Phosphine intoxication following oral exposure of horses to aluminum phosphide–treated feed

Easterwood, Leslie; Chaffin, M. Keith; Marsh, Peggy S.; Porter, Brian F.; Barr, Catherine

doi:10.2460/javma.236.4.446

Cited by 23 publications

(14 citation statements)

References 9 publications

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“…In experimental models, AlP may alter glucose homeostasis; it signifi cantly decreases plasma glucose in AlP-treated rats (55) and horses (56). Hypoglycaemia has also been reported in other studies (40,(57)(58)(59).…”

Section: Electrolyte and Metabolic Abnormalitiesmentioning

confidence: 60%

A Systematic Review of Aluminium Phosphide Poisoning

Mehrpour¹,

Jafarzadeh

Abdollahi

2012

Archives of Industrial Hygiene and Toxicology

163

214

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Every year, about 300,000 people die because of pesticide poisoning worldwide. The most common pesticide agents are organophosphates and phosphides, aluminium phosphide (AlP) in particular. AlP is known as a suicide poison that can easily be bought and has no effective antidote. Its toxicity results from the release of phosphine gas as the tablet gets into contact with moisture. Phosphine gas primarily affects the heart, lungs, gastrointestinal tract, and kidneys. Poisoning signs and symptoms include nausea, vomiting, restlessness, abdominal pain, palpitation, refractory shock, cardiac arrhythmias, pulmonary oedema, dyspnoea, cyanosis, and sensory alterations. Diagnosis is based on clinical suspicion, positive silver nitrate paper test to phosphine, and gastric aspirate and viscera biochemistry. Treatment includes early gastric lavage with potassium permanganate or a combination with coconut oil and sodium bicarbonate, administration of charcoal, and palliative care. Specifi c therapy includes intravenous magnesium sulphate and oral coconut oil. Moreover, acidosis can be treated with early intravenous administration of sodium bicarbonate, cardiogenic shock with fl uid, vasopresor, and refractory cardiogenic shock with intra-aortic baloon pump or digoxin. Trimetazidine may also have a useful role in the treatment, because it can stop ventricular ectopic beats and bigeminy and preserve oxidative metabolism. This article reviews the epidemiological, toxicological, and clinical/pathological aspects of AlP poisoning and its management.

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Section: Electrolyte and Metabolic Abnormalitiesmentioning

confidence: 60%

A Systematic Review of Aluminium Phosphide Poisoning

Mehrpour¹,

Jafarzadeh

Abdollahi

2012

Archives of Industrial Hygiene and Toxicology

163

214

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“…Veterinarians, veterinary nurses and animal owners, who handle animals with phosphine poisoning can also be affected and sickened by phosphine gas (Easterwood et al . ).…”

Section: Discussionmentioning

confidence: 97%

“…) causing further toxicosis through inhalation in subjects exposed to the breath or vomitus of poisoned animals or humans (Easterwood et al . ; CDC , O'Malley et al . ; Lodde et al .…”

Section: Introductionmentioning

confidence: 99%

Phosphine poisoning in free‐range local chickens: a case report

Muraina

Oladipo²,

Akanbi

et al. 2018

Veterinary Medicine & Sci

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Phosphine poisoning is rarely reported in poultry, and its diagnosis is a great challenge for veterinary toxicologists and pathologists. A case of phosphine toxicosis in local, free range chickens is reported. Fourteen dead chickens (age ≥6 months old) were presented to the veterinary clinic for necropsy. The history revealed that the chickens were normally fed with guinea corn grains, but were suspected to have been fed boiled rice laced with poison. The clinical signs observed were ruffled feathers, somnolence, anorexia and high mortality. The disease ran a 2‐day course with mortality pattern of four chickens the first day, six overnight and 14 the following day. Necropsy findings showed generalized vascular congestion and haemorrhage in the lungs and visceral organs, with the crop and gizzard filled with guinea corn and rice grains and greenish‐yellow faecal material in the intestinal lumen. The presence of widespread congestion and petechial haemorrhages on visceral organs with the microscopic pulmonary congestion, and diffuse intraparabronchial presence of air sac macrophages, strongly suggested an acute toxic cause of death. Chemical tests on the crop contents of the dead chickens were positive for phosphine gas. This report will contribute to a better understanding of the clinical signs and lesions presented in cases of acute phosphide rodenticide exposure in domestic chickens, with a brief review of the forensic literature.

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“…Aluminium phosphide, a common fumigant for stored grains, is also able to release to phosphine and cases of poisoning have been reported in horses (Easterwood et al . ). The exact mechanism of phosphine toxicity has not been elucidated yet.…”

Section: Rodenticidesmentioning

confidence: 97%

Long‐established and emerging pesticide poisoning in horses

Nagy

Cortinovis²,

Spicer

et al. 2018

Equine Veterinary Education

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Summary Poisoning is a frequent problem in domestic animals. Horses are the third most commonly affected species and pesticides are one of the main causes of toxicosis. Here within are reviewed the most frequent toxicoses where it emerges that the main causes are misuse and accidental exposure. Rodenticides, acetylcholinesterase insecticides followed by herbicides are the main cause of toxicosis and effects of emerging chemicals are being reported. Metaldehyde is still a problem, together with methiocarb. No information has been reported on poisoning with pesticide mixtures.

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Phosphine intoxication following oral exposure of horses to aluminum phosphide–treated feed

Cited by 23 publications

References 9 publications

A Systematic Review of Aluminium Phosphide Poisoning

A Systematic Review of Aluminium Phosphide Poisoning

Phosphine poisoning in free‐range local chickens: a case report

Long‐established and emerging pesticide poisoning in horses

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