• S J Wort and T W Evans.
• Unit of Critical Care, Imperial College School of Medicine, Royal Brompton Hospital, London, UK.
• Br. Med. Bull. 1999 Jan 1;55(1):30-48.

AbstractThe majority of deaths amongst critically ill patients requiring intensive care are attributable to sepsis and its sequelae: septic shock, the systemic inflammatory response syndrome (SIRS) and the acute respiratory distress syndrome (ARDS). Patients within the ICU who develop these conditions and fail to survive succumb to multiple organ dysfunction syndrome (MODS). ARDS is considered to be the pulmonary component of MODS and is characterized by pulmonary hypertension, often in the setting of systemic hypotension. Endothelial cells, normally responsible for modulating vascular tone, becomes dysfunctional in sepsis. Pro-thrombotic, pro-inflammatory and vasoactive mediators are released including nitric oxide (NO), endothelins (ETs) and products of cyclo-oxygenase metabolism. It is probably the disordered production of these mediators in vascular beds that results in MODS. This review highlights recent research in this area with particular emphasis on possible therapeutic options.

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