Corrosive Poisons

Corrosives: Intro - Burn Basics

• Corrosive poisons: Destroy tissues by chemical action on contact.

• Classification:

  • Strong Acids (e.g., $H_2SO_4$, $HNO_3$): Cause coagulative necrosis (dry, hard eschar). Pain often immediate.
  • Strong Alkalis (e.g., $NaOH$, $KOH$): Cause liquefactive necrosis (soft, soapy, deep lesion). Pain may be delayed.

• Burn severity factors: Concentration, quantity, contact duration, tissue penetration.

⭐ Vitriolage, the act of throwing acid (commonly $H_2SO_4$), is a specific offense under BNS Section 124 (voluntarily causing grievous hurt by acid) and Section 125 (voluntarily throwing or attempting to throw acid).

Acid Corrosives - Fierce Fiends

• Mechanism: Coagulative necrosis, forming a firm, dry eschar; limits deeper penetration.
• Symptoms: Intense burning pain (mouth to stomach), dysphagia, odynophagia. Vomitus often dark ("coffee-ground").
• Stomach: Hard, leathery, contracted; perforation less common than alkalis. Pyloric stenosis (late).
• Examples:
  • $H_2SO_4$ (Sulphuric): "Vitriolage"; black/brown burns.
  • $HNO_3$ (Nitric): Yellow skin/mucosa (xanthoproteic reaction).
  • Carbolic Acid (Phenol): Whitish eschar, carbolic odor, green urine (carboluria).
  • Oxalic Acid: Hypocalcemia, renal damage (calcium oxalate crystals).

⭐ Nitric acid ($HNO_3$) causes characteristic yellow staining of tissues due to the xanthoproteic reaction with proteins.

Alkali Corrosives - Melting Menace

• Mechanism: Liquefactive necrosis (saponification, protein dissolution).
• Penetration: Deeper than acids; "melting" tissue.
• Symptoms: Intense pain, dysphagia, vomiting. Mucosa: slimy, swollen, greyish-white.
• Complications:
  • Perforation (oesophageal/gastric, often delayed).
  • Strictures: Common, severe (esp. oesophagus).
  • Laryngeal edema.
• Examples: NaOH (Caustic Soda), KOH (Caustic Potash), Ammonia, Carbonates.
• Management:
  • Dilute: Milk/water (small amounts, cautiously).
  • ⚠️ NO emetics, NO lavage.
  • Endoscopy: Within 12-24 hrs (or when stable).

  ⭐ Alkalis cause liquefactive necrosis, resulting in deeper penetration and a higher risk of severe strictures and perforation than acids.

Acids vs. Alkalis - Dueling Damage

• Acids (e.g., $H_2SO_4$, $HCl$)
  • Necrosis: Coagulative (eschar formation, limits penetration)
  • Pain: Immediate, severe
  • Site: Stomach (pylorus, antrum) > esophagus
  • Vomiting: Common, coffee-ground
  • Strictures: Hourglass stomach; less common in esophagus
• Alkalis (e.g., $NaOH$, $KOH$)
  • Necrosis: Liquefactive (saponification, deep penetration)
  • Pain: Delayed, may be less intense initially
  • Site: Esophagus > stomach
  • Vomiting: Less common
  • Strictures: Common, severe in esophagus

⭐ Alkalis cause deeper burns and have a higher risk of perforation and long-term esophageal strictures compared to acids due to liquefactive necrosis allowing deeper tissue penetration. 📌 Acids = Coagulative; Alkalis = Liquefactive (mnemonic: ACid ALkali).

Corrosives: Mgmt & MLC - Manage & Report

• Management:
  • Secure ABCs, IV access.
  • ⚠️ Contraindicated: Emesis, lavage, charcoal.
  • Dilution: Small sips water/milk (early, cautious).
  • Analgesia, IV fluids, PPIs.
  • Early endoscopy (<24-48h) for grading (Zargar).
  • No clearly established therapeutic protocol for corrosive esophagitis. Steroids (controversial), antibiotics (if confirmed infection).
  • Surgery for perforation/severe necrosis.
• Medico-Legal (MLC):
  • Inform police immediately. If patient leaves/absconds against medical advice, inform police immediately. Give police 24h notice before discharge.
  • Record dying declaration if indicated.
  • Preserve evidence (samples, clothing).
  • Detailed documentation.

⭐ Gastric lavage and emesis are absolutely contraindicated in corrosive poisoning due to risks of re-injury and aspiration.

High‑Yield Points - ⚡ Biggest Takeaways

• Corrosives: strong acids (e.g., H₂SO₄, HNO₃) & alkalis (e.g., NaOH, KOH).
• Acids cause coagulative necrosis (forms eschar); Alkalis cause liquefactive necrosis (deeper penetration).
• Sulphuric acid (Vitriolage): black, leathery burns. Nitric acid: yellow stains (xanthoproteic).
• Stomach in acid poisoning: hard, shrunken, often blackened. Alkali poisoning: soft, gelatinous, hemorrhagic.
• Perforation risk is higher with alkalis due to deeper tissue damage.
• Laryngeal edema is a common, often fatal, complication.
• Gastric lavage and emetics are generally contraindicated.