Critical care : the official journal of the Critical Care Forum
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Following intravenous administration, vancomycin is poorly metabolized and is mainly excreted unchanged in urine. Total body clearance is thus dependent on the kidney, and is correlated with glomerular filtration rate and creatinine clearance. ⋯ The aim of the present review is to establish guidelines for handling this drug in such patients. We indicate how and when plasma concentrations of vancomycin should be determined in dialysis patients.
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The ability of the isolated lung tissue to take up glucose and to release lactate is potentially similar to that of other body tissues. Nonetheless, when lung lactate exchange was assess in vivo in normal humans, no measurable lactate production could be detected. ⋯ Potential mechanisms of lactate production by the injured lung may include not only the onset of anaerobic metabolism in hypoxic zones, but also direct cytokine effects on pulmonary cells and an accelerated glucose metabolism in both the parenchymal and the inflammatory cells infiltrating lung tissue. In addition, as skeletal muscle, lung tissue may show metabolic adaptations in response to systemic mediators and may contribute to the systemic metabolic response to severe illness even in the absence of direct tissue abnormalities.
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The native kidney has a major role in lactate metabolism. The renal cortex appears to be the major lactate-consuming organ in the body after the liver. Under conditions of exogenous hyperlactatemia, the kidney is responsible for the removal of 25-30% of all infused lactate. ⋯ In some cases, this increase can result in an exacerbation of metabolic acidosis. If bicarbonate-buffered replacement fluids are used, a significant correction of the acidosis or acidemia can also be achieved. The clinician needs to be aware of these renal effects on lactate levels to understand the pathogenesis of hyperlactatemia in critically ill patients, and to avoid misinterpretations and unnecessary or inappropriate diagnostic or therapeutic activities.
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The present review introduces the notion of statistical power and the hazard of under-powered studies. The problem of how to calculate an ideal sample size is also discussed within the context of factors that affect power, and specific methods for the calculation of sample size are presented for two common scenarios, along with extensions to the simplest case.
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Inadequate splanchnic perfusion is associated with increased morbidity and mortality, particularly if liver dysfunction coexists. Heart failure, increased intra-abdominal pressure, haemodialysis and the presence of obstructive sleep apnoea are among the multiple clinical conditions that are associated with impaired splanchnic perfusion in critically ill patients. Total liver blood flow is believed to be relatively protected when gut blood flow decreases, because hepatic arterial flow increases when portal venous flow decreases (the hepatic arterial buffer response [HABR]). ⋯ Unfortunately, no drugs are yet available that increase total hepato-splanchnic blood flow selectively and to a clinically relevant extent. The present review discusses old and new concepts of splanchnic vasoregulation from both experimental and clinical viewpoints. Recently published trials in this field are discussed.