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 Table of Contents  
Year : 2018  |  Volume : 2  |  Issue : 4  |  Page : 150-151

Wernicke's encephalopathy after sleeve gastrectomy

1 Department of Medicine, Hamad General Hospital, Hamad Medical Corporation; Weill Cornell Medical College, Doha, Qatar
2 Weill Cornell Medical College, Doha, Qatar

Date of Web Publication17-Jan-2019

Correspondence Address:
Dr. Abdul Aziz Zafar
Department of Internal Medicine, Hamad General Hospital, Hamad Medical Corporation, P. O. Box: 3050, Doha
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/LJMS.LJMS_28_18

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As bariatric surgery is becoming a more sought-after treatment for morbid obesity, Wernicke's Encephalopathy (WE) is becoming more recognized complication of bariatric surgery. WE is a classic triad of symptoms of ataxia, ophthalmoplegia, and acute confusion due to thiamine deficiency. Bariatric surgery has its own complications in the form of vitamin deficiencies. Thiamine deficiency following bariatric surgery can present as WE. We present a case of 20-year-old young man, who presented after a short period of 3 months after sleeve gastrectomy with symptoms of diplopia and dizziness. The diagnosis was confirmed by the immediate resolution of the neurological symptoms after thiamine administration.

Keywords: Bariatric, thiamine deficiency, Wernicke's encephalopathy

How to cite this article:
Zafar AA, Al-Mohtasib Y, Hussein M, Elzouki AN. Wernicke's encephalopathy after sleeve gastrectomy. Libyan J Med Sci 2018;2:150-1

How to cite this URL:
Zafar AA, Al-Mohtasib Y, Hussein M, Elzouki AN. Wernicke's encephalopathy after sleeve gastrectomy. Libyan J Med Sci [serial online] 2018 [cited 2022 Oct 7];2:150-1. Available from: https://www.ljmsonline.com/text.asp?2018/2/4/150/250302

  Introduction Top

Morbid obesity is defined as a body mass index of over 40 kg/cm2, which worsens a patient's quality of life due to complications such as hypertension, diabetes mellitus, stroke, and osteoarthritis.[1],[2],[3] Bariatric procedures for the treatment of morbid obesity are the most commonly performed gastrointestinal procedures these days. Nearly, half a million bariatric procedures are performed annually throughout the world.[3] Sleeve gastrectomy has increased in prevalence from 0% in 2003-28% in 2011[4] WE is a rare but very important complication after bariatric surgery. Literature search has revealed about 118 reported cases so far. Neurological disturbances of both central and peripheral nervous system occur in approximately 5%–16% of patients subjected to bariatric surgery.

Thiamine (Vitamin B1) is a coenzyme and is involved in the metabolism of glucose, fatty acids, and neurotransmitters. It is estimated that the incidence of thiamine deficiency following bariatric surgery is approximately 18%.[5] Failure to take inadequate food supplements, food avoidance, can pose major risk factors for developing neurological complications. Body stores of thiamine can be depleted within 6 weeks, so most cases of thiamine deficiency symptoms such as WE and polyneuropathy may present about 2 months after bariatric surgery. WE was reported for the first time in 1981 resulting from bariatric surgery for morbid obesity.

In this case report, we present one of WE cases due to thiamine deficiency postlaparoscopic sleeve gastrectomy. The patient presented with dizziness, eye symptoms and with numbness in the lower limbs 3 months after surgery and losing 40 Kg of weight.

  Case Report Top

A 20-year-old man, s/p Laparoscopic sleeve gastrectomy in April 2017. He presented to the emergency department with dizziness and diplopia for 3 days' duration. For 3 months' postgastrectomy, the patient was in his normal state of health. Seven days before admission, he started to feel numbness in both his lower limbs. This started in his feet and progressed upward involving both thighs. After that, he developed dizziness and vertigo, which was episodic and was unrelated to head movement. He was nauseous and had bilious vomitus for 3 times. Intermittent diplopia with the blurring of vision was also associated during this period. No history of focal weakness, headache or LOC, urinary or stool incontinence, dysphagia or dysphasia. Apart from occasional heartburn, he did not have any fever, rash, tinnitus, shortness of breath, chest pain, diarrhea, constipation, polyuria, or polydipsia. No history of recent trauma or unsteadiness. He lost 40 kg over the past 3 months and was noncompliant to vitamin supplements. Before surgery, the patient had a BMI of 44.5 as his Weight was 138 kg and Height 176 cm. He had been unable to lose weight by diet, exercise, or medications. His excessive weight was affecting his personal, social, and professional life. The patient was a university student, living with his family. His diet included only juices and soups as he was concerned about gaining weight again. He did not do exercise regularly. He had been smoking half a pack a day for the past 6 years. He did not drink alcohol or use any illicit drugs. On physical examination, he was apyrexial, heart rate 80 bpm, SBP 120 mmHg, DBP 79 mmHg, and SpO 298%

The patient was alert conscious oriented to time, place, and person with the intact higher mental exam. Cranial nerves: Eye exam. Reactive pupils, no nystagmus or ophthalmoplegia, normal eye movement, no double vision, and 5/7/8/9/10/11/12 nerves were intact. The speech was normal. Power was 5/5 in both upper and lower limbs. Sensations: Decreased below umbilicus with hyporeflexia in right lower limb and areflexia in left lower limb. Planters were downgoing bilaterally. Gait was normal, and Cerebellar signs were negative. Other systems were unremarkable for Neck, Chest, Cardiovascular and Abdomen.

His complete blood count, Urea and electrolytes, liver function test, C-reactive protein, erythrocyte sedimentation rate, and glucose were normal. Apart from low Vitamin D of 17, his copper, zinc, selenium, iron, folate, and B12 were well within normal ranges. Computer tomography head was unremarkable and MRI head with contrast did not show focal parenchymal changes, demyelination or signal abnormality in the brain. Posterior fossa structures appeared unremarkable. The right maxillary sinus large retention cyst/polyp is noted.

On clinical grounds, the diagnosis of Thiamine deficiency was made, and the patient was started on thiamine 500 mg as a replacement therapy for 3 days then to continue on 100 mg once daily. The patient was given multivitamin and Vitamin D supplements as well. The patient had a dramatic response to therapy and his diplopia and dizziness improved the next day.

  Discussion Top

WE is a condition affecting the central nervous system due to deficiency of the B vitamins reserves in particular B1 (Thiamine). Classically, WE is a triad of ophthalmoplegia, ataxia, and confusion. Only in 10% of cases, all the three signs are present. Other signs symptoms can be bilateral 3rd nerve palsies, horizontal and vertical nystagmus, papilledema, blurred vision, vision loss, impaired or hearing loss, fatigability, apathy, dysphagia, Hypotension, Hypothermia, memory impairment, and stupor can occur.[6] Mostly, the malnourished alcoholics are affected, but a variety of diseases can lead to WE.

Although 94% of WE cases were seen within 6 months after surgery, this disease may appear 3 weeks after surgery, especially when the patient progress to solid foods suffering from vomits, or even can present after a long time like 72 weeks of surgery.[5] Diagnosis can be made by blood tests such as Blood thiamine concentration or Erythrocyte transketolase activity.[7] Imaging studies like MRI showing hyperintense areas on T2 (medial thalamus, periventricular zone, or mammillary bodies),[8] but low sensitivity prevents exclude the diagnosis when no changes are demonstrated, as in our case. MRI can be helpful, but still, the main approach to diagnose thiamine deficiency is by clinical diagnosis especially in those with a known history of gastrectomy or known alcoholic patients.

In this case, the patient presented after 3 months of sleeve gastrectomy and the diagnosis was made on mostly clinical presentation and improvement with treatment. Although thiamine level is not available, we have confirmed our diagnosis by ruling out other vitamin and minerals deficiencies and MRI with contrast which was unremarkable. The diagnosis was confirmed with immediate resolution of symptoms with thiamine replacement therapy.

To conclude, it is utmost important to give due consideration to the nutritional status of the patient after bariatric surgery. In general, all the vitamins and in particular thiamine should be given as supplements. WE should be considered immediately if a patient presents with neurological symptoms after a few weeks of bariatric surgery.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Zafar A. Wernicke's encephalopathy following roux en Y gastric bypass surgery. Saudi Med J 2015;36:1493-5.  Back to cited text no. 1
Jeong HJ, Park JW, Kim YJ, Lee YG, Jang YW, Seo JW, et al. Wernicke's encephalopathy after sleeve gastrectomy for morbid obesity – A case report. Ann Rehabil Med 2011;35:583-6.  Back to cited text no. 2
Oudman E, Wijnia JW, van Dam M, Biter LU, Postma A. Preventing wernicke encephalopathy after bariatric surgery. Obes Surg 2018;28:2060-8.  Back to cited text no. 3
Pardo-Aranda F, Perez-Romero N, Osorio J, Rodriguez-Santiago J, Muñoz E, Puértolas N, et al. Wernicke's encephalopathy after sleeve gastrectomy: Literature review. Int J Surg Case Rep 2016;20:92-5.  Back to cited text no. 4
Ragab OA, El Fath Belal AA, Al-Malt AM, Nosair NA, Mohamed ES. Wernickes Encephalopathy and polyneuroradiculopathy after bariatric surgery – A case report bariatric surgery: A case report. J Neurol Exp Neurosci 2018;4:11-4.  Back to cited text no. 5
Sullivan J, Hamilton R, Hurford M, Galetta S, Liu G. Neuro-ophthalmic findings in Wernickés encephalopathy after gastric bypass surgery. Neuro Ophtalmol 2006;30:80-9.  Back to cited text no. 6
Available from: http://www.harmonesmatter.com/thiamine-deficiency-testing. [Last accessed on 2018 May 05].  Back to cited text no. 7
Zuccoli G, Gallucci M, Capellades J, Regnicolo L, Tumiati B, Giadás TC, et al. Wernicke encephalopathy: MR findings at clinical presentation in twenty-six alcoholic and nonalcoholic patients. AJNR Am J Neuroradiol 2007;28:1328-31.  Back to cited text no. 8


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