In Patient’s with Alcohol Use Disorder What is the Best Dose and Route of Thiamine to - PowerPoint Presentation

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In Patient’s with Alcohol Use Disorder What is the Best Dose and Route of Thiamine to Prevent WE

ACKNOWLEDGEMENTSOmer Yusuf, Aaron Guinn, Carol Cooke.

METHODThe search strategy was focussed on trying to accumulate as many academic papers as possible.A “concept map” of all the key terms in the search can be seen in table 1 below.One RCT was found from 2001. There is also a Cochrane review that was done on the topic “to determine the optimum form, dose, and duration of thiamine treatment for WE.”

INTRODUCTIONThiamine is essential to carbohydrate metabolism and acute thiamine deficiency can severely impact parts of the brain resulting in Wernicke’s Encephalopathy (WE). The two most common presentations related to alcohol use disorder (AUD): The high-risk patient with alcohol use disorder with multiple co-morbidities often presenting malnourished and unwell. The other is the low risk relatively healthy uncomplicated patient with alcohol use disorder. In Manitoba thiamine dose and route varies from patient to patient with no formal protocol. The purpose of this assessment was to try and find an optimal route and dose of thiamine for the patient with AUD to prevent WE.

ResultsThe clinical question was broken into two parts:What is the optimal route regarding thiamine administrationWhat is the optimal dose to prevent development of WEOptimal route:Daily thiamine requirements in a healthy person are 1.1-1.2mgIf a healthy person was to consume 100mg TID they would maximally absorb 13.5mgPatient’s with AUD will have a 70% reduction in absorption of thiamine through their GI tract and a further 50% reduction with concomitant alcohol ingestionFurthermore, the enzymes required to absorb thiamine in the digestive system require thiamine as a cofactor compounding the thiamine deficiencyStudies examining people with AUD after oral thiamine show no increase in CSF levels of thiamine due to such poor intestinal absorption which was a stark contrast to those who received parenteral thiamineOral thiamine in those patients with AUD with co-morbidities and malnourishment would not be sufficient to prevent WEOptimal Dose:RCT from St. Vincent’s Hospital in Australia in 2001 that was double blinded comparing 5, 20, 50, 100 and 200mg doses of thiamine IM OD for 2 days in patients in alcohol detoxResult suggested that 200mg of IM thiamine showed superior performance on the delayed alteration (DA) task which has shown to be sensitive to Wernicke Korsakoff Syndrome (WKS) in humans and animalsWith the exact dose still uncertain it appears that 200mg IV/IM is the minimum needed in order to prevent WKS

Christian Palaschuk, Omer Yusuf

RFHS / Max Rady College of Medicine

Alcohol use disorder

Thiamine

Wernicke’s encephalopathy

alcohol use

alcohol abuse

alcoholi*ethanol abuseethanol usealcohol dependencealcohol dependencyalcohol addictionThiamineVitamin B1Vitamin B 1BetaxinThiamijectProsultiamineFursultiamin*CocarboxylaseAneurin Wernicke*Korsakoff SyndromeAlcoholic Korsakoff SyndromeWernicke Korsakoff syndrome

Table 1: Concept map of key terms for clinical question of “In patients with an alcohol use disorder presenting to the ED, what is the best dose and route of Thiamine to prevent development of Wernicke’s encephalopathy?

ConclusionResearch supports parenteral thiamine treatment to prevent development of WE in high risk patientsOral thiamine can be used to prevent WE in the low risk patient with AUDThe exact dose is still uncertain but the research suggests a minimum of 200mg parenterally would be needed to prevent WE in the at high risk groupThiamine doses in the low risk group can be 100mg