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Many household products meant for specific applications are the common indoor
toxicants that pose threat to pets and children. Household products are formulations of
complex chemical mixtures with multiple active ingredients. Although many products are not
highly toxic, cleaning substances, disinfectants, cosmetics, personal care products and some of
the commonly used over the counter drugs are common sources of toxicological exposure
particularly to pet animals.
The common route of exposure of the household hazardous compounds to an animal
may be dermal, oral, ocular or inhalational. When an animal exposed to a high concentration of
household product resulting in abnormal clinical signs is presented to the clinic, essential
information to obtain from the owner includes full trade name of the product, ingredients listed
on the product label and their concentration, the exposure amount and the duration of exposure,
the progression of clinical signs in relation to the time of exposure and any treatment or first aid
given by the owner before presenting to the vet. Owner may also be advised to bring the
product container as sample of the suspected agents whenever possible, for easier
identification of the chemical ingredient.
Even with this information, it may be still difficult to assess the situation as: a) the toxicity
of many household products are always not predictable on the basis of physical and chemical
characteristics of the individual ingredient. b) the interactions between ingredients within a
single product and between different products when present in combination further complicate
the toxicological risk assessment.
The clinical toxicology of some of the important indoor toxicants and other miscellaneous
household products is described with the general line of management and treatment especially
with reference to pet animals.
RODENTICIDES
Treatment: If the exposure has occurred within the last 24 hours, emetics, activated charcoal,
and cathartics are warranted. Once the clotting factors are depleted, aggressive treatment is
necessary, since synthesis of clotting factors takes at least 12 hours. The cat is given IV
transfusions of blood or plasma and vitamin K. The form of vitaminK, Vitamin K 1 , which is
immediately available for the synthesis of new clotting factors should always be administered;
but not vitamin K3. Vitamin K1, Phytonadione is administered 2-5mg/kg/day,PO or SC, in
divided doses, with a fatty food for 20-30 days, depending on the amount ingested. IV and IM
routes are not preferred as they pose anaphylactic and life threatening haemorrhage risk
respectively.
Zinc phosphide: After ingestion, the liberated phosphine gas in the acidic gastric environment,
directly damages capillary endothelium and erythrocyte membranes within the lungs, liver and
kidneys, which leads to increased vascular permeability with resulatant cardiovascular
collapse. Clinical signs noticed are anorexia, lethargy, weakness, abdominal pain, vomition,
recumbency, whole body tremors, seizures and death. Inducing vomition, administering
activated charcoal, saline cathartic and the supportive treatment with IV fluids, sodium
bicarbonate, calcium gluconate, corticosteroids, and dextrose is recommended.
Bromethalin: is the active ingredient in rat poisons, results in vomition, tremors, posterior
paresis porogressing to ascending paralysis. CNS depression and coma. Induction of emesis,
orogastric lavage , repeated doses of activated charcoal every 4 to 6 hours for three days, and
supportive therapy with IV fluids, anticonvulsants, muscle relaxant (methocarbamol, up to
220mg/kg/day,IV toeffect) , oxygen supplementation is recommended along with mannitol
(0.5-1g/kg;IV) and furosemide(1mg/kg,IV) if cerebral oedema is present.
INSECTICIDES
Amitraz: It is the active ingredient in anti-tick and anti-mite products; poisoning occurs
commonly from ingestion of a tick collar. Clinical signs include ataxia, bradycardia, CNS
depression, vomition, diarrhoea, and seizures. Treatment involves cardiovascular support with
decontamination (emesis, activated charcoal, saline cathartic) and repeated injections of
yohimbine (0.1mg/kg,.IV) or atepamizole (50µg/kg,IM) or tolazoline (4mg/kg,IV) to reverse
its adrenergic agonistic effects or physical retrieval of the collar through endoscopy Atropine
sulphate is to be avoided as it can potentially increase the viscosity of respiratory secretions
and may promote the absorption of the toxic compound.
Pyrethrins and pyrethroids: The onset of toxicosis occurs within 1 to 4 hours after dermal
and subsequent oral exposure, manifested by clinical signs of depression, hypersalivation,
muscle tremors, vomiting, ataxia, dypsnea, and anorexia. Treatment includes bathing, and a
combination of emetics, and activated charcoal. Diazepam or methocarbamol to control muscle
tremors and seizures, and atropine to control hypersalivation is recommended. Insect repellent;
Diethyltoluamide (DEET)poisoning has similar signs and similar treatment.
Organophosphates and carbamates : The clinical signs noticed with these groups are
salivation,lacrimation, excessive bronchial secretions, vomiting and diarrhoea, muscle
tremors,respiratory paralysis,, CNS depression, seizures, miosis, and hyperactivity.. Atropine
sulfate to alleviate respiratory distress, enzyme reactivator, Pralidoxime chloride (only in
organophosphates poisoning) and atropine sulfate are administered to counteract cholinergic
signs. However, overdoses or rapid IV administration of pralidoxime can cause tachycardia,
and cardiac arrhythmias as well as depression.
FERTILISERS
They have moderate toxic potential depending on the type and amount ingested. Many are
composed of urea or ammonium salts, phosphates, nitrates, potash and metal salts. Clinical
signs of ingestion include vomition, diarrhoea, metabolic acidosis, diuresis, electrolyte
disturbances: hyperkalemia, hyperphosphatemia, hyperammonemia and hyperosmolarity.
(Nitrate/nitrites cause formation of methhemoglobin). Treatment is symptomatic with milk, egg
white, water, emesis induction, gastric lavage, antiemetics, IV fluid to control hydration,
electrolyte imbalance and blood pressure.
Fire extinguisher fluids contain chloro bromomathane or methyl bromide, which if ingested are
converted in to methanol causing CNS excitation, depression, aspiration pneumonitis and
hepatorenal damage. Emesis and orogastric lavage are contraindicated. Flushing the eyes and
skin with water or normal saline solution, gastroprotectants, antiemetics, IV fluids and oxygen
supplementation or mechanical ventilation has been recommended.
GRAPES
The mechanism of toxicity being unknown, even small amount of grapes can be toxic to dogs.
Clinical signs like vomition, diarrhoea (with visible grapes in fecal matter), hypertension,
lethargy appear within 24 hours of ingestion, leading to signs of acute renal failure (polyuria,
polydipsia,vomition) and anuria. Treatment involves gastric lavage, gastroprotectants,
antiemetics with repeated doses of activated charcoal, calcium channel blockers ( amlodipine ,
diltiazem) to control hypertension and IV fluid therapy for maintaining renal perfusion. In
cases of severe oliguric or anuric renal failure, dopamine, furosemide and mannitol can be
useful in increasing urine output along with peritoneal or hemodialysis.
They contain sulfoxide compounds that can cause oxidative damage of RBCs leading to
anemia, methhemoglobinemia and intravascular hemolysis, manifestd by clinical signs like
tachypnoea, tachycardia, vomition, diarrhoea, pale mucous membranes,weakness,
haemoglobinuria. IV fluid diuresis, induction of emesis, gastric lavage, activated charcoal and
cathartic administration is indicated, with blood transfusion in case of severe anaemia.
MUSHROOMS
Evans R.J (1996). Toxic hazards to cats. In Vet. Clin. North .Am. (Small Anim. Pract.): pp 251-
259
Jane.G.Owens and David.C. Dorman. (1997). Common household hazards for small animlas.
Veterinary Medicine, Feb : pp 140-148
Jane.G.Owens and David.C. Dorman. (1997). Drug poisononig in small animals. Veterinary
Medicine, Feb : pp 149-157
Kore.A.M (1997). Over the counter analgesic drug toxicoses in small animals. Veterinary
Medicine, Feb : pp 158-165
Lorgue .G ,Lechenet J and Riviere .A (1996). Clinical veterinary toxicology .Blackwell science
publishers, UK.
Michael E. Peterson and Patricia A. Talcott.(2006). Small animal toxicology, second edition, .
Elsevier saunders Inc, USA.pp 223-344