Zinc phosphide was discovered as a chemical in 1740, and its use as a rodenticide was documented as early as 1911. Although zinc phosphide is most commonly and readily available in pelleted form, typically gray in color, and in containers designed to facilitate subterranean placement for the control of gophers and moles, both aluminum phosphide and magnesium phosphide remain available as well. Formulations may include pastes, powders, grains, and pellets, and they range in concentration from 0.5% to 10%. Phosphides remain stable for up to 2 years; a persistently wet environment, however, could decrease stability to 3 weeks to several months.
As with other products, nontarget species typically are exposed by direct ingestion of the bait product itself, although relay toxicity after ingestion of prey or carrion remains theoretically possible, given the very narrow margin of safety. Lethal doses in dogs have been suggested at 20–40 mg/kg, and one-tenth of the lowest lethal dose is widely accepted as a toxic dose requiring decontamination, monitoring, and care.
Phosphides react in the liquid gastric environment to produce phosphine gas. Zinc phosphide requires an acidic pH < 4 to hydrolyze to the toxic phosphine gas, whereas magnesium and aluminum phosphides may do so at a neutral pH. The gas itself is severely corrosive, very rapidly resulting in spontaneous vomiting with or without blood. As a consequence, species that cannot vomit (eg, horses and rabbits) are likely to be at increased risk for severe clinical signs and potentially death. The liberated phosphine gas is then quickly absorbed from both the GI tract and respiratory mucosa, and it carries a very distinct decaying-fish or garlic odor. The gas poses substantial risk to humans, and animal owners should be instructed to transport pets to the clinic with open windows for ventilation purposes, in the event that spontaneous vomiting occurs. Staff exposure should be limited as much as is practically possible, and adequate ventilation should be established and maintained at all times. Any symptomatic human should be evaluated by a medical professional and human poison control contacted out of an abundance of caution.
Once systemically absorbed, phosphine gas exacts extensive oxidative damage to multiple organ systems; it may also disrupt aerobic respiration and cellular energy production at the mitochondrial level, and it may inactivate acetylcholinesterase. Clinical signs of phosphide poisoning can include lethargy, severe GI distress that may be hemorrhagic in nature, ataxia, tremors, seizures, hyperesthesia, pulmonary edema (tachypnea or dyspnea), pallor, shock, tachycardia or bradycardia, renal and hepatic damage, disseminated intravascular coagulopathy, and methemoglobinemia. Clinical signs may occur within minutes of exposure or, rarely, take up to 24 hours to appear. In severe cases, cardiovascular collapse and death may occur within 5 hours after exposure.
Pre-decontamination care and decontamination:
Raising of gastric lumen pH
Feeding should be avoided because food results in gastric acid secretion and lower pH.
Magnesium hydroxide is favored for rapid effect, transitioning to aluminum hydroxide for more sustained effect.
Animal owners may give calcium carbonate antacids orally before transport.
Induction of emesis in a controlled, well-ventilated environment within 1–2 hours of ingestion in clinically normal patients only
Gastric lavage, with caution, may be considered in clinically affected patients.
A single dose of activated charcoal with sorbitol, in patients that are clinically normal and have a low risk of aspiration
Diagnostic tests:
Baseline CBC, serum biochemical analysis, urinalysis, venous blood gas analysis
Coagulation profile in severely affected patients
ECG, if cardiovascular signs are noted
Thoracic radiographs, if respiratory changes are noted
Close monitoring of vitals and blood pressures
Monitoring of serum biochemical analysis and venous blood gas analysis in clinically affected patients
Liver profile 3–5 days after ingestion
Treatment:
Antacids (aluminum hydroxide, magnesium hydroxide, or calcium carbonate) for 3–5 days
Gastroprotectants (proton pump inhibitors, H2 blockers, sucralfate, or combination thereof) for 5–7 days in clinically normal patients, or for 14–21 days in clinically affected patients
IV fluid therapy for 24 hours or until clinical signs resolve
N-acetylcysteine in clinically affected patients or cases of large exposure, to act as a free radical scavenger, diluted to 5% or less and given IV through a 0.2-mcm filter: 140–280 mg/kg loading dose, followed by 70 mg/kg every 6 hours for 7–17 doses, depending on clinical progression
Methocarbarbamol (55–220 mg/kg, IV, to effect, or as a CRI at 10 mg/kg/h) as needed for tremors
Anticonvulsants as needed for seizures
Hepatoprotectants as needed
Supportive care as determined by clinical course
The prognosis is favorable in dogs that remain clinically normal 12 hours after ingestion and in dogs that are clinically affected without progression of clinical signs over 24 hours. The prognosis is guarded in cases of multiorgan involvement. In a single retrospective study across 5 years and 362 patients, the survival rate was found to be 98.3%.1
References
Gray SL, Lee JA, Hovda LR, Brutlag AG. Potential zinc phosphide rodenticide toxicosis in dogs: 362 cases (2004-2009). J Am Vet Med Assoc 2011; 239: 646–51.
