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Explanation :WE is a reversible biochemical lesion of the CNS caused by overwhelming metabolic demands being made upon depleted B-vitamin reserves, in particular thiamine (B1). Although, usually associated with chronic alcoholism, WE can occur in the setting of poor nutrition caused by any other condition The classic triad of WE includes acute confusion, ataxia and ophthalmoplegia. However the triad is present in only 10% of patients with WE. Thus if the classic triad is used for diagnosis, WE will be missed or the diagnosis will be delayed till the classic triad becomes obvious Thiamine deficiency in alcohol abusers results from inadequate intake and reduced GI absorption. Thiamine absorption is significantly reduced in malnourished alcoholic abusers. Thus parenteral treatment is needed.

Explanation :Caused by acute and severe CNS deficiency of thiamine (chronic def lead to Beri beri) Thiamine is a cofactor for several key enzymes important in energy metabolism and production of ATP Alcohol withdrawal causes CNS over activity leading to increased need for thiamine. Thiamine deficiency cause brain cell death by inhibiting metabolism in brain regions with high metabolic requirements and high thiamine turnover. WE may be precipitated in susceptible patients by administration of intravenous glucose before thiamine supplementation as glucose lead to utilisation of thiamine. Oral B-vitamin replacement is both inadequate and ineffective owing to limited gastrointestinal absorption in alcohol misusers. Parenteral B-vitamin replacement is therefore required. The classic triad of WE includes acute confusion, ataxia and ophthalmoplegia. However the triad is present in only 10% of patients with WE. Thus if the classic triad is used for diagnosis, WE will be missed or the diagnosis will be delayed till the classic triad becomes obvious. A high index of suspicion is therefore needed and the presence of only one sign should be sufficient to assign a diagnosis and commence treatment.

Explanation :WE is a reversible biochemical lesion of the CNS caused by overwhelming metabolic demands being made upon depleted B-vitamin reserves, in particular thiamine (B1). Malnourished hospitalized patients on IV dextrose is also prone to develop WE and must be on the differential diagnosis if they become confused. Dietary requirement of thiamine is only 1-2 mg daily. Atrophy of the mamillary bodies on MRI is a highly specific finding in WE and Korsakoff syndrome and is present in most cases and can be detected within a week of onset of WE. Mental changes- confusion, disorientation, inattentiveness, drowsiness, obtundation, semi coma, coma. Mental changes are most common and may be the only sign of WE. These changes are however non specific and may be caused by alcohol intoxication or withdrawal.

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MCQ On Wernicke’s encephalopathy

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