospective analysis of the case records of all pregnancies that resulted in the birth of an infant with a positive direct antiglobulin test on the cord red cells born to Rh(D) negative women between 1 April 1985 and 31 March 1990. Setting Obstetric units in the South East Scotland region and the South East Scotland Regional Blood Transfusion Service Antenatal Laboratory. Main outcome measures The causes and clinical consequences of maternal immunisation to the Rhesus (D) antigen. Results Between 1985 and 1990, 80 pregnancies resulted in the birth of an infant sensitised with anti‐D on the cord red cells. There were no deaths due to haemolytic disease, but considerable resources were deployed in obstetric and neonatal care for these pregnancies. Sufficient data were available to categorise the cause of maternal immunisation in 70 pregnancies. Seven cases were due to immunisation by pregnancy before 1970. Sixty‐three cases could be attributed to failure of the Rhesus programme: 10 cases (16%) were due to failure to implement the programme adequately, the other 53 cases (84%) were due to failure of the current guidelines to provide adequate protection. Late immunisation in an uncomplicated pregnancy was the single commonest identifiable cause. Conclusions It is likely that substantial further reductions in Rhesus (D) immunisation and haemolytic disease of the newborn will require changes in the Rhesus prevention programme. In particular the role of antenatal prophylaxis requires detailed consideration.

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887noticeable improvement in about two thirds of the remainder. About one sixth of the total cases showed slight or no improvement.4 These differences between their and our results were mainly due to an inadequate dose of the drug being given for an inadequate time. We found that nodular lesions responded quickly and depigmented macules very slowly. Our high dose and longer duration of treatment were based on the fact that sodium stibogluconate is quickly excreted in the urine and six hours after an intravenous injection blood concentrations have fallen to less than 1% of peak values. The danger of cumulative toxicity might be exaggerated.5We thank Dr R S Jha, department of pathology; Mr R J Sharma, technician;and Mr C P Singh, who typed the manuscript. We received financial support from the United Nations Development Programme/World Bank/World Health Organisation special programme for research and training in tropical disease.