| Abstract [eng] |
Background. Wernicke encephalopathy (WE) is an acute neurological syndrome caused by thiamine deficiency. First described by Karl Wernicke in 1881, the disease is characterized by a triad of symptoms—encephalopathy, ataxia, and ocular disturbances. WE is underdiagnosed (80 % of cases identified post-mortem) and inadequately treated (20 % mortality rate in the acute phase). Poor treatment and diagnostic outcomes necessitate better education on this topic. Aim. This article aims to comprehensively review and summarize the scientific literature on WE, according to the latest diagnostic and treatment recommendations. Materials and methods. A literature review was conducted, searching PubMed, ClinicalKey, Cochrane Library, and UpToDate databases using English keywords "Wernicke encephalopathy," "Wernicke-Korsakoff syndrome," and "thiamine deficiency". Thirty-four English-language publications were analysed. Results. Alcohol abuse is the main cause of thiamine deficiency resulting in WE however, up to 26 % of cases have non-alcoholic origins. Various conditions including hyperemesis gravidarum, anorexia nervosa, oncological diseases, bariatric surgery, or hypermetabolic states, can cause WE. The classic triad rarely occurs in its entirety; various autonomic dysregulations accompany typical symptoms with Korsakoff's syndrome developing later. Diagnosis is clinical, based on the Caine criteria, with magnetic resonance imaging recommended for confirmation. Treatment for WE is based on intravenous thiamine replacement therapy. The prognosis is poor, with 17-20 % mortality in the acute phase and 85% experiencing severe residual symptoms. Conclusions. Inadequate diagnosis of WE is often attributed to its atypical presentation and varied etiological factors. Better education on this topic is crucial for improving outcomes by ensuring timely diagnosis and adequate treatment. |
