In patients with acute fulminant hepatic failure, progression to grade IV encephalopathy is associated with a progressive rise in intracranial pressure, eventually resulting in brainstem herniation. Precipitating causes such as variceal bleeding or occult infection should be sought and promptly corrected. Clinical signs of raised intracranial pressure such as pupillary dilatation or flexor or extensor posturing are unreliable as they may occur too late for treatment, and in any case may be disguised by the use of opioid infusions to obtund autonomic responses and neuromuscular blockade to facilitate mechanical ventilation. Intracranial pressure monitoring is the ideal method for detection and management, but the substantial risk of intracranial hemorrhage associated with these devices means that the coagulopathy must be corrected first, and this can be difficult to achieve. Control of intracranial pressure in the absence of normal renal function is likely to require continuous ultrafiltration.

Cerebral hemorrhage may also occur spontaneously, and will require CT or magnetic resonance imaging for diagnosis. Other causes of impaired cerebral function include hypoglycemia and rapid shifts in sodium balance. Hyponatremia may be induced by excessive use of mannitol, and hypernatremia by sodium-containing colloids or dialysis. Central pontine myelinolysis may be induced by rapid correction of hyponatremia.

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