Definition: Encephalopathy that occurs secondary to thiamine (vitamin B1) deficiency. While Wernicke encephalopathy is reversible with treatment, it can progress to the irreversible Korsakoff’s syndrome if left untreated.

Without thiamine, the Krebs cycle breaks down leading to ATP depletion affecting the brain and heart

Acetyl-CoA enters the Krebs cycle and ATP is produced

Thiamine is a cofactor for the enzyme pyruvate dehydrogenase

2 of above components is diagnostic

Elevated lactate levels are common due to interruption of the Krebs cycle ( Donnino 2007

Hypotension and hypothermia may be seen

All three features present in < 10% of patients ( Donnino 2007

Patients will have a history of malnutrition or malabsorption

Ophthalmoplegia can improve in hours while altered mental status and ataxia are frequently more delayed in improvement if they improve at all

Unclear how long this provides protection for. Best estimates are about 1-2 weeks ( Hoffman 2015

Should be provided to all groups at risk of thiamine deficiency (see above)

IV better than IM as many patents have diminished muscle mass making absorption less predictable

Parenteral route recommended as many of these patients have abnormal GI absorption

Wernicke encephalopathy is characterized by ataxia, altered mental status and ophthalmoplegia but patients are unlikely to have all these components

Suspect Wernicke encephalopathy in any patient that is at risk of malnutrition or malabsorption and has any one of the classic symptoms

Prophylactic administration of thiamine 100 mg IV/IM to at risk patients can prevent development of the disease