الفهرس 
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Abstract
Hepatic encephalopathy constitutes a spectrum of neuropsychiatric abnormalities, beginning with subtle psychomotor changes and progressing to confusion with asterixis, somnolence, and then coma, arising in patients with impaired liver function or portosystemic shunting.
It is a pathognomonic feature of liver failure and a common cause of admission to emergency departments. It affects the quality of life of both patient and relatives.
There are several methods of classifying hepatic encephalopathy , The most common clinical classification used to describe the severity of hepatic encephalopathy is the West Haven criteria ,This describes the hepatic encephalopathy progressing through its four stages, from mild lack of awareness to coma.
Overt hepatic encephalopathy affects approximately 20% of patients with liver cirrhosis each year, Covert hepatic encephalopathy also has a poor prognosis, with increased risk of hospitalization and progression to overt hepatic encephalopathy or mortality.
Neurological examination is often normal in stages 1-2 of hepatic encephalopathy, but hyperreflexia and extensor posturing may develop later, together with a positive Babinski sign.
In liver cirrhosis seizures are less common than in acute liver failure (when they warn of developing cerebral edema). and suggest causes such as electrolyte derangement (for example, hypoglycemia, hypomagnesaemia), alcohol withdrawal, stroke, or encephalitis.
Hepatic encephalopathy can develop due to liver failure from any cause.It is postulated that its pathogenesis is related to the effects of nitrogenous waste products on the brain, particularly ammonia and glutamine.
Muscle volume depletion (sarcopenia) contributes to the development of encephalopathy, since muscle represents an alternative site of ammonia detoxification.
There is no specific test for hepatic encephalopathy, and the diagnosis should be made on clinical grounds through the exclusion of other conditions that can mimic or be confused with hepatic encephalopathy .
Computed tomography or magnetic resonance imaging should be performed in all patients in whom a diagnosis of hepatic encephalopathy is being considered, in order to exclude other conditions such as intracranial hemorrhage or space occupying lesions. Positron emission tomography has been used experimentally and may have a role, but this remains undefined. Electroencephalography is used to investigate for the presence of seizures and should be considered if subclinical seizures are suspected.
The management of hepatic encephalopathy depends on its type and severity. Many patients with covert hepatic encephalopathy may not require treatment unless the condition is thought to be adversely affecting quality of life.(American Association for the Study of Liver and European Association for the Study of the Liver )
Episodes of overt hepatic encephalopathy can be shortened with appropriate treatment and further events prevented.
Many patients presenting acutely with overt hepatic encephalopathy will have an underlying precipitant, such as gastrointestinal bleeding, infection, diuretic overdose, or use of sedating medication.
The first stage in management is to address the causes of hepatic encephalopathy by stopping precipitating drugs, treating infection, etc. However, a substantial proportion of patients will have no identified cause. (EASL-AASLD) also it is recommended by the International Society for Hepatic Encephalopathy and Nitrogen Metabolism that 1.2-1.5 g/kg of protein is given in small meals distributed throughout the day, with a late night snack of complex carbohydrates
The EASL-AASLD guidelines recommend that lactulose is used as a first line agent in episodes of overt hepatic encephalopathy and then continued to prevent further episodes
Advances in treatment in recent decades have been due to the use of oral antibiotics to modulate gut flora, thus reducing ammonia production like neomycin and rifaximin
The EASL-AASLD guidance recommend rifaximin for secondary prophylaxis of overt hepatic encephalopathy in patients who have had further episodes while taking lactulose. There is no evidence for the use of rifaximin alone.
Patients whose hepatic encephalopathy does not respond to optimal medical treatment, in the form of lactulose and rifaximin, may be considered for embolization of portosystemic shunts, which can be under taken percutaneously
Liver transplantation should be considered in all suitable candidates presenting with hepatic encephalopathy especially if they have had two admissions for hepatic encephalopathy in the past six months in the absence of comorbidities that would preclude surgery