Published online by Cambridge University Press: 24 July 2019
Hepatic encephalopathy (HE) is a complex neuropsychiatric disorder, manifestations of which range from subtle abnormalities demonstrable only on neuropsychometric testing, such as mild cognitive impairment, psychomotor slowing, and impaired bimanual and visuomotor coordination (referred to as minimal HE or MHE), through to overt manifestations such as disruption of the sleep cycle, disturbed attention span, change in personality, confusion, disorientation, and coma. Aside from the uncommon patient with HE due to a congenital deficiency of an urea cycle enzyme, in whom liver function is otherwise normal, HE occurs as a consequence of severe acute or chronic liver disease or in the setting of porto-systemic venous shunting, the latter arising either spontaneously, usually in the presence of portal venous hypertension complicating cirrhosis, or iatrogenically, following portal venous hypertension-decompressive shunt procedures, both surgical and radiologically placed. Irrespective of the clinical setting in which it arises, the severity of overt HE is traditionally graded using systems such as the West Haven criteria [1] (Table 30.1).
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