Hepatic Encephalopathy: Therapeutic Dichotomy

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Background
In 2014, the American Association for the Study of Liver Diseases (AASLD) and European Association for the Study of the Liver (EASL) published a new set of practice guidelines for Hepatic Encephalopathy (Vistrup et al., 2014). These guidelines define Hepatic Encephalopathy (HE) as “a brain dysfunction caused by liver insufficiency and/or portosystemic shunting, and manifests as a wide spectrum of neurological/psychiatric abnormalities ranging from subclinical alterations to coma” (Vistrup et al.). Until recently, there had been limited consensus on the diagnostic criteria for HE, but now there are classifications and descriptive criteria for the neurological and psychiatric abnormalities associated with each stage of HE (Dharl & Bajaj, 2015). The recent advances made by the AASLD-EASL have created a systematic and uniform approach to diagnosis HE (Dharl & Bajaj, 2015). The diagnosis for HE is done through identifying the underlying etiology, clinical severity, time course, and presence or absence of precipitating factors (Dharl & Bajaj). The AASLD-EASL guidelines recommend that the underlying etiology be identified first (Dharl & Bajaj). There are three
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As defined by the American Liver Foundation, cirrhosis “is the scarring of the liver with hard scar tissue replacing soft healthy tissue” (American Liver Foundation, 2015). Cirrhosis can be caused by multiple conditions including alcoholism, non-alcoholic fatty liver disease, Hepatitis C and genetic diseases such as Wilson’s Disease (ALF, 2015). In a study released by the Chronic Liver Disease Foundation (CLDF), “ patients with cirrhosis from alcoholism have more brain deterioration with HE compared to non-alcoholic cirrhosis patients” (Ahluwalia et al., 2015). Almost half of patients with cirrhosis will be diagnosed with HE during their clinical course, some repeatedly (Vistrup et

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