bubble_chart Overview

Keratomalacia is a condition caused by severe vitamin A deficiency, leading to early drying and degeneration of the corneal and conjunctival epithelium. In advanced stages, necrosis and disintegration of the corneal stroma occur. It is most commonly seen in children under 3 years old and often affects both eyes.

bubble_chart Etiology

The main cause is vitamin A deficiency, which can lead to the following situations:

1. The intake of vitamin A is insufficient to meet the body's minimal requirements, such as poor food preparation during artificial feeding or weaning, malnutrition; or due to fever, wasting diseases, lack of parental hygiene knowledge, or inappropriate "dietary restrictions," such as measles, pneumonia, etc.

2. Poor absorption of vitamin A, where the child suffers from digestive tract diseases, such as gastroenteritis, indigestion, dysentery, etc., preventing the absorption of vitamin A.

3. Excessive consumption, where the child's rapid growth and development or excessive consumption during illness increases the demand for vitamin A, leading to a deficiency state.

bubble_chart Pathological Changes

In the early stage, the goblet cells of the conjunctival membrane disappear, the epithelial cells undergo hyaline degeneration, and pigmentation occurs. In the late stage [third stage], the superficial layer of epithelial cells becomes flattened and thickened, the nuclei disappear, and the cells are arranged in a wavy pattern, indicating keratinization changes.

The dry plaques contain secretions from the meibomian glands, epithelial debris, fat, and dry bacilli. Due to the keratinization of epithelial cells, the surface becomes rough and uneven, presenting a foamy appearance.

The early changes of the corneal membrane are similar to those of the conjunctival membrane. In the advanced stage, the keratinized epithelial cells slough off, the anterior elastic layer undergoes necrosis and disappears, the stromal layer develops edema, and leukocyte infiltration and necrosis occur, which may be accompanied by hypopyon.

bubble_chart Clinical Manifestations

Vitamin A deficiency not only causes degeneration of the conjunctival and corneal epithelium but also leads to varying degrees of tissue changes in other epithelial systems of the body, such as the skin, digestive tract, respiratory tract, urinary tract mucous membranes, and even tissues derived from epithelial evolution like the tarsal glands and lacrimal glands. The most significant effects occur in the mucous membranes of the respiratory and digestive tracts, potentially leading to pneumonia, bronchitis, enteritis, and systemic symptoms such as dry skin, emaciation, limb weakness, hoarseness, and diarrhea. The ocular symptoms primarily involve a special dry state of the conjunctiva, particularly in the palpebral fissure area, and necrotic changes in the corneal stroma. The pathological process is divided into four stages.

1. Night Blindness Stage: The earliest subjective symptom reported by patients is the loss of dark adaptation function in dim environments, making vision much blurrier at night than during the day, commonly referred to as "chicken blindness" or "nyctalopia." This is mainly due to vitamin A deficiency, which deprives the rod cells in the retinal neuroepithelium of the raw materials needed to produce rhodopsin, leading to impaired dark adaptation. Infants and young children may struggle to express this symptom due to their age.

2. Pre-Dryness Stage: The bulbar conjunctiva loses its normal luster, and the corneal surface becomes dull. The subconjunctival vessels take on a distinctive bluish-purple hue. If the lower eyelid is held open for 10 seconds, the hazy state of the conjunctival and corneal surfaces rapidly worsens. The conjunctiva loses elasticity, and when the eyeball moves, centrifugal wrinkles appear on the bulbar conjunctiva. Corneal sensitivity significantly declines, and the blink reflex becomes sluggish, accelerating the progression of xerosis. At this stage, scraping smears of bulbar conjunctival epithelial cells can reveal keratinized granules and numerous dry bacilli. Early diagnosis and treatment at this stage are crucial for rapid recovery.

3. Dryness Stage: The bulbar conjunctiva becomes noticeably dry, and distinctive silvery-white foamy triangular plaques may appear on the conjunctiva in the palpebral fissure area, with their bases facing the cornea, known as Bitot's spots. Morphologically, these dry patches resemble solidified mineral oil and cannot be moistened by tears. They typically appear symmetrically on the temporal side of the bulbar conjunctiva in both eyes, and later may also appear on the nasal side. The conjunctiva in the lower eyelid and fornix, as well as the semilunar fold, may exhibit a grayish-blue pigmentation due to melanin growth in the epithelial layer, a unique ocular feature of vitamin A deficiency.

The corneal surface loses its luster, appearing foggy and opaque, like frosted glass. In the palpebral fissure area, the corneal margin connects with the conjunctival dry patches. The corneal periphery may show accompanying pigmentary changes. Corneal sensation may be completely lost, and photophobia becomes pronounced.

4. Corneal Softening Stage: The bulbar conjunctiva becomes rough, thickened, and markedly wrinkled. Corneal infiltration and opacity worsen, turning grayish-yellow or yellowish-white. The cornea rapidly undergoes autolysis, forming ulcers, with hypopyon appearing. Within 1–2 days, the entire corneal tissue may dissolve and perforate, ultimately leading to corneal adhesion leukoma, complete corneal staphyloma, or flattened cornea, resulting in eyeball atrophy and total blindness.

bubble_chart Treatment Measures

The treatment principles are to improve nutritional status, prevent secondary infection of the corneal membrane, and seize the most effective treatment window, which is the early dry stage.

1. Actively treat systemic diseases.

2. Improve nutritional status by selecting foods high in vitamin A, such as liver, eggs, fish, and dairy products. Administer oral vitamin A, as well as complex vitamins B and C. For patients with digestive disorders who cannot absorb oral supplements, provide vitamin A injections.

3. Apply cod liver oil drops locally three times daily, combined with antibiotic eye ointment. Dilate the pupils when necessary, including in the affected eye. During examinations, avoid applying pressure to the eyeball to prevent perforation.

bubble_chart Prevention

1. Strengthen publicity and education, popularize maternal and child health knowledge, ensure reasonable feeding, and correct picky eating habits to provide infants and young children with proper nutrition.

2. When infants and young children suffer from chronic wasting diseases, gastrointestinal diseases, or sexually transmitted diseases, in addition to actively treating the primary conditions, appropriate supplementary nutritious foods should be provided to prevent unreasonable dietary restrictions. If symptoms such as difficulty opening the eyes are observed, an eye examination should be conducted to achieve early detection and timely treatment, avoiding further deterioration of the condition.