When time is brain: a systematic review about Wernicke encephalopathy as a dramatic consequence of thiamin deficiency in hyperemesis gravidarum.

Nausea and vomiting affect up to 80% of all pregnancies, sometimes so severely that the condition of hyperemesis gravidarum (HG) is established. HG may in addition be a predisposing factor for Wernicke encephalopathy (WE), a severe and life-threatening condition due to vitamin B1 (thiamin) deficiency. If untreated, WE may progress to Korsakoff's syndrome, an irreversible cognitive disorder. We reported a case that recently occurred at our clinic and performed a systematic review of the literature to investigate the clinical presentation, maternal and perinatal outcomes and treatment of WE in women with HG. METHODS: We performed a systematic review of case series and case reports searching the Medline database on Pubmed from inception until December 2021. We used as search terms (Wernicke encephalopathy) OR (Wernicke-Korsakoff syndrome) AND (hyperemesis gravidarum) AND (pregnancy) AND (thiamin deficiency). Articles were considered eligible for inclusion in our review if they described at least one case of WE due to thiamin deficiency in relation to HG. An overall of 82 cases of WE due to HG in pregnancy from 66 manuscripts, including our own, were selected. RESULTS: The maternal mean age was 26.38 ± 5.23 years, while mean gestational week at hospitalization was 14.57 ± 4.12 after a mean of 6.6 ± 3.14 weeks of vomiting duration. WE manifestation occurred at a mean gestational age of 16.54 ± 3.06 weeks. Regarding clinical presentation, ocular signs and symptoms were reported by 77/82 (93.9%) women, 61/82 (74.4%) presented with ataxia and 63/82 (76.8%) with confusion. Dysarthria affected 15/82 women (18,3%), while muscular weakness was present in 36/82 (43.9%) and impaired reflexes in 42/82 (51.2%). Memory impairment involved 25/82 (30.5%) of the study population. Almost all cases reported a thiamin administration treatment, however data regarding the clinical course of the neurological condition and the perinatal outcomes were often missing and showed a great heterogeneity when reported. CONCLUSION: WE is a challenging diagnosis, as its clinical presentation is nonspecific. A high clinical suspicion and the awareness of its possible predisposing conditions such as HG may help clinicians to get a prompt diagnosis and starting treatment, which are vital to prevent possible life-impairing neurological sequelae.

The importance of thiamine (vitamin B1) in humans.

Thiamine (thiamin, B1) is a vitamin necessary for proper cell function. It exists in a free form as a thiamine, or as a mono-, di- or triphosphate. Thiamine plays a special role in the body as a coenzyme necessary for the metabolism of carbohydrates, fats and proteins. In addition, it participates in the cellular respiration and oxidation of fatty acids: in malnourished people, high doses of glucose result in acute thiamine deficiency. It also participates in energy production in the mitochondria and protein synthesis. In addition, it is also needed to ensure the proper functioning of the central and peripheral nervous system, where it is involved in neurotransmitter synthesis. Its deficiency leads to mitochondrial dysfunction, lactate and pyruvate accumulation, and consequently to focal thalamic degeneration, manifested as Wernicke's encephalopathy or Wernicke-Korsakoff syndrome. It can also lead to severe or even fatal neurologic and cardiovascular complications, including heart failure, neuropathy leading to ataxia and paralysis, confusion, or delirium. The most common risk factor for thiamine deficiency is alcohol abuse. This paper presents current knowledge of the biological functions of thiamine, its antioxidant properties, and the effects of its deficiency in the body.

Can thiamine substitution restore cognitive function in alcohol use disorder?

AIMS: While clinical consequences of thiamine deficiency in alcohol use disorder (AUD) are severe, evidence-based recommendations on dosage, type of administration and duration of thiamine substitution (TS), and its' target levels remain sparse. This study aimed to compare the effect of two best practice TS regimens on thiamine blood levels (i.e. thiamine pyrophosphate, TPP) and cognitive function. METHODS: In 50 patients undergoing in-patient alcohol-withdrawal treatment, TPP levels were determined at baseline and end of weeks 1, 2 and 8 following administration of oral TS (3 × 100 mg/day for 7 days followed by 1 × 100 mg/day thereafter) either with or without preceding intravenous TS (3 × 100 mg/day for 5 days). An extensive psychiatric assessment was conducted at baseline, including an evaluation of AUD severity and depressive symptoms. Additionally, cognitive function and depressive symptoms were repeatedly evaluated. RESULTS: Relevant increases (mean increase by 100.2 nmol/l [CI 76.5-123.8], P < 0.001) in peripheral blood TPP levels were observed in all patients at the end of weeks 1 and 2. Furthermore, no relevant difference between the intravenous and the oral group was found (average difference between increases: 2.3 nmol/l, P = 0.912). Importantly, an association between the 'extent of the response' to TS and the performance in a memory task was revealed in secondary analyses. CONCLUSION: TS was associated with improving cognitive function in patients with AUD, independently of the substitution regime. Thus, in clinical practice, oral TS might be a sufficient but obligatory medication to prevent cognitive decline in AUD in the absence of Wernicke-Korsakoff Syndrome.

Fetal demise and Wernicke-Korsakoff syndrome in a patient with hyperemesis gravidarum: a case report.

BACKGROUND: Wernicke-Korsakoff syndrome is a neuropsychiatric disorder caused by thiamine deficiency composed of two related disorders accounting for an acute presentation and chronic progression. Hyperemesis gravidarum presents a significant risk factor for Wernicke-Korsakoff syndrome as symptoms may rapidly progress in the setting of pregnancy. We present the first-reported case of hyperemesis-gravidarum-associated Wernicke encephalopathy in a patient in the first half of pregnancy in which a missed diagnosis led to septic shock, fetal demise, and eventual profound Korsakoff syndrome. CASE PRESENTATION: We present the case of a 33-year-old primigravid African American woman at 15 weeks gestational age who initially presented at a community emergency department with nausea and vomiting that ultimately progressed to severe hyperemesis-gravidarum-associated Wernicke-Korsakoff syndrome, fetal demise, and septic shock. The patient received a total of 6 weeks of high-dose parenteral thiamine. Magnetic resonance imaging of the head and formal neuropsychological assessment following treatment plateau confirmed the diagnosis of Wernicke-Korsakoff syndrome. CONCLUSIONS: The multisystem complications seen in severe thiamine deficiency can delay timely administration of high-dose thiamine, particularly in pregnancy, in which the classic triad of Wernicke-Korsakoff syndrome may not raise clinical suspicion due to rapid progression of neurological sequelae in this population. We advise a low threshold for parenteral thiamine repletion in pregnant women with persistent vomiting as hyperemesis gravidarum-induced severe thiamine deficiency can result in Wernicke-Korsakoff syndrome, sepsis, and fetal demise.

Wernicke encephalopathy and beriberi disease presenting as STEMI-equivalent.

Thiamine deficiency is commonly associated with malnutrition, alcoholism and bariatric surgery. Thiamine deficiency can manifest in different ways, especially in developing countries: as peripheric neuropathy, as Wernicke encephalopathy or as beriberi disease. The authors present the case of a 72-year-old male, with a hiatal hernia that led to thiamine deficiency due to malnutrition. The initial clinical manifestation was an ST-elevation myocardial infarct equivalent, an ECG with a shark-fin pattern that evolved to a Wellens type B pattern. The patient evolved with severe altered mental status. A Wernicke encephalopathy diagnosis was confirmed by MRI; the patient was medicated with high-dose thiamine, with quick recovery, both neurologic and cardiac. The clinical history and response to treatment confirm the diagnosis of Wernicke encephalopathy and beriberi disease.

SLC19A1 Genetic Variation Leads to Altered Thiamine Diphosphate Transport: Implications for the Risk of Developing Wernicke-Korsakoff's Syndrome.

AIMS: Wernicke-Korsakoff syndrome (WKS) is commonly associated with chronic alcohol misuse, a condition known to have multiple detrimental effects on thiamine metabolism. This study was conducted to identify genetic variants that may contribute to the development of WKS in individuals with alcohol dependence syndrome through alteration of thiamine transport into cells. METHODS: Exome sequencing data from a panel of genes related to alcohol metabolism and thiamine pathways were analysed in a discovery cohort of 29 individuals with WKS to identify possible genetic risk variants associated with its development. Variant frequencies in this discovery cohort were compared with European frequencies in the Genome Aggregation Database browser, and those present at significantly higher frequencies were genotyped in an additional cohort of 87 alcohol-dependent cases with WKS and 197 alcohol-dependent cognitively intact controls. RESULTS: Thirty non-synonymous variants were identified in the discovery cohort and, after filtering, 23 were taken forward and genotyped in the case-control cohort. Of these SLC19A1:rs1051266:G was nominally associated with WKS. SLC19A1 encodes the reduced folate carrier, a major transporter for physiological folate in plasma; rs1051266 is reported to impact folate transport. Thiamine pyrophosphate (TPP) efflux was significantly decreased in HEK293 cells, stably transfected with rs1051266:G, under thiamine deficient conditions when compared with the efflux from cells transfected with rs1051266:A (P = 5.7 × 10-11). CONCLUSION: This study provides evidence for the role of genetic variation in the SLC19A1 gene, which may contribute to the development of WKS in vivo through modulation of TPP transport in cells.

Bromisoval-induced bromism with status epilepticus mimicking Wernicke's encephalopathy: report of two cases.

BACKGROUND: Bromine compounds are used in several drugs, including over-the-counter drugs. They sometimes cause intoxication known as bromism. Although the acute neurological symptoms and sequelae of bromism vary, few reports have mentioned acute encephalopathy. CASE PRESENTATION: We report two cases of bromisoval-induced bromism with status epilepticus. Presence of pseudohyperchloremia and history of over-the-counter medication use guided the diagnosis. In the acute phase, our patients showed bilateral medial thalamic lesions on magnetic resonance imaging. The imaging findings were similar to those of Wernicke's encephalopathy. Although these findings improved in the chronic phase, neuropsychiatric sequelae, such as confabulation and amnesia, occurred. CONCLUSION: Bromism can cause acute encephalopathy, and it is important to differentiate it from Wernicke-Korsakoff syndrome.

Síndrome de Wernicke-Korsakoff y otras patologías asociadas al déficit de tiamina / Wernicke-Korsakoff syndrome and other diseases associated with thyamine deficiency

El síndrome de Wernicke-Korsakoff es la consecuencia más conocida del déficit de tiamina; se asocia frecuentemente a pacientes con un consumo crónico y excesivo de alcohol, pero puede deberse a cualquier causa que produzca déficit de tiamina.La enfermedad está infradiagnosticada, por lo que es fundamental tener una alta sospecha clínica, principalmente en los pacientes que no presentan consumo de alcohol como factor de riesgo. El diagnóstico sigue siendo eminentemente clínico, con la dificultad de una elevada variabilidad clínica. Las pruebas complementarias sirven para apoyar el diagnóstico y descartar otras causas que puedan producir sintomatología similar, siendo la resonancia magnética la prueba de imagen más rentable.El tratamiento se basa en la administración de tiamina, que debe iniciarse precozmente, de forma parenteral y a las dosis adecuadas en todos los pacientes con clínica compatible, sin esperar a confirmar el diagnóstico. (AU)

Wernicke-Korsakoff syndrome is the best known consequence of thiamine deficiency, frequently associated with patients with chronic and excessive alcohol consumption, but it can be produced by any cause that produces thiamine deficiency.The disease is underdiagnosed so it is essential to have a high clinical suspicion, mainly in patients who do not have alcohol consumption as a risk factor. For this, the diagnosis continues to be eminently clinical, with the difficulty of high clinical variability. Complementary tests are used to support the diagnosis and rule out other causes that can produce similar symptoms, with magnetic resonance imaging being the most cost-effective imaging test.Treatment is based on the administration of thiamine, which should be started early, and parenterally at the appropriate doses, in all patients with compatible symptoms, without waiting to confirm the diagnosis. (AU)

What is the Korsakoff syndrome? - a paper in tribute to Prof Alwyn Lishman.

INTRODUCTION: Alwyn Lishman was interested in how memory research could be applied to clinical psychiatry. After a brief review of his major contributions, this paper will focus on his research on the alcoholic Korsakoff syndrome. It will consider how his findings relate to contemporary debates, particularly on how the syndrome should be defined, and its relationship to broader alcohol-induced cognitive impairments. METHODS: A review of the contribution of Alwyn Lishman, Robin Jacobson and colleagues to our knowledge of Korsakoff's syndrome, together with a review of the pertinent recent literature. RESULTS: Lishman and colleagues followed earlier authors in defining the Korsakoff syndrome in terms of disproportionate memory impairment, but they also noted a variable degree of IQ, frontal-executive, and timed visuo-spatial impairment in their cases. More recent authors have included such features in their definitions of the syndrome. Lishman also argued for a specific "alcoholic dementia". The present paper argues that recent definitions of the Korsakoff syndrome confound its core and associated features, and also fail to recognise the multifactorial basis of alcohol-related brain damage. CONCLUSIONS: Korsakoff's syndrome is best defined in terms of disproportionate memory impairment, and more widespread cognitive impairment is best encompassed within "alcohol-related brain damage".

[Wernicke-Korsakoff syndrome and other diseases associated with thyamine deficiency]. / Síndrome de Wernicke-Korsakoff y otras patologías asociadas al déficit de tiamina.

Wernicke-Korsakoff syndrome is the best known consequence of thiamine deficiency, frequently associated with patients with chronic and excessive alcohol consumption, but it can be produced by any cause that produces thiamine deficiency. The disease is underdiagnosed so it is essential to have a high clinical suspicion, mainly in patients who do not have alcohol consumption as a risk factor. For this, the diagnosis continues to be eminently clinical, with the difficulty of high clinical variability. Complementary tests are used to support the diagnosis and rule out other causes that can produce similar symptoms, with magnetic resonance imaging being the most cost-effective imaging test. Treatment is based on the administration of thiamine, which should be started early, and parenterally at the appropriate doses, in all patients with compatible symptoms, without waiting to confirm the diagnosis.

Temporal Cognitive and Brain Changes in Korsakoff Syndrome.

OBJECTIVE: To investigate cognitive and brain changes in patients with Korsakoff syndrome (KS) over months and up to 10 years after the diagnosis. METHODS: Two groups of 8 patients with KS underwent neuropsychological, motor, and neuroimaging investigations, including structural MRI and 18F-fluorodeoxyglucose-PET. The KSC group, recruited at Caen University Hospital, was examined early after the KS diagnosis (KSC-T1) and 1 year later (KSC-T2). The KSR group, recruited at nursing home at Roubaix, was evaluated 10 years after the diagnosis. Longitudinal comparisons in KSC explored short-term changes, while cross-sectional comparisons between KSC-T1 and KSR informed about long-term changes. RESULTS: No cognitive, motor, or brain deterioration occurred over time in patients with KS. There was no clear improvement either, with only modest recovery in the frontocerebellar circuit. Compared to the norms, KSC-T1 had severe episodic memory impairments, ataxia, and some executive dysfunctions. They also presented widespread atrophy and hypometabolism as well as cerebellar hypermetabolism compared to 44 healthy matched controls. Episodic memory remained significantly impaired in KSC-T2 and KSR. Contrary to KSC at T1 and T2, KSR had preserved inhibition abilities. Atrophy was similar but less extended in KSC-T2 and even more limited in KSR. At all times, the thalamus, hypothalamus, and fornix remained severely atrophied. Hypometabolism was still widespread in KSC-T2 and KSR, notably affecting the diencephalon. Cerebellar metabolism decreased over time and normalized in KSR, whereas motor dysfunction persisted. CONCLUSION: In KS, structural and metabolic alterations of the Papez circuit persisted over time, in accordance with the irreversible nature of amnesia. There was neither significant recovery as observed in patients with alcohol use disorder nor progressive decline as in neurodegenerative diseases.

Unraveling Apathy in Korsakoff Syndrome Patients Receiving Long-Term Care With and Without Cerebrovascular Comorbidity.

BACKGROUND: Korsakoff syndrome (KS) is a severe neuropsychiatric disorder caused by acute deficiency of vitamin B1 and concomitant alcoholism. Patients with KS are particularly vulnerable for cerebrovascular comorbidity. KS is characterized by cognitive and neuropsychiatric symptoms, one of which is apathy. Apathy is a pathological lack of goal-directed behaviors, goal-directed cognitions, and goal-directed emotions. Cerebrovascular accidents are known to carry a risk for developing apathy. Apathy has a dramatic effect on the autonomy and daily lives of patients suffering from this condition. METHODS: We assessed general apathy and related subconstructs in fifteen patients with KS, fifteen patients with KS and cerebrovascular comorbidity who reside in a 24-hour care facility, and fifteen healthy controls. RESULTS: Compared with healthy controls, both KS patient groups showed higher levels of apathy as rated by a close informant. We found no difference between both KS patient groups and the healthy control group on the self-report section of the Pleasant Activities List, suggesting that motivation is still intact in KS patients. It is important to note a discrepancy was found between self-reporting and proxy reporting on this list. KS patients with cerebrovascular comorbidity showed more severe emotional blunting compared to both KS patients without cerebrovascular comorbidity and healthy controls. The competency to consent was lower in patients compared with healthy controls, but no difference was found between KS patients with cerebrovascular comorbidity and those without. CONCLUSIONS: Our results suggest that KS patients show increased levels of general apathy compared with healthy controls. Patients show a diminished competency to consent and increased emotional blunting, while motivation is not compromised. Cerebrovascular comorbidity in KS forms a high risk for emotional blunting. The results of this study suggest that apathy is a severe problem in KS. More attention in both the literature and clinical practice would benefit this complex patient population.

The thin line between reality and imagination: The imagination inflation effect in Korsakoff's syndrome.

OBJECTIVE: The imagination inflation effect, which is a form of memory distortion, occurs when imagining an event that never happened may increase the tendency to falsely remember that it really occurred. We investigated this effect in Korsakoff's syndrome. METHOD: Our procedures consisted of 2 sessions and a recognition test. In Session 1, patients with Korsakoff's syndrome and controls listened to statements of actions (e.g., "hold the pen"), enacted the actions, or imagined performing the actions. In Session 2, participants imagined statements of actions from Session 1 as well as new statements of actions once or 3 times. On the recognition test, participants had to decide whether statements of actions were or were not enacted during Session 1. RESULTS: Analysis demonstrated that imagining performing the actions increased the tendency of both patients with Korsakoff's syndrome and controls to falsely recall the actions as having been enacted. DISCUSSION: Our findings suggest that patients with Korsakoff's syndrome are prone to the imagination inflation effect, an effect that can be attributed to difficulties with source monitoring. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

Wernicke-Korsakoff syndrome: Focus on low-threshold diagnosis and prompt treatment in the primary care setting.

The authors present the case of an inpatient hospitalized at the Veterans Affairs psychiatric unit diagnosed with Wernicke-Korsakoff syndrome to promote awareness of this prevalent yet often underdiagnosed and undertreated condition. Although Veterans present with a unique predisposition for alcohol abuse, it remains problematic in the general population as well. Analysis from 2000 to 2003 reveals alcohol use in the past month in Veterans at 56.6% and 50.8% in comparable non-Veterans. According to the National Survey on Drug Use and Health, it is estimated that of those who are 18 and older, 86.4% have used alcohol, 26.9% have engaged in binge drinking in the past month, 7% engaged in heavy alcohol use in the past month, and 6.2% (15.1 million) carried the diagnosis of alcohol use disorder., The lifetime prevalence of alcohol abuse in the general population is estimated to be between 4.5% and 13.2%. Primary care providers should maintain a high degree of vigilance in evaluating patients for timely diagnosis and prompt treatment of those suspected to have thiamine deficiency. Indeed, Wernicke's encephalopathy carries a significant level of morbidity and mortality associated with the syndrome, even in cases when it does not present with all of the classic signs. This article aims to raise the primary and ambulatory care provider's ability to recognize the condition, emphasize a low threshold to treat, and highlight current treatment recommendations.

Pellagra and Alcohol Dependence Syndrome: Findings From a Tertiary Care Addiction Treatment Centre in India.

AIM: To define the prevalence and clinical presentation of pellagra, a multi-systemic disease caused by the deficiency of niacin, in patients admitted to a tertiary addiction treatment centre in southern India, with alcohol dependence syndrome (ADS)-(ICD10). METHODS: Review of the health records of 2947 patients who received inpatient care for ADS between 2015 and 2017. RESULTS: Out of 2947, 31 (1%) were diagnosed with pellagra. Nearly two-thirds (64.5%) of those with pellagra were from a low-income group. Of the clinical-triad of pellagra, all patients had dermatitis, more than half (58%) had delirium, a minority (19%) had diarrhoea. Nearly two-thirds (61%) had presented in a complicated-withdrawal state. Associated conditions included peripheral neuropathy (32%); Wernicke's encephalopathy (26%); seizures (16%).Seventeen (54%) had BMI <18.5 kg/m2. Treatment was a high dose of parenteral vitamins including niacin (mean dose: 1500 mg/day) for an average of 7.5 days followed by oral multivitamin supplements. All had complete resolution of pellagrous symptoms by the end of the three weeks of inpatient care. CONCLUSIONS: Pellagra is an acute medical condition, frequently encountered in the context of alcohol dependence and poverty. It often presents with other disabling and life-threatening comorbidities like delirium tremens and Wernicke's encephalopathy. The classical triad of pellagra is only seen in a minority of cases. Thus a high index of suspicion is required lest pellagra may remain undiagnosed. Prompt identification and treatment with a high dose of niacin in combination with other vitamins result in complete recovery.

Preserved re-experience of discrete emotions: Amnesia and executive function.

Amnesic patients can re-experience emotions elicited by forgotten events, suggesting that brain systems for episodic and emotional memory are independent. However, the range of such emotional memories remains under-investigated (most studies employing just positive-negative emotion dyads), and executive function may also play a role in the re-experience of emotions. This is the first investigation of the intensity of the emotional re-experience of a range of discrete emotions (anger, fear, sadness, and happiness) for a group of amnesic patients. Twenty Korsakoff syndrome (KS) patients and 20 neurologically normal controls listened to four novel emotional vignettes selectively eliciting the four basic emotions. Emotional experience was measured using pen-and-paper Visual Analogue Mood Scales and episodic memory using verbal recollections. After 30 min, the recollection of stories was severely impaired for the patient group, but the emotional re-experience was no different from that of controls. Notably, there was no relationship between episodic recall and the intensity of the four emotions, such that even profoundly amnesic patients reported moderate levels of the target emotion. Exploratory analyses revealed negative correlations between the intensity of basic emotions and executive functions (e.g., cognitive flexibility and response inhibition) for controls but not patients. The results suggest that discrete emotions can be re-experienced independently of episodic memory, and that the re-experience of certain discrete emotions appears to be dampened by executive control. KS patients with absent or mild cognitive symptoms should benefit from emotion-regulation interventions aimed at reducing the recognized affective burden associated with their episodic memory deficit.

Visuospatial declarative learning despite profound verbal declarative amnesia in Korsakoff's syndrome.

Korsakoff's syndrome (KS) is a neuropsychiatric disorder characterised by severe amnesia. Although the presence of impairments in memory has long been acknowledged, there is a lack of knowledge about the precise characteristics of declarative memory capacities in order to implement memory rehabilitation. In this study, we investigated the extent to which patients diagnosed with KS have preserved declarative memory capacities in working memory, long-term memory encoding or long-term memory recall operations, and whether these capacities are most preserved for verbal or visuospatial content. The results of this study demonstrate that patients with KS have compromised declarative memory functioning on all memory indices. Performance was lowest for the encoding operation compared to the working memory and delayed recall operation. With respect to the content, visuospatial memory was relatively better preserved than verbal memory. All memory operations functioned suboptimally, although the most pronounced disturbance was found in verbal memory encoding. Based on the preserved declarative memory capacities in patients, visuospatial memory can form a more promising target for compensatory memory rehabilitation than verbal memory. It is therefore relevant to increase the number of spatial cues in memory rehabilitation for KS patients.

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

Beyond Thiamine: Treatment for Cognitive Impairment in Korsakoff's Syndrome.

BACKGROUND: Wernicke's encephalopathy is a condition whose treatment many consultation-liaison psychiatrists know quite well. Less clear, however, is the treatment of its dementia disorder descendent, the Korsakoff's syndrome (KS). OBJECTIVE: This article seeks to review treatment options and provide recommendations for consultation-liaison psychiatrists treating cognitive impairment in KS. METHODS: In this nonsystematic review, we reviewed PubMed, CINAHL Plus, and Google Scholar for published reports and studies regarding treatment of KS. RESULTS: The literature revealed case reports and placebo-controlled trials of various medications for treatment of KS, though the samples sizes were small and were mostly case reports. There is more attention devoted toward medications used in other dementia disorders, such as donepezil and memantine. The literature revealed more studies around behavioral interventions recommended for treatment of memory impairment in KS and they focused on cognitive remediation and environmental adaptation, such as the use of PDAs or alarms. CONCLUSIONS: There is no single, well-studied intervention proven effective as a primary treatment for cognitive impairment in KS. An approach of using environmental modifications in a well-structured living environment, combined with various cognitive interventions, such as pictorial associations, and perhaps a trial of donepezil or memantine, likely represents the best strategy for treating long-term cognitive impairment in KS.