Satevia

Signalment: 3 month old, Chihuahua

History: Acute onset of weakness and lethargy. Owners also observed difficulty breathing (dyspnea).
Exam: Tachypnea (rapid breathing), pale mucous membranes, weak, lethargic, muffled heart sounds bilaterally.

Lab testing:

(Normals)
pcv/tp:22/5.0>35/>6
Prothrombin time:>220 seconds12 – 17 seconds
Pulse oximeter~85%>95%

Upon further discussion with the owners, it was found that the puppy had eaten rat bait poison approximately 3 days prior to presentation.The owners believed that the poison was an anticoagulant.

Diagnosis: Anticoagulant rodenticide toxicity with resultant hemothorax (bleeding into the chest cavity).

Prognosis: Guarded to poor due to ongoing hemorrhage and late stage of toxicity.

Treatment: An intravenous catheter was placed on arrival and oxygen therapy was instituted. Following approval of necessary care by the owners, a plasma transfusion was started. We administered a total of 20mls of fresh frozen plasma intravenously (provides important clotting factors to stop the ongoing hemorrhage). Vitamin K1 was also administered during the plasma transfusion (antidote).

Approximately 4 hours after presentation, the puppy was observed becoming progressively dyspneic suggesting that too much blood had accumulated within the chest cavity to allow normal lung inflation. The pulse ox was 88% (measurement of oxygen concentration in the blood) on room air but dyspnea was also observed with supplemental oxygen.

Thoracocentesis was performed (placing a needle into the chest to remove the blood) and approximately 35mls of blood was removed from each side of the chest. We attempted to collect blood in an anticoagulant for possible auto-transfusion (transfusing the same blood back into the animal) but the blood clotted. Breathing immediately improved but mucous membranes were becoming pale again.

PCV/TP: 11/3.5

Due to the quantity of blood removed from the chest and the subsequent severe anemia observed, a whole blood transfusion was administered (60mls) intravenously. Mucous membrane color improved and “Satevia” was upgraded to stable condition by 8am the next morning. No further problems were observed. The Animal Hospital of Rowlett continued to provide oxygen and monitor the breathing through the day. “Satevia” was discharged later that afternoon with a prescription of vitamin K1 capsules.

Mechanism of toxicity: The agent in the rat poison (brofidacoum, warfarin, others) selectively bind to vitamin K receptors in the liver and prevents the production of specific clotting factors. Without these factors, we will eventually see some area of uncontrolled hemorrhage. The areas of bleeding can be into the chest cavity, abdomen, stomach, urine, eyes or from a small cut or bruise. If all bleeding is internal, the only signs observed might be difficulty breathing, pale gums and lethargy. Hemorrhage will be fatal unless treated in the initial stages of bleeding.

Discussion: Unfortunately, anticoagulant rodenticide toxicity is a fairly common ailment observed at the emergency clinic. The rat poison is readily found and eaten by curious pets with bleeding signs developing ~3 days after ingestion. The PT test can quickly confirm any suspected exposures by measuring the efficiency of the clotting system. If the PT is significantly prolonged and exposure is possible, a presumed diagnosis can be made.
“Satevia” was already bleeding on arrival so blood product transfusions were necessary to stop the bleeding. Plasma provides clotting factors and proteins for those animals and whole blood also provides red blood cells. Vomiting and activated charcoal are of little use by this time because the toxin has already being digested and absorbed. The antidote (vitamin K1) is administered in high concentrations for the next 2-3 weeks to overwhelm the binding sites in the liver thus pushing the toxin compounds off the receptor sites in the liver. This allows the liver to make the much needed cloting factors again. If the vitamin K1 is discontinued too early, the signs could re-develop. This duration of action of the toxin depends on which exact compound was in the product. Some components will have effects lasting several weeks and others may only last a week or so.

Treatment options:
Acute ingestion (owner recognizes the ingestion within the first few hours)
Prognosis: good/excellent
1. Decontaminate – induce vomiting.
2. Prevent absorption – administer activated charcoal
3. Administer antidote – vitamin K1
4. Confirm prolonged PT and baseline PCV/TP.

> 3 days ingested (often presenting with an ongoing critical hemorrhage)
Prognosis: guarded/poor
1. Plasma and/or blood transfusions
2. Administer antidote.
3. Possible thoracocentesis if severe hemothorax encountered.

Important Facts:

Keep all poisons away from areas that are even remotely accessable to pets or children.
If your pet ingests a poison, call your veterinarian or local emergency facility and inform immediately.
Not all poisons should be vomited; please call your veterinarian first before inducing vomiting at home.
Bring the packaging of the poison with you so your veterinarian can read the ingredient list.

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