How can I differentiate between hepatic encephalopathy and other causes of altered mental status in a patient?

To differentiate hepatic encephalopathy (HE) from other causes of altered mental status, focus on clinical context, characteristic features, and targeted investigations.

HE typically occurs in patients with known or suspected liver disease, especially cirrhosis or acute liver failure, and presents with a spectrum of neuropsychiatric symptoms ranging from subtle cognitive impairment to coma ¹. The presence of precipitating factors such as gastrointestinal bleeding, infection, electrolyte disturbances, or medication changes supports HE diagnosis ¹.

Clinically, HE often manifests with asterixis (flapping tremor), disorientation, altered sleep patterns, and personality changes, which are less common in other causes of encephalopathy ¹. In contrast, other causes of altered mental status (e.g., metabolic, infectious, structural brain lesions) may lack these specific signs and have different clinical contexts ².

Laboratory investigations are crucial: elevated serum ammonia levels support HE but are not diagnostic alone, as ammonia can be elevated in other conditions (Sargent, 2007). Liver function tests and coagulation profiles indicating hepatic dysfunction strengthen the suspicion of HE ¹. Neuroimaging (CT or MRI) is important to exclude structural brain causes of altered mental status ².

Response to empirical treatment with lactulose or rifaximin can also help differentiate HE, as improvement in mental status following ammonia-lowering therapy is characteristic (Sargent, 2007).

In summary, differentiation relies on identifying underlying liver disease, typical clinical features such as asterixis, exclusion of other causes via imaging and labs, and response to specific HE treatments ¹,² (Sargent, 2007).