Cases reported "Wernicke Encephalopathy"

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1/16. Acute Wernicke's encephalopathy following bariatric surgery: clinical course and MRI correlation.

    postoperative complications and nutritional deficits resulting from bariatric surgery can lead to severe vitamin-deficiency states, such as Wernicke's encephalopathy (WE). patients with acute WE generally present with the classic clinical triad of inattentiveness, ataxia, and ophthalmoplegia. We describe a patient who presented with acute WE at 2 months after laparoscopic bariatric surgery. Initial MRI of the brain demonstrated the characteristic injuries of WE, and repeat imaging showed resolution after 4 months of thiamine supplementation, at which time the patient had normal gait but persistent memory deficits. Even with early recognition and aggressive therapy, acute WE commonly results in permanent disability due to the irreversible cytotoxic effects on specific regions of the brain. Since the clinical onset of acute WE follows a predictable time-course in post-bariatric surgery patients with malnutrition, we recommend prevention by administration of parenteral thiamine beginning at 6 weeks postoperatively in malnourished patients.
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2/16. Wernicke's encephalopathy in a malnourished surgical patient: clinical features and magnetic resonance imaging.

    We report a clinical and neuroradiological description of a severe case of Wernicke's encephalopathy in a surgical patient. After colonic surgery for neoplasm, he was treated for a long time with high glucose concentration total parenteral nutrition. In the early post-operative period, the patient showed severe encephalopathy with ataxia, ophthalmoplegia and consciousness disorders. We used magnetic resonance imaging (MRI) to confirm the clinical suspicion of Wernicke's encephalopathy. The radiological feature showed hyperintense lesions which were symmetrically distributed along the bulbo-pontine tegmentum, the tectum of the mid-brain, the periacqueductal grey substance, the hypothalamus and the medial periventricular parts of the thalamus. This progressed to typical Wernicke-korsakoff syndrome with ataxia and memory and cognitive defects. thiamine deficiency is a re-emerging problem in non-alcoholic patients and it may develop in surgical patients with risk factors such as malnutrition, prolonged vomiting and long-term high glucose concentration parenteral nutrition.
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3/16. Wernicke's encephalopathy with hyperemesis and ketoacidosis.

    BACKGROUND: avitaminosis can result from the acute malnutrition associated with prolonged pregnancy-related hyperemesis. Serious complications may arise from thiamine deficiency under these circumstances. CASE: We review the relevant literature and describe a case with central nervous system involvement presenting with typical manifestations of Wernicke's encephalopathy, apparently precipitated by a combination of hyperemesis gravidarum, diabetic ketoacidosis, and intravenous glucose administration. CONCLUSION: While this life-threatening complication is rare, it is important for all who care for obstetric patients to be aware of it and alert to its development. Early recognition is critical given the need to treat affected women expeditiously to help avoid potentially fatal adverse consequences. Prophylactic thiamine supplementation should be considered in the care of gravidas with hyperemesis.
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4/16. Wernicke's encephalopathy after gastric bypass that masqueraded as acute psychosis: a case report.

    Wernicke's encephalopathy was originally described more than a decade ago. It has been reported after many causes of malnutrition. This case presents a patient with thiamine deficiency after gastric bypass, although unusual in itself, further complicating the case was the initial diagnosis of acute psychosis that was scheduled for electroconvulsive therapy. After recognition and intervention, the patient was successfully treated with thiamine replacement and parenteral nutrition.
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5/16. Wernicke's encephalopathy in a patient with schizophrenia.

    Clinically, we most often associate Wernicke's encephalopathy (WE) with an alcohol abusing population. However, it is important to consider other causes of malnutrition and vitamin deficiency as risk factors for the development of this disorder. We present a case of a 51-year-old man with schizophrenia and malnutrition who presented with delirium, ophthalmoplegia, and seizures. He responded rapidly to the administration of IV thiamine. Because of the high rate of mortality and morbidity, WE should be high on the differential of any patient at risk for malnutrition or with ophthalmoplegia, regardless of alcohol history. This is particularly important in psychiatric patients where the syndrome may be masked and thus treatment delayed.
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6/16. Wernicke's encephalopathy in association with complicated acute pancreatitis and morbid obesity.

    A young obese female with acute pancreatitis complicated by pseudocyst formation and intermittent gastric outlet obstruction, who had been maintained on high-calorie enteral feeds, developed a sudden onset of confusion and ophthalmoplegia associated with papilloedema and retinal haemorrhages. A possible diagnosis of Wernicke's encephalopathy (WE) was made, and the patient was treated with parenteral thiamine. Clinical resolution was complete. Any patient with suspicious or unusual neurological symptoms and signs associated with possible malnutrition, hyperemesis or malabsorption should be given intravenous thiamine without delay to avoid the potential morbidity and mortality associated with undiagnosed WE.
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7/16. Wernicke's encephalopathy in acquired immune deficiency syndrome (AIDS): a case report.

    A 40-year-old male, with established AIDS developed cachexia and dementia. At autopsy opportunistic infections were found. An additional neuropathological finding was Wernicke's encephalopathy. Although malnutrition is common in AIDS patients, it seems that Wernicke's encephalopathy is rare in AIDS. Nevertheless, it is suggested that a therapeutic trial with parenteral thiamine may be useful in AIDS patients with amnestic syndrome and dementia.
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8/16. Wernicke's encephalopathy during total parenteral nutrition: observation in one case.

    A patient operated for toxic megacolon secondary to ulcerative colitis developed a Wernicke syndrome (thiamine deficiency) during the postoperative period despite the administration of the usually recommended doses of vitamin B1 during total parenteral nutrition (TPN) treatment. Vitamin B1 deficiency should be checked in order to evaluate the patients' nutritional condition before starting TPN, especially those suffering from severe chronic malnutrition. Routine administration of vitamin B1 in repletion doses may be reasonably proposed in order to avoid the development of a Wernicke syndrome which is potentially lethal in a short time if not recognized and corrected in time.
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9/16. Catastrophic weight loss after vertical banded gastroplasty: malnutrition and neurologic alterations.

    The case of a patient with severe vomiting and very rapid weight loss following vertical banded gastroplasty (VBG) (almost 50% of original weight in 11 months) and who suffered severe neurological and nutritional disorders is reported. All abnormal findings with the exception of nystagmus, disappeared during enteral nutritional support with a complete diet and vitamin supplementation. The alterations found in this case may have been related to the very rapid weight loss, which resulted in protein calorie malnutrition and, probably, in one or more vitamin deficiencies. This complication may be preventable by early nutritional intervention in subjects undergoing gastric reduction surgery and who exhibit very rapid weight loss and intractable vomiting.
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keywords = malnutrition
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10/16. Jakob-Creutzfeldt disease associated with wernicke encephalopathy.

    Wernicke disease (WD) is a complication of alcoholism and malnutrition and usually presents acutely and is characterized by disturbances of consciousness, paralysis of the external ocular muscles, and ataxia. The disease results from deficiency of vitamin B 1, or thiamine, an essential coenzyme in intermediate carbohydrate metabolism. On the other hand, Jakob-Creutzfeldt disease (J-C) results from infection with an unconventional agent with a long incubation period and is characterized by a rapidly progressive dementia and histologically by a spongiform encephalopathy associated with neuronal destruction and pronounced astrogliosis. Combination of both diseases has not been reported in the literature previously and their relationship is uncertain. We present 3 cases with this interesting association and consider their relationship.
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