Paraquat

Widely available highly toxic herbicide that generates reactive oxygen species which cause extensive injury to:

• Lungs
• Kidneys
• Liver

Epidemiology and Risk Factors

Pathophysiology

Key pharmacology of paraquat:

• Highly hydrophilic
  • Rapid gut absorption
  • Poor skin absorption
• Rapidly inactivated in soil
  Leads to popularity as a herbicide, as planting can occur immediately.
• Pulmonary accumulation
• Rapid renal clearance of unchanged drug

Aetiology

Clinical Features

Features of Paraquat Toxicity

System	Mild	Moderate	Severe
General			Multi-organ failure Death
Respiratory	Haemoptysis Mucous membrane ulceration	Pulmonary oedema Day 1-3. Pulmonary haemorrhage Pulmonary fibrosis Day 3-7.
Neurological	Tremors	Convulsions
Renal	AKI	ATN
GIT	Nausea Vomiting Diarrhoea Intestinal haemorrhage	Hepatotoxicity Haematemesis

Assessment

History:

Exam:

Investigations

Bedside:

Laboratory:

• Blood
  • Plasma paraquat assay
  • FBE
  • UEC
• Urine
  • Sodium dithionite
    Qualitative measure; urine turns blue on exposure.

Imaging:

Other:

Diagnostic Approach and DDx

Management

• Early management essential to avoid pulmonary fibrosis and death
• Give oral absorbents
• Target mild hypoxia

Resuscitation:

• B
  • Avoid hyperoxia
    SpO₂ >88% acceptable, minimise O₂.

Specific therapy:

• Pharmacological
  • Absorbents
    • Fullers earth
      30% 250ml Q4H until seen in stools.
    • Activated charcoal
      If Fullers earth not available.
  • Antioxidants
    • Salicylate
    • Acetylcysteine
• Procedural
  • Extracorporeal filtration
    Both RRT and plasma exchange are generally ineffective due to rapid pulmonary redistribution.
• Physical
  • Remove contaminated clothes
  • Wash skin with soap and water

Supportive care:

Disposition:

Preventative:

Marginal and Ineffective Therapies

Anaesthetic Considerations

Complications

• Death
  In >50%.

Prognosis

Key Studies

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References