Intoxications

Question 1

Important things to note when you receive an intoxication patient. (5)

Answer 1

What toxin?
How much of the toxin?
When was it ingested?
If possible have the toxin or package brought to the clinic.
A good source of information (toxicology and its management books)

Question 2

Emergency management of an intoxication.

Answer 2

ABCDs! (airway, breathing, circ., dysfunction)

Supportive care and treatment:
Monitoring and supportive care
Fluid therapy
Cardiovascular support
Gastrointestinal support
Neurological support
Analgesia/sedation
etc.

Question 3

Ocular decontamination

Answer 3

• Physiological saline ideal (e.g. contact lens solution)
• Tepid tap water
• flushing for min.15-20min
• Maximize decontamination
• Reduce secondary injury to cornea
• Immediate veterinary care is needed, ask them to come in promptly.
• Prevent rubbing/Elizabethan collar

Question 4

Dermal decontamination

Answer 4

• Prevent transdermal absorption
• Prevent oral re-exposure secondary to grooming - bathe the animal!
• don’t forget the Eyes!
• Protect yourself and instruct the owner

Oil-based toxicities
- Tepid water and liquid dish soap
- Clip hair

Caustic, acidic or alkaline toxicities
- Gentle decontamination with tepid water
- Do not scrub! Do not use high pressure water sprays!
- Do not “neutralize”!

Risk of hypothermia with cooling
- Increases the effect of pyretroids and pyrethrins on CNS (household insecticides and products to control insects on pets or livestock)

• Not too warm water though because can cause Vasodilation and toxin canmove through the skin faster.

Question 5

Gastrointestinal decontamination

Answer 5

Before considering emesis get a complete history.

Consider
* Underlying med. problems
* Symptomatic patients
* Corrosive vs caustic agent
* Hydrocarbons: gasoline, kerosine, motor oil etc. (no emesis induction in these!)

Be aware of possible complications.
* Aspiration pneumonia
* Hematemesis
* Caustic or corrosive injury to esophagus, oropharynx or GIT

Question 6

Emesis

Answer 6

The earlier the better (ideal is within 120 min).
* Mainly useless after 4h (1-2h ideal)

Except:
* Large wads of xylitol gum
* Large amounts of chocolate (even 6h is okay but meds are max 1 h due to high solubility)

• Grapes and raisins
• Massive ingestion that can cause concretion (fish oil capsules, iron-vitamins)
• Ingestions that can form a bezoar or foreign body (blood or bone meal; fire starter logs).
• Drugs that delay gastric emptying (e.g. opioids).

Question 7

Emesis at home

Answer 7

3% hydrogen peroxide
* Direct gastric irritation
* 1-2ml/kg; do not exceed 50ml
* Induction in 5-10min

Table salt
* No longer recommended by veterinarians nor human doctors.
* Risk of hypernatremia

7% Syrup of Ipecac
* No longer recommended by veterinarians nor human doctors.
* Severe hematemesis, lethargy, diarrhea, depression.

Question 8

Emesis at the clinic (4)

Answer 8

• Ropinirol (Clevor)
• Apomorphine
• Xylazine
• Dexmedetomidine

Note: after use of one of the above, use an “antidote”, metoclopramide (primperan), ondansetron or maropitant etc.

Question 9

When to consider gastric lavage? (4)

Answer 9

Symptomatic patient with changed
mental status.

Need for controlled decontamination

Material large in size

Large toxic ingestions of tablets/capsules approaching LD 50

Question 10

Complications and contraindications of gastric lavage. (4+3)

Answer 10

Complications:
Risk of sedation
Aspiration pneumonia
Hypoxemia
Mechanical injury

Contraindications:
Corrosive agent
Hydrocarbon agent
Sharp objects

Question 11

Describe Activated charcoal use.

Answer 11

• Act as an absorbent and prevent systemic absorption
• Dose 1-5g/kg
• Often with cathartic (a medication that acts similarly to a laxative)
• Ideally should not mix with food but in practice…
• Toxicant must come in direct contact with the charcoal so Toxicant must be in the stomach.
• Currently ideal timeframe 0-60min post-ingestion
• charcoal Binds poorly with: alcohol, sugar alcohol (sorbitol), glycols, strong acids, strong bases, metals, lithium, sodium, iron,
  lead, arsenic, fluorine, boric acid, inorganic materials.

Question 12

Clinical signs of nicotine intoxication?

Answer 12

Tremors, constricted pupils,
drooling and vomiting,
hallucinations, excitement,
diarrhea, twitching and
seizures in more severe cases,
high or low heart rate depending on dose, high blood pressure but falls in
circulatory collapse in high doses.

Coma and death possible in very severe cases.

Question 13

Treatment of nicotine intoxication?

Answer 13

Induced vomiting if about an hour from ingestion.

Gastric lavage and activated charcoal
administration can aid preventing nicotine absorption.

+ Supportive treatment, IV fluids and e.g.
anticonvulsants or anti-nausea drugs.

Question 14

Clinical signs of grape and raisin intoxication.

Answer 14

vomiting and/or diarrhea within 6-12 hours,
lethargy, anorexia,
abdominal pain, dehydration,
polydipsia, tremors and
oliguric or anuric renal failure which develops within 24-72 hours.

Question 15

Treatment of grape and raisin intoxication.

Answer 15

induce emesis
give activated charcoal
aggressive fluid therapy
monitor electrolytes
poss. give diuretics
(this tox. can cause acute renal failure)

Question 16

Clinical signs of ethylene glycol intoxication (antifreeze)?

Answer 16

First 12 hours: nausea, vomiting and mental dullness.

After apparent recovery, signs of kidney failure within 12-72h.

By 72-96 hours, anuric kidney failure develops, with painful and enlarged
kidneys.

Question 17

Accumulation of ethylene glycol toxic metabolites causes

Answer 17

metabolic acidosis and further
organ damage.

Oxalic acid binds to minerals like calcium in the kidneys and forms calcium oxalate crystals, causing irreversible tubular necrosis and acute kidney failure.

Question 18

Another trick for diagnosing ethylene glycol toxicosis is to use

Answer 18

a Wood’s lamp–which emits ultraviolet light.

Most commercial antifreeze contains a compound which fluoresces under ultraviolet light; this is included so that car mechanics can detect potential antifreeze leaks.

Question 19

Treatment of ethylene glycol toxicosis.

Answer 19

Aim is to decrease absorption and metabolism of ethylene glycol, increasing
excretion of the unmetabolised form.

• Within 1-2h of ingestion, Emesis or gastric lavage

Ethanol administration iv: Competitively prevents formation of toxic metabolites.
* IV fluid therapy: 4-Methylprazole (fomepizole), 20% ethanol boluses or
30% ethanol constant-rate infusion.
* Gastrointestinal support

Dosages vary between species and symptoms being exhibited.

Prognosis: If treatment is received within 4-8h post ingestion, full recovery is possible
If not, acute kidney failure and death may follow.

Question 20

Bromethalin is

Answer 20

a Non-anticoagulant, neurotoxic rodenticide.

Bromethalin exerts toxicity by uncoupling oxidative phosphorylation in mitochondria, thereby decreasing ATP synthesis. CNS is the target organ, and the toxicity is characterized by cerebral edema, convulsions, and paralysis.

Question 21

Clinical signs of bromethalin poisoning.

Answer 21

High doses -> Convulsant form
Signs develop within 2-12 hours.
Seizures, Anorexia
Hyperexcitability, Circling
Hyperthermia, Hyperesthesia
Muscle tremors
Almost always leads to death.

Low doses -> Paralytic form
Signs develop within 12-24 hours.
Anorexia, Ataxia
Posterior paresis, Tremors
Decreased mentation, Vomiting
Nystagmus, Anisocoria
Can worsen over 1-2 weeks.

Question 22

Treatment & prognosis of bromethalin poisoning.

Answer 22

Early low-dose, non-clinically affected patients:
- induce emesis if ingestion within 4h
- activated charcoal to prevent further absorption (given multiple times, every 6-8 hours)
- prognosis is good

High-dose, clinically affected patients:
- for decontamination: gastric lavage and enema
- for tremors Methocarbamol (IV or CRI)
- for seizures, anticonvulsants
- to reduce cerebral edema and intracranial pressure Mannitol (IV)
- prognosis is guarded or poor, but recovery is possible within weeks.

Question 23

what is methocarbamol

Answer 23

sold under the brand name Robaxin among others, is a muscle relaxant used to treat acute, painful musculoskeletal spasms in a variety of musculoskeletal conditions.

Question 24

Mechanism of action behind anti-coagulant rodenticides.

Answer 24

Anticoagulant rodenticides interfere with the liver’s production of clotting factors by inhibiting the enzyme that recycles vitamin K1, which is essential for blood clotting.

This leads to a depletion of active clotting factors, preventing normal blood clotting and resulting in internal hemorrhage

Question 25

Clinical signs of Anticoagulant rat poison intoxication.

Answer 25

During the first 36–72h following ingestion of the anticoagulant, the patient is usually clinically normal as the clotting factors are slowly depleted.

In animals with some underlying illnesses hemorrhage can occur as early as 24–48h
following exposure.

Clinical signs: Lethargy, weakness, anemia, difficulty breathing (dyspnea), coughing & hemoptysis.

Bleeding into body cavities or joints, external hemorrhage (GI tract, surgical sites, orifices).

Abdominal distention, bruising, hematomas, muffled heart sounds.

Central nervous system signs in severe cases.

Sudden death in cases of severe internal bleeding – hypovolemic shock!

Question 26

Treatment & prognosis for Anticoagulant rat poison intoxication.

Answer 26

Induced vomiting is effective within 4–8h of ingestion. If vomiting is not successful or contraindicated, oral vitamin K1 should be started.

• Asymptomatic patients: start prophylactic vitamin K1 or monitor patient’s PT. If PT is normal at 72h, no treatment is needed.
  If PT increases, start vitamin K1 treatment.

PT monitoring should not occur while administering vitamin K1, can lead to false readings.

• Vitamin K1: 3–5 mg/kg twice per day. Duration of treatment depends on the specific rodenticide.
• Symptomatic patients: stabilization, oxygen treatment and blood or plasma transfusions. Oral vitamin K1 treatment.
  Hospitalization until PT normalizes.

Prognosis of ingesting anticoagulant rodenticides depends on if the patient is able to survive the first 48hours of acute coagulopathy. If the patient survives, the prognosis improves.

Question 27

Pathophysiology of xylitol intoxication.

Answer 27

hypoglycemia occurs due to xylitol’s direct stimulation of insulin secretion from the pancreas (seen within 10-15 mins).

The mechanism of hepatic necrosis is unknown, but hypothesized either by ATP depletion or by production of reactive oxygen species during the metabolism of xylitol in the liver.

Question 28

Clinical signs of xylitol intoxication.

Answer 28

Vomiting
Diarrhea
Lethargy
Weakness
Seizures
Potentially death

(measurement of severe hypoglycemia can put you on the right track + anamenesis)

Question 29

Treatment of xylitol intoxication.

Answer 29

Emesis (not in case of 100% xylitol products over 30 mins ago, or in case neuro signs are present).

IV fluids + dextrose bolus, then parenteral fluids containing 2.5-5% dextrose.

Monitoring of blood glucose every 1-4h and liver enzymes.

Small frequent meals, as long as patient isn’t vomiting.

Drugs: Liver protectant/supportive + antiemetics.

Good prognosis with lower doses and prompt treatment.
Fair to guarded prognosis with larger ingestions.
Guarded prognosis for patients with liver failure.

Question 30

Permethrin use in dogs and cats.

Answer 30

Permethrin is widely used as an ectoparasitic for dogs, but it’s highly toxic to cats.

Cats lack the liver enzyme glucuronyl transferase, which is needed to break down permethrin efficiently, leading to toxic accumulation in their bodies.

Some cats are so sensitive that even
brief contact with a dog treated with a spot-on product containing concentrated permethrin (45%–65% permethrin) can cause symptoms of toxicity.

Question 31

Clinical signs of permethrin intoxication.

Answer 31

Paresthesia in all animals after dermal application. Ear twicthing, paw/tail licking, hiding and hyperexcitability.

In cats: weakness, tremors, shaking, ataxia, seizures and paralysis. Severe poisoning signs including seizures, tremors and in extreme cases death.

• In dogs: nervousness, rubbing of application site, agitation, shaking of legs and mild muscle fasciculation can occur if overdosed.

Question 32

Treatment of permethrin intoxication.

Answer 32

• intravenous fluid support to maintain electrolyte balance
• thermoregulation support
• decontamination by washing
• benzodiazepines for seizure control
• intravenous lipid emulsion (off-label use) can be considered
• methocarbamol (muscle relaxant) to reduce tremors

Prognosis: Depends on severity of the exposure and time of treatment initiation. When caught early and managed effectively, recovery is often achievable.

Question 33

Clinical signs of Paracetamol intoxication in small animals

Answer 33

vomiting, anorexia, diarrhea, respiratory distress and signs of shock.

Cats have more methemoglobinemia and dogs, hepatotoxicity with GI and CNS signs, but either syndrome is possible in both species.

Question 34

Treatment of Paracetamol intoxication in small animals

Answer 34

induce vomiting within 2 hours of ingestion,

administer activated charcoal,

antioxidants therapy with N-acetylcysteine 140mg/kg I/V initial dose.

Prognosis depends on the amount of acetaminophen ingested and the amount of time before treatment begins.

Question 35

Paracetamol intoxication in small animals.
Signs of methemoglobinemia include

Answer 35

shock (tachycardia, tachypnea, hypothermia, weakness, collapse), brown MMs, respiratory distress, cyanosis, lethargy, coma and face & paw edema.

Question 36

Pathophysiology of lily intoxication in small animals.

Answer 36

True lilies are nephrotoxic to cats but may cause GIT upset in dogs.

Hybrid lilies are toxic to both cats and
dogs, causing GIT upset and possibly other symptoms.

The mechanism of action and toxin are unknown. However, the toxin is water-soluble and acts very rapidly, causing severe acute kidney injury (AKI) that targets
the renal tubules provoking necrosis.

Three systems are affected: renal, GIT, and nervous.

Question 37

Signs of lily intoxication in small animals.

Answer 37

Clinical picture develops within 6 to 12 hours after ingestion.

Early signs show vomiting, anorexia and lethargy followed by signs of AKI: polyuria/oliguria/anuria, dehydration, diarrhea and depression.

Some cats express CNS signs with ataxia, head pressing, disorientation, tremors and seizures. In some rare cases, the animal
may develop pancreatitis.

Question 38

Treatment of lily intoxication in small animals.

Answer 38

Induce vomiting (before symptoms start)

IV-fluid therapy: at least for 48-72 hours, isotonic crystalloids, initially at 2-3x maintenance for 48 hours then adjust accordingly to patient’s needs.

activated charcoal for binding toxins & cathartic for increasing bowel movements (if not dehydrated / diarrhea)

Other treatment considerations: diazepam (seizures), gastroprotectants, antiemetics, analgesics

Good to excellent if cat is treated in less than 18h + 48-72h of fluid therapy. Poor to grave if delayed treatment in more than 18h → chronic kidney injury may occur.

Question 39

What is metaldehyde and its pathophysiology in small animals?

Answer 39

Metaldehyde is a chemical used in slug and snail bait and is often a blue-green pellet.

Metaldehyde decreases the concentration of gamma-aminobutyric acid, an inhibitory neurotransmitter that causes CNS excitation.

Decreased concentrations of serotonin (5-hydroxytryptamine) and norepinephrine in the CNS decrease the threshold for seizures.

Question 40

Clinical signs of metaldehyde intoxication.

Answer 40

Signs can appear in a few minutes and up to 3 hours. Dose-dependent signs and similar in most species.

Early signs (within 1-3 hours of ingestion): hyperesthesia (heightened sensitivity to stimuli), hyperthermia, restlessness, anxiety, severe muscle tremors and ataxia.

Progressive signs: Seizures, tachycardia, tachypnea, hypersalivation, vomiting, diarrhea, mydriasis, nystagmus (cats), cyanosis, acidosis and coma, leading to death without treatment.

Question 41

Treatment of metaldehyde intoxication.

Answer 41

No specific treatment, but supportive care during the first 24h results in full recovery of most patients in 2-3 days’ time.

care includes; IV fluids, sedation and anesthesia.

Activated charcoal is used for gastric lavage
and decontamination.

Cold water provisions are used to treat the hyperthermia.

Question 42

pathophysiology of chocolate toxicosis small animals.

Answer 42

Toxic ingredient in chocolate is 2 methylxanthines: theobromine and caffeine, both constituents contribute to chocolate toxicosis.

Theobromine and caffeine competitively inhibit cellular adenosine receptors, resulting in CNS stimulation, diuresis, and tachycardia.

Methylxanthines also increase intracellular calcium levels by increasing cellular calcium entry and inhibiting intracellular sequestration of calcium by the sarcoplasmic reticulum of striated muscle. The net effect is increased strength and contractility of skeletal and cardiac muscle.

Question 43

Clinical signs of chocolate toxicosis small animals.

Answer 43

• Usually within 6–12 hours of ingestion.
• GI tract: vomiting and diarrhea
• Cardiovascular: tachycardia, arrhythmias, and hypertension
• CNS: ataxia, muscle tremors, seizure activity and hyperexcitability
• Renal/urological: polyuria, polydipsia and urinary incontinence
• Respiratory: tachypnea, respiratory failure
• Endocrine/metabolic: hypokalemia

Death generally due to cardiac arrhythmias, hyperthermia, or respiratory failure.

Question 44

Treatment of chocolate toxicosis small animals.

Answer 44

Induce emesis if patient is not yet showing clinical signs.

Activated charcoal, gastric lavage if indicated

Supportive care and treatment of seizures with benzos, lidocaine for ventricular arrhythmias, beta blockers if tachyarrhythmias.