PEDIATRICS Vol. 7 No. 6 June 1951, pp. 865-872
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Round Table Discussion

RECENT ADVANCES IN THE TREATMENT OF BLOOD DYSCRASIAS IN CHILDREN

MILA PIERCE M.D., I. DAVIDSOHN M.D., EDITH POTTER M.D., WILLIAM J. SCOTT M.D., and JAMES B. SNOW M.D.

Chairman Pierce: I wish to emphasize that your participation in the discussion is cordially invited. It is the desire of the Program Committee that the Round Table provide an opportunity for all of us to share our experience. The specialists whom we have invited to join us and who are well known to us have kindly indicated their willingness to take part in the discussion. Dr. I. Davidsohn is the attending hematologist at Mt. Sinai Hospital; Dr. Edith Potter is the pathologist at Chicago Lying-in Hospital. The subject for discussion this morning will be limited to a discussion of acute hemolytic anemia of the newborn, or erythroblastosis fetalis—hematologic and pathologic aspects of the disease. All the hemolytic anemias have certain common characteristics. Erythrocytes are destroyed, anemia follows, hepatic function is disturbed by anoxia, and further impaired by the demand for the excretion of excessive quantities of blood pigment. Bilirubinemia follows. The hematopoietic centers compensate for blood destruction by delivery of reticulated erythrocytes or normoblasts to the blood and extramedullary erythropoiesis may result. In the acute hemolytic anemias this chain of events is initiated by a plasma factor while the cells themselves are normal. The plasma factor may be (1) an antibody; (2) a toxin of bacterial or spirochetal origin; (3) a chemical, or (4) a hormone. In the chronic types of hemolytic anemias there is often a familial or racial abnormality of the erythrocytes which predisposes it to the hemolytic effects of a plasma factor. Examples of hemolytic anemia resulting from these various causes are seen in the newborn. (1) Erythroblastosis fetalis or hemolytic disease of the newborn is due to the antigen antibody reaction caused by incompatibility of blood groups of mother and baby; (2) hemolytic anemia due to bacterial toxin may result from sepsis, bronchopneumonia or congenital lues; (3) in congenital hemolytic icterus, the splenic or hormonal factor together with erythrocytes which are spheroids rather than discs in the cause of the anemia.