Hydrops Fetalis Caused by Massive Maternofetal Transplacental Hemorrhage

Abstract

Chronic massive fetomaternal transplacental hemorrhage is a documented cause of nonimmune hydrops fetalis. The present authors describe a remarkable instance of such a hemorrhage that produced heart failure and hydrops in utero. The mother was a 31-year-old healthy woman (group A Rh-positive blood) in her second pregnancy, the first having resulted in a normal full-term delivery. The pregnancy was uneventful until the 31st week of gestation, when she noted a rapid increase in abdominal girth. She was referred 5 days later for fetal assessment. The real-time ultrasound scan demonstrated a fetus with ascites, hepatosplenomegaly, placental edema, and early skin edema. Maternal serum, tested against a red cell panel including the husbands's red cells, by enzyme and indirect antiglobulin methods, showed no red cell antibodies. A Kleinhauer acid elution test revealed that 5.4 per cent of her circulating red cells were of fetal origin, indicating that a potentially exsanguinating fetal transplacental hemorrhage had occurred. With evidence of massive fetal transplacental hemorrhage, the cause of the hydrops was believed to be severe anemia, hepatic erythropoiesis, portal obstruction, and hepatocellular damage. The patient was delivered promptly by cesarean section. The infant, a 2700-gm girl, looke plethoric. She became cyanotic and required prompt endothracheal intubation and positive-pressure ventilation with 100 per cent oxygen. She had moderate generalized edema and clinical evidence of ascites. Her liver was firm and palpable 2.5 cm below the right costal margin. Moist crepitations were audible throughout both lungs. The heart sounds were indistinct, and a gallop rhythm was heard. After tracheal intubation and positive-pressure ventilation, abdominal paracentesis was performed. Forty millili-ters of yellow ascitic fluid were aspirated, and more ascitic fluid drained through the paracentesis wound subsequently. After paracentesis, an 8 French catheter was placed in the umibilical vein, and an exchange transfusion was begun with compatible 24-hour-old group O, Rh-negative blood, partially packed to a hemoglobin concentration of 140 to 150 g per liter. Initial portal venous blood gas values were pH 7.18, pO2 43 torr, and pCO2 68 torr. As the exchange transfusion progressed, the baby's color and blood gas values improved. Shortly after the commencement of exchange transfusion, the cord blood hemoglobin concentration and hem-atocrit were reported to be 205 and 0.63 gm/liter, respectively, which refuted the original diagnosis of hydrops related to fetal anemia, portal obstruction, and hepatocellular damage. Because of the plethora and the likelihood of hypervolemia and hyperviscosity, the transfusion was continued until the equivalent of one blood volume of the infant (200 ml) had been exchanged. A 10 per cent (20 ml) blood volume deficit was left at the end of the exchange transfusion. Postexchange hemoglobin and hematocrit were 155 and 0.52 gm/liter, respectively. Total serum protein and albumin concentrations in the cord and preexchange samples were 58 and 33 gm/liter and 62 and 38 gm/liter, respectively, which excluded hy-poproteinemia as the cause of the fetal hydrops. Just as the exchange transfusion was completed, the laboratory notified the authors that, whereas 5.4 per cent of the red cells circulating in the mother were Kleihauer positive and therefore of fetal origin, 90 per cent of the red cells in the cord and preexchange blood samples were Kleihauer negative and probably of maternal origin. A chest radiograph taken shortly after completion of the exchange transfusion showed cardiomegaly and pulmonary congestion. An echocardiogram revealed a structurally normal heart with a probable (unconfirmed) pericardial effusion. The infant was given digoxin and furosemide and maintained on positive-pressure artificial ventilation. Diuresis was prompt and the crepitations disappeared. She was taken from the ventilator on the 4th day. Another chest radiograph on the 5th day showed a normal heart and lungs. The infant reached her lowest weight (2000 gm, 26 per cent below her birth weight) at 6 days of age. She was discharged from the hospital 18 days after birth, clinically well, breast feeding, and gaining weight. When seen at 7 months of age, she appeared to be a healthy baby. The placenta weighed 560 gm. On its cut surface were extensive areas of infarction, with areas of intervillous hemorrhage. In sections taken from an excavated lesion below the insertion of the umbilical cord, seven stem vessels of fetal origin were identifiable. Microscopic examination of these vessels showed areas of rupture and tearing of their walls. The minor blood group populations in the mother and infant were readily detected by a capillary blood grouping