Fluid clearance from the lungs of newborns, infants and children

Abstract

In 1976 I was a first year paediatric resident assigned to the neonatal intensive care unit of the Winnipeg Children’s Hospital. One of my first patients was a newborn infant who had been born after 28 weeks gestation. She nearly died from her hyaline membrane disease and then just as her lung disease was improving she developed florid pulmonary edema as blood flooded into her lungs through a widely patent ductus arteriosus (PDA). I was fascinated by her clinical course and chagrined by how little we really knew about the mechanisms of her lung disease. My lecture will outline some new information that I and my colleagues have discovered over the past 25 years using molecular biology, biochemistry, electrophysiology, cell biology, physiology and bed-side clinical research techniques. My initial work, during post-doctoral research training with Robert Mellins at Columbia University and as a young faculty member at McMaster University, was to investigate mechanisms that caused, and the consequences of, high permeability and high pressure pulmonary edema in the newborn and adult lung. The pathophysiologic consequences of my patient’s PDA were investigated in large animal and human studies involving the recruitment and distention of the pulmonary circulation under normoxic and hypoxic conditions and the effect of increased pulmonary blood flow on lung lymph flow in normal and acutely injured lungs (e.g. Our lab then developed of a new technique that could be utilized at the bedside (99mTc-DPTA clearance from the lung) to show in 1984 for the first time, showed there was an increased alveolar capillary permeability in neonatal respiratory distress syndrome (RDS), the most common acute respiratory disease in premature infants.