Wernicke’s Encephalopathy and Polyradiculoneurpathy after Bariatric Surgery: A Case Report

Belal, A; Al-Malt, Ayman M.; Nosair, Nahla A; Mohamed, Ehab Shawky

doi:10.17756/jnen.2018-034

Cited by 3 publications

(2 citation statements)

References 13 publications

(13 reference statements)

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“…Continuous vomiting depletes vitamin B1 levels in 3 -6 weeks. Vitamin B1 deficiency presents with neurologic impairments as in Wernicke's encephalopathy and polyneuropathy [11,12]. Altered levels of Magnesium can be seen in WE since the active form of thiamine: thiamine pyrophosphate, requires Magnesium as a cofactor [8].…”

Section: Discussionmentioning

confidence: 99%

Wernicke’s Encephalopathy: An Overlooked Cause

Muzangwa¹,

Rivera²,

Jurcik³

et al. 2019

J Neurol Exp Neurosci

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A 66-year-old female patient with a past medical history of obesity and ORBERA @ intragastric balloon placement presented with Wernicke's encephalopathy (WE) features without social history of alcoholism. The patient was subjected to ORBERA @ balloon bariatric procedure in Egypt and subsequently developed episodes of uncontrolled emesis which prompted removal of the intragastric balloon placement one month later. Two weeks after removal of the intragastric balloon placement, vomiting still persisted. Patient suddenly developed altered mental status and weakness which prompted admission to our hospital. Initial clinical examination was largely inconclusive, bilateral horizontal nystagmus was noted after subsequent days. A tentatively diagnosis of WE was made based on clinical presentation and magnetic resonance imaging (MRI) scan results; vitamin B1 (thiamine) levels were ordered but were still pending. Empiric treatment with vitamin B1 infusion was initiated which resulted in improvement of both motor function and cognitive functions. Patient was given 200 mg IV TID for 8 days, then 100 mg po for 6 months. Patient was also started on folic acid and vitamin B12. WE diagnosis was supported one week later after lab results showed low vitamin B1 level (21 nmol/L). The patient was sent to rehabilitation center for 6 weeks then was able to be discharged home with a 6-month supply of vitamin B1 supplements. On discharge, memory deficits, loss of appetite and docility were noted.

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Section: Discussionmentioning

confidence: 99%

Wernicke’s Encephalopathy: An Overlooked Cause

Muzangwa¹,

Rivera²,

Jurcik³

et al. 2019

J Neurol Exp Neurosci

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“…[ 50 ] It is estimated that the prevalence of thiamine deficiency after bariatric procedures is about 18%. [ 51 ]…”

Section: Thiamine Deficiency After Gastrectomymentioning

confidence: 99%

Wernicke encephalopathy: An updated narrative review

Elzouki

Habas

Farfar

et al. 2023

Saudi J Med Med Sci

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Wernicke’s encephalopathy (WE) and Korsakoff Syndrome (KS) are distinct neurological disorders that may have overlapping clinical features. Due to the overlap, they are collectively known as Wernicke–Korsakoff syndrome. WE is related to diencephalic and mesencephalic dysfunction due to thiamine. WE typically manifests as confusion, ophthalmoplegia, nystagmus, and gait ataxia (Wernicke’s triad), although they may not consistently occur together. Although WE mostly occurs in alcoholics, other etiologies, such as post-bariatric surgery, must be considered. Early diagnosis and therapy by intravenous thiamine are essential to prevent WE complications and to reduce morbidity and mortality. Therefore, physicians’ and patients’ awareness of WE is essential for early diagnosis and therapy. Accordingly, this narrative review aimed to provide an update on WE by reviewing articles published between April 2015 to April 2022 about the etiology, pathophysiology, diagnosis, and WE management updates. EMBASE, PubMed, Google Scholar, Google, and Scopus search engines were used to conduct the literature search.

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