• Ophthalmic Pearls

    Management of Bitot’s Spots

    Written By: Umesh Krishna, MD, Sumana J. Kamath, MD, and Madhurima K. Nay­ak, MD
    Edited by Sharon Fekrat, MD, and Ingrid U. Scott, MD, MPH

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    Vitamin A deficiency (VAD) can cause a range of ocular mani­festations, known collectively as xerophthalmia, including night blindness, conjunctival and corneal xerosis, and keratomalacia, and is an important cause of preventable blindness. The major cause of VAD is malnutrition, followed by malabsorption.1

    The World Health Organization has classified the ocular manifestations of VAD as follows2:

    XN Night blindness
    X1A Conjunctival xerosis
    X1B Bitot’s spots
    X2 Corneal xerosis
    X3A Corneal ulceration <1/3 of surface
    X3B Corneal ulceration >1/3 of surface
    XS Corneal scarring
    XF Xerophthalmic fundus

    This article will focus on X1B, Bitot’s spots.

    Bitot's Spots
    BITOT’S SPOTS. Conjunctival lesion, temporal to the cornea, shows typical dry, foamy appearance.


    Bitot’s spots, first described by the French physician Pierre Bitot in 1863 in debilitated children,3 are an important sign for diagnosing vitamin A deficien­cy (VAD). Bitot’s spots are typically dry-appearing triangular patches of xerosed conjunctiva with a layer of foam on the surface, usually located temporal to the cornea (Fig. 1). These lesions are not wetted by the tear film. Bitot’s spots are more extensive than le­sions caused by focal conditions of the ocular surface such as trachoma, burns, and pemphigoid.4

    Chart 1: Evaluation of Bitot's Spots


    Vitamin A is required for the devel­opment of normal epithelium. VAD causes Bitot’s spots through meta­plasia of the conjunctival epithelium and tangles of keratin admixed with Corynebacterium xerosis, which dwell in the stratum corneum of the conjunc­tiva. The typical foamy appearance is due to gas produced by these bacteria.5 Histologically, Bitot’s spots show kerati­nization, irregular maturation, inflam­matory infiltration, and accumulation of gram-positive bacilli.6

    In developing countries, primary VAD is mainly caused by malnour­ishment,1 particularly from decreased intake of provitamin carotenoids. Preg­nant and lactating women and young children are at greatest risk, owing to higher nutritional demands. Further, in children with measles, VAD increases morbidity and mortality.

    In developed countries, VAD is usually secondary to gastrointestinal disorders that cause malabsorption or impaired storage or transport of vitamin A, including liver, bowel, or pancreatic disease.7 Deficiency may also occur in people following strict vegetarian or vegan diets.

    Causes. The major underlying causes of VAD may be summarized as follows.8,9

    Reduced intake

    • Inadequate food supply
    • Alcoholism
    • Mental illness
    • Dysphagia

    Impaired absorption

    • Crohn’s disease
    • Celiac sprue
    • Pancreatic insufficiency
    • Short bowel syndrome
    • Chronic diarrhea

    Disordered transport

    • Abetalipoproteinemia

    Reduced storage

    • Liver disease
    • Cystic fibrosis

    Role of zinc. Zinc deficiency may also be involved with the pathogenesis of secondary VAD. Inadequate zinc can depress the hepatic synthesis of retinol-binding protein (RBP), which is required for mobilization of retinol from the liver. In addition, zinc may play a role in the conversion of beta-carotene to retinol via the enzyme 15-15 dioxygenase.10

    Table 1: Vitamin A Treatment Regimens


    In addition to an ocular examination, the evaluation of a patient with Bitot’s spots involves a careful history, general health exam, and laboratory investiga­tions to determine the underlying cause (Chart 1). In patients presenting with Bitot’s spots, evaluate first for malnutri­tion in the younger age group and for malabsorption in the elderly.

    History. The clinician should query the patient or guardian on aspects of the social or medical history potential­ly associated with reduced intake or impaired absorption of vitamin A. Rel­evant factors include age, diet, weight loss, alcohol intake, gastrointestinal disorders or surgery, and night blind­ness or other ocular conditions.

    General exam. This should include assessment of the patient’s build and weight, signs of jaundice, and abdomi­nal palpation to rule out hepatomegaly.

    Ocular exam. The clinician should look for possible subconjunctival fi­brosis and symblepharon. The status of the ocular surface may be evaluated by means of Schirmer test, rose bengal, or lissamine green staining, and conjunc­tival impression cytology.

    Blood tests. Serum RBP measure­ment is relatively simple, is inexpensive, has high specificity and sensitivity, and can be done in less-advanced labora­tories.11 The reference range is 30 to 75 mg/L.

    Serum vitamin A/retinol. The refer­ence range is 30 to 80 μg/dL.

    Serum zinc. The reference range is 75 to 120 μg/dL.

    Table 2: RDA of Vitamin A


    High-dose vitamin A is the treatment for all individuals with xerophthalmia and for infants or children with severe malnutrition or measles. See the treat­ment regimens in Table 1.

    Improvement of Bitot’s spots is seen within 2 weeks of high-dose vitamin A therapy. However, the retinal mani­festations of vitamin A deficiency are slower to respond to treatment, with night blindness and dark adaptation problems often persisting for 4 weeks.12


    1 Sharma A at al. Int J Prev Med. 2014;5(8):1058-1059.

    2 Sommer A. Vitamin A Deficiency and Its Con­sequences. Geneva: WHO; 1995. http://apps.who.int/iris/handle/10665/40535.

    3 Shukla M, Behari K. Indian J Ophthalmol. 1979;27(2):63-64.

    4 Sihota R, Tandon R. Diseases of the conjuncti­va. In: Parson’s Diseases of the Eye, 20th ed. New Delhi: Elsevier India; 2007:178.

    5 Ferrari G et al. N Engl J Med. 2013;368(22):e29.

    6 Sommer A et al. Arch Ophthalmol. 1981;99(11):2014-2027.

    7 Ahad MA et al. Eye. 2003;17(5):671-673.

    8 Rubino P et al. Case Rep Ophthalmol Med. 2015. doi:10.1155/2015/181267.

    9 Fernando-Langit A, Ilsen PF. Clin Refract Op­tom. 2008;19(3):86-93.

    10 Tinley CG et al. J Cyst Fibros. 2008;7(4):333-335.

    11 Mahmood K et al. Saudi J Gastroenterol. 2008;14(1):7-11.

    12 Ross DA. J Nutr. 2002;132902S-2906S. http://jn.nutrition.org/content/132/9/2902S.full.


    Dr. Krishna is a resident, Dr. Kamath is a professor, and Dr. Nayak is senior resident in the department of ophthalmology, Kasturba Medical College, Mangalore, Manipal University, Karnataka, India. Relevant financial disclosures: None.