New horizons (Baltimore, Md.)
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Liver failure is commonly encountered in the critically ill, septic patient. This hepatic dysfunction occurs as a wide spectrum of abnormalities, ranging from mild chemical derangements to fulminant liver failure. The syndrome of multiple system organ system failure due to sepsis is often complicated by alterations in splanchnic/hepatic function. ⋯ The functions of these pathophysiologically produced factors include extensive autocrine, paracrine, and endocrine effects. Evidence suggests that adequate resuscitation during sepsis, which is measured by systemic end-points, may result in inadequate splanchnic blood flow and oxygen delivery. The addition of serial measurements of splanchnic end-points may limit the hepatic failure encountered in multiple system organ failure due to sepsis.
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Traditionally, shock has been recognized or diagnosed by subjective signs and symptoms, particularly in septic shock, where transition from localized to systemic infection and then to septic shock may be gradual and subtle. Management has been directed toward normalizing these subjective symptoms as well as BP, heart rate, urine output, hematocrit, central venous pressure, and blood gases. The major problem is that restoration to normal values of these secondary aspects of shock do not correct the underlying tissue perfusion defect. ⋯ Specifically, when the optimal values of cardiac index, DO2, and VO2 used as therapeutic goals were attained in 8 to 12 hrs, there was marked and significant reduction in mortality and morbidity rates. This finding was also confirmed in 12 prospective, controlled trials, four of which were randomized. We conclude that driving septic shock patients into the survivors' patterns improves outcome, as has been shown in other shock syndromes.(ABSTRACT TRUNCATED AT 400 WORDS)
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The pro-inflammatory cytokines, tumor necrosis factor (TNF) and interleukin-1 (IL-1), are widely assumed to participate in the initial systemic manifestations of sepsis. While the toxicities of excessive cytokine activity have been well described in animal models, clinical evaluations often fail to detect circulating forms of these mediators in critically ill patients. It is now evident that a diverse array of host mechanisms serve to attenuate or block excessive cytokine influences. ⋯ Recombinantly derived forms of these natural cytokine antagonists have proven effective in preventing many of the adverse consequences of sepsis. Prospective clinical trials of these agents are currently underway. While results of such trials are not fully available at present, it is likely that one or more therapies directed against TNF and IL-1 may prove effective in the management of septic shock.
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Hypovolemia is one of the principal defects contributing to cardiovascular instability and circulatory failure during septic shock. Fluid infusion is the mainstay of initial resuscitation. ⋯ Crystalloids and colloids are equally effective, although the volume of fluids required with crystalloids is two to four times that of colloids. In older patients, where high filling pressures may be required for optimal hemodynamic effect, colloids may be associated with a lower frequency of pulmonary edema.
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When fluid administration is not sufficient to restore hemodynamic stability, inotropic agents may be given to restore the tissue perfusion pressure and to increase oxygen delivery (DO2) to the cells. Dopamine remains the drug of choice in the resuscitation of septic shock but norepinephrine can also have a place in the treatment of profound cardiovascular collapse or severe right ventricular failure. ⋯ The potential of other adrenergic agents (such as dopexamine) or nonadrenergic agents (such as phosphodiesterase inhibitors) is also discussed in this article. Inotropic therapy should be guided not only by measurements of systemic BP but also by repeated assessments of the metabolic function of organs.