Ocular Chemical Burns



  • Chemical exposure to the eye can result in rapid, devastating, and permanent damage and is one of the true emergencies in ophthalmology.
    • Alkali burns: more severe; alkaline compounds are lipophilic and penetrate rapidly into eye tissue; saponification of cell membranes leads to necrosis and may cause injury to lids, conjunctiva, cornea, sclera, iris, and lens.
    • Acid burns: less severe; associated anions from acidic compounds cause protein denaturation, 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



  • Estimated 5 to 6 cases/100,000 persons per year (accounting for 11–22% of all ocular injuries)
  • Median age is 32 years, but children between the ages of 1 and 2 years represent the highest-risk group.
  • Male > female
  • Most common in workplace and residential settings

Etiology and Pathophysiology

  • Alkaline compounds (pH >7)
    • Alkali burns are twice as common as acid burns.
    • Typical sources include ammonia (most common), calcium hydroxide (lime), sodium/potassium hydroxide (lye), and ammonium hydroxide.
    • Lipophilic compounds that penetrate into deep structures dissociate into cations and hydroxide. Hydroxide causes saponification of fatty acids in cell membranes, leading to cell death. Cations cause hydration of glycosaminoglycans, leading to hydration of collagen, rapid shortening and thickening of collagen fibrils, and resultant corneal opacification and acute elevation in intraocular pressure (IOP).
    • Long-term elevation in IOP may occur from accumulation of inflammatory debris within the trabecular meshwork.
    • Penetration into deep structures may affect perfusing vessels, leading to ischemia.
  • Acidic compounds (pH <7)
    • Typical sources include sulfuric acid (most common), sulfurous acid, hydrochloric acid, acetic acid, hydrofluoric acid.
    • Anion leads to protein denaturing and protective barrier formation by coagulation necrosis forming an eschar. This more superficial mechanism of injury reduces further tissue penetration but may lead to more prominent scarring.
    • Hydrofluoric acid is an exception. In its nonionized form, it behaves like an alkaline substance that can penetrate the corneal stroma and lead 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.

Risk Factors

  • Industrial work, including in chemical labs
  • Construction work (plaster, cement, whitewash)
  • Use of cleaning agents (drain cleaners, ammonia)
  • Automobile battery explosions (sulfuric acid)
  • Any risk factor for assault

General Prevention

  • Safety glasses/goggles to safeguard eyes
  • Safe handling training for occupational exposures

Commonly Associated Conditions

Facial (including eyelids) cutaneous chemical or thermal burns

There's more to see -- the rest of this topic is available only to subscribers.