This issue of Liver Transplantation features an interesting article by Sotil et al. 1 that further substantiates the clinical significance of hepatic encephalopathy (HE) and its potential effect on patient functioning in the years following liver transplantation (LTX). With the implementation of the Model for End-Stage Liver Disease (MELD) system of organ allocation, HE was not included in the MELD score for prioritizing patients for LTX because it was not found to influence short-term survival.2 However, Sotil et al. suggest that beyond the prediction of survival, pre-LTX HE has important implications for persisting neurological deficits post-LTX. Their point is well taken. Transplant outcomes have largely moved beyond mere survival to improving patient quantity and quality of life. In this context, the importance of HE cannot be overemphasized. Diagnosing HE is essential to improving treatment and prognosticating about the potential for recovery following LTX. Clinicians, patients, and families alike need to be aware of the signs and symptoms of HE in order to prepare for LTX and the post-LTX recovery. Although the current study by Sotil et al. highlights the critical issue of the persistence of post-LTX cognitive impairment, it additionally raises the yet unanswered question of whether early identification and treatment could prevent or at least minimize these persisting effects. Several key points on HE deserve further discussion.
IDENTIFYING AND DEFINING HE PRIOR TO LTXAs proposed by Ferenci et al. 3 in the 2002 final report of the working party on HE, every effort should be made to better define and quantify the degree of HE. This is especially important for patients undergoing evaluation for listing for LTX and for patients on the waiting list for LTX. HE is a complex neuropsychiatric syndrome characterized by a constellation of signs and symptoms, which can include alteration of consciousness (up to and including stupor or coma), cognitive impairment, confusion/disorientation, affective/emotional dysregulation, psychosis, behavioral disturbances, bioregulatory disturbances, and disturbances of the motor system represented by asterixis, extrapyramidal symptoms, tremor, increased tendon reflexes, increased muscle tone, ataxic gait, bradykinesia, slurred speech, or incoordination. Although Sotil et al.1 relied on the diagnosis of overt HE, the current definition of HE emphasizes that it reflects a continuum of symptoms, with subclinical HE lying at the minimal end of the spectrum.3 Although gross disorientation and bizarre behavior (eg, lack of restraint, inappropriate behavior, psychotic symptoms, and nocturnal ramblings) are easily identifiable, minimal symptoms can manifest as slight deficits in attention and personality or mood changes most often noticed only by family or those who know the patient well. Thus, in addition to clinical interviews of the patient and family about such subtle changes, subclinical HE by definition will be revealed only by psychometric testing. Neuropsychological tests of ...