Paraquat poisoning: the rationale for current treatment regimes.

The critical events leading to death from the ingestion of paraquat are absorption from the gastrointestinal tract, active accumulation in the lung almost certainly preceded by acute renal failure and redox cycling in the lung which initiates certain, as yet unidentified, biochemical events leading to cell death with subsequent destruction of the lung and death from anoxia. Present evidence suggests that absorption of paraquat is rapid and the use of absorbents more than 6 hours after ingestion is likely to be ineffective. Further work is needed to characterize the mechanism of absorption and to identify an innocuous chemical which could be added to formulations of paraquat to inhibit absorption; this approach may be the best solution to the problem of paraquat poisoning. Steps to actively remove paraquat from the systemic circulation will probably only succeed in a small number of patients taking moderate doses and developing early renal failure. The 'window' for such treatment may be as narrow as 6-18 h after ingestion. This 'window' would also operate for chemicals designed to inhibit the pulmonary uptake of paraquat. The biochemical events leading to paraquat-induced cell death are not sufficiently defined to permit the design of treatments to prevent or reverse these processes.