Wernicke Encephalopathy After Bariatric Surgery: a Literature Review.

Wernicke encephalopathy (WE) is an acute neurological disorder classically characterized by ataxia, ophthalmoplegia, and altered mental status. This is caused by thiamine deficiency and is usually seen in malnourished populations. However, with the advent and rise of bariatric surgery in the last 50 years, WE has become an increasingly recognized and potentially deadly complication. Here, we review the populations at risk, clinical presentation, and the incidence of WE in the bariatric surgery population from 1985 to 2023. While the predominant procedure shifts throughout the years, the overall incidence of WE per 100,000 cases for the following procedures are sleeve gastrectomy (1.06), gastric band (1.16), RYGB (4.29), and biliopancreatic diversion with duodenal switch (8.92). Thus, early intervention and post-operative supplementation is recommended to prevent WE.

What is the optimum thiamine dose to treat or prevent Wernicke's encephalopathy or Wernicke-Korsakoff syndrome? Results of a randomized controlled trial.

BACKGROUND: The primary cause of Wernicke-Korsakoff syndrome (WKS) is thiamine deficiency, and more than 90% of cases are reported in alcohol-dependent patients. While observational studies show parenteral thiamine administration drastically reduced WKS-related mortality, relevant treatment trials have never been conducted to determine the optimum thiamine dose. METHODS: Two double-blind, parallel groups, randomized controlled trials (RCTs) were conducted to determine the optimal thiamine dose required for (1) the prevention of Wernicke's encephalopathy (WE), the acute phase of WKS, in asymptomatic but "at-risk" alcohol misuse patients (Study 1) and (2) the treatment of WE in symptomatic alcohol misuse patients (Study 2). Each study had a dosage regimen comprising three parenteral thiamine doses that were allocated at a ratio of 1:1:1. Study 1: Asymptomatic At-Risk patients (N = 393) received either 100 mg daily, 100 mg thrice daily, or 300 mg thrice daily, for 3 days. Study 2: Symptomatic patients (N = 127) received either 100 mg thrice daily, 300 mg thrice daily, or 500 mg thrice daily, for 5 days. Cognitive function was the primary outcome, assessed using the Rowland Universal Dementia Assessment Scale, two Cogstate subtests, and an adapted Story Memory Recall test. Secondary analyses examined differences in neurological function (ataxia, oculomotor abnormalities, and confusion) at follow-up. RESULTS: No significant differences were observed between any of the dosage conditions for either Study 1 or Study 2 on cognition or neurological functioning. This real-world study found that having a clinically unwell target population with high comorbidity and multiple presentations, coupled with challenges in cross-cultural assessment is likely to complicate RCT findings. CONCLUSIONS: The results of this study showed no clear benefit of high dose thiamine over intermediate or lower doses of thiamine, over the time intervals examined, for the treatment and prevention of cognitive and neurological abnormalities related to WKS. Several study limitations temper the interpretation of these findings. Nevertheless, the absence of conclusive evidence for the superiority of high-dose thiamine supports a recommendation for patient-specific treatment, while ensuring that the potential impact of other biochemical factors (e.g., magnesium and other B vitamin deficiencies) are considered and corrected if necessary.

A view from the acute hospital: managing patients with alcohol problems.

Regular heavy consumption of alcohol is associated with a wide range of physical, psychological and social problems. All health-care clinicians should be able to screen for and detect problematic levels of alcohol consumption in their patients, and deliver an effective brief intervention. When patients with alcohol dependence are admitted to hospital there must be an assessment of whether medication is required to prevent withdrawal symptoms and potential delirium tremens and withdrawal seizures. Medically assisted alcohol withdrawal using a long-acting benzodiazepine such as chlordiazepoxide should be carefully monitored and titrated to effect, and the clinician should be aware of the risk of Wernicke-Korsakoff syndrome and other complications. Abstinence from alcohol is usually only the first step in treatment, and effective linkage to community alcohol services is an important step.

Thiamine Substitution in Alcohol Use Disorder: A Narrative Review of Medical Guidelines.

AIMS: Patients with alcohol use disorder (AUD) frequently suffer from cognitive deficits ranging from mild symptoms to most severe forms. Wernicke encephalopathy (WE), caused by thiamine deficiency, is a potentially fatal syndrome characterized by the clinical triad of ophthalmoplegia, ataxia, and confusion. WE frequently presents in patients with AUD and, if left untreated, can progress to Wernicke-Korsakoff syndrome, which constitutes severe anterograde amnesia, confabulation, and behavioral abnormalities. Due to oftentimes indistinct clinical presentation, WE remains undiagnosed in up to 80% of cases. We conducted a review of current treatment guidelines for AUD in order to identify recommendations for the use of thiamine. METHODS: Three different keyword combinations ("alcohol treatment guideline," "alcohol withdrawal guideline," and "alcohol treatment recommendation") were entered in PubMed and Scopus, additional guidelines were searched screening the online sites of the respective agencies or societies. In total, 14 guidelines were included. RESULTS: Thiamine was mentioned in all but one of the reviewed publications. Specifications on application modalities and indications varied considerably. While the majority of reviewed guidelines recommended parenteral thiamine only for patients at high risk for WE, some gave no information regarding the application form or dosage. CONCLUSION: Substitution of parenteral thiamine in individuals with suspected WE is a well-established treatment regimen. However, suggestions according to guidelines vary widely. Furthermore, hardly any evidence-based recommendations exist on a more general use of thiamine as a preventative intervention in individuals with AUD. Further research is of utmost importance to raise awareness for this potentially undervalued problem.

Cuidados de enfermagem a um paciente alcoolista portador da síndrome de Wernicke-Korsakoff: estudo de caso / Cuidados de enfermería a paciente alcohólico con síndrome de Wernicke-Korsakoff: presentación de um caso / Nursing care approach towards an alcoholic patient bearing the Wernicke-Korsakoff syndrome: case study

Introduction: Wernicke-Korsakoff Syndrome (WKS) is one of the most serious consequences of alcohol abuse. The cognitive impact of the pathology is derived from alcoholic neurotoxicity and thiamine deficiency, which can progress to stupor, coma and death. Objective: Performing a case study regarding an alcoholic patient bearing the WKS, and also designing a nursing care plan. Methods: It is a case study with a qualitative approach that assesses an alcoholic patient bearing the WKS. The study was performed at the Hospital Universitário Oswaldo Cruz (HUOC) in Recife, Brazil, over the period from February to March 2016. Results: We were able to identify 14 nursing diagnoses, as follows: chronic confusion/memory deficit/disturbed thought processes/ impaired verbal communication; impaired walking/risk of tumble down; self-care deficit; nutrition smaller than the needs/fatigue; excessive fluid volume/impaired tissue integrity; bleeding risk; impaired skin integrity; ineffective tissue perfusion. Conclusion: The nursing professionals have singular importance with regards to both the execution of health education actions as well as the alcoholics' treatment, thus preventing the complications of the disease

Introdução: A síndrome de Wernicke-Korsakoff (SWK) é uma das mais graves consequências do abuso de álcool. O impacto cognitivo da patologia é derivado da neurotoxicidade alcóolica e deficiência de tiamina, podendo progredir para estupor, coma e morte. Objetivo: Realizar um estudo de caso de paciente alcoolista portador de SWK e construir um plano de assistência de enfermagem. Métodos: Estudo de caso com abordagem qualitativa. O estudo foi realizado no Hospital Universitário Oswaldo Cruz (HUOC), em Recife, Brasil, fevereiro a março de 2016. Resultados: Identificamos 14 diagnósticos de enfermagem: confusão crônica/memória prejudicada/ processos do pensamento perturbados/comunicação verbal prejudicada; deambulação prejudicada/risco de quedas; déficit no autocuidado; nutrição desequilibrada menor que as necessidades/fadiga; volume excessivo de líquido/integridade tissular prejudicada; risco de sangramento; integridade da pele prejudicada; perfusão tissular ineficaz. Conclusão: A enfermagem tem especial importância na execução das ações de educação em saúde e tratamento de alcoolistas prevenindo as complicações da doença

Introducción: El síndrome de Wernicke-Korsakoff (WKS) es una de las más graves consecuencias del abuso del alcohol. El impacto de trastorno cognitivo se deriva de la neurotoxicidad alcohólica y la deficiencia de tiamina, que puede progresar a estupor, coma y muerte. Objetivo: Realizar un estudio de caso de un paciente con SWK alcohólica y construir un plan de atención de enfermería. Métodos: Un estudio de caso con enfoque cualitativo. El estudio se realizó en el Hospital Universitario Oswaldo Cruz (HUOC) en Recife, Brasil, entre febrero y marzo de 2016 Resultados: Se identificaron 14 diagnósticos de enfermería: confusión crónica/deterioro de la memoria/ procesos de pensamiento perturbados/alteración de la comunicación verbal; alteración de la deambulación/riesgo de caídas; déficit de autocuidado; la nutrición desequilibrada menos necesita/fatiga; volumen excesivo de líquido/ la integridad del tejido deteriorado; riesgo de sangrado; alteración de la integridad de la piel; la perfusión tisular ineficaz. Conclusión: La enfermería tiene especial importancia en la implementación de las iniciativas de educación en la salud y el tratamiento de alcohólicos prevención de las complicaciones de la enfermedad

Thiamine Prescribing and Wernicke's Encephalopathy Risk Factors in Patients With Alcohol Use Disorders at a Psychiatric Hospital.

BACKGROUND: Alcohol use disorder (AUD) is the leading cause of thiamine deficiency and can lead to Wernicke's encephalopathy (WE). WE has a higher prevalence of development in patients with AUD, and current recommendations emphasize parenteral administration of thiamine. Our objective was to characterize thiamine utilization in patients with AUD who were prescribed thiamine and evaluate if those who received oral thiamine had risk factors for the development of WE. METHODS: This retrospective chart review enrolled adults admitted to a psychiatric hospital from October 2014 through September 2015 diagnosed with AUD as per the International Classification of Diseases, Ninth Edition (ICD-9). The cohort was divided on the basis of route of thiamine administration (nonparenteral vs. parenteral) and was then screened retrospectively for risk factors for WE. Descriptive data and measures of central tendency were utilized to assess the objectives. RESULTS: The majority of patients were white male individuals, with a mean age of 48 years. Of the 226 patients, 201 (89%) were prescribed oral thiamine. Of the first 100 patients who received oral thiamine, 36% had risk factors for WE, with the most common risk factor being malnutrition. A χ analysis revealed that WE risk factors did not influence route of thiamine administration (χ=2.148, df=1, P=0.143). No patients were diagnosed with WE during their admission; however, 8 patients received parenteral thiamine at a treatment dose indicated for WE. CONCLUSIONS: Parenteral thiamine is underutilized in patients with AUD and risk factors for WE. Education is needed to enhance thiamine prescribing and evaluation of risk factors for WE in this population. A thiamine prescribing protocol has been developed for further thiamine optimization.

Preventing Wernicke's encephalopathy in anorexia nervosa: A systematic review.

Anorexia nervosa (AN) is a common eating disorder that affects 2.9 million people worldwide. Not eating a balanced diet or fasting can cause neurological complications after severe vitamin B1 malnourishment, although the precise signs and symptoms of Wernicke's encephalopathy (WE) are not clear. Our aim was to review the signs and symptoms of WE in patients with AN. We searched MEDLINE, EMBASE, Scopus, and PiCarta on all case descriptions of WE following AN. All case descriptions of WE in AN, irrespective of language, were included. Twelve WE cases were reviewed, suggesting that WE following AN is still a relatively rare neuropsychiatric disorder. WE is characterized by a triad of: mental status change, ocular signs, and ataxia. In alcoholism, this triad is present in 16% of cases, but eight out of 12 AN cases presented themselves with a full triad of symptomatology. Importantly, patients often had a more complex triad than has been previously described, involving vertigo, diplopia, and the consequences of refeeding syndrome. The development of a full triad and additional symptomatology suggests a late recognition of signs and symptoms of WE in AN. A complicating factor is the overlap between symptoms of thiamine deficiency and the symptoms of WE. Specifically, patients who show rapid weight loss are vulnerable for the development of WE. Eating disorders, such as AN, can lead to WE. Prophylactic thiamine checks and treatment in patients with AN are relevant, and in case of suspicion of WE, adequate parenteral thiamine supplementation is necessary.

Preventing Wernicke Encephalopathy After Bariatric Surgery.

Half a million bariatric procedures are performed annually worldwide. Our aim was to review the signs and symptoms of Wernicke's encephalopathy (WE) after bariatric surgery. We included 118 WE cases. Descriptions involved gastric bypass (52%), but also newer procedures like the gastric sleeve. Bariatric WE patients were younger (median = 33 years) than those in a recent meta-analysis of medical procedures (mean = 39.5 years), and often presented with vomiting (87.3%), ataxia (84.7%), altered mental status (76.3%), and eye movement disorder (73.7%). Younger age seemed to protect against mental alterations and higher BMI against eye movement disorders. The WE treatment was often insufficient, specifically ignoring low parenteral thiamine levels (77.2%). In case of suspicion, thiamine levels should be tested and treated adequately with parenteral thiamine supplementation.

[Thiamine (vitamin B1) treatment in patients with alcohol dependence]. / Le traitement par thiamine (vitamine B1) dans l'alcoolodépendance.

Thiamine deficiency (vitamin B1) is common in patients with alcohol dependence. Cognitive impairments may be an early consequence of thiamine deficiency. Wernicke's encephalopathy is underdiagnosed and undertreated. In patients with established Wernicke's encephalopathy, parenteral thiamine 200-500mg three times a day should be given for 3-5 days, followed by oral thiamine 250-1000mg/day. In patients with suspected Wernicke's encephalopathy, parenteral thiamine 250-300mg should be given two times a day for 3-5 days, followed by oral thiamine 250-300mg/day. In patients at high risk of thiamine deficiency, parenteral thiamine 250-500mg/day should be given for 3-5 days, followed by oral thiamine 250-300mg/day. In patients at low risk (with uncomplicated alcohol dependence), oral thiamine 250-500mg/day should be given for 3-5 days, followed by oral thiamine 100-250mg/day.

[Wernicke encephalopathy: Guiding thiamine prescription]. / Thiamine et encéphalopathie de Gayet-Wernicke : quelles règles de prescription ?

BACKGROUND AND AIM: Wernicke's encephalopathy (WE) is a medical emergency. The objective of this paper is to systematically review the literature published over the past 15 years pertaining to prophylactic and curative treatment of WE with thiamine. METHODS: A systematic literature search was performed using Medline to include all studies published between January 1, 2000 and December 31, 2015. RESULTS: Of the 316 abstracts identified, 20 met the final inclusion criteria. The evidence on the use of prophylactic thiamine was quite heterogeneous. The use of thiamine in this context largely depended on the evaluation of an individual's risk of developing WE. Use of prophylactic thiamine in low-risk patients is not universally indicated. When prescribed in this sub-population, the oral route is suggested but may be insufficient owing to its limited intestinal absorption and the high risk of non-compliance. High-risk patients need parenteral treatment with a recommended posology of 250 mg daily for 3 to 5 days. Intramuscular route is preferred in the outpatient setting, whereas intravenous route is suggested for inpatients. In cases where the diagnosis of WE is suspected or confirmed, a curative treatment with high-dose IV thiamine is justified. The evidence widely accepted in the literature is much clearer in this condition, with treatment regimens consisting of 500 mg IV 3 times daily for 3 to 5 days, followed by 250 mg IV daily for a minimum of 3 to 5 additional days. CONCLUSION: The literature does indicate that thiamine should be prescribed at high dosages, with the parenteral routes indicated in hospital settings and in high-risk patients. Based on the current literature review, we suggest treatment algorithms guiding thiamine prescription for WE.

Prevention of delirium in trauma patients: are we giving thiamine prophylaxis a fair chance?

BACKGROUND: Delirium is associated with increased morbidity and mortality in injured patients. Wernicke encephalopathy (WE) is delirium linked to malnutrition and chronic alcoholism. It is prevented with administration of thiamine. Our primary goal was to evaluate current blood alcohol level (BAL) testing and thiamine prophylaxis in severely injured patients. METHODS: We retrospectively reviewed the cases of 1000 consecutive severely injured patients admitted to hospital between Mar. 1, 2009, and Dec. 31, 2009. We used the patients' medical records and the Alberta Trauma Registry. RESULTS: Among 1000 patients (mean age 48 yr, male sex 70%, mean injury severity score 23, mortality 10%), 627 underwent BAL testing at admission; 221 (35%) had a BAL greater than 0 mmol/L, and 189 (30%) had a BAL above the legal limit of 17.4 mmol/L. The mean positive BAL was 41.9 mmol/L. More than 4% had a known history of alcohol abuse. More patients were assaulted (20% v. 9%) or hit by motor vehicles (10% v. 6%) when intoxicated (both p < 0.05). Most injuries occurred after falls (37%) and motor vehicle collisions (33%). Overall, 17% of patients received thiamine prophylaxis. Of the 221 patients with elevated BAL, 44% received thiamine prophylaxis. Of those with a history of alcohol abuse, 77% received thiamine prophylaxis. CONCLUSION: Despite the strong link between alcohol abuse, trauma and WE, more than one-third of patients were not screened for alcohol use. Furthermore, a minority of intoxicated patients received adequate prophylaxis against WE. Given the low risk and cost of BAL testing and thiamine prophylaxis and the high cost of delirium, standard protocols for prophylaxis are essential.

CONTEXTE: Le délire est associé à une morbidité et une mortalité accrues chez les traumatisés. L'encéphalopathie de Wernicke (EW) est un délire associé à la malnutrition et à l'alcoolisme chronique que l'on peut prévenir en administrant de la thiamine. Notre objectif principal était d'évaluer le recours actuel aux tests d'alcoolémie et au traitement prophylactique à la thiamine chez les grands traumatisés. MÉTHODES: Nous avons passé en revue de manière rétrospective 1000 cas consécutifs d'hospitalisation pour traumatismes graves entre le 1er mars 2009 et le 31 décembre 2009. Nous avons utilisé les dossiers médicaux des patients et le Registre des traumatismes de l'Alberta. RÉSULTATS: Sur 1000 patients (âge moyen 48 ans, sexe masculin 70 %, indice moyen de gravité des traumatismes 23, mortalité 10 %), 627 ont subi un test d'alcoolémie à leur admission; 221 (35 %) présentaient un taux d'alcoolémie supérieur à 0 mmol/L et 189 (30 %) avaient un taux d'alcoolémie au-dessus de la limite permise de 17,4 mmol/L. Le taux moyen des tests d'alcoolémie positifs était de 41,9 mmol/L. Plus de 4 % de ces cas avaient des antécédents d'alcoolisme. Les patients qui étaient sous l'effet de l'alcool ont davantage été victimes d'agressions (20 % c. 9 %) ou d'accidents impliquant un véhicule (10 % c. 6 %; tous deux p < 0,05). La majorité des traumatismes ont été causés par des chutes (37 %) ou des accidents de la route (33 %). Dans l'ensemble, 17 % des patients ont reçu un traitement prophylactique à la thiamine. Parmi les 221 patients qui présentaient un taux d'alcoolémie élevé, 44 % ont reçu de la thiamine en prophylaxie. Parmi ceux qui présentaient des antécédents d'abus d'alcool, 77 % ont reçu un traitement prophylactique à la thiamine. CONCLUSION: Malgré le lien étroit entre abus d'alcool, traumatismes et EW, plus du tiers des patients n'ont subi aucun test d'alcoolémie. En outre, seule une minorité de patients intoxiqués ont reçu une prophylaxie adéquate contre l'EW. Compte tenu des risques faibles et des coûts peu élevés du test d'alcoolémie et de la prophylaxie par thiamine et des coûts élevés occasionnés par les épisodes de délire, il est essentiel d'instaurer des protocoles standard de prophylaxie.

Experimentally-induced Wernicke's encephalopathy modifies crucial rat brain parameters: the importance of Na+, K+ -ATPase and a potentially neuroprotective role for antioxidant supplementation.

Wernicke's encephalopathy (WE) is a serious neuropsychiatric syndrome caused by chronic alcoholism and thiamine (T) deficiency. Our aim was to shed more light on the pathophysiology of WE, by introducing a modified in vivo experimental model of WE and by focusing on changes provoked in the total antioxidant status (TAS) and three crucial brain enzyme activities in adult rats. Rats were placed on ethanol (EtOH) consumption (20 % v/v) for a total of 5 weeks. By the end of the third week, rats were fed a T-deficient diet (TDD) and were treated with pyrithiamine (PT; 0.25 mg/kg) for the remaining 2 weeks. Following the induction of WE symptomatology, rats were treated with three consecutive (every 8 h) injections of saline or T (100 mg/kg) and were sacrificed. Brain homogenates were generated and used for spectrophotometrical evaluation of TAS and enzymatic activities. Additionally, in vitro experiments were conducted on brain homogenates or pure enzymes incubated with T or neuromodulatory antioxidants. Pre-exposure to EtOH provided a successful protocol modification that did not affect the expected time of WE symptomatology onset. Administration of T ameliorated this symptomatology. WE provoked oxidative stress that was partially limited by T administration, while T itself also caused oxidative stress to a smaller extent. Brain acetylcholinesterase (AChE) was found inhibited by WE and was further inhibited by T administration. In vitro experiments demonstrated a potential neuroprotective role for L-carnitine (Carn). Brain sodium-potassium adenosine triphosphatase (Na(+),K(+)-ATPase) activity was found increased in WE and was reduced to control levels by in vivo T administration; this increase was also evident in groups exposed to PT or to TDD, but not to EtOH. In vitro experiments demonstrated a potential neuroprotective role for this Na(+),K(+)-ATPase stimulation through T or L-cysteine (Cys) administration. Brain magnesium adenosine triphosphatase (Mg(2+)-ATPase) activity was found decreased by prolonged exposure to EtOH, but was not affected by the experimental induction of WE. Our data suggest that T administration inhibits AChE, which is also found inhibited in WE. Moreover, increased brain Na(+),K(+)-ATPase activity could be a marker of T deficiency in WE, while combined T and antioxidant co-supplementation of Cys and/or Carn could be neuroprotective in terms of restoring the examined crucial brain enzyme activities to control levels.

Preventing long-term brain damage in alcohol-dependent patients.

An inadequate supply of thiamine (vitamin B) to the brain can result in Wernicke's encephalopathy, which is an acute neuropsychiatric disorder This article explains the known risk of thiamine deficiency in people who are dependent on or misuse alcohol. The importance of making parenteral vitamin supplements available to patients in a community alcohol service is outlined. A project that has provided intramuscular thiamine supplementation to reduce the likelihood of long-term brain damage is described.

A novel scoring system to guide risk assessment of Wernicke's encephalopathy.

BACKGROUND: Thiamine deficiency in patients who abuse alcohol can cause Wernicke's encephalopathy (WE). Thiamine supplements are given to prevent this complication. Guidelines exist for giving thiamine supplementation in the inpatient population. However, similar guidelines are not available for clinicians detoxifying patients in the community, and consequently, assessment of risk of WE and prophylaxis can be inconsistent. METHODS: A scoring system to assess risk of WE was developed and evaluated by comparing practice before and after introduction of the system. One hundred and twenty-six cases requiring alcohol detoxification were examined: 94 before introduction of the scoring system and 32 afterward. RESULTS: Before introduction of the scoring system, a risk assessment for developing WE was performed in 30% of patients and parenteral thiamine prescribed in 32%. After introduction of the scoring system, risk assessment and administration of parenteral thiamine increased to 100 and 75%, respectively. There was 1 probable case of WE before introduction of the scoring system and none afterward. CONCLUSIONS: We conclude that assessment of WE is often inadequate, leading to inadequate thiamine administration. The new scoring system allows simple, structured risk assessment for WE and thus guides appropriate thiamine administration. This is of most value to clinicians treating the consequences of alcohol dependence in the community.

Appraisal of the Glasgow assessment and management of alcohol guideline: a comprehensive alcohol management protocol for use in general hospitals.

BACKGROUND: Guidelines exist for the management of alcohol withdrawal syndrome (AWS) but few have been assessed as to their suitability for general hospitals. The Glasgow Assessment and Management guideline for alcohol has been specifically developed for use in this context. AIM: To determine if this alcohol assessment guideline aids the management of AWS in general hospitals. DESIGN: The four components of the Glasgow Assessment and Management of Alcohol guideline were evaluated. This included the use of the Fast Alcohol Screening Test (FAST) to identify at risk patients, a risk stratification strategy to indicate fixed dose or symptom-triggered benzodiazepine treatment, the Glasgow Modified Alcohol Withdrawal Scale (GMAWS) for symptom-triggered treatment and a clear recommendation for vitamin prophylaxis of Wernicke's encephalopathy. METHODS: FAST scores were assessed along with the CAGE (cut down, annoyed, guilty and eye-opener) screening tool to ascertain if a single screening tool could identify hazardous and dependent drinking. The GMAWS and Clinical Institute Withdrawal Assessment for Alcohol (CIWA-Ar) were compared between two medical units. A staff survey of the two AWS tools was also carried out. RESULTS: FAST was able to identify both probable hazardous and dependent drinking. The GMAWS was reliable and gauged both physical and cognitive aspects of AWS. Staff generally preferred the GMAWS-based treatment as opposed to CIWA-Ar management and welcomed the Guideline as a whole. CONCLUSION: The Glasgow Guideline aids the management of patients with AWS in an acute hospital setting. It allows early identification of at risk patients and directs effective therapeutic intervention.

Glucose before thiamine for Wernicke encephalopathy: a literature review.

BACKGROUND: The prevailing teaching in medical school curricula and in medical textbooks is that if thiamine deficiency is suspected, thiamine supplementation should be given before administering glucose. OBJECTIVE: We sought to evaluate the published evidence describing the commonly held belief that thiamine supplementation must be given before glucose in hypoglycemic patients to prevent Wernicke encephalopathy. METHODS: Articles were identified through computerized searches of MEDLINE and other online sources. Pertinent references were traced back to their sources and also included in the literature review. The quality and content of each article was evaluated by the authors using the American Academy of Emergency Medicine literature review guidelines. RESULTS: Nineteen papers were ultimately identified and evaluated. No evidence rose above the level of case report/series. There were 13 case reports/series, 4 animal studies, and 2 expert opinion articles. True clinical research about the question of whether or not a glucose load can precipitate acute onset of Wernicke encephalopathy is lacking. CONCLUSIONS: Mounting case report evidence suggests that prolonged glucose supplementation without the addition of thiamine can be a risk factor for the development of Wernicke encephalopathy. Based on our findings, a delay in giving glucose to hypoglycemic patients cannot be recommended at this time, although prompt thiamine supplementation after or concurrent with a return to normoglycemia is recommended.

The clinical management of hyperemesis gravidarum.

Hyperemesis gravidarum is a severe and disabling condition with potentially life-threatening complications. It is likely to have a multifactorial etiology which contributes to the difficulty in treatment. Treatment is supportive with correction of dehydration and electrolyte disturbance, antiemetic therapy, prevention and treatment of complications like Wernicke's encephalopathy, osmotic demyelination syndrome, thromboembolism, and good psychological support. There are abundant data on the safety of antihistamines, phenothiazines, and metoclopromide in early pregnancy and treatment should therefore not be withheld on the basis of teratogenicity concerns. Thiamine replacement is indicated in hyperemesis gravidarum to prevent development of Wernicke's encephalopathy.

Wernicke's encephalopathy: a preventable cause of maternal death.

Wernicke's encephalopathy is a rare cause of maternal death. It is a difficult diagnosis to make but prevention and treatment is straightforward. Severe thiamine deficiency causes Wernicke-Korsakoff syndrome. Correct diagnosis and treatment with thiamine will decrease the case fatality rate.