Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

ACUTE

suspected Wernicke's encephalopathy

1st line – stabilisation/resuscitation + parenteral thiamine

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ACUTE
|
suspected Wernicke's encephalopathy
1st line – 

stabilisation/resuscitation + parenteral thiamine

Following any required stabilisation and resuscitation, all patients with suspected Wernicke's encephalopathy should be treated with parenteral administration of high-dose thiamine to avoid permanent neurological injury, and subsequent Korsakoff's psychosis, or death.[1][23]​ However, given the lack of quality evidence and global consensus for dosing, preparation, and timing, there is often significant variability in thiamine administration in emergency treatment.[1][69][80][81]​​ In the absence of randomised controlled trial data affirming a specific dose, high doses of thiamine are favoured given the favourable risk-benefit ratio.[1][82]

Treatment duration is guided by clinical response. Ophthalmoplegia is likely to be the first sign to respond following thiamine repletion, with complete recovery after a few hours except for a residual fine horizontal nystagmus in up to 60% of patients.[17]​ Ataxia may resolve over several days but can be incomplete. Improvement in mental status often takes several weeks to be observed. 

The European Federation of Neurological Societies advise that urgent parenteral administration of thiamine should be continued until there is no further improvement in signs and symptoms. However, the UK National Institute of Health and Care Excellence (NICE) recommends that treatment be continued for a minimum of 5 days, unless Wernicke's encephalopathy is excluded.[1][66]

The most common adverse effect associated with parenteral administration of thiamine is injection site reactions, which tend to be mild and self-limited.[85]​ Although rare, anaphylaxis has been observed following parenteral administration of thiamine.[82][85][86] Patients should be monitored for severe adverse reactions or anaphylaxis and administration should be immediately stopped where noted. 

Some guidance suggests that thiamine must be administered before any glucose infusion as intravenous dextrose may precipitate Wernicke's encephalopathy in thiamine-deficient individuals.[1][23] However, there is a lack of consensus regarding this approach and little evidence to suggest that glucose administration should be delayed if it is required.[87]​ If the patient is acutely symptomatic from hypoglycaemia, parenteral thiamine should be administered concurrently with (or as soon as possible following) glucose-containing intravenous fluids.[64]

Primary options

thiamine: 200-500 mg intravenously/intramuscularly every 8 hours for 2-7 days, followed by 250 mg intravenously/intramuscularly every 24 hours for 3-5 days, then 100 mg orally once daily until no longer at risk

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Plus – vitamin/mineral supplementation

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ACUTE
|
suspected Wernicke's encephalopathy
Plus – 

vitamin/mineral supplementation

Treatment recommended for ALL patients in selected patient group

Nutritional deficits should be corrected in patients with alcohol-use disorders and those with other risk factors for Wernicke's encephalopathy.[80][83]​​[84]​ Magnesium deficiency often coexists alongside thiamine deficiency and its correction is critical given it is a cofactor required for normal functioning of several thiamine-dependent enzymes.[48] Supplementation with water-soluble vitamins, especially niacin (vitamin B3) and pyridoxine (vitamin B6), is also recommended as patients with Wernicke's encephalopathy are often deficient in these vitamins.[23] Various vitamin and/or mineral supplements exist; consult your local drug information source for more information.

ONGOING

high risk for thiamine deficiency

1st line – long-term thiamine supplementation

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ONGOING
|
high risk for thiamine deficiency
1st line – 

long-term thiamine supplementation

Patients at high risk for thiamine deficiency may benefit from supplementary low-dose thiamine either parenterally or orally, depending on clinical circumstances.[1][66]​ This includes patients with chronic alcohol-use disorder or history of alcohol intoxication; with repeated vomiting, or poor oral intake; who are hospitalised; with a history of Wernicke's encephalopathy; who are immunocompromised with cancer or receiving chemotherapy; who have had recent gastrointestinal surgery (particularly bariatric surgery); on chronic haemodialysis. 

Formal guidance for longer-term therapy is lacking but thiamine supplementation may be continued for up to several months depending on the clinical picture and the patient’s risk factors.[23]

Primary options

thiamine: 100-200 mg orally/intramuscularly once daily

More

Plus – vitamin/mineral supplementation

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ONGOING
|
high risk for thiamine deficiency
Plus – 

vitamin/mineral supplementation

Treatment recommended for ALL patients in selected patient group

Nutritional deficits should be corrected in patients with alcohol-use disorders and those with other risk factors for Wernicke's encephalopathy.[80][83]​​[84]​​ Magnesium deficiency often coexists alongside thiamine deficiency and its correction is critical given it is a cofactor required for normal functioning of several thiamine-dependent enzymes.[48] Supplementation with water-soluble vitamins, especially niacin (vitamin B3) and pyridoxine (vitamin B6), is also recommended as patients with Wernicke's encephalopathy are often deficient in these vitamins.[23] Various vitamin and/or mineral supplements exist; consult your local drug information source for more information.

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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