The Royal College of Physicians Report on Alcohol: Guidelines for Managing Wernicke's Encephalopathy in the Accident and Emergency Department

Thomson, Allan D.

doi:10.1093/alcalc/37.6.513

Cited by 347 publications

(342 citation statements)

References 43 publications

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“…The major treatment goals for withdrawal delirium are to control agitation, decrease the risk of seizures, and decrease the risk of injury and death with the use of the methods outlined in Table 3. 7,9,13,[18][19][20][21][22][23] Because of the high prevalence of agitation among patients with withdrawal delirium and the potential lethal outcomes, treatment is best carried out in a locked inpatient ward or an ICU.…”

Section: Components Of Scale Most Severe Manifestationsmentioning

confidence: 99%

Recognition and Management of Withdrawal Delirium (Delirium Tremens)

2014

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A t some time in their lives, 20% of men and 10% of women in most Western societies will have an alcohol-use disorder, which is defined as repetitive alcohol-related problems in at least 2 of 11 areas of life. 1,2 These conditions can decrease the life span by a decade and are associated with severe impairments in social functioning, as well as high rates of medical problems. Although alcohol-related conditions occur in persons from all social strata and affect more than 20% of patients in most medical settings, 2,3 few physicians have been adequately trained in identifying and treating these serious problems.About 50% of persons with alcohol-use disorders have symptoms of alcohol withdrawal when they reduce or discontinue their alcohol consumption; in 3 to 5% of these persons, grand mal convulsions, severe confusion (a delirium), or both develop. 1 It is essential that clinicians know how to prevent, recognize, and treat these severe withdrawal states to minimize costly hospitalizations and avoidable deaths.

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Section: Components Of Scale Most Severe Manifestationsmentioning

confidence: 99%

Recognition and Management of Withdrawal Delirium (Delirium Tremens)

2014

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“…Los niveles de tiamina normales no excluyen el diagnóstico de EW, ya que existe una relación con mutaciones en el gen del transportador de tiamina (20,21) y adicionalmente, su medición es difícil en el contexto de los paises en vias de desarrollo. En nuestra institución es necesaria la remisión internacional de la muestra, con resultado disponible luego de 10 días de la toma, además son necesarias algunas condiciones técnicas difíciles de cumplir en pacientes sintomáticos (análisis de la muestra antes de 24 horas de la recolección, toma en ayuno mínimo de 8 horas y sin infusiones dextrosadas, entre otras).…”

Section: Discussionunclassified

“…Aunque no existe un consenso acerca de la dosis y forma de preparación, es claro que el tratamiento se debe realizar vía parenteral ya que la tiamina se absorbe en el duodeno a una velocidad limitada y la cantidad máxima vía oral que puede absorberse en una dosis es de sólo 4.5 mg (21). La vida media de la tiamina es 96 minutos por lo que la administración en varias dosis (dos o tres) puede lograr una mejor penetración cerebral que con una sola dosis (12).…”

Section: Discussionunclassified

“…Hay evidencia que dosis entre 100 -250 mg no reestablecen el nivel óptimo de tiamina (23), no mejoran los signos clínicos (24) y no previenen la muerte (25). En nuestro caso se administró una dosis inicial de 500mg de tiamina IV en 100 cc de DAD al 5% en 30 minutos cada 8 horas por 3 días (21,26). Se continuó con 250 mg IV diarios por 5 días, obedeciendo la recomendación de 3 -5 días hasta la mejoría clínica o hasta que el paciente tolere la vía oral (12); posteriormente se administró reposición vía oral con 300 mg una vez al día.…”

Section: Discussionunclassified

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Encefalopatía de Wernicke secundario a hiperémesis gravídica: la importancia del diagnóstico temprano

NIETO

Burgos

Echeverry

et al. 2018

Rev. chil. obstet. ginecol.

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RESUMENIntroducción: La hiperémesis gravídica (HG) es una condición frecuente en el embarazo, que puede resultar en complicaciones potencialmente letales como la encefalopatía de Wernicke (EW), síndrome que al ser reconocido y tratado tardíamente puede traducirse en una alta morbi-mortalidad materna y fetal. Objetivo: Describir el primer caso de EW secundario a HG en Colombia y realizar una revisión de la literatura publicada sobre su diagnóstico y tratamiento. Materiales y métodos: Se describe un caso de EW secundario a HG en el que se brindó un manejo interdisciplinario. Se realizó una revisión de la literatura con los términos "encefalopatía de Wernicke", "hiperémesis gravídica" y "embarazo" incluyendo reportes de casos, series de casos, artículos de revisión, investigaciones originales o cartas al editor en inglés, español y francés, en donde se analizaron el método y tiempo del diagnóstico, pauta de tratamiento y estado funcional final. Resultados: Se incluyeron 69 publicaciones y se identificaron 89 casos. En 23 de ellos se presentó pérdida gestacional, sólo en el 12,4% de los casos se reportó el nivel de tiamina, de los cuales en el 90% se encontraba disminuido y de los casos en donde se reportó estado funcional final en el 5,9% la gestante falleció. Conclusión: La EW secundaria a HG es una complicación potencialmente letal. Debe sospecharse ante cualquier alteración neurológica e historia de emesis persistente. El diagnóstico y tratamiento oportuno interdisciplinario son fundamentales para disminuir el riesgo de secuelas que limitan la capacidad funcional con alto impacto en la calidad de vida.PALABRAS CLAVE: Encefalopatía de Wernicke; Hiperemesis gravídica; Tiamina; Embarazo. ABSTRACTIntroduction: Hyperemesis gravidarum (HG) is a frequent condition in pregnancy, which can result in potentially lethal complications such as Wernicke encephalopathy (WE), a syndrome that can be translated into a high maternal and fetal morbidity and mortality if it is recognized and treated late. Objective: To describe the first case of WE due to HG in Colombia and to review the published literature about its diagnosis and treatment. Materials and methods: We describe a case of WE due to HG with an interdisciplinary approach. A review of the literature was performed with the terms "Wernicke's encephalopathy", "hyperemesis gravidarum" and "pregnancy" including case reports, case series, review articles, original investigations or letters to the editor in English, Spanish and French, where the method and time of the diagnosis, treatment regimen and sequelae were analyzed.

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“…The reason that alcoholics are prone to develop thiamine deficiency relates to decreased oral intake of food and the direct effects of alcohol on intestinal transport of thiamine (Gastaldi et al, 1989). The resulting reduced thiamine stores and impaired thiamine utilization impair normal central nervous system function (Thomson et al, 2002). Phillips et al (1987) have speculated that the withdrawal effects of highly intoxicating levels of alcohol contribute to the disruption of white matter integrity .…”

Section: Introductionmentioning

confidence: 99%

Interaction of Thiamine Deficiency and Voluntary Alcohol Consumption Disrupts Rat Corpus Callosum Ultrastructure

Sullivan

Stankovic

et al. 2007

Neuropsychopharmacol

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The relative roles of alcohol and thiamine deficiency in causing brain damage remain controversial in alcoholics without the WernickeKorsakoff syndrome. Experimental control over alcohol consumption and diet are impossible in humans but can be accomplished in animal models. This experiment was designed to differentiate the separate and combined effects on the macro-and ultrastructure of the corpus callosum of thiamine deficiency and voluntary alcohol consumption. Adult male alcohol-preferring (P) rats (9 chronically alcoholexposed and 9 water controls) received a thiamine-deficient diet for 2 weeks. There were four groups: five rats previously exposed to alcohol were treated with pyrithiamine (a thiamine phosphorylation inhibitor); five rats never exposed to alcohol were treated with pyrithiamine; four alcohol-exposed rats were treated with thiamine; and four rats never exposed to alcohol were treated with thiamine. On day 14, thiamine was restored in all 18 rats; 2 weeks later the 10 pyrithiamine-treated rats received intraperitoneal thiamine. The rats were perfused 61 days post-pyrithiamine treatment at age 598 days. Brains were dissected and weight and volumes were calculated. Sagittal sections were stained to measure white matter structures. The corpus callosum was examined using transmission electron microscopy to determine density of myelinated fibers, fiber diameter, and myelin thickness. The corpus callosum in the alcohol/ pyrithiamine group was significantly thinner, had greater fiber density, higher percentage of small fibers, and myelin thinning than in the alcohol/thiamine and water/thiamine groups. Several measures showed a graded effect, where the alcohol/pyrithiamine group had greater pathology than the water/pyrithiamine group, which had greater pathology than the two thiamine-replete groups. Across all 16 rats, thinner myelin sheaths correlated with higher percentage of small fibers. Myelin thickness and axon diameter together accounted for 71% of the variance associated with percentage of small fibers. Significant abnormalities in the alcohol/pyrithiamine group and lack of abnormality in the alcohol-exposed/thiamine-replete group indicate that thiamine deficiency caused white matter damage. The graded abnormalities across the dually to singly treated animals support a compounding effect of alcohol exposure and thiamine depletion, and indicate the potential for interaction between alcohol and thiamine deficiency in human alcohol-related brain damage.

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The Royal College of Physicians Report on Alcohol: Guidelines for Managing Wernicke's Encephalopathy in the Accident and Emergency Department

Cited by 347 publications

References 43 publications

Recognition and Management of Withdrawal Delirium (Delirium Tremens)

Recognition and Management of Withdrawal Delirium (Delirium Tremens)

Encefalopatía de Wernicke secundario a hiperémesis gravídica: la importancia del diagnóstico temprano

Interaction of Thiamine Deficiency and Voluntary Alcohol Consumption Disrupts Rat Corpus Callosum Ultrastructure

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