• D E Fry.
• Department of Surgery, University of New Mexico School of Medicine, Albuquerque, NM, USA. dfry@salud.unm.edu
• Surg Infect (Larchmt). 2000 Jan 1; 1 (3): 155-61; discussion 161-3.

AbstractIn the past, our approach to multiple organ failure in the injured or critically ill surgical patient was driven by attempts to simplify a complex process. Early studies focused on uncontrolled invasive infection (sepsis) as the driving force of multiple organ dysfunction syndrome (MODS). However, some patients with adequately controlled infection and those without sepsis nevertheless develop MODS and signs of systemic inflammation. This discrepancy led to investigations of systemic activation of inflammation by a wider variety of biological modulators than just infection. Despite the apparent involvement of biological modulators such as endotoxin, tumor necrosis factor, and interleukin-1 receptor in MODS, agents that neutralize these modulators have failed to thwart the progression of sepsis, septic shock, and organ failure. A new paradigm suggests that, in the critically ill patient at risk for organ failure, an integrated process propagates an excessive systemic inflammatory response and/or an inadequate compensatory anti-inflammatory response. Future studies should examine the balance between these two processes at the level of the individual patient with organ failure. Careful stratification of individual patient responses to inflammatory stressors may be an essential step for creating better strategies for therapeutic interventions that can restore balance between the pro-inflammatory and anti-inflammatory processes in the critically ill patient and possibly prevent organ failure.

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