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Surviving accidental paraquat ingestion: a limited evidence zone

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A 17-year-old youth accidentally ingested paraquat, a herbicide which is an uncommon but potentially highly lethal cause of poisoning. He was initially managed at a regional hospital where, upon advice from a Victorian Poisons Information Centre toxicologist, he was commenced on dexamethasone, continuous venovenous haemodiafiltration (CVVHDF), and N-acetyl cysteine (NAC) and sodium salicylate infusions. He was transferred to a transplant centre for consideration of lung transplantation where he was maintained on CVVHDF, dexamethasone and NAC for 2 weeks. Fortunately, despite ingestion of a potentially lethal dose of paraquat at 36.48 mg/kg, he recovered with mild restrictive respiratory deficits, steroid side effects, and oropharyngeal burns as sequelae.

Paraquat toxicity primarily damages the respiratory and renal systems. In the alveolar epithelium, absorbed paraquat concentrations can be up to 10–20 times the serum paraquat levels.1 Here it undergoes oxidation to form superoxide radicals leading to progressive pulmonary fibrosis. In the kidneys, paraquat induces acute tubular necrosis, which impairs its elimination and further increases lung concentrations. The ingestion of greater than 20 mg/kg of paraquat, which represents only 10–20 mL of a 20% w/w solution typically leads to acute kidney injury (AKI) and progressive pulmonary fibrosis causing death in 1–3 weeks.2

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