Case Presentation: A 38-year-old female presented with 4-weeks of intractable nausea with non-bloody, non-bilious vomiting and 6-days of vertigo. She was initially hospitalized for nausea and vomiting 4 weeks ago. She underwent a CT abdomen-pelvis, upper gastrointestinal series, and an esophagogastroduodenoscopy (EGD); no cause for her symptoms was identified and she left against medical advice. Her symptoms persisted and she developed vertigo, prompting return to the hospital. She described her vertigo as constant. She also had bilateral blurred vision. She denied other neurologic symptoms. Eight weeks ago, she underwent laparoscopic gastric bypass in Mexico. On presentation, her temperature was 36.7o C, blood pressure was 109/85 mmHg, and pulse was 98 bpm. Physical exam revealed bilateral decreased visual acuity, vertical nystagmus in all directions of gaze, and 4 out of 5 strength in all extremities. Labs demonstrated low vitamin A (16.7 mcg/dL), copper (0.53 mcg/mL), vitamin B1 (<70 nmol/L); and normal zinc, vitamins B3 / B6 / B12 / D / E / K, thyroid stimulating hormone, cortisol, anti-nuclear antibody, antineutrophil cytoplasmic antibodies, heavy metals screen, serum IgG, and cerebrospinal fluid cell count / protein / glucose / IgG / oligoclonal bands / aquaporin-4 antibody / anti-myelin oligodendrocyte glycoprotein antibody. Her brain MRI with and without contrast showed bilateral optic nerve atrophy. Her optic neuropathy was from vitamin A deficiency and her nystagmus and global weakness were from thiamine and copper deficiencies, all from inadequate supplementation post-gastric bypass. She was started on total parenteral nutrition and vitamin supplementation with resolution of her symptoms and normalization of her vitamins A / B1 and zinc levels.

Discussion: Nutritional deficiencies commonly occur after bariatric surgery with an estimated post-operative prevalence of 16% per year.1 Neurologic complications associated with these deficiencies can develop as early as days-to-weeks post-operatively. Vitamin A, copper, and thiamine are particularly vulnerable to rapid depletion after bariatric surgery.2-5 Vitamin A deficiency presents with vision loss due to optic neuropathy and often occurs in patients who have undergone Roux-en-Y bypass.2,6 Copper deficiency is associated with ataxia, weakness, fatigue, numbness, and paresthesia. Thiamine (vitamin B1) deficiency may present with polyneuropathy, oculomotor dysfunction, ataxia, and/or encephalopathy.1 Several factors contribute to the development of acute nutritional deficiencies after bariatric surgery. Despite obesity, preoperative nutritional status is often suboptimal in patients scheduled for bariatric surgery. Existing nutritional deficiencies can be quickly exacerbated by malabsorption after the procedure. Additionally, protracted vomiting after the procedure prevents patients from receiving appropriate vitamin supplementation, allowing for further depletion of stores.1 Excessive alcohol use has also been associated with rapid development of nutritional deficiencies following bariatric surgery.1

Conclusions: General internists should maintain a high level of suspicion for severe vitamin deficiencies in patients with new neurologic symptoms days-to-weeks following bariatric surgery. In these circumstances, prompt testing with a broad nutritional panel and empiric supplementation with vitamins A / D / E / K / B1 / B3 / B6 is warranted, as appropriate repletion may prevent permanent neurological deficits.