Synopsis
Diagnose Wernicke encephalopathy clinically, deliver immediate high-dose parenteral thiamine and cofactor support, and distinguish persistent Korsakoff amnesia from intoxication, withdrawal and other causes of encephalopathy.
- Wernicke encephalopathy is an acute thiamine-deficiency brain disorder and a medical emergency; the complete triad of confusion, eye signs and ataxia is absent in many patients.
- Suspect it in alcohol dependence, malnutrition, prolonged vomiting, hyperemesis, bariatric surgery, cancer, starvation, dialysis or another state of depleted intake or increased requirement.
- Operational clinical recognition improves when at least two of dietary deficiency, ocular abnormality, cerebellar dysfunction and altered mental state or memory impairment are present.
Key red flags
Coma, airway compromise, hypothermia, hypotension or severe hypoglycaemia requires simultaneous resuscitation and intravenous thiamine rather than transfer to a routine detoxification setting.
Investigation priorities
Identify risk plus mental, ocular, cerebellar and nutritional features and initiate treatment immediately.
Management branches
A nutritionally vulnerable patient has confusion, eye signs, gait dysfunction or memory change.
- Perform ABC assessment, check capillary glucose and temperature, identify ocular and gait findings and seek trauma, infection, withdrawal and liver clues.
- Administer high-dose intravenous thiamine immediately through the local Wernicke protocol and give glucose without delay if hypoglycaemic.
Key medicines
Intravenous thiamineFor suspected Wernicke encephalopathy, use the current hospital high-dose regimen, commonly 300–500 mg intravenously three times daily for 3–5 days, then continue guided by clinical response and national guidance.
Oral thiamine after stabilisationContinue an oral dose and duration from the local alcohol or nutrition pathway after the parenteral course, often in divided daily dosing while malnutrition or alcohol risk persists.