The management of renal failure in patients at risk of cerebral edema/hypoxia.

Intermittent modes of renal replacement therapy have been shown to cause an increase in intracranial pressure in susceptible patients, including those with acute liver failure and cerebral edema from trauma or post neurosurgery. Such changes are due to the combination of adverse effects on cerebral oxygen delivery and/or cerebral perfusion pressure and the generation of an osmotic gradient between plasma and cerebral tissues. With continuous renal replacement therapy (CRRT) these cardiovascular and cerebrovascular changes are generally much reduced. Patients with hepatic failure and those postneurosurgery are at risk of fatal intracranial hemorrhage. A drawback of CRRT is the need for anticoagulation of the extracorporeal circuit. Epoprostenol appears to confer a reduced risk of hemorrhage without reducing circuit lifespan in these patients compared with the effects of standard and fractionated heparins. Lactate metabolism is often impaired in patients with severe liver failure and the use of lactate-buffered hemofiltration replacement dialysis fluids, even at the reduced rates used in CRRT, may result in hyperlactatemia and failure to correct acid-base deficits; therefore, "lactate-free" fluids are to be preferred. The introduction of CRRT in the management of patients with acute renal failure complicated by cerebral edema has been associated with greater patient stability and improved outcome.