Ophthalmologic Approach to Chemical Burns
- Author: J Bradley Randleman, MD; Chief Editor: Hampton Roy Sr, MD more...
Background
Chemical injuries to the eye represent one of the true ophthalmic emergencies. While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or acidic compounds. Alkali injuries are more common and can be more deleterious. Bilateral chemical exposure is especially devastating, often resulting in complete visual disability. Immediate, prolonged irrigation, followed by aggressive early management and close long-term monitoring, is essential to promote ocular surface healing and to provide the best opportunity for visual rehabilitation.[1, 2, 3] See the image below.
Severe chemical injury with early corneal neovascularization. Pathophysiology
The severity of this injury is related to type, volume, concentration, duration of exposure, and degree of penetration of the chemical. The mechanism of injury differs slightly between acids and alkali.[4]
Acid injury
Acids dissociate into hydrogen ions and anions in the cornea. The hydrogen molecule damages the ocular surface by altering the pH, while the anion causes protein denaturation, precipitation, and coagulation. Protein coagulation generally prevents deeper penetration of acids and is responsible for the ground glass appearance of the corneal stroma following acid injury. Hydrofluoric acid is an exception; it behaves like an alkaline substance because the fluoride ion has better penetrance through the stroma than most acids, leading to more extensive anterior segment disruption.[4]
Alkali injury
Alkaline substances dissociate into a hydroxyl ion and a cation in the ocular surface. The hydroxyl ion saponifies cell membrane fatty acids, while the cation interacts with stromal collagen and glycosaminoglycans. This interaction facilitates deeper penetration into and through the cornea and into the anterior segment. Subsequent hydration of glycosaminoglycans results in stromal haze. Collagen hydration causes fibril distortion and shortening, leading to trabecular meshwork alterations that can result in increased intraocular pressure (IOP). Additionally, the inflammatory mediators released during this process stimulate the release of prostaglandins, which can further increase IOP.[5] See the image below.
Alkali burn. Note the severe conjunctival reaction and stromal opacification blurring iris details inferiorly. Epidemiology
Frequency
United States
Chemical injuries are responsible for approximately 7% of work-related eye injuries treated at US hospital emergency departments.[6] More than 60% of chemical injuries occur in workplace accidents, 30% occur at home, and 10% are the result of an assault.[7]
Mortality/Morbidity
As many as 20% of chemical injuries result in significant visual and cosmetic disability; only 15% of patients with severe chemical injuries achieve functional visual rehabilitation.
Race
No overall racial predilection exists; however, young black males are more likely to have high-concentration, high-impact alkaline chemical injuries secondary to assault.[8]
Sex
Males are 3 times more likely to experience chemical injuries than females.[7]
Age
Chemical injuries can strike any population; however, most injuries occur in patients aged 16-45 years.[6, 7]
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