Acute Lung Injury: The Pathophysiology

Abstract

Acute lung injury (ALI) is a serious clinical problem. The aspiration of vomitus or the inhalation of smoke are responsible for a high rate of morbidity and mortality in the clinical population. Changes secondary to mechanical manipulation of the airway also play a critical role in the clinical outcome of many patients [1]. Smoke inhalation is a primary factor in the mortality of fire victims [2]. We have developed an ovine model which allows us to study ALI [3]. Immediately after inhalation injury, induced by the insufflation of cotton smoke into the ovine model, the airway shows a marked hyperemia and an increase in microvascular permeability, leading to tracheobronchial edema [4]. Similar findings have been seen in canine preparations after endotracheal insufflation with artificial smoke [5]. The diagnosis of inhalation injury in humans is often made after observing the appearance of airway hyperemia [6]. Consequently, the observations in sheep are similar to those seen in humans with ALI. Other forms of ALI are also associated with an airway hyperemia. An elevated bronchial blood flow was noted with acute exposure to ozone [7]. Similar pulmonary problems have been reported with acid aspiration [8] and mechanical damage induced by endotracheal tubes and the use of ventilators [9, 10].