Rodenticide Toxicity Flashcards
What are some possible toxic principles of anticoagulant rodenticide toxicity? What is its mechanism of action?
- 1st gen = Warfarin
- 2nd gen = Brodifacoum, Bromdialone
- indandione = Diphacinone
inhibits vitamin K1 epoxide reductase, which prevents activation of vitamin K-dependent coagulation factors (II, VII, IX, X)
What are some signs of rodenticide toxicity?
- hemorrhage into abdomen, retroperitoneum, pleural space, and lung
- hemorrhagic shock - pale MM, prolonged CRT, tachycardia, weak pulses
- abdominal distention
- respiratory distress
When are clinical signs of rodenticide toxicity most commonly observed?
3-7 days after ingestion (compounds can persist for 4-6 weeks
- takes 3-7 days to deplete remaining coagulation factors
What are 3 ways of diagnosing rodenticide toxicity?
- prolonged prothrombin time (PT) - takes 36-72 hours to deplete factor VII (shortest half-life)
- prolonged partial thromboplastin time (aPTT) - takes 3-5 days
- rodenticide toxicology screen for definitive diagnosis
How are dogs with recent known ingestions of rodenticide treated?
- emesis if ingestion within 2-4 hours
- activated charcoal +/- sorbitol if ingested within 8-12 hours
- treat with vitamin K1 for 4 weeks OR check PT 36-72 hours after ingestion to determine if it is needed
- check PT 48-72 hours after completion of vitamin K1 therapy
How are dogs with known or possible previous ingestion of rodenticide treated?
- immediately perform PT
- only induce emesis if PT is normal
- administer vitamin K1 for 4 weeks
- activated charcoal
- check PT 48-72 hours after completion of vitamin K1 therapy
What are 6 parts to treating dogs presenting with hemorrhage secondary to coagulopathy due to rodenticide ingestion?
- plasma infusion (+/- RBC infusion) - vitamin K1 can take >24 hours to be effected, plasma offers immediate hemostasis (typically 10-15 mL/kg)
- thoracocentesis with hemorrhage into pleural space +/- autotransfusion
- O2 support or mechanical ventilation
- isotonic crystalloids and/or colloids
- vitamin K1 SQ or oral and continue for 4 weeks
- check PT 48-72 hours after completion of vitamin K1 therapy
What is the mechanism of action of bromethalin rodenticides? What does this result in?
inhibits oxydative phosphorylation and ATP production, especially in neurons
loss of ability to maintain osmotic gradients, cerebral edema, and increased intracranial pressure
What are signs of high and low doses of bromethalin rodenticide toxicity?
HIGH - tremors, seizures, hyperexcitability, and hyperthermia soon after ingestion (<12 hours)
LOW - ascending paralysis beginning in the hindlimb seen days to weeks after ingestion
How does treatment for acute and chronic presentation of bromethalin rodenticide toxicity compare?
ACUTE - GI decontamination with emesis or gastric lavage and activated charcoal
CLINICAL SIGNS - seizure treatment/prophylaxis, Mannitol +/- Furosemide to reduce cerebral edema, incline plane 30 degrees to promote venous return
What is the toxic principle of cholecalciferol rodenticides? What does toxicity result in?
precursor converted into active vitamin D after ingestions
increased intestinal absorption of calcium and mobilization from bones —> severe hypercalcemia, hyperphosphatemia, organ injury
When do clinical signs of cholecalciferol rodenticide toxicity typically appear? What is seen?
within 36 hours
- acute renal failure - PU/PD
- GI upset
- cardiac arrhythmias
How is cholecalciferol rodenticide toxicity diagnosed?
presence of:
- hyperphosphatemia (12 hours)
- hypercalcemia (24 hours)
- azotemia (36-48 hours)
How are acute and chronic cases of cholecalciferol rodenticide toxicity treated?
ACUTE = emesis and activated charcoal
CHRONIC =
- hypercalcemia - saline diuresis, loop diuretic, corticosteroids, bisphosphonates (Pamidronate), calcitonin
- azotemia - supportive care for acute renal failure (poor prognosis!)
