Pathophysiology and diagnosis

In human oral paraquat poisoning, full recovery can be expected if ingestion is less than 20 mg/kg, death may occur on ingestion of 20 to 40 mg/kg, and death usually occurs if more than 40 mg/kg is ingested (Val.§...M...§L 1987).

Paraquat actively accumulates in the lung. The mechanisms of toxicity are suspected to be lipid peroxidation in biological membranes caused by superoxide free radicals generated from the oxidoreduction of paraquat.

Immediately after ingestion, vomiting and diarrhea with the blue-green pigment of the formulation occur. Painful erosions of oral and pharyngeal mucosa and the gastrointestinal tract become evident within 1 to 2 days. Moderate renal and hepatic dysfunction may also appear. Hypoxemia due to pulmonary edema and alveolitis occurs within a few days of ingestion, and develops into intractable pulmonary fibrosis resulting in death within a period of weeks. The central nervous system disturbances do not develop until the severe hypoxemia progresses. If ingestion is massive, patients die of cardiac failure within a few days.

Adding a grain of sodium hydroxide and the smallest spatula blade full of sodium dithionite to 10 ml of urine or gastric aspirate produces a blue coloration if 1 ppm or more of paraquat is present. The results of this test on urine on admission roughly predict the severity of poisoning.

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