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CASE FILES – Diquat Herbicide

Herbicide bottle in open field

Toxicology Case Files from the Utah Poison Control Center

Teaching Points
  • Diquat is a bipyridyl herbicide that acts as a potent generator of reactive oxygen species
  • Activated charcoal, hemodialysis, and antioxidants are treatment options, but evidence is limited to case reports
  • Ingestion of even 1 ounce of concentrated 20% diquat may be fatal
Case Presentation

A 3-year-old male ingested 2 sprays of Spectracide Weed & Grass Killer from a premixed, ready-to-use retail product containing diquat dibromide 2.3%. He coughed and choked and vomited immediately after. He had 4 more episodes of vomiting within the next few hours.

In the emergency department, he appeared well, with no further episodes of vomiting. He had no evidence of mucosal injury. Serial chemistry panels over the next 24 hours were normal except for a slightly elevated chloride. The patient continued to do well, was tolerating oral intake, and was discharged home with poison center follow-up.

Diquat Toxicity

Diquat and paraquat are both contact herbicides. Paraquat is not allowed for household use or residential application in the United States. Paraquat is more toxic than diquat, with mortality rates of 50% even in accidental ingestion. Diquat is permitted for household use, with retail formulations generally supplied as a 2.3% solution at most. Commercial diquat products are more concentrated, up to 20%.

Both paraquat and diquat have similar mechanisms of toxicity. They undergo “redox cycling,” whereby they continuously generate superoxide radicals in the presence of molecular oxygen. They are potent irritants and may cause significant mucosal injury.

Diquat toxicity is most commonly associated with acute kidney injury. Paraquat toxicity is usually more severe and is classically associated with significant lung injury. In severe cases, seizures, coma, and death may occur.

Formal testing for diquat and paraquat is unavailable. However, a simple qualitative test may be used by adding sodium dithionite to plasma or urine. Color change to green (diquat) or blue (paraquat) is indicative of significant quantities of either compound. Many labs do not stock this reagent, but poison centers or a toxicologist may be able to assist with testing. This reagent is not currently available at any area hospitals in Utah.

Case reports utilize numerous different therapies to treat diquat toxicity. Diquat binds activated charcoal, so prompt administration is recommended with antiemetics to control vomiting. Diquat is renally eliminated but has high intrinsic clearance. There are almost no data using modern hemodialysis as most data come from old cases of charcoal hemoperfusion. However, hemodialysis would be reasonable if instituted early after a large, potentially life-threatening ingestion.

Antioxidants may have a role in limiting diquat toxicity, but evidence is severely lacking to support any particular therapy. N-acetylcysteine, corticosteroids, and vitamin E could be considered. Use of supplemental oxygen should be minimized and only used for confirmed hypoxemia.

Using very conservative estimates of 5 mL in each spray, the child may have ingested up to 120 mg of diquat. Mild toxicity with GI symptoms and mild kidney injury occurs with diquat ingestions of <50 mg/kg. Ingestion of 50-200 mg/kg is potentially serious or fatal with refractory shock, renal and hepatic failure, and intracranial hemorrhage. Ingestion of >200 mg/kg is likely fatal within 24-48 hours (Saeed 2001).

  1. Saeed SA, Wilks MF, Coupe M. Acute diquat poisoning with intracerebral bleeding. Postgrad Med J. 2001 May;77(907):329-32. doi: 10.1136/pmj.77.907.329. PMID: 11320278; PMCID: PMC1742045.

Author: Michael Moss, MD, FAACT, Medical Director, Utah Poison Control Center