Ruble A. Mason

Coagulation changes in eclampsia: Their frequency and pathogenesis

The maternal coagulation mechanism has been investigated in an effort to identify its role, if any, in the pathogenesis of eclampsia. Thrombocytopenia was identified in 28 of 95 cases (29 per cent), a prolonged thrombin time in 19 of 38 (50 per cent), abnormally elevated serum fibrinogen-fibrin degradation products in two of 65 (3 per cent), and circulating fibrin monomer in one out of 20 (5 per cent). Overt hemolysis was rare (2 per cent). Thus the pattern as well as the degree of change in the maternal coagulation mechanism differed remarkably from that typical of severe abruptio placentae and of prolonged retention of a dead fetus, the classic obstetric models of fast and slow disseminated intravascular coagulation. It is concluded that the coagulation changes when present in eclampsia are effect rather than cause. Moreover, the changes may evolve primarily from platelet adherence at sites of vascular endothelial damage as the consequence of segmental vasospasm and vasodilatation rather than be triggered by the escape of thromboplastin from the placenta into the maternal circulation.

The effects of maternal sickle cell hemoglobinopathies and sickle cell trait on reproductive performance

Abstract Reproductive performances have been analyzed for 797 black women whose red cells contain sickle cell hemoglobin. Fifty pregnancies in 34 women with sickle cell anemia yeilded only 27 infants who survived; there were no maternal deaths, but morbidity was frequent and often intense. Seventy-eight pregnancies in 43 women with sickle cell-hemoglobin C disease culminated in the births of 68 infants who survived; serious maternal morbidity was common, and 2 women died. Thirty-two infants survived from 37 pregnancies in 21 women with sickle cell-beta thalassemia disease; maternal morbidity was comparable to that with sickle cell-hemoglobin C, disease but there were no maternal deaths. The pregnancy experiences for women with sickle cell trait were not different from those of black women whose red cells do not sickle except for twice the frequency of significant bacteriuria. Thus, the only major cause for special concern by women with sickle cell trait who contemplate reproduction is their potential for transmission of one gene for sickling to the off spring.

On reducing the frequency of severe abruptio placentae

At Parkland Memorial Hospital the frequency of abruptio placentae so severe as to kill the fetus has decreased from 1 in 420 deliveries during 1956 through 1969 to 1 in 830 during 1974 through 1989. Major factors in this reduction were elimination of very high parity and a marked increase in the percentage of Latin American women, in whom the risk was 1 in 1473 deliveries compared with 1 in 595 for black women and 1 in 876 for white women. Abdominal trauma was encountered rarely, as was fetoplacental-to-maternal hemorrhage sufficient to impair fetal perfusion seriously. Abnormal development of Müllerian ducts and uterine myomas were encountered rarely. Neither red blood cell macrocytosis characteristic of folate deficiency nor iron deficiency could be implicated in the genesis of severe abruptio placentae. Abruptio placentae recurred in 12% of subsequent pregnancies and proved fatal to the fetus in 7%, unchanged from our earlier experience.

Mechanisms of hemolysis and anemia associated with acute antepartum pyelonephritis

Anemia develops in about a fourth of women whose pregnancy is complicated by pyelonephritis, although its exact mechanism has not been defined clearly. In this study of 18 women with antepartum pyelonephritis, although only a third had anemia (hematocrit p

Prophylactic transfusions of normal red blood cells during pregnancies complicated by sickle cell hemoglobinopathies

Prophylactic transfusions of normal donor red cells were administered during 37 pregnancies to women with sickle cell anemia, sickle cell-hemoglobin C disease, or sickle cell-beta thalassemia disease. Once the diagnosis was confirmed, the transfusions were administered intermittently throughout the rest of the pregnancy in such amounts and at such frequencies that no more than 60% of the circulating red cells contained hemoglobin S and the hematocrit was above 25. The maternal mortality rate was zero and maternal morbidity as the consequence of the sickle cell hemoglobinopathy was minimal. The perinatal mortality rate was appreciably reduced when compared to that previously observed without prophylactic transfusions but perinatal morbidity was still excessive. Evidence that the intrauterine environment was compromised, in spite of the transfusions consisted of an increased frequency of growth-retarded fetuses, of meconium staining of amnionic fluid, and of ominous decelerations of fetal heart rate. Morbidity from the transfusions was troublesome. Nonetheless, it is concluded tentatively that both the mother with a sickle cell hemoglobinopathy and her fetus are likely to benefit from prophylactic transfusions of normal donor red cells administered during one pregnancy according to the protocol employed in this study.