ECC toxicology Flashcards
most common way animals are exposed to toxins
- 75-90% oral exposure, followed by dermal exposure
General Management of Acute Intoxication
- History & triage
- Physical examination: ABCDs of patient stabilization*
- 1° treatment: decontamination (gastrointestinal, dermal, ocular)
- minimize further toxicant absorption
- promote excretion of toxicant from body - Specific antidotes
- intralipid emulsion therapy - Symptomatic supportive care
Telephone Triage: Key Questions
Ø Signalment: species, breed, age, health history
Ø BW: estimate vs. historical
Ø Known (witnessed) vs. potential exposure
Ø Specific product: active ingredient, form (XR, SR, LA), max vs. min amount
Ø Estimated exposure time (time elapsed since exposure)
Ø Patient’s condition:
- level of consciousness
- respiratory status
- seizures, muscle tremors
Ø Animal poison control centers - case file #, home treatment given
Telephone Triage: Consultation
Ø Safe removal from poisoning area: ↓ further exposure
Ø Do not administer internet-based home remedies
Ø At-home emesis induction?
- consult veterinarian
- animal poison control helpline
Ø Nearest veterinary facility: prompt emesis induction?
Ø Bring product for verification
Ø Call pharmacy for total quantity prescribed & back-count
Triage & Physical Examination
- first things to check
- Airway
- Breathing 3. Circulation 4. Dysfunction
ØAddress immediate life-threatening concerns before decontamination
Toxicologic Decontamination
- purpose
Ø To prevent further toxin absorption + enhance elimination
Gastrointestinal Decontamination methods
- Emesis induction
- Gastric lavage
- Activated charcoal ± cathartic
- Whole bowel irrigation
Emesis Induction: Effectiveness depends on?
- Physical properties of toxicants
- gel caps, antiemetic effects, delay gastric emptying - Time elapsed from toxin ingestion
-»_space; rapid emesis,»_space; gastric recovery
- ideal: < 1 hour
- little value: > 4 hours - Volume of gastric contents
- Emetic agent
- not effective: unsuccessful emesis after 2 doses
Emesis Induction: Indications
Ø Asymptomatic patient
- recent ingestion (<1-2 hours)
- unknown time of ingestion
Ø Toxicants that retain in stomach
- grapes, raisins, chocolate, xylitol gum, massive ingestions, FB, bezoar
Emesis Induction: Contraindications
Ø Symptomatic patient, underlying medical conditions
- CNS depression, tremors, seizures, agitation, hypoglycemia, respiratory distress
- megaesophagus, laryngeal paralysis, upper airway disease, hx of aspiration
Ø Corrosive (caustic) toxicants, sharp objects
- lime removal products, ultra-bleach, batteries, oven cleaning chemicals, lye
Ø Petroleum distillates / hydrocarbon toxicants
- gasoline, kerosene, torch oil, transmission fluid, motor oil
Ø Brachycephalic breeds*
Emesis Induction: Agents
At-home:
- 3% hydrogen peroxide
- cats: no safe, effective emetic agents
- also, salt, soaps…
Veterinary:
- apomorphine
- ⍺2-agonists (dexmedetomidine, xylazine)
Emesis Induction: No Longer Recommended methods
- direct stimulation
- syrup of ipecac
- liquid dishwashing detergent
- dry mustard powder
- table salt
3% Hydrogen Peroxide - how does it work for emesis? dont use when? how fast does it work?
Ø MOA: direct irritation of oropharynx & gastric mucosa
Ø Dosage: 1-2 mL/kg PO, up to 2 doses in dogs
- not recommended in cats
Ø Onset: within 10 mins, most effective post-meal
Apomorphine - how does it work for emesis? what animals? how fast? when not reccomended?
Ø MOA: direct CRTZ stimulation + emetic center depression
Ø 1° emetic agent in dogs, ↓ efficacious in cats
Ø Onset: within 4-6 mins
Ø Reversal: naloxone
Ø Not recommended: metaldehyde
Alpha 2-Agonists- how does it work for emesis? which drugs? how fast? adverse effects?
Ø MOA: centrally acting ⍺2-agonist activity
Ø Dexmedetomidine: 5.5x more success
- reversal atipamezole
Ø Xylazine:
- reversal yohimbine
Ø Onset: within 10 mins
Ø Adverse effects: sedation, respiratory depression
Gastric Lavage - what is this and how does it work? how useful?
Ø Remove toxicants from stomach by irrigation
Ø Practical clinical success: questionable (transport to facility)
- 15-20 mins: 29-38% drug recovery
- >1 hour: 9-13% drug recovery
Ø Labor intensive, low yield
Ø Potentially life-saving procedure
Gastric Lavage: Indications
Ø Unproductive or contraindicated emesis induction
- comatose, sedate, tremors, seizures
Ø Massive ingestions
- FB obstruction (e.g. bone meal, blood meal, kitty litter)
- Bezoar/concretion (e.g. iron tablets, unbaked yeast bread dough, xylitol gum)
Ø Approaching LD50
Ø Narrow safety margin, severe clinical signs
- Ca2+ channel blockers, 𝛽-blockers, cholecalciferol, organophosphates, baclofen, macrocyclic lactones, metaldehyde
Gastric Lavage: Contraindications
Ø Corrosive toxicants
- oropharynx/esophagus/gastric perforation with orogastric tube placement
Ø Petroleum distillates / hydrocarbon toxicants
- highly volatile, low-viscosity liquids > severe aspiration pneumonia
Ø Sharp objects (sewing needles)
Ø Post-surgical/medical conditions
Gastric Lavage: Complications
Ø Aspiration pneumonitis/pneumonia
Ø Sedation/GA risks
- hypoxemia, hypercapnia (hypoventilation)
- hypothermia, laryngospasm
- arrhythmias, sudden death
Ø Mechanical injuries
- mouth, oropharynx, esophagus, stomach
- esophageal, GI perforation
Activated Charcoal ± Cathartic
- how does this work? when is it effective? vs not? how soon after ingestion should we give?
Ø MOA: physically binds to toxicant in GIT, ↓ absorption
Ø Effective against large non-polar compounds
- NOT heavy metals, alcohols (e.g. ethylene glycol, xylitol)
Ø ↓↓ particle size, ↑↑ surface area
- oral suspension/slurries»_space; effective than tablets, capsules
Ø Dosage: 1-5 g/kg PO once, with cathartic
- speeds expulsion of charcoal-toxicant moiety from GIT
- ↓ significant desorption
Ø Beneficial even as late as 6 hours post ingestion
Activated Charcoal: Multidose - how to give? complications?
Ø Repeat 1-2 g/kg PO q 6 hours for 24 hours, without cathartic
Ø Complications:
- aspiration pneumonia
- dehydration, constipation
- fluid, electrolyte, acid-base abnormalities (hypernatremia)
- interferes endoscopic visualization
- corneal abrasions (accidental contact)
ØPrepare owners: black stool, black vomitus
AC ± Cathartic: Contraindications
Ø Symptomatic, underlying medical conditions
- CNS depression, diminished gag reflex, compromised airway
- megaesophagus, laryngeal paralysis, upper airway disease - GI obstruction, perforation, ileus, stasis
Ø Dehydration, hypovolemia, hypernatremia (GI free water loss)
- renal disease, diabetes mellitus/insipidus, psychogenic polydipsia
Ø Corrosive/caustic agents, hydrocarbons, salt toxicosis
- paintballs, homemade play dough, ocean water, table salt
Cholestyramine - what is it? method of action?
ØBile acid sequestrant, anti-lipemic agent
ØMOA: binds intestinal bile acid & lipoprotein > insoluble complex >
prevents toxin absorption, interrupts enterohepatic recirculation
Cholestyramine adverse effects and contraindications
Ø Wide safety margins, adverse effects:
- nausea
- hypoproteinemia
- steatorrhea
- loss of fat-soluble vitamins (supplement Vit K1)
Ø Contraindicated: complete biliary obstruction
Intravenous Lipid Emulsion (ILE)
- what is it and when is it used? MOA?
Ø Triglycerides + phospholipids emulsifier + glycerin + plant oil
Ø Lipophilic drug toxicities, cardiotoxicities, neurotoxicities
ØExact MOA unknown:
1. “lipid shuttle” theory
- forms chylomicron-like droplets in plasma > expand plasma’s lipid phase > sequester xenobiotic molecules from target tissues (brain, heart) > shuttles elsewhere: storage, metabolism, excretion > ↓ clinical signs, ↑ toxin clearance
2. Improve myocardial performance
- deliver free fatty acids (preferred substrate) to myocardium
Intravenous Lipid Emulsion (ILE) complications
- infection (bacterial contamination)
- hypersensitivity reactions
- pancreatitis, hyperlipidemia, corneal lipidosis - hemolysis
Advanced Therapies for decontamination
Blood purification therapies
- hemodialysis
- plasmapheresis
- hemoperfusion
Symptomatic Supportive Care for toxicity includes…
- Fluid therapy
- GI support
- Cardiovascular support
- CNS support
- Hepatoprotectants
- etc.
Clinical Signs of marijuana Intoxication
- lethargy, CNA depression, disorientation
- ataxia, incoordination
- vomiting, hypersalivation
- urinary incontinence
- hypothermia, mydriasis, bradycardia, hypotension
- hyperesthesia
- wtc.
Diagnostic Tests for marijuana toxicity
v Gold standard: gas / liquid chromatography mass spectrometry
v No reliable, or validated, point-of-care tests
> human tests not reliable
Decontamination for marijuana
v Induce emesis
‒ Within 30-60 minutes from ingestion
‒ Reverse nausea with maropitant
v Activated charcoal 1-4 g/kg PO
‒ Enterohepatic recirculation
Symptomatic Treatment
- what do we use for nausea
Maropitant
Ondansetron
Symptomatic Treatment
for bradycardia
Atropine
Symptomatic Treatment
for CNS excitement
Butorphanol
Acepromazine
Prognosis for marijuana toxicity
v Recovery: within 24-36 hours, up to 72 hours (dose dependent)
v Good with supportive care
v No long-term adverse effects
v Rare mortality
> THC butter: 2 deaths
