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Med Clin N Am 92 (2008) 795–812

Hepatic Encephalopathy
Santiago J. Munoz, MDa,b,*

Division of Hepatology, Department of Medicine, Albert Einstein Medical Center, Philadelphia, PA 19141, USA b Jefferson Medical College, Philadelphia, PA 19107, USA

Hepatic encephalopathy (HE) is a syndrome of neuropsychiatric dysfunction caused by portosystemic venous shunting, with or without intrinsicliver disease [1]. Patients with HE often present with the onset of mental status changes ranging from subtle psychologic abnormalities to profound coma. Several hypotheses have been proposed to explain the mental impairment associated with portosystemic shunting and liver disease. Clinicians diagnosing HE frequently have the opportunity to intervene and reverse severe HE, even hepatic coma. Therecent advances in understanding and management of HE are the subject of this article.

Epidemiology and clinical significance HE is a common complication of advanced cirrhosis. Between one third to one half of hospitalizations for cirrhosis are related to HE [2]. The frequency of hospitalization for HE has nearly doubled over the last decade, with lengths of stay between 5 and 7 days [2].Patients with HE often have other manifestations of end-stage liver disease, such as ascites, jaundice, or gastrointestinal variceal bleeding. HE can also develop as an isolated manifestation of decompensated cirrhosis. HE usually signals advanced liver failure, and is often considered a clinical indication for evaluation for liver transplantation [3]. HE may disable the patient from employment,driving, and self-care, and require involvement of family or household members in the care of affected patients. The clinical importance of HE is underscored by the frequent reversibility of the precipitating factors.

* P.O. Box 403, Moorestown, NJ 08057. E-mail address: 0025-7125/08/$ - see front matter Ó 2008 Elsevier Inc. All rights reserved. doi:10.1016/



Risk factors Severe, acute, or chronic liver disease and portosystemic venous shunting are the sine qua non for the development of HE. The more advanced the liver disease, the more likely the development of HE. Patients with cirrhosis who have minimal HE (formerly known as ‘‘subclinical’’ HE) are at risk of developing overt HE [4]. Placement of a transjugularintrahepatic portosystemic shunt (TIPS) is also a risk factor. Patients who have diabetes mellitus or malnutrition seem to develop HE more frequently with cirrhosis [5]. HE is an essential component of acute liver failure [6]. Severe hyperammonemia (O150–200 mmol/L) with acute liver failure can cause cerebral edema that contributes to HE [7]. Patients with portal vein thrombosis and extensiveportosystemic shunting without significant parenchymal liver disease occasionally develop HE. Other risk factors can precipitate HE (Box 1). Types of hepatic encephalopathy HE is clinically classified into three major categories, according to the underlying hepatic condition (Table 1) [8]. Type A occurs in patients with acute liver failure. Type B occurs in patients without intrinsic liver disease butwith large, noncirrhotic, portosystemic shunting. Type C is related to underlying cirrhosis with portosystemic shunting. Type C is the most common form. It can be episodic or persistent. Episodic HE can lead to repeated hospitalizations, often caused by precipitating factors (see Box 1). The HE Box 1. Precipitating factors for hepatic encephalopathy Dehydration Gastrointestinal bleeding Infections(especially spontaneous bacterial peritonitis, urinary tract, skin, or pulmonary) Constipation Excessive dietary protein Central nervous system acting drugs Hypokalemia Renal failure Urinary obstruction Hyponatremia Surgery Transjugular intrahepatic portal-systemic shunt Superimposed liver injury (acute hepatitis, drug-induced liver injury) Hepatocellular carcinoma Terminal liver disease...
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