Critical care : the official journal of the Critical Care Forum
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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.
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Data obtained from net organ balance studies of glucose production lead to the classic view according to which glucose homeostasis is mainly ensured by the liver, and renal glucose production only plays a significant role during acidosis and prolonged starvation. Renal glucose release and uptake, as well as the participation of gluconeogenic substrates in renal gluconeogenesis, were recently re-evaluated using systemic and renal arteriovenous balance of substrates in combination with deuterated glucose dilution. Data obtained using these methods lead one to reconsider the magnitude of renal glucose production as well as its role in various physiological and pathological circumstances. These findings now conduce one to consider that renal gluconeogenesis substantially participates in postabsorptive glucose production, and that its role in glucose homeostasis is of first importance.
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Despite decades of resuscitating patients with intravenous fluids in intensive care units, it is somewhat surprising that very little consensus exists regarding the type of fluid physicians should choose. Factors that influence decisions are often local culture or politics, hospital administrators, history (i.e. 'I've always done it this way') and budgets, as opposed to strong evidence. ⋯ As such, in the future, clinicians will need to consider other factors when making their decision. In addition, large-scale quality randomised studies are desperately needed to guide clinicians.