Diagnosis Of Wernicke's Encephalopathy Research Articles

Wernicke Encephalopathy Caused by Avoidance-Restrictive Food Intake Disorder in a Child: A Case-Based Review.

Wernicke encephalopathy (WE) is an acute and potentially fatal neuropsychiatric disorder resulting from thiamine deficiency: its etiology and clinical presentation can be heterogeneous and arduously recognized, especially in children and adolescents. An 8-year-old girl arrived to the emergency room with ataxic gait, nystagmus, and mental confusion after a 10-day history of repeated severe vomiting; her recent clinical history was characterized by restricted nutrition due to a choking phobia, which caused substantial weight loss. Brain magnetic resonance imaging revealed a bilaterally increased T2 signal in the medial areas of the thalami and cerebral periaqueductal region. Diagnosis of WE based on clinical and neuroradiological findings was established and confirmed after labwork showing low serum thiamine. Following psychiatric evaluation, the patient was also diagnosed with avoidance-restrictive food intake disorder (ARFID), which required starting cognitive behavioral therapy and introducing aripiprazole. The patient displayed improvement of the radiological findings after one month and complete resolution of her neurological symptoms and signs. Eating disorders like ARFID might forerun acute signs of WE; this possibility should be considered even in pediatric patients, especially when atypical neurological pictures or feeding issues come out.

Bilateral hearing loss as the initial presentation of reversible Wernicke's encephalopathy with splenial lesion.

Wernicke's encephalopathy (WE) is an acute neurological syndrome resulting from thiamine (vitamin B1) deficiency. It has been recognized increasingly in non-alcoholic patients, such as in the condition of malnutrition. Recent literature has shed light on uncommon symptoms and neuroimaging findings. We reported a case of a 44-year-old male who initially presented with bilateral hearing loss, and exhibited abnormality in the splenium of the corpus callosum on magnetic resonance imaging(MRI) diffusion-weighted imaging sequence. On the following day the patient developed new symptoms, including unstable walking, double vision and hallucination. The subsequent brain MRI demonstrated lesions involving periaqueductal grey matter and bilateral medial thalamus, indicating the diagnosis of WE. Empirical treatment with intravenous thiamine resulted in complete clinical and radiological resolution. To the best of our knowledge, the current case is the first report of WE in literature with uncommon but reversible manifestations. This case warns us to maintain a heightened level of suspicion for WE in malnourished patients with neurological deficits, despite the possibility of atypical presentations encompassing bilateral hearing disturbances and unusual neuroradiological results. Early diagnosis and timely administration of thiamine in WE are likely to lead to a favorable outcome and full recovery.

Особенности диагностики энцефалопатии Вернике: клинический случай

Wernicke's encephalopathy (WE) is a rare neurological disorder caused by vitamin B1 (thiamine) deficiency and is associated with a significant risk of developing persistent neurological deficiency, chronification, disability and ultimately death if the aetiopathogenetic therapy with high doses of vitamin B1 is initiated late. Objective: to raise awareness among physicians about the characteristics of clinics, diagnostics and treatment of Wernicke's encephalopathy. Materials and methods. Retrospective analysis of the medical records of a patient with alcoholic Wernicke's encephalopathy. Results. This paper presents the own clinical observation of a patient with newly diagnosed alcoholic Wernicke's encephalopathy, clinical manifestations and MRI picture, describes the main features of aetiology and pathogenesis of this pathological process. Conclusion. An important role in the diagnosis of WE is played by the correct collection of anamnestic data and magnetic resonance imaging (MRI) of the brain, which has a sufficiently high specificity and is the only diagnostic method that allows this disease to be identified with high reliability. Thus, it is the thorough collection of anamnesis and the timely MRI examination that allow the doctor to point in the right direction of the diagnostic search in a timely manner.

Coordination and Cognition in Pure Nutritional Wernicke's Encephalopathy with Cerebellar Degeneration after COVID-19 Infection: A Unique Case Report.

Alcoholic cerebellar degeneration is a restricted form of cerebellar degeneration, clinically leading to an ataxia of stance and gait and occurring in the context of alcohol misuse in combination with malnutrition and thiamine depletion. However, a similar degeneration may also develop after non-alcoholic malnutrition, but evidence for a lasting ataxia of stance and gait and lasting abnormalities in the cerebellum is lacking in the few patients described with purely nutritional cerebellar degeneration (NCD). We present a case of a 46-year-old woman who developed NCD and Wernicke's encephalopathy (WE) due to COVID-19 and protracted vomiting, resulting in thiamine depletion. We present her clinical course over the first 6 months after the diagnosis of NCD and WE, with thorough neuropsychological and neurological examinations, standardized clinical observations, laboratory investigations, and repeated MRIs. We found a persistent ataxia of stance and gait and evidence for an irreversible restricted cerebellar degeneration. However, the initial cognitive impairments resolved. Our study shows that NCD without involvement of alcohol neurotoxicity and with a characteristic ataxia of stance and gait exists and may be irreversible. We did not find any evidence for lasting cognitive abnormalities or a cerebellar cognitive-affective syndrome (CCAS) in this patient.

500: DIAGNOSIS OF WERNICKE ENCEPHALOPATHY IN A PATIENT WITH UNDERLYING PSYCHIATRIC ILLNESS

Introduction: Wernicke’s encephalopathy (WE) is an acute neuropsychiatric syndrome caused by thiamine deficiency. Common causes include alcohol use, bariatric surgery, and hemodialysis. Description: Our case involves a 65-year-old female who initially presented with seizure-like activity. Subsequent presentations over months included dysphagia, behavioral changes, and confusion. Initial workup with EEG, CT head, MRI brain, CT soft tissue neck, and endoscopy was unremarkable. Further history revealed that after her mother’s death four months prior, she began to self-isolate and reduce oral intake. Patient was evaluated by psychiatry and was diagnosed with conversion disorder. The clinical course was complicated by worsening neurological symptoms and respiratory distress requiring mechanical ventilation. Repeat MRI brain showed increased T2 FLAIR signal in the periaqueductal gray matter and along the dorsomedial thalamus consistent with WE. Patient was started on thiamine and showed symptomatic improvement. Discussion: WE is a triad of oculomotor dysfunction, ataxia, and confusion. In an observational study by Chamorro et al, 92.7% of cases were due to excessive alcohol intake, 47.1% due to malnutrition, and 5.9% due to psychiatric illness. The diagnosis of WE is primarily clinical, yet the classic triad is reported in only 10% of cases. The most consistent characteristic is a change in mental status. Caine et al developed the clinical diagnostic criteria, which include dietary deficiencies, oculomotor abnormalities, cerebellar dysfunction, and altered mentation or mild memory impairment. A case series based on this criteria found that clinical features of WE vary between alcohol and non–alcohol-related etiologies. The classic triad was more common in alcoholics than in non-alcoholics. One of the main challenges is the rate of underdiagnosis, which can be due to a lack of clinical suspicion or atypical presentation. Hence, MRI is a useful test to support the diagnosis of WE with a sensitivity of 53% and specificity of 93%. MRI may demonstrate lesions with increased symmetrical signal intensity in the periaqueductal region, medullary bodies, medial thalami, and the tectum of the midbrain. Diagnosis of WE should be considered in patients with psychiatric illnesses and atypical neurologic presentation.

Is there a time window for MRI in Wernicke encephalopathy - a decade of experience from a tertiary hospital.

Wernicke encephalopathy (WE) is a neuropsychiatric syndrome caused by thiamine deficiency. Despite its low sensitivity, brain magnetic resonance imaging (MRI) is the most useful diagnostic technique. Our aim was to investigate whether the timing of the imaging study, and thiamine replacement can influence brain MRI findings in these patients. Retrospective observational study of hospitalized patients between January/2008 and December/2020 with a clinical diagnosis of WE. Data from clinical presentation, diagnostic features, therapeutic approach, and outcomes were collected. We identified 41 patients (55 ± 13.3years) with WE. Brain MRI was performed in 36 patients, and one third had T2/FLAIR hyperintensities suggestive of WE. We found an association between a history of poor diet and periventricular hyperintensities (p = 0.023), especially on the ventral surface of the thalamus and the periaqueductal region. It was found that the odds of having a typical imaging of WE decreased by 5.3% for each additional unit (100mg) of thiamine administered (p = 0.046)(95% CI [0.89, 0.99]). On the other hand, the number of days from clinical presentation was not found to be a viable predictor (p = 0.254) (95% CI [0.88, 1.03]) Recovery was positively correlated with the total dose of thiamine received until discharge (p = 0.020). MRI hyperintensities seem to be dependent on the timing of thiamine correction and, particularly, on the thiamine dosage prescribed at admission. Nevertheless, thiamine replacement should not be delayed, as its timely prescription is associated with a better prognosis at discharge.

Bilateral papilledema with vision loss due to post–COVID-19–induced thiamine deficiency: illustrative case

BACKGROUNDBilateral papilledema with vision loss is considered a neurosurgical emergency due to high intracranial pressure. However, it may not be the only cause of papilledema. The authors reported an association among coronavirus disease 2019 (COVID-19), bilateral papilledema, blindness, and Wernicke’s encephalopathy (WE).OBSERVATIONSAn 18-year-old woman presented to the neurosurgery service with rapid profound vision loss and bilateral papilledema. She had COVID-19 3 months earlier with subsequent loss of smell (anosmia) and taste (ageusia), which resulted in hyperemesis and a 43-lb weight loss. Examination revealed ataxia, horizontal nystagmus, and blindness. Magnetic resonance imaging and magnetic resonance venography of her brain were normal. Presumptive diagnosis of WE was made, and she was treated with intravenous thiamine with restoration of vision within 48 hours. Patient’s thiamine level was less than half the normal value.LESSONSNeurosurgeons should be aware of this unique correlation between papilledema and vision loss and its association with WE due to post–COVID-19 hyperemesis and weight loss from anosmia and ageusia.

Wernicke encephalopathy with epileptic seizures during pregnancy

ABSTRACT A 22-year-old woman was admitted to the emergency department with headache, dizziness, and numbness on the left side of the body. Neurologic examination revealed gaze-evoked nystagmus. Cranial magnetic resonance imaging, venous and arterial magnetic resonance angiography were normal. Generalized epileptogenic activity was observed in the electroencephalography. The erythrocyte thiamine transketolase levels were found to be 13 u/L. She received intravenous thiamine. On discharge, she had no neurologic sequelae. The diagnosis of Wernicke encephalopathy in our patient is based on increased thiamine requirement due to pregnancy, nystagmus, low transketolase level, and reversal of symptoms after thiamine replacement. .

Fedratinib Does Not Inhibit Thiamine Uptake or Induce Experimental Wernicke's Encephalopathy in Nonclinical Studies

Introduction:Despite compelling efficacy data from Phase II and Phase III trials, clinical development of fedratinib was halted in 2013 after 8 of 670 treated patients presented with neurological symptoms suggestive of Wernicke's encephalopathy (WE). WE is a neurological disorder that develops due to thiamine deficiency that is treated or prevented simply by using thiamine supplementation. Autopsy studies indicate WE has a prevalence between 0.8-2.8% in the general population with a higher rate in MPN and cancer patients. Confirming a diagnosis of WE is complicated by comorbidities in patients with myeloproliferative neoplasms (MPN) including a high incidence of stroke, hepatic encephalopathy secondary to hepatic extramedullary hematopoiesis or sepsis related to marrow failure in an elderly population. Analysis of patients in fedratinib trials by a panel of neurology and neuroradiology experts indicates that between 1-5 patients of 670 treated experienced WE, less than what might be expected based on historical norms.WE is commonly caused by either poor nutritional status or chronic alcohol use. The most common non-hematological adverse events for fedratinib are nausea, vomiting and diarrhea, suggesting they may be exacerbating factors for malnutrition in patients. Nonetheless, inhibition of thiamine transporter (THTR) has been proposed as a putative mechanism based on Caco-2 studies. Interpretation of data from these studies is complicated based on use of protein-free culture medias that don't replicate protein binding of drug in patients (96% protein bound) and for which the drug is sparingly soluble. No CNS lesions that would be predictive of WE were reported in the IND-enabling toxicology studies with fedratinib, but subtle neurological signs or histology signs may not be clear to non-experts.To evaluate the potential of fedratinib to inhibit thiamine uptake, thiamine transporter studies were run using previously published methods with Caco-2 cells that overexpress thiamine transporters with the significant exception that they were performed using human FBS rather than cell culture media. This addresses concerns about protein binding, solubility and replicates conditions experienced by patients. Further, to evaluate the potential of fedratinib to induce WE non-clinically, rats were dosed orally with 40 mg/kg fedratinib (140% of 500 mg patient dose by allometric scaling) daily for 28 days with careful monitoring of neurological signs of disease followed by evaluation of brains for any signs of lesions consistent with WE.Results:Fedratinib had no effect on THTR-1 at concentrations up to 30 µM (6-12X higher than Cmax at highest dose of drug). Fedratinib IC50 against THTR-2 was >30 µM. This indicates that fedratinib does not inhibit either thiamine transporter at plasma concentration achievable in patients. This is consistent with patient data in which plasma thiamine levels were normal for the 161 patients sampled at end of treatment in the fedratinib clinical studies.In rats dosed orally with 40 mg/kg fedratinib for 28 days, there was no observed ataxia, opisthotonus, nystagmus, loss of righting reflex or any other overt neurological signs of thiamine deficiency. Examination of the brains of these animals found no lesions consistent with focal damage to vulnerable areas of brain, e.g. thalamus, inferior colliculus or brainstem. There was no difference in weight gain in these animals compared to control animals. This data indicates that at doses comparable or higher than the highest fedratinib dose used in phase III studies, there is no nonclinical evidence that fedratinib induces thiamine deficient disease.Conclusion:Transporter studies performed in the presence of human serum indicate that fedratinib does not inhibit thiamine transport at clinically achievable concentrations. This is consistent with plasma thiamine data available from patients. Rodent studies indicate that fedratinib does not induce thiamine deficient disease when administered orally at clinically relevant concentrations. Notably, rats are incapable of emesis, so this model doesn't account for effects of gastric distress. In total, these data suggest that fedratinib does not increase the risk of thiamine deficiency, beyond its potential to exacerbate malnutrition through poor management of preventable GI adverse events. DisclosuresHood:Impact Biomedicines, Inc.: Employment, Equity Ownership. Hazell:Impact Biomedicines, Inc.: Research Funding; University of Montreal Neurosciences: Employment.

Case Series of Potential Wernicke's Encephalopathy in Patients Treated with Fedratinib

Introduction:In the phase III study, JAKARTA I, the JAK2 inhibitor, fedratinib, elicited responses in 47% (400mg) and 50% (500mg) of patients with intermediate 2 or high risk myelofibrosis (MF). In JAKARTA II, 53% of MF patients who were resistant and 63% of patients who were intolerant to ruxolitinib responded to fedratinib, indicative of clinical benefit for the majority of patients not responding to standard therapy. Fedratinib development was discontinued after the FDA placed a clinical hold on November 15, 2013 as a result of neurological symptoms, suggestive of Wernicke's encephalopathy (WE) in 8 of 670 subjects, exposed to fedratinib.WE develops in the setting of thiamine deficiency and is typified by diplopia, ataxia, confusion and characteristic brain MRI findings. Confirming a diagnosis of WE is complicated by comorbidities in patients with myeloproliferative neoplasms (MPN) including a high incidence of stroke, hepatic encephalopathy secondary to hepatic extramedullary hematopoiesis or sepsis related to marrow failure in an elderly population. While autopsy studies indicate that rates of WE range from 0.8-2.8% of the general population, the incidence in MPN patients is reportedly 3-fold higher. WE can be diagnosed based on clinical signs and specific MRI findings; prevented by ensuring that nutritional status is not exacerbated by nausea and vomiting; and treated with thiamine.To evaluate the epidemiology of potential WE subjects treated with fedratinib, we conducted a retrospective analysis of the 8 fedratinib-treated subjects. Patient demographics, clinical signs together with thiamine levels, when available, and MRI scans were evaluated to determine the likelihood of WE and elucidate contributory factors by an independent expert panel.Results:Eight patients (1 male, 7 females) from 7 countries and 5 fedratinib trials were identified. Median age was 69.1 years (IQR 67-71). Of these patients, 6 had MF, 1 had polycythemia vera and 1 had metastatic head and neck cancer. Based on retrospective analysis of clinical reports, thiamine levels and MRI results the data was either inconclusive or not supportive of WE in three patients, one of which likely had hepatic encephalopathy. Of the remaining 5 patients, 1 clearly had WE, 2 likely had WE, and 2 had inconclusive diagnosis. All potential WE patients had preceding protracted nausea and vomiting suggesting this as a contributing factor to malnutrition and thiamine deficiency.Concerning the 3 subjects thought to have WE: one was severely malnourished and refused gastrostomy during study suggesting malnutrition as a cause of thiamine deficiency. The two other likely WE patients had preceding sustained nausea and vomiting with recovery from neurological deficits while continuing fedratinib treatment suggesting fedratinib did not inhibit thiamine uptake. Consistent with that, mean patient thiamine levels from 161 patients available at end of treatment were normal and in vitro experiments in the presence of human serum show fedratinib at physiologically achievable levels does not inhibit thiamine transport.The two other patients that may have had WE had preceding nausea and vomiting; one developed neurological symptoms while not on drug and the other developed disseminated metastases, including an edematous brain metastases, preceding neurological symptoms confounding the diagnosis.Conclusion:Across 9 fedratinib trials enrolling 670 MPN or solid tumor patients between 3 to 5 patients experienced WE (0.4-0.7%). The overall prevalence of WE observed was less than published levels for a patient population of this size. For the 5 potential WE patients, one subject had malnutrition related to protracted nausea and vomiting as well as clinical signs and MRI findings consistent with WE. Additionally, 2 other subjects likely experienced WE, both of which recovered without a dose interruption suggesting fedratinib does not inhibit thiamine absorption. The remaining 2 had an unclear diagnosis with 2 of 3 experts believing the data were either inconclusive or not supportive of WE. Notably, one of the patients was not on fedratinib at the time of neurological symptoms. In total, these data suggest that fedratinib does not increase the risk of thiamine deficiency beyond its potential to exacerbate malnutrition through poor management of preventable GI adverse events. DisclosuresHarrison:Novartis: Honoraria, Research Funding, Speakers Bureau; Gilead: Consultancy, Speakers Bureau; Shire: Speakers Bureau; Celgene: Consultancy; CTI: Speakers Bureau. Mesa:Galena Biopharma, Inc.: Consultancy; Promedico: Research Funding; Novartis Pharmaceuticals Corporation: Consultancy; Celgene Corporation: Research Funding; CTI BioPharma Corp.: Research Funding; Gilead Sciences, Inc.: Research Funding; Incyte Corporation: Research Funding; Ariad: Consultancy. Hood:Impact Biomedicines, Inc.: Employment, Equity Ownership. Bykowski:Impact Biomedicines, Inc.: Consultancy, Honoraria. Zuccoli:Impact Biomedicines, Inc.: Consultancy, Honoraria. Brewer:Elan: Other: Advisory Board; Bristol-Myers Squibb: Other: Advisory Board; Avanir: Other: Advisory Board; Novartis: Other: Advisory Board; Genentech: Other: Advisory Board; Eli Lilly: Other: Advisory Board; CorTechs Labs, Inc.: Equity Ownership; Human Longevity, Inc.: Equity Ownership.

Reversible Wernicke encephalopathy caused by hyperemesis gravidarum in the second trimester of pregnancy: a case report

Wernicke encephalopathy is a potentially life-threatening neurologic syndrome caused by acute thiamine (vitamin B1) deficiency. It is usually associated with excessive alcohol consumption. Less frequently, this syndrome can be caused by persistent vomiting. This is a case report of a 33-year-old woman diagnosed with Wernicke encephalopathy (WE) during the second trimester of pregnancy. The presence of neurological and ophthalmological symptoms in the context of hyperemesis gravidarum led us to evoke the diagnosis of WE, and it was confirmed when specific lesions were found in the brain magnetic resonance imaging (MRI). Luckily for our patient, WE was diagnosed promptly and the signs were reversible after thiamine supplementation. In conclusion, any first line care taker or midwife must know the symptoms of Wernicke encephalopathy because prompt diagnosis and treatment can lead to recovery

Wernicke's encephalopathy in a child with abdominal tuberculosis

Wernicke's encephalopathy (WE) is an acute neurological disorder, potentially fatal if untreated, caused by thiamine deficiency. A 15-year-old female patient with choledocholithiasis, cholecystitis and abdominal tuberculosis on antitubercular therapy presented with poor oral intake, bilious vomiting and encephalopathy. A prompt diagnosis of WE was made and confirmed by brain magnetic resonance imaging. The patient recovered completely after the administration of thiamine.

Anesthetic management of a parturient with Wernicke's encephalopathy secondary to hyperemesis gravidarum for cesarean section

Wernicke's encephalopathy (WE) secondary to hyperemesis gravidarum (HG) is a rare but a known complication. A delay in diagnosis and treatment often results in long-term neurological sequelae. Critical care management of these patients is reported in the literature, but their anesthetic management for cesarean section is lacking. We report the case of a 28-year-old parturient who presented with HG in the first trimester of pregnancy and was managed conservatively. She later developed nystagmus, weakness, and cognitive dysfunction, and a diagnosis of WE secondary to HG was established. The patient was later posted for cesarean section in view of persistent quadriparesis and cognitive impairment at term gestation. General anesthesia was the preferred anesthesia technique of choice. Obstetric patients with preexisting neurological disease for cesarean section become a special subpopulation for anesthesiologists with their unique anesthetic challenges.

Thiamine Dosing for the Treatment of Alcohol-Induced Wernicke's Encephalopathy: A Review of the Literature.

Objective: To determine the most appropriate thiamine replacement regimen by evaluating safety and efficacy of the drug specific to alcohol-induced Wernicke's encephalopathy (WE). Data Sources: A comprehensive literature search was conducted using PubMed, MEDLINE, Scopus, and ProQuest between January and August 2020 using the following keyword and Boolean search terminology: "thiamine" AND "alcohol" AND (encephalopathy OR korsakoff). Study Selection and Data Extraction: Randomized control trials; prospective, observational, and retrospective cohort analyses; and case reports and series were included in this evaluation. A confirmed diagnosis of alcohol-induced WE and treatment with parenteral or intramuscular (IM) thiamine were required for inclusion. Data Synthesis: Six publications composed of 138 patients were evaluated in this review, in which a wide variety of thiamine supplementation strategies were employed. Clinical diagnostic criteria varied significantly between publications. Doses ranged from 100 to 1500 mg intravenous thiamine and up to 300 mg IM thiamine, with no apparent difference in patient outcomes. All patients who received thiamine experienced symptom improvement, and adverse drug events were minimal. Conclusions: Despite the clinical controversy regarding the appropriate thiamine supplementation regimen, the heterogeneity of published works combined with symptom resolution across the gamut of dosing strategies makes a definitive consensus elusive. Clinicians should continue to provide parenteral or IM thiamine in doses of ≥100 mg to patients with confirmed alcohol-induced WE.

Comprehensive review of Wernicke encephalopathy: pathophysiology, clinical symptoms and imaging findings.

Wernicke's encephalopathy (WE) is a severe and life-threatening illness resulting from vitamin B1 (thiamine) deficiency. The prevalence of WE has been estimated from 0.4 to 2.8%. If not treated properly, severe neurologic disorders such as Korsakoff psychosis and even death may occur. The classical triad of clinical symptoms (abnormal mental state, ataxia, and ophthalmoplegia) is found in only 16-33% of patients on initial examination. The originally described underlying condition of WE is alcoholism, but it accounts for about 50% of causes of WE. Nonalcoholic patients are also affected by WE and likely to present symptoms and radiological imaging findings different from patients with alcoholism, which further complicates the diagnosis of WE. Being familiar with predisposing causes, symptoms and radiological imaging findings of WE is important for radiologists and clinicians when making the diagnosis to start immediate treatment. This review discusses pathophysiologies, underlying causes, clinical symptoms, imaging findings and their mimics.

SUN-596 A Rare Presentation of Early Onset Wernicke Encephalopathy Following Sleeve Gastrectomy

Background: Wernicke encephalopathy (WE) has been reported after malabsorptive bariatric surgeries but is an uncommon complication of sleeve gastrectomy. Since 2011, the number of patients receiving a sleeve gastrectomy has tripled, with almost 60% of patients undergoing bariatric surgery receiving a sleeve gastrectomy in 2017 (1). We present a case of WE in a young woman as a rare and early complication of sleeve gastrectomy. Clinical Case: A 32-year old female with a past medical history significant for hypertension, pseudotumor cerebri, and morbid obesity status post sleeve gastrectomy two months prior presented to the emergency department with complaints of blurry vision and lower extremity numbness. Physical examination showed sluggish light reflex and decreased extraocular movements. Given history of pseudotumor cerebri, patient underwent a therapeutic lumbar puncture with removal of 13 ml of CSF. Opening pressure was 20 cm of water and patient experienced no relief of her symptoms. Ophthalmology consult did not offer an explanation for the blurry vision. MRI-brain with and without contrast showed findings highly suggestive of WE. It showed faint linear symmetric hyperintensities along the bilateral mesial thalamus, dorsal midbrain and periaqueductal gray matter, which were determined to be acute in nature in comparison with a MRI performed three weeks prior. Upon further investigation, thiamine level was low at 43.6 nmol/L [66.5 – 200] confirming the diagnosis of WE. Thiamine supplementation was started immediately and patient reported improvement of her vision the next day with return to baseline in 3 days. Conclusion: There have been a handful of cases of WE reported in literature as a complication of sleeve gastrectomy. Zheng, L also reported a case of WE 7 weeks after sleeve gastrectomy (2). Although sleeve gastrectomy does not directly affect the primary absorptive pathway of thiamine in the gastrointestinal tract, it is imperative to consider WE in patients presenting with suspicious neurologic symptoms after a recent sleeve gastrectomy. WE was suspected in our case due to typical MRI findings and neurological presentation after bariatric surgery, which was later confirmed by low serum thiamine level. Early detection and thiamine supplementation resulted in complete reversal of symptoms in our patient. WE is a rare but severe and preventable consequence of bariatric surgery that warrants attention given its rapid onset and detrimental course. Reference: (1) Estimate of Bariatric Surgery Numbers, 2011-2017. (2018, June 26). Retrieved from https://asmbs.org/resources/estimate-of-bariatric-surgery-numbers. (2) Zheng, L. (2016).Wernicke Encephalopathy and Sleeve Gastrectomy. American Journal of Therapeutics, 23(6).

Wernicke's encephalopathy due to malnutrition and parenteral nutrition in a patient with cerebral infarction

Introduction:Wernicke's encephalopathy (WE) is a severe neuropsychiatric disorder, which results from a nutritional deficiency of thiamine. The occurrence of WE is rarely reported in patients with cerebral infarction, who often have complications of malnutrition. Cerebral infarction is a neurological disease, patients with cerebral infarction may show symptoms such as disturbance of consciousness and gait instability, which is difficult to differentiate from WE. Thus, early recognition and differential diagnosis of WE are important. We report a rare case of cerebral infarction patient who developed WE due to malnutrition and parenteral nutrition.Patient concerns:A 65-year-old woman was admitted to our hospital with cerebral infarction. She had lost 15 kg of weight in the past month or so and was diagnosed with malnutrition. In order to correct malnutrition, parenteral nutrition and intravenous glucose without thiamine were administered. Cognitive dysfunction, laloplegia, sleep rhythm inversion, somnolence and bilateral lower limbs weakness were presented 20 days after admission.Diagnosis:Brain magnetic resonance imaging confirmed the diagnosis of WE.Interventions:The patient was given thiamine and nutrition support therapy.Outcomes:The patient's cognitive impairment, laloplegia and sleep condition improved within 4 days. Neurological status continued to improve and physical activity recovered gradually within 2 weeks. She received rehabilitation training when her condition was relatively stable, and her muscle strength of limbs and physical function gradually improved.Conclusion:Infarction-related malnutrition may result in nutrient deficiency-related neurological complications, such as WE. Thus, it is important to pay close attention to the nutritional status of patients with cerebral infarction. In addition, early recognition and differential diagnosis of WE in patients with infarction-related malnutrition are necessary, early treatment of replete thiamine supplementation and nutrition support therapy can reduce the risk of WE and improve the prognosis.

Triad of Wernicke's Encephalopathy in an Alcohol Withdrawal Patient - A Case Report

Wernicke’s encephalopathy (WE) is an acute neurological condition with psychiatric manifestations characterized by the classic triad of confusion, ophthalmoplegia and ataxia. The presence of all features of the classic triad in one patient is uncommon and not present in up to 90% of patients with WE. Early diagnosis and management of WE is important for better outcome and improved quality of life in these patients. This case reports a rare presentation of all the symptoms of the triad of WE in one patient with Alcohol Dependence Syndrome.

WERNICKE ENCEPHALOPATHY AFTER GASTRIC BYPASS: A SURPRISING ETIOLOGY OF ALTERED MENTAL STATUS PROGRESSING TO CARDIAC ARREST

SESSION TITLE: Wednesday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/23/2019 09:45 AM - 10:45 AM INTRODUCTION: Wernicke’s Encephalopathy (WE) after bariatric surgery is more frequent than commonly understood. Doctors and patients must be aware of the risk and predisposing factors for WE to effectively prevent this potentially fatal condition. In this case, we present a patient with a late diagnosis of WE, with altered mental status resulting in eventual cardiac arrest and intubation. CASE PRESENTATION: A 63-year-old woman was brought to the ED after being found at home confused. She had no history of alcohol use. She exhibited disconjugate gaze and mental slowing, but was otherwise neurologically intact. CT brain demonstrated no acute changes and labs were normal. The patient had a sleeve gastrectomy 2 months prior, and a history of depression and anxiety. Family reported that following bariatric surgery she had poor oral intake and frequent vomiting. She was admitted for confusion and dehydration, and diagnosed with a UTI. She remained altered and on hospital day 9 the patient suffered a cardiac arrest of unclear etiology and CPR was started. She was intubated and transferred to the ICU, where she remained minimally responsive for several days. A brain MRI then demonstrated evidence of WE, specifically T2 FLAIR hyperintense signal abnormalities involving the mammillary bodies, medial thalami, periaqueductal area, and around the third ventricle. Intravenous thiamine was started immediately. Over the next few days, her mental status slowly began to recover. DISCUSSION: WE is primarily associated with malnutrition and chronic alcohol use, however hyperemesis gravidarum or bariatric surgery recovery can also produce the syndrome. Patients who undergo bariatric surgery are at risk of multiple vitamin deficiencies; B1 deficiency is common enough to have garnered the nickname “bariatric beriberi”. The classic triad for WE consists of ataxia, nystagmus, and confusion. The underlying pathophysiology is related to severe thiamine deficiency, and symptoms can be precipitated by glucose loading causing lactic acidosis in the medial thalamus resulting in neuronal damage. In a 2008 review of 84 existing cases, 94% occurred within the first 6 months post-surgery. As with our patient, MRI revealed lesions in 47% of patients. In 2007, another review found WE was most likely to occur between 4 and 12 weeks after surgery; our patient presented with symptoms at 8 weeks post-surgery. A case series from Southern Europe reported a preventive intervention after biliopancreatic diversion; no WE cases were observed after initiating administration of large doses of thiamine to patients reporting small food intakes during early postoperative weeks. CONCLUSIONS: Our patient’s altered mentation seems to have begun after diminishing PO intake for days at home. Given the risk for WE with progression to severe altered mental status, providers should consider thiamine deficiency in altered patients with recent bariatric surgeries. Reference #1: Aasheim ET. Wernicke Encephalopathy After Bariatric Surgery. Annals of Surgery. 2008;248(5):714-720. https://doi.org/10.1097/SLA.0b013e3181884308. Reference #2: Sonal S, Abhay K. Wernicke encephalopathy after obesity surgery Neurology Mar 2007, 68 (11) 807-811; https://doi.org/10.1212/01.wnl.0000256812.29648.86 DISCLOSURES: No relevant relationships by Mitchell Brown, source=Web Response No relevant relationships by Amy Wolfe, source=Web Response

Four Cases of Wernicke's Encephalopathy Following Hematopoietic Stem Cell Transplantation

To make through introduction of Wernicke's encephalopathy (WE) following hematopoietic stem cell transplantation (HSCT) in terms of clinical characteristics, diagnostic process and treatment. The clinical charactaristics, diagnostic and therapeutic process and prognostic follow-up in 4 patients diagnosed of WE following HSCT between January 2016 to January 2017 at Department of Hematology, Chinese Aerospace Center Hospital were retrospectively analyzed. Four patients included 2 ALL and 2 AML, and 3 males and 1 female, their age ranged from 8 to 20 years old. 4 patients accouted for about 3% of all petients who received HSCT at that time. Typical triad syndrome consisting of ocular motility disorders, ataxia, global confusion was seen in only 1 patient. However, confusion and heterophthongia as onset of this complication were seen in all patients. Cerebral computed tomograph scan was universally unremarkable and useless. Cerebral MRI scan disclosed that typical involvement including thalamus, fourth ventricle, third ventricle, middle cerebral aqueduct was seen in 3, while untypical site including mamillary body was in the remaining 1 patient. All received vitamin B1 supplement therapy by intramuscular injection at a dose of 100 mg each day. Initial response was observed at 2, unknown, 3, 4 days after treatment and all obtained complete remission within 2 weeks without any event of relapse after median follow-up period of 8 (7-12) months. Any recipient of HSCT with clinical signs or symptoms of central nervous system should receive vitamin B1 supplementary therapy immediately to decrease risk of mortality of WE even if the diagnosis of WE is uncertain.