Injuries from Sulphuric Acid, Nitric Acid, and Hydrochloric Acid

Comparative Table

Detailed Breakdown

1. Sulphuric Acid (H₂SO₄) — Most Severe Injury

• Mechanism: Three simultaneous actions — (a) coagulation of proteins, (b) dehydration of tissues (extraction of water from cells), and (c) an exothermic reaction on contact with water/tissue moisture, generating intense heat. It is also a strong oxidising agent.
• Skin burn: Deep, black/brown eschar. The thermal component worsens skin burns beyond pure chemical injury.
• Ingestion: Stomach is converted into a soft, spongy black mass that disintegrates on touch. Squamous epithelium is relatively more resistant than columnar epithelium. Lesser curvature most involved. Pyloric spasm occurs. Perforation is common (7–12 days post-exposure).
• Time course of injury:
  • Acute inflammatory stage: 4–7 days
  • Granulation stage: 4–7 days
  • Perforation: 7–12 days
  • Cicatrisation/stricture: 3 weeks to years
• PM findings: Black/dark eschar on mouth, tongue; corrosion/haemorrhage in upper GI tract and respiratory system; sulphurous odour; acid haematin formation in stomach.
• Cause of death: Circulatory collapse, glottic oedema/spasm, peritonitis from gastric perforation, toxaemia.

2. Nitric Acid (HNO₃) — The Yellow Acid

• Mechanism: Coagulative necrosis like sulphuric acid, plus the xanthoproteic reaction — nitric acid reacts with aromatic amino acids in proteins to form trinitrophenol, producing a characteristic yellow/yellowish discolouration.
• Skin burn: Yellow eschar — pathognomonic of nitric acid.
• Ingestion: Signs and symptoms similar to H₂SO₄ but with added features:
  • More eructation and greater abdominal distension due to gas (NO₂/NO) formation
  • Yellow staining of clothes, tongue, and teeth
  • Xanthoproteic reaction less prominent on stomach mucosa (masked by acid haematin → dark brown colour)
• Inhalation of fumes (HNO₃ fumes/NO₂): Lacrimation, photophobia, sneezing, coughing, dyspnoea, asphyxia. This is a distinguishing clinical feature — fume toxicity is prominent.
• PM findings: Yellow discolouration of affected area; stomach mucosa swollen and soft with desquamation, haemorrhage, ulceration; perforation less common than H₂SO₄ but can occur; leakage causing chemical peritonitis.

3. Hydrochloric Acid (HCl) — Least Severe of the Three

• Mechanism: Purely coagulative necrosis (monoprotic acid — releases one proton per molecule). No dehydrating property, no exothermic reaction, no oxidising action — hence less tissue destruction compared to H₂SO₄.
• Skin burn: White to grey-brown eschar.
• Ingestion: Coagulative necrosis of oesophagus, stomach, and duodenum; histologically, superficial necrosis with relatively preserved tissue architecture — important forensic distinction from H₂SO₄, which causes transmural destruction.
• Fumes: HCl fumes are irritant to mucous membranes (lacrimation, cough) but less toxic systemically than NO₂ fumes from HNO₃.
• Tongue/mucosa: Greyish discolouration.
• Fatal dose is highest (30–40 mL) reflecting lower potency per unit volume compared to H₂SO₄.

Key Forensic Distinguishing Features (at a glance)

Medico-Legal Notes

• Vitriolage (throwing acid, usually at the face) most commonly involves H₂SO₄ due to its availability and severity.
• All three acids are most commonly ingested with suicidal intent; accidental splash/ingestion also occurs.
• The colour of the eschar/stain is the single most useful distinguishing sign at the scene and on post-mortem examination.
• All three eventually cause stricture formation as a late complication of GI tract injury.
• Death from acid ingestion results in a characteristic pattern: hardened, grey-firm outer aspect of GI organs with relatively more normal deeper tissue (coagulation barrier effect), most pronounced with H₂SO₄.