Eicosanoids, Cytokines and Altered Metabolic Control in the Evolution of the Posttraumatic Host Defense Failure Syndromes: Adult Respiratory Distress Syndrome and Multiple Organ Failure Syndrome

Abstract

Trauma of sufficient magnitude to induce a large volume of tissue injury and hypovolemic hemorrhagic shock results in a disparity between oxygen delivery and the oxygen consumption required to maintain cellular metabolic processes. As a result an oxygen debt is produced which forces the body cells into an anaerobic metabolic phase with increased production of lactic acid and a significant degree of metabolic acidemia [1]. The magnitude of this oxygen debt and the resultant metabolic acidemia have been shown to be quantitative predictors of mortality and the severity of the ischemic insult in experimental hemorrhagic shock [1] and also in blunt multiple trauma [2]. Initiation of hypovolemic, hemorrhagic shock has also been shown to induce bacterial translocation from the gut [3] and significant levels of circulating endotoxin have been demonstrated in humans following shock-producing traumatic injury [4]. Such shock patients have also been shown to have a higher incidence of postinjury sepsis and an increased frequency of development of the pulmonary failure syndrome known as adult respiratory distress syndrome (ARDS) or renal or hepatic failure, as well as a significant incidence of myocardial dysfunction. The various sequences of organ failures which occur have been characterized as the multiple organ failure syndrome (MOFS) [4].