Diagnosis, Therapy and Prevention of Wernicke's Encephalopathy
A. Ivashynka
National Neurology and Neurosurgery Research Centre, Minsk, Belarus
Search for more papers by this authorR. Tanasescu
Colentina Hospital, University of Medicine and Pharmacy, Carol Davila, Bucharest, Romania
Search for more papers by this authorM. A. Leone
Azienda Ospedaliero-Universitaria Maggiore della Carita, Novara, Italy
Search for more papers by this authorA. Ivashynka
National Neurology and Neurosurgery Research Centre, Minsk, Belarus
Search for more papers by this authorR. Tanasescu
Colentina Hospital, University of Medicine and Pharmacy, Carol Davila, Bucharest, Romania
Search for more papers by this authorM. A. Leone
Azienda Ospedaliero-Universitaria Maggiore della Carita, Novara, Italy
Search for more papers by this authorNils Erik Gilhus MD, PHD
Department of Clinical Medicine, University of Bergen, Norway
Department of Neurology, Haukeland University Hospital, Bergen, Norway
Search for more papers by this authorMichael P. Barnes MD, FRCP
University of Newcastle, Newcastle upon Tyne, UK
Hunters Moor Neurorehabilitation Ltd, Newcastle upon Tyne, UK
Search for more papers by this authorMichael Brainin MD
Department of Clinical Medicine and Prevention, Austria
Center for Clinical Neurosciences, Donau-Universität Krems, Austria
Department of Neurology, Landesklinikum Donauregion Tulln, Tulln, Austria
Search for more papers by this authorSummary
Backround: Although Wernicke encephalopathy (WE) is a preventable and treatable disease it often remains undiagnosed.
Objectives: To create practical guidelines for diagnosis, management and prevention of the disease.
Methods: we searched Medline, EMBASE, LILACS and the Cochrane Library.
Recommendations: (1) The clinical diagnosis of WE should take into account the different presentations of clinical signs between alcoholics and non-alcoholics (Level C); although prevalence is higher in alcoholics, WE should be suspected in all clinical conditions which could lead to thiamine deficiency (good practice point). (2) The clinical diagnosis of WE in alcoholics requires two of the following four signs: (a) dietary deficiencies, (b) eye signs, (c) cerebellar dysfunction, and (d) either an altered mental state or mild memory impairment (Level B). (3) Total thiamine in a blood sample should be measured immediately before its administration (good practice point). (4) MRI should be used to support the diagnosis of acute WE in alcoholics and non-alcoholics (Level B). (5) Thiamine is indicated for the treatment of suspected or manifest WE. It should be given, before any carbohydrate, 200 mg three times daily, preferably intravenously (Level C). (6) The overall safety of thiamine is very good (Level B). (7) After bariatric surgery we recommend follow-up of thiamine status for at least 6 months (Level B) and parenteral thiamine supplementation (good practice point). (8) Parenteral thiamine should be given to all at-risk subjects admitted to the Emergency Room (good practice point). (9) Patients dying from symptoms suggesting WE should have an autopsy (good practice point).
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