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ISU Student Experience

Zinc Phosphide Toxicity

Written by: Anna Herriott • 2022 Scholar


Max is a 11-year-old, male neutered Dachshund mix dog who presented to Iowa Veterinary Specialties after ingesting approximately 1/3 cup of mole repellent. He ingested it in the yard about 2-4 hours prior to presentation. He had one incident of vomiting at home after the ingestion – the vomit was described as granular and sandy. Max had no diarrhea prior to presentation. Max had eaten a milk bone and drank some water since the ingestion. The owner reported that Max had been trembling and lethargic since the ingestion.

Physical Exam

Temperature: 101.1 F
Heart Rate: 174 beats per min
Respiration Rate: 42 breaths per min
Mucus Membrane: Pink
Capillary Refill Time: < 2 seconds
Systolic Blood Pressure: 120mmHg
Weight: 6.7 kg

Upon presentation, Max was tachycardic, was drooling, had dental disease, and cataracts in both eyes. The rest of the physical exam was unremarkable.
Blood was drawn for a complete blood count (CBC) and a chemistry panel. The CBC showed lymphopenia and the chemistry panel revealed high ALKP (liver enzyme) levels. Elevated ALKP can be a sign of liver dysfunction. The rest of the initial bloodwork was unremarkable.


Because of his recent mole repellant ingestion and presenting clinical signs, Max was diagnosed with zinc phosphide toxicity. The lowest lethal dose of zinc phosphide in canines is about 20-40mg/kg, and 2-4mg/kg is accepted as a toxic dose. In Max’s case, the exact dose ingested was unknown.

A dangerous component of zinc phosphide consumption is its ability to hydrolyze phosphine gas at an acidic pH. Phosphine gas is very corrosive, smells like decaying fish, and will result in spontaneous vomiting when it is released in the stomach. This gas poses a risk to humans if inhaled, so keeping the animal in a well-ventilated area, or taking the animal outside to vomit is important for the safety of caretakers.


Because a zinc phosphide ingestion requires intense monitoring, care, and decontamination, Max was hospitalized. Initial decontamination procedures included anti-nausea medication (Cerenia), aluminum hydroxide, and activated charcoal. Aluminum hydroxide is an antacid and phosphate binder, so it decreases phosphate levels and reduces stomach acid production. Since phosphine gas requires an acidic pH of <4 to hydrolyze phosphine gas, reducing stomach acid production will increase the gastric pH, making the ingested zinc phosphide less toxic. Activated charcoal was administered because it will bind the toxic compounds in the Max’s stomach, and prevent them from being absorbed into the bloodstream. Max was then treated with IV fluid therapy, started on a hepato-protectant drug (S-Adenosylmethionine), and kept on aluminum hydroxide. He was also fasted because consumption of food would result in gastric acid secretion, lowering the gastric pH, leading the zinc phosphide to more readily hydrolyze phosphine gas.

In addition to treatments, Max’s electrolytes and blood pressure were monitored every 6 hours and a chemistry panel was done every 24 hours.

About 24 hours after presentation, Max became hypokalemic. His potassium level was 4.8mmol/L in the initial bloodwork and had dropped to 3.3mmol/L 24 hours later. Max’s IV fluids were supplemented with an additional 20mEq/L KCl (potassium chloride). Max also developed progressively elevated liver values.

48 hours after presentation, Max was still hypokalemic and his liver enzymes had further elevated. Acetylcysteine, an additional hepato-protectant, as well as a gastro-protectant drug (pantoprazole) were added to his treatment plan at this time.

Shortly after that, Max vomited a large amount of yellow liquid. At this point, an AFAST (abdominal focused assessment with sonography for trauma) was performed, showing a subjectively thickened bladder and a gallbladder halo sign. This gallbladder halo sign lead to concern for pancreatitis secondary to zinc accumulation caused by the zinc phosphide ingestion. Max was started on ondansetron to treat vomiting and sucralfate to protect the stomach. He was also given gabapentin for pain.
Throughout the following day, Max’s mentation became duller and more lethargic. He also had bloody diarrhea. Max was humanely euthanized 3 days after presentation.


  • Dekker, M., Shell, L., & Gwaltney-Brant, S. (2019, February 8). Zinc Phosphide Toxicosis (Canine). VIN. Retrieved July 14, 2022, from https://www.vin.com/members/cms/project/defaultadv1.aspx?pid=607&id=4953224
  • Peterson, M. E., Talcott, P. A., & Peterson, M. E. (2013). Small animal toxicology. Elsevier.
  • Siow, J. W. (2018). Zinc toxicosis in a dog secondary to prolonged zinc oxide ingestion. Open Veterinary Journal, 8(4), 458. https://doi.org/10.4314/ovj.v8i4.17

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