Related Subjects:
|Drug Toxicity - clinical assessment
|Metabolic acidosis
|Aspirin or Salicylates toxicity
|Ethylene glycol toxicity
|Ethanol toxicity
|Methanol toxicity
|Ricin toxicity
|Carbon Tetrachloride Toxicity
|Renal Tubular Acidosis
|Lactic acidosis
|Iron Toxicity
|Tricyclic Antidepressant Toxicity
|Opiate Toxicity
|Carbon monoxide Toxicity
|Benzodiazepine Toxicity
|Paracetamol (Acetaminophen) toxicity
|Amphetamine toxicity
|Beta Blocker toxicity
|Calcium channel blockers toxicity
|Cannabis toxicity
|Cyanide toxicity
|Digoxin Toxicity
|Lithium Toxicity
|NSAIDS Toxicity
|Ecstasy toxicity
|Paraquat toxicity
|Quinine toxicity
|SSRI Toxicity
|Theophylline Toxicity
|Organophosphate (OP) Toxicity
|Toxin elimination by dialysis
|Drug Toxicity with Specific Antidotes
Carbon tetrachloride (CCl₄) is a toxic halogenated hydrocarbon once used in cleaning agents, refrigerants, and fire extinguishers.
It is now largely banned due to its potent hepatotoxic and nephrotoxic effects.
Absorption occurs via ingestion and inhalation (rapid) or dermal exposure (slower).
🔎 About
- Formerly used in dry-cleaning, fire extinguishers, and industrial solvents.
- Now restricted worldwide due to carcinogenicity and organ toxicity.
- Main organs affected: liver, kidneys, brain, and lungs.
⚙️ Aetiology / Mechanism
- Metabolised by cytochrome P450 enzymes in hepatocytes → formation of free radicals (trichloromethyl, CCl₃·).
- Free radicals cause lipid peroxidation, mitochondrial damage, and centrilobular (zone 3) hepatic necrosis.
- Secondary injury to renal tubules and CNS depression also occurs.
🩺 Clinical Features
- Onset within hours after exposure.
- GI symptoms: nausea, vomiting, diarrhoea, abdominal pain.
- CNS: dizziness, headache, confusion, seizures, coma.
- Hepatic: tender hepatomegaly, jaundice, acute liver failure.
- Renal: oliguria → anuria, haematuria, proteinuria (acute tubular necrosis).
- Respiratory: pulmonary oedema after high inhaled dose.
- Dermal/ocular: burning, erythema, conjunctival irritation.
🔬 Investigations
- Bloods: ↑ AST, ALT, bilirubin, prolonged PT/INR (hepatic necrosis).
- Renal: ↑ creatinine, proteinuria, haematuria, glucosuria.
- Urine output: oliguria or anuria in severe cases.
- Arterial blood gases: metabolic acidosis possible.
💊 Management
- Immediate: ABC, remove from exposure, high-flow oxygen, decontaminate skin/eyes with copious irrigation.
- GI decontamination: Activated charcoal if recent ingestion (within 1 hour).
- Antidote: N-acetylcysteine (NAC) is recommended (same protocol as paracetamol overdose) to counter oxidative stress.
- Supportive: IV fluids for renal protection, monitor electrolytes and urine output.
- Severe cases: consider haemodialysis for refractory renal failure; liver transplant if fulminant hepatic failure develops.
- Avoid alcohol (induces CYP450 and worsens toxicity).
⚠️ Prognosis
- Mild exposures may recover fully.
- Severe poisoning can lead to fulminant hepatic failure, multi-organ dysfunction, and death within days.
📚 References
