Encefalopatía hepática

RESUMO

Mental deterioration in patients with fulminant hepatitis is a poor prognosis sign. Patients in stages III or IV with stupor or coma have cerebral edema. The increase in cerebral fluid eventually leads to endocraneal hypertension. Brain edema is not the cause of encephalopathy, only when the structures are displaced or intracraneal pressure increases, pupilary abnormalities, abnormal caloric reflexes and myoclonic seizures appears. Significant elevation of intracraneal pressure can be asymptomatic leading to temporal lobe herniation and death. Liver transplantation has changed the prognosis, and subdural and epidural monitoring has been developed in order to evaluate this problem optimally. Monitoring of cerebral perfusion pressure (mean arterial pressure - endocraneal pressure) to assess brain flow is essential. Values of less than 40mmHg imply cerebral ischemia. In patients with cirrhosis encephalopathy has several stages, and sleep disturbances can present very early. Asterixis is a sensible but not specific sign and the classic "faetor hepaticus" is not frequent. Most of the time a precipitating factor can be identified: gastrointestinal bleeding, sedatives, iuremia, infections, constipation, high protein intake and hypokalemia, chronic porto-systemic encephalopathy is mainly related to spontaneous porto-systemic collaterals or surgically created shunts. The most important pathogenetic factors are: ammonia, glutamate, increase cerebral serotonine, increase GABA tone and recently the presence of endogenous benzodiazepines. New therapeutic modalities included the administration of flumazenil, vegetable protein, lactulose and sodium benzoate...