- Last edited on July 30, 2020
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- | ====== Wernicke–Korsakoff 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 findings, has 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/|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.]])] | ||
+ | ==== 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 ===== | ||
- | * CBC, lytes, Cr | + | * B12, thiamine (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 cases, 200mg IV thiamine x 3 days, followed by oral supplementation is appropriate. Those with suspected Wernicke’s encephalopathy should receive thiamine 100mg IM/IV x 3 days, then 300mg PO x 3-12 months. Don’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|Day, G. 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/|Thomson, A. 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).]] | ||