The development of the replacement transfusion for the prevention of brain damage associated with elevated levels of bilirubin in the blood has prompted numerous papers related to this procedure. The present report deals with a frequently observed phenomenon occurring during exchange transfusion, which seldom attracts attention until a disastrous episode takes place. This was our experience, and it therefore seemed desirable to re-evaluate the pathophysiology associated with pressure changes in the umbilical vein of the neonate.
This report will present a case of marked negative pressure in the umbilical vein of a neonate exhibiting inspiratory stridor of partial airway obstruction, and also the physiologic data from some animal experi ments to demonstrate this phenomenon.
CASE REPORT
Infant B was the second-born, male twin of a 24-year-old, Rh-negative, gravida 4, para 3 mother. At term the maternal Rh antibody titer was 1:32. The membranes ruptured spontaneously 48 hours prior to delivery. Labor was induced with oxytocin (Pitocin) administered intravenously. Twin Infant A was delivered spontaneously, unassisted; it was then found that twin B presented as a "transverse lie." This second twin was delivered in 15 minutes by version and extraction. Respiration was initiated after endotracheal aspiration and was normal for 1 hour, after which an inspiratory stridor was noted associated with moderate cyanosis. The stridor and cyanosis improved with oxygen-mist therapy. The baby weighed 2,930 gm and the blood was Rh-positive and Coombs' positive, as was the blood of his twin. Bilirubin in the serum at birth was 3 mg/100 ml; hemoglobin, 14.5 gm/100 ml.