Paraquat is a fast acting, potent, and non-selective contact herbicide. Paraquat poisoning, resulting in serious damage to various organs, may be caused by ingestion of just one teaspoon of paraquat. Paraquat poisoning is frequently fatal.
The amount of paraquat ingested dictates the extent of organs damage and symptoms . Ingestion of more than 50 to 100 ml of 20% (w/v) liquid concentrate is very likely to cause multi-system organ failure (pulmonary, cardiac, renal, and liver) and death within a few hours to days following ingestion .
Immediate symptoms include pain and swelling of the mouth, throat, and upper airway. Ingestion of a small quantity of paraquat causes pulmonary and renal toxicity over a period of 2 to 6 days. Pulmonary toxicity is characterized by acute alveolitis and pulmonary edema over a period of 1 to 3 days, followed by an aggressive development of pulmonary fibrosis. Manifestations of acute renal failure (e.g., decreased urinary output, severely elevated creatine, cystatin C, and BUN levels) and/or liver toxicity (jaundice and elevated transaminases levels) are also common  .
Some degree of gastrointestinal (GI) toxicity is almost always present in those with paraquat ingestion. GI symptoms may include mucosal lesions of the mouth and tongue (‘paraquat tongue’), pharynx, esophagus, and stomach within the first several days of ingestion. Abdominal pain, nausea, vomiting, and/or diarrhea may also be present. Patients that present with mediastinitis and/or pneumomediastinum secondary to esophageal perforation have a high mortality rate .
Clinicians should first obtain a thorough history that includes the patient's comorbidities, the strength and quantity of paraquat ingested, and the time of ingestion  . The physical exam includes an inspection of the patient's skin and eyes for signs of topical contact, the mouth and pharynx for irritation or ulcerations, auscultation of the chest for crackles which may indicate alveolitis, and the palpation of the abdomen.
The patient's vital signs should be continuously monitored, including respiratory rate and oxygen saturation levels given the high likelihood of pulmonary injury. An arterial blood gas test may be used to evaluate resultant lung injury. A low PaCO2 with concurrent tachypnea indicates the progression of hypoxia. PaO2 steadily declines as paraquat-induced lung injury proceeds; a PaO2 less than 60 mmHg has been associated with a significant rise in mortality .
Quantitative serum and urine paraquat levels should be obtained to ascertain the degree of intoxication . The concentration of paraquat in the body relative to the time of paraquat ingestion predicts the likelihood of death . The dithionite urine test becomes positive for paraquat about six hours following a large ingestion . The serum level usually peaks one hour after ingestion, followed by a rapid decline as it is redistributed to other compartments in the body.
A chest radiography may be performed in patients with symptoms indicative of acute lung injury, hypoxia, hyperventilation, and/or crackles on admission, but it has weak sensitivity. A high-resolution computed tomography of the chest could be performed to ascertain the extent of lung injury, about one week after ingestion   .