Paraquat toxicity

Background

Paraquat is an herbicide that has a rapid and large distribution and can be fatal even with small ingestions. It has a high case-fatality rate (>50%) which makes it a frequent means of suicide in the developing world, as well as a dangerous accidental occupational exposure.

Paraquat exerts its toxic effects via multiple proposed mechanisms, including lipid peroxidation and generation of reactive oxygen species, direct mitochondrial toxicity, and apoptosis.

Clinical Features

Paraquat Tongue (Credit: wikitox.org)

Overall, pulmonary and renal toxicities predominate and are the primary cause of mortality. GI toxicity is nearly universal and is probably an underrecognized cause of mortality secondary to erosion and perforation.

• Gastrointestinal: predominate early
  • Paraquat tongue
  • Esophageal and gastric erosion
  • Nausea and vomiting
• Pulmonary: occurs due to distribution to pneumocytes
  • Pneumonitis
  • Pulmonary fibrosis (delayed)
• Multiorgan failure
  • Acute renal failure
  • Hepatic necrosis
  • Myocardial necrosis
  • Internal bleeding

Evaluation

Note: patients who present in extremis after an ingestion will not survive regardless of management and should be treated palliatively.

ABC's

• Airway: consider early aggressive intubation for any respiratory distress or large (>100mL) ingestions
• Breathing: CXR, O2. Avoid aggressive oxygen therapy if not necessary due to increased free radical production
• Circulation: may develop early shock and require aggressive inotropic support

Laboratory Evaluation

• CBC
• BMP
• LFTs and coagulation tests
• VBG or ABG
• UA: high concentrations of paraquat in the urine will cause it to appear blue

Diagnostics

• CXR
• EKG
• consider CT if stable to evaluate for perforation/mediastinitis