Affiliation:
1. Joseph S. Barr Pediatric Intensive Care Unit, Children's Service and the Anesthesia Service, Massachusetts General Hospital; the Children's Hospital Medical Center; and the Department of Pediatrics and Anesthesia, Harvard Medical School, Boston
Abstract
Two children, ages 9 and 2½ years, with clinical diagnoses of laryngotracheitis (croup) and epiglottitis, respectively, developed florid pulmonary edema without evidence of cardiac enlargement. Both children responded to vigorouS therapy, which included endotracheal intubation, mechanical ventilation with high oxygen concentrations and positive end expiratory pressure, diuretics, and support of the intravascular volume with colloid infusions.
Swan-Ganz catheterization was performed in the child with epiglottitis to elucidate any hemodynamic malfunction. Pulmonary artery occluded pressure was found to be normal.
We postulate that pulmonary edema may be the result of any of three major physiologic alterations: alveolar hypoxia, increased alveolar-capillary transmural pressure gradient, and a catechol-mediated shift of blood volume from the systemic to the pulmonary circulation. These alterations acting in concert would increase the volume of blood presented to the pulmonary capillaries, the pore size in those capillaries, and the hydrostatic pressure gradient promoting transudation. Failure of pulmonary lymphatics to effectively clear this fluid would result in pulmonary edema.
Although pulmonary edema associated with acute upper airway obstruction is unusual, physicians should be alerted to its possible appearance and the need for early and vigorous therapeutic measures.
Publisher
American Academy of Pediatrics (AAP)
Subject
Pediatrics, Perinatology, and Child Health
Cited by
19 articles.
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