[Hepatic encephalopathy in liver cirrhosis].

Hepatic encephalopathy (HE) is a common and serious complication of liver cirrhosis, associated with significant morbidity and mortality. Pathophysiologically, it results from a complex interplay of hyperammonemia, systemic inflammation, neuroinflammatory processes, and microbial dysbiosis. Clinically, HE ranges from subtle cognitive impairments (minimal HE) to coma (grade 4 HE). Diagnosis requires thorough clinical assessment and the use of specialized testing methods, particularly to detect subclinical alterations. In everyday practice, ammonia levels have limited diagnostic value but may be useful for differential diagnosis. The acute treatment of overt hepatic encephalopathy (OHE) is primarily based on the administration of lactulose, optionally supplemented with intravenous L-ornithine-L-aspartate. For secondary prophylaxis lactulose is the treatment of choice and in patients with recurrent episodes, the combination of rifaximin and lactulose is well established. Nutritional recommendations are a key component of therapy, especially to prevent sarcopenia. In cases of refractory HE or recurrent relapses despite guideline-based treatment, liver transplantation should always be considered. In general, early detection and individualized management of HE is essential to preserve and improve quality of life, prognosis, and functional independence of the affected patients.