Abstract

In the 1960s, hyaline membrane disease (HMD) was the major cause of neonatal death in the United States. Boston, Geller, and Smith (1) reported 100% mortality if neonates had Pao2s of less than 100 mm Hg in the first 12 hours after birth, and Stahlman and associates (2) reported a 70% mortality if neonates were breathing 100% oxygen in the first 12 postnatal hours. Included among the deaths were infants who weighed more than 1,800 g at birth. Outcomes were similar in other centers. Available care often consisted of administering oxygen, intravenous fluids, and antibiotics and keeping patients warm. As a last ditch effort, some babies were mechanically ventilated. Knowledge of the physiology of neonates and of their disease processes increased rapidly during this period. Smith (3) and Nelson and colleagues (4) demonstrated that neonates who had HMD had low lung compliance and a reduced functional residual capacity. Stahlman, (5) Rudolph and associates, (6) and many others demonstrated abnormalities in ventilation or the cardiovascular systems of affected neonates. John Clements isolated surfactant from the lung, (7) and Mary Ellen Avery and Jerry Mead (8) demonstrated a deficiency of surfactant in the lungs of neonates who died of HMD. Surfactant deficiency was associated with atelectasis. In detailed pulmonary and cardiovascular studies of neonates who had HMD, Chu and associates (9) demonstrated that a significant portion of the problem with this disease was due to mismatching of ventilation and perfusion and that grunting was an effort to counteract atelectasis (Figure). The development of neonatal intensive care units (NICUs) in the early 1960s, such as that created by Dr. Mildred Stahlman at Vanderbilt University, provided an environment in which sick neonates could be cared for, questions could be asked and answered, and physiologic measurements (such as those used by Stanley …

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