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Paraquat poisoning

Darren M Roberts, MBBS, PhD, FRACP
Nicholas A Buckley, MD, FRACP
Section Editors
Stephen J Traub, MD
Michele M Burns, MD, MPH
Deputy Editor
Jonathan Grayzel, MD, FAAEM


Paraquat ingestion is a leading cause of fatal poisoning in many parts of Asia, Pacific nations, and the Americas [1]. Paraquat is a rapidly-acting, nonselective herbicide that is relatively inexpensive. These characteristics contribute to its widespread use in much of the developing world.

Paraquat is reasonably safe to use in agriculture: dermal or spray exposure generally causes only limited, localized injury [2]. However, accidental or deliberate ingestion has an extremely high case-fatality rate [3]. Largely for this reason, paraquat has been restricted in many parts of the world. In the rural areas of countries where it remains readily available, it is a common method for intentional self-poisoning [1].

Diquat is a related herbicide that is often formulated with paraquat. There are relatively few reports of diquat poisoning, but it appears to involve mechanisms and manifest clinical features similar to those of paraquat [4]. While evidence is limited, the treatment of diquat poisoning is generally the same as that for paraquat poisoning.

The presentation and management of paraquat poisoning will be reviewed here. General approaches to the assessment of the poisoned patient are discussed separately. (See "General approach to drug poisoning in adults" and "Initial management of the critically ill adult with an unknown overdose".)


Chemically, paraquat and diquat are classified as bipyridyl compounds. After absorption, paraquat is concentrated inside many cells where it undergoes redox cycling, a process involving repetitive enzyme-mediated cycling between paraquat and paraquat radicals. A by-product of this process is a superoxide radical, a highly reactive oxygen species, which can cause direct cellular damage or react further to form other reactive oxygen species and nitrite radicals [5]. Redox cycling consumes NADPH, one of the cell’s key antioxidant defenses. The resultant oxidative stress created by the production of free radicals and the depletion of NADPH directly causes cell damage (via lipid peroxidation, mitochondrial dysfunction, necrosis and apoptosis) and triggers a pronounced secondary inflammatory response.

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Literature review current through: Oct 2017. | This topic last updated: Aug 23, 2016.
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