Surgical infections
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Surgical infections · Jan 2000
ReviewEpidemiology of multiple organ dysfunction syndrome in critical surgical illness.
Multiple organ dysfunction syndrome (MODS) is a major cause of morbidity and mortality in surgical intensive care units (SICUs). Multiple organ dysfunction syndrome remains the most important factor associated with mortality in the SICU. Illness severity scores such as the Acute Physiology and Chronic Health Evaluation-III (APACHE III) and the magnitude of the systemic inflammatory response syndrome (SIRS) at the time of SICU admission are useful in stratifying patients at risk for MODS and subsequent mortality. ⋯ Despite the prognostic utility of SIRS/MODS, definitions of dysfunction of individual organs have shortcomings. The problem with quantitating MODS lies in the inability to adequately define organ dysfunction, especially of the gastrointestinal tract, liver, and central nervous system. Biological indicators of organ dysfunction may prove to be better markers for MODS in the future.
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Surgical infections · Jan 2000
ReviewMultiple organ dysfunction syndrome: past, present and future.
In 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. ⋯ 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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Surgical infections · Jan 2000
Biography Historical Article Classical ArticleEffect of preoperative neomycin-erythromycin intestinal preparation on the incidence of infectious complications following colon surgery. 1973.
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Surgical infections · Jan 2000
ReviewMolecular biology of multiple organ dysfunction syndrome: injury, adaptation, and apoptosis.
Injury will equal or surpass communicable disease in the year 2020 as the number one cause of lost disability-adjusted life-years worldwide. The major cause of "late death" after trauma is organ dysfunction, commonly as a complication of shock or sepsis. The pathophysiology of injury-induced organ dysfunction is poorly characterized but has been linked to systemic inflammation as a result of infection (either obvious or occult) or massive tissue injury (systemic inflammatory response syndrome, SIRS). ⋯ We hypothesize that a complete understanding at the molecular level of the stress responses induced by injury will aid in the development of therapeutic strategies for treating MODS in the critically ill surgical patient. This paper reviews recent data from our Cellular Injury and Adaptation Laboratory relevant to our understanding of MODS pathophysiology, particularly as it relates to stress-induced cell death by apoptosis. Our data suggest that inhibition of stress-induced apoptosis may improve survival after severe injury.
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Multiple organ failure (MOF) is currently the most common cause of late death after injury and surgery. The pathogenesis of MOF remains incompletely understood but in all likelihood results from a combination of dysregulated balance between inflammatory response and immune function, maldistribution of microcirculatory blood flow, and ischemia/reperfusion injury. ⋯ However, as recent clinical trials have shown, studies demonstrating an improvement in outcome from use of these therapeutic agents are difficult to design. The purpose of this article is to discuss the evolution, clinical course, and pathogenesis of MOF, to attempt to better define and quantitate MOF, and to describe recent studies aimed at identifying an at-risk study population for improved treatment and prevention strategies for MOF.