- Darren M Roberts, MBBS, PhD, FRACP
Darren M Roberts, MBBS, PhD, FRACP
- Clinical Toxicologist, Royal Prince Alfred Hospital
- Nephrologist, Canberra Hospital
- Associate Professor, Australian National University
- Nicholas A Buckley, MD, FRACP
Nicholas A Buckley, MD, FRACP
- Professor of Clinical Pharmacology
- University of Sydney Medical School
- Clinical Toxicologist
- Royal Prince Alfred Hospital
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- Stephen J Traub, MD
Stephen J Traub, MD
- Section Editor — Toxicology
- Associate Professor of Emergency Medicine
- Mayo Medical School
- Michele M Burns, MD, MPH
Michele M Burns, MD, MPH
- Section Editor — Pediatric Toxicology
- Assistant Professor of Pediatrics and Emergency Medicine
- Harvard Medical School
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Jonathan Grayzel, MD, FAAEM
- Senior Deputy Editor — UpToDate
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Paraquat ingestion is a leading cause of fatal poisoning in many parts of Asia, Pacific nations, and the Americas . 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 . However, accidental or deliberate ingestion has an extremely high case-fatality rate . 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 .
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 . 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".)
PHARMACOLOGY AND CELLULAR TOXICOLOGY
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 . 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.
Subscribers log in hereLiterature review current through: Sep 2017. | This topic last updated: Aug 23, 2016.References
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- PHARMACOLOGY AND CELLULAR TOXICOLOGY
- CLINICAL FEATURES OF POISONING
- Physical examination and basic monitoring
- LABORATORY EVALUATION AND DIAGNOSTIC IMAGING
- General testing
- Specific testing for paraquat exposure
- DIFFERENTIAL DIAGNOSIS
- Initial resuscitation
- Gastrointestinal decontamination
- Topical and inhalation exposure
- Specific treatments and antidotal therapy
- - Indications for extracorporeal therapies
- - Antiinflammatory and immunosuppressive therapy
- - Antioxidant therapy
- Ongoing management
- Medical management versus palliative care
- PEDIATRIC CONSIDERATIONS
- ADDITIONAL RESOURCES
- SOCIETY GUIDELINE LINKS
- SUMMARY AND RECOMMENDATIONS