Common Agents - Culprit Chemicals
- Corrosives:
- Acids (e.g., HCl, $H_2SO_4$ in toilet/battery cleaners): Coagulative necrosis (limits penetration).
- Alkalis (e.g., NaOH, KOH in drain/oven cleaners): Liquefactive necrosis (deep penetration). 📌 Alkali = Liquefactive, Looser tissue.
- Hydrocarbons:
- Kerosene, turpentine, gasoline, petroleum distillates.
- Mechanism: CNS depression, pulmonary aspiration leading to chemical pneumonitis.
⭐ Kerosene aspiration pneumonitis is often more severe than systemic toxicity from ingestion.
- Pesticides:
- Organophosphates (e.g., Malathion, Chlorpyrifos): Irreversible acetylcholinesterase (AChE) inhibition.
- Carbamates (e.g., Carbaryl, Propoxur): Reversible AChE inhibition.
- Pyrethroids (e.g., Permethrin, Allethrin): Sodium channel modulation (prolonged opening).
- Rodenticides:
- Zinc phosphide: Releases phosphine ($PH_3$) gas (mitochondrial toxin).
- Warfarin-type (Superwarfarins): Anticoagulant (Vitamin K epoxide reductase inhibition).
- Cleaning Agents:
- Bleach (Sodium hypochlorite, $NaOCl$): Oxidizing agent, irritant. Mixing with acids releases $Cl_2$ gas. $Cl_2 + H_2O \rightleftharpoons HOCl + HCl$.
- Detergents (Anionic, Cationic, Non-ionic): GI upset. Cationic (e.g., benzalkonium chloride) can be corrosive.
- Disinfectants (e.g., Phenols, Cresols): Cellular toxicity, neurotoxicity, hepatotoxicity.
- Medications (Accidental Ingestion):
- Paracetamol (Acetaminophen): Hepatotoxicity via NAPQI metabolite.
- Iron tablets: Direct GI corrosive effects, systemic iron toxicity (mitochondrial damage).
Clinical Features & Diagnosis - Toxic Tell-Tales
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General: ABCDE, history (source, amount, time), vital signs.
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Key Toxidromes & Features:
Toxin Clinical Features Diagnostic Pointers Corrosives Oral/pharyngeal burns, dysphagia, drooling, stridor, hematemesis, chest/abdominal pain. Signs of perforation (rigid abdomen, shock). Endoscopy (within 6-24h, ideally 12h); Zargar classification (Grade 0-IV). Hydrocarbons Coughing, choking, dyspnea, grunting, tachypnea. Chemical pneumonitis (fever, hypoxia). CNS: lethargy, seizures. Kerosene/gasoline odor. CXR for pneumonitis. Organophosphates Cholinergic crisis: 📌 DUMBBELS (Diarrhea, Urination, Miosis, Bronchospasm/Bronchorrhea, Bradycardia, Emesis, Lacrimation, Salivation/Sweating) / SLUDGE. Muscle fasciculations, weakness. Garlic-like odor. ↓RBC/Plasma cholinesterase. Carbamates Similar to OPs (cholinergic), but generally shorter duration and less severe. Reversible cholinesterase inhibition. Clinical diagnosis. Bleach (NaOCl) Irritant: oral, esophageal, gastric. Nausea, vomiting. Mixing with acid → $Cl_2$ gas (lung injury); with ammonia → chloramine gas. History of exposure/mixing. -
Other Clues: Specific odors (e.g., bitter almonds - cyanide), skin changes, pupillary signs.
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Investigations: CBC, electrolytes, LFTs, RFTs, ABG, ECG. Chest X-ray (hydrocarbons). Specific toxin levels if available.

- Corrosive Ingestion Management Flowchart:
⭐ Absence of oral burns does not rule out significant esophageal injury, especially with alkali ingestion (e.g., drain cleaners).
Management Principles - Toxin Takedown
Core Principles (📌 ABCDE):
- Airway, Breathing, Circulation: Prioritize supportive care.
- Decontamination: Skin, eye, GI.
- Antidotes: Specific, if available.
- Enhanced Elimination: Rarely for common household chemicals.
Decontamination Strategies:
- Skin/Eye: Copious irrigation immediately.
- GI Decontamination:
- Emesis: ⚠️ Contraindicated: Corrosives, hydrocarbons, ↓LOC.
- Gastric Lavage: Limited utility; ⚠️ Contraindicated: Corrosives, hydrocarbons, >1 hr post-ingestion.
- Activated Charcoal: Ineffective for corrosives, hydrocarbons, metals, alcohols. Consider for specific pesticides/medications.

Specific Poisoning Management:
- Corrosives (Acids/Alkalis):
- ⚠️ DO NOT neutralize, induce emesis, or perform lavage.
- Supportive care, NPO, early endoscopy (<24 hrs).
- Hydrocarbons (Kerosene, Petrol):
- ⚠️ DO NOT induce emesis. Risk of aspiration pneumonitis.
- Supportive care, manage pneumonitis (monitor CXR).
- Organophosphates (OP)/Carbamates:
- Full decontamination. Atropine (2-5 mg IV, repeat PRN). Pralidoxime (OPs only: 1-2 g IV).
⭐ Pralidoxime is most effective if given early in organophosphate poisoning (ideally <24-48 hours), before "aging" of the enzyme-phosphate complex.
High‑Yield Points - ⚡ Biggest Takeaways
- Organophosphates: Cholinergic crisis (DUMBELS). Antidotes: Atropine, Pralidoxime.
- Caustics: Acids cause coagulation, Alkalis liquefaction necrosis. No emesis. Early endoscopy.
- Hydrocarbons (Kerosene): Risk chemical pneumonitis. Avoid emesis/lavage (low viscosity). CXR key.
- Carbon Monoxide: Tissue hypoxia, cherry-red skin (late). Dx: COHb levels. Treat: 100% O2, HBOT.
- Methanol/Ethylene Glycol: High AGMA, ↑ osmolar gap. Methanol: visual loss. EG: renal failure. Antidote: Fomepizole.
- Paracetamol: Hepatotoxicity. Antidote: N-acetylcysteine (Rumack-Matthew nomogram).
- Iron: GI bleed, shock, metabolic acidosis. Chelator: Deferoxamine.
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