Hepatic encephalopathy clinical presentation

The diagnosis of hepatic encephalopathy is made on clinical grounds. Plasma ammonia concentrations are rarely helpful, either for diagnosis or for monitoring the patient s disorder normal ammonia concentrations are helpful in excluding hepatic encephalopathy as a cause of cerebral dysfunction. An exception is a patient who presents with acute encephalopathy of unknown cause. Elevated ammonia concentrations in that situation suggest acute hepatic failure or Reye s syndrome. 

Several strategies to treat alcoholic liver disease have been evaluated. Prednisolone may improve survival in patients with hepatic encephalopathy. Nutrients such as S-adenosylmethionine and polyunsaturated lecithin have been found to have beneficial effects in nonhuman primates and are undergoing clinical trials. Other medications that have been tested include oxandrolone, propylthiouracil, and colchicine. At present, however, none of these drugs is approved for use in the United States for the treatment of alcoholic liver disease. The current... 

In the case of chronic liver disease, episodic HE and persistent HE were defined and the term minimal hepatic encephalopathy (MHE) was coined to replace the hitherto inappropriate term subclinical encephalopathy . It is expected that this new system of classification will help to dispel the confusion frequently present in current textbook definitions and to facilitate multi-centre clinical trials in HE. 

The major aims of interventional procedures for portal hypertension are prophylactic and emergent treatment of variceal bleeding, control of hepatic encephalopathy, and treatment of refractory ascites. Hypersplenism associated with hematological disorder is an additional clinical problem in patients with portal hypertension. At present, the main primary embolotherapies available for portal hypertension are balloon-occluded retrograde transvenous obliteration (BRTO) and partial splenic embolization (PSE). In Japan, BRTO has recently been applied for gastric varices instead of either endoscopic treatment or transhepatic intrahepatic portosystemic shunt (TIPS) procedure, and numerous studies have reported that this method has an excellent success rate. Its efficacy for control of hepatic encephalopathy has also been demonstrated. 

The clinical situation deteriorates rapidly febrile temperatures and leucocytosis as well as subicterus are observed there are also signs of encephalopathy. An arterial murmur can often be heard on auscultation, since the tumour is mainly supplied with blood from the hepatic artery. A sudden blossoming of vascular spider naevi is frequently seen with underlying cirrhosis. Virchow s lymphadenopathy may be present. (84) Fever and leucocytosis frequently occur in tumour necrosis. Clinical findings include ... 

If the patient with kidney failure also has cirrhosis or some other form of hver failure, this additional ammonia load may present a stress that cannot be adequately handled by the diseased liver. The result may be increased blood and central nervous system ammonia levels with development of encephalopathy (Fraser Arieff, 1985). Thus, patients with cirrhosis and end-stage kidney disease are at particular risk for developing encephalopathy since both conditions act synergistically to increase both blood and central nervous system ammonia. It should also be noted that plasma urea and serum creatinine do not always adequately reflect renal function in patients with severe liver disease. Recent studies suggest that many patients who have cirrhosis, ascites, and normal plasma urea and creatinine may in fact have severe renal functional impairment (Gines et al., 1988 Papadakis Arieff, 1987 Takabatake et al., 1988). In such individuals, differentiation of hepatic from uremic encephalopathy on clinical grounds may be difficult. 

At present, the important clinical indication areas for therapy with thiamine are the beriberi of alcoholics and Wernicke s encephalopathy (Korner and Vollm 1976). In both cases, therapy is started with daily doses of at least 50-100 mg (in severe cases up to 200 mg) thiamine administered parenterally. Therapy is then continued with oral doses of 100-300 mg daily. Neuritis accompanying pregnancy responds particularly well to vitamin therapy. In some severe disorders of the intermediate metabolism (e.g., diabetic acidosis, severe hepatic malfunction), the necessary phosphorylation of thiamine in the organism is no longer ensured. Thiamine has, therefore, to be administered directly in its active form, thiamine pyrophosphate (TPP, cocarboxylase). Instances of toxicity of thiamine have been reported, primarily showing effects on the cardiovascular and nervous systems (Un-NA 1972 DiPalma and Ritchie 1977). 

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