- Keratomalacia is a severe, sight-threatening eye disorder resulting from profound vitamin A deficiency, characterized by softening and ulceration of the cornea, which may progress rapidly to corneal perforation and irreversible blindness if not treated promptly.
- It represents an advanced stage of xerophthalmia, a spectrum of ocular manifestations due to vitamin A deficiency, and is most commonly observed in young children in developing countries where malnutrition is prevalent. Though rare in industrialized nations, keratomalacia remains a significant public health issue in parts of Africa, Southeast Asia, and regions with limited access to nutrient-rich food.
- The pathophysiology of keratomalacia involves the breakdown of epithelial integrity and collagen structure in the cornea. Vitamin A plays a critical role in maintaining healthy epithelial tissues, particularly those of the eye, by regulating cell differentiation and mucin production. In the absence of adequate vitamin A, the conjunctiva and cornea become dry and keratinized, eventually leading to corneal xerosis. As the deficiency progresses, the corneal tissue becomes necrotic and liquefied, a process referred to as keratomalacia. This degeneration is further aggravated by secondary infections, poor tear production, and lack of immune defense, all of which contribute to rapid tissue destruction.
- Clinically, keratomalacia often begins with night blindness (nyctalopia) and progresses through stages of conjunctival dryness, Bitot’s spots (foamy patches on the conjunctiva), and corneal dryness. In keratomalacia, the cornea may appear cloudy, ulcerated, or even collapsed, and the globe of the eye may lose its shape due to the liquefaction of corneal stroma. The condition can affect one or both eyes and is frequently bilateral in severe nutritional deficiency. Children with keratomalacia may also exhibit signs of protein-energy malnutrition such as stunted growth, lethargy, and recurrent infections.
- Diagnosis is primarily clinical and based on the distinctive appearance of the cornea, the presence of other xerophthalmic signs, and a history of dietary deficiency or malnutrition. Laboratory tests may reveal low serum retinol levels, although these may be affected by concurrent infections or inflammation. In endemic areas, keratomalacia should be considered a medical emergency due to the speed with which it can lead to irreversible blindness.
- Treatment involves immediate administration of high-dose vitamin A, typically following the World Health Organization (WHO) protocol: 200,000 IU orally on diagnosis, followed by the same dose on the next day and again two weeks later. In cases where oral absorption may be impaired or the child is too ill to take medication orally, intramuscular injection may be used. Topical antibiotics, lubricating eye drops, and sometimes corneal transplantation may be required to manage corneal damage, although visual recovery is often limited if treatment is delayed.
- Prevention of keratomalacia hinges on ensuring adequate vitamin A intake, especially in vulnerable populations such as young children and pregnant or lactating women. Public health measures such as vitamin A supplementation programs, fortification of staple foods, promotion of breastfeeding, and nutrition education have proven effective in reducing the incidence of keratomalacia and associated child mortality.
