4.2 Household Toxicants

Question 1

acid vs alkali burns

Answer 1

-acids cause coagulation necrosis > a barrier to further penetration
-alkalis cause liquefaction necrosis > facilitates rapid, deep dissolution of tissue (much more severe)

Question 2

how are soaps made? what toxic signs do they cause?

Answer 2

• Made by reacting alkali with fat
• Primarily GI signs
• Alkali may cause caustic burns
• Homemade soaps, dishwasher detergents often contain free alkali (lye = NaOH/KOH)

Toxicity generally low, ingestion uncommon

Question 3

treatment options for ingestion of soap

Answer 3

• Emesis (only if non-alkali)
• Dilution (oral milk or water)
• Fluids/electrolytes if vomiting/diarrhea severe (or if cardiac signs)

Question 4

what are non-ionic detergents? how toxic are they? what signs do they cause when ingested?

Answer 4

e.g. many hand dishwashing detergents, shampoos, some laundry detergents
* Generally low toxicity
* Usually GI signs, mild corneal damage
* Ingestion is uncommon

Question 5

what is a treatment for ingestion of non-ionic detergents?

Answer 5

• Decontamination (flush skin/eyes)
• Dilution (oral milk or water)
• Fluids if vomiting/diarrhea severe

Question 6

what are anionic detergents? how toxic are they? what issues do they cause when ingested?

Answer 6

e.g. sulfates, sulfonates in laundry detergent automatic dishwasher detergents, some shampoos
* Toxicity mild to moderate (usually not fatal)
* Esophageal damage a major concern
* Ocular lesions more severe
* Ingestion uncommon but very harmful, intravascular hemolysis possible

Question 7

how do we treat ingestion of anionic detergents?

Answer 7

• Decontamination (flush skin/eyes)
• Dilution (oral milk/water)
• Activated charcoal
• Fluids if vomiting/diarrhea severe

Question 8

what are cationic detergents? how toxic are they? what problems do they cause when ingested?

Answer 8

• Quaternary ammonium compounds
• e.g. some detergents, fabric softeners, sanitizers
• Toxicity high to extreme
• Severe oral & esophageal caustic burns, severe ocular damage
• Profuse salivation, hematemesis, weakness, seizures, coma, death

Question 9

how do we treat ingestion of cationic detergents? What should we be careful of, in particular?

Answer 9

• Decontamination (flush skin/eyes)
• Dilution/deactivation (milk, egg whites)
• Activated charcoal?
• Fluids to correct electrolyte imbalances
• DO NOT INDUCE VOMITING
• DO NOT NEUTRALIZE ALKALI WITH ACID > heat > burns

Question 10

how toxic are other alkali products such as toilet bowl and drain cleaners, or bleach? what sort of effects do they cause? how can they be treated and what is the prognosis?

Answer 10

• Ingestions of these products are rare but contact can occur with spills
• Toxicity HIGH to EXTREME
• Effects similar to cationic detergents or
  worse
• May obliterate esophagus; gastric perforation
• Dilution & supportive care
• AC will not bind**
• Analgesics to control severe pain
• Prognosis grave

Question 11

what is the timeframe and mechanism of ibuprofen toxicosis? what signs do we see?

Answer 11

Ibuprofen toxicosis: 30 minutes to 3 hours after ingestion
 GI adverse effects are seen at lower doses, e.g. gastric ulcers (higher doses > multiple organ toxicity)
> Inhibits gastric mucus secretion, increases gastric acid production > ulceration & hemorrhage
 Higher doses cause renal vasoconstriction, kidney damage, bleeding may be seen due to inhibition of platelet function
 Corticosteroids exacerbate NSAID toxicity; do not use concurrently!!!

Question 12

**why do corticosteroids exacerbate NSAID toxicity? what are the mechanisms of these two drugs?

Answer 12

Mechanism:
Phospholipids > arachadonic acid
=>leukotrines > inflammation
OR
=>prostaglandins > inflammation

-Steroids block the synthesis of arachadonic acid from phospholipids
-NSAIDS (eg. ibuprofen) block the synthesis of prostaglandins from arachadonic acid
>compounding effect?

Question 13

most common signs of ibuprofen toxicosis

Answer 13

Most common signs: (worse if pre-existent dz present)
 GI (vomiting, anorexia, diarrhea, melena)
 Depression, ataxia
 Renal
> Gastric hemorrhage less common in cats, primary signs usually renal

Question 14

ibuprofen toxicosis treatment

Answer 14

 If detected early, treatment aimed at reducing absorption (emesis, activated charcoal, cathartics)
 IV fluids may be required to ensure adequate renal perfusion
 GI perforations require surgery
 Severe blood loss may necessitate transfusion

Omeprazole: proton pump inhibitor - inhibits gastric acid secretion > shortens recovery time

Misoprostol: PGE1 analogue that protects GI mucosae, decreases gastric acid secretion, increases bicarbonate secretion (more of a preventative)

Question 15

what doses of acetaminophen (tylenol) cause toxicity?

Answer 15

Dogs: therapeutic dosage is 15 mg/kg TID
Toxicity seen with acute dosages of ~600 mg/kg, and occasionally with chronic therapy

Cats: far more sensitive, drug is not used therapeutically
Toxicity seen at dosages as low as 10 mg/kg

Question 16

**what is the mechanism of acetaminophen toxicosis?

Answer 16

Metabolism in dogs:
Most of the drug is conjugated via hepatic glucuronidation & sulfation pathways to yield non- toxic metabolites > excreted in urine & bile > also some enterohepatic recycling

Ordinarily only a small minority of molecules undergo P450 metabolism > toxic intermediate metabolite NAPQI (N-acetyl benzoquinoneimine) that is then conjugated with glutathione

Glucuronidation & sulfation pathways are finite, so high doses result in increasing P450 metabolism

Acetaminophen also inhibits glutathione synthesis
> even more unconjugated toxic metabolite accumulates

Cats are deficient in enzymes required for hepatic glucuronidation, so even higher amounts of NAPQI toxic metabolite accumulate > essentially no safe dose

Question 17

how can we treat an acetaminophen overdose?

Answer 17

Within limits, glutathione conjugation can inactivate this reactive intermediate > administer source of glutathione (n-acetylcysteine) > minimizes hepatic damage

Question 18

what specifically does acetaminophen toxicosis damage? what clinical signs will we see in dogs and cats?

Answer 18

Metabolite directly damages plasma membranes
> damage most severe in liver, blood

Dogs: clinical signs are those of hepatic injury (vomiting, anorexia, tachycardia, tachypnea)

Cats: feline RBCs far more prone to oxidative injury (different hemoglobin structure)
> methemoglobinemia is the most prominent feature of feline acetaminophen toxicity

Question 19

treatment steps for acetamiphen toxicosis and prognosis?

Answer 19

Treatment
1. minimize absorption (emesis or gastric lavage, followed by activated charcoal)
2. supportive therapy (for electrolyte disturbances, etc.)
3. source of glutathione (N-acetyl-cysteine) to speed conjugation of toxic metabolites > administer immediately to affected cat; repeat every 4 hours for 5 treatments

Prognosis depends on dose and delay before treatment

Question 20

most common illicit drug conumed by animals, and most important thing to do with client in cases of illicit drug consumption

Answer 20

• Most common is dog eating marijuana (particularly edibles)
• Whatever the source, important to gain trust of client in order to help animal

Question 21

effects of marijuana consumption on pets? signs? recovery time?

Answer 21

• Rarely fatal
• Stimulates cannabinoid receptor 1 in brain
• CNS signs: bradycardia, depression, ataxia, mydriasis; also urinary incontinence, vomiting, hypothermia, other
• Supportive care – control temperature; recovery may take up to 5 days

Question 22

what are the effects of amphetamine consumptions? how do we treat?

Answer 22

Amphetamines: treat narcolepsy, ADD
* CNS stimulation: seizures
* Arrhythmias
* Supportive treatment and AC (inhibit enterohepatic recycling)

Question 23

what can result in a false positive for amphetamines in a urine drug test?

Answer 23

• Decongestants containing pseudoephedrine can result in false positives on urine drug tests

Question 24

what do barbituates do? what are the signs of overdose and how do we treat?

Answer 24

Barbiturates: sedatives, anticonvulsants
* CNS depression, extreme hypotension
* Supportive treatment, emesis (not if unconscious)/gastric lavage + AC

Question 25

what do benzodiazepines do? what are the signs of overdose and how do we treat? Antidote?

Answer 25

Benzodiazepines: anti-anxiety medications
* CNS depression
* Supportive treatment
* Antidote: flumazenil

Question 26

what does cocaine do? what are the signs of overdose and how do we treat?

Answer 26

• Causes CNS stimulation
• May be combined with lidocaine, amphetamines, caffeine, heroin, strychnine
• Very rapidly absorbed: decontamination only useful if caught right away
• Supportive care: diazepam for seizures, beta blocker for tachyarrhythmia, control temperature

Question 27

what does LSD do? what are the signs of overdose and how do we treat?

Answer 27

LSD
* CNS stimulation or depression
* Supportive care
* Gastric lavage/AC may worsen signs?

Question 28

what do opiods do? what are the signs of overdose and how do we treat?

Answer 28

Opioids
* Respiratory depression may be fatal
* Emesis, AC, gastric lavage
> Opioids cause pylorospasm – may remain in stomach for a few hours
* Naloxone, the antidote for opioid overdose, is a competitive mu opioid–receptor antagonist that reverses all signs of opioid intoxication.

Question 29

what do PCP and ketamine do? what are signs of overdose and how do we treat?

Answer 29

PCP (Phencyclidine) and Ketamine
* Inhibit NMDA receptors in brain – mimics schizophrenia
* Increased muscle tone, HR, BP
* Abnormal facial expressions, jaw snapping, salivation, seizures, blank staring
* Supportive treatment, control seizures

Question 30

what is an easy way to test animals for consumption of illicit drugs?

Answer 30

MANY HUMAN URINE DRUG TESTS WORK ON ANIMALS
*note – risk of false negatives, particularly with THC toxicities

Question 31

why is gasoline consumed by animals? what are associated concerns? what does it do to the body?

Answer 31

• May drink out of curiosity, dermal exposure > licking
• Main concern is aspiration: can dissolve tissues within minutes
• Less than 1 mL of volatile hydrocarbon > widespread destruction of alveolar membranes > pulmonary edema, necrosis, agonal death
• CNS depression

Question 32

how should we treat gasoline consumption? what should we not do? what is the prognosis?

Answer 32

• DO NOT INDUCE VOMITING/gastric lavage > aspiration may occur upon emesis > fatal
• Treatment is supportive (e.g. oxygen, decontamination of skin)
• Prognosis with aspiration or coma is poor/grave

Question 33

why do animals consume ethylene glycol antifreeze? what are the effects/ mechanism of toxic action? how much is fatal?

Answer 33

• Ethylene glycol a major toxicant of small
  animals
• Sweet taste – animals drink from spills in garages, on driveways
• 1.5 mL/kg fatal to cats – groom from paws
• Hepatic alcohol dehydrogenase enzymes convert it to organic acids (e.g. formic, oxalic acid) > metabolic acidosis
• Oxalic acid crystallizes in renal tubules > calcium oxalate crystals cause renal tubular necrosis > renal failure (1d cats, 3d dogs)
• Clinical signs of renal failure, vomiting, CNS depression, dehydration

Question 34

clinical signs of ethylene glycol antifreeze consumption?

Answer 34

• Clinical signs of renal failure, vomiting, CNS depression, dehydration

Question 35

how can we treat ethylene glycol antifreeze consumption? what is the prognosis?

Answer 35

Ethylene glycol
* EG metabolized by alcohol dehydrogenase (ADH)
* Ethanol uses up ADH – vodka was often the choice for treatment before an antidote was available
> E.g. dogs tx with 5.5 mL/kg/hr IV of a 20% vodka solution (half vodka, half sterile saline)
* BETTER TX: Main goal is early prevention of metabolism with fomepizole antidote (ADH inhibitor) – prevents oxalic acid formation
> May work for brake fluid ingestion as well
* Prolonged fluid therapy (days) may be needed
* OFTEN FATAL

Question 36

what are the effects of porpylene glycol consumption on animals? mechanism of action? signs? treatment and prognosis?

Answer 36

Propylene glycol is less harmful to animals, is found in de-icing fluids for cars and also in low amounts in some foods!
* ADH converts it to lactic acid > acidosis may be fatal, but no calcium oxalate crystals
* Reacts with hemoglobin to form heinz bodies (especially in cats) that can persist for several weeks
* Treat with supportive fluid therapy
* Prognosis depends on delay prior to treatment
* No specific antidote

Question 37

effects of methanol consumption? where is it found, what does it do, what is the mechanism? how do we treat?

Answer 37

Methanol is less harmful to animals than it is to primates/humans
* Windshield washer fluid, rubbing alcohol
* CNS depression; blindness not observed in most non-primate species
* Coverted in liver to formaldehyde and formic acid (toxic in primates, but domestic species convert it to C02 and water)
* No specific antidote
* Monitor; fluid therapy to correct electrolyte imbalances, if necessary

This See-No-Evil Monkey Emoji is your reminder this mostly affect primates, and causes blindness and CNS depression