eMedicine Specialties > Psychiatry > Adult
Wernicke-Korsakoff Syndrome: Treatment & Medication
Updated: May 29, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
Wernicke encephalopathy is a medical emergency. Prompt recognition of the symptom complex and a high index of suspicion are crucial to ensure early treatment. Parenteral thiamine (100 mg) is the treatment of choice. Early treatment can rapidly reverse the ophthalmoplegia and improve ataxia/dysequilibrium and early mental confusion, as well as prevent development of the amnestic state. In advanced cases, where severe prolonged deficiency has led to permanent structural damage, permanent deficits are most often manifested as the amnestic state and severe ataxia.
After the initial IV dose, continue daily doses of thiamine (100 mg) as IV, IM, or oral doses depending on patient status. Supplementation of electrolytes, particularly magnesium and potassium (often low in people with alcoholism), may be required in addition to thiamine. Magnesium acts as a cofactor for many enzymes (eg, transketolase for the conversion of thiamine to thiamine pyrophosphate) and, therefore, its deficiency may lead to refractory response to thiamin supplementation.14 In patients who are chronically malnourished, the remainder of the B vitamins also should be supplemented. Administration of intravenous glucose to patients who are severely malnourished can exhaust their supply of thiamine and precipitate Wernicke-Korsakoff syndrome. Thus, good practice demands administration of thiamine prior to glucose infusion in patients at high risk for Wernicke-Korsakoff syndrome.
Emergency psychiatry hospitalization and evaluation is indicated when the patient is having active psychotic symptoms that pose a danger to self or others. Many such patients also meet the criteria of grave disability (ie, inability to provide basic needs such as food and shelter). In such cases, however, the patient should generally be medically and neurologically stable prior to transfer to a psychiatric facility, where acute medical work-up and monitoring may be available (eg, IV access, neuroimaging, nutritionist, neurology consultation). In most cases, patients with psychotic symptoms may require inpatient medical hospitalization and psychiatric consultation. Once medically stabilized, patients may need continued psychiatric care if severe psychotic symptoms persist.
In patients with comorbid acute alcohol withdrawal, treatment with IV/IM thiamine occurs concurrently with the indicated alcohol withdrawal procedures.
Consultations
Long-term alcohol use is the most common etiology for Wernicke-Korsakoff syndrome, and abstinence provides the best chance for recovery. Referral to an alcohol recovery program should be part of the treatment regimen. Inpatient treatment versus outpatient rehabilitation depends on the needs of the individual and risks of relapse. Several other risk factors for Wernicke-Korsakoff syndrome are recognized (see Causes). Patients with these risk factors also could benefit from referral or consultation to help prevent future episodes.
Diet
A balanced diet should be resumed as early as possible. Vitamin and electrolyte supplementation should be adhered to in addition to a well-balanced diet initially, and supplementation can be tapered as the patient resumes normal intake and demonstrates symptomatic improvement.
Activity
Due to gait abnormalities, unassisted ambulation is discouraged during the initial phase of treatment. Patients may require physical therapy evaluation for gait assistance. Gait abnormalities may be permanent, depending on the severity at initial presentation and the timeliness of therapy.
Medication
Wernicke-Korsakoff syndrome is a result of thiamine deficiency. The treatment is replacement of this essential vitamin. The usual dose is 100 mg/d PO/IV/IM. However, the dosing and duration of thiamine treatment has not been sufficiency studied. In a systematic review from the Cochrane Database, Day et al only found 2 randomized studies that were of sufficient quality.15 There was a significant difference in favor of 200 mg/d, as compared to 5 mg/d, when the outcomes were measure after 2 days.
Overall, the current standard-of-care involves use of thiamine 100 mg/d for acute prophylaxis. Duration of treatment varies greatly and depends on the comorbid conditions and etiology. For example, thiamine would be administered indefinitely for patients with absorption problems. However, when use as prophylaxis for acute alcohol withdrawal/detoxification, thiamine could be discontinued once dietary intake is adequate. When in doubt, a serum thiamine level may be obtained to guide treatment.
For persistent cognitive impairment (eg, Korsakoff dementia), cognitive enhancers such as acetylcholinesterase inhibitors and memantine have demonstrated some benefit.16,17 However, the findings were negative in one small comparison study with rivastigmine.18
Nutrients
In treating this disorder, the objective is to replenish vitamin B-1 stores. In adults, 60-180 mEq of potassium, 10-30 mEq of magnesium, and 10-40 mmol/L of phosphate per day appear necessary to achieve optimum metabolic balance.
Thiamine (Thiomalate)
Water-soluble vitamin that combines with adenosine triphosphate to form the coenzyme thiamine pyrophosphate, which is necessary for carbohydrate metabolism. The B vitamins are readily absorbed from the GI tract (except in cases of malabsorption syndromes). Alcohol inhibits absorption of thiamine, which occurs primarily in the duodenum.
Adult
100-200 mg PO/IV/IM
Pediatric
Not established
May alter theophylline, uric acid, and urobilinogen laboratory values
Documented hypersensitivity
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Sensitivity reactions can occur (intradermal test dose is recommended in suspected sensitivity); deaths have resulted from IV use; sudden onset or worsening of Wernicke encephalopathy following glucose intake may occur in patients who are thiamine deficient; administer before or together with dextrose-containing fluids in suspected thiamine deficiency
Magnesium sulfate
Cofactor in a number of enzyme systems, it also is involved in neurochemical transmission and muscular excitability. Patients with chronic alcoholism and patients who are malnourished usually have inadequate magnesium stores.
Adult
2-4 g IV at rate of 1 g/h initially, switch to PO when tolerated; dose is determined by level of deficiency
Pediatric
Not established
Concurrent use with nifedipine may cause hypotension and neuromuscular blockade; may increase neuromuscular blockade observed with aminoglycosides and potentiate neuromuscular blockade produced by tubocurarine, vecuronium, and succinylcholine; may increase CNS effects and toxicity of CNS depressants, betamethasone, and cardiotoxicity of ritodrine
Documented hypersensitivity; heart block; Addison disease; myocardial damage; severe hepatitis
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
Possible alteration of cardiac conduction, leading to heart block in digitalized patients; monitor respiratory rate, deep tendon reflex, and renal function when electrolyte is administered parenterally; magnesium may produce significant hypertension or asystole, so caution is needed when administering dose; in overdose, calcium gluconate, 10-20 mL IV of 10% solution, can be administered as antidote for clinically significant hypermagnesemia
Potassium acid phosphate (K-Phos)
Essential for transmission of nerve impulses, contraction of cardiac muscle, maintenance of intracellular tonicity, skeletal and smooth muscles, and maintenance of normal renal function. Gradual potassium depletion occurs via renal excretion, through GI loss, or because of low intake. Patients with chronic alcoholism and patients who are malnourished usually have inadequate nutrient stores. Potassium depletion sufficient to cause a 1-mEq/L drop in serum potassium requires a loss of about 100-200 mEq of potassium from the total body store.
Adult
10 mEq/h IV, switch to PO when tolerated; dose is determined by level of deficiency
Pediatric
Not established
Concurrent use with ACE inhibitors may result in elevated serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; in patients taking digoxin, hypokalemia may result in digoxin toxicity; caution if discontinuing potassium administration in patients maintained on digoxin
Hyperkalemia; renal failure; conditions in which potassium retention is present; oliguria or azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency
Pregnancy
A - Fetal risk not revealed in controlled studies in humans
Precautions
High plasma concentrations may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels; monitor potassium replacement therapy whenever possible by continuous or serial ECG
More on Wernicke-Korsakoff Syndrome |
| Overview: Wernicke-Korsakoff Syndrome |
| Differential Diagnoses & Workup: Wernicke-Korsakoff Syndrome |
 Treatment & Medication: Wernicke-Korsakoff Syndrome |
| Follow-up: Wernicke-Korsakoff Syndrome |
| References |
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Further Reading
Keywords
Wernicke-Korsakoff syndrome, Wernicke encephalopathy, Wernicke's encephalopathy, polioencephalitis hemorrhagica superioris, Korsakoff's psychosis, Korsakoff psychosis, amnestic-confabulatory state, psychosis polyneuritica, thiamine deficiency, confusion, ataxia, nystagmus, alcoholism, Korsakoff amnestic state, confabulation, Korsakoff dementia, nutritional deficiency
