Ocular Chemical Burns

Ocular Chemical Burns is a topic covered in the 5-Minute Clinical Consult.

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Basics

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 its associated anion causes 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

Epidemiology

  • Predominant age: can occur at any age, peak from 20 to 40 years of age
  • Predominant sex: male > female

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

Etiology and Pathophysiology

  • Acidic compounds
    • Anion leads to protein denaturing and protective barrier formation by coagulation necrosis forming an eschar. 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 hydroxide
    • Hydroxide causes saponification of fatty acids in 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 that leads to an acute elevation in intraocular pressure secondary to shrinking and contraction of the cornea and sclera.
    • Long-term elevation in intraocular pressure may occur from accumulation of inflammatory debris within the trabecular meshwork.
    • Penetration into deep structures may also affect perfusing vessels, leading to ischemia of affected area.
Sources of Alkaline and Acidic Compounds

Alkaline CompoundsTypical Sources
Calcium hydroxide (lime)Cement, whitewash
Sodium hydroxide (lye)Drain cleaner, airbags
Potassium hydroxide (lye)Drain cleaner
AmmoniaCleaning agents
Ammonium hydroxideFertilizers
Acidic CompoundsTypical Sources
Sulfuric acidCar batteries
Sulfurous acidBleach
Hydrochloric acidChem labs, swimming pools
Acetic acidVinegar
Hydrofluoric acidGlass polish

Risk Factors

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

General Prevention

Safety glasses to safeguard eyes

Commonly Associated Conditions

Facial (including eyelids) cutaneous chemical or thermal burns

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Citation

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TY - ELEC T1 - Ocular Chemical Burns ID - 116411 ED - Baldor,Robert A, ED - Domino,Frank J, ED - Golding,Jeremy, ED - Stephens,Mark B, BT - 5-Minute Clinical Consult, Updating UR - https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116411/all/Ocular_Chemical_Burns PB - Wolters Kluwer ET - 27 DB - Medicine Central DP - Unbound Medicine ER -