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We followed the clinical course of 23 infants with bronchopulmonary dysplasia (BPD) on home oxygen therapy during the first year of life in order to monitor patterns of growth, need for hospital readmission, and improvement in oxygenation. Oxygenation was assessed by serial, resting, awake, and room air transcutaneous PO2 (tcPO2) measurements at clinic visits. Weight gain was poor, with boys growing below the fifth percentile and girls growing at the tenth percentile. Ten of the 23 infants (43%) required rehospitalizations. There were no deaths. Fourteen of the 23 infants (61%) were taken off supplemental oxygen by 12 months corrected age, at a mean age of 7.9 months. Mean rate of improvement in tcPO2 was 3 torr/month, but wide individual variation was found. Infants off of oxygen treatment at 12 months corrected age grew at a significantly greater rate than those still requiring oxygen supplementation (p less than 0.02). Infants with right ventricular hypertrophy (RVH) by electrocardiogram tended to resolve their RVH while on home oxygen therapy. We conclude that infants with BPD on home oxygen therapy generally show steady improvement in oxygenation, but grow poorly and require frequent hospitalizations.

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Fifty newborn infants of less than 33 weeks' gestation were followed prospectively from birth with serial coagulation and real-time ultrasound studies. A significant association of hypocoagulability in the first four hours of life with subsequent onset or progression of intraventricular or other clinical hemorrhages was documented. Abnormalities included lower values for fibrinogen, platelet count, antithrombin III, and factor VIII with higher values for fibrin monomer and longer Laidlaw whole blood clotting times. These abnormalities tended to correct spontaneously in surviving infants. An association between gestational complications and incidence of hypocoagulability and intracranial hemorrhage (ICH) was noted. Babies of preeclamptic mothers had fewer abnormalities and babies born to mothers with premature rupture of membranes and suspected amnionitis manifested more hypocoagulability and more severe intracranial hemorrhages.