World journal of surgery
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Multiple organ failure (MOF) is considered to be the leading cause of death after severe trauma. Although there is extensive literature on MOF, little is known about the pattern, sequence, and onset of this clinical syndrome. The first goal of this clinical study was to define MOF; the second was to assess the typical onset, sequence, and pattern of MOF; and the third was to define certain risk factors for the development of MOF in 342 multiple trauma patients. ⋯ Significant renal failure and the need for dialysis decreased to < 5%; other signs of organ dysfunction (gastric, central nervous system) are difficult to verify. Typical risk factors for the development of MOF after severe trauma are the severity, type, and distribution of injury as well as the indicators of prolonged hemorrhagic shock (elevated lactate levels). The main therapeutic efforts, therefore, should be the effective treatment of traumatic hemorrhagic shock during the initial phase, adequate resuscitation, optimal oxygenation, and early surgical treatment.
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Throughout this issue of World Journal of Surgery are recommendations and descriptions of therapy to prevent the development of multiple organ failure (MOF). The subjects include advances in monitoring; circulatory, pulmonary, and gut support; blood treatment; immune modulation; and control of the inflammatory process. ⋯ New therapeutic agents such as growth factors, glucan, ketaconazole, and antithrombin III are described. Finally, methods to support organ function before it fails (circulation, lungs, and kidneys) are described.
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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.