Non-Metallic Poisons

Corrosives - Burn & Churn

Corrosives cause chemical burns and tissue destruction on contact, primarily affecting the gastrointestinal tract.

• Post-mortem: Characteristic staining (e.g., H2SO4 blackish, HNO3 yellowish), corrosion, ulceration, perforation of GIT; strictures (if survived initially).
• Medico-legal: Vitriolage (acid assault, commonly H2SO4) covered under BNS Sections 124 and 125 (voluntarily causing grievous hurt by acid attack); accidental or suicidal ingestion.

⭐ Vitriolage, or acid throwing, most commonly involves the use of sulfuric acid (H2SO4) due to its strong corrosive properties and availability. BNS Sections 124-125 specifically address acid attacks with enhanced penalties.

Cyanide & H₂S - Breath Takers

Cyanide ($HCN$)

• Sources: Cassava, Rosaceae seeds, industrial (electroplating), burning plastics/wool.
• MoA: Inhibits cytochrome oxidase C (Fe³⁺) → histotoxic anoxia.
• S/S: Rapid; bitter almond odor (inconstant); dyspnea, seizures, coma, rapid death.

  ⭐ The fatal dose of Hydrogen Cyanide ($HCN$) for an adult is approximately 50-60 mg, and death can occur within minutes.

• PM: Cherry-red lividity (inconstant); bitter almond odor (stomach); mucosal erosions.
• Tests: Prussian blue (tissues); Sodium picrate paper.
• Legal: Toxicological evidence admissible under BSA Sections 45-51; autopsy procedures per BNSS Section 174.

Hydrogen Sulfide ($H_2S$)

• Sources: Decaying organic matter (sewers), industrial (petroleum, paper).
• MoA: Inhibits cytochrome oxidase (like $HCN$).
• S/S: Rotten egg odor (olfactory fatigue ↑ conc.); rapid collapse, respiratory paralysis, pulmonary edema.
• PM: Greenish brain/organs (sulfmethemoglobin); strong rotten egg odor.

Phosphorus - Glow & Groan

• Forms:
  • Yellow/White: Highly toxic (Fatal dose: 1 mg/kg or 50-100 mg for adults, potentially as low as 8 mg).
  • Red: Relatively non-toxic.
• Mechanism: Potent protoplasmic poison → widespread cellular damage (liver, kidneys, heart, GIT).
• Signs & Symptoms (Triphasic):
  • Stage 1: Severe GI irritation (garlic odor, burning pain), vomiting (may glow - phosphorescence).
  • Stage 2: Symptom-free interval (deceptive).

    ⭐ Phosphorescent (glowing) vomitus/feces ("smoking stool syndrome") is characteristic, though not always present.

  • Stage 3: Systemic toxicity: jaundice, acute liver failure, hemorrhages, cardiovascular collapse, convulsions.
• Post-mortem:
  • Jaundice, pervasive garlic odor.
  • Fatty degeneration of liver ("nutmeg liver" / "phosphorus liver").
  • Widespread hemorrhages (skin, serosa, organs).
  • Phosphorescent viscera (if examined promptly in dark).
• Diagnosis: GC-MS or HPLC for detection and quantification of phosphorus metabolites in biological samples (modern methods replacing historical Mitscherlich's test).

Carbon Monoxide - Silent Snuffer

• Sources: Incomplete combustion (fires, faulty heaters, vehicle exhaust in enclosed spaces).
• Mechanism: Binds hemoglobin (affinity 200-250x > $O_2$), forming carboxyhemoglobin ($COHb$), causing tissue hypoxia.
• Signs/Symptoms:
  • Headache, dizziness, nausea, confusion, weakness, LOC, coma.
  • Cherry-red discoloration often post-mortem finding, not always present in living patients at lower $COHb$ levels.
• Post-mortem:
  • Cherry-red/bright pink blood, tissues, organs.
  • Brain edema.
  • Bilateral symmetrical globus pallidus necrosis (delayed death/chronic).
• Diagnosis: Spectroscopic analysis for $COHb$; direct blood $COHb$ levels, co-oximetry, arterial blood gas analysis for metabolic acidosis.

⭐ Bilateral symmetrical globus pallidus necrosis is a strong indicator in survivors of severe CO poisoning with later neurological sequelae, though not exclusive to CO poisoning.

High‑Yield Points - ⚡ Biggest Takeaways

• Phosphorus poisoning: Garlic odor, luminous vomitus/feces, phossy jaw (chronic).
• Cyanide: Bitter almond odor, cherry-red postmortem, inhibits cytochrome oxidase. Antidotes: Nitrites, Thiosulfate.
• Carbon Monoxide (CO): Cherry-red discoloration, forms carboxyhemoglobin (Hb affinity 200-300x > O2).
• Organophosphates (OPC): Inhibit AChE, causing cholinergic crisis (SLUDGE). Antidotes: Atropine, Oximes.
• Methanol: Toxic formic acid metabolite causes optic neuritis, blindness, acidosis. Antidote: Ethanol.
• Corrosive Acids: Cause coagulative necrosis; Alkalis cause liquefactive necrosis.
• Paraquat: Herbicide causing progressive pulmonary fibrosis ("Paraquat lung").