Abstract
Critical illness in adults is often followed by acute lung injury (ALI). The most severe form of ALI, termed Acute Respiratory Distress Syndrome (ARDS), has a mortality rate of about 50% in most series and higher than 90% when it is associated with severe sepsis and multiple system organ failure (1). Among the clinical conditions associated with the development of ARDS, sepsis is the most common and lethal. Despite recent advances in critical care medicine, the current therapeutic approach for ALI and ARDS is just supportive, not curative. Significant improvements in supportive treatment in the intensive care unit (e.g., more specific antibiotic treatment, improved mechanical ventilation, improved monitoring of circulation, better nursing care, etc.) are mainly responsible for improvements in survival in ARDS and sepsis. However, the incidence of sepsis is rising while a third of septic patients will succumb to this devastating syndrome (2). The septic insult results in a complex cascade of inflammatory mediators, such as cytokines, that is initiated by the organisms themselves or by their soluble products. Although cytokine production is not unique to systemic infection, measurement of circulating inflammatory mediators can confirm the presence of host inflammation, but may not distinguish crucial pathways involved in disease progression and outcome (3).
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