Rodenticide Flashcards
(32 cards)
Cholecalciferol: Forms & Sources
FORMS
o Plant derived: Ergocalciferol (D2)
o Animal derived: Cholecalciferol (D3)
SOURCES:
- Ingestion of rodenticides
- Human medicine ingestion ( psoriasis cream)
- Pet food (Blue buffalo 2010)
Cholcalciferol: Toxic dose (acute vs chronic)
Acute ingestion: Exposure to rat/mouse bait in the backyard.
Chronic ingestion: Kitty that licks psoriasis cream off the owners arm.
o Toxic lethal dose depends on the biochemical form
o Vitamin D3 is 10 times more potent than D2
o Single oral lethal dose ~ 13 mg/kg
0.1 mg/kg mild GI signs
> 0.5 mg/kg hypercalcemia, renal failure
Cholecalciferol: What predispositions make dog more succeptible?
Primary renal failure, Addisons ( animals prone to hypercalcemia)
Cholecalciferol: Mechanism of Toxicity
Vitamin D absorbed/ingested-> LIVER( 25hydroxyvitaminD)-> KIDNEY (1,25-di-hydroxyvitamin D)-> Vitamin D receptors in SI, Colin, & Lungs activated
GUT - Calcium & Phosphorus absorption increase
Kindneys- Calcium renal absorption increases ( increase Phosphorous too)
BONE-If you have low calcium floating around in the body, the Vit D is going to help increase resorption of calcium from the bone, so that you can increase that calcium
Hypercalcemia Differentials
HARD IONS o H: Hypercalcemia of malignancy (lymphoma, multiple myeloma, adenocarcinoma of anal glands) Hyperparathyroidism o A: Addison’s disease, aluminum tox o R: Renal failure – throws off Ca:P ratio o D: Vitamin D tox – vitamin D is needed to absorb Ca. too much vit D = too much Ca absorbed o I: Iatrogenic, Idiopathic o O: Osteolytic disease like HOD (hypertrophic osteodystrophy) o N: Neoplasia (osteosarcoma), metastatic bone disease such as mets from a mammary tumor o S: Spurious
o Hypercalcemia of malignancy o Hypoadrenocrticism o Chronic kidney disease o Primary hyperparathyroidism o Osteolytic bone disease o Ingestion of Vitamin D ointments (psoriasis cream) o Granulomatous disease
Cholecalciferol Toxicity early signs (12-36 hrs)
- Depression, weakness, anorexia
Thennnn
• Vomiting, polyuria/polydipsia, constipation, dehydration – bc we have CS of renal disease
• Dark Feces ( GI ulceration)
Cholecalciferol : Later Clinical signs
• Acute kidney injury, oliguria/anuria
-Calcification of the renal tubules
• ECG changes
-Shortened QT, prolonged PR intervals
• Hematemesis/melena
-Grave prognosis , GI Mineralization and ulceration
Cholecalciferol: What should be monitored in Minimum database?
o Monitor total calcium
- 15-18mg/dL (Normal 9.5-11.5)
o ionized calcium
-calcium/phosphorus product that is greater than 60 - 70 -mineralization
o phosphorus
o BUN
o Creatinine
o UA
- IsosthenuriaCholecalciferol : Treatment in acute ingestion
o Acute ingestion (<6 hours)
- Induce emesis
- Activated charcoal
- Monitor calcium at baseline and q 24-48 hours for 5-7 days
Cholecalciferol: What does Supportive care look like for this toxicity
IV fluids - NaCl
- high levels of fluids to correct dehydration, volume expansion, and the sodium will induce calciuresis
Phosphate binders
- if animal is eating, used to bind phosphorus before its absorbed into the system
antiemetic therapy
- animals vomit a lot want to decrease electrolyte disturbances
Antacids
- in case there are Gi ulcers due to mineralization
Cholecalciferol: What does Supportive care look like for this toxicity ( 2)
Glucocorticoids
- decrease calcium absorption from bones & GI. After HARDIONS ruled out. No tumors,
Furosemide
- animal must be well hydrated first
Biphostphonate ( Pamidronate)
- Alendronate: cats use this for Primary Hypercalcemia
- Inhibits osteoclastic bone resorption
- Reduces calcium concentration within 48 hours
- Given as Iv infusion, must have IV fluid bolouses too, because can be Nephrotoxic
Salmon Calcitonin
- Inhibits osteoclast activity reducing resorption of calcium from bones
- Risk of anaphylaxis
Bromethalin: What is it? What systems does in affect?
- Used in Rat, gopher… etc poisoning
- neurotoxic ( w/ no antidote)
Bromethalin Toxic dose
Cats are more sensitive
- LD50 ~0.5 mg/kg in cats
- 5 mg/kg in dogs
o Clinical signs are seen at much lower doses
- Cats ~ 0.2 mg/kg
- Dogs ~1 mg/kg
Bromethalin Toxokinetics : What part of the body is it distributed to most?
Gi tract absorption
- Peak plasma levels 4 hrs
Liver metabolization
- desmethylbromethalin is the toxic metabolite
Throughout body - Highest in Body fat
Bromthalin : Clinical signs of the primary target of the drug. Acute vs Delayed onset
Primary target:CNS
- Depression, abnormal behavior, ataxia, tremors, seizures
Dose dependent clinical signs ACUTE >LD50 2-24 hrs post injection • Severe muscle tremors • Hyperthermia • Seizures • Hyperesthesia
Delayed onset neurological signs Days- 2 weeks, less toxic dose • Hind limb ataxia/paresis • Patellar hyperreflexia • Mild to severe CNS depression • Seizure---- Coma
Bromethalin: Minimum Database information
CBC/CHEM EEG - Not pathognomonic for Bromethalin toxicity - Seizure foci - Cerebral edema and hypoxia
Bromethalin Antemortem and postmortem Confirmatory tests
o Antemortem:
Exposure history
Appropriate clinical signs
o Postmortem:
Diffuse vacuolization of white matter
Bromethelin residues in the fat, liver, kidney and brain tissue
Bromethalin: No antidote so how do we treat?
- Reduce GI absorption
- Emesis within 1 hour- Only to alert, neurologically normal animals
- Activated Charcoal - Repeat every 4-6 hours for at least 2-3 days
2a. Provide Symptomatic and supportive Care
- Mannitol, hypertonic saline
- Keep head elevated 30°
- No jugular venipuncture
2b. Control Seizures
- Phenobarbital
- Keppra
- Midazolam/diazepam/lorazepam PRN or CRI
Anticoagulant Rodenticides: What is the source of these rodenticides
1st Gen: Warfarin Based, rats becae resistant
2nd Gen: More toxic: brodifacoum, difenacoum, bromadiolone, indandione
- Last longer than the previous, problem with exposure to animals and
children
Anticoagulant Mechnaism of Toxicity
- Secondary intoxication- uncommon ( cat eats a mouse thats eaten the toxin)
- coagulopathy -mVitamin K depletion clotting factors effected include:
- 7 , 2, 9, 10
- 7 has the shortest half-life so the prothrombin time is first prolonged
- 7 , 2, 9, 10
Anticoagulant Rodenticide : Clinical signs seen?
lag period between exposure and clinical signs shown
- 3-5 days
Depletion of coagulation factors
- 7 ( halflife 6.2 hrs) , 9, 10, 2
Presenting complaint:
- Lethargy, anorexia, dyspnea, hemoptysis, lameness
Physical Exam : may bleed from anywhere ( often the lungs- 50% of the time) - hematomesis, epistaxis, dyspnea May bleed into joints - lameness Bleed in GI - Bloody Diarrhea, Vomitting blood
Anticoagulant Rodenticide: What are the results of some of the minimum database tests?
Blood samples before treatment
CBC (depending on the progression of the disease)
- Thrombocytopenia, Mild anemia
Serum Chemistry
Coagulation Panel
- Aptt & Pt prolonged
Prothrombin Time
- Extrinsic pathway measurement ( including factor VII)
- Prolonged first 48 hrs, prolonged before APTT
Blood Typing, cross match
- May need to do blood transfusion
Imaging
- Rads( dtr source of bleeding) , Abdominal Ultrasound
confirmatory Testing
- Gas chromatography ( takes a couple days, useful in legal cases
Anticoagulant Rodenticide: Treatment for acute ingestion ( Within 1st Few hrs )
o Induce emesis
- For acute ingestion we’re going to induce vomiting, decontaminate, check PT 48 hrs later, if prolonged start in Vit K, if not prolonged (which is more likely) carry on, is normal.
o Decontaminate with activated charcoal
Anticoagulant Rodenticide: Treatment for acute ingestion ( Within 1st Few hrs ) But we find that after 48 hrs the Pt is prolonged
• Oral Vitamin K (phytonadione)
- 2.5 mg/kg orally every 12 hours
- 4 weeks
• Recheck PT 48 hours after last dose of vitamin K, If still prolonged
- Continue for additional 1-2 weeks
