Article Date: 8/1/2011

Ocular Surface Disease From Vitamin A Deficiency
Treatment Plan

Ocular Surface Disease From Vitamin A Deficiency

By William L. Miller, OD, PhD, FAAO

As a worldwide entity, hypovitaminosis A or vitamin A deficiency is second only to protein calorie malnutrition as a nutritional disorder. Although more common in developing countries, in developed countries it can occur in patients who have psychiatric disease, eating disorders, alcoholism, and in patients adhering to a particular food fad or residing in geographic areas that suffer from poor nutritional health. In addition, conditions and/or surgeries that interfere with fat absorption such as cystic fibrosis and gastric bypass surgery may also lead to a depletion of vitamin A.

Effects of Vitamin A Deficiency

A significant issue often discussed in vitamin A deficiency is its impact on retinal rod photoreceptor function and, in particular, nyctalopia. However, it is its impact on mucous membranes that causes severe debilitating problems leading to blindness and death in severe untreated cases.

Xerosis of the conjunctival and corneal surface will lead to severe dry eye and scarring. A loss of corneal luster will be the initial biomicroscopic sign with possible fluorescein or lissamine green staining of the cornea and/or conjunctiva. As the deficiency progresses, the cornea may take on a “peau d'orange” appearance, indicating a keratinization of this surface. Fluorescein pooling may be evident between the keratinized areas on the corneal surface. The conjunctiva and cornea may also demonstrate frothy areas comprised of keratinized cells admixed with bacteria or fungi commonly called Bitot's spots. These spots can be removed, but the underlying keratinized areas will remain and the frothy spots will re-form with time.

Conjunctival Bitot's spots in children younger than age 6 indicate an active vitamin A deficiency, but in older children their presence may indicate a previous or chronic suboptimal level of vitamin A. Conjunctival signs in children are more indicative of a deficiency than in adults because other known factors such as ultraviolet radiation, aging, smoking, and environmental factors can cause thickening changes in the conjunctiva. Along with conjunctival staining, a loss of goblet cells can be seen after impression cytology of the conjunctival surface.

Treatment Strategies

Treatment of hypovitaminosis A is aimed at re-establishing sufficient quantities of the vitamin through massive supplementation. Guidelines for supplementation are age dependent and outlined by the World Health Organization. Our primary responsibility in suspected patients is to refer them to their primary care provider or internist for evaluation. Current RDA levels for vitamin A are 700 mcg (retinol activity equivalents [RAE]) and 900 mcg (RAE) for females and males, respectively, older than age 14. Massive oral supplementation in severely deficient individuals will be nearly 200,000 IU vitamin A (110mg retinol palmitate or 66mg retinol acetate). For mild deficiency, multivitamins or vitamin A alone may be indicated.

Dry eye symptoms may be alleviated with topical supplementation, but systemic dosing is essential to address the root cause. Topical vitamin A and its derivatives have been suggested to promote ocular surface healing and to aid in dry eye symptoms. However, most studies in this regard have been conducted in an animal model with sparse information available in humans (Kubo et al, 2000; Johansen, 1998, Kim et al 2009). CLS

For references, please visit www.clspectrum.com/references.asp and click on document #189.


Dr. Miller is an associate professor and chair of the Clinical Sciences Department at the University of Houston College of Optometry. He is a member of the American Academy of Optometry and the AOA where he serves on its Journal Review Board. You can reach him at wmiller@uh.edu.

Contact Lens Spectrum, Issue: August 2011