Household toxins (Proceedings)

Pets' eating and grooming habits, species inherent sensitivities to certain chemical/foods, and owners' attitudes are helpful in preventing accidental exposures. Similar hand-to-mouth behavior observed in children is the expected with pets. All precautions – properly store all hazardous chemicals, personal human medication, read medication labels, and know the need for, and seek immediate veterinary care - should be taken in preventing access of pet to hazardous substances.

Household Toxins Under the kitchen sink

Bleaches

Disinfectants, deodorizers, water purifiers

Sodium hypochloride (main component) of varying concentrations (3%, 6% and sometimes 50%).

Sodium peroxide/perporate (non-chlorine bleach).

Low oral toxicity (vomiting and diarrhea).

Detergents

Non-ionic (hand washing detergents, shampoos)

Anionic (laundry detergents)

Both of low oral toxicity

Cationic detergents (quaternary ammonium compounds)

High oral toxicity:

Muscle fasciculation, CNS depression and at times, seizures are manifested.

Corrosive at high concentrations

Emesis and/or gastric lavage are contraindicated.

Mothballs

Contain either naphthalene (more toxic) or para-dichlorobenzene. Cats are very sensitive.

Naphthalene: Vomiting, met-hemoglobinemia, Heinz body anemia, CNS stimulation, and rarely hepatic signs.

Paradichlorobenzene: No met-hemoglobinemia and/or Heinz body anemia. Could be hepato-toxic (phenol metabolites)

Easily diagnosed – history of ingestion and/or mothball odor in breath and vomitus.

Treat symptomatically.

Pine Oils

Mixture of terpene alcohols. LD50 of 1-2.5 ml/kg body weight (cats - more sensitive).Vomiting, hyper salivation, ataxia, weakness, CNS depression, renal failure, shock, and death. Emetics are contraindicated (aspiration pneumonia).Modeling dough and De-icing salt (Na ion) toxicity

Prevalence – Occurs infrequently but when do so, the dog is mainly affected.

Lethal dose (dogs) approximately 3.7 g/kg body weight.

High mortality (renal/gastrointestinal congestion and gastrointestinal inflammation).

Ice-melt exposure

Product ingredients: Sodium chloride (4g/kg), potassium chloride, magnesium chloride, calcium carbonate, and calcium magnesium acetate (some may contain urea).

Clinical signs

Vomiting (30% of cases), hypersalivation, diarrhea, lethargy, tremor, thirst polydipsia/polyuria, and dehydration, muscular rigidity, convulsions, coma, renal failure, shock, hyperchloremia, mixed metabolic and respiratory acidosis.

Treatment

Vomiting (perfuse) is common therefore emesis is not recommended. Anti-emetics recommended instead. Gastric lavage may enhance absorption (dissolution). Surgical removal – animal unable to withstand anesthesia. Adsorbents – not useful

Lower sodium concentration slowly (Rapid reduction may lead to cerebral edema). Small amounts of water at frequent intervals. Perenteral fluid if required – 5% dextrose or 2.5% dextrose in 0.45 % saline – recovery may take several days. Monitor sodium and chloride concentrations; renal function.

Aspirin (Acetylsalicylic acid)

Anti-inflammatory: Dogs - (25 mg/kg 3X daily); Anti-thrombic: - (0.5 mg/kg 2X daily)

Analgesic: – (10-20 mg/kg 2X daily); Antipyretic; Causes emesis in dogs @50 mg/kg q12h

Its use in cats – severe caution (possible toxicity. 10 mg/kg q48h for pain and fever. Cats are glucuronosyl-transferase deficient, thus reduced aspirin metabolism and toxicity results.

Clinical signs (Dogs)

Vomiting, restlessness progressing to CNS depression, seizure, and coma. Respiratory alkalosis >> metabolic acidosis.

Clinical signs (cats)

CNS depression, anorexia, vomiting, gastric hemorrhage. Toxic hepatitis, anemia, bone marrow hypoplasia, hyperpyrexia and Heinz body anemia.

Treatment: Emetic activated charcoal, osmotic cathartic (GI decontamination).

Correct acid base balance. Slow IV bicarbonate for metabolic acidosis. Alkaline urine – increased excretion "ion trapping"

Acetaminophen (Tylenol)

Antipyretic, Analgesic, but not anti-inflammatory

Well tolerated by dogs (toxic dose 600 mg/kg). The liver is the target organ for toxicity.

Cats – extremely sensitive. The liver is not the target organ for toxicity. Toxic dose reported to be 50-100 mg/kg. One 325mg tablet (possible toxic response), followed by a second within 24 h. could be lethal.

Clinical signs (dogs)

CNS depression, anorexia, vomiting, abdominal pain, icterus, dark colored urine/mucous membranes, with death in 4-5 days post exposure.

Clinical signs (cats):

Cyanosis, met-hemoglobinemia, dyspnea, facial and paw edema, CNS depression, hypothermia, salivation/vomiting, generalized weakness and death 12-48 h post exposure.

Treatment

Symptomatic and supportive - N-acetyl-cysteine (140 mg/kg PO or IV initially. Repeat in 6h then dose at 70-mg/kg q6h. Ascorbic acid (30 mg/kg PO). Blood transfusion thought helful. Poor prognosis

Ibuprofen (motrin, advil)

Analgesic/Anti-inflammatory

Very toxic to dogs (slow excretion) > 100 mg/kg. Gastrointestinal irritation, renal failure and hemorrhage are reported at 8 mg/kg/day.

Recommended safe dose: 5 mg/kg (2 divided doses)

Cats: Toxicity reported at > 50 mg/kg

Clinical signs

Vomiting, depression, abdominal pain, ataxia gastric ulcer (> 80 mg/kg), renal failure (> 300 mg/kg), and sudden death (> 800 mg/kg).

Pathophysiology: Like all Non-steroidal anti-inflammtory drugs (NSAID), ibuprofen affects Cyclo-oxygenase synthesis >> altered prostaglandin synthesis >> altered microcirculation, thereby causing direct GI irritation.

Treatment

Emetic, Activated charcoal; cimetidine (tagamet); an H2 blocker which decrease gastric acid production; Sucralfate (carafate) synthetic disaccharide binds denuded mucosa and seems to be prostaglandin protective?

Tricyclic Antidepressants: Amitriptyline (elavil, endep, amitril), Clomipramine (anafranil clomicalm. Developed in the 1950s and are still in use today.Toxic dose: >15 mg/kg (considered lethal). Readily absorbed from the gastrointestinal tract – prolonged absorption due to their anti-cholinergic effects. Peak plasma level reached with in 2-8h (extended delays can be expected).

Highly lipophilic therefore widely distributed - brain, heart, lungs, and liver.

Highly protein bound, cross placenta, and distributed in milk.

Hepatic metabolism and undergo enterohepatic recirculation. Variable T1/2 (9-84h).

Excretion - primarily urine, some in feces and bile.

Pathophysiology: Organ systems affected – cardiovascular and Neurological systems.

Inhibit fast sodium channels in ventricular myocardium >>> slowing of ventricular depolarization >> prolongation of QRS intervals (similar to quinidine, an ant arrhythmic drug) >> ventricular tachycardia or fibrillation (bradycardia, cardiac arrhythmias, and severe hypotension).

Inhibit nor epinephrine, dopamine, and serotonin reuptake.

Anticholinergic effects (hyperactivity, decreased gastrointestinal motility, decreased mucous secretions and seizures).

Clinical signs

Seen within 1h post ingestion (rapid onset and progression) – vomiting, hyperexcitabilty, hyperthermia, tremors, seizures >>> lethargy ataxia, bradycardia, coma, cardiac arrhythmia and death from cardiac failure.

Diagnosis

History of exposure, clinical signs, detection of tricyclic antidepressant in plasma, serum, whole blood, and/or urine.

Differential diagnosis

Amphetamine, cocaine, methylxanthines, herbal preparations (ma huang or guarana root), quinidine, propranolol and albuterol.

Treatment

Emesis induction should be done with caution (rapid development of clinical signs). Can cause seizures and possible aspiration in poisoned animals. Sedate and administered activated charcoal. Cathartic - Sodium sulfate NOT magnesium sulfate (slow gut motility, more magnesium absorbed). Repeat activated charcoal since tricyclic antidepressants undergo enterohepatic recirculation.

Avoid using atropine – anticholinergic effects of tricyclic antidepressants.

Monitor animals and give bicarbonate (acidosis, or cardiac toxicity). Cardiac toxicity reversed by elevating blood pH.

Treat seizures with diazepam or Phenobarbital

Good supportive (fluids, thermoregulation) care essential

Loratidine (Claritin)

Non-sedating histamine H1- receptor antagonist. Chemically related to the tricyclic antidepressants, therefore overdose could lead to ventricular arrhythmias.

Peak plasma concentration reached in 1-1.5h post-ingestion. It is 97-99% plasma protein bound.

Liver metabolism (minor active metabolite). With an elimination T1/2 of 7.8-15h.

Excreted into breast milk

Selective peripheral histamine H1- receptor antagonist with no substantial cerebral and autonomic nervous system effects.

Illicit Drugs (Stimulants)

Cocaine, Phencyclidine (PCP, angel dust, hog) – Sernyl (human use), Ketamine, Myristin and Elemicin

Methylxanthine

Caffeine, Theobromine and Theophylline: Components of tea, coffee, medications, soft drinks, and chocolate – sweetened/unsweetened baking chocolate (the primary component of which is theobromine).

Theobromine

Occur naturally in many plants found throughout the world. Examples include cocoa, tea and coffee plants. Theobromine is the predominant methylxanthine found in cocoa beans - present in all chocolate products. The amount of theobromine in the finished product depends on the type of chocolate used and the serving size.

Effect on domestic animals

In domestic animals, especially dogs, chocolate may harm the heart, kidneys and central nervous system. This is because dogs metabolize/excrete theobromine slowly. The effect of theobromine (diuretic and cardiac stimulant) on dogs and some other pets is serious.

Peak serum level reached 1.5h (dogs and cats); Elimination T1/2: 5.7h (dogs); 7.8h (cats).

10% excreted unchanged in urine.

Pharmacological actions

CNS stimulation, Cardiac muscle stimulation, Smooth muscle relaxation (bronchial in particular)

Diuresis. For most species the reported LD50 methylxanthine is 100-300 mg/kg bodyweight.

200-500-mg/kg-body weight (lethal in dogs)

Ingesting 2.25 ounces baking chocolate or 20 ounces milk chocolate could poison 10 kg dog.

Slow absorption, peak plasma level in about 10h.(dogs); 3h (human).

Clinical signs (within hours of ingestion of a toxic dose)

Vomiting, diarrhea, polyuria, weakness, hyperexcitability, tremors, seizure, and coma. Death from seizures and cardiac arrhythmias.Secondary pancreatitis reported in some cases.

Pathophysiology: Inhibits cyclic nucleotide phosphodiesterases and antagonize receptor-mediated action of adenosine resulting in cerebral cortical stimulation and seizures, myocardial contraction, smooth muscle relaxation, and diuresis.

Diagnosis

History of exposure, Clinical signs

Methylxanthines in stomach content, plasma, serum, urine, and liver of poisoned animal.

Stable in plasma or serum – room temperature (7 days); refrigerated (14 days); frozen (4 months).

Theobromine detected in serum 3-4days post-initial exposure.

Treatment

No specific antidote, therefore the goals are to sustain basic life support, decreased further absorption, increased excretion of absorbed methylxanthine, and relief of seizures, respiratory difficulties and cardiac dysfunction.

     • Emesis (maybe difficult in seizure animal) activated charcoal q3-6h (enter hepatic circulation).

     • Control seizures (valium, pentobarbital)

     • Monitor arrhythmias and treat as necessary

     • Fluid therapy in case of dehydration

     • Avoid steroids – decrease methylxanthine excretion.

     • With early intervention, prognosis is good.

Amitraz (mitaban, preventic flea and tick collar)

A topical miticide (Alpha-adrenergic agonist and a weak monoamine oxidase inhibitor - formamidine insecticide), used in the control of demodex, fleas and other ectoparasites in dogs, cattle and swine. Horses and cats are very sensitive to its use and therefore it use in these species are prohibited. In horses it use is associated with impacted colic, depression, in-coordination and death within 24 of exposure

In dogs, hypotension, mydriasis, hypothermia, bradycardia, hypoperistalsis, ataxia, sedation, vasoconstriction, vomiting diarrhea and hyperglycemia are reported clinical signs associated with excessive exposure.

Treatment

Yohimbine 0.45 mg/lb or 0.1 mg/kg IV is reported to reverses the signs of Amitraz toxicity.