Paraquat Poisoning

Other trade names: Crisquat — Dextrone — Dexuron — Gramoxone Extra — Herba-xone — Ortho Weed and Spot Killer — Sweep

Introduction

Paraquat poisoning (Image sourced from Bristol Biomed Image Archive with permission)

Paraquat is the trade name for a widely used herbicide, named variously as N, N’-dimethyl-4, 4’-dipyridinium dichloride, N, N’-dimethyl-4, 4’-bipyridinium dichloride or N, N’-dimethyl-4, 4’-bipyridyl. It is a non-selective and so is used to kill fast growing weeds amongst crops. Its use has been banned in the E.U since July of 2007 but it is still used by authorized personnel in the U.S and with no supervision at all in some other countries.

It is extremely poisonous to animals and has been known to cause death by chronic poisoning, which is usually accidental, but it has also been seen in acute malicious poisonings. It is also toxic to humans and many cases of illness and death have been recorded worldwide.

Mechanism of toxicity
Paraquat concentrates in alveoli type I and II cells by an energy dependant transport system.
High concentration of Paraquat once accumulated into lung or renal cells then results in redox cycling and generation of free radicals, which cause damage to the air-blood barrier leading to lung damage.

Depending on dose, acute or chronic damage can occur. Oedema and haemorrhage are acute lesions and fibroplasia and change of alveolar cells from type I to type II are signs of chronic damage.
It can also cause pulmonary oedema and congestion and hyaline membrane formation. Inflammatory infiltration will eventually lead to progressive diffuse pulmonary fibrosis.
Additional extrapulmonary lesions to note following paraquat intoxication are necrosis of the adrenal zona glomerulosa and renal tubular epithelium.

Clinical Signs

Initial signs include vomiting, lethargy and anorexia. There will be obvious acute gastrointestinal disturbance. Respiratory signs such as dyspnoea, stertor and coughing, as well as other signs of respiratory distress and failure.

On physical examination, there may be evidence of hypertension. On blood results, signs of renal and hepatic failure will be evident, as well as hyperlipidaemia.

Diagnosis

History of exposure to toxin and clinical examination.

Histological examination of stomach, kidneys, urine or liver in acute cases as well as microscopy of lungs for fibrous alveoli in chronic cases.

Treatment

There is no antidote for this poison.

The animal should be given an emetic followed by activated charcoal in acute cases where the animal has been found and brought into a vets immediately.

Supportive care for clinical signs such as fluid therapy and placement in an oxygen cage if respiratory signs are very severe. Diuresis with fluids can be used to increase renal excretion.

Prognosis

Poor if not treated early in acute stage.

References

Cope RB, Eildfell RJ, Valentine BA, White KS, Cooper BJ, Oncken A (2004) Fatal Paraquat Poisoning in Seven Portland, Oregon, Dogs. Veterinary and Human Toxicology. October; 46 (5): 258-264
Darke PG, Gibbs C, Kelly DF, Morgan DG, Pearson H, Weaver BM (1977) Acute Respiratiry Distress in the Dog Associated with Paraquat Poisoning. Veterinary Record. April ; 100(14):275-7
Klaassen, C.D (1996) Casarett and Doull's Toxicology The Basis Science of Poisons (Fifth Edition)

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