Difference between injuries from sulphuric acid , nitric acid, hcl. As per Fmt subject topic corrosive poisons
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forensic medicine toxicology corrosive poisons sulphuric acid nitric acid hydrochloric acid injuries differences FMT
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HCl hydrochloric acid corrosive poison PM findings forensic medicine stomach eschar signs
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Corrosive Poisons: H₂SO₄ vs HNO₃ vs HCl — Forensic Medicine & Toxicology
General Mechanism (All Three Mineral Acids)
All three act as corrosive poisons through:
- Extraction of water from tissues (hygroscopic action)
- Coagulation/denaturation of cellular proteins
- Conversion of Hb → Acid Haematin (dark brown-black discoloration)
- Chiefly local action on tissues contacted
Comparative Table at a Glance
| Property | Sulphuric Acid (H₂SO₄) | Nitric Acid (HNO₃) | Hydrochloric Acid (HCl) |
|---|---|---|---|
| Synonyms | Oil of Vitriol | Aqua Fortis, Red Spirit of Nitre | Muriatic Acid |
| Appearance | Heavy, oily, colourless, non-fuming, hygroscopic | Colourless/yellowish, acrid, choking odour | Colourless, fuming |
| Fatal Dose | 10–15 ml (conc.) | 20–30 ml | 15–20 ml (some texts 30–40 ml) |
| Fatal Period | 12–24 hours | 12–24 hours | 18–36 hours |
| Tongue colour | Swollen, blackish/brownish | Yellowish (Xanthoproteic reaction) | Greyish → brownish/black |
| Teeth | Chalky white | Yellowish | Chalky white |
| Skin burns | Black/brown eschar | Yellow staining | Whitish/grey burns |
| Perforation risk | Most common | Less common than H₂SO₄ | Least common |
| Gas/fumes inhalation | Less volatile | Marked — fumes cause lacrimation, photophobia, sneezing, cough, dyspnoea | Fumes cause coryza, conjunctivitis, corneal ulcers, bronchitis |
1. Sulphuric Acid (H₂SO₄)
Physical Properties
- Heavy, oily, colourless, odourless, non-fuming, strongly hygroscopic liquid
Mechanism of Injury
- Extreme dehydration of tissues + coagulation of proteins → charring/carbonisation
- Converts Hb → acid haematin (black)
Signs & Symptoms
- Intense burning pain in mouth, throat, chest, abdomen
- Vomiting of black/brown material (haematemesis)
- Swollen, blackened lips, tongue, and oral mucosa
- Voice becomes hoarse and husky
- Abdomen distended and tender
- Mind remains clear until death
- Circulatory collapse, shock
Post-Mortem Findings
External:
- Burns around lips, mouth, chin with black/brown eschar
- Staining of clothes brown/black
Internal:
- Stomach converted into a soft, spongy, black mass that disintegrates on touch
- Lesser curvature most involved
- Spasm of pylorus
- Mucosal ridges more damaged than intervening furrows
- Perforation (7–12 days if survives acutely)
- Corrosion and inflammation of larynx and trachea
- Squamous epithelium of oesophagus relatively resistant; columnar epithelium of stomach is more vulnerable
- Chalky appearance/consistency of teeth
- Carbonisation/charring (pathognomonic of concentrated H₂SO₄)
Time Course of Injury
| Stage | Timing |
|---|---|
| Acute inflammatory | 4–7 days |
| Granulation | 4–7 days |
| Perforation | 7–12 days |
| Cicatrisation/stricture | 3 weeks to years |
Cause of Death
- Circulatory collapse
- Spasm/oedema of glottis
- Perforation of stomach (chemical peritonitis)
- Toxaemia
2. Nitric Acid (HNO₃)
Physical Properties
- Colourless or yellowish liquid with acrid, penetrating, choking odour
- Fuming — produces reddish-brown nitrogen dioxide fumes
Distinguishing Feature: Xanthoproteic Reaction
- Nitric acid reacts with proteins → forms trinitrophenol (picric acid)
- Results in characteristic yellow staining of skin, mucous membranes, teeth, tongue, and clothes
- This is the hallmark of HNO₃ poisoning — unique to this acid
Signs & Symptoms
- Similar to H₂SO₄ but with additional features:
- Yellow staining of tongue, teeth, clothes
- More eructation and greater abdominal distension (due to gas formation — NO₂ gas produced)
- Inhalation of fumes → lacrimation, photophobia, sneezing, coughing, dyspnoea, asphyxia
Post-Mortem Findings
- Generally similar to H₂SO₄, but:
- Yellow discolouration of skin, mucosa, tongue, oesophagus (Xanthoproteic reaction)
- Xanthoproteic reaction may be masked in deeper tissues by dark brown acid haematin
- Stomach wall: swollen, soft with desquamation, haemorrhage, ulceration
- Perforation less common than with H₂SO₄
- Corrosion of mucous membranes may appear brown/black due to acid haematin formation
- Upper small intestine shows irritation
Cause of Death
- Same as H₂SO₄ + risk of asphyxia from inhaled fumes causing pulmonary oedema
3. Hydrochloric Acid (HCl)
Physical Properties
- Colourless, fuming, odourless (concentrated form has pungent odour)
- Least viscous of the three — less likely to remain in contact
Key Feature
- Less corrosive than H₂SO₄ or HNO₃ in equivalent concentrations
- No unique colour reaction — mucosa becomes grey-white initially, then turns brown/black
Signs & Symptoms
- Similar burning pain, haematemesis
- Mucous membrane initially grey or grey-white, later brown or black
- Chronic inhalation of fumes → coryza, conjunctivitis, corneal ulcers, pharyngitis, bronchitis, inflammation of gums, loosening of teeth
Post-Mortem Findings
External:
- Burns around mouth, less severe than H₂SO₄
Internal:
- Stomach contains brownish fluid
- Whole stomach mucosa folds are brownish (diffuse involvement — vs. lesser curvature predominance in H₂SO₄)
- Mucosa shows greyish/brownish discolouration (no yellow, no charring)
- Stomach perforation least common among the three mineral acids
- Oesophageal stricture is the main long-term complication
Cause of Death
- Similar to H₂SO₄ — circulatory collapse, glottic oedema, peritonitis
Key Differentiating Points — Summary for Exams
| Feature | H₂SO₄ | HNO₃ | HCl |
|---|---|---|---|
| Tongue colour | Black/Brown | Yellow | Grey → Brown |
| Skin staining | Black/Brown | Yellow | Whitish |
| Stomach colour | Black, disintegrating | Brown/black (yellow masked) | Brownish (whole stomach) |
| Stomach involvement | Lesser curvature > rest | Diffuse | Diffuse, whole mucosa |
| Perforation | Most common | Less common | Least common |
| Unique sign | Charring/carbonisation | Xanthoproteic reaction (yellow) | Chronic fume toxicity (corneal ulcers, dental erosion) |
| Gas production | Minimal | Yes (NO₂ — bloating, dyspnoea) | Fumes (HCl gas) |
| Volatility/Fumes | Non-fuming | Fuming (toxic NO₂) | Fuming (less toxic) |
| Hygroscopic | Strongly | Moderate | Low |
| Medicolegal | Vitriolage (acid attacks) | Less common | Drain cleaner ingestion |
Medicolegal Aspects (Common to All Three)
- Suicidal ingestion is the most common mode
- Accidental — industrial splash injuries
- Vitriolage — throwing acid on another person's face (most common with H₂SO₄ due to availability and high viscosity which causes it to adhere to skin)
- All produce coagulative necrosis (unlike alkalis which cause liquefactive necrosis)
- Stricture formation is the main long-term complication for all three (oesophageal/pyloric)
- Diagnosis confirmed by chemical analysis of viscera
Sources: GMCH Forensic Medicine lecture notes on Corrosive Poisons; Reddy's Essentials of Forensic Medicine; Modi's Medical Jurisprudence & Toxicology — standard FMT curriculum references.
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