Der Anaesthesist
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Sepsis results from the host response to infection. While a localized and controlled inflammatory reaction helps to control infection, a dysregulated response may lead to multiple organ failure and determines the course and prognosis of the septic patient. Despite intensive care, mortality remains as high as 54% for severe sepsis and septic shock. ⋯ Nevertheless, several seminal studies have indicated that early and systematic supportive therapy according to pathophysiological principles, most notably early goal-directed therapy, low-dose hydrocortisone and activated protein C, can disrupt dysfunctional cascades and can favourably influence the course of the disease. In parallel, efforts to better define nationwide epidemiology and treatment habits for severe sepsis by the German competence network "SepNet" indicate that therapy of severe sepsis is generally in poor compliance with guidelines, while the personal perception of physicians in charge would suggest high rates of adherence. Thus, strategies of change management, such as implementation of sepsis bundles are warranted to achieve a better standard of care toward the aim of the "surviving sepsis campaign", i.e. a reduction of mortality by 25% within the next 5 years.
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Acute renal failure in critically ill patients in the intensive care unit is associated with high morbidity and mortality which is independent of the underlying etiology. Despite improvements in intensive care medicine and renal replacement therapy, patients with acute renal failure have much higher morbidity and mortality rates than patients without acute renal failure in the intensive care unit. In this overview, we summarize the literature on the incidence and mortality of patients with acute renal failure in the intensive care unit. Furthermore, we discuss timing of the initiation of renal replacement therapy, patient outcome with different renal replacement therapies and the adequate dialysis dose to be delivered.
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Ketamine is the only intravenous anesthetic that causes an increase in mean arterial pressure without compromising cardiac output. These beneficial effects are basically linked to stimulation of the sympathetic nervous system, inhibition of adenosine triphosphate-sensitive potassium channels and interactions with the nitric oxide pathway. Experimental and clinical studies have shown that ketamine exerts antiinflammatory properties by inhibiting the release of proinflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6. ⋯ In view of the current literature ketamine appears to represent a beneficial therapeutic option for long-term sedation of patients with arterial hypotension resulting from sepsis and systemic inflammatory response syndrome (SIRS). However, it has to be taken into account that ketamine inhibits endothelial nitric oxide synthase, thereby potentially aggravating impaired (micro) regional blood flow in sepsis. Future studies are required to investigate the role of ketamine in the treatment of patients with sepsis and SIRS.