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The conquest of Rh disease.

We now have the means of preventing Rh hemolytic disease in newborn infants. Worldwide studies have proven that the administration of a y-globulin preparation containing anti-Rh (anti-D) antibodies to Rh-negative women post partum prevents Rh isoimmunization. Without such treatment approximately 15% of women at risk (Rh-negative mothers with Rh-positive babies) will produce antibodies. Problems remain, however. The existing programs are not totally effective and failures still occur. At present most of these failures result from error or oversight within the program. Ideally, every Rh-negative woman who has delivered an Rh-positive baby should be tested and if her serum does not contain anti-D antibodies she should receive anti-D-containing y-globulin. In Canada this has been Rh immune globulin (Connaught Laboratories, Toronto). In several reported series the percentage of women injected has varied from 70% to more than 99% .. For example, if only 80% of a population of women at risk are injected with Rh immune globulin, approximately 3% of that population will become isoimmunized. The problem is greater following abortion. Rh isoimmunization occurs in approximately 4% of Rhnegative women who abort and is prevented if anti-D-containing y-globulin is administered following the abortion. However, compliance in the treatment of cases after an abortion has been less than that after delivery.1 Accordingly, every effort must be made to develop a system whereby women who have aborted, either spontaneously or by therapeutic intervention, receive protection. Since it is difficult to determine the Rh status of the fetus in such cases, all Rh-negative women who abort should be treated. Another cause of failure is massive transplacental hemorrhage at delivery. There is evidence to suggest that the 300 pg-dose of anti-D recommended in Canada will not prevent Rh isoimmunization in mothers who have received more than 30 mL of fetal blood by transplacental hemorrhage (approximately 1 in 300 deliveries). Such bleeds can be easily detected by routine testing of maternal blood for the presence of fetal erythrocytes by the Kleihauer technique. When a fetal bleed has been detected and quantitated, the appropriate additional dose of anti-D containing y-globulin (10 ,ig of antiD/mL of fetal blood) can be given. Accordingly, the following recommendations can be made: 1. All Rh-negative women who have delivered an Rh-positive baby should receive a protective dose of anti-Dcontaining y-globulin. 2. All Rh-negative women should receive a protective dose of anti-D 'yglobulin after an abortion or amniocentesis. 3. All Rh-negative women should be screened post partum for massive transplacental hemorrhage; when there is evidence that this has occurred, the dose of anti-D-containing y-globulin should be increased to provide a minimum of 10 ,.g of anti-D per millilitre of transplacental hemorrhage. If the above recommendations are applied most cases of Rh isoimmunization will be prevented. Is this the end of the problem? The answer is no, since it now appears that a proportion of women at risk will produce antibodies before delivery. For them prevention post partum will be too late. The problem of antepartum isoimmunization is the subject of two papers presented by Bowman and his associates in this issue of the Journal (pages 623 and 627). In the first of these papers, the Winnipeg group point out that in 1.8% of Rh-negative women at risk (63 of 3533) antibodies developed prior to delivery. Although the antibodies were often weak when first detected, the severity of antepartum isoimmunization did not differ significantly from that appearing post partum. It was found that the severity of disease in subsequent infants was not significantly different from that occurring in the infants of women who had been immunized post partum. Most of these women were isoimmunized after the 28th week of gestation. It was therefore reasonable to consider whether such cases of isoimmunization could be prevented by administering anti-D-containing y-globulin at the 28th and 34th weeks of pregnancy. There is now ample evidence that such treatment is safe to the mother and fetus.1 The Winnipeg group now describe the exciting results of such a study in which they found that of 1357 women treated none produced antibodies; one would expect from earlier data that 24 of this number would have produced antibodies. The study described by Bowman and associates used historical rather than concurrent controls. Nevertheless, reports from elsewhere suggest that the incidence of antepartum isoimmunization in untreated women does vary from 1 % to 2% *1 Furthermore, studies performed in Sweden (F. Bartsh and M. Hermann: personal communication, 1977), Australia (M. Davey: personal communication, 1977) and Hamilton (M. Blajchman and A. Zipursky: unpublished study, 1977) support the observation of Bowman and colleagues concerning the effectiveness of antepartum protection. Bowman and coworkers point out that although an injection at the 28th and 34th weeks of pregnancy will prevent most cases of antepartum isoimmunization, there