• U.S.

Medicine: The Unnecessary Illness

4 minute read
TIME

On the surface, Joan and her husband Bob seemed compatible. But biologically, they were not. Bob’s blood was Rh-positive, Joan’s negative−meaning that she lacked the Rh factor* present in most blood. The difference had no adverse effect on their first child, an Rh-positive boy born in a Louisville hospital two years ago. But their second, born last year, suffered from a condition called erythroblastosis fetalis, which destroyed his red blood cells, leaving him severely anemic with an accumulation of toxic substances in his tiny body. Soon after birth, he died.

The case is not unusual. Twelve percent of all American marriages pair an Rh-negative woman with an Rh-positive man. Of the 3.3 million deliveries that take place in the U.S. each year, 260,000 result in the birth of an Rh-positive baby to an Rh-negative mother, and of these babies, at least 10% are likely to be afflicted with some degree of Rh disease. The irony is that this threat is unnecessary. Medicine has an effective weapon against Rh disease.

The first child of a positive-negative couple is usually unaffected. But if the baby is Rh-positive, and the chances are 3 in 5 that he will be, then there is an increasing chance of trouble in later pregnancies. Exposure to Rh-positive fetal blood, which may leak across the placenta or enter the maternal blood stream as a result of hemorrhage during delivery, can cause the Rh-negative mother to become sensitized, or “immunized,” against future Rh-positive babies and produce antibodies that attack and destroy the babies’ red blood cells.

Mildly affected babies may be only slightly anemic and recover fully from the jaundice, or yellowing, that characterizes their condition. Those with more serious cases of erythroblastosis fetalis suffer from the presence in the blood of too many erythroblasts, or immature red blood cells. Unable to do mature cells’ work of carrying oxygen to the body’s cells, the overworked blood-producing tissues−liver, spleen and other organs−swell and contribute to congestive heart failure, eventually causing death. The most seriously afflicted infants, however, are usually stillborn.

Once, the only treatment for Rh disease was to replace virtually the entire fetal blood supply with massive transfusions before or shortly after birth. Now prevention is possible in the form of a blood extract called Rh immune globulin. Developed independently by research teams in England and the U.S. nearly a decade ago, the globulin acts as a vaccine to curtail the Rh-negative woman’s production of antibodies and greatly reduces the risks to future Rh-positive children.

But Dr. John Gorman, one of the American researchers, warns that the vaccine works only if the woman is not already immune to Rh factor. He recommends that the globulin be given automatically to every woman within 72 hours of her first delivery, abortion or miscarriage if tests show that she is Rh-negative and the baby is Rh-positive. Says he: “You’ve got to get in during the time that the window is open.”

Most doctors and hospitals routinely use this vaccine on Rh-negative women following the birth of Rh-positive babies. Connecticut has established a registry to show which patients need the inoculation and which have received it. Despite such precautions, many women leave the hospital with a built-in immunity to their offspring.

Rh disease is not a major problem in Africa−nearly all black Africans (like most blacks in the U.S.) are Rh-positive. In other countries, it remains a persistent though preventable ailment.The World Health Organization estimates that 75% of the Rh-negative women in Britain now receive the vaccine. But in Italy, the vaccine is now given to only 30%, while in Venezuela, only 5% of Rh-negative mothers get the shots. Even in the U.S., where 85% are now protected, the gap is still significant. Only half of the women now undergoing abortions receive Rh immune globulin after their operations.

These gaps are unfortunate. Used properly, the vaccine is nearly 99% effective.

* A substance on the surface of red blood cells that is crucial, along with the A, B and O factors, in matching blood types.

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