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Thomas ST Li

Updated on 23 April 2006


  • The most important bipyridyl herbicide for killing weed
  • Completely denatured in contact with earth
  • Available in liquid concentrate, granules, aerosol


Chemical properties

  • Extremely soluble in water, insoluble in most organic solvent
  • Not volatile, sprayed droplets too large to enter lung
  • Potentially lethal if swallowed
  • Directly caustic
  • Suppress reduction of NADP®NADPH during photosynthesis in plant & production of superoxide, singlet oxygen, peroxide radicals. Destroy cell membrane


Clinical manifestations

Depends on route of absorption

  • GI absorption: high potential for GI injury and multiple organ failure
  • Skin contact  and inhalation: unlikely to cause significant systemic reactions
  • uGI tract: Ulceration of oral cavity, pharynx and oesophagus. Esophageal perforation is possible.
  • uSkin: skin rash
  • uRespiratory tract: epistaxis, haemoptysis, pneumothorax, pneumomediastinum and subcutaneous emphysema
  • Systemic toxicity
    Acute renal failure
    Acute heart failure
    Acute pulmonary oedema (in 24 – 48 hours)
    Metabolic acidosis (cardiac failure, adrenal insufficiency, hypotension, hypoxaemia, renal failure)


Depends on the dose of paraquat

Mild poisoning

  • < 20 mg paraquat /kg body weight
  • Asymptomatic or vomiting and diarrhoea
  • Minimal renal and hepatic dysfunction
  • Decrease in pulmonary diffusion capacity
  • Complete recovery expected

Moderate poisoning

  • > 20 mg but < 40 mg paraquat / kg body weight
  • Immediate: vomiting
  • Hours: Diarrhoea, abdominal pain, oropharyngeal ulceration
  • 1 – 4 days: acute renal failure, hepatic derangement, hypotension and tachycardia
  • 1 – 2 weeks: cough, haemoptysis, pleural effusion, pulmonary fibrosis
  • Majority of cases die within 2 to 3 weeks from respiratory failure

Acute fulminant poisoning

  • > 40 mg paraquat per kg
  • Immediate: vomiting
  • Hours to days: diarrhoea, abdominal pain, renal and liver failure, GI ulceration, pancreatitis, myocarditis, hypotension, coma and convulsion
  • Death from multi-organ failure in 4 days

Diagnosis of paraquat poisoning

  • Urine sodium dithionite test: reduction of paraquat by sodium dithionite under alkaline solution to form blue radical ion. Colour change to dark blue indicates significant paraquat ingestion
  • Plasma paraquat level by spectrophotometry, gas chromatography, high pressure liquid chromatography and radioimmunoassay




  • Assessement of Airway, breathing and circulation
  • Gastrointestinal decontamination
    • Gastric lavage with (bentonite and Fuller’s earth (15% solution, 1 litre for adult, 15 ml/kg for children))
      Activated charcoal 100 g for adults, 2 g/kg for children
      Add mannitol or magnesium sulfate as purgative
  • Anti-emetic
  • Rehydration
  • Maintain low FiO2
  • Analgesia
  • Mouth care

Increase elimination of paraquat

  • Charcoal haemoperfusion: efficacy controversial
  • Can be used for patient with moderate severity of poisoning
  • < 6 to 10 hours after ingestion
    • In-vitro study showed that elimination by charcoal haemoperfusion is more effective than haemodialysis resulting in lower paraquat concentration
    • Higher rate of reduction of plasma paraquat concentration is also associated with survival

Anti-inflammatory therapy

  • First reported by Addo (Lancet 1986)
  • 72 patients with paraquat (10 ml 20%-24%) poisoning
  • Fuller’s earth, activated charcoal
  • High dose of dexamethasone & cyclophosphamide
  • 72% survived
  • Could not be repeated by Perriens (Human Exp Toxicol 1992)
  • Recent randomized trial from Taiwan (Lin JL et al Crit Care Med 2006) demonstrated reduction of mortality from paraquat poisoning if aggressive pulse methylprednisolone and cyclophosphamide is used together with continuous dexamethasone

    Regimen of treatment suggested by Lin JL et al Crit Care Med 2006 as follows:

    • Activated charcoal via nasogastric tube
    • 2 courses of charcoal haemoperfusion within 24 hours of ingestion
    • Pulse cyclophosphamide 15 mg/kg/day in 200 ml 5% dextrose infused for 2 hours for consecutive 2 days
    • Pulse methylprednisolone 1 g in 200 ml 5% dextrose over 2 hours per day for 3 days
    • Dexamethasone 5 mg IV Q6H until PaO2 ³ 11.5 kPa
    • If PaO2 < 8.6 kPa, repeat pulse methylprednsiolone 1 g in 200 ml 5% dextrose over 2 hours for 3 days and pulse cyclophosphamide 15 mg/kg/day IV over 2 hours for 1 day ( if WBC> 3000m-3)

Prognosis of paraquat poisoning

None of the prognostication model has been prospectively validated

Urine dithionite test:

  • Scherrmann found that patients with negative or pale blue urine on dithonite test had mortality of 14% and 89% died if the urine was navy or dark blue
  • However, urine test might give false result if patient has poor renal function as a result of preexisting renal dysfunction or paraquat related renal dysfunction

Plasma paraquat level

Many hospitals do not have plasma paraquat level assay

If available, paraquat nomogram from Jones, Proudfoot can be used to predict survival

Hart et al also produced probability curves for prediction of mortality

These nomograms are available in a recent review article on paraquat poisoning Eddleston M QJM 2003


Eddlestone et al Prospects for treatment of paraquat-induced lung fibrosis with immunosuppressive drugs and the need for better prediction of outcome: a systematic review Q J M 2003; 96: 809-824

Lin JL et al Repeated pulse of methylprednisolone and cyclophosphamide with continuous dexamethasone therapy for patients with severe paraquat poisoning Crit Care Med 2006; 34 : 368-373

Centers for Disease Control and Prevention | Facts about Paraquat

© Thomas Li, May 2006

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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