Current opinion in critical care
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Curr Opin Crit Care · Oct 2002
ReviewOutcome of cardiac surgery patients with complicated intensive care unit stay.
Risk stratification has become an essential element in the practice of cardiac surgery. Several studies have identified preoperative risk factors for adverse outcome. However, outcome is mostly defined by 30-day mortality and morbidity. ⋯ By reviewing the recent data reported in the literature, we can identify a number of preoperative predictive factors for complicated ICU stay, including advanced age, chronic obstructive pulmonary disease, preoperative low ejection fraction, previous myocardial infarction, reoperation, renal failure, combined surgery (coronary artery bypass grafting plus valve surgery), low hematocrit, and neurologic impairment. Short- and long-term outcomes are dependent on the type of postoperative complication. Unfortunately, data regarding the long-term outcome in these situations are very scarce.
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Surgical infections in the critically ill patient population are a significant cause of morbidity and mortality. Intra-abdominal and surgical soft-tissue infections are responsible for a significant proportion of the disease burden. ⋯ The diagnosis and management of these infections require a high index of suspicion, prompt surgical intervention, and adequate antibiotic therapy and resuscitation. Therefore, these infections present a challenge to the intensivist caring for a critically ill patient.
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The nature of myocardial dysfunction during sepsis and septic shock has been investigated for more than half a century. This review traces the evolution of scientific thought regarding this phenomenon during this period with particular emphasis on the current understanding of both the clinical manifestations and the molecular/cellular basis of septic myocardial dysfunction in critically ill patients. Current data suggest, contrary to older literature, that patients with septic shock develop a hyperdynamic circulatory state after fluid resuscitation and maintain this hyperdynamic circulatory state until death or recovery. ⋯ Available evidence suggests that myocardial hypoperfusion is not responsible for septic myocardial depression, because examination of humans with septic shock demonstrates increased myocardial perfusion, and animal models of septic shock appear to maintain myocardial high-energy phosphates. A circulating factor or factors, including the cytokines tumor necrosis factor alpha and interleukin-1beta, appear to have a significant role in the phenomenon. In addition, septic myocardial depression appears to be mediated in part through combinations of nitric oxide-dependent and -independent alterations of basal and catecholamine-stimulated cardiac myocyte contractility.