Intraabdominal infection: pulmonary failure

Since its first description in 1967, the mortality of the adult respiratory distress syndrome (ARDS) has remained unchanged despite the increasing sophistication of supportive techniques. Few patients now die of refractory hypoxemia, the majority succumbing to the multiple systems organ failure syndrome, commonly due to sepsis. Sepsis is both the most common cause of ARDS, usually involving the abdomen, and the most frequent complication, usually affecting the lungs. ARDS is, thus, increasingly seen as the pulmonary component of multiple systems organ failure, triggered by the systemic response to sepsis. In critically ill patients, impairment of hepatic function and of the barrier function of the gut mucosa allows translocation of endotoxin derived from the aerobic Gram-negative bacteria within the gut. This releases mediators which are responsible for the activation of cellular and humoral cascades, resulting in the pathological changes seen in ARDS. This sequence of events underlines the importance of therapies directed at abnormal colonization of the gastrointestinal tract and elimination of the gut endotoxin pool. Selective decontamination of the digestive tract is attractive in that it attacks the problem from 2 sides: first, by eliminating colonization, it appears effective in preventing secondary infection and, second, it may also play a role in reducing the enteric endotoxin pool. Recent descriptions of pathological oxygen supply dependency in both ARDS and septic patients emphasize the similarity of pathophysiological abnormalities in the 2 conditions. Intensive supportive therapy to achieve adequate oxygen transport and aggressive investigation and surgical management of septic foci are the cornerstones of management of the established syndrome.