Paraquat Poisoning


  • highly toxic herbicide
  • common agent in suicide in 3rd world, especially Asia (lethal in small amounts, cheap, available)
  • leading single agent causing death from pesticide poisoning in many countries including Sri Lanka
  • occurs sporadically elsewhere
  • >50% case fatality rate



  • Paraquat is rapidly but incompletely absorbed and then largely eliminated unchanged in urine within 12–24h
  • volume of distribution of 1.2–1.6 l kg−1
  • Kinetics of distribution into target tissues can be described by a two-compartment model with time-dependent elimination from the central compartment. The lungs may be considered a third compartment from which elimination is very slow.


  • Paraquat generates reactive oxygen species which cause cellular damage via lipid peroxidation, activation of NF-κB, mitochondrial damage and apoptosis in many organs.
  • actively taken up against a concentration gradient into lung tissue leading to pneumonitis and lung fibrosis.
  • Paraquat also causes renal and liver injury.


Risk assessment

  • Ingestion of large amounts of liquid concentrate (>50–100 ml of 20% ion w/v) results in fulminant organ failure and death (hours to days)
  • Ingestion of smaller quantities usually leads to toxicity in the two key target organs (kidneys and lungs) developing over the next 2–6 days (still >50% mortality)

Clinical features

  • ulceration of the mucous membranes (paraquat tongue), esophageal perforation
  • nausea
  • sweating
  • vomiting
  • tremors
  • convulsions
  • pulmonary oedema
  • cardiovascular collapse
  • renal failure (early)
  • liver dysfunction with abnormal LFTs
  • acute alveolitis over 1–3 days followed by a secondary fibrosis (3-7 days) with death at up to 5 weeks


As indicated

  • paraquat assay
  • sodium dithionite test on urine (if changes colour to blue -> confirms urine paraquat concentration >1 mg l−1,  indicates a very poor prognosis)
  • FBC, UEC, LFTs, lipase, coags (multi-organ dysfunction)
  • CT Chest
  • endoscopy


  • Fullers earth (non-plastic clay): 30%, 250mL Q 4 hourly -> until comes out in stools
    Activated Charcoal
  • early NGT recommended (due to mucosal injury)
  • avoid gastric lavage (caustic injury, and unlikely to provide any benefit)
  • titrate O2 (can worsening pulmonary fibrosis, mild hypoxia is acceptable e.g. SpO2 >88%)
  • immediate plasma exchange or haemofiltration (not likely to change outcome – distribution to the lungs occurs <2h)
  • immune suppression with cyclophosphamide, MESNA, methylprednisolone and dexamethasone to dampen inflammatory reaction (unproven)
  • Antioxidants such as acetylcysteine and salicylate might be beneficial through free radical scavenging, anti-inflammatory and NF-κB inhibitory actions (no evidence)
  • patients in extremis should be palliated

References and Links

  • Gawarammana IB, Buckley NA. Medical management of paraquat ingestion. Br J Clin Pharmacol. 2011 Nov;72(5):745-57. PMC3243009.

CCC 700 6

Critical Care


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