NEPHROTOXICANT TABLE
TOXIN SOURCE vetgirlontherun.com
MECHANISM OF ACTION
CLINICAL SIGNS
CLIN PATH FINDINGS
TOX TEST
TREATMENT
PROGNOSIS
Serum parathyroid hormone (iPTH) – will be suppressed and low Total Ca ++ and iCa ++ – elevated 25(OH)D 3 and 1,25(OH) 2 D 3 levels elevated
Signs result from hypercalcemia: depression, lethargy, weakness, anorexia, vomiting, malaise, hematemesis, PU/PD, uremic halitosis, constipation, melena, dehydration AKI usually 2-3d post-exposure due to soft tissue mineralization of renal tubules
Rodenticides OTC or Prescription Vitamin D 3 Psoriasis creams (calcipotriene) e.g. Dovonex®, Calcitrene®, Sorilux®
Hypercalcemia Hyperphosphatemia Azotemia Metabolic acidosis
>0.1-0.5 mg/kg can result in clinical signs and hypercalcemia, respectively LD 50 85 mg/kg (dog) Minimum acute toxic dose in dogs of calcipotriene is 37 μ g/kg BW
If no hypercalcemia, conservative treatment but aggressive decontamination: • emesis • activated charcoal • cholestyramine Limited fluid therapy Clinpath monitoring q24h x 2-3d: • SDMA • BUN/creatinine • Ca/Phosphorous • iCa ++ If hypercalcemia present, then calciuresis tx: • hospitalization • IV fluids (0.9% NaCl) • furosemide • prednisone • zoledronic acid • calcitonin (hard to find) • pamidronate Fomepizole (4-MP antidote) is the therapy of choice in which EG ingestion is suggested, and data supports use of higher doses of fomepizole in cats suspected of ingestion DOGS: 4-MP – 20 mg/kg IV 1st dose; 15 mg/kg at 12h; 15 mg/kg at 24h; 5 mg/kg at 36h CATS: 4-MP – 125 mg/kg IV 1st dose; 31.25 mg/kg at 12h; 31.25 mg/kg at 24h; 31.25 mg/kg IV at 36h 7% ethanol solution can be used if 4-MP unavailable (remove 175mls from 1L bag of saline and add 175ml of 80-proof vodka OR remove 74mls from 1L bag of saline and add 74mls of 190-proof grain alcohol) – use only “clear” alcohols • loading dose 8.6 ml/kg (600 mg/kg) 7% ethanol slowly IV • follow with CRI of 1.43 ml/kg/hr (100 mg/kg/hr) IV for 24-36h
Hypercalcemia: Vitamin D precursor of activated Vit D 3 leading to calcium reabsorption from kidneys, bone and GI tract
Cholecalciferol/ Vitamin D 3 Products
Stage 1 (0.5-12h): Signs similar to alcohol poisoning – ataxia, hypersalivation, nausea, vomiting, seizures, PU/PD, metabolic acidosis Stage 2 (12-24h): Signs seem to “resolve” from Stage 1 but severe internal injury – dehydration, tachycardia and tachypnea Stage 3 (12-24h in CATS and 36-72h in DOGS): Severe AKI, severe anorexia, lethargy, hypersalivation, uremic halitosis, coma, depression, vomiting and seizures
Antifreeze (95% EG), Windshield de-icing agents, motor oils, hydraulic brake fluid, developer solutions, paints, some industrial solvents
High osmolal gap seen as early as 1 hour after ingestion High anion gap and normochloremic acidosis w/in 3 hours of ingestion Chemistry changes: • low iCa ++ • hypoglycemia • hyperphosphatemia • azotemia Calcium monohydrate crystals in the urine may present as early as 3-6 hours from ingestion and is considered “diagnostic”
Alcohol dehydrogenase (ADH) converts EG to glycoaldehyde and organic acids (glycolic acid and oxalic acid) –> calcium oxalate crystalluria –> AKI
Ethylene Glycol (EG)
• Excellent - dogs treated by 5 hours following ingestion • Good - cats treated by 3 hours following ingestion • Grave without hemodialysis – azotemic patients The minimum lethal dose of undiluted EG is 4.2 - 6.6 ml/kg in the dog and 1.5 ml/kg in the cat. DOGS: 4.4 ml/kg –> AKI CATS: 1.4 ml/kg –> AKI
EG or metabolites are only accurate within 24h of ingestion Cats can have false negative results Rare false positives for EG with propylene glycol, sorbitol, mannitol, alcohol, etc. Woods lamp on vomitus, paws, mouth as many products will fluoresce
Made with FlippingBook - Online Brochure Maker