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JAMA Ophthalmology Clinical Challenge
May 2016

Conjunctival Lesions and Vision Impairment After Gastrointestinal Surgery

Author Affiliations
  • 1Texas College of Osteopathic Medicine, University of North Texas Health Science Center, Fort Worth
  • 2Brazos Eye Surgery of Texas, Waco
JAMA Ophthalmol. 2016;134(5):597-598. doi:10.1001/jamaophthalmol.2015.4129
Case

A woman in her early 40s sought ophthalmological care after a referral from an optometrist for bilateral eye pain, substantial eye watering, bilateral conjunctival lesions, and decreased vision, which she described as dim once the room was darkened. She had little to no improvement over the last few months with an artificial tear solution. She claimed to be in good health and denied any concurrent medical conditions. She had undergone a weight loss procedure known as a duodenal switch the year prior.

On ophthalmologic examination with a Snellen eye chart, her visual acuity was best corrected to 20/40 OD and 20/30 OS. Her pupils were normal without afferent pupillary defect. She had a marked uptake of lesions, which were revealed with lissamine green stain on the conjunctivae, and an overall appearance of diffuse punctate keratopathy. She had bilateral conjunctival lesions with a foamy appearance both temporally and nasally (Figure). The lenses were clear, and ophthalmoscopy revealed no abnormal findings. Macular optical coherence tomography revealed normal contour with a bilateral cube volume of 9.4 mm3 and a central subfield thickness of 220 and 222 μm for the right and left eyes, respectively. Visual field testing revealed general constriction bilaterally.

Figure.
Conjunctival lesion stained with lissamine green. The lesions were located on temporal and nasal bulbar conjunctivae bilaterally (arrowhead [original magnification ×2.5]).

Conjunctival lesion stained with lissamine green. The lesions were located on temporal and nasal bulbar conjunctivae bilaterally (arrowhead [original magnification ×2.5]).

Box Section Ref ID

What Would You Do Next?

  1. Order anti-Ro and anti-La antibody testing

  2. Measure vitamin levels, including vitamin A (retinol)

  3. Biopsy lesions to rule out malignancy or premalignancy

  4. Ask the patient if she is taking any antibiotics or anticonvulsants

Read the Discussion.

Discussion
Diagnosis

Bitot spots associated with vitamin A deficiency

What to Do Next

B. Measure vitamin levels, including vitamin A (retinol)

After evaluation, it became clear that the patient had a malabsorption syndrome from her weight loss procedure manifesting as ocular symptoms. We immediately measured her levels of vitamins A, D, E, and K and found that she had markedly decreased levels of vitamin A (retinol) and vitamin K and a suboptimal vitamin D level. She was referred for an electroretinogram and dark adaptation that revealed significantly diminished rod function and a final dark threshold 100 000 times higher than the normal threshold. The differential diagnosis of conjunctival lesions, as in this case, may include Sjögren syndrome, squamous conjunctival neoplasia, or Stevens-Johnson syndrome, although not as highly suspected following an intestinal bypass. In each case, management would include ordering anti-Ro and anti-La antibodies, performing a biopsy of a lesion, or removing any causal medications, respectively.

In 1995, the World Health Organization estimated 250 million children to have vitamin A deficiency and nearly 3 million to have xerophthalmia, making it the leading cause of preventable blindness worldwide.1 Vitamin A (retinol) is a fat-soluble vitamin that is vital in maintaining visual function. In the retina, retinol functions as a substrate for rhodopsin in rods and cones. On ocular surfaces, retinol induces the RNA synthesis necessary for normal cell division and maturation.

Xerophthalmia is defined as the ocular manifestations of vitamin A deficiency, including conjunctival and corneal xerosis, Bitot spots, keratomalacia, and corneal scarring. Bitot spots (Figure) are xerotic conjunctival lesions usually located temporally and are often a late clinical manifestation of vitamin A deficiency. Histologically, the lesion is characterized by a loss of goblet cells, an irregular maturational sequence, and disorganization of basal cell layers as a result from keratinizing metaplasia.2,3

Bariatric surgery has rapidly gained popularity in the United States for its benefits of pronounced weight loss, enhanced quality of life, and diminished long-term mortality. A duodenal switch is a procedure that removes a portion of the stomach and bypasses the majority of the small bowel, inducing both restriction and malabsorption to favor excessive weight loss. Common complications include gastroesophageal reflux, dumping syndrome, and vitamin deficiencies.4

A duodenal switch is becoming an increasingly plausible alternative to the traditional gastric bypass, with data showing significant weight reduction in the superobese population. Unfortunately, a duodenal switch has been associated with significantly lower vitamin A and vitamin D levels compared with a gastric bypass.5,6 Of importance, the effects of the vitamin deficiency may not surface for a long period of time after the procedure. In some cases, visual symptoms of hypovitaminosis A have not surfaced until 18 years after various weight loss procedures.7

Although xerophthalmia is quite rare in developed countries, ophthalmologists should be familiar with this presentation because it will likely become more common with the increased popularity of gastrointestinal bypass surgery. The continued misdiagnosis of xerophthalmia in the patient could have ultimately led to blindness or severe corneal ulceration. Therefore, the importance of linking such ocular findings with a past history of weight loss surgery in a timely manner is imperative. Furthermore, these findings warrant a full laboratory workup, including the measurement of vitamin A, D, E, and K levels and an investigation of bleeding and bone density.

Patient Outcome

The patient was referred to our gastroenterology department, which recommended parenteral vitamin A therapy indefinitely until revision surgery could be performed. The patient self-reported complete resolution of visual and ocular symptoms but has not been seen owing to the fact that she was lost to follow-up.

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Article Information

Corresponding Author: Kyle A. Kirkland, BS, Texas College of Osteopathic Medicine, University of North Texas Health Science Center, 3500 Camp Bowie, Fort Worth, TX 76107 (kyle.kirkland@live.unthsc.edu).

Published Online: March 31, 2016. doi:10.1001/jamaophthalmol.2015.4129.

Conflict of Interest Disclosures: All authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and none were reported.

References
1.
Word Health Organization (WHO).  Global Prevalence of Vitamin A Deficiency in Populations at Risk 1995-2005: WHO Global Database on Vitamin A Deficiency. Geneva, Switzerland: WHO; 2009.
2.
Sommer  A.  Xerophthalmia and vitamin A status.  Prog Retin Eye Res. 1998;17(1):9-31.PubMedGoogle ScholarCrossref
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Pirie  A.  Xerophthalmia.  Invest Ophthalmol. 1976;15(5):417-422.PubMedGoogle Scholar
4.
Hess  DS, Hess  DW.  Biliopancreatic diversion with a duodenal switch.  Obes Surg. 1998;8(3):267-282.PubMedGoogle ScholarCrossref
5.
Aasheim  ET, Björkman  S, Søvik  TT,  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.PubMedGoogle ScholarCrossref
6.
Søvik  TT, Aasheim  ET, Taha  O,  et al.  Weight loss, cardiovascular risk factors, and quality of life after gastric bypass and duodenal switch: a randomized trial.  Ann Intern Med. 2011;155(5):281-291.PubMedGoogle ScholarCrossref
7.
Chae  T, Foroozan  R.  Vitamin A deficiency in patients with a remote history of intestinal surgery.  Br J Ophthalmol. 2006;90(8):955-956.PubMedGoogle ScholarCrossref
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