Encefalopatía hepática

Abstract

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, uremia, 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.

Acute hepatic failure represents one of the most dramatic clinical pictures in internal medicine. Most of the time the patient is very young and the picture evolves very rapidly. The most common causes are viral hepatitis (A, B, C), drug toxicity with halothane, non steroidal antinflammatory agents, isoniazide and suicidal attempts with acethaminophen in England. Other causes are hepatic ischemia, malignant infiltration of the liver, mushroom poisoning and Wilson disease in young people. The clinical picture includes variable jaundice, rapidly progressive encephalopathy, non palpable liver, bleeding diathesis, hypoglycemia, renal failure and infections. The most severe complication is brain edema and endocraneal hypertension that frequently determines the prognosis. Recent advances in management include: mannitol for endocraneal hypertension, early dialysis, H2 blockers, barbiturate coma in cases refractory to treatment. Finally liver transplantation in stage III or II coma by centers with good experience can obtain excellent results, with survival rates of 70-75% not obtainable by other therapeutic modalities