Case #026

The triad of confusion, ocular abnormalities and ataxia in a malnourished heavy drinker is Wernicke encephalopathy, though all three features are present together in only about a third of cases, relying on the complete triad is the commonest reason it is missed. Bilateral lateral rectus palsies with nystagmus, a broad-based ataxic gait and global inattention with preserved consciousness are the pattern here. A normal ammonia and preserved consciousness argue against hepatic encephalopathy, and an undetectable ethanol level excludes simple intoxication. The critical error is visible in the fifth clue: dextrose was given before thiamine. Thiamine is an essential cofactor for pyruvate dehydrogenase and transketolase, and a glucose load in a deplete patient exhausts the remaining stores and precipitates deterioration: glucose must always follow thiamine, never precede it. Hypomagnesemia compounds this, since magnesium is required for thiamine-dependent enzymes to function, and encephalopathy will not resolve until it is corrected. The MRI changes are highly specific but insensitive; normal imaging never excludes the diagnosis, which is clinical. That is the whole argument for treating now: high-dose intravenous thiamine, at doses far above oral supplementation and before any further glucose-containing fluid, with magnesium replaced alongside it or the enzymes it feeds will not run. Thiamine is cheap and close to harmless, while untreated disease carries roughly 20% mortality and leaves a large proportion of survivors with irreversible Korsakoff amnesia. Set against that, waiting for imaging or for the full triad is not caution but a decision to accept the worse outcome.