Hepatic encephalopathy diagnosis

In suspected subclinical hepatic encephalopathy, psychometric tests are extremely important for the diagnosis and cannot be substituted by other examination procedures (e.g. anamnesis, inspection, laboratory analysis, imaging). 

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As far as the costs are concerned, a one-year course of prophylactic treatment including the necessary follow-up checks and possible early treatment of commencing water retention is less expensive than 3 or 4 days hospitalization. This solely economic viewpoint is hkewise true for prophylactic measures used in hepatic encephalopathy as well as for its early diagnosis and successful therapy at the practitioner s surgery. 

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. 

Colquhoun S, Lipkin C, Connelly C. The pathophysiology, diagnosis, and management of acute hepatic encephalopathy Adv Intern Med 2001 46 155-76. 

Diagnosis Hepatic encephalopathy likely secondary to elevated ammonia levels. 

Percy Veere s symptoms and laboratory abnormalities did not slowly subside over the next 6 weeks as they usually do in uncomplicated viral hepatitis A infections. Instead, his serum total bilirubin, ALT, AST, and alkaline phosphatase levels increased further. His vomiting became intractable, and his friend noted jerking motions of his arms (asterixis), facial grimacing, restlessness, slowed mentation, and slight disorientation. He was admitted to the hospital with a diagnosis of hepatic failure with incipient hepatic encephalopathy (brain dysfunction caused by accumulation of various toxins in the blood), a rare complication of acute type A viral hepatitis alone. The possibility of a superimposed acute hepatic toxicity caused by the use of acetaminophen was considered. 

Since hepatic myelopathy does not respond to the classical ammonia lowering therapy of hepatic encephalopathy, transplantation should be considered as soon as the diagnosis is made. With successful liver transplant, the patient has a chance of improvement (Weissenbom et al., 2003). 

The diagnostic work-up of a patient with suspected hepatic encephalopathy should include in any case a cerebral computed tomography. Subdural haematoma and also parenchymal bleeding are rare but significant complications of liver cirrhosis that must be ruled out before the diagnosis of HE is made. 

The fasting venous plasma ammonia concentration is useful in the differential diagnosis of encephalopathy when it is unclear if encephalopathy is of an hepatic origin. It is especially helpful in diagnosing Reye s syndrome and the inherited disorders of urea metabolism. However, it is not a useful test to use in patients with laiown liver disease. 

Differential diagnosis of typhoid fever includes other Salmonella infections, leptospirosis, schistosomiasis, disseminated tuberculosis, malaria, brucellosis, viral hepatitis. Yersinia enterocolitis, influenza, lymphoma, toxoplasmosis, infectious mononucleosis, tuphus, encephalopathy and connective-tissue disorders. 

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