Paraquat toxicity

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Paraquat toxicity is highly lethal. ❌ Avoid high-dose oxygen therapy acutely, as it worsens free radical damage and accelerates pulmonary fibrosis.

ℹ️ About

• Paraquat (1,1-dimethyl-4,4-bipyridylium dichloride) is a widely used herbicide, found in weed killers such as Gramoxone, Weedol, and Pathclear. 🌱
• Highly toxic when ingested: as little as 10–15 mL of 20% concentrate can be fatal. ⚠️
• 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. 🌍

Pathophysiology 🧬

• Redox cycling: Paraquat undergoes repeated redox reactions, generating superoxide anions and reactive oxygen species (ROS). ⚡
• Pulmonary accumulation: Actively taken up by alveolar type I & II pneumocytes → intense oxidative stress → alveolitis → progressive pulmonary fibrosis.
• Renal injury: Proximal tubular necrosis from direct toxicity and oxidative stress → acute kidney injury (AKI).
• GI tract: Corrosive injury causes painful oral, oesophageal, and gastric ulceration → perforation risk. 😣
• Systemic: Multi-organ failure due to widespread oxidative damage and mitochondrial dysfunction.

Clinical Presentation 🩺

• Early (0–24h): Severe nausea, vomiting, diarrhoea, oral & pharyngeal ulceration (painful swallowing).
• Intermediate (24–72h): Worsening renal impairment (oliguria, ↑urea/creatinine), hepatic dysfunction, respiratory distress.
• Late (>72h): Progressive pulmonary fibrosis → hypoxaemia, ARDS-like picture, respiratory failure.
• Complications: Oesophageal perforation, mediastinitis, pneumomediastinum. ⚠️

Investigations 🔬

• 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 💉

• ABCs: Critical care admission; continuous monitoring.
• Decontamination: Activated charcoal 100 g (or Fuller's earth if available) ASAP within 1h. ⏱️
• Supportive therapy: IV fluids for renal protection; careful fluid balance. ⚖️
• Oxygen: ❌ Avoid high FiO₂ unless severe hypoxia (SpO₂ <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 (<4–6h), 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. 🍊

Prognosis 📉

• Extremely poor if >6 g ingested or paraquat plasma levels high on nomogram.
• Under 1.5 g rarely fatal; between 1.5–6 g → ~60–70% mortality.
• Mortality often due to progressive pulmonary fibrosis → patients suffocate despite initial survival. 🫁
• No proven antidote; outcome depends on dose, early decontamination, and supportive care.

Clinical Pearls ✨

• 🚑 Any suspected paraquat ingestion warrants immediate referral to intensive care and toxicology services.
• 📈 Severity is dose-dependent; but even small amounts can be fatal in low body weight or with comorbidities.
• 🫁 The unique teaching pearl: oxygen accelerates lung damage — examiners love this fact.
• 👩‍⚕️ Prognosis is so poor in severe cases that palliative discussions may be needed early.