Inhaled nitric oxide in advanced paraquat intoxication

No effective treatment is available for adult respiratory distress syndrome, pulmonary hypertension and progressive lung fibrosis in severe paraquat poisoning. A potentially beneficial effect of nitric oxide inhalation on the mean pulmonary artery pressure and gas exchange in a subject with advanced paraquat intoxication is reported. Eight days after the suicidal ingestion of an unknown dose of paraquat, a 52-year-old female had a [PaO.sub.2] [less than or equal to] 50 mm Hg despite ventilation with an [FiO.sub.2] of 1 and a positive end-expiratory pressure of 14 to 18 cm [H.sub.2O]. After administration of 25 ppm nitric oxide, [PaO.sub.2] increased and the mean pulmonary artery pressure and the right-to-left shunt decreased. Discontinuation of nitric oxide resulted in rapid reversal. Ventilatory function was stabilized for three days during nitric oxide inhalation but the patient developed massive pleural effusions and died on d 11 during an interruption of nitric oxide therapy. The response of serious paraquat intoxications to nitric oxide therapy may merit further study. A remarkable post-mortem finding was extensive myonecrosis supporting prolonged muscular retention of paraquat with toxic myopathy or neuromyopathy as a late manifestation of paraquat toxicity.
INTRODUCTION Severe paraquat intoxication is associated with high lethality due to progressive respiratory failure and pulmonary fibrosis (1-3). Paraquat is reduced by NADPH to a rather stable diradical, which induces [...]