World journal of surgery
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Mediators play a key role in the development of systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome, and multiple organ failure of vital organs. In this short review, we update our knowledge on these mediator networks. First, we summarize the stimuli that occur during severe trauma (intraoperative stress), including polymorphonuclear neutrophil-derived tissue-damaging substances, complement activation products, and adherence molecules such as selectins. ⋯ Second, we describe the mediators, including cytokines, nitric oxide, phospholipase A2, platelet-activating factor, and procoagulatory substances, that are released during sepsis. The release of mediators depends primarily on the severity of the trauma, shock, or sepsis and secondarily on the activation of the various cascades of mediators during posttraumatic/postoperative complications. The mediators are thus of decisive importance regarding the intensity of organ damage and the outcome.
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Progress in the care of the critically ill patient with life-threatening infection has been hampered by inconsistent, often confusing terminology. The clinical syndrome of sepsis-familiar to all yet definable by none-describes a highly heterogeneous group of disorders with different causes and differing prognoses. The imminent availability of mediator-directed therapy has created a sense of urgency to develop better methods for delineating discrete clinical syndromes and to modulate the host response, which may bring both benefit and harm, depending on the clinical circumstances. ⋯ The development of cogent conceptual frameworks for classification of the septic response in critically ill patients is more than a question of linguistic pedantry. Optimal therapy presupposes identification of an homogeneous patient population with a characteristic disease process and a predictable response to an intervention. Although progress has been made in identifying such groups of critically ill patients, the disappointing results of clinical trials of agents that so clearly demonstrate efficacy in animal models indicates that considerable work remains.
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Multiple organ failure (MOF) stems from a complex interaction between the host's immune response and inadequate tissue perfusion. Prevention of MOF therefore addresses these two components. The risk of inflammation is reduced through treatment of any infection and early stabilization of traumatized regions. ⋯ Once MOF has developed, treatment turns to support of individual organs. Unfortunately, there is no single treatment for MOF that seems to reverse the associated trend of high mortality. Survival is more likely when the cause of MOF can be found and eliminated.
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World journal of surgery · May 1996
ReviewUpdate on the mechanisms of immune suppression of injury and immune modulation.
Major trauma results in massive impairment of immunologic reactivity, the clinical consequence of which consists in the high susceptibility of the traumatized individual toward serious infection. Whereas parts of the immune system are stimulated within a systemic, nondiscriminant, excessive whole-body inflammation, other functions within the complex of cell-mediated immunity (CMI) are dramatically paralyzed. Immune abnormalities in the aftermath of trauma occur in a sequence of states of cellular activation and within a complex order of events that is not yet well understood. ⋯ Immune modulatory interventions, depending on the immune abnormalities seen in the traumatized host, should be started as early as possible after trauma in a preventive fashion to protect against organ tissue destruction. Ideally, it should protect all cellular host defense compartments from hyperactivation as well as from exhaustion. We do believe that only a combination of drugs can effectively control the posttraumatic dyshomeostasis of the various cell systems.
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World journal of surgery · May 1996
ReviewRole of the gut in multiple organ failure: bacterial translocation and permeability changes.
It is clear that increased gut permeability and bacterial translocation play a role in multiple organ failure (MOF). Failure of the gut barrier remains central to the hypothesis that toxins escaping from the gut lumen contribute to activation of the host's immune inflammatory defense mechanisms, subsequently leading to the autointoxication and tissue destruction seen in the septic response characteristic of MOF. However, the role of the gut is more than that of a sieve, which simply allows passage of bacteria and endotoxin from the gut lumen to the portal or systemic circulation. ⋯ A vicious cycle of increased intestinal permeability, leading to toxic mediator release, resulting in a further increase in gut permeability is generated. Additionally, the systemic and local inflammatory cells that become activated in the gut contribute to the systemic response characteristic of the sepsis syndrome and MOF. Thus even if the immune inflammatory system, rather than the gut, is the "motor of" MOF, the gut remains one of the major pistons that turns the motor.