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Table of Contents
Year : 2021  |  Volume : 3  |  Issue : 1  |  Page : 36

Acute nutritional optic neuropathy following bariatric surgery

Department of Ophthalmology, Centro Hospitalar Entre o Douro e Vouga, Santa Maria da Feira, Portugal

Date of Submission11-Sep-2021
Date of Acceptance21-Sep-2021
Date of Web Publication17-Nov-2021

Correspondence Address:
Dr. Jeniffer Jesus
Praceta Metalomecânica no 10, RC direito Fração J, 3800-235, Aveiro
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pajo.pajo_111_21

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Given the increasing incidence of obesity, bariatric procedures are gaining attention during the past decades, being one of the most effective methods of long-term weight loss. Nutritional optic neuropathy (NON) following bariatric surgeries is a rare but devastating complication caused by a complete lack or inadequate supply of nutrients for the normal function of nerve fibers. We report a case of bilateral anterior NON after a Single Anastomosis Duodenoileal Bypass with Sleeve Gastrectomy, and present a review of the literature about neuro-ophthalmic complications associated with these procedures. Bariatric surgery may constitute an established risk factor for NON and both patient and physician have to be aware of the importance of closely monitoring vitamin depletions and neurologic and visual symptoms.

Keywords: Bariatric surgery, nutritional optic neuropathy, obesity, vitamin deficiencies

How to cite this article:
Jesus J, Soares R, Matias MJ, Miranda V, Aguiar C, Chibante-Pedro J. Acute nutritional optic neuropathy following bariatric surgery. Pan Am J Ophthalmol 2021;3:36

How to cite this URL:
Jesus J, Soares R, Matias MJ, Miranda V, Aguiar C, Chibante-Pedro J. Acute nutritional optic neuropathy following bariatric surgery. Pan Am J Ophthalmol [serial online] 2021 [cited 2022 Oct 7];3:36. Available from: https://www.thepajo.org/text.asp?2021/3/1/36/330602

  Introduction Top

At present, bariatric surgery has become one of the most effective treatment options for obesity, which is a major global public health problem.[1] Bariatric procedures can be divided into restrictive, malabsorptive, and mixed procedures.[2] Restrictive procedures, such as sleeve gastrectomy (SG) or adjustable gastric banding, reduce oral intake by decreasing gastric volume, causing early satiety. On the other hand, malabsorptive procedures, such as biliopancreatic diversion, involve the creation of a tubular stomach similar to SG but divide the gastrointestinal (GI) tract at two points, which can predispose more to malabsorption states. Mixed procedures, such as gastric bypass or SG with duodenal switch, include both techniques at the same time. Despite the positive effects associated with weight loss, namely the reduction of obesity-associated comorbidities and mortality; bariatric procedures are associated with significant risks given the possibility of early and late complications, requiring careful multidisciplinary management.

Due to the anatomic alterations, guidelines to evaluate patients in the pre- and postoperatory period were developed. In the postoperatory period, adequate vitamin supplementation and a regular follow-up with vitamin levels screening are real concerns to prevent nutritional deficiencies and reduce significant risks resulting from malabsorption.

According to the literature, up to 16% of patients after various types of bariatric procedures suffer from neurological complications.[3] The most common nutritional deficiency is hypovitaminosis A. Other nutrient deficiencies include Vitamins B12, B1, C, D, E, and K, folate, iron, selenium, zinc, and copper. From these, nutritional optic neuropathy (NON) after bariatric surgery is often associated with copper or B12 deficiencies, and usually develops 1.5–3 years after surgery.[4],[5]

To emphasize the importance of this pathology, we present a case of a 40-year-old female patient who developed bilateral NON in the early postoperative period caused by a severe deficiency of B6 Vitamin, after a single-anastomosis duodeno-ileal bypass with sleeve gastrectomy (SADI-S), a mixed procedure. In addition, we present a review of the literature about neuro-ophthalmic complications related to bariatric procedures.

  Case Report Top

A 40-year-old woman with a history of SADI-S one month before presented to the emergency department with vomits and nausea complaints for 2 days. After a normal summary analytic study, gasometry, and abdominopelvic computerized tomography, she was discharged with a symptomatic treatment regimen and an indication of surveillance. Nausea and vomit remained and 3 weeks later (2 months after surgery), she returned to the emergency department with associated complaints of blurred vision in the previous 6 days. Since the surgery, she had been on oral supplementary multivitamin regimen with Bariatric®, and she lost 31 kg, at this time weighing 101 kg. On examination, she was slightly encephalopathic with slowness of responses. Pupillary reflexes were normal. The right eye (RE) and left eye (LE) visual acuity (VA) was counting fingers, and she presented with bilateral horizontal nystagmus in all positions, evoked in levoversion and dextroversion. Fundoscopy revealed bilateral optic nerve edema. However, due to the general status of weakness and vomiting, she was unable to cooperate in performing retinography or optical coherence tomography (OCT).

Neurologic examination emphasized the encephalopathic status with lack of attention. When the orthostatic position was tried, she revealed instability in the standing position with enlargement of the base. The clinic presentation corresponded to a Wernicke's syndrome with NON, and she was oriented for further investigation.

Brain computed tomography was normal. Laboratory investigations revealed severe deficiency of Vitamin B6 (<9 nmol/L [normal, 23–172.5]) and included Vitamin A: 0.35 mg/l (normal, 0.30–1.00); B1: 2.2 μg/dL (normal, 2.0–7.2); Vitamin B12: 733 pg/mL (normal, 213–816); Vitamim D: 6.80 ng/mL (normal, 10.00–65.00); and folic acid: 3.9 ng/mL (3.0–20.0).

The patient was hospitalized for vitaminic supplementation with intravenous thiamine (3000 mg 3id), intramuscular Neurobion® 3id, Bariatric®, and folic acid (5 mg per os, id).

One week later, her VA improved to <20/400 in the RE and 20/400 in the LE, maintaining nystagmus, now with a vertical upbeat component in all positions of the gaze. Ishihara plates were 0/17 in the RE and 1/17 in the LE. Fundoscopy revealed a slight pallor of the right optic disc with normal OCT [Figure 1]. Goldmann's visual field revealed a tubular field in the LE and was impossible to perform in the RE [Figure 2]. At this time, she presented with right upper limb dysmetria, gait ataxia needing third-person support, despite the improvements in the standing position. She was maintained on a treatment regimen of Neurobion®, Bariatric®, and folic acid 5 mg per os id. In addition to the continuous follow-up in ophthalmology, neurology, endocrinology, and general surgery, the patient began a multidisciplinary rehabilitation program where she learned how to orientate and perform basic daily tasks, through a multidisciplinary approach of neuropsychology, physical medicine and rehabilitation, and physiotherapy. At this time, analytic study revealed Vitamin A: 0.32 mg/l (normal, 0.30-1.00); B1: 9.50 μg/dL (normal, 2.0–7.2), B6: <9 nmol/L (normal, 23–172.5), Vitamin B12: >2000 pg/mL (normal, 213–816); Vitamin D: 6.80 ng/mL (normal, 10.00–65.00); and folic acid: 5.7 ng/mL (3.0-20.0). The patient performed magnetic resonance imaging of the brain and orbita which were both normal, and Vigantol® id was added to the treatment.
Figure 1: Macular optical coherence tomography reveals areas of normal macular thickness. Note thicker areas closer to the ON due to ON edema

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Figure 2: Goldmann's Perimetry of the left eye 4 weeks after the first presentation revealing a generally depressed visual field

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Four months later, her general status improved, as well as her VA, which was at this time <20/400 in the RE and 1/10 in the LE. The nystagmus persisted similar to the last observation, and fundoscopy revealed slight temporal pallor bilaterally. ON OCT revealed RNFL deficits in temporal quadrants [Figure 3]. Goldman's perimetry in the RE remained impossible to realize, and in the LE showed visual field improvements [Figure 4]. Laboratory investigations revealed Vitamin A: 0.33 mg/l (normal, 0.30–1.00); B1: 5.10 μg/dL (normal, 2.0–7.2), B6: 20.5 nmol/L (normal, 23–172.5), Vitamin B12: 317 pg/mL (normal, 213–816); Vitamin D: 11.10 ng/mL (normal 10.00–65.00), Vitamin E: 11.20 μg/ml (normal 5.00 – 20.00); folic acid: 15.5 ng/mL (3.0-20.0); and Zinc: 53.6 μg/dL (normal 68.0–120.0). The remaining study was unremarkable. She remained on the treatment with vitamin supplementation.
Figure 3: Optic nerve optical coherence tomography revealing temporal atrophy of RNFL 4 months later

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Figure 4: Evolution of Goldmann's perimetry 4 months later. Note the generally depressed visual field in the RE and the improvements of the left eye

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On her last neuro-ophthalmology visit, 14 months after the first episode, her weight was 78 kg. She revealed improvements in cognitive issues and presented autonomy for daily living practices. Her VA was CF in the RE and 20/400 in the LE with optic nerve pallor bilaterally. Optic nerve OCT revealed a slight decrease in Retinal Nerve Fiber Layer (RNFL) in the LE, and a loss of fixations in the RE [Figure 5]. Macular OCT is still normal, but the patient cannot fixate to perform ON OCT. The nystagmus disappears. The electromyography revealed incipient axonal polyneuropathy due to the absence of potentials in the medial plantar digital nerves bilaterally, without other lesions. The patient remained in the rehabilitation program and vitamin supplementation with a close monthly follow-up.
Figure 5: Optic nerve optical coherence tomography 14 months after the first episode revealing a bilateral worsening of RNFL atrophy, with loss of fixations in the right eye

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  Discussion Top

Besides these risk factors, bariatric procedures have emerged recently as a new cause of NON due to the worldwide increase in the search for surgical treatments against obesity, a serious and growing public health problem.

Bariatric procedures, associated with GI malabsorption of vitamins and microelements, may be a well-established risk factor for NON, mainly in cases with adverse effects after surgery, such as vomiting, food intolerance or noncompliance, or GI disorders.[6]

Reviewing the relevant literature on bariatric surgery is a complex challenge because it crosses numerous specialties, including ophthalmology, neurology, general surgery, and physical medicine and rehabilitation. [Table 1] shows all published clinical cases of NON after bariatric surgery caused by different nutritional deficiencies. Becker et al. reviewed the neurological complications of nutritional deficiency after bariatric surgery caused by Vitamin A, B complex, D, and E, copper, and folate. Three years later, Moss et al. published a review of ophthalmology, neurology, general surgery, obesity, endocrinology, nutrition, psychiatry, and neurosurgery literature, and highlighted the importance of recognizing early signs of NON, because vitamin deficiencies may have some different presentations, such as nystagmus, optic neuropathy, nyctalopia and/or ophthalmoparesis, and may be developed weeks to years after surgery.[15]
Table 1: Chronological review of noncase-reports associated with bariatric procedures

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Regarding the neuro-ophthalmic syndromes after bariatric surgery, the best characterized is Wernicke's encephalopathy, characterized by the triad ataxia, confusion, and nystagmus.[15] Our case presented with a complete triad, in addition to blurred vision. As shown by laboratory tests, the main deficiencies in our case were primary Vitamin B1 and B6. However, several studies showed that optic neuropathy following bariatric surgery can also be caused by copper and Vitamin B12, E, and A insufficiencies.[16] Due to the body stores of the nutrients, Vitamin B6 and B1 deficiencies typically present in weeks to months following surgery. In contrast, B12 deficiency typically presents over 1 year following surgery and copper deficiency over 3 years and up to over 20 years.[15]

The risk factors for nutritional complications after bariatric surgery include treatment noncompliance, vomiting, severe diarrhea, inadequate food intake, or excessive alcohol consumption. In our case, the patient went twice to the emergency department with a 3-week history of nausea and vomiting, which originated poor nutritional status.[15],[17] The diagnosis is clinically supported by laboratory tests, at the minimal suspicion of vitamin depletion or patient symptoms.

Although the mechanism for the development of NON is uncertain, the rationale for the development of NON is especially due to reduced transketolase activity, a thiamine-dependent enzyme, throughout the nervous system, being responsible for degeneration of the papillomacular bundles and consequent development of optic neuropathy.[3]

Despite the high incidence of nutritional deficiencies, and the well-described neurological consequences post bariatric surgery, the majority of nutrient depletions could be asymptomatic.[15] As a result, it is crucial to prescribe long-term appropriate vitamin supplementation and to make a close follow-up with regular screenings. The ophthalmologist has to be aware of the symptoms of NON, such as central scotoma or blurred vision, knowing that many cases are also associated with other neurological symptoms, such as sensory neuropathies. In our case, VA did not improve despite the implementation of appropriate supplementation, probably as a consequence of too late diagnosis. Thus, even if the bariatric surgery occurred in a distant past, with the first evidence or if there is any early sign of NON, nutritional deficiency, food intolerance, or GI disorders, an empirical and immediate supplementation with vitamins should be initiated, in parallel with laboratory testing.

At a time when the management of obesity continues to be a serious challenge for modern medicine, this clinical case and the reviewed cases reinforce the importance of vigilance for vitamin depletions after bariatric procedures, mainly in patients with food intolerance, and highlight the necessity of prompt treatment, even in the absence of laboratory confirmation, to improve the overall prognosis and reduce the possibility of irreversible consequences.

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

Expert Panel Members, Michael D. Jensen MD, Donna H. Ryan MD, Karen A. Donato SM, Caroline M. Apovian MD, FACP, Jamy D. Ard MD, Anthony G. Comuzzie PhD, Frank B. Hu MD, PhD, FAHA, Van S. Hubbard MD, PhD, John M. Jakicic PhD, Robert F. Kushner MD, Catherine M. Loria PhD, FAHA, Barbara E. Millen DRPH, RD, Cathy A. Nonas MS, RD, F. Xavier Pi-Sunyer MD, MPH, June Stevens PhD, Victor J. Stevens PhD, Thomas A. Wadden PhD, Bruce M. Wolfe MD, Susan Z. Yanovski MD. Executive summary: Guidelines (2013) for the management of overweight and obesity in adults: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Obesity Society Published by the Obesity Socie. Obesity 2014;22:3-5. [doi: 10.1002/oby. 20821].  Back to cited text no. 1
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Becker DA, Balcer LJ, Galetta SL. The neurological complications of nutritional deficiency following bariatric surgery. J Obes 2012;2012: 1-2.  Back to cited text no. 3
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Naismith RT, Shepherd JB, Weihl CC, Tutlam NT, Cross AH. Acute and bilateral blindness due to optic neuropathy associated with copper deficiency. Arch Neurol 2009;66:1025-7.  Back to cited text no. 5
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Stroh C, Weiher C, Hohmann U, Meyer F, Lippert H, Manger T. Vitamin A deficiency (VAD) after a duodenal switch procedure: A case report. Obes Surg 2010;20:397-400.  Back to cited text no. 7
Santos-García D, Abella J, De Domingo B, De La Fuente-Fernández R. Leber hereditary optic neuropathy associated with malabsorption syndrome after bariatric surgery. J Neuro-Ophthalmol 2009;29:75-6. [doi: 10.1097/WNO.0b013e3181989cb0].  Back to cited text no. 8
Theeler BJ, Wilson DJ, Crawford CM, Grazko M. Optic neuropathy and a reversible splenial lesion after gastric bypass: Shared pathophysiology? J Neurol Sci 2010;291:92-4.  Back to cited text no. 9
Chacko JG, Rodriguez CJ, Uwaydat SH. Nutritional optic neuropathy status post bariatric surgery. Neuro-Ophthalmology 2012;36;165-7. [doi: 10.3109/01658107.2012.700993].  Back to cited text no. 10
Ramos-Leví AM, Sánchez-Pernaute A, Rubio Herrera MA. Dermatitis and optic neuropathy due to zinc deficiency after malabsortive bariatric surgery. Nutr Hosp 2013;28:1345-7.  Back to cited text no. 11
Yarandi SS, Griffith DP, Sharma R, Mohan A, Zhao VM, Ziegler TR. Optic neuropathy, myelopathy, anemia, and neutropenia caused by acquired copper deficiency after gastric bypass surgery. J Clin Gastroenterol 2014;48:862-5.  Back to cited text no. 12
Shah AR, Tamhankar MA. Optic neuropathy associated with copper deficiency after gastric bypass surgery. Retin Cases Brief Rep 2014;8:73-6.  Back to cited text no. 13
Sawicka-Pierko A, Obuchowska I, Hady RH, Mariak Z, Dadan J. Nutritional optic neuropathy following bariatric surgery. Wideochir Inne Tech Maloinwazyjne 2014;9:662-6.  Back to cited text no. 14
Moss HE. Bariatric surgery and the neuro-ophthalmologist. J Neuroophthalmol 2016;36:78-84.  Back to cited text no. 15
Bhasker AG, Kantharia N, Baig S, Priya P, Lakdawala M, Sancheti MS. Management of Nutritional and Metabolic Complications of Bariatric Surgery. Springer Nature Singapore Pte Ltd: Springer Singapore; 2021. doi:10.1007/978-981-33-4702-1.  Back to cited text no. 16
Kumar P, Hamza N, Madhok B, De Alwis N, Sharma M, Miras AD, et al. Copper deficiency after gastric bypass for morbid obesity: A systematic review. Obes Surg 2016;26:1335-42.  Back to cited text no. 17


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1]


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