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cl:wernicke-korsakoff [on July 30, 2020]
cl:wernicke-korsakoff [on February 19, 2022] (current)
psychdb [Thiamine Storage]
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-====== WernickeKorsakoff Syndrome ======+====== Wernicke ​Encephalopathy and Korsakoff Syndrome ======
 {{INLINETOC}} {{INLINETOC}}
  
 ===== Primer ===== ===== Primer =====
-**Wernicke-Korsakoff Syndrome** (WKS) is a syndrome ​due to thiamine (vitamin B1) deficiency, commonly found in chronic alcoholism. This primarily alcohol-induced ​amnestic ​disorder ​results in necrotic lesions to the mammillary bodies, thalamus, and brainstem. The syndrome itself consists of 2 components:​ Wernicke’s encephalopathy (WE), ​and Korsakoff’s amnesia (KA),​ hence the combined name Wernicke-Korsakoff Syndrome.+**Wernicke-Korsakoff Syndrome** (WKS) is a neuropsychiatric ​syndrome ​caused by thiamine (vitamin B1) deficiency, commonly found in chronic alcoholism. This primarily alcohol-induced disorder ​is characterized by amnesia, confabulation,​ disorientation,​ and neurological findings. WKS occurs due to necrotic lesions to the mammillary bodies, thalamus, and brainstem. The syndrome itself consists of 2 components:​ **Wernicke encephalopathy (WE)**and **Korsakoff’s amnesia (KA)**, hence the combined name **Wernicke-Korsakoff Syndrome**.
  
 +== History ==
 +<alert type="​info"​ icon="​fa fa-book fa-lg fa-fw">​
 +See also: **[[https://​pubmed.ncbi.nlm.nih.gov/​23157990/​|Isenberg-Grzeda,​ E. et al. (2012). Wernicke-Korsakoff-syndrome:​ under-recognized and under-treated. Psychosomatics,​ 53(6), 507-516.]]**
 +</​alert>​
 +
 +
 +== Epidemiology ==
 +  * The prevalence is estimated to be up to 2% among the general population and as high as 12.5% in patients with alcohol use disorders.[([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC4979979/​|Isenberg-Grzeda,​ E., Alici, Y., Hatzoglou, V., Nelson, C., & Breitbart, W. (2016). Nonalcoholic thiamine-related encephalopathy (Wernicke-Korsakoff syndrome) among inpatients with cancer: a series of 18 cases. Psychosomatics,​ 57(1), 71-81.]])]
 +  * Autopsy studies indicate that Wernicke is frequently undiagnosed during life, and is first diagnosed postmortem in over 80% of case.[([[https://​pubmed.ncbi.nlm.nih.gov/​20642790/​|Galvin,​ R., Bråthen, G., Ivashynka, A., Hillbom, M., Tanasescu, R., & Leone, M. A. (2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology, 17(12), 1408-1418.]])][([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC4578911/​|Flynn,​ A., Macaluso, M., D’Empaire,​ I., & Troutman, M. M. (2015). Wernicke’s encephalopathy:​ increasing clinician awareness of this serious, enigmatic, yet treatable disease. The primary care companion for CNS disorders, 17(3).
 +]])]
 +
 +== Prognosis ==
 +  * Wernicke encephalopathy is an acute presentation that when identified and treated in a timely manner, can lead to quick improvement of symptoms.
 +    * Failure to diagnose and treat Wernicke encephalopathy can result in death in up to 20% of patients
 +  * If untreated, up to 75% may develop Korsakoff syndrome (irreversible cognitive impairment),​ and the chance of full recovery is low[([[https://​www.cmaj.ca/​content/​186/​8/​E295|Day,​ G. S., & Del Campo, C. M. (2014). Wernicke encephalopathy:​ a medical emergency. Cmaj, 186(8), E295-E295.]])] (but not impossible[([[https://​pubmed.ncbi.nlm.nih.gov/​15746545/​|Carota,​ A., & Schnider, A. (2005). Dramatic recovery from prolonged Wernicke-Korsakoff disease. European neurology, 53(1), 45-46.]])]).
 +    * Wernicke-Korsakoff syndrome thus is sometimes referred to as alcoholic dementia or alcohol-related dementia.
 +
 +== Comorbidity ==
 +  * [[addictions:​alcohol:​1-use-disorder|Alcohol use disorder]] is highly common.
 +    * In industrialized countries, 90% of the cases of thiamine deficiency are associated with alcohol use disorder.[([[https://​pubmed.ncbi.nlm.nih.gov/​16384871/​|Thomson,​ A. D., & Marshall, E. J. (2006). The natural history and pathophysiology of Wernicke'​s encephalopathy and Korsakoff'​s psychosis. Alcohol and Alcoholism, 41(2), 151-158.]])]
 +    * However! This is not a disease that affects only alcohol users, most cases of missed WKS are in those without an alcohol misuse history.
 +  * Thiamine deficiency also presents in several syndromes other than Wernicke’s encephalopathy,​ including cardiac beriberi, neuropathic beriberi.
 +
 +== Risk Factors ==
 +  * [[addictions:​alcohol:​1-use-disorder|Alcohol use disorder]], cancer patients,​[([[https://​pubmed.ncbi.nlm.nih.gov/​23157990/​|Isenberg-Grzeda,​ E., Kutner, H. E., & Nicolson, S. E. (2012). Wernicke-Korsakoff-syndrome:​ under-recognized and under-treated. Psychosomatics,​ 53(6), 507–516.]])] gastrointestinal surgery (e.g. - bariatric, gastric bypass), hyperemesis gravidarum, and starvation/​fasting are risk factors.[([[https://​pubmed.ncbi.nlm.nih.gov/​20642790/​|Galvin,​ R., Bråthen, G., Ivashynka, A., Hillbom, M., Tanasescu, R., & Leone, M. A. (2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology, 17(12), 1408-1418.]])]
 +
 +===== Underdiagnosis =====
 +  * Wernicke encephalopathy may be overlooked in 68% of patients with alcoholism and 94% of patients without alcoholism (e.g. - cancer patients).[([[https://​www.cmaj.ca/​content/​186/​8/​E295|Day,​ G. S., & Del Campo, C. M. (2014). Wernicke encephalopathy:​ a medical emergency. Cmaj, 186(8), E295-E295.]])][([[https://​pubmed.ncbi.nlm.nih.gov/​23157990/​|Isenberg-Grzeda,​ E., Kutner, H. E., & Nicolson, S. E. (2012). Wernicke-Korsakoff-syndrome:​ under-recognized and under-treated. Psychosomatics,​ 53(6), 507–516.]])]
 +
 +===== Diagnosis =====
 +WKS is a clinical diagnosis. Although often described as a triad (oculomotor abnormalities,​ cerebellar dysfunction,​ and an altered mental state) in the classic literature, it is rare for all three clinical signs to be present. [([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC4979979/​|Caine,​ D., Halliday, G. M., Kril, J. J., & Harper, C. (1997). Operational criteria for the classification of chronic alcoholics: identification of Wernicke'​s encephalopathy. Journal of Neurology, Neurosurgery & Psychiatry, 62(1), 51-60.]])] Less than 16% of individuals with WKS will have all three signs. Neuroimaging findings may help in confirming the diagnosis but it is not diagnostic.
 +
 +==== Caine Criteria ====
 +In 1997, Caine et al. proposed that a diagnosis can be made when patients have any ''​2''​ of the following 4 features:​[([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC486695/​|Caine,​ D., Halliday, G. M., Kril, J. J., & Harper, C. (1997). Operational criteria for the classification of chronic alcoholics: identification of Wernicke'​s encephalopathy. Journal of Neurology, Neurosurgery & Psychiatry, 62(1), 51-60.]])]
 +  - Nutritional deficiency
 +  - Ocular signs
 +  - Cerebellar signs
 +  - Altered mental status or mild memory impairment
 +
 +==== Signs and Symptoms ====
 +  * A dramatic improvement of neurologic signs often indicates adequate treatment and confirms the clinical diagnosis of Wernicke encephalopathy.[([[https://​www.cmaj.ca/​content/​186/​8/​E295|Day,​ G. S., & Del Campo, C. M. (2014). Wernicke encephalopathy:​ a medical emergency. Cmaj, 186(8), E295-E295.]])]
 ===== Terminology ==== ===== Terminology ====
-<panel type="​info"​ title="​Wernicke'​s ​vs. Korsakoff's" no-body="​true">​ +Classically,​ Wernicke encephalopathy is an acute presentation,​ while Korsakoff syndrome is a late, chronic manifestation of Wernicke encephalopathy that typically presents as anterograde and retrograde amnesia with preserved long-term memory.  
-Wernicke'​s Encephalopathy ​                                                                                                                                                                                                                                                                                                                                             ​Korsakoff'​s Syndrome/​Amnesia ​                                                                                                                                                                                                                                                       ​+ 
-<​HTML><​ul><​li>​Acute, but reversible</​li><​li>​The classic triad of:</​li><​ul><​li>​eye ​abnormalities (nystagmus, oculomotor paralysis, paralysis of conjugate gaze), CN VI palsy AKA lateral gaze palsy (lateral rectus)</​li><​li>​Ataxia of stance and gait</​li><​li>​Mental status changes, including withdrawal, confusion, retro/​anterograde amnesia</li></​ul></​ul></​HTML> ​ ​| ​<​HTML><​ul><​li>​Chronic and only 20% of cases is reversible with treatment</​li><​li>​Anterograde amnesia ​and confabulations</li><​li>​Cannot occur during an acute delirium or dementia and must persist beyond usual duration of intoxication or withdrawal management</​li></​ul></​HTML> ​ |+<panel type="​info"​ title="​Wernicke vs. Korsakoff" footer="​* = Cannot occur during an acute delirium or dementia and must persist beyond usual duration of intoxication or withdrawal management" no-body="​true"​
 +<​mobiletable 1
 +                                    ​Course ​                                                      ^ Symptoms ​                                                                                                                                                                                                                                                                               ​
 +^ Wernicke Encephalopathy (WE)      ​| Acute, but reversible ​                                       ​| ​The classic triad of: \\ • Eye abnormalities (nystagmus, oculomotor paralysis, paralysis of conjugate gaze), CN VI palsy AKA lateral gaze palsy (lateral rectus) ​\\ • Ataxia of stance and gait \\ • Mental status changes, including withdrawal, confusion, retro/​anterograde amnesia ​ | 
 +^ Korsakoff'​s Syndrome/Amnesia (KS)*  | Chronic and only 20% of cases are reversible with treatment ​ | • Anterograde amnesia ​\\ • Confabulations\\ • Personality changes ​                                                                                                                                                                                                                      | 
 +</mobiletable>
 </​panel>​ </​panel>​
 +===== Pathophysiology =====
 +<alert type="​info"​ icon="​fa fa-book fa-lg fa-fw">​
 +See also: **[[https://​pubmed.ncbi.nlm.nih.gov/​16384871/​|Thomson,​ A. D., & Marshall, E. J. (2006). The natural history and pathophysiology of Wernicke'​s encephalopathy and Korsakoff'​s psychosis. Alcohol and Alcoholism, 41(2), 151-158.]]**
 +</​alert>​
  
-===== Physical Exam ===== +==== Thiamine Absorption and Storage ​==== 
-In patients with chronic alcoholism ​with //only// an ataxic gait and stance found on physical exam, and no other neurological findingshas alcoholic cerebellar degeneration ​(midline cerebellar degeneration).+  * The daily thiamine requirement for healthy individuals is between 1 and 2 mg per day, and is related to overall carbohydrate intake. 
 +    * The thiamine requirement increases ​with alcohol misuse. 
 +    * There are several mechanisms behind this, including inadequate dietary intake, malabsorption of thiamine from the gastrointestinal tract due to alcohol’s effects, and impaired utilization of thiamine in the cells. 
 +  * Since the body stores are only between 30 and 50 mg of thiamine, it is estimated that this store is depleted in 4–6 weeks.[([[https:​//pubmed.ncbi.nlm.nih.gov/16384871/|ThomsonA. D., & Marshall, E. J. (2006). The natural history and pathophysiology of Wernicke'​s encephalopathy and Korsakoff'​s psychosis. Alcohol ​and Alcoholism41(2), 151-158.]])] 
 +==== Vitamin B1 (Thiamine) Deficiency ==== 
 +<WRAP group> 
 +<WRAP half column>​ 
 +  * Thiamine is a cofactor in the decarboxylation of pyruvate. Thiamine is needed for pyruvate to enter the citric acid cycle, which allows for aerobic metabolism of glucose to adenosine triphosphate (ATP).  
 +  * Lack of ATP production in areas of the brain susceptible to thiamine depletion thus leads to neuronal death 
 +    * This can result in damage to the limbic system, specifically the mammillary bodies and anterior/​medial thalamus. 
 +</​WRAP>​
  
 +<WRAP half column>
 +<callout type="​tip"​ title="​A Quick Review on Vitamins"​ icon="​true">​
 +Vitamins are either water-soluble (vitamins B and C), or fat-soluble (vitamins A, D, E, K)
 +  * **Fat-soluble vitamins** are dependent on absorption from the ileum and pancreas. Toxicity is easier with fat soluble vitamins because these vitamins accumulate in fat. Malabsorption syndromes such as cystic fibrosis and/or celiac disease) can result in fat-soluble vitamin deficiencies.
 +  * **Water-soluble vitamins** are usually important coenzymes in cellular processes or precursors to coenzymes. All are excreted easily from the body, except for vitamins B12 and B9. B vitamin deficiency can result in glossitis, dermatitis, and diarrhea. For certain vitamin B deficiencies (B1 and B12), there can be neuropsychiatric and cognitive symptoms as well. Broadly, the B vitamins include:
 +    * [[cl:​wernicke-korsakoff|B1 (thiamine)]]
 +    * B2 (riboflavin)
 +    * B3 (niacin)
 +    * B5 (pantothenic acid)
 +    * [[meds:​antidepressants:​maoi:​home#​vitamin-b6-pyridoxine-deficiency|B6 (pyridoxine)]]
 +    * B7 (biotin)
 +    * B9 (folate)
 +      * Is stored in the liver between 3 to 4 months
 +    * [[cl:​vitamin-b12-cyanocobalamin-deficiency|B12 (cobalamin)]]
 +      * Is stored in the liver between 3 to 4 years
 +</​callout>​
 +</​WRAP>​
 +</​WRAP>​
 +
 +===== Differential Diagnosis =====
 +  * **Other medical issues resulting in thiamine deficiency**
 +    * Although thiamine deficiency often occurs in the context of alcohol use disorders, it can also occur in eating disorders, malnutrition,​ hyperemesis gravidarum, chronic vomiting, extreme dieting, and cancer patients[([[https://​pubmed.ncbi.nlm.nih.gov/​23157990/​|Isenberg-Grzeda,​ E., Kutner, H. E., & Nicolson, S. E. (2012). Wernicke-Korsakoff-syndrome:​ under-recognized and under-treated. Psychosomatics,​ 53(6), 507–516.]])] undergoing chemotherapy.
 +  * **[[cl:​1-delirium|Delirium]]**
 +    * Confusion and memory impairment may be due to delirium
 +  * **[[cl:​tbi|Traumatic brain injury]]**
 +    * There is a risk of the Wernicke being missed in patients with acute head injury. A history of alcohol use may not be available, and the signs and symptoms of Wernicke encephalopathy may be misattributed to the head injury.[([[https://​pubmed.ncbi.nlm.nih.gov/​9719389/​|Cook,​ C. C., Hallwood, P. M., & Thomson, A. D. (1998). B vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol and Alcoholism, 33(4), 317-336.]])]
 +  * **[[addictions:​alcohol:​4-other|Alcohol-induced psychosis]]**
 +  * **[[geri:​dementia:​home|Neurodegenerative disorders]]**
 ===== Investigations ===== ===== Investigations =====
-  * CBClytes, Cr +  * B12thiamine (not all laboratories may have thiamine available) 
-  * GGT indicator of acute liver injury from EtOH use, for detecting people ​drinking > 4 drinks/day +  * CBC, electrolytes,​ creatinine, ​GGT (indicator of acute liver injury from alcohol ​use, for individuals ​drinking > 4 drinks/day), AST, ALT, ALP, GGT 
-  * AST, ALT, ALP, GGT +  Elevated ​AST/ALT ratio may be suggestive of alcoholic liver disease.[([[https://​pubmed.ncbi.nlm.nih.gov/​15208167/​|Nyblom,​ H., Berggren, U., Balldin, J., & Olsson, R. (2004). High AST/ALT ratio may indicate advanced alcoholic liver disease rather than heavy drinking. Alcohol and alcoholism, 39(4), 336-339.]])]
-    * AST ALT x 3 (in EtOH hepatitis) +
-    * AST/ALT ratio also > 2+
   * INR   * INR
-  ​B12 and thiamine+ 
 + 
 +===== Physical Exam ===== 
 +  ​Nystagmus ​and ophthalmoplegia are the most common ocular findings in Wernicke.[([[https://​pubmed.ncbi.nlm.nih.gov/​20642790/​|Galvin,​ R., Bråthen, G., Ivashynka, A., Hillbom, M., Tanasescu, R., & Leone, M. A. (2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology, 17(12), 1408-1418.]])] 
 +  * In patients with chronic alcohol use disorder with //only// an ataxic gait and stance found on physical exam, and no other neurological findings, they most likely have alcoholic cerebellar degeneration (midline cerebellar degeneration). 
 + 
 + 
 +==== Neuroimaging ==== 
 +  * [[neurology:​mri|MRI]] brain may show mammillary body atrophy, volume loss in the thalamus, volume loss in the corpus callosum. 
 +    * Lesions from Wernicke are characterized by petechial hemorrhages and can be often found with a symmetrical distribution around the cerebral aqueduct, third ventricle, and fourth ventricle.[([[https://​pubmed.ncbi.nlm.nih.gov/​27799475/​|Hattingen,​ E., Beyle, A., Müller, A., Klockgether,​ T., & Kornblum, C. (2016). Wernicke encephalopathy:​ SWI detects petechial hemorrhages in mammillary bodies in vivo. Neurology, 87(18), 1956-1957.]])] 
 +  * CT head are unfortunately poor at identifying mammillary body lesions and thus not recommended.[([[https://​pubmed.ncbi.nlm.nih.gov/​20642790/​|Galvin,​ R., Bråthen, G., Ivashynka, A., Hillbom, M., Tanasescu, R., & Leone, M. A. (2010). EFNS guidelines for diagnosis, therapy and prevention of Wernicke encephalopathy. European Journal of Neurology, 17(12), 1408-1418.]])] 
  
 ===== Treatment ====== ===== Treatment ======
-<callout ​type="success">{{fa>​arrow-circle-right?color=green}} ​See also article: **[[addictions:​alcohol|]]**</callout+<alert type="info" icon="​fa ​fa-book fa-lg fa-fw"> 
-It is important ​to supplement ​patients with PO or IV thiamine. Thiamine 100mg TID should be prescribed as ongoing supplementary therapy in alcohol use disorder patients identified as at risk for thiamine deficiency. [([[http://​rebelem.com/​should-you-prescribe-oral-thiamine-for-chronic-alcoholics/​|RebelEM:​Should You Prescribe Oral Thiamine for Chronic Alcoholics?​]])] ​For the more severe cases200mg IV thiamine x 3 daysfollowed by oral supplementation is appropriateThose with suspected ​Wernicke’s encephalopathy ​should receive thiamine 100mg IM/IV x 3 daysthen 300mg PO x 3-12 monthsDon’t forget to give fluids as well!+See also: 
 +  * **[[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC4578911/​|Flynn,​ A. et al. (2015). Wernicke’s encephalopathy:​ increasing clinician awareness of this serious, enigmatic, yet treatable disease. The primary care companion for CNS disorders, 17(3).]]** 
 +  * **[[https://​pubmed.ncbi.nlm.nih.gov/​15746545/​|Carota,​ A., & Schnider, A. (2005). Dramatic recovery from prolonged Wernicke-Korsakoff disease. European neurology, 53(1), 45-46.]]** 
 +</​alert>​ 
 + 
 +<alert icon="​fa fa-arrow-circle-right ​fa-lg fa-fw" type="​success">​ 
 +See also article: **[[addictions:​alcohol:home]]** 
 +</alert
 + 
 +Thiamine resupplementation ​is the primary treatment. Oculomotor deficits should resolve over hours to days, while cognitive impairment may resolve within days to weeks. Most patients ​will exhibit some residual deficits.[([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC1031727/​|Foster,​ J. B. (1989). The Wernicke-Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition. Journal of Neurology, Neurosurgery,​ and Psychiatry, 52(10), 1217.]])] 
 + 
 + 
 +==== IV Thiamine ==== 
 +  * Treatment is with intravenous thiamine therapy, but the optimum dosage remains controversial.[([[https://​pubmed.ncbi.nlm.nih.gov/​17681641/​|Donnino,​ M. W., Vega, J., Miller, J., & Walsh, M. (2007). Myths and misconceptions of Wernicke’s encephalopathy:​ what every emergency physician should know. Annals of emergency medicine, 50(6), 715-721.]])] Some clinicians base dosing from a study published by Cook et al. in 1998, which recommended up to 1 g of thiamine daily to achieve a clinical response.[([[https://​pubmed.ncbi.nlm.nih.gov/​9719389/​|Cook,​ C. C., Hallwood, P. M., & Thomson, A. D. (1998). B vitamin deficiency and neuropsychiatric syndromes in alcohol misuse. Alcohol and Alcoholism, 33(4), 317-336.]])][([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC5354137/​|Nishimoto,​ A., Usery, J., Winton, J. C., & Twilla, J. (2017). High-dose parenteral thiamine in treatment of Wernicke'​s encephalopathy:​ case series and review of the literature. in vivo, 31(1), 121-124.]])][([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC3545191/​|Thomson,​ A. D., Guerrini, I., & Marshall, E. J. (2012). The evolution and treatment of Korsakoff'​s syndrome. Neuropsychology review, 22(2), 81-92.]])] 
 +  * In individuals with suspected clinical signs of Wernicke, they should be prescribed thiamine 500mg IV x 3 days (some may prescribe as high as 500mg TID), followed by 250mg IV x 3 days (some may prescribe as high as 250mg TID) followed by oral supplementation 100mg PO daily.[([[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC3545191/​|Thomson,​ A. D., Guerrini, I., & Marshall, E. J. (2012). The evolution and treatment of Korsakoff'​s syndrome. Neuropsychology review, 22(2), 81-92.]])] 
 +    * A significant improvement in neurologic symptoms ​or cognitive function helps confirm the diagnosis. 
 +  * Most patients should thereafter have indefinite oral thiamine ​supplementation (i.e. - 100 mg thiamine daily) until there is resolution of their nutritional compromise.[([[https://​pubmed.ncbi.nlm.nih.gov/​17681641/​|Donnino,​ M. W., Vega, J., Miller, J., & Walsh, M. (2007). Myths and misconceptions of Wernicke’s encephalopathy:​ what every emergency physician should know. Annals of emergency medicine, 50(6), 715-721.]])] 
 + 
 + 
 +==== Oral Thiamine ​==== 
 +  * Remember that oral thiamine is difficult to absorb, so even for individuals with adequate oral intake, IV administration is recommended. In individuals with gut absorption changes (e.g. - bariatric surgery), IV supplementation is a must. 
 +    * It could also be argued that in general, the oral doses of thiamine are so low, and that is that it would provide a negligible effect on symptoms. 
 +  * In situations where IV thiamine is not available, thiamine 300mg PO TID could be prescribed. 
 +  * In low risk patients, thiamine ​100mg TID should be prescribed as ongoing supplementary therapy in alcohol use disorder patients identified as at risk for thiamine deficiency.[([[http://​rebelem.com/​should-you-prescribe-oral-thiamine-for-chronic-alcoholics/​|RebelEM:​Should You Prescribe Oral Thiamine for Chronic Alcoholics?​]])] ​ 
 + 
 + 
 +===== Guidelines ===== 
 +<alert icon="​fa fa-arrow-circle-right fa-lg fa-fw" type="​success">​ 
 +See also: **[[teaching:​clinical-practice-guidelines-cpg|]]** 
 +</​alert>​ 
 + 
 +{{page>​teaching:​clinical-practice-guidelines-cpg#​wernicke-encephalopathy&​nouser&​noheader&​nodate&​nofooter}} 
 + 
 +===== Resources ===== 
 +  * [[https://​www.emra.org/​emresident/​article/​wernicke/​|EM Resident: Detecting Wernicke-Korsakoff Syndrome]] 
 +  * [[https://​www.cmaj.ca/​content/​186/​8/​E295|DayG. S.& Del Campo, C. M. (2014). Wernicke encephalopathy: a medical emergency. Cmaj, 186(8), E295-E295.]] 
 +  * [[https://​www.ncbi.nlm.nih.gov/​pmc/​articles/​PMC3545191/​|ThomsonA. D., Guerrini, I., & Marshall, E. J. (2012). The evolution and treatment of Korsakoff'​s syndrome. Neuropsychology review, 22(2), 81-92.]] 
 +  * [[https://​www.cochrane.org/​CD004033/​DEMENTIA_thiamine-for-prevention-and-treatment-of-wernicke-korsakoff-syndrome-in-people-who-abuse-alcohol|Day,​ E. et al. (2013). Thiamine for prevention and treatment of Wernicke‐Korsakoff Syndrome in people who abuse alcohol. Cochrane Database of Systematic Reviews, (7).]]