Wernicke encephalopathy in alcohol dependence
Wernicke encephalopathy is triggered by ingestion of carbohydrate (orally or intravenously) in patients with thiamine deficiency before thiamine has been adequately supplemented1. In severe cases, brain injury may occur; brain magnetic resonance imaging (MRI) may identify oedema of the mammillary bodies, and sometimes bleeding in specific areas. Persisting brain damage can result in Korsakoff syndrome and, very rarely, death.
Wernicke encephalopathy should be suspected if any of the following features are presentHaber, 2021:
- delirium (approximately 80% of patients)
- ataxia (approximately 20 to 25% of patients)
- eye signs (nystagmus or ophthalmoplegia) (approximately 30% of patients).
Wernicke encephalopathy can occur independently or with other causes of delirium, including alcohol intoxication, withdrawal and hepatic encephalopathyHaber, 2021.
Prompt treatment of Wernicke encephalopathy reduces the likelihood of permanent neurological damage. Give high doses of intravenous or intramuscular thiamine promptly if any clinical signs are present; see the Gastrointestinal guidelines for dosages. Exclude coagulopathy and severe thrombocytopenia before using the intramuscular route. Oral thiamine supplementation is not adequate in Wernicke encephalopathy.
Thiamine requires magnesium as a cofactor; even high thiamine doses may not have optimal effect if a patient has untreated hypomagnesaemia. See Identifying adults at risk of refeeding syndrome for a list of patients at high risk of electrolyte abnormalities (including hypomagnesaemia). Some patients may not be visibly wasted but may have low serum magnesium concentrations from use of medications such as proton pump inhibitors. Check serum electrolyte concentrations (calcium, magnesium and phosphate) or administer preventive magnesium concurrently with thiamine; see Hypomagnesaemia for intravenous regimens. Concurrent treatment of hypokalaemia is also important.