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|Metabolic acidosis
|Aspirin or Salicylates toxicity
|Ethylene glycol toxicity
|Ethanol toxicity
|Methanol toxicity
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|Cannabis toxicity
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|Digoxin Toxicity
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|Paraquat toxicity
|Quinine toxicity
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|Drug Toxicity with Specific Antidotes
Paraquat toxicity is highly lethal. β Avoid high-dose oxygen therapy acutely, as it worsens free radical damage and accelerates pulmonary fibrosis.
About
- Paraquat (1,1-dimethyl-4,4-bipyridylium dichloride) is a widely used herbicide, found in weed killers such as Gramoxone, Weedol, and Pathclear. π±
- Highly toxic when ingested: as little as 10β15 mL of 20% concentrate can be fatal. β οΈ
- Absorbed rapidly from the GI tract; tissue accumulation occurs in the lungs and kidneys.
- Toxicity is worse in developing countries where paraquat use is less tightly regulated. π
Pathophysiology π§¬
- Redox cycling: Paraquat undergoes repeated redox reactions, generating superoxide anions and reactive oxygen species (ROS). β‘
- Pulmonary accumulation: Actively taken up by alveolar type I & II pneumocytes β intense oxidative stress β alveolitis β progressive pulmonary fibrosis.
- Renal injury: Proximal tubular necrosis from direct toxicity and oxidative stress β acute kidney injury (AKI).
- GI tract: Corrosive injury causes painful oral, oesophageal, and gastric ulceration β perforation risk. π£
- Systemic: Multi-organ failure due to widespread oxidative damage and mitochondrial dysfunction.
Clinical Presentation π©Ί
- Early (0β24h): Severe nausea, vomiting, diarrhoea, oral & pharyngeal ulceration (painful swallowing).
- Intermediate (24β72h): Worsening renal impairment (oliguria, βurea/creatinine), hepatic dysfunction, respiratory distress.
- Late (>72h): Progressive pulmonary fibrosis β hypoxaemia, ARDS-like picture, respiratory failure.
- Complications: Oesophageal perforation, mediastinitis, pneumomediastinum. β οΈ
Investigations π¬
- Blood paraquat concentration: Correlates strongly with outcome; nomograms exist but availability is limited.
- CXR/CT: Early may be normal; later shows diffuse interstitial infiltrates, fibrosis.
- ABG: Metabolic acidosis + progressive hypoxia.
- U&E: Rising creatinine = poor prognosis.
- LFTs: Hepatic dysfunction common.
- FBC: Often non-specific but may show inflammatory changes.
Management π
- ABCs: Critical care admission; continuous monitoring.
- Decontamination: Activated charcoal 100 g (or Fuller's earth if available) ASAP within 1h. β±οΈ
- Supportive therapy: IV fluids for renal protection; careful fluid balance. βοΈ
- Oxygen: β Avoid high FiOβ unless severe hypoxia (SpOβ <90%). Oxygen fuels ROS-mediated injury. Use lowest oxygen concentration compatible with life.
- Immunosuppression: Some centres trial high-dose steroids + cyclophosphamide to limit pulmonary fibrosis; evidence mixed.
- Renal replacement therapy: Haemodialysis or haemoperfusion may remove paraquat if started very early (<4β6h), but often too late by presentation.
- Antioxidants: Trials of vitamin C, vitamin E, and N-acetylcysteine (NAC) have shown limited benefit but sometimes used as adjuncts. π
Prognosis π
- Extremely poor if >6 g ingested or paraquat plasma levels high on nomogram.
- Under 1.5 g rarely fatal; between 1.5β6 g β ~60β70% mortality.
- Mortality often due to progressive pulmonary fibrosis β patients suffocate despite initial survival. π«
- No proven antidote; outcome depends on dose, early decontamination, and supportive care.
Clinical Pearls β¨
- π Any suspected paraquat ingestion warrants immediate referral to intensive care and toxicology services.
- π Severity is dose-dependent; but even small amounts can be fatal in low body weight or with comorbidities.
- π« The unique teaching pearl: oxygen accelerates lung damage β examiners love this fact.
- π©ββοΈ Prognosis is so poor in severe cases that palliative discussions may be needed early.