Citation

Traber DL, Linares HA, Herndon DN, Prien T. Burns 1988; 14(5): 357-364.

Affiliation

University of Texas Medical Branch, Galveston.

Copyright

(Copyright © 1988, Elsevier Publishing)

DOI

unavailable

PMID

3067821

Abstract

The inhalation of smoke results in a series of pathophysiological events involving the respiratory and circulatory systems. Upper airway injury is mainly the result of heat damage. The lesions of the tracheobronchial and parenchymal areas are more related to the chemicals present in the smoke. The initial damage of the tracheobronchial mucosa results in chemotaxis of leucocytes into the airway tissues, with release of inflammatory mediators and formation of exudative materials. Bronchial oedema, bronchoconstriction, and bronchial obstruction by cast materials develop. The pulmonary microvasculature shows a permeability type of lesion, which is the result of mediator release from entrapped polymorphonuclear cells. This parenchymal lesion may relate to the tracheobronchial damage and be the result of a reperfusion injury. The systemic changes which have been identified relate to an increase in microvascular permeability and a reduction of myocardial contractility secondary to the inhalation of the toxic products of smoke. These latter findings may help to explain the difficulty encountered in resuscitating some of the burn victims who have concomitant inhalation injury.

Language: en