Ophthalmologic Approach to Chemical Burns

Updated: Apr 11, 2017
  • Author: Mark Ventocilla, OD, FAAO; Chief Editor: Andrew A Dahl, MD, FACS  more...
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Overview

Background

Chemical injuries to the eye represent one of the true ophthalmic emergencies, wherein time is truly critical. While almost any chemical can cause ocular irritation, serious damage generally results from either strongly basic (alkaline) compounds or strongly acidic compounds. Alkali injuries are more common and can be more clinically challenging, with a significant potential for long-term morbidity. 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 neovascu Severe chemical injury with early corneal neovascularization.
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Pathophysiology

The severity of this injury is related to chemical composition, pH, 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 in the cornea. This usually occurs when a strong acid has a pH of less than 4. The hydrogen molecule damages the ocular surface by altering the pH, while the anion causes protein denaturation, precipitation, and coagulation. Protein coagulation creates a barrier and thus 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 are lipophilic and can penetrate cell membranes. They 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, in turn, result in increased intraocular pressure (IOP), sometimes permanent. 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 Alkali burn. Note the severe conjunctival reaction and stromal opacification blurring iris details inferiorly.
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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] Thus, 90% result from accidental exposures. Safety glasses can help prevent injuries, but industrial accidents often involve chemicals under high pressure. Safety glasses are not of much defense in this setting. 

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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