Abstract
Purpose
This case report aims to highlight the potential for severe ocular complications due to vitamin A deficiency (VAD) following bariatric surgery, emphasizing the importance of long-term nutritional monitoring and compliance. We present a case report of corneal ulceration and ocular surface keratinization occurring eight years post-biliopancreatic diversion with duodenal switch (BPD-DS) and discuss its management in the context of limited access to intramuscular vitamin A therapy.
Observations
VAD can present years after bariatric surgery and cause severe ocular complications. In this case, inconsistent multivitamin intake led to xerophthalmia and progressive vision loss, thus highlighting the importance of long-term adherence to supplementation in patients with a history of bariatric surgery. Due to a nationwide shortage of intramuscular vitamin A at the time, high-dose oral therapy was used. Despite being well tolerated, the condition progressed to the point of requiring surgical intervention. This case highlights the importance of early detection, timely treatment, and long-term nutritional monitoring in bariatric patients to prevent irreversible vision loss.
Conclusions and importance
VAD can present years after bariatric surgery and cause serious ocular risks. While oral supplementation showed potential, it was insufficient to prevent surgical intervention. This case report aims to raise awareness of post-surgical risks to vision and highlight the importance of long-term nutritional monitoring and early diagnosis in patients with a history of bariatric surgery.
Keywords: Vitamin A deficiency, Bariatric surgery, Ocular complications, Corneal ulceration, Nutritional supplementation, Keratoplasty
1. Introduction
We present a patient with nyctalopia, severe corneal ulceration, and complete ocular surface keratinization in one eye caused by hypovitaminosis A eight years following gastric bypass surgery. The patient had been on multivitamin supplementation but reported irregular intake prior to presentation. Due to a nationwide backorder of intramuscular vitamin A solution, we treated the patient with over-the-counter oral vitamin A supplements (200,000 IU initial dose, after initial dose, 10,000 IU as maintenance daily until vitamin A levels are normalized).
2. Case report
A 35-year-old male presented with pain, foreign body sensation, nyctalopia, and progressive visual loss OS. Past medical history was significant for a biliopancreatic diversion with duodenal switch (BPD-DS) eight years previously. The patient denied any addictions, alcohol use, or digestive problems, but mentioned noncompliance with his multivitamin intake. Past ocular history was significant for a persistent corneal infection OS for four months despite treatment with doxycycline, topical moxifloxacin six times a day, and over the counter multivitamin supplements by an external physician. This was his first occurrence of ocular symptoms.
At presentation, best-corrected visual acuity (BCVA) was 20/50 OD and counting fingers (CF) OS. Intraocular pressure was 11 mmHg OD measured with Tono-Pen (Reichert Technologies, Depew, NY, USA) device technique; the patient reported pain OS and could not tolerate applanation or even finger tension. Slit lamp examination revealed severe bilateral xerosis and conjunctival keratinization OU (Fig. 1A), and presence of corneal ulcer OS with an estimated diameter size of 2.3mm (Fig. 1B). Dilated fundus examination was normal OD and could not be performed OS due to corneal opacity. B-scan ultrasonography OS was normal.
Fig. 1.
(A) Slit lamp photo showing conjunctival keratinization OD (blue arrow). (B) Slit lamp photo showing a central cornea ulcer OS (estimated size 2.3mm). (C) Despite receiving antibiotic treatment, cornea perforation occurred one week later (estimated size 3.4mm).
A cotton swab cornea culture was performed, as well as a blood test due to a suspicion of vitamin deficiency. Two weeks later, cornea cultures revealed a pan-sensitive Pseudomonas aeruginosa infection OS, and blood testing showed markedly low serum vitamin A levels (<0.06 mg/dl; normal range 32.5–78 mg/dl). Anti-dsDNA, ANA, ANCAS Sjogren's SSA and SSB were all negative or normal.
The patient was diagnosed with xerophthalmia OU and corneal ulceration OS secondary to hypovitaminosis A. Due to a nationwide backorder of intramuscular vitamin A, it was decided to start oral vitamin A supplementation. The patient was given 200,000 IU as an initial dose, then 10,000 IU as maintenance daily. This supplementation was well tolerated by the patient.
However, despite treatment with tobramycin and vancomycin eye drops, the corneal ulcer OS progressed to melting and eventual perforation, with an estimated size of 3.4mm one week following initial presentation (Fig. 1C). An emergency penetrating keratoplasty was performed, during which an amniotic membrane was applied to facilitate epithelialization and mitigate inflammatory responses at the ocular surface. This was complicated by a graft re-infection occurring two weeks postoperatively. Due to the complex nature of the patient's condition and the lack of success with both topical and surgical treatment approaches, conjunctival flap surgery and cryotherapy was performed (Fig. 2).
Fig. 2.
Conjunctival flap/amniotic membrane.
Despite these interventions, the patient developed conjunctival flap retraction with corneal melting and the formation of a descemetocele. Consequently, one month after initial presentation, a subsequent therapeutic corneal transplant was performed using a graft diameter of 13–14 mm, accompanied by cataract removal and amniotic membrane placement. Two months after initial presentation, and one month after the second corneal transplant OS, examination OD showed improvement, with BCVA 20/25 and resolution of conjunctival keratinization (Fig. 3). Examination OS showed BCVA hand motions (HM) with a slow-healing corneal transplant and no recurrent corneal infections. Unfortunately, the patient was lost to follow-up after initial management, and subsequent assessment of vitamin A level normalization or long-term clinical status could not be completed. A timeline summarizing the clinical course is shown in Fig. 4.
Fig. 3.
(A) Resolution of conjunctival keratinization after oral vitamin A treatment OD. (B) Post-corneal transplantation OS.
Fig. 4.
Timeline of Clinical events.
3. Discussion
Bariatric surgery is a popular and effective method to achieve significant weight loss and improve outcomes for individuals suffering from obesity, with an estimated 280,000 Americans having undergone bariatric surgery in 2022.1 Despite its popularity, bariatric surgery comes with several important risks, including nutritional deficiency.2
Various vitamin deficiencies have been documented following bariatric surgery, with vitamin A deficiency (VAD) particularly prevalent after procedures like the duodenal switch.3 VAD following bariatric surgery has been reported to initially present six months after surgery and can persist even with adequate vitamin supplementation.4 In gastric bypass patients, VAD is associated with ocular complications such as nyctalopia (68 %), decreased visual acuity (39 %), xerosis (38 %), and eye pain or foreign body sensation (23 %).5
Xerophthalmia is one of the top causes of preventable blindness globally, particularly in developing countries with insufficient vitamin A intake from the diet.6 Cases are rare in developed nations like the United States where vitamin A is abundant in everyday foods and instead typically result from issues in vitamin A metabolism, such as following gastric surgery.
While vitamin deficiencies typically manifest within the first few months to two years following bariatric surgery,4 a previous case report of a 68-year-old female described ocular complications due to VAD ten years after bariatric surgery.6 Another case report of a 41-year-old female LASIK patient described corneal ulceration due to VAD ten years following bariatric surgery; similar to our case, this patient reported noncompliance with nutritional supplementation.7
This case differs from previously reported cases of ocular complications following bariatric surgery in several important aspects. First, the delayed time course between bariatric surgery and ocular symptoms was understood to occur as a result of recent noncompliance with multivitamin intake, highlighting the importance of long-term nutritional management in bariatric patients. Second, intramuscular vitamin A was not available at the time of presentation, which posed a significant challenge in management and prolonged the visual recovery process. Finally, surgical management was complicated by rapidly progressive corneal ulceration with melting and perforation, while the occurrence of graft re-infection further increased surgical complexity and the risk of poor outcomes, making this case both technically challenging and clinically instructive.
International guidelines recommend oral vitamin A supplementation for VAD in patients without gastrointestinal impairment.8 In our case, a history of bariatric surgery suggests reduced ability to absorb fat-soluble vitamins such as vitamin A, making intramuscular administration the preferred treatment. However, due to a nationwide backorder of intramuscular vitamin A at the time, we were compelled to use oral administration.
In patients with fat-soluble vitamin malabsorption who cannot access intramuscular vitamin A, alternative strategies may include high-dose oral water-miscible or water-soluble vitamin A formulations, which can improve bioavailability compared to traditional fat-based preparations.9,10 Additionally, ensuring close nutritional counseling, including addressing dietary fat intake and monitoring serum retinol levels, can help guide individualized therapy. Where feasible, hospital-supervised supplementation may also improve adherence in patients at risk of poor outpatient compliance.11
Further research is needed to optimize oral replacement protocols in bariatric surgery patients with ocular complications. Combination treatment (intramuscular plus oral vitamin A) has been reported, as in the case of a short bowel syndrome patient with corneal ulceration and VAD who demonstrated resolution of ocular symptoms with intramuscular vitamin A administration initially, followed by oral supplementation for maintenance.12 Unfortunately, our patient demonstrated poor compliance with multivitamin supplementation prior to presentation, and oral supplementation during the treatment period was insufficient. Although improvement was observed on OD with resolution of conjunctival keratinization, but no healing response on the OS due to infection. A key limitation of this case report is that the patient became lost to follow-up and vitamin A normalization was not confirmed. This limits our ability to draw firm conclusions about long-term outcomes and reduces the generalizability of our observations. Therefore, the findings should be interpreted as descriptive and hypothesis-generating. While this case suggests the importance of considering long-term nutritional management in similar clinical scenarios, it does not establish causality and should be viewed as an illustrative example underscoring the need for further study.
This case report presents a case of VAD-induced xerophthalmia occurring eight years following bariatric surgery due to multivitamin noncompliance prior to presentation for visual symptoms, highlighting the importance of long-term nutritional management in patients with a history of bariatric surgery in order to prevent complications such as irreversible vision loss.
CRediT authorship contribution statement
Jose Miguel Mora Correa: Writing – review & editing, Writing – original draft, Methodology, Formal analysis. Arslon Humayun: Writing – review & editing, Writing – original draft, Visualization, Validation. Stephen G. Schwartz: Writing – review & editing, Validation, Supervision. Jaime D. Martinez: Writing – review & editing, Visualization, Validation, Supervision, Formal analysis.
Patient consent
Written consent to publish this case has not been obtained. This report does not contain any personal identifying information.
Authorship
All authors attest that they meet the current ICMJE criteria for Authorship.
Declaration of generative AI and AI-assisted technologies in the writing process
During the preparation of this work the author(s) used ChatGPT (ChatGPT4, OpenAI, San Francisco, CA, USA) service in order to polish grammar and spelling. After using this tool/service, the author(s) reviewed and edited the content as needed and take(s) full responsibility for the content of the published article.
Funding
Supported by NIH Center Core Grant P30EY014801 (Institutional); Research to Prevent Blindness- Unrestricted Grant GR004596 (Institutional).
Declaration of competing interest
The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgements
None.
References
- 1.Clapp B., Ponce J., Corbett J., et al. American society for metabolic and bariatric surgery 2022 estimate of metabolic and bariatric procedures performed in the United States. Surg Obes Relat Dis. 2024;20(5):425–431. doi: 10.1016/j.soard.2024.01.012. [DOI] [PubMed] [Google Scholar]
- 2.Aasheim E.T., Björkman S., Søvik T.T., et al. Vitamin status after bariatric surgery: a randomized study of gastric bypass and duodenal switch. Am J Clin Nutr. 2009;90(1):15–22. doi: 10.3945/ajcn.2009.27583. [DOI] [PubMed] [Google Scholar]
- 3.Jalilvand A., Blaszczak A., Needleman B., Hsueh W., Noria S. Vitamin A deficiency in patients undergoing sleeve gastrectomy and gastric bypass: a 2-year, single-center review. J Laparoendosc Adv Surg Tech. 2020;30(1):20–30. doi: 10.1089/lap.2019.0627. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Eckert M.J., Perry J.T., Sohn V.Y., et al. Incidence of low vitamin A levels and ocular symptoms after Roux-en-Y gastric bypass. Surg Obes Relat Dis. 2010;6(6):653–657. doi: 10.1016/j.soard.2010.02.044. [DOI] [PubMed] [Google Scholar]
- 5.Feroze K.B., Kaufman E.J. Stat Pearls. Stat Pearls Publishing; Treasure Island, FL: 2024. Xerophthalmia.https://www.ncbi.nlm.nih.gov/books/NBK431094/ Retrieved from. [Google Scholar]
- 6.De Salvo G., Maguire J.I., Lotery A.J. Vitamin A deficiency-related retinopathy after bariatric surgery. Graefe’s Arch Clin Exp Ophthalmol. 2012;250(6):941–943. doi: 10.1007/s00417-011-1715-8. [DOI] [PubMed] [Google Scholar]
- 7.Donaldson K.E., Fishler J. Corneal ulceration in a LASIK patient due to vitamin A deficiency after bariatric surgery. Cornea. 2012;31(12):1497–1499. doi: 10.1097/ICO.0b013e318243e4ac. [DOI] [PubMed] [Google Scholar]
- 8.World Health Organization Vitamin A deficiency and xerophthalmia: report of a joint WHO/USAID meeting. World Health Organ Tech Rep Ser. 1976;590:1–88. [PubMed] [Google Scholar]
- 9.Decker G.A., Swain J.M., Crowell M.D., Scolapio J.S. Gastrointestinal and nutritional complications after bariatric surgery. Am J Gastroenterol. 2007;102(11):2571–2581. doi: 10.1111/j.1572-0241.2007.01421.x. [DOI] [PubMed] [Google Scholar]
- 10.Blomhoff R., Green M.H., Green J.B., Berg T., Norum K.R. Vitamin A metabolism: new perspectives on absorption, transport, and storage. Physiol Rev. 1991;71(4):951–990. doi: 10.1152/physrev.1991.71.4.951. [DOI] [PubMed] [Google Scholar]
- 11.Liljeberg E., Andersson A., Blom Malmberg K., Nydahl M. High adherence to oral nutrition supplements prescribed by dietitians: a cross-sectional study on hospital outpatients. Nutr Clin Pract. 2019;34(6):887–898. doi: 10.1002/ncp.10243. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Fieldhouse H., Nestel A., Theron B., Knox Cartwright N. Corneal perforation due to vitamin A deficiency in a patient with short bowel syndrome. BMJ Case Rep. 2021;14(9) doi: 10.1136/bcr-2021-242776. [DOI] [PMC free article] [PubMed] [Google Scholar]




