Anticoagulant Rodenticide Toxicity – Another Great Pretender
Katherine Earl, DVM, CVA
A five-year-old female spayed Australian shepherd presented with a 24-hour history of lethargy and increased respiratory rate and effort. The owners were unaware of any toxin exposure or trauma. On presentation, the dog had mild tachycardia with harsh bronchovesicular sounds appreciated bilaterally. Bloodwork was unremarkable outside of a mild thrombocytopenia (140,000) not confirmed on differential. Thoracic radiographs were obtained (Figure 1, 2).
Figure 1: Right lateral thoracic radiograph.
Figure 2: Ventrodorsal thoracic radiograph.
The receiving emergency veterinarian interpreted the radiographs as demonstrating possible dynamic tracheal collapse, and the patient was discharged after receiving butorphanol with a course of hydrocodone. The radiologist’s interpretation was pending.
The dog returned for reassessment the following day due to lack of improvement in clinical signs. On repeat examination the dog was noted to have pale mucous membranes, tachycardia and tachypnea with increased expiratory effort. A TFAST was performed revealing marked bilateral pleural effusion. The radiologist’s report from the prior day’s radiographs suggested the possibility of tracheal mucosal hemorrhage and scant pleural effusion. Repeat questioning of the owners revealed there was rodenticide on the property, but was removed earlier in the week. A PT and PTT were performed, both out of range with repeat bedside bloodwork revealing a PCV/TS of 29% / 6.4 g/dL. The dog received a matched unit of packed red blood cells and fresh frozen plasma and was started on oral vitamin K1. The patient did well and was discharged for at-home care with a course of vitamin K1 after 24 hours of hospitalization.
Decision Tree for Anticoagulant Rodenticide Exposure
This case serves as a reminder of the subtle ways that anticoagulant rodenticide can present in our patient population as this patient bled initially into the trachea mucosa – a unique presentation. Despite phasing out of anticoagulant rodenticides in favor of bromethalin, these toxins are still in the environment and we need to maintain an index of suspicion for possible exposure, especially in cases that do not add up.
Anticoagulant rodenticides work by inhibiting vitamin K epoxide reductase in the liver resulting in blockage of vitamin K production. Without vitamin K, certain clotting factors (II, VII, IX and X) and anti-thrombotic factors (Protein C, Protein S, Protein Z) are not produced. These proteins become depleted within 48 to 72 hours after toxin ingestion and signs of coagulopathy become apparent. Animals will bleed into potential spaces in the body typically with no external sign of hemorrhage. Due to the delayed onset of clinical signs, it is important to press the owners to think of any potential exposure in the past week, not just 24-hours.