Paraquat

CAS RN: 4685-14-7

Treatment Overview

0.4.2 ORAL EXPOSURE
  • A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    • 1) Following decontamination, supportive care is the mainstay of care. Immunosuppressive therapy (glucocorticoids and cyclophosphamide) should be administered to a patient at risk of moderate or severe pulmonary toxicity and those with symptoms consistent with moderate to severe toxicity.
  • B) MANAGEMENT OF SEVERE TOXICITY
    • 1) Following decontamination, supportive care is the mainstay of care. Aggressive fluid resuscitation should aim to replace fluid losses and maintain renal blood flow in order to augment toxin elimination. Early hemoperfusion may reduce mortality. Immunosuppressive therapy (eg, cyclophosphamide, methylprednisolone and dexamethasone) should be administered to treat the acute inflammatory process associated with paraquat poisoning that can lead to lung injury and death (see IMMUNOSUPPRESSIVE THERAPY). Prolonged QT interval has been reported following paraquat exposure. In patients with QT prolongation, monitor serum electrolytes including potassium, calcium and magnesium in patients with significant overdose; correct any abnormalities.
  • C) DECONTAMINATION
    • 1) PREHOSPITAL: DERMAL EXPOSURE: Remove contaminated clothing and wash thoroughly with soap and water.
    • 2) HOSPITAL: DERMAL EXPOSURE: Remove contaminated clothing and wash thoroughly with soap and water. Care should be taken not to abrade the skin because disruption of the stratum corneum may lead to increased toxin absorption. INGESTION: Patients with a recent ingestion should receive nasogastric suction with a soft, small gauge tube in order to remove any liquid remaining in the stomach. After gastric decontamination with an NG tube, aggressive antiemetic therapy should be provided to facilitate administration of the adsorbent agent. Patients with an ingestion within the last 24 hours should be given one of the following: ACTIVATED CHARCOAL: DOSE: ADULT: 50 to 100 g; CHILD: 1 g/kg); BENTONITE CLAY (7% solution): DOSE: ADULT: 100 to 150 g; CHILD less than 12 years of age: : 2 g/kg; or FULLER'S EARTH (30% solution) DOSE: ADULT: 100 to 150 g; CHILD less than 12 years of age: 2 g/kg). AVOID: Gastric lavage is NOT recommended because of corrosive injuries imparted by the solution itself may increase the risk of iatrogenic perforation. OCULAR EXPOSURE: Copious irrigation with saline or sterile water and ophthalmology consultation.
  • D) AIRWAY MANAGEMENT
    • 1) Airway support should be considered for patients with severe CNS depression or those at risk of aspiration.
  • E) ANTIDOTE
    • 1) There is NO antidote available for paraquat toxicity.
  • F) IMMUNOSUPPRESSIVE THERAPY
    • 1) SUMMARY: Several small studies suggest that immunosuppressive therapy can reduce the mortality rate of severe paraquat poisoning. Different strategies have been recommended.
    • 2) PULSE THERAPY: This protocol suggests the following: ACTIVATED CHARCOAL: Gastric lavage followed by administration of 1 g/kg of activated charcoal in 250 mL of magnesium citrate in patients presenting within 24 hrs. HEMOPERFUSION: Two 8 hours courses of activated charcoal hemoperfusion within 24 hrs of paraquat ingestion. After hemoperfusion, administer IV cyclophosphamide 15 mg/kg/day in 200 mL D5NS infused over 2 hrs for 2 consecutive days. Also administer 1 g methylprednisolone in 200 mL D5NS infused over 2 hrs daily for 3 consecutive days. After the initial pulse therapy, administer dexamethasone 5 mg IV every 6 hrs until PaO2 is 80 mmHg (11.5 kPa) or greater. If PaO2 is less than 60 mmHg (8.64 kPa), repeat IV methylprednisolone 1 g in 200 mL D5NS infused over 2 hours daily for 3 consecutive days. If WBC is greater than 3000/m(
    • 3) and it has been 2 weeks since the initial pulse of cyclophosphamide, repeat IV infusion of cyclophosphamide 15 mg/kg in 200 mL D5NS infused over 2 hrs as a single dose. Then continue IV dexamethasone 5 mg every 6 hrs until PaO2 is 80 mmHg (kPa 11.
    • 5) or greater. Then reduce dexamethasone dose gradually.
    • 3) ALTERNATIVE THERAPIES: Other treatment methods have included the following: High-dose therapy includes the same initial treatment (activated charcoal and hemoperfusion) as pulse therapy along with high-dose cyclophosphamide (5 mg/kg
      • /d) and dexamethasone 24 mg/d for 14 days. Another method includes early decontamination and 15 mg/kg of cyclophosphamide in D5NS in 200 mL infused over 2 hrs for 2 days and methylprednisolone 1 g in 200 mL D5NS IV infused over 4 hrs and repeated for 3 consecutive days. Mesna (15 mg/kg) was also administered over 4 days to avoid side effects to cyclophosphamide.
  • G) HYPOTENSION
    • 1) Treat hypotension with isotonic fluid resuscitation until the patient is felt to be euvolemic, followed by addition of vasopressors in standard doses. Cardiac dysrhythmias should be treated according to typical ACLS protocols.
  • H) OXYGEN THERAPY
    • 1) In general, oxygen therapy should be withheld until the PaO2 is below 50 mmHg, because supplemental oxygen may lead to increased production of oxygen free radicals and increased pulmonary toxicity. Lung transplantation may be considered late in the course for patients with severe pulmonary injury and subsequent hypoxia after the serum paraquat concentration is zero.
  • I) NAUSEA AND VOMITING
    • 1) Treatment is supportive with care to ensure replacement of gastrointestinal fluid losses. Antiemetics should be provided liberally (Ondansetron: Adult: 4 to 8 mg IV; Children: 0.15 mg/kg IV). Stress ulcer prophylaxis should be provided, since patients are likely to have corrosive injury due to the ingestion.
  • J) ACUTE TUBULAR NECROSIS
    • 1) Renal injury is due to acute tubular necrosis and is largely reversible. Adequate fluid resuscitation is key to limiting secondary renal injury. Hemodialysis for oliguric renal failure is occasionally necessary as a temporizing measure until renal function improves.
  • K) SEIZURES
    • 1) Seizures should be treated with benzodiazepines.
  • L) ENHANCED ELIMINATION
    • 1) Hemoperfusion may increase survival if initiated early (ideally within 5 hours), based on data from retrospective studies. Both hemoperfusion and hemodialysis have been shown to increase paraquat clearance. Hemoperfusion is the preferred method of extracorporeal elimination, if available.
  • M) PATIENT DISPOSITION
    • 1) HOME CRITERIA: Patients with dermal exposures involving a small body surface area to intact skin that do not have local symptoms or mucous membrane involvement can be managed at home with simple soap and water decontamination.
    • 2) OBSERVATION CRITERIA: Patients with dermal, "lick", "sip" or "taste" exposures can be observed for 6 hours and evaluated for evidence of caustic injuries.
    • 3) ADMISSION CRITERIA: Any patient with an intentional ingestion should be admitted to the hospital for monitoring. Patients with corrosive injury or other systemic toxicity should be admitted.
    • 4) CONSULT CRITERIA: A toxicologist should be consulted for all ingestions and all dermal exposures involving more than minimal body surface area. Appropriate medical subspecialties should be consulted to aid in the support of specific organ dysfunction due to toxicity.
  • N) PITFALLS
    • 1) Failure to consider decontamination early in patients with ingestion can lead to significant absorption and progression of toxicity with no effective treatment. Failure to provide immunosuppressant therapy may lead to increased pulmonary toxicity.
  • O) TOXICOKINETICS
    • 1) Following an ingestion, absorption is rapid and peak serum paraquat concentrations occur within 2 hours. Paraquat is cleared primarily through the kidneys within the first 12 to 24 hours. Dermal absorption through intact skin is minimal. Mucous membrane and ocular exposures may lead to minimal systemic absorption though local tissue damage may be significant.
  • P) DIFFERENTIAL DIAGNOSIS
    • 1) Ingestion of other herbicide products, such as glyphosate, should be considered because they may lead to similar cardiovascular toxicity though pulmonary and renal impairment are uncommon. Other inhalational exposures leading to chemical pneumonitis should be considered in patients presenting with pulmonary toxicity since this is a later finding in paraquat toxicity. Primary medical etiologies of pulmonary fibrosis should be considered if there is not a history of paraquat ingestion.
0.4.3 INHALATION EXPOSURE
  • A) There have been no substantiated cases of paraquat poisoning due to inhalation of "fumes." Inhalation of spray mist does occur, but the droplets are usually large and deposit in the upper respiratory tract where they cause local irritant effects. Although pulmonary toxicity has not been reported after inhalation exposure, supplemental oxygen should be avoided unless significant hypoxia develops.
0.4.4 EYE EXPOSURE
  • A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
0.4.5 DERMAL EXPOSURE
  • A) OVERVIEW
    • 1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).
    • 2) Paraquat is well absorbed through abraded or injured skin; fatalities following skin exposure have occurred. Medical personnel must take precautions so as not to become contaminated.
Find more information on this substance at: PubChem, PubMed