Abstract
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent points on a spectrum of acute hypoxic respiratory failure that are distinguished by the severity of associated hypoxemia. The hallmark of ALI/ARDS is an increase in pulmonary capillary permeability resulting from epithelial and endothelial injury; a variety of inflammatory mediators are involved in the pathogenesis, including toxic oxygen radicals, cytokines, and eicosanoids. Patients with ALI/ARDS are at high risk for malnutrition because the underlying disease increases caloric expenditure and promotes the loss of lean body mass; this, in turn, has adverse effects on pulmonary and immune function. The type of fatty acids (FA) that comprise the cell membrane of alveolar macrophages and neutrophils is influenced by dietary fat intake; this, in turn, impacts on the nature of eicosanoid mediators produced during ALI/ARDS. Diets high in linoleic acid (LA) promote an inflammatory response by stimulating production of arachidonic acid and its derived eicosanoids. Nutritional supplementation with ω-3 FA can lessen the inflammatory response and be of therapeutic benefit in patients with ALI/ARDS. This article reviews the pathology and pathophysiology of acute hypoxemic respiratory failure, summarizes animal and human studies that delineate the effects of modified FA solutions, and provides clinical recommendations for the nutrition support of patients with ALI/ARDS.
Get full access to this article
View all access options for this article.
