Description

• Chemical exposure to the eye can result in rapid, devastating, and permanent damage, and is one of the true emergencies in ophthalmology.
• Separate alkaline from acid chemical exposure:
  • Alkali burns: More severe. Alkaline compounds are lipophilic, penetrating rapidly into eye tissue; saponification of cells leads to necrosis and may produce injury to lids, conjunctiva, cornea, sclera, iris, and lens (cataracts).
  • Acid burns: Acid usually does not damage internal structures because protein denatures, creating a barrier to further acid penetration. (Hydrofluoric acid is an exception to this rule; see below.) Injury is often limited to lids, conjunctiva, and cornea.
• System(s) affected: Nervous; Skin/Exocrine
• Synonym(s): Chemical ocular injuries

Epidemiology

• Predominant age: Can occur at any age, peak from 16–25 years of age
• Predominant sex: Male > Female

• Estimated 300/100,000 per year
• Alkali burns twice as common as acid burns

Risk Factors

• Construction work (plaster, cement, whitewash)
• Use of cleaning agents (drain cleaners, ammonia)
• Automobile battery explosions (sulfuric acid)
• Industrial work (many possible agents)
• Alcoholism
• Any risk factor for assault (~10% of injuries due to deliberate assault)

General Prevention

Safety glasses to safeguard eyes

Pathophysiology

• Acidic compounds:
  • Anion leads to protein denaturing and protective barrier. This more superficial mechanism of injury tends to have prominent scarring that may lead to vision loss:
    • Hydrofluoric acid is an exception. In its nonionized form, it behaves like an alkaline substance, capable of penetrating the corneal stroma and leading to extensive anterior segment lesions. When ionized, it may combine with intracellular calcium and magnesium to form insoluble complexes, leading to potassium ion movements and cell death. Once systemically absorbed, severe hypocalcemia can occur.
• Alkaline compounds:
  • Lipophilic compounds that penetrate into deep structures on disassociation into cations and OH^-
  • OH^- causes saponification of cell membranes, leading to cell death.
  • Cation causes hydration of glycosaminoglycans, leading to corneal opacification, and hydration of collagen, resulting in rapid shortening and thickening of collagen fibrils. Elevated intraocular pressure secondary to distortion of trabecular meshwork may occur.
  • Penetration into deep structures may also affect perfusing vessels, leading to ischemia of affected area.

Etiology

Sources of alkaline and acidic compounds

Commonly Associated Conditions

Facial (including eyelids) cutaneous chemical or thermal burns