Thiamine Dosing for the Treatment of Alcohol-Induced Wernicke’s Encephalopathy: A Review of the Literature

Abstract

Objective: To determine the most appropriate thiamine replacement regimen by evaluating safety and efficacy of the drug specific to alcohol-induced Wernicke’s encephalopathy (WE). Data Sources: A comprehensive literature search was conducted using PubMed, MEDLINE, Scopus, and ProQuest between January and August 2020 using the following keyword and Boolean search terminology: “thiamine” AND “alcohol” AND (encephalopathy OR korsakoff). Study Selection and Data Extraction: Randomized control trials; prospective, observational, and retrospective cohort analyses; and case reports and series were included in this evaluation. A confirmed diagnosis of alcohol-induced WE and treatment with parenteral or intramuscular (IM) thiamine were required for inclusion. Data Synthesis: Six publications composed of 138 patients were evaluated in this review, in which a wide variety of thiamine supplementation strategies were employed. Clinical diagnostic criteria varied significantly between publications. Doses ranged from 100 to 1500 mg intravenous thiamine and up to 300 mg IM thiamine, with no apparent difference in patient outcomes. All patients who received thiamine experienced symptom improvement, and adverse drug events were minimal. Conclusions: Despite the clinical controversy regarding the appropriate thiamine supplementation regimen, the heterogeneity of published works combined with symptom resolution across the gamut of dosing strategies makes a definitive consensus elusive. Clinicians should continue to provide parenteral or IM thiamine in doses of ≥100 mg to patients with confirmed alcohol-induced WE.

What is the optimum thiamine dose to treat or prevent Wernicke's encephalopathy or Wernicke–Korsakoff syndrome? Results of a randomized controlled trial

“…The results of this study showed no clear benefit of high dose thiamine over intermediate or lower doses of thiamine for the treatment and prevention of cognitive and neurological abnormalities related to WE (synonymous with acute WKS) over the time interval examined. In the absence of conclusive evidence for the superiority of high dose thiamine, these findings support a recommendation that treatment of alcohol‐induced WE should be patient‐specific (Smith et al, 2020) and include an investigation of other confounding comorbidities that may impact thiamine replacement (e.g., hypomagnesemia, sepsis, or other metabolic disturbance).…”

Acute Ethanol Intoxication: Αn Overlooked Cause of High Anion Gap Metabolic Acidosis With a Marked Increase in Serum Osmolal Gap

“…Intravenous isotonic crystalloid fluids can be administered to patients with symptoms of volume depletion or hypotension [ 19 ]. Parenteral thiamine should be administered to all comatose patients due to ethanol intoxication in order to prevent or treat Wernicke's encephalopathy (usual doses in prevention ranging from 100 mg to 250 mg or higher in established encephalopathy) [ 20 ].…”

Non-alcoholic Wernicke encephalopathy in an esophageal cancer patient receiving radiotherapy: A case report

“…Once a diagnosis of Wernicke encephalopathy is suspected, it is advisable to administer thiamine as early as possible to prevent permanent neurological damage[ 20 ]. Although there are no published guidelines for the treatment of Wernicke encephalopathy in non-alcoholics patients, intravenous thiamine supplementation in the acute stage is currently recommended.…”