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Alkali Eye Injury

Also known as: Alkali Burn of the Eye

Exposure to a base (sodium hydroxide, potassium hydroxide, ammonia, calcium hydroxide as lime and plaster, magnesium hydroxide in flares and fireworks, cement). Alkali burns are the commonest and most damaging chemical eye injury.

  • Mechanism: hydroxyl ions saponify cell membrane lipids and hydrolyse collagen; ammonia (lipid soluble) penetrates the anterior chamber within seconds; sodium hydroxide causes deep penetration within minutes; lime causes persistence of particles in the fornix with ongoing release.
  • Consequences: liquefactive necrosis, corneal stromal haze, endothelial loss, trabecular damage with glaucoma, lens opacity, ciliary body damage (hypotony), limbal stem cell destruction.
  • Natural course: acute phase (first 7 days), early repair (days 7 to 21: risk of corneal melt, ulceration, persistent epithelial defect), and late repair (after 3 weeks: scarring, vascularisation, symblepharon, glaucoma).

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