Paraquat or N, N′-dimethyl-4, 4′-bipyridinium dichloride is a very common potent herbicide. Ingestion causes mucosal damage, gastrointestinal (GI) perforation, and renal and hepatic failure. In large quantity, it can even cause pulmonary, cardiac, and CNS toxicity [1, 2]. A patient may complain of burning sensation of the mouth, nausea, yellowing of the eyes, breathing difficulty, decreased urine output, and erythematous tongue covered with necrotic sluff (Fig. 1). Ingestion of paraquat causes peroxidation of the lipid cell membrane and mitochondrial complex I (NADH-ubiquinone oxidoreductase) by free oxygen radical leading to apoptosis [2]. Current treatment is supportive and consists of gastric decontamination, steroids, and N-acetyl cysteine as free radical scavenger. Hemoperfusion and hemodialysis is considered in patients with renal failure and pulmonary edema [1, 2]. The presence of paraquat tongue should warrant a clinician to carefully look for GI perforation, mediastinitis, pneumothorax, and pneumomediastinum (Fig. 2). Early identification and treatment is important as paraquat has a very high mortality.
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