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50 Years Ago in The Journal of PediatricsTHE ‘‘PULMONARY HYALINE MEMBRANE’’ AS A MANIFESTATION OF HEART FAILURE

IN THE NEWBORN INFANT

Lendrum F.C. J Pediatr 1955;47:149-56

Dr Lendrum provides a careful description of the clinical and pathologic findings associated with hyaline membrane disease (HMD)in preterm infants. He winds along intellectual paths that take him from the fetal circulatory transition, lung fluid clearance, anoxia-induced pulmonary hypertension, unequal ventilation, resorption ‘‘atelectasis,’’ patent ductus arteriosis, and surface forces—perilouslyclose to the ‘‘truth’’—before concluding that the disorder is caused by left heart failure. He recommends a treatment regimen focused tocareful positioning to ‘‘achieve harmonious alliance between the physician and the gravitational field.’’ Veering from the path leading tosurface tension and pulmonary surfactant, he proposes a treatment of HMD based on that for heart failure. He was not alone. Infantswith respiratory distress syndrome (RDS) in the 1950s were often treated with digitalis in hopes of improving respiratory-hemodynamicstatus. In spite of the shortcomings of his final conclusion, his description of the disorder contains accurate observations consistent withanatomic and physiologic abnormalities in HMD. Although the concepts that the fetal left ventricle is undeveloped and fails, thatnegative pressure rather than positive pressure can inflate the lung in HMD, and that venous stasis leads to congestive heart failure in thisdisorder may be spurious, he carefully described the potential importance of alveolar edema, unequal and ‘‘proximal’’ ventilation,hypoxia-induced pulmonary hypertension, and the fetal circulation, which all contribute to the pathogenesis of respiratory failure andhypoxemia associated with HMD.

Now routinely used in clinical practice, exogenous surfactant suffices to improve alveolar stability, unequal ventilation, and pulmonaryvascular resistance during the usually successful treatment of HMD. We have learned to trust the performance of the preterm heart,especially in the first days of respiratory adaptation. Left ventricular failure is not associated with RDS until pulmonary vascular resistantfalls and left to right shunting occurs across a patent ductus arteriosis. Indeed, pulmonary congestion, typical of infants dying in the firstdays of life with HMD, is caused primarily by the lack of pulmonary surfactant that is required for maintenance of alveolar volumes andnormal alveolar capillary permeability. In addition to surfactant replacement, careful resuscitation and ventilation, appropriate fluid andelectrolyte balance, proper handling and positioning, and management of the ductus arteriosis remain fundamental to the improvedoutcomes of preterm infants with HMD.

Jeffrey A. Whitsett, MDChief, Section of Neonatology, Perinatal and Pulmonary Biology

Cincinnati Children’s Hospital Medical CenterCincinnati, OH 45229-3039

Mildred T. Stahlman, MDProfessor of Pediatrics and Pathology

Director, Division of NeonatologyVanderbilt University School of Medicine

Nashville, TN 37232-2585

YMPD158810.1016/j.jpeds.2005.04.056

220 Ostrom et al The Journal of Pediatrics � August 2005