Injuries from Sulphuric Acid, Nitric Acid, and Hydrochloric Acid — A Comparison

Core Mechanism (All Three)

"Exposure to acidic compounds can produce protein denaturation and subsequent coagulative necrosis. In theory, the eschar limits the depth by which an acid can penetrate." — Rosen's Emergency Medicine

• Acids are proton donors that dissociate into free H⁺ ions in solution
• H⁺ ions denature tissue proteins → coagulum/eschar forms
• The eschar acts as a self-limiting barrier (unlike alkali burns where liquefaction allows deeper penetration)
• Injury severity correlates with concentration, pH (<3), duration of contact, and volume

Comparison Table

Individual Acid Details

1. Sulphuric Acid (H₂SO₄)

• Produces a black or brown eschar
• Concentrated H₂SO₄ is highly hygroscopic — it absorbs water from tissues and generates heat (exothermic hydration), adding a thermal burn component on top of the chemical burn
• Drain cleaners can contain up to 93% H₂SO₄ — even brief contact causes deep coagulative burns
• On ingestion: causes severe oropharyngeal, esophageal, and gastric burns; stomach is more commonly involved than with alkali (antrum/pylorus especially affected)
• Inhalation of sulfur trioxide/sulfuric acid aerosols → acid aerosol lung injury

2. Nitric Acid (HNO₃)

• Produces a characteristic yellow eschar due to the xanthoproteic reaction (nitration of aromatic amino acids — tyrosine — in proteins) — this is diagnostically distinctive
• Yellow staining of skin/mucosa is a hallmark
• Generates nitrogen dioxide (NO₂) fumes, which can cause delayed pulmonary edema — potentially fatal; onset may be hours after exposure
• Workers exposed to nitric acid fumes may appear well initially, then develop severe pulmonary edema 4–24 hours later
• Industrial relevance: used in fertilizer production, metal etching, explosives manufacturing

3. Hydrochloric Acid (HCl)

• Produces a white to gray-brown eschar
• Highly volatile at room temperature — releases HCl gas, which severely irritates the upper airways, eyes, and mucous membranes
• Inhalation causes: intense laryngospasm, bronchospasm, chemical tracheobronchitis, and pulmonary edema
• Toilet bowl cleaners contain up to 26% HCl; industrial/swimming pool cleaners up to 31%
• On ingestion: esophageal injury less common than with alkali; stomach (pylorus) more commonly injured

Shared Features (All Three)

• Coagulative necrosis — eschar formation limits (but does not prevent) deep penetration
• Ocular exposure → corneal injury, potentially permanent vision loss
• Ingestion → oropharyngeal burns, esophageal burns (less severe than alkalis), gastric burns (pyloric stricture common late complication)
• Dermal burns → severity correlates with concentration and contact time; thin skin areas (face, genitalia) more vulnerable
• Management: Remove from exposure, copious water irrigation (decontamination), no neutralization (exothermic risk), supportive care; endoscopy for ingestion

Key Distinguishing Points (Summary)