Other Rodenticides Flashcards
Phosphide rodenticides
-Zinc phosphide, aluminium phosphide, magnesium phosphide (Zn most toxic)
-pellets, treated grains, powders
-2-5% formulations (2% in SK)
-stable in dry environments for several years (less persistent in wet, low risk of secondary poisoning)
Toxicity of phosphide rodenticides
Typically 20-40mg/kg BW for most species
Mechanism of phosphide rodenticides
- Phosphide rodenticides enter stomach
- results in release of phosphine gas
- Phosphine gas is irritating and causes oxidative damage to multiple organs (liver, kidney, lungs, heart, brain)
Onset of phosphide rodenticides
Fast, 15 mins post ingestion
Clinical signs of phosphide rodenticides
- Severe GI distress (vomiting, diarrhea, hematemesis, hematochezia)
*colic signs in horses because can’t vomit
-shock, pale MM (arrythmias and cardio collapse)
-profuse sweating
-CNS (lethargy, hyperexcitation (tremors, seizures)
-Pulmonary edema (tachypnea, dsypnea, cyanosis)
-death within 3-48hrs
-delayed kidney or liver failure
-characteristic odour (rotten fish/garlic)= acetylene
Signs in clinical pathology for phosphide rodenticide
-dehydration
-elevated liver enzymes
-azotemia
-metabolic acidosis
-elevated blood zinc
Is there an antidote for phosphide rodenticides?
No
Management for phosphide rodenticide toxicity
- decontaminate in well ventilated area
- IVFT, gastroprotectants, hepatoprotectants/antioxidants, oxygen
- seizure control
- monitor with CBC, blood gas, xrays, liver chem, PT/PTT
Specific management for zinc phosphide
Need to neutralize stomach acid
-carbonate antacids
-dilute sodium bicarbonate
How to diagnose phosphide rodenticides?
-history and clinical signs
-detection of phosphine gas in stomach contents, vomit, liver, kidney
-PM lesions: hemorrhagic GIT, pulmonary edema, hepatocellular necrosis and steatosis
Prognosis for phosphide rodenticide toxicity
Better prognosis if symptomatic patients survive 24hrs
Phosphine gas in humans
Toxic (at 0.03ppm, death at 7ppm)
-need to be aware when tubing a horse or if an animal is vomiting in clinic
Symptoms of phosphide toxicity in humans
-dizziness
-lethargy
-nausea
-vomiting
-cough
-dyspnea
- liver failure symptoms (jaundice, delirium)
-coma
Sources of vitamin D3 (cholecalciferol) toxicity
-rodenticides
-human ointments and supplements
-certain plants (day blooming jessamine, yellow oatgrass)
-feed mixing errors
Cholecalciferol rodenticide percentage
Typically 0.075%
Mechanism of cholecalciferol toxicity
Disruption of calcium and phosphorus homeostasis leading to hypercalcemia = resulting in dystrophic mineralization and multi organ damage
Toxicokinetic factors for cholecalciferol
-lipophilic
-long elimination half life
-EHC
Metabolism of cholecalciferol
Role of calcitriol
-increased intestinal absorption
-increased tubular reabsorption
-increased bone resorption
*hypercalcemia &hyperphosphatemia
Onset of cholecalciferol
12+ hours post ingestion
Clinical signs of cholecalciferol toxicity
-weakness, lethargy
-anorexia
-vomiting and diarrhea
-PU/PD
-hyperphosphatemia &hypercalcemia (12 hrs after)
-azotemia (24hrs after ingestion)
-iso/hyposthenuria (72hrs after)
-metastatic calcification= kidneys, soft tissues= kidney injury and renal failure
Management for cholecalciferol toxicity
-decontamination if not contraindicated
-dose dependent treatment (SQ fluids, CBC,
-specific treatments for clinical symptoms
Treatments for hypercalcemia
-IVFT
-prednisone
-furosemide
Treatments for hypercalcemic gastritis
GI protectants
What is contraindicated for use with cholecalciferol?
-Ca containing fluids = LRS
-Thiazide diuretics
Diagnosis for cholecalciferol
-history
-bloodwork
Differential diagnosis for cholecalciferol
Hypercalcemia from neoplasm, hyperparathyroidism, kidney disease
*Acute kidney disease= due to ethylene glycol, grapes, lilies, NSAIDs, aminoglycosides
Prognosis for cholecalciferol toxicity
Good with early decontamination and supportive therapy
*guarded to poor with development of renal failure
PM lesions of cholecalciferol toxicity
-soft tissue mineralization (kidneys, GIT, aorta, striated muscle)
-Histo: degeneration and necrosis of renal tubules & calcium accumulation (Von kossa stain)
