Journal of Burn Care & Research

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Journal of Burn Care & Rehabilitation:
September/October 2001 - Volume 22 - Issue 5 - pp 347-351
Features: Burn Prevention Forum

Paraquat Poisoning in a Burn Patient

Gear, Andrew J. L. MD; Ahrenholz, David H. MD; Solem, Lynn D. MD

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Abstract

Paraquat is a bipyridyl compound widely used as a contact herbicide. Since its introduction in 1962, hundreds of deaths have occurred, usually after suicidal or accidental ingestion. Death after dermal absorption of paraquat is uncommon, but has occurred after either contact with undiluted paraquat, disruption of skin integrity, or prolonged exposure. It is the purpose of this case report to describe a patient who had fatal dermal paraquat absorption after a crop-dusting accident in which he sustained 37% TBSA burns. After 9.5 hours of cutaneous exposure, a paraquat level of 0.169 mg/ml was obtained at 20 hours, the standard lethal dose at 16 hours being 0.16 mg/ml. In light of the apparently irreversible pathophysiology of paraquat poisoning with plasma levels as low as 3 mg/L, prevention and early intervention are the best treatments. Our patient may have survived an otherwise routine thermal injury had his wounds been aggressively irrigated in the field.

Paraquat (1,1'dimethyl-4-4'-bipyridylium dichloride) is a broad-spectrum, contact herbicide and desiccant. Since its introduction in 1962, hundreds of deaths have resulted from suicidal or accidental ingestion. 1 In the agricultural setting, paraquat's corrosive effects have been well documented, including nose-bleeds after inhalation, nail damage, skin burns, and eye effects such as conjunctivitis and inflammation of the eyelid. Occupational systemic poisoning with paraquat has been rare.

The first reported case of death caused by to dermal absorption of paraquat was reported in 1974. 3 Since that time, 11 fatal cases have been documented. 4 Systemic toxicity after dermal absorption of paraquat appears to require either 1) contact with undiluted paraquat, 2) disruption of skin integrity, or 3) prolonged contact with dilute paraquat, as demonstrated by the 11 documented cases. Pulmonary fibrosis is the final common pathway of paraquat toxicity, occurring because of selective uptake of paraquat by type II alveoli and subsequent generation of free radicals.

Medical interventions, which have included attempts at forced diuresis such as hemodialysis, and antidotes that either prevent the uptake of paraquat into the lung, increase the efflux of paraquat from the lung, prevent the redox cycling or reduce its consequences, or reduce the fibrous reaction, have proven largely ineffective once a certain systemic level of paraquat had been obtained. In a retrospective review of 42 case reports, no patient with a plasma level greater than 3 mg/L survived, despite therapeutic interventions. The purpose of this case report is to describe a patient who suffered fatal paraquat poisoning after dermal absorption after a crop-dusting accident in which he sustained 37% TBSA burns.

©2001The American Burn Association

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