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.
- Give high-dose parenteral thiamine immediately when Wernicke disease is suspected; oral absorption is unreliable in the acute high-risk state and laboratory confirmation must not delay therapy.
- If hypoglycaemia is present, treat it immediately and administer thiamine before or alongside carbohydrate as soon as possible; do not withhold life-saving glucose while sourcing thiamine.
- Check and replace magnesium because thiamine-dependent enzymes require it, and identify phosphate, potassium, infection, liver disease, head injury and withdrawal occurring at the same time.
- Korsakoff syndrome is a persistent amnestic disorder with severe new-learning impairment, variable remote-memory loss, executive dysfunction, apathy and confabulation that often follows inadequately treated Wernicke episodes.
- After acute treatment, continue nutrition, alcohol treatment, cognitive rehabilitation, safeguarding and supported-living assessment; thiamine prevents further injury but does not reliably reverse established Korsakoff disability.
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.
Focal deficit, head trauma, seizure or anticoagulant use requires urgent brain imaging because subdural haemorrhage or stroke can coexist with alcohol-related risk.
Fever, neck stiffness, hypoxia or haemodynamic instability requires infection and critical-illness evaluation alongside empirical Wernicke treatment.
Autonomic hyperactivity, hallucinations and seizure during alcohol cessation can indicate severe withdrawal or delirium tremens requiring a separate monitored benzodiazepine pathway.
Refusal of food, medication or accommodation in profound amnesia requires decision-specific capacity assessment and safeguarding rather than assuming an informed choice.
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.
- Check magnesium, phosphate, potassium, renal and liver function and replace important abnormalities while planning controlled nutrition.
- Admit and reassess frequently; continue parenteral therapy for the guideline-defined course unless the diagnosis is excluded and investigate competing causes in parallel.