## Chemical Injury Severity Classification **Key Point:** Alkali (base) injuries are more destructive than acid injuries because they penetrate deeper into ocular tissues and cause progressive damage even after initial exposure. ### Mechanism of Alkali Injury Sodium hydroxide and other strong alkalis: 1. Saponify (dissolve) lipids in cell membranes 2. Denature proteins irreversibly 3. Penetrate through corneal stroma and reach anterior chamber 4. Cause liquefactive necrosis with ongoing tissue destruction 5. Lead to severe scarring, symblepharon, and vision loss ### Comparison: Acid vs. Alkali Injuries | Feature | Acid Injury | Alkali Injury | |---------|-----------|---------------| | **Mechanism** | Coagulative necrosis (protein precipitation) | Liquefactive necrosis (saponification) | | **Penetration** | Superficial (limited by coagulum barrier) | Deep (progressive, no barrier) | | **Prognosis** | Better (often reversible) | Worse (permanent damage) | | **Scarring** | Mild to moderate | Severe (symblepharon, entropion) | | **Severity** | Less severe | Most severe | | **Examples** | HCl, H₂SO₄, acetic acid | NaOH, KOH, ammonia | **Clinical Pearl:** Acid injuries form a protective coagulum that limits further penetration, whereas alkali injuries dissolve this natural barrier and continue damaging tissues for hours after exposure. **High-Yield:** In alkali burns, the cornea may appear deceptively clear initially but undergoes progressive melting and perforation due to ongoing collagenase activity and tissue necrosis. ## Management Principle Both require immediate copious irrigation, but alkali injuries require: - Prolonged irrigation (30+ minutes) - Chelation therapy (EDTA) to remove metal ions - Aggressive anti-inflammatory treatment - Close monitoring for late complications (cataract, glaucoma, corneal scarring) 
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