Nitric oxide inhalation for paraquat-induced lung injury

When ingested, concentrated paraquat can cause either rapid death from multisystem failure and cardiovascular shock or delayed death from progressive pulmonary fibrosis. Diquat ingestion does not usually cause pulmonary fibrosis, but produces early onset acute renal failure.

A 52-year-old male ingested approximately 50 mL of a solution containing 13% paraquat and 7% diquat (about 6650 mg of paraquat and 3500 mg of diquat), and subsequently developed adult respiratory distress syndrome and pulmonary fibrosis. Survival prediction employing the criteria of Hart et al. for paraquat plasma levels was 30%. From the probable amount of paraquat ingested, severe toxicity was expected. The clinical course was not consistent with significant diquat toxicity. Treatment included oral Fuller's earth, forced diuresis, hemofiltration, N-acetylcysteine, methylprednisolone, cyclophosphamide, vitamin E, colchicine, and delayed continuous nitric oxide inhalation. The patient recovered and pulmonary function was subsequently normal.

It is unclear which, if any, of the above treatments contributed to recovery, but the encouraging outcome suggests a possible benefit of nitric oxide inhalation in paraquat poisoning which deserves further study.