Encefalopatía de Wernicke / Wernicke's encephalopathy

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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 (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.

Thiamine in the treatment of Wernicke encephalopathy in patients with alcohol use disorders.

Wernicke encephalopathy is an acute, reversible neuropsychiatric emergency due to thiamine deficiency. Urgent and adequate thiamine replacement is necessary to avoid death or progression to Korsakoff syndrome with largely irreversible brain damage. Wernicke Korsakoff syndrome refers to a condition where features of Wernicke encephalopathy are mixed with those of Korsakoff syndrome. Although thiamine is the cornerstone of treatment of Wernicke encephalopathy, there are no universally accepted guidelines with regard to its optimal dose, mode of administration, frequency of administration or duration of treatment. Currently, different dose recommendations are being made. We present recommendations for the assessment and treatment of Wernicke encephalopathy based on literature review and our clinical experience.

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.

Biomarkers in alcohol misuse: their role in the prevention and detection of thiamine deficiency.

In Western countries alcohol misuse is the most frequent cause of thiamine (vitamin B1) deficiency (TD) and consequent neuro-impairment. Studies have demonstrated that between 30 and 80% of alcoholics are thiamine deficient, and this puts them at risk of developing the Wernicke-Korsakoff (WK) syndrome. The relative roles of alcohol and TD in causing brain damage remain controversial and it is important to try to determine the role played by each factor. Animal studies support an additive effect of alcohol exposure and TD, and indicate the potential for interaction between alcohol and TD in human alcohol-related brain damage. Early diagnosis of alcohol-related TD is therefore an important aspect of effective intervention and treatment. Alcohol biomarkers provide a direct and indirect way of estimating the amount of alcohol being consumed, the duration of ingestion and the harmful effects that long-term alcohol use has on body functions. Appropriate use of these markers is very helpful when considering a diagnosis of alcohol-related TD.

The impact of prolonged hunger strike: clinical and laboratory aspects of twenty-five hunger strikers.

BACKGROUND: Hunger strike is a very serious entity which may lead to severe diseases and death. AIMS: The aim of this study is to document the clinical, neurophysiological, neuroradiological, and neuropsychological aspects of prolonged hunger strike. MATERIAL AND METHOD: We investigated the clinical and laboratory characteristics of 25 hungerstrikers hospitalized during refeeding process. One sample t-test, independent samples t-test, Mann-Whitney and Pearson correlation tests were used for statistical analyses. RESULTS: Twelve of them had a continuous hunger strike ranging between 190-366 days. The other 13 had quitting intervals for various reasons with a continuous hunger ranging between 65-265 days with a total hunger duration of 153-382 days. The mean loss of body mass index (BMI) was 40.98 +/- 9.3%. Imbalance, sleep disorders, somatosensory disturbances, and adynamia were the most common complaints. At admission, one third experienced ophthalmoparesis, about half of them had paresis, one quarter had truncal ataxia. At discharge 16% had persistent ophthalmoparesis and 36% nystagmus. Only four patients (16%) could walk independently. There was no serious MRI, EEG findings. Most prominent EMG findings were the decrease in median and sural nerve cnap, median and fibular cmap, and fibular ncv values. They showed mild impairment in MMTS and most of them had attention deficit and frontal type memory impairment. CONCLUSION: It can be concluded that vitamin B intake, independent of the quantity and timing, lowers the morbidity and mortality of hunger strikers.

Thiamine (vitamin B1) deficiency and associated brain damage is still common throughout the world and prevention is simple and safe!

Many different population groups throughout the world have thiamine deficiency and are at risk of developing severe neurological and cardiac disorders. Alcoholics are most at risk but other important clinical groups should be monitored carefully. The most severe, potentially fatal disease caused by thiamine deficiency is the neurological disorder Wernicke-Korsakoff syndrome. This can be difficult to diagnose and many cases remain undiagnosed. Treatment with thiamine generally results in a dramatic clinical improvement. Thiamine supplementation of stable food products like flour is an effective, simple and safe public health measure that can improve the thiamine status of all population groups.

The natural history and pathophysiology of Wernicke's Encephalopathy and Korsakoff's Psychosis.

AIMS: To identify the early clinical indications of thiamine deficiency and to understand the factors involved in the development of the amnesic state in alcohol-dependent individuals with thiamine deficiency. It is hoped that this will highlight the need for clinicians to treat alcohol-dependent patients prophylactically with parenteral thiamine and thus prevent the development of Korsakoff's Psychosis (KP). METHOD: We have reviewed the natural history and pathophysiology of Wernicke's Encephalopathy (WE) in both human and animal studies together with any contributory factors that may predispose the individual to thiamine deficiency. A further understanding of these problems is provided by recent studies into the metabolic consequences of thiamine deficiency and alcohol misuse. CONCLUSIONS: Where WE is due to thiamine deficiency alone (i.e. in the absence of alcohol misuse) KP rarely supervenes following thiamine replacement therapy. Successful treatment or prophylaxis of WE in alcohol dependence probably depends on a number of inter-related issues and is not simply a matter of early and adequate thiamine treatment. If sufficient alcohol-related neurotoxicity has occurred by the time of diagnosis, then this may be the more important or limiting factor with respect to the long-term outcome. This possible obstacle to complete recovery should not prevent every attempt being made to provide the patient with optimum brain thiamine replacement.

Thiamin treatment and working memory function of alcohol-dependent people: preliminary findings.

BACKGROUND: Wernicke-Korsakoff syndrome (WKS) is most often seen in people who are alcohol dependent. Treatment with thiamin may rapidly resolve acute symptoms. However, much evidence suggests that identification of WKS on clinical examination is relatively insensitive when compared with diagnosis at postmortem. No study has investigated the therapeutic effect of thiamin in a sample of alcohol-dependent people without the clinical triad of acute WKS. METHODS: We conducted a randomized, double-blind, multidose study of thiamin treatment in 107 subjects who were detoxifying from alcohol. Five groups of subjects were assessed with the Mini-Mental State Examination and were examined for the presence of neurological signs. Subjects were given different doses of intramuscular thiamin for two consecutive days. The posttreatment performance of these groups then was examined on a test of working memory derived from comparative neuropsychology, namely, the delayed alternation task. This test has been established as sensitive to the neuropathology of WKS. RESULTS: Pretreatment measures of mental status and neurological signs were equivalent across groups. Groups were equated with respect to the background variables of age, education, typical daily alcohol consumption, and years of drinking. On the posttreatment measure, a superior performance was found in the group that received the highest dose of thiamin, compared with the other four treatment groups. CONCLUSIONS: A therapeutic relationship between dose and working memory performance was indicated. These results have important implications for the management and prevention of WKS, but further investigations are needed to substantiate the nature of the therapeutic relationship.

Mechanisms of vitamin deficiency in chronic alcohol misusers and the development of the Wernicke-Korsakoff syndrome.

The classic signs of vitamin deficiency only occur in states of extreme depletion and are unreliable indicators for early treatment or prophylaxis of alcoholic patients at risk. Post-mortem findings demonstrate that thiamine (vitamin B1) deficiency sufficient to cause irreversible brain damage is not diagnosed ante mortem in 80-90% of these patients. The causes of vitamin deficiency are reviewed with special attention to the inhibition of oral thiamine hydrochloride absorption in man caused by malnutrition present in alcoholic patients or by the direct effects of ethanol on intestinal transport. As the condition of the patient misusing alcohol progresses, damage to brain, liver, gastrointestinal tract, and pancreas continue (with other factors discussed) to further compromise the patient. Decreased intake, malabsorption, reduced storage, and impaired utilization further reduce the chances of unaided recovery. Failure of large oral doses of thiamine hydrochloride to provide an effective treatment for Wernicke's encephalopathy emphasizes the need for adequate and rapid replacement of depleted brain thiamine levels by repeated parenteral therapy in adequate doses.

Prevention and treatment of Wernicke-Korsakoff syndrome.

Wernicke's encephalopathy (WE) is both common and associated with high morbidity and mortality and yet there is evidence that appropriate and effective prophylaxis and treatment are often not given. Effective treatment and prophylaxis may only be achieved by use of parenteral vitamin supplements, since oral supplements are not absorbed in significant amounts. Although there are rare anaphylactoid reactions associated with the use of parenteral thiamine preparations, the risks and consequences of inadequate prophylaxis and treatment, in appropriately targeted groups of patients, are far greater. It is therefore proposed that all in-patient alcohol withdrawal should be covered by prophylactic use of parenteral thiamine, that there should be a low threshold for making a presumptive diagnosis of WE, and that there is a need for guidelines to assist physicians in appropriate management of this common clinical problem.

A survey of the current clinical practice of psychiatrists and accident and emergency specialists in the United Kingdom concerning vitamin supplementation for chronic alcohol misusers.

Although it is well known that B-vitamin deficiencies directly affecting the brain are common in alcohol misuse, no concise guidelines on the use of vitamin supplements in alcohol misusers currently exist in the UK. The purpose of this study was to assess current practice and opinion among UK physicians. Questionnaires were completed by a total of 427 physicians comprising Accident and Emergency (A&E) specialists and psychiatrists, with a response rate of 25%. The main findings were that vitamin deficiency was perceived as being uncommon amongst alcohol misusers (<25%) and there was no consensus as to which B vitamins are beneficial in treatment or the best method of administration of B-vitamin supplementation. The majority of psychiatrists favoured oral administration for prophylaxis against the Wernicke-Korsakoff syndrome in chronic alcohol misusers and parenteral therapy in patients with signs of Wernicke-Korsakoff syndrome. Whilst only just over half the A&E specialists expressed a preference, most favoured parenteral therapy in both cases. Most respondents did not currently have a unit policy/protocol on the management of vitamin supplementation in chronic alcohol misusers. Overall, the findings suggest that there is wide variation in current practice and highlight the need for guidelines in this area.

Wernicke-Korsakoff syndrome in Sydney hospitals after 6 years of thiamin enrichment of bread.

OBJECTIVES: To estimate the incidence of Wernicke's encephalopathy (WE) and Korsakoff's psychosis (KP) before and after the introduction of thiamin enrichment of bread in Australia. DESIGN AND SUBJECTS: Inpatient records were examined in 17 major public general hospitals in greater Sydney for the 4 years 1993-96 (inclusive) with the International Classification of Diseases (ICD) 9 diagnoses 265.1 (WE), 291.1 and 294.0 (KP). Relevant clinical data were recorded on a specially designed form so that cases could be classified as confirmed or probable WE, confirmed or probable KP, confirmed or probable Wernicke-Korsakoff syndrome (WE + KP) or not WE or KP. The average number of cases of WE + KP was 38 acute (new) cases and 69 total (acute + chronic) cases per annum for all the hospitals combined. RESULTS: This study used the same methods as our earlier retrospective examination of Wernicke-Korsakoff cases in essentially the same hospitals for 1978-93. Records for 1993 were thus pulled twice and, while individual cases (using hospital index number) did not always coincide, the total numbers for 1993 were 69 and 70. For the 5 years after 1991 the number of acute cases of WE and KP in Sydney hospitals was 61% of the number for the 5 years before 1991 (P<0.01). There is, however, no continuing downward trend. CONCLUSIONS: These results are consistent with a 40% reduction of the incidence of acute WE and KP since bread has been enriched with thiamin. The disease complex has, however, not been eliminated. To achieve this, further public health action would be needed, such as addition of thiamin to beer.