Encefalopatía hepática en perros y gatos

Abstract

Hepatic encephalopathy (HE) in dogs and cats is a complex metabolic disturbance of the central nervous system that may result from hepatic failure, urea cycle enzyme defi ciency, or portosysistemic shunting. As a result, the metabolic and detoxifi cation functions of the liver are impaired and/or bypassed and the unaltered constituents of the portal blood go directly into the systemic circulation. The pathogenesis of hepatic failure-associated encephalopathy is complex. Probably, the HE is a syndrome in which take part multiple factors that can have different importance according the clinical situation. The key points to consider in the pathogeny of HE are: a) neurotoxins; b) alterations of neurotransmission systems; and c) astrocytes alterations. Clinical signs of HE include obtunded mental status, abnormal behavior, compulsive pacing, head-pressing, visual defi cits and seizure activity. Other clinical signs consistent with hepatic failure, as weight loss, anorexia, vomiting, diarrhea and polyuria-polydipsia, are often present. Diagnosis of HE is based upon documenting hepatic dysfunction in a patient with neurologic defi cits typical of a metabolic encephalopathy. Although there are multiple methods, the preferred is per-rectal scintigraphy. Treatment for HE is directed at reducing the level of gut-derived toxins and controlling seizures, if present; but treatment of the underlying hepatic disorder is the key to controlling signs of neurologic dysfunction. This article describes the major developments described so far regarding the pathophysiology of hepatic encephalopathy and therapeutic strategies