MANAGEMENT OF TOXICITY OF COMMON

HOUSEHOLD HAZARDOUS SUBSTANCES IN

DOGS AND CATS

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.
SOAPS AND DETERGENTS
Hand soaps, shampoos, spray cleaners, dishwashing liquids, powders, laundry products,
disinfectants, fabric softeners and sanitizers are the common products under this category.
Soaps: Bath soaps and bar soaps usually have low toxic potential and cause mild
gastroenteritis with vomition, on ingestion. Treatment involves a) use of demulcents and
diluents: milk, rinsing with water for dermal and ocular exposure. b) induction of emesis if
soap is non alkaline( noncorrosive), if there is no spontaneous vomition within thirty minutes of
ingestion c) symptomatic treatment for diarrhoea and vomition, maintenance of fluid and
electrolyte balance.
Detergents: are surfactants: agents that lower the surface tension of the water to enable it to
wet surfaces moré efficiently. They mainly contain inorganic ingredients such as phosphates,
silicates or carbonates. Based on their degree of ionization, when in solution they have been
classified in to nonionic, cationic and anionic detergents. Nonionic detergents generally have
low order of irritaion and low toxicity, being non corrosive. .Based on their degree of
ionization, when in solution they have been classified in to nonionic, cationic and anionic
detergents. Anionic and cationic detergents are corrosive and highly toxic. Nonionic detergents
(alkyl ethoxylate, alkyl phenoxylate, poly ethoxyethanols; sources: shampoos, dishwash
detergents, laundry detergents) generally have low order of irritaion and toxicity, being non
corrosive. Anionic (alkylsodium sulfate, alkyl sodium sulfonate, dioctyl sodium sulfosuccinate,
sodium lauryl sulfate; sources: shampoos, dishwash detergents, laundry detergents) and
cationic (benzethenium chloride, benzalkonium chloride, alkyl dimethyl zene,cetirimide, cetyl
pyridinium chloride; sources: fabric softeners, germicides, disinfectants, sanitizers) detergents
(Quaternary ammonium compounds) are corrosive and highly toxic. Ethanol and isopropanol,
which are often found in cationic detergent preparations significantly enhance gastrointestinal
absorption and damaged skin favours percutaneous absorption.
Toxicity related clinical signs are vomition, diarrhoea, gastrointestinal discomfort,
intravascular hemolysis in impaired liver condition, dermal irritation, corneal damage ; Oral-
Corrosive damage, salivation, haematemesis, muscle weakness, respiratory and CNS
depression, seizures, collapse, comapredominantly seen with cationic detergents. Treatment
involves dilution with milk, water, egg white, administering activated .charcoal, saline
cathartics, fluids, antibiotic, analgesics and thorough washing the skin with soap and water and
eye lavage with isothermic isotonic saline for 20minutes.
Shampoos: Selenium sulfide shampoos have low toxic potential, primarily causing
gastroenteritis; treated by gastric decontamination, dilution with egg white, milk, activated
charcoal. Zinc based (zinc pyridinethione) antidandruff shampoos are more toxic, resulting in
gastroenteritis; retinal detachment on ocular exposure. Gastric decontamination; emesis
induction, lavage along with IV fluids and thorough eye rinsing with saline is the therapy.
CORROSIVES
Corrosive products are either acidic or alkaline agents depending on their pH in
solution.. Strongly alkaline or basic compounds tend to produce more severe injury than acidic
materials; because contact with acids induces immediate intense acidic burns and pain, and
most of the animals do not ingest significant quantities. Alkaline products produce liquifactive
necrotic lesions, which are more deeply penetrating than the localized coagulative necrosis
produced by acids.
Acidic corrosive (Hydrochloric acid, sulfuric acid, nitric acid, phosphoric acid, sodium
bisulfite) product examples are antirust compounds, toilet bowl cleaners, automobile batteries,
gun barrel cleaning fluid and swimming pool cleaning agents. Alkaline (sodium hydroxide,
potassium hydroxide, sodium carbonate, potassium carbonate, ammonium hydroxide,
potassium permanganate) product examples are drain cleaners, washing products, liquid
cleansers and toilet bowl products.
On dermal and ocular exposure: serious burns, extremely painful, corneal/conjuctival
necrosis, perforation and opacity which may not be evident immediately. On ingestion:
corrosive burns of mucosal membranes appear firstly as milky white or grey, which later turns
to wrinkled black. Animal may vocalize or depressed; manifest pain by panting, inability to
swallow. Haematemesis, abdominal pain, polydypsia, and respiratory distress, and shock,
secondary pneumonia from aspiration of vapors, gastrointestinal bleeding, perforation and
fistula are the other signs observed depending on the severity.
Treatment: Oral dilution with egg white, milk or water, skin and eyes thourghly
flushed with copious water and sterile saline respectively; therapy for shock: IV fluids, steroids
within 48 hours, which reduce the fibroblastic activity and inflammation, reduce the stricture
from circumferential alkaline burns. Analgesics and antibiotics prophylactically in animals
with perforations. Contraindications: 1. Attempts to neutralize burns chemically, as
exothermic reactions produce elevated local heat and thermal burns.. 2. Gastric lavage and
induction of emesis 3. Charcoal is ineffective in binding to caustics
DISINFECTANTS
Disinfectants found in cleaning products include quaternary ammonium compounds,
phenol, pine oil, bleaches, and alcohols; are more toxic than soaps and detergent compounds
Phenols: are aromatic alcohols derived from coal tar, highly reactive and corrosive contact
poisons; denatures and precipitates cellular proteins of all contacting cells. They are generally
nephrotoxic, hepatotoxic and neurotoxic; rapidly absorbed through ingestion, inhalation or
skin. Cats are highly sensitive to phenolic compounds. Sources of phenolic compounds include
flooring materials, coal tar, creosote, tar paper.
The dermal exposure results in intense pain, areas of coagulative necrosis; treated by
glycerol, polyethylene glycol washing, thorough rinsing with water , dressings soaked in 0.5%
sodabica. The ocular exposure results in clinical signs like corrosive burns of mouth,
oropharynx, oesophagus. vomition, salivation, hyperactivity, ataxia, panting, weakness, tremor,
coma, seizures, methhaemoglobinaemia, respiratory alkalosis, severe liver and kidney damage.
Treatment is by demulcents-milk, egg white, gastric lavage and emesis(contraindicated in
severe damage) activated charcoal, saline cathartic, 1% methylene blue, 4mg/kg;IV; ascorbic
acid 20mg/kg,PO; N-acetyl cysteine 140mg/kgIV, 70mg/kg PO. q,id for 3 days. Ocular
exposure is treated by sterile saline wash
Bleaches: Most household bleach preparations contain sodium hypochlorite. Calcium
hyp[ochlorite and trichloroisocyanuric acid are present in industrial strength bleaching
solutions, swimming pool chlorine products and chlorine laundry bleaches. Non chlorine
bleach preparations or colorfast bleaches contain sodium peroxide, sodium perborate or
enzymatic detergents. Chlorine bleaches are hazardous when mixed with strong acids or
ammonia solutions as they release chlorine and chloramine gas respectively, which are severe
respiratory and eye irritants. Generally, the toxicity of bleaches is of lower degree, resulting
in irritation of oropharynx, salivation, vomition and abdominal pain. Bleaching of hairs,
pulmonary irritation- coughing, dyspnoea and retching on inhalation may also be seen.
Nonchlorine bleach products, (sodium perborate, sodium peroxide) are alkaline and severe
gastric irritatants causing renal damage and CNS excitation, depending on the amount
ingested. Treatment: Milk and water orally; washing with soap and rinsing with abundant
water/sterile saline on dermal/ocular exposure. Induction of emesis and orogastric lavage is
contraindicated to avoid the risk of causing further oesophageal irritation. Acidic antidote
medications should not be used as they enhance tissue penetration and injury by forming
hypochlorous acid. Milk of magnesia (2-3ml/kg) can be administered and other clinical signs
are treated symptomatically.
Pine oils and turpentines: Pine oils are mixture of terpene alcohols derived from pine wood
distillation. Turpentine is derived from pine oil, and is used as paint thinner. Pine oil based
compounds may contain small amount of phenol derivatives. Cats are most susceptible to these
agents. Pine oils are directly irritating to pharyngeal , oral and dermal an ocular mucous
membranes resulting in pain and erythema.. Clinical signs: Ocular exposure: blepharospasms,
epiphpora, photosensitivity, conjuctival erythema.. Dermal: Irritation, pain, erythema.
Ingestion: vomition, salivation, ataxia, CNS and respiratory depression, hypotension,
myoglobinuria, renal failure, shock, aspiration pneumoinia.
Treatment involves dilution with milk, egg white or water orally and rinsing with
copious water , activated charcoal and saline cathartics are indicated.. Emetics and gastric
lavage are contraindicated. Symptomatic and supportive therapy for maintenance of renal
perfusion, acid-base and electrolyte balance is followed.
Boric acid: It is the active ingredient in many ant and roach killers. Clinical signs include
vomition (blue-green vomitus), renal damage, CNS excitation and depression. Treatment
involves gastric decontamination with emesis induction, gastroprotectants (activated charcoal is
ineffective) and cathartics. IVfluid therapy and antiemetics are administered.
Deodorants: They are composed of aluminum chloride and aluminum chlorohydrate; which
have moderate toxicity potential. Ingestion can cause oral irritation, necrosis, gastroenteritis
and nephrosis.; which can be treated by orogastric lavage, antiemetics and gastroprotectant
drugs.
Denture cleaners: Sodium perborate being the active ingredient, can cause mucous
membrane irritation and CNS depressant. Treatment includes gastric decontamination along
with emesis induction, cathartic administration, IV fluid therapy, gastroprotectant and
antiemetic drug , if necessary. Activated charcoal is ineffective in ingestion of this toxin.
SOLVENTS AND ALCOHOLS
Acetone: Product sources: nail polish remover, varnishes, glues. Though relatively low in
toxicity , it can be absorbed orally, inhalation or by dermal application. Clinical signs
simulate ethanol intoxication, with higher degree of CNS depression. Ataxia, vomition,
stupor, hyperglycemia, ketonemia, metabolic acidosis, acetone odour in breath and coma if
severe, which needs to be differentiated from acute diabetic coma. Treatment is symptomatic. If
recently ingested (within 2 hours) induction of emesis, with activated charcoal and saline
cathartics; IV fluids containing sodium bicarbonate to manage acidosis is recommended.
Alcohols: The most commonly encountered alcohols include isopropanol, methanol and
alcohol. Sources of alcohols include perfumes,cologne, grooming products (isopropanol),
antifreeze products, automotive wind shield clesnser, consumer products (methanol) and
alcoholic beverages, cosmetics, mouthwashes ,common baker’s and brewer’s yeast (ethanol).
Activated charcoal ineffective in binding to the alcohols; should not to be used in therapy.
Clinical signs noticed are CNS and respiratory depression acidosis, ataxia, hypothermia,
cardiac arrest, coma; which is treated by emesis induction, (if < 2 hrs); IV fluid Ringers
lactate/ saline solution with NaHCO3(1-3mEq/kg). Ethanol reduces severity of methanol
poisoning.
Ethylene glycol: Sources: Automobile radiator antifreeze, heat exchange fluids, photographic
developing solutions. Clinical signs: CNS depression, ataxia, renal failure signs, vomition,
crystalluria, hypothermia. Treatment: Emetics activated charcoal, saline cathartic, diuretics, IV
NaHCO3. Ethanol (5.5ml of 20% ethanol in saline/kg IV)acts as competitive inhibitor of
alcohol dehydrigenase, prevents oxidation of ethylene glycol in to oxalic acid. 4-methyl
pyrazole , which acts as non competitive inhibitor of alcohol dehydrogenase, is given at the
rate of 20mg/kgIV of 5 % solution
Petroleum distillates: The compounds include cyclohexane, alkanes and alkenes. Sources:
gasoline (petrol), kerosene, motor fuels, solvent paints and vehicles for pesticides. Because of
low surface tension, chance of aspiration is most common. Dermal exposure may result in
dermatitis. Oral exposure results in aspiration pneumonia, cough, hyperthermia, cyanosis, CNS
depression and pulmonary oedema. Emetics and oily purgatives are contraindicated, as they
increase the risk of aspiration. Gastric lavage and activated charcoal should be reserved for
ingestion of large amount (2ml/kg) or when other toxicants are present. Oxygen therapy, rest ,
flushing the skin and eyes with water and IV fluids to maintain hydration and electrolyte
balance is recommended. Other solvents (eg: acetone, turpentine) or other hydrocarbons should
not be used for removing the petroleum distillates from skin.
METALS
Most commonly, Lead is the major source of toxicity among the metals, resulting in acute or
chronic toxicity upon ingestion. The sources of lead are paints, batteries, solder, plumbing
supplies, lubricating material, ceramic containers, Pb pipes, toys, inks, dyes, used oil from
vehicles that burn leaded gasoline. The clinical signs noticed are Acute- CNS excitability
signs, convulsions, behavioural changes, ataxia, tremor, blindness. Chronic- gastrointestinal
disturbance signs, vomition, pica,diarrhoea,abdominal pain. Treatment is by administering Ca
disodium EDTA, 25mg/kg, q.i.d, SC diluted in 10% dextrose ,Oral D-penicllamine,
110mg/kg/day, 1-2 weeks, Dimercaptosuccinic acid(DMSA), 10mg/kg,t.i.d.
Zinc (zinc oxide) present in food and beverages stored in galvanized containers, diapers,
rubber products, cosmetics, sunscreen lotions,batteries, electrical equipments, textiles, pennies
and transportation crates may result in clinical signs like CNS depression, vomition, diarrhoea,
icterus, anemia, pica. Emesis induction, Chelation therapy with Ca disodium
EDTA(110mg/kg/day,SC in 4 divided doses) or D-Penicillamine (110mg/kgPO) and
supportive therapy is followed..
BATTERIES
Automotive or dry cell batteries contain sulfuric acid, that can be irritating on contact with
eyes, skin and gastrointestinal tract., which is treated accordingly as with acid exposure.The
sources of small disc/button batteries include batteries used in calculators, cameras, hearing
aids, watches , the content being mainly mercuric oxide. The dry cell batteries , commonly
used in toy flash lights, may contain the alkaline ( NaOH, KOH; alkaline batteries) or acidic
compounds (ammonium chloride, manganese dioxide, heavy metals- Li, Ni, Zn, Ag, Cd) in
them.
On ingestion, most of the intact batteries pass through digestive tract within 24 to 36
hours without producing any major adverse effects, except for mechanical obstruction
occasionally. Gastrointestinal distress may occur resulting from retention and obstruction,
which has to be diagnosed by radiography and has to be corrected by endoscopy and surgery .
If battery is chewed and split apart, it may cause corrosive damage depending on the chemical
content in it. Timely surgical intervention together with the administration of saline
cathartics, enemas and appropriate chelation therapy with specific chelating agents if any (eg:
DMSA or D-Penicillamine as for Pb), can minimize the corrosive damage caused.
CYANOACRYLATE ADHESIVES ( SUPERGLUE)
Uncured cyanoacrylate adhesives form an almost instantaneous bond on contact with
hair/skin resulting in annoyance and frustration of the animal. Cured ones are nontoxic upon
ingestion
 Treatment: Dermal : Exposed areas are soaked with warm soapy water as quickly as
possible. and with acetone for several minutes, if area is away from face or eye. The hairs may
be clipped to reduce the tension on skin. The surfaces should not be pulled apart, with direct
opposing actions.Ocular : Eyelid/eyeball is thoroughly washed with warm water and Elizabeth
collar is applied to prevent self trauma. The animal will be able to open eyes on its own with no
residual tissue damage within 2-3 days and hence forceful manipulation should not be done.

MATCHES, FIREWORKS AND MOTHBALLS

Matches contain 40-60% potassium chlorate in match heads, are generally non toxic . It
is an oxidizing agent and can cause methhaemoglobinemia.The signs are manifested with
ingestion of about 20matches. Mothballs contain naphthalene and paradichlorobenzene, which
have high toxic potential. The toxicity results in vomition, CNS stimulation, seizures,
methhaemoglobinemia and hepatic toxicity. Emesis should not be induced. Diazepam, IV
fluids, N-acetyl cysteine and liver protectants are the agents employed in the line of therapy.
Fireworks are relatively harmless if swallowed. Fireworks contain
oxidizing agents (nitrates and chlorates: potassium nitrate, potassium chloride,sodium nitrite,
potassium perchlorate, sulfur, various hydrocarbons) and metals(mercury, copper, strontium,
barium, phosporous); which cause haemorrhagic gastroenteritis and methhemoglobinemia
upon ingestion.. Emesis induction, activated charcoal, saline cathartic and treatment of
methHbnemia (1% methylene blue) is recommended.

OVER THE COUNTER DRUGS AND MEDICATIONS

Importrant drug toxicoses encountered in pets include cough and cold medicaments, vitamins
and mineral supplements, methyxanthines, antidepressants, bronchodilators, antiasthma
medications, NSAIDS, pesticides and herbal medicinal products
Cough and cold medications: These agents mainly contain antihistaminics, decongestants,
antitussives, expectorants and analgesic. Toxicity signs are mainly related to the sedative
effects of antihistaminics, in addition to dry mucous membrane, ataxia, salivation and vomition,
which are treated symptomatically.. Dogs, more commonly being exposed than cats, to
decongestant pseudoephedrine, show signs of sympathetic overstimulation like hyperactivity,
vomition, mydriasis, tachycardia, hyperthermia, disorientation and seizures.Treatment involves
induction of emesis within one hour of ingestion. Tachycardia is controlled with beta blocker
propranolol, 0.02-0.06mg/kg, slow IV and the reflex bradycardia controlled by atropine
sulphate, 0.02-0.04mg/kg.IV; anticonvulsant, diazepam is given at a total dose of 2.5-10mg,
IV.
Methylxanthines: The common sources are coffee, tea, chocolates, cola/soft drinks,
analgesic, asthma and cold medications. Dogs are most commonly poisoned by ingestion of
coffee beans, chocolate and tablets. Caffeine, theophyllline and theobromine are the primary
toxic agents. Clinical signs are seen within 1-4 hours of ingestion, manifested by vomition,
diarrhoea, polyuria, weakness, hyperexcitability, tremors, seizures, coma and death resulting
from cardiac tachyarrhythmias.
If ingestion is less than 2 hours, emetics administration followed by, activated
charcoal and saline cathartic is indicated. Since methylxanthines undergo enterohepatic
recycling, charcoal should be administered every 3-6 hours until symptoms disappear.
Antiarrythmics (lidocaine, without epinephrine; 1-2mg/kg,IV- loading dose; 40-60mg/kg/min
infusion rate, slow IV- as maintenance dose) or beta blocker (metoprolol; 0.1-
0.3mg/kg,PO,tid) to control arrhythmia ; Diazepam or Phenobarbital to control seizures and
fluid therapy to maintain hydration and electrolyte balance is recommended. Corticosteroids
and erythromycin should be avoided as they decrease urinary excretion of methylxanthines.
Antianxiety,Antideppressants and other psychotic drugs: Amitryptilline, nortryptilline,
protriptylline, imipramine, clomopramine, trimipramine and desipramine are commonly
prescribed human psychotherapeutic tricyclic antidepressant (TCA) medications. Toxicity
results in pronounced parasympathetic, anticholinergic and antihistaminic effects. The signs
include hyper excitability, vomition, ataxia, tremors, seizures and pulmonary oedema.
Magnesium sulphate should not be used as it may lead to magnesium toxicity; sodium sulphate
is the suitable agent . Activated charcoal should be administered at three hourly
intervals until asymptomatic. Symptomatic therapy is given to the animal with anticonvulsants,
antiarrythmics and sodium bicarbonate; 2-3mEq/kg, IV; to control acidosis.
Bronchodilators: Commonly prescribed β2 agonists like albuterol, salbutamol, salmetrol,
metaproterenol, in the form of tablets, antiasthma.inhalers, nebulisers powder sprays are the
main source. In addition to being, β2 agonistic, they also activate β1 receptor in heart and CNS.
The clinical signs are anxiety, vomition, tachycardia, ventricualr arrhythmia, muscle weakness,
twitching, anxiety and hypokalemia. Emetics and adsorbents within 2 hours of exposure,
diazepam or acepromazine to control muscle twitching; IV fluids; potassium supplementation
and specific β1 blocker propranolo(0.1-1mg/kg,tid,IV) is recommended
NSAIDS : Aspirin, ibuprofen and paracetamol are the most common OTC analgesic and
antipyretic drugs, with cats being extremely sensitive to their toxicity. Since NSAIDS are
weak acids, alkalinisation of urine with sodium bicarbonate encourages their excretion. Blood
may be given in conjuction with fluid therapy. Soft and highly palatable food should be offered
to the reluctant animal.
Aspirin : Clinical signs of aspirin toxicoses in cats are dose-dependant and may include CNS
depression, anorexia, vomiting, gastric hemorrhage, haematemesis , toxic hepatitis, anemia,
bone marrow hypoplasia, hyerpnea and hyperpyrexia, hyperthermia, hyperglycemia, and
glycosuria. Early in the syndrome, respiratory alkalosis may develop secondarily to the
salicylate-induced metabolic acidosis. This would cause hyperventilation, which inturn,
stimulates renal secretion of bicarbonate. Thrombocytopenia, anemia, and Heinz bodies are
evident in cats with chronic exposure. Incordination, loss of balance and falling,
hypersensitivity and loss of appetite are also some clinical signs.
Treatment is by GI decontamination with emetics, activated charcoal and cathartics, within 4
hours of ingestion. Acid-base imbalance is corrected with a slow infusion of sodium
bicarbonate, carefully monitored and adjusted to avoid pulmonary edema being developed..
The resulting hyperthermia should be controlled by external cooling; the use of antipyretic
drugs should be avoided. If this is still not enough, or as in a severe acute case of poisoning,
peritoneal dialysis with an osmotic alkaline fluid may be needed. Treatment for the
gastrointestinal mucosa include histamine receptor antagonists like ranitidine, synthetic PG
analogs like misoprostol to control the inflammation and mucosal damage..
Paracetamol: Toxicity Signs: Dirty brown colored gums, dyspnoea, haematuria, jaundice
,facial and paw edema , cyanosis, hypothermia, and vomiting. Less common signs include
coma, generalized weakness, and death. Normally, methemoglobin is reduced to hemoglobin
by glutathione, but in the presences of a toxic amount of acetaminophen, glutathione synthesis
is reduced, and insufficient free glutathione is available to reduce methemoglobin and bind the
reactive metabolite, consequently, the tissues are starved for oxygen due to
methaemoglobinaemia
Treatment: If ingestion is less than 2 hours, emetics, activated charcoal and saline or osmotic
cathartic. Are admionistered. If severe cyanosis is present, oxygen therapy should
administered, and the animal should be subject to as little stress as possible.IV administration
of acetylcysteine, 140mg/kg/hr for 7 hours; Acetylcysteine is a precursor of glutathione,
thereby facilitating the detoxification of the reactive intermediate. Ascorbic acid, 30 mg/kg
orally to reduce methemoglobinemia to Hb. Supportive care including fluid therapy for
possible metabolic acidosis is also recommended.
Other drugs used for NSAID toxicosis include H2 antagonists like ranitidine(2mg/kg, tid,
IV,Po), cimetidine; proton pump iinhibitors like omeprazole(0.7mg/kg,sid,PO); antiemetics like
metoclopramide(0.2-0.4mg/kg, tid,PO,IM); ulcer healing agent like sucralfate (0.5-1g,
bid,PO)and PGE analog misoprostol(2-5µg/kg,tid,PO).
Oral contraceptives: They contain steroids which are modifications oestrogen and
progesterone molecules. Oestrogens can be toxic to the bonemarrow and cause irreversible
aplastic anaemia, leucopenia and thrombocytopenia. Treatment involves decontamination and
symptomatic therapy.
Xylitol: is a sweetener used in sugar free products, chewing gum being the most common
source. It induces hypoglycemia by stimulating insulin secretion, resulting in weakness, ataxia,
seizures and collapse. It is treated by inducing emesis, administering activated charcoal, 50%
dextrose , IV and liver tonics.
Benzoyl peroxide: is the active ingredient in many OTC acne prerparations. Exposure results
in hydrogen peroxide production, gastroenteritis, gastric dilatation, dermal irritation and
blistering. Gastroprotectants and antiemetics are indicated and emesis should not be induced.
Ingestion of the following products is unlikely to result in toxicities, though large quqantities
may cause mechanical obstruction of gastrointestinal tract. Examples: cured cyanoacrylate
glues, silica gel packets, lipsticks, ball point pen, chalk, indelible markersd, newspapers, water
colours, pencil lead(graphite), petroleum jelly, calamine lotion, ink etc.
Vitamin and mineral preparations
In general,ingestion of multivitamin preparations rarely result in toxicosis. Vitamin A, vitamin
D and iron are of toxicological significance with accidental exposure or overdosage.
Multivitamin medications are the main sources of vitamin D and vitamin A. Gestational
supplements, multivitamins and lawn fertilizers are the source s of Iron and iron salts.
Ingestion can result in severe depression, vomition, haematemesis, diarrhoea, bloody stools,
abdominal pain, tremors, shock and death due to myocardial and hepatic toxicity.
Treatment includes cardiovascular support in the form of IV fluid , antiarrythmic drug; emesis
induction, Gastric lavage ( activated charcoal - ineffective) Gastric protectants( sucralfate)and
chelation therapy with Deferoxamine, 15mg/kg/hour,IV infusion.

RODENTICIDES

Anticoagulants:Warfarin, coumateryl,bromadiolone, diphenadione and brodifacoum are class

of rodenticides interfering with vitamin K epoxide reductase, which is responsible for
converting "inactive" vitamin K to its "active" state. Dogs and Cats, though not poisoned
directly, may eat rats or mice slowed down by their last meal of the bait. Clinical signs: The
clinical signs appear one to four days after ingestion. Depression, weakness, staggering, pallor,
dyspnea, coughing, and subcutaneous hematomas are seen. Hematemesis, epistaxis, melena,
ataxia, paresis, seizures, and sudden death have also been observed.

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 K1 , 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.

Cholecalciferol (Vitamin D3 ): is another rodenticide which can increase absorption of

calcium and phosphorus from the intestinal tract, increase osteoclastic reabsorption of bone,
and increase renal distal tubular reabsorption of calcium, all resulting in persistent
hypercalcemia and hyperphosphatemeia. Clinical Signs: appear within 12- 36 hours after
ingestion. Initially anorexia, depression, vomiting, muscle weakness, and constipation are seen,
with hypertension, polyuria, and polydipsia being exhibited later.. Mineralization of cardiac
and renal tissues eventually leads to cardiac or renal failure.
Treatment: Emetics, activated charcoal and cathartics are indicated.. Furosemide (2-
6mg/kgSC,IV,IM every 8-12 hours) is given to assist in renal calcium excretion, prednisolone
(2-6mg/kg, IM ,PO every 12 hours)aids in decreasing both osteoclastic activity and
gastrointestinal calcium absorption. Calcitonin (4-6IU, IM or SC) is injected every two to three
hour to help lower plasma calcium levels, and aluminum or magnesium hydroxide (5-
10ml/kgPO, every 4-6 hours) will help lower plasma phosphorus levels by preventing
gastrointestinal absorption. Long term treatment may include a low calcium diet until calcium
and phosphorus levels have stabilized.

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.

LIQUID FIRE EXTINGUISHERS

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.

ONIONS, GARLIC AND CHIVES

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

The ingestion of mushrooms commonly causes activation of autonomic nervous system,

resulting in tremors, agitation, restlessness, vomition,salivation, lacrimation, urination,
defecation and seizures., including hepatic toxicity in some cases. Inducing emesis, within 2
hours; administering activated charcoal, fluid therapy, skeletal muscle relaxants,
anticonvulsants and hepatoprotective agents has been recommended as line of therapy.
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