Thiamine Repletion in Alcohol Abuse

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Author: Alexandria Gregory, MS-3
Saint Louis University School of Medicine
AAEM/RSA Social Media Committee

Thiamine deficiency is commonly seen in patients with a history of chronic alcohol use and can have significant consequences if untreated. Therefore, repletion of thiamine in these patients is crucial, and appropriate administration should begin in the emergency department (ED).

Thiamine Deficiency in Alcohol-Dependent Patients
Thiamine deficiency is common in alcohol-dependent patients for several reasons. First, those who drink alcohol excessively tend to have poor nutritional intake overall. Their nutritional intake may be further worsened if they have chronic vomiting and diarrhea due to alcohol ingestion. Additionally, alcohol damages the gastrointestinal tract, impairing absorption of vitamins and minerals. Patients often have associated hypomagnesemia, which decreases efficient utilization of thiamine, as magnesium acts an activator for thiamine. Alcohol-dependent patients may also have decreased hepatic storage of thiamine due to impaired liver function.[1]

Manifestations of Thiamine Deficiency
There are several clinical manifestations of thiamine deficiency, which are more commonly seen in alcoholics, but can occur in other patient populations, such as pregnant women or patients with HIV. Beriberi can occur in the “dry” and “wet” forms. Dry beriberi presents primarily with polyneuropathy that can have both sensory and motor impairments. Wet beriberi typically presents with cardiomyopathy, edema, and heart failure, but can also have associated polyneuropathy.[2]

Wernicke encephalopathy (WE) is a feared complication of thiamine deficiency, and consists of the classic triad of confusion, ataxia, and opthalmoplegia/nystagmus. It is potentially reversible if thiamine is repleted. However, because the symptoms of WE are similar to that of alcohol intoxication, the diagnosis may be missed if a patient is thought to simply be intoxicated.[3]

Korsakoff’s psychosis is considered a late manifestation of WE, and presents as amnesia, often with confabulation, though the patient has an intact sensorium and preservation of long-term memory. Korsakoff’s may develop even in the absence of a WE diagnosis, which suggests that the patient previously had WE that went undiagnosed and untreated.[3] Recovery is rare, and the disease is typically treated with acetylcholinesterase inhibitors or memantine, an N-methyl-D-aspartate (NMDA) receptor antagonist, with the goal of slowing the progression of dementia.

How should we replete thiamine?
To prevent and treat the clinical manifestations of thiamine deficiency, it is important to administer thiamine appropriately, beginning in the ED. A healthy adult typically requires 1.1-1.5 mg of thiamine per day, and deficiency occurs within approximately two to three weeks.[4] While absorption of oral (PO) thiamine can reach 4.5 mg per dose in a healthy patient, most malnourished alcoholics will absorb only 0.8 mg per dose, or less if they recently consumed alcohol.[5] For this reason, parenteral—intramuscular (IM) or intravenous (IV)—administration is recommended. Furthermore, parenteral administration is more rapid, which becomes particularly important when treating WE. Despite this recommendation, however, only a minority of patients receive thiamine parenterally. Reasons for this include physicians not being aware of the recommendation, as well as physicians being concerned about possible adverse reactions from parenteral administration, such as anaphylaxis and rash.[5] However, a slow infusion of thiamine (over approximately thirty minutes) has been shown to significantly reduce the risk of adverse reactions, and in many cases, the benefits outweigh the risks even if an adverse reaction were to occur.[6]

The order of thiamine administration in relation to that of glucose is also an important consideration. Thiamine is a cofactor in the breakdown of glucose for energy, so providing glucose without its cofactor will result in the buildup of unusable/toxic metabolites as well the inability to complete glycolysis efficiently. The phrase “thiamine before glucose” has been emphasized in medical school curriculum for years, but should not be taken as an absolute. While prolonged administration of glucose in the absence of thiamine has been shown to precipitate or worsen WE, a single dose of glucose does not have this effect.[7] Therefore, emergent administration of glucose should not be withheld if thiamine is not immediately available as well.

Given all of these considerations, the overall recommendation for thiamine administration in alcohol use disorder is the following:

  • Prophylaxis: 250 mg thiamine IM daily for 3-5 days
  • Established Wernicke-Korsakoff: 500 mg thiamine IV or IM three times a day for at least two days. This should be continued until there is clinical improvement.[8]

However, these recommendations do not necessarily work in the ED, since continued parenteral administration cannot be done at home. Therefore, it is important to determine whether a patient is at high risk for developing WE, and, if so, to consider admitting the patient for further management. High-risk patients are those with a history of chronic alcohol use and symptoms such as confusion, decreased consciousness, and ataxia, as well as severely hypoglycemic patients with a history of chronic alcohol use.[6] For low-risk patients or those requiring prophylaxis only, it is recommended that the patient receive a dose of IM thiamine in the ED, which can then be transitioned to 100 mg PO thiamine daily until the patient’s nutritional status improves.[7]

The appropriate administration of thiamine can significantly affect a patient’s prognosis; there is a mortality rate of approximately 20% in those with WE who do not receive proper thiamine repletion, and Korsakoff’s can develop in up to 85% of patients who receive inadequate doses of thiamine.[6] Therefore, a simple practice change—proper thiamine administration—can have a significant impact.

Pearls and Pitfalls

  • Don’t assume all patients who present with confusion, ataxia, and nystagmus are drunk—though Wernicke encephalopathy is rare, it is important to diagnose and treat.
  • Thiamine should be given IV or IM due to poor oral absorption seen in chronic alcohol use.
  • If your patient in the ED is severely hypoglycemic, don’t hesitate to treat with a dose of glucose. However, do initiate thiamine repletion prior to continuing glucose infusion, as this can precipitate/worsen Wernicke encephalopathy.


1. Thomson AD, Ryle PR, Shaw GK. Ethanol, thiamine and brain damage. Alcohol Alcohol. 1983;18:27.

2. Tanphaichitr V. Modern nutrition in health and medicine, 9th, Shils M (Ed), Lippincott, Philadelphia 2000.

3. Guerrini I, Mundt-Leach R. Preventing long-term brain damage in alcohol-dependent patients. Nurs Stand. 2003;19:43-6.

4. Thomson AD. Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome. Alcohol Alcohol. 2000;35(Suppl. 1):2-7.

5. Cook CCH, Hallwood PM, Thomson AD. B vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alchol Alcohol. 1998;33:317-336.

6. Thomson AD, Cook CCH, Touquet R, Henry JA. The Royal College of Physicians report on alcohol: guidelines for managing Wernicke’s encephalopathy in the Accident and Emergency Department. Alcohol Alcohol. 2002;37:513-21.

7. Donnino MW, Vega J, Miller J, Walsh M. Myths and misconceptions of Wernicke’s encephalopathy: what every emergency physician should know. Ann Emerg Med. 2007;50(6):715-21.

8. Agabio R. Thiamine administration in alcohol-dependent patients. Alcohol Alcohol. 2005;40(2):155-6.