Presentation of Wernicke encephalopathy in patient secondary to one anastomosis gastric bypass. Case report and literature review.

Wernicke encephalopathy, which is caused by a thiamine deficiency, occurs in 0.8-2% of the population. Only 16% present the typical triad of this disease: nystagmus, confusion and ataxia. We present the case of a postoperative patient with a one anastomosis gastric bypass with reoperation undergoing a Roux-en-Y gastric bypass that begins with confusion and nystagmus on her third postoperative day. The diagnosis of Wernicke encephalopathy is made by imaging, and vitamin B1 is administered with total improvement of nystagmus and altered state of consciousness (lethargy, bradypsychia, bradylalia).

La encefalopatía de Wernicke se produce por una deficiencia de tiamina se presenta en un 0.8-2% de la población. Solo el 16% de los casos presentan la tríada típica de esta enfermedad: nistagmo, confusión y ataxia. Presentamos el caso de una paciente operada de bypass gástrico de una anastomosis con reintervención convirtiendo a bypass gástrico en Y de Roux que en su tercer día de posoperatorio comienza con confusión y nistagmo. Se realiza por imagen el diagnóstico de encefalopatía de Wernicke se administra vitamina B1 con mejoría total del nistagmo y alteración del estado de consciencia (letargia, bradipsiquia, bradilalia).

Atypical Wernicke's encephalopathy without mental status changes following bariatric surgery in an adolescent patient.

Morbid obesity is a systemic disease which can result in chronic complications, including hypertension, diabetes mellitus, depression, osteoarthritis and low self-esteem in the adolescent population.Bariatric surgery can be indicated to treat more severe forms of obesity, but these procedures are not without long-term risks. Therefore, adequate preoperative and postoperative care, which includes preoperative psychosocial evaluation for compliance, ongoing nutrition counselling and vitamin and micronutrient supplementation, is required for all patients, especially adolescent patients, who generally may not comply with medical therapies and/or be able to developmentally fully appreciate or comprehend the health consequences of their behaviours, prior to as well as after bariatric surgery to prevent complications.Thiamine pyrophosphate, an active form of thiamine (also known as vitamin B1, a water-soluble vitamin), which functions as a coenzyme in glucose and energy metabolism, is one such vitamin that requires supplementation postoperatively. It is mandatory for glucose to be administered concomitantly with thiamine, as glucose alone can precipitate Wernicke's encephalopathy (WE) in thiamine-deficient individuals. WE is a medical emergency, with a mortality rate of up to 20%. WE is best understood as a classic triad of mental confusion, gait ataxia and eye movement abnormalities, and atypical WE or Wernicke's syndrome (WS) is seen when the classic triad is not present. Cases that meet some, but do not necessarily meet all three criteria, are referred to as atypical WE or WS which can lead to delayed diagnosis. Atypical WE has an incidence of 19% which can lead to misdiagnosis of a preventable medical emergency with fatal complications.The following case reviews the consequences of post-bariatric thiamine supplementation therapy non-adherence and resulting in a deficiency in an adolescent patient.

Infrequent but serious? Beriberi And Thiamine deficiency among adolescents and young adults after bariatric surgery.

BACKGROUND: Thiamine deficiency (TD) among adolescents following metabolic and bariatric surgery (MBS) has not been assessed. OBJECTIVE: We assessed TD among adolescents following MBS. SETTING: University Hospital. METHODS: A retrospective chart review was conducted for all adolescents and young adults (aged 10-25 years) who had MBS and subsequently presented with TD at our institution (n = 30). Diagnosis used clinical, laboratory, brain imaging, and neurophysiology criteria. Of 1575 patients, 7 subsequently had TD. Another 23 adolescents had MBS at private hospitals or overseas and presented at our institution with TD. RESULTS: Based on MBS undertaken at our institution, TD prevalence was .45 cases per 100 MBS. The mean age of patients was 19.5 ± 3.23 years, 53.3% were male, 96.7% had sleeve gastrectomy, and time from MBS to admission averaged 4.97 ± 11.94 months. Mean weight loss from surgery to admission was 33.68 ± 10.90 kg. Associated factors included poor oral intake (90%), nausea and vomiting (80%), and noncompliance with multivitamins (71%). Signs and symptoms included generalized weakness, nystagmus, numbness, and paraparesis (83.3%-80%). Seven patients had Wernicke encephalopathy full triad; 16 displayed a mixed picture of Wernicke encephalopathy and dry beriberi; and there were no cases of wet beriberi. Half the patients achieved complete resolution of symptoms, whereas 47% and 40% had residual weakness or persistent sensory symptoms, respectively. There was no mortality. Most common concurrent nutritional deficiencies were of vitamins K, D, and A. CONCLUSIONS: This is the first in-depth study of TD among adolescents after MBS. Although TD is uncommon among adolescents after MBS, it is serious, requiring diligent suspicion and prompt treatment. Bariatric teams should emphasize compliance with multivitamin regimens and follow it up.

Diplopia after Sleeve Gastrectomy: The Canary in the Coal Mine.

Wernicke's encephalopathy (WE) is a neurologic emergency requiring timely intravenous thiamine supplementation to prevent permanent neurologic deficits. Historically, the WE diagnosis was limited to individuals with alcohol use disorder. However, it is now widely recognized to occur in patients who are chronically malnourished, post-bariatric surgery, pregnant with hyperemesis gravidarum, and with severe anorexia nervosa. Here we present a young woman who developed WE after undergoing a recent sleeve gastrectomy followed by protracted emesis for several days. This case underscores the importance of performing a thorough neurological review of systems and physical exam in high-risk patients and having a low clinical threshold to initiate appropriate thiamine treatment.

Non-alcoholic Wernicke's Encephalopathy mimicking neuromyelitis optica spectrum disorder in a young woman: a case report and literature review.

Wernicke's encephalopathy is an under-recognized life-threatening disease caused by thiamine (vitamin B1) deficiency. It has historically been related to chronic alcoholic intake but other causes of malnutrition, such as invasive gastric surgery and hyperemesis, have been linked to the onset of this illness over the years, often presenting with atypical clinical manifestations.  Herein we report a case of a young obese woman affected by non-alcoholic Wernicke's Encephalopathy following a minimally invasive gastrointestinal surgery. She showed an unusual clinical profile characterized by prominent subacute neuro-ophthalmological involvement which combined to her juvenile age, overweight condition and brain lesions, have made diagnosis challenging due to similarities with Neuromyelitis Optica Spectrum Disorder.   Our case underscores the relevance of prompt diagnosis in order to prevent the development of irreversible neuropathological changes and to avoid the use of a long-term immunosuppressive treatment.

A Case of Wernicke's Encephalopathy After Sleeve Gastrectomy.

BACKGROUND: Wernicke's encephalopathy, resulting from thiamine deficiency, is a rare but serious neurological complication of bariatric procedures. A clinical and radiologic diagnosis is often difficult, and thiamine blood tests are not broadly available. Only a few cases of Wernicke's encephalopathy after sleeve gastrectomy have been reported in the literature, nonetheless, subjects can be underdiagnosed, and their cases can be underreported. CASE PRESENTATION: We present the case of a 20-year-old female patient who developed Wernicke's encephalopathy after sleeve gastrectomy for grade II obesity with metabolic complications. She was presented to the Emergency Department showing confusion, gait ataxia and horizontal nystagmus two months after surgery. Persistent vomiting and lack of compliance with vitamin intake were reported. Cerebral MRI showed acute bilateral lesions in the periaqueductal and periventricular regions. Parenteral thiamine supplementation was administered, obtaining a progressive resolution of altered mental status, motor ataxia, and nystagmus. She was discharged on oral thiamine supplementation and underwent a multidisciplinary rehabilitation program, since anterograde, retrograde, and working memory impairment persisted. After a 2-year follow-up, she was compliant with a balanced fractionated diet and vitamin supplementation. A new cerebral MRI showed regression of the neuroradiological findings, but minimal memory impairment remained. CONCLUSION: Wernicke's encephalopathy is a concrete possibility after sleeve gastrectomy and should always be suspected in patients with recurrent vomiting, poor nutritional intake, and non-compliance to vitamin supplementation. Immediate and aggressive thiamine supplementation is mandatory to prevent patients from irreversible neurological impairment, even though full recovery is not always achieved.

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.

Can depressed cancer patients with a borderline thiamine concentration develop deficiency within a short time period?

BACKGROUND: Despite increasing reports of thiamine deficiency (TD) among cancer patients, there remain some patients with borderline thiamine concentrations (BTC). However, it is unclear whether such patients subsequently develop TD. METHODS: Here, we report cases of cancer patients progressing to TD within a short time period after presentation with BTC (24-28 ng/ml). CASE 1: A 49-year-old female with lung cancer. During treatment for depression, the patient showed a decreased appetite, and a blood sample revealed BTC (25 ng/ml). Fourteen days later, she reported a continued loss of appetite, and despite the absence of the 3 classical signs of Wernicke encephalopathy (WE), additional testing showed a thiamine level of 23 ng/ml, leading to a diagnosis of TD. CASE 2: A 65-year-old female developed depression during chemotherapy for angiosarcoma. Her blood sample revealed BTC (25 ng/ml). Seven days later, despite the absence of the classical signs of WE, a further testing revealed a thiamine level of 20 ng/ml. CASE 3: A 41-year-old female developed depression during chemotherapy for ovarian cancer. No loss of appetite was observed, but a blood sample revealed BTC (25 ng/ml). Seven days later, despite the absence of the classical signs of WE or decreased appetite, further testing revealed a thiamine level of 19 ng/ml. SIGNIFICANCE OF RESULTS: Depressed cancer patients with BTC may develop TD within a short time frame. To prevent TD, health-care professionals should maintain an awareness of its potential and the need for regular testing of thiamine level or prophylactic replacement therapy.

Wernicke-Korsakoff Syndrome in a Young Adult on Dialysis Who Showed Bilateral Ganglia Lesions.

A 30-year-old man admitted with renal dysfunction (serum creatinine, 8.19 mg/dL) was diagnosed with immunoglobulin A nephritis through a renal biopsy. He was treated with intravenous methylprednisolone pulse therapy and urgent hemodialysis, and eventually, he underwent maintenance hemodialysis. On day 108, he developed amnesia. Magnetic resonance imaging revealed bilateral basal ganglia lesions. Wernicke encephalopathy (WE) was diagnosed based on decreased serum thiamine concentration (12.8 µg/dL; reference range, 24-66 µg/dL). Thiamine replacement therapy was initiated, but the Wernicke-Korsakoff syndrome persisted. Careful monitoring of thiamine is required in patients undergoing dialysis. In addition, patients with WE may exhibit bilateral basal ganglia lesions.

A case report of Wernicke Korsakoff syndrome in a patient with cholangiocellular carcinoma: An underestimated cause of encephalopathy in cancer patients.

INTRODUCTION: Wernicke's encephalopathy, a disorder caused by thiamin deficiency, is characterized by a classical triad of encephalopathy, ataxia, and ophthalmoplegia. Although alcoholism is the most common predisposing factor, it can also be associated with nonalcoholic states (hyperemesis gravidarum, intestinal obstruction, bariatric surgery, and others). This work presents a case of nonalcoholic Wernicke-Korsakoff syndrome diagnosed in a cholangiocellular carcinoma patient and literature review. CASE REPORT: A 65-year-old male patient with a history of cholangiocellular carcinoma (Klatskin tumor) was treated with radiotherapy at the operation site after Roux-en-Y hepaticojejunostomy. During follow-up, the patient developed gastric outlet obstruction and was diagnosed with peritoneal carcinomatosis after a palliative gastrojejunostomy. As the patient could not tolerate oral nutrition during hospitalization, total parenteral nutrition was administered. After 10 days of admission, the patient showed decreased response to verbal stimuli as well as bilateral horizontal nystagmus, lethargy, and disorientation. Furthermore, the patient displayed confabulation. Clinical and imaging findings were consistent with Wernicke's encephalopathy. Therefore, treatment with intravenous thiamin replacement was initiated. The patient's encephalopathy regressed on the second day after treatment, and he recovered the place-person-time orientation. In the following month, the abnormal imaging findings were almost entirely resolved. CONCLUSION: In order to prevent irreversible brain damage induced by chronic thiamin deficiency, thiamin replacement therapy with parenteral nutrition solutions should be included as a treatment for hospitalized cancer patients unable to receive enteral nutrition for a long time.

Cystic fibrosis associated with Wernicke's encephalopathy in an older adult.

Here we report the first case of an association between cystic fibrosis and Wernicke's encephalopathy. The patient had a history of cystic fibrosis diagnosed in her early 60s associated with pancreatitis and chronic lung disease. She presented with a traumatic hip fracture requiring operative repair. On examination, she was found to have bilateral nystagmus. MRI revealed enhancement of the mammillary bodies. Laboratory results were notable for thiamine deficiency, which in context of the radiographic and physical examination findings, confirmed a diagnosis of Wernicke's encephalopathy. The cause of her low thiamine was thought to be poor dietary intake, weight loss and malabsorption associated with exocrine pancreatic insufficiency in the setting of a history of recurrent pancreatitis. The patient had complete resolution of her symptoms with the initiation of thiamine supplementation and pancreatic enzymes. Although classically associated with fat soluble vitamin deficiencies, there are increasing reports of water-soluble vitamin deficiencies associated with cystic fibrosis.

Wernicke's encephalopathy in advanced cancer.

This 54-year-old woman with metastatic breast cancer presented with severe confusion, incontinence and self-neglect. MRI suggested Wernicke's encephalopathy (WE) without any history of alcohol misuse. The patient's symptoms seemed to not respond to acute treatment. Cancer progression was assumed to be causing her condition and she was discharged to a nursing home with community palliative care team follow-up. This case demonstrates the natural course of cancer-associated WE and eventual improvement with thiamine therapy. It also illustrates a role for specialist palliative care follow up for patients discharged to a nursing home for expected end-of-life care.

Wernicke encephalopathy after Roux-en-Y gastric bypass in a young patient.

We report a case of Wernicke encephalopathy (WE) in a woman in her 20s who had Roux-en-Y gastric bypass surgery for severe obesity, which resulted in a severe depletion of the patient's thiamine reserve and development of WE syndrome, we also emphasise the importance of prompt diagnosis of this serious complication in addition to the importance of adequate therapy.

Can the Ketogenic diet lead to Wernicke's encephalopathy?

BACKGROUND: Wernicke's encephalopathy (WE), a neurological disorder due to the deficiency of thiamine, is often underdiagnosed in the pediatric population. The classic triad of mental status changes, oculomotor abnormality, and ataxia is observed in only 16-21% of all pediatric presentations. Wernicke's is most often associated with alcohol dependence, but also malignancy, parenteral nutrition, and gastrointestinal (GI) malformations. The correlation between following a Ketogenic diet and acquiring Wernicke's, however, has not previously been reported. CASE REPORT: A 16-year-old previously healthy male presented with an eleven-day history of neurological deficits and GI upset. The patient had recently lost one hundred pounds while following a "ketogenic" diet. He was subsequently diagnosed with Wernicke's, received intravenous thiamine, and was transferred to the inpatient rehabilitation, where he received extensive diet education. After making significant functional improvement, he was discharged home. RELEVANCE: This case illustrates the importance of including Wernicke's in the differential diagnosis when a pediatric patient presents with neurological deficits after rapid weight loss. Wernicke's encephalopathy may be fatal in the pediatric population, therefore, it must be treated immediately if clinically suspected. Children presenting with Wernicke's would benefit from early intervention, intensive inpatient rehabilitation, and comprehensive education regarding the role of food and exercise on weight loss and health.

A rare case of Wernicke encephalopathy in stage IV gastric cancer.

A 38-year-old male with stage IV gastric adenocarcinoma presented with abdominal pain, nausea, bilious non-bloody vomiting, and lethargy. He was found to have an ileus and was treated appropriately with bowel rest and nasogastric tube decompression. However, the patient was also noted to have confusion and nystagmus. While he was abstinent from alcohol for 20 years, he was found to have Wernicke Encephalopathy (WE) as a result of malnutrition from the underlying malignancy.

Alcoholic Liver Disease Among Patients with Wernicke Encephalopathy: A Multicenter Observational Study.

BACKGROUND: data regarding the association between Wernicke encephalopathy (WE) and alcoholic liver disease (ALD) are scarce in spite of alcohol consumption being the main risk factor for WE. AIMS: to describe the frequency of ALD in a cohort of patients diagnosed with WE and alcohol use disorders (AUDs) and to compare the characteristics of WE patients with and without ALD. METHODS: we conducted an observational study in 21 centers through a nationwide registry of the Spanish Society of Internal Medicine. WE Caine criteria were applied and demographic, clinical, and outcome variables were analyzed. RESULTS: 434 patients were included in the study, of which 372 were men (85.7%), and the mean age was 55 ± 11.8 years. ALD was present in 162 (37.3%) patients and we found a higher percentage of cases with tremor, flapping and hallucinations in the ALD group. A total of 22 patients (5.0%) died during admission (7.4% with ALD vs 3.7% without ALD; P = 0.087). Among the ALD patients, a relationship between mortality and the presence of anemia (Odds ratio [OR]=4.6 Confidence interval [CI]95% 1.1-18.8; P = 0.034), low level of consciousness (OR=4.9 CI95% 1.1-21.2; P = 0.031) and previous diagnosis of cancer (OR=10.3 CI95% 1.8-59.5; P = 0.009) was detected. Complete recovery was achieved by 27 patients with ALD (17.8%) and 71 (27.8%) without ALD (P = 0.030). CONCLUSION: the association of WE and ALD in patients with AUDs is frequent and potentially linked to differences in clinical presentation and to poorer prognosis, as compared to alcoholic patients with WE without ALD.