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Severe forms of ocular surface chemical burns are responsible for conjunctivalisation and neovascularisation of the cornea often associated with recurrent corneal erosions.1 This hallmark of limbal stem cell deficiency (LSCD) can be associated with a variable destruction of the corneal stroma leading to heavy scarring or perforation in the worst cases. Conjunctival lesions can also be responsible for severe sequelae such as symblepharons and dry eyes. The prognosis of severe forms has improved during the last decade as a result of amniotic membrane transplantation (AMT) and the use of auto-2 or allo-3 limbal stem cell transplantation (LSCT). The severity of ocular surface chemical burns varies with the causative agent and the duration of exposure. The penetration depth in the anterior segment correlates with the pH, especially for alkalis.
Acid burns (pH<4): strong acids such as sulfuric acid, found in car batteries, or chlorhydric acid, used for swimming-pool cleaning, will denature, precipitate and coagulate corneal proteins. Protein coagulation generally acts as barrier preventing deeper penetration. It is responsible for a ‘ground glass’ appearance of the cornea.
Alkali burns (pH>10): strong bases such as baking soda or ammonia are lipophylic. They dissociate into a hydroxyl ion and a cation, and will destroy the epithelium, the stroma and the endothelium while they saponify cell membrane fatty acids.1 Hydroxyl ions will denature the collagen matrix. Penetration will keep occurring long after the initial exposure. In 5–15 min, strong bases can reach the anterior chamber and damage the iris, lens, iridocorneal angle and ciliary body.
Hydrofluoridric acid, a weak acid found in antirust solutions, is an exeption. In its nonionised form, it behaves like an alkaline substance, penetrating the corneal stroma and leading to extensive anterior segment lesions. When it becomes ionised it will combine with intracellular calcium and magnesium ions, and …
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