Toxicoses caused by household products (Proceedings)


Household products are generally made from complex chemical mixtures.

Household products are generally made from complex chemical mixtures. Because of this, it is important that the client is instructed to bring the source (original container) of the suspect ingested chemical. As the chemical components vary, the therapy of the animals before clinical signs develop may vary from the therapy after clinical signs develop.

Soaps, detergents and cleaning agents.

Soaps are generally low in toxicity when ingested but home made soaps and laundry soaps may be very caustic because of the alkalinity and cause corrosive damage. Commercial soaps may cause vomiting and diarrhea because of GI irritation. Non-ionic products such as hand dishwashing detergents and some shampoos have a low order of toxicity, depending upon the route of exposure. 

Anionic detergents such many laundry detergents and dishwasher detergents, are slightly to moderately toxic because of their alkalinity. Cationic detergents such as fabric softeners, germicidal agents and sanitizers should be considered high to extremely toxic. The severity and location of the damage depend on the type and amount of chemical ingested. The corrosive agent may damage only the mucosa or submucosa or it may injure all esophageal layers.

Tissue damage occurs in three phases: an acute phase, marked by edema and inflammation; a latent phase, characterized by ulceration, exudation, and tissue sloughing; and a chronic phase of diffuse scarring. Endoscopy may be used to determine the extent of the injury in patients with a history of chemical ingestion and an oropharynx that appears abnormal. However, endoscopy use is controversial because of the risk of perforating the damaged esophagus.

Treatment of these ingested toxicants is directed towards diluting the ingesta with milk or water. The use of neutralizing substances are controversial as the neutralization involves an exothermic reaction resulting in heat which may be detrimental to the patient. Gastric lavage is contraindicated and activated charcoal is an inefficient binding agent. Depending upon the severity of injury to the pharynx, a tracheotomy may be required. IV fluid therapy is required in most cases. Some animals will require a esophagostomy tube for alimentation. The use of corticosteroids is controversial in that in some human studies in treating patients with caustic oral- esophageal burns, the corticosteroids were ineffective. The theory behind their use is corticosteroids reduce stricture formation by fibrous connective tissue.


Disinfectants include phenolics, pine oil and turpentine, and bleaches. Chemically, phenol is a colorless or whitish crystalline compound with a characteristic odor. It is moderately soluble in water and benzene, and is very soluble in alcohol, chloroform and oils. Phenol has a melting point of 40 C when pure, considerably higher when contaminated. It is an acid with a pKa of 9.9. It should be stored in closed containers and protected from light to prevent oxidation. Phenol and phenolic products should be handled with gloves. All animals are susceptible to phenol toxicity, including humans. The cat has a higher incidence of phenol toxicity, probably due grooming habits, and especially due to a deficiency of the enzyme, glucuronyl transferase

Phenol is a general protoplasmic poison and causes necrosis of skin and mucous membranes without forming a limiting membrane and is considered a corrosive agent. Phenol is considered a systemic toxicant as it first stimulates and then depresses the CNS. GI demulcents (milk or eggs) should be given at home by the owner prior to transporting their pet. For dermal exposures, glycerol followed by washing with a mild liquid dish detergent and a thorough rinsing with water is best. For ocular exposures, the eyes much be flushed with isothermic isotonic saline. Aggressive supportive care is necessary.

Pine oils and turpentine are fairly toxic substances and are readily absorbed from the GI tract. Pine oils are very irritating to mucous membranes and ocular exposure causes marked irritation of the structures of the eye. Ingestion results in nausea, hypersalivation, bloody vomiting and abdominal pain. Systemic effects seen include CNS depression and weakness, ataxia, hypotension and respiratory depression.

Aspiration pneumonia may occur during ingestion or emesis, but it may also occur from absorption and deposition of the pine oil in the lungs. Lesions seen include pulmonary edema, centrilobular hepatic necrosis and renal cortical necrosis. Treatment should directed towards prompt dilution by milk, egg white or water followed th GI decontamination. Gastric lavage should not be done. Supportive treatment with fluids to maintain renal function and prevent hypotension and appropriate pain medication. Dermally exposed animals should be bathed.


Bleaches contain 3% to 6% sodium hypochlorite. Sodium hypochlorite is a strong oxidizer and when it reaches the acidic stomach, hypochlorous acid is produced and causing coagulation of the local protein in the gastric mucosa. The clinical signs of bleach ingestion include: irritation of the oropharynx, salivation, vomiting and abdominal pain. These animals may smell of “bleach.” Treatment should consist of demulcents (milk and egg white) or water. The bleach should not be neutralized. Treatment as for other caustics should be implemented.

Ethylene glycol

Ethylene glycol in antifreeze and Propylene glycol (PG) (1,2- propanediol)(Sierra®)(“The Safer Antifreeze”) intoxications often occur in pets. The clinical signs may be biphasic. Two - 4 hours following ingestion of EG there may be a transient exhilaration followed by marked CNS depression marked by ataxia, abnormal placing and righting reflexes within 4-7 hours Nausea, vomiting, anorexia, polydipsia and polyuria resulting in dehydration are often seen up to the time of development of coma. Animals often survive the initial intoxication and may return to near normal within 12 hours. There is generally a recurrence of the more severe signs within 24 hours.

A terminal metabolic acidosis (pH = 7.3 or less) occurs with congestion of mucous membranes. Heart and respiratory rates are often increased, but the terminal events include bradycardia with ectopic activity. Animals surviving longer than 24 - 36 hours will develop signs of uremia with oliguria or complete anuria indicating complete renal failure. There is usually a progressive increase in BUN as well as hyperkalemia and acidosis. Urine sediment may contain small birefringent crystals, best observed under polarized light.

Treatment of EG intoxicated animals is most successful if initiated within 24 hours of ingestion.  Therapy consists of: GI decontamination, administration of fomepizole (20 mg/kg followed by 15mg/kg at 12 and 24 hours following the initial administration); and correction of acid/base and fluid imbalances. Ethanol can be used but it causes CNS depression. Peritoneal dialysis if undertaken will require 28 - 30 days of continual therapy.

Solvents and alcohols

Acetone is a highly flammable common solvent in nail polish removers, varnishes, glues and rubber cement. It can be absorbed through the skin or inhaled but the most common route of exposure is ingestion. The clinical signs following exposure resemble ethanol ingestion but acetone is more of a CNS depressant. Other signs include ataxia, vomiting, stupor and coma. Hyperglycemia and ketonemia with acidosis are often present. Treatment is largely symptomatic along with appropriate alkalinizing solutions. The half-life of acetone in the dog is long and it may take 2-3 days before improvement is seen.

Isopropyl alcohol is commonly used in the household as a skin disinfectant. It is also used in cosmetics and other grooming agents. The clinical signs are similar to ethanol, but isopropyl alcohol is biotransformed by alcohol dehydrogenase to acetone which also has a long half-life. Other signs include ataxia, vomiting, stupor and coma. Hyperglycemia and ketonemia with acidosis are often present. Treatment is largely symptomatic along with appropriate alkalinizing solutions.

Methanol or wood alcohol, similar to acetone, isopropyl alcohol, is a CNS depressant and produces similar clinical signs. Methanol, like ethanol is biotransformed by alcohol dehydrogenase but major product is formaldehyde which further goes to formic acid. in humans. This has not been seen as problematical in dogs and the treatment is as for ethylene glycol.


Miscellaneous hazards


Chocolate contains methyl xanthines similar to those found in coffee and tea. TheobromineTheobromine  is found chocolate, cocoa beans, cocoa bean hulls, colas, and tea. Milk chocolate contains 44 mg/oz and unsweetened baking chocolate contains 390 mg/oz. CaffeineCaffeine  is found coffee, tea, chocolate, colas, and human stimulants such as NoDoz®. Theophylline is found in  tea, and human and veterinary preparations as a bronchodilator). The  LD50 of theobromine in  dogs  is 250 - 500 mg/kg (0.67 - 1.33 oz of baking chocolate/kg body weight), but deaths have been reported after ingesting115 mg/kg.

The LD50 of caffeine in dogs is 140 mg/kg. Both are rapidly absorbed from GI tract, and excreted in urine. Somebiotransformation occurs in liver. Xanthines may be reabsorbed from urinary bladder. While caffine is more toxic than theobromine, caffeine is excreted 4 times more rapidly which makes it less of a problem. The primary effect of xanthines is thenhibition of cellular phosphodiesterase causing an increase in cyclic AMP.

The clinical Signs seen in caffeine intoxication include: vomiting, diuresis, restlessness and hyperactivity; Tachycardia and tachypnea may be present along with ataxia, cyanosis, cardiac arrhythmias, and seizures. Death is not common, although may occur due to cardiovascular  collapse. The inital clinical signs in theobromineTheobromine  (chocolate) in dogs are: vomiting, diarrhea, diuresis (sometimes reported as urinary incontinence), hyperactivity, and sometimes depression.

Cardiac arrhythmias may develop along with hyperthermia, ataxia, muscle tremors, seizures and coma sometimes terminating in death. Additionally Abdominal pain, hematuria, muscle weakness, bradycardia, and dehydration are sometimes present. Post mortem lesions are nonspecific and may consist of gastroenteritis and congestion of organs. Chronic theobromine ingestion may cause fibrotic cardiomyopathy.

The diagnosis of intoxications is made by the history and identification of xanthines in serum, plasma, tissue, urine, or stomach contents. Very small amounts remain in feces. There are no specific antidotes for methylxanthine intoxications. General treatment along with supportive care for shock is indicated. The marked muscle tremors or seizures may be treated with diazepam IV. The electrical activity of the heart should be monitored and treated accordingly. Catheterization of urinary bladder is necessary to prevent reabsorption.


Xylitol occurs in small amounts as a natural intermediary during the conversion of L-xylulose to D-xylulose.  It also occurs in low concentrations in fruits and vegetables. Xylitol has been advocated for use by diabetics and low-carbohydrate dieters. It is anti-carcinogenic. Xylitol is most commonly found in baked goods, desserts, toothpaste, other oral care products, and sugar-free gums and candies. It can be purchased as granulated powder for cooking and baking. It is rapidly absorbed from stomach and is distributed throughout the body. Some formulations are slow release so absorption takes place over several hours.

Xylitol stimulates the pancreas to release insulin causing a rapidly occurring hypoglycemia. The clinical signs often develop within 30-60 minutes following ingestion and include: weakness, ataxia, collapse, and seizures. Some animals may develop acute hepatic necrosis during therapy, and the cause is unknown. These animals may develop a hemorrhagic syndrome with other signs of hepatic failure. There may be may be no gross lesions, but dogs with hepatic failure may have widespread petechial or ecchymotic hemorrhages on serosal surfaces or gastrointestinal tract hemorrhages.

The diagnosis is made from a history of ingestion, identification of fragments of chewing gum or other sources of xylitol, or most commonly by a profound hypoglycemia. The treatment of these patients, if early, includes inducing emesis and administration of activated charcoal. The oral feeding of small amounts of sugar or sugar-containing meals may be done if the hypoglycemia is present but  no clinical signs are evident. Once the clinical signs are evident, 50% dextrose should be given rapidly, IV, with continuous dextrose infusion until patients blood glucose returns to normal and is spontaneously maintained. The response from clinical effects is usually rapid and within 12-24 hours.

Homemade play dough

Homemade play dough may contain high concentrations of sodium chloride. Clinical signs associated with ingestion of this dough may include: vomiting, polydipsia, polyuria, tremors, hyperthermia and seizures. Treatment should consist of normal GI decontamination procedures and monitoring the blood sodium levels. Correcting the hypernatremia normally takes 48 to 72 hours as the sodium levels should not be reduced more rapidly than 0.5 to 1 mEq/L/hour. This can be done by the administration of isotonic fluids.


Paintballs contain many ingredients such as polyethylene glycol, glycerin, sorbitol, and mineral oil. Ingestions will cause vomiting, diarrhea, ataxia and tremors. Also tachycardia, hyperactivity, blindness and seizures have been reported. Paintballs induce hypernatremia, hypercloremia, acidosis and hypokalemia. The patients should receive GI decontamination and isotonic fluids for correcting the acidosis and hypokalemia. The clinical signs often resolve within 24 hours of instituting the supportive measures.


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