What is paraquat poisoning?

Paraquat Poisoning: Clinical Features and Management

Paraquat poisoning is a life-threatening condition caused by ingestion or exposure to the herbicide paraquat, characterized by multi-organ damage primarily affecting the lungs, kidneys, and liver, with no specific antidote and mortality rates exceeding 90% in cases of significant ingestion.

What is Paraquat?

Paraquat (N,N'-dimethyl-4'-bipyridinium dichloride) is a highly toxic, non-selective contact herbicide widely used in agriculture. Despite its agricultural benefits, paraquat presents severe human health risks:

• Chemical structure: Quaternary ammonium compound
• Commercial forms: Typically available as concentrated solutions
• Mechanism of action: Potent redox cycler that generates free radicals and reactive oxygen species
• Primary toxicity: Causes direct cellular damage through lipid peroxidation and oxidative stress 1

Routes of Exposure

• Ingestion (most common and dangerous route)
• Dermal absorption (through damaged skin)
• Inhalation (rare but possible)
• Injection (subcutaneous, intravenous, or intraperitoneal - extremely rare) 2

Clinical Features

Paraquat poisoning severity can be classified into three categories based on ingested amount 2:

1. Mild Poisoning (<20 mg paraquat ion/kg body weight)

• Asymptomatic or limited to gastrointestinal symptoms
• Complete recovery expected

2. Moderate to Severe Poisoning (20-40 mg paraquat ion/kg body weight)

• Initial gastrointestinal symptoms
• Progressive renal failure (may recover)
• Delayed pulmonary fibrosis (may take days or weeks to develop)
• High mortality rate, death usually occurs within 2-3 weeks

3. Acute Fulminant Poisoning (>40 mg paraquat ion/kg body weight)

• Severe gastrointestinal symptoms
• Multiple organ failure (cardiac, respiratory, hepatic, renal, adrenal, pancreatic, neurological)
• Death within hours to days

Organ-Specific Effects

Gastrointestinal System:

• Painful burning of mouth and throat
• Nausea, vomiting, abdominal pain
• Ulceration of oral mucosa, esophagus, and stomach
• Gastrointestinal hemorrhage

Respiratory System:

• Progressive pulmonary fibrosis (hallmark of paraquat poisoning)
• Hypoxemia requiring oxygen (caution: oxygen may worsen toxicity)
• Acute respiratory distress syndrome (ARDS)

Renal System:

• Acute kidney injury
• Tubular necrosis
• Electrolyte disturbances

Hepatic System:

• Hepatocellular necrosis with cholestatic lesions 3
• Elevated liver enzymes

Other Systems:

• Metabolic acidosis
• Cardiac arrhythmias
• Central nervous system effects (seizures, coma)

Diagnostic Approach

1. History and clinical presentation:

   • Exposure history (amount, time, intent)
   • Characteristic symptoms (oral ulceration, respiratory distress)

2. Laboratory tests:

   • Qualitative urine test for paraquat (dithionite test)
   • Quantitative blood paraquat levels (if available)
   • Complete blood count, electrolytes
   • Liver and kidney function tests
   • Arterial blood gases
   • Chest imaging (may be normal initially)

Management

Critical first steps:

1. Decontamination:

   • Remove contaminated clothing
   • Wash exposed skin thoroughly
   • For ingestion: gastric lavage if within 1-2 hours of ingestion
   • Activated charcoal or fuller's earth administration

2. Supportive care:

   • Fluid resuscitation
   • Electrolyte management
   • Renal replacement therapy if renal failure develops

3. Oxygen therapy caution:

   • In paraquat poisoning, oxygen should only be given if the saturation falls below 85% and should be reduced or stopped if saturation rises above 88% 3
   • Oxygen can paradoxically worsen paraquat toxicity by enhancing free radical production

4. Enhanced elimination:

   • Hemoperfusion (most effective if started within 2-4 hours of ingestion)
   • Hemodialysis for renal failure management

5. Potential therapies (limited evidence):

   • Immunosuppression with cyclophosphamide and corticosteroids
   • Antioxidants (N-acetylcysteine, vitamin E)
   • Lung transplantation (rarely an option due to rapid progression)

Prognosis

• No specific antidote exists 4
• Mortality rate approaches 95% for significant ingestions
• Survival depends on amount ingested, time to treatment, and quality of supportive care
• Long-term survivors often have permanent pulmonary and gastrointestinal complications

Prevention

• Strict regulation of paraquat availability
• Proper storage away from food and beverages
• Education about dangers and proper handling
• Use of appropriate personal protective equipment
• Consideration of less toxic herbicide alternatives

Key Points to Remember

• Paraquat poisoning is one of the most lethal poisonings with extremely high mortality
• The lung is the primary target organ with progressive fibrosis being the hallmark
• Do not administer high-concentration oxygen unless absolutely necessary
• Early and aggressive decontamination is crucial
• Supportive care remains the mainstay of treatment
• Prevention is paramount given the poor outcomes despite treatment