ECC toxicology

Question 1

most common way animals are exposed to toxins

Answer 1

• 75-90% oral exposure, followed by dermal exposure

Question 2

General Management of Acute Intoxication

Answer 2

1. History & triage
2. Physical examination: ABCDs of patient stabilization*
3. 1° treatment: decontamination (gastrointestinal, dermal, ocular)
   - minimize further toxicant absorption
   - promote excretion of toxicant from body
4. Specific antidotes
   - intralipid emulsion therapy
5. Symptomatic supportive care

Question 3

Telephone Triage: Key Questions

Answer 3

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

Question 4

Telephone Triage: Consultation

Answer 4

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

Question 5

Triage & Physical Examination
- first things to check

Answer 5

1. Airway
2. Breathing 3. Circulation 4. Dysfunction
   ØAddress immediate life-threatening concerns before decontamination

Question 6

Toxicologic Decontamination
- purpose

Answer 6

Ø To prevent further toxin absorption + enhance elimination

Question 7

Gastrointestinal Decontamination methods

Answer 7

1. Emesis induction
2. Gastric lavage
3. Activated charcoal ± cathartic
4. Whole bowel irrigation

Question 8

Emesis Induction: Effectiveness depends on?

Answer 8

1. Physical properties of toxicants
   - gel caps, antiemetic effects, delay gastric emptying
2. Time elapsed from toxin ingestion
   -&raquo_space; rapid emesis,&raquo_space; gastric recovery
   - ideal: < 1 hour
   - little value: > 4 hours
3. Volume of gastric contents
4. Emetic agent
   - not effective: unsuccessful emesis after 2 doses

Question 9

Emesis Induction: Indications

Answer 9

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

Question 10

Emesis Induction: Contraindications

Answer 10

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*

Question 11

Emesis Induction: Agents

Answer 11

At-home:
- 3% hydrogen peroxide
- cats: no safe, effective emetic agents
- also, salt, soaps…

Veterinary:
- apomorphine
- ⍺2-agonists (dexmedetomidine, xylazine)

Question 12

Emesis Induction: No Longer Recommended methods

Answer 12

• direct stimulation
• syrup of ipecac
• liquid dishwashing detergent
• dry mustard powder
• table salt

Question 13

3% Hydrogen Peroxide - how does it work for emesis? dont use when? how fast does it work?

Answer 13

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

Question 14

Apomorphine - how does it work for emesis? what animals? how fast? when not reccomended?

Answer 14

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

Question 15

Alpha 2-Agonists- how does it work for emesis? which drugs? how fast? adverse effects?

Answer 15

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

Question 16

Gastric Lavage - what is this and how does it work? how useful?

Answer 16

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

Question 17

Gastric Lavage: Indications

Answer 17

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

Question 18

Gastric Lavage: Contraindications

Answer 18

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

Question 19

Gastric Lavage: Complications

Answer 19

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

Question 20

Activated Charcoal ± Cathartic
- how does this work? when is it effective? vs not? how soon after ingestion should we give?

Answer 20

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&raquo_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

Question 21

Activated Charcoal: Multidose - how to give? complications?

Answer 21

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

Question 22

AC ± Cathartic: Contraindications

Answer 22

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

Question 23

Cholestyramine - what is it? method of action?

Answer 23

ØBile acid sequestrant, anti-lipemic agent
ØMOA: binds intestinal bile acid & lipoprotein > insoluble complex >
prevents toxin absorption, interrupts enterohepatic recirculation

Question 24

Cholestyramine adverse effects and contraindications

Answer 24

Ø Wide safety margins, adverse effects:
- nausea
- hypoproteinemia
- steatorrhea
- loss of fat-soluble vitamins (supplement Vit K1)
Ø Contraindicated: complete biliary obstruction

Question 25

Intravenous Lipid Emulsion (ILE)
- what is it and when is it used? MOA?

Answer 25

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

Question 26

Intravenous Lipid Emulsion (ILE) complications

Answer 26

• infection (bacterial contamination)
• hypersensitivity reactions
• pancreatitis, hyperlipidemia, corneal lipidosis - hemolysis

Question 27

Advanced Therapies for decontamination

Answer 27

Blood purification therapies
- hemodialysis
- plasmapheresis
- hemoperfusion

Question 28

Symptomatic Supportive Care for toxicity includes…

Answer 28

• Fluid therapy
• GI support
• Cardiovascular support
• CNS support
• Hepatoprotectants
• etc.

Question 29

Clinical Signs of marijuana Intoxication

Answer 29

• lethargy, CNA depression, disorientation
• ataxia, incoordination
• vomiting, hypersalivation
• urinary incontinence
• hypothermia, mydriasis, bradycardia, hypotension
• hyperesthesia
• wtc.

Question 30

Diagnostic Tests for marijuana toxicity

Answer 30

v Gold standard: gas / liquid chromatography mass spectrometry
v No reliable, or validated, point-of-care tests
> human tests not reliable

Question 31

Decontamination for marijuana

Answer 31

v Induce emesis
‒ Within 30-60 minutes from ingestion
‒ Reverse nausea with maropitant

v Activated charcoal 1-4 g/kg PO
‒ Enterohepatic recirculation

Question 32

Symptomatic Treatment
- what do we use for nausea

Answer 32

Maropitant
Ondansetron

Question 33

Symptomatic Treatment
for bradycardia

Answer 33

Atropine

Question 34

Symptomatic Treatment
for CNS excitement

Answer 34

Butorphanol
Acepromazine

Question 35

Prognosis for marijuana toxicity

Answer 35

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