Pulmonary and ductal hemodynamics in studies of simulated diaphragmatic hernia of fetal and newborn lambs

Abstract

Congenital Posterolateral Diaphragmatic Hernia is associated with ipsilateral pulmonary hypoplasia and blood flow to the affected lung remains diminished into late childhood. 1 Although this unilateral pulmonary hypoplasia is physiologically significant, it is probably not primarily responsible for the high mortality of congenital diaphragmatic hernia. The major immediate threat to a baby's life is the tension effect of the herniated abdominal viscera, but even after successful reduction of these organs, a greater than 50% mortality occurs. The mortality and morbidity is often due to continuing and progressive hypoxemia and metabolic acidosis. Several authors 2–4 have reported pulmonary hypertension, patent ductus arteriosus and variable right-to-left shunting in babies with diaphragmatic hernias. Right-to-left shunting via a patent ductus may contribute significantly to increasing hypoxemia and acidosis in addition to the efect of pulmonary hypoplasia. To test this hypothesis, we have developed a simplified fetal model to simulate diaphragmatic hernia and permit studies of pulmonary and ductal hemodynamics. The fetal lamb was chosen for studies of the pathophysiology of diaphragmatic hernia because pulmonary development in fetal lambs occurs late in gestation and because many studies have been made of normal pulmonary function in newborn lambs. 5–8 This cumulative data is available for comparison with laboratory models of pulmornary abnormalities. These studies were therefore designed to test our belief that right-to-left shunting via the patent ductus arteriosus (PDA) is due to persistent fetal circulation and associated with altered blood flow to the hypoplastic lung.