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Paraquat Poisoning: ‘What We Do and Do Not Know.’

Arora Navneet, Sarthak Wadhera, Deba Prasad Dhibar

Paraquat is a quaternary compound used as an herbicide for destroying weed and is highly toxic for humans. Its ingestion leads to multi-organ dysfunction, leading to liver insufficiency and lung fibrosis, which are life-threatening due to respiratory failure. A Pubmed, EMBASE, Ovid, and Cochrane library search was done, all authors reviewed all literature and relevant studies, and data were included in references. Paraquat is available in commercial 20% concentrate form, as 2.5% granules, and 0.2% aerosol. Mortality rates are as high as 65% in patients who ingest concentrated formulation compared to 4% in those who ingest diluted solution (25% w/v). Paraquat undergoes redox-cycling to generate reactive oxygen species leads to its toxic effects. This highly reactive oxygen and nitrite species result in multi-organ toxicity which is maximally seen in the lungs. Absorption occurs primarily through the small intestine. Peak concentration in plasma and maintenance of plasma paraquat levels are the two main factors that decide its concentration in the lungs. The destructive phase is followed by the proliferative phase, in which there is the presence of extensive fibrosis. High dose intake leads to acute respiratory distress syndrome, myocardial necrosis, cerebral edema, and renal failure, which leads to multi-organ failure. The diagnosis of paraquat poisoning is based on history. Simple bedside methods like urine or plasma dithionate tests are used to assess systemic paraquat toxicity. Management stands on four pillars which are reducing absorption, supportive care, antioxidant therapy, and immunosuppression.