Cerebral herniation is a leading cause of death in patients with fulminant hepatocellular failure. Classical signs of elevated intracranial pressure are often absent in these patients. A reliable noninvasive method by which the presence of cerebral edema could be determined is much needed. To assess the efficacy of computed tomography of the brain in this setting, we compared the radiographic findings to the intracranial pressure measured by an epidural monitor in patients with fulminant hepatic failure. Unfortunately, a considerable difference existed between the presence of cerebral edema diagnosed by computed tomography of the brain and elevation of the intracranial pressure. Our observations suggest that in patients with fulminant hepatic failure and advanced hepatic encephalopathy, computed tomography of the brain is of little value in detecting cerebral edema. Pressure monitoring is most important to establish the presence and guide the therapy of intracranial hypertension. (HEPA- TOLOGY 1991; 13:209-212.)
The frequency of cerebral edema occurring in fulminant hepatic failure ranges from 50% to 85% (1-5). Cerebral herniation has been implicated as the cause of death in 30% to 50% of patients with fulminant hepatic failure (1-6). Classical signs of elevated intracranial pressure (ICP) such as headache, explosive vomiting, bradycardia and papilledema are often absent in the setting of fulminant hepatic failure. There is little correlation between the elevation of ICP and the clinical signs of cerebral edema ( 3 , 4 , 7 , 8 ) . In one study, only the changes in pupillary responses (assessed every 5 min by experienced observers) were found to be useful indicators of ICP (7). In addition to cerebral edema, these patients may have impaired mental function caused by hepatic encephalopathy, a metabolic disorder that does not lead to brain herniation but further confounds the evaluation of the neurological status (7, 8). Decorticate and decerebrate posturing that may result from hepatic