Canine toxicology

Canine toxicology

1. Chocolate

   • Theobromine is a naturally occuring stimulant found in cocoa beans
   • methylxanthines
   • Metabolised slowly = toxicity
   • Ingested - absorbed by GI tract - metabolised by liver - stimulates CNS
   • Inhibits cellular adenosine receptors = cell hyeractivity = tremors and seizures
   • Affects the heart: tachycardia, hypertension, arrhythmias
   • Clinical signs: vomiting, abdominal tenderness, hypersalivation, PUPD, excitability, sometimes bradycardia, ataxia, muscle rigidity, tachypnoea, hyperthermia, cyanosis, real dysfunction
   • Milk = 50g/kg, Dark = 5g/kg, white = less toxic.
   • Toxicity: eat large amount or long-term exposure
   • Onset of signs: rapid: within 1hr
   • Treatment: induce emesis promptly. Supportive care: IVFT, management of clinical signs including seizure management (benzodiazepines) and continual monitoring. Halflife is 17.5hrs so clinical signs can persist. Use activated charcoal
   • Prevention: owner education
   • Prognosis: favourable if rapid action is taken and owners are aware of the dangers

2. Metaldehyde

   • Commonly used in gardens to kill slugs and are blue/green pellets
   • Often eaten by intuitive dogs and cause convulsions
   • Unsteady on feet, twitchy, rapidly deteriorate; convulsions, respiratory failure and death

3. Warfarin

   • For rat/mice infestations
   • Exposure can cause severe bruising or bleeding with effects not seen fr several days
   • Not all rodenticides are anticoagulants so determine the type
   • Treatment = vitamin K1

4. Grapes and raisins

   • Significant toxicity = acute renal failure
   • Related to metabolic disruption causing nephrotoxic changes
   • All parts are poisonous
   • 8g/kg
   • Within 2 hours of ingestion: vomiting, diarrhoea, lethargy and polydipsia
   • Within 24 hours-several days: signs of ACR, anorexia, lethargy, depression, abdominal pain and hypovolaemia
   • Serum biochemistry: elevated urea, creatinine and phosphorous.
   • Reduced urine production
   • Diagnosis: history of exposure, clinical signs, development of AFR.
   • Treatment: prompt, initial decontamination = induce emesis, activated charcoal (1-3g/kg orally), fluid diuresis over the intial 48 hours to prevent ARF, monitor renal parameters for up to 3 days
   • Prevention: owner education
   • Onset of signs : 2hrs
   • Prognosis: guarded if ARF

5. Paracetamol

   • Toxic when exceeds 100mg/kg
   • Accidental ingestion or overdose
   • Cummulative effect if owner is medication at home
   • Metabolised in the liver - metabolites bing to lipid components of hepatic cell membranes = injury and death
   • Cells: oxidative stress = hepatocellular necrosis and liver failure
   • RCB damage due to metabolites = haemolysis. Heinz body formation and methaemoglobin = haemoglobin = non-functional
   • Excess methaemoglobin = brown mm, dyspnoea
   • Signs expected within 12 hours: lethargy, vomiting, dyspnoea,
   • Within 24 hours: facial and limb swelling due to hypoproteinaemia following acute hepatic damage, seizures, incoordination
   • Acute liver failure: jaundice, abdominal pain, coma, death
   • Treatment: induce emesis within 2-3 hours, oral administration of activated charcoal (1-3g/kg), IVFT, monitoring of hepatic parameters, cimetidine (5-10mg/kg) to prevent ongoing hepatic damage as inhibits oxidative liver damage and aids in reducing toxins metablism. Acetylcysteine (parvolex): to reduce liver damage, if given within 8 hoursog ingestion (140mg/kg IV), deactivated toxic metabolites. Full blood transfusion if has methaemoglobin. IV methylene blue: (1-2mg/kg) artificially restore iron in haemoglobin, has side effects. oral ascorbic acid (30mg/kg) can convert methaemoglobin back to haemoglobin. Basic nursing care
   • Diagnosis: clinical signs, history, blood levels but results are delayed, assess methaemoglobin
   • Prognosis: recovery is possible if treatment is prompt/aggressive, a number have permananet liver damage, if high dose; guarded/fatal