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Journal List > West J Med > v.148(1); Jan 1988

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West J Med. 1988 January; 148(1): 33–36.
PMCID: PMC1026006
Copyright notice
New Developments in the Pathogenesis of Smoke Inhalation-Induced Pulmonary Edema
Mark L. Witten, PhD, Stuart F. Quan, MD, Richard E. Sobonya, MD, and Richard J. Lemen, MD
Abstract
Smoke inhalation causes most of the deaths in fire-related injuries, with pulmonary edema as a major determinant in the outcome of smoke-inhalation injury. The pathophysiology of pulmonary edema is thought to be related to the products of incomplete combustion. Damage to the integrity of the alveolar epithelium is one of the determinants of the development of smoke-induced pulmonary edema. In recent studies using lung clearance of aerosolized pentetic acid (DTPA [diethylenetriaminepentaacetic acid]) labeled with technetium Tc 99m to assess the permeability of the alveolar epithelium, several factors were identified that may increase a person's susceptibility to smoke-induced acute lung injury. These are increased initial alveolar permeability and alterations in the number and activity of alveolar macrophages. Clinical measurement of 99mTcDTPA clearance may provide a sensitive and convenient method for the early detection and serial assessment of smoke-induced alveolar epithelial permeability changes.
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Selected References
These references are in PubMed. This may not be the complete list of references from this article.
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