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Common household hazards (Proceedings)


Baits may come in the form of gels injected with a preloaded syringe or incorporated into a plastic housing. The bait may be mixed with food stuffs such as peanut butter, jelly, and bread crumbs to attract the insects. Most of the insecticides used in these products are of low mammalian toxicity; exposure to these insecticides cause little more than gagging or vomiting.

Ant and roach baits

Baits may come in the form of gels injected with a preloaded syringe or incorporated into a plastic housing. The bait may be mixed with food stuffs such as peanut butter, jelly, and bread crumbs to attract the insects. Most of the insecticides used in these products are of low mammalian toxicity; exposure to these insecticides cause little more than gagging or vomiting. The exceptions are avermectin/abamectin in ivermectin-sensitive dog breeds and arsenic. In addition, ingestion of the plastic or metal housing may present a foreign body hazard.

Birth control pills

Contraceptive pills generally come in 28 tablet packs with 21 hormone tablets (estrogen and/or progesterone) and 7 placebo tablets. Most hormone pills contain 0.035 mg of estrogen or less. In general, estrogen doses of less than 1 mg/kg are not of concern. At higher doses, bone marrow suppression may be seen. However, due to the low estrogen content of the pills, estrogen exposure is generally not sufficient to require treatment. Some placebos may contain an iron supplement; elemental iron doses of >20 mg/kg may require decontamination and other treatments.

Silica gel packets

Desiccant packs are included as moisture absorbents. They are found in shoeboxes, new sweaters, electronics, lamps, medications and food. Most ingestions will not cause clinical signs, although a mild gastrointestinal upset may occur. If a large amount is ingested, a potential for a foreign body or osmotic diarrhea exists. Ingestion of the intact packet may cause a gastrointestinal obstruction.

Glow-in-the-dark sticks and jewelry

Glow-in-the-dark items, including glo-sticks and glo-jewelry, are novelty items sold at fairs, carnivals, novelty stores. The primary luminescent agent in is dibutyl phthalate (n-butyl phthalate), an intensely bitter plasticizer of low toxicity (LD50 >8000 mg/kg in rats). Signs generally occur within seconds of the pet biting into the item. Cats may display profuse salivation and foaming, with occasional retching and/or vomiting. Cats may show dramatic behavioral effects such as hyperactivity, aggression, head shaking, hiding, and agitation. Rarely, transient panting, dyspnea, tremors and urinary incontinence have been seen in cats. In contrast, dogs may show no reaction or may have mild salivation or retching, with behavioral effects being rarely reported. In all cases, signs are generally self-limiting and should resolve once the pet gets the taste of the product out of their mouth. The exposure is managed by diluting the taste of the dibutyl phthalate using milk or highly palatable food (e.g. canned tuna). Any chemical that has gotten on skin or fur should be bathed or wiped off to prevent re-exposure when the animal grooms themselves; taking the pet into a darkened room will aid in identifying the luminescent chemical on the skin or coat. For ocular exposure, copious flushing of the eyes is recommended.

Non-ionic and anionic detergents

Non-ionic and anionic detergents are found in a wide variety of household products, including body and hand soaps, shampoos, dishwashing detergents, various household cleaners, etc. These products are gastrointestinal and ocular irritants with few to no systemic effects under most circumstances. Clinical signs consist of hypersalivation, vomiting, and diarrhea, and are generally mild and self limiting, although ingestion of large quantities may result in more severe vomiting (± blood) requiring veterinary intervention. Bar soaps swallowed whole take a while to dissolve in the GI tract, so signs may persist for a few days. In cats, respiratory compromise may occur if they groom undiluted detergents off of their coats; this most commonly occurs when they walk through or have shampoos or liquid dish soaps spilled onto their coats and then groom the areas. Cats may present mildly to moderately dyspneic with moist lung sounds. In more severe cases, radiographic indications of mild pulmonary edema may be seen. Most recover quickly with symptomatic care, although cats with previously-existing respiratory disease may have more pronounced signs and require more extensive treatment. This syndrome has also been seen with the use of 'natural' sodium laurel sulfate flea drops in cats.



Products containing acids include cleaning agents, anti-rust compounds, etching compounds, automotive batteries, and pool sanitizers. The relative toxicity of an acid, as well as other corrosives, is related to its concentration and decreases with dilution. Acids produce localized coagulation necrosis of tissue and generally produce immediate pain upon exposure, which helps to limit ingestion. In most cases, clinical signs occur almost immediately upon exposure. Oral exposure results in oral pain, vocalization, dysphagia, vomiting (± blood), abdominal pain, and irritation or ulceration of oral and/or esophageal mucosa. Lesions often appear milky white to gray initially, then gradually turn black. Esophageal and gastric ulceration are uncommon, but possible with large exposures. Dermal exposure results in dermal irritation or ulceration, accompanied by intense local pain. Inhalation of acid fumes may result in dyspnea, pulmonary edema, tracheobronchitis or pneumonitis. Ocular exposure may result in corneal erosion or ulceration.


Common sources of alkaline products include drain openers, automatic dishwasher detergents, alkaline batteries, toilet bowl cleaners, swimming pool products, and radiator cleaning agents. Agents with pH greater than 11 should be considered to be capable of causing significant corrosive injury. Alkaline agents penetrate local tissue rapidly and deeply, causing liquefactive necrosis. Unlike acidic products, very little pain may be felt upon initial contact with an alkaline product. Therefore, an animal may continue to ingest the alkaline agent and cause more extensive gastrointestinal injury. Clinical signs may not develop immediately, and it may require up to 12 hours for the full extent of tissue damage to become apparent. Acute signs include depression, hypersalivation, anorexia, oral inflammation or ulceration, smacking of lips, tongue flicking, dysphagia, vomiting (± blood), abdominal pain, and melena, hyperthermia (>104 F), esophageal and/or pharyngeal ulceration. Inhalation may result in coughing, dyspnea, and moist lung sounds. Sequelae can include esophageal perforations or strictures and pleuritis or peritonitis from leakage of ingesta through perforated mucosa. The absence of oral burns does not preclude the development of esophageal burns. Endoscopy may used to evaluate esophageal injury, although delaying endoscopy for 12 hours will allow the full extent of the burns to develop.

     Cationic detergents

Cationic detergents are contained in fabric softeners, some potpourri oils, hair mousse, algaecides, germicides and sanitizers. Cationic detergents are more toxic than non-ionic/anionic detergents and can cause extensive systemic and local effects at levels as low as 2% or less. Local tissue injury caused by cationic detergents resembles that seen with exposure to alkaline products. In addition, cationic detergents can cause systemic toxicity including CNS depression, coma, seizures, hypotension, muscular weakness and fasciculations, collapse, pulmonary edema, and metabolic acidosis; the mechanism of these signs is not known.

     Treatment of corrosives

Treatment of corrosive exposure is similar regardless of the type. Attempting to chemically neutralize an acid or alkali agent with a weak alkali or acid, respectively, is contraindicated, as this may stimulate an exothermic reaction that will exacerbate tissue injury. Treatment of oral exposure includes immediate dilution with water or milk. Gastric lavage and induction of emesis are contraindicated due to the risk of increasing corrosive injury. Activated charcoal is ineffective for caustic agents and should not be used. Feeding soft food for a few days post exposure may prevent worsening of the irritation. Treatment of oral lesions should include antibiotics to prevent infection; pain management (opioids), sucralfate slurries to treat oral, esophageal or gastric ulcers; intravenous fluids to maintain hydration; and provision for nutritional support (e.g. gastrostomy tube). The use of corticosteroids to decrease inflammation and esophageal stricture formation is controversial, as steroids will delay wound healing and may increase susceptibility to infection. Dermal exposures should be treated with copious flushing with clear water for 15 minutes. For ocular exposures, eyes should be flushed with room temperature water or sterile saline solution for 15 minutes, followed by fluorescein staining. Animals with significant respiratory signs (coughing, dyspnea, etc.) should be monitored for a minimum of 24 hours for the development of pulmonary edema. Supplemental oxygen or other respiratory supportive care should be used as needed.


There are three main alcohols of concern: Ethanol found in beverages, some liquid medications, and bread dough; methanol found in windshield cleaner "antifreeze"; and isopropanol found in rubbing alcohol and some alcohol-based flea sprays. All alcohols are rapidly absorbed orally; dermal absorption can also occur. Inhalation, particularly of concentrated fumes in a confined area, can also cause systemic signs. Signs develop rapidly, often within 30-60 minutes, and include vomiting, ataxia, tremors, hypothermia, hypoglycemia, acidosis, aspiration pneumonia, respiratory depression, and coma. Methanol, in humans and other primates, can cause blindness but this is not an issue in dogs and cats. Due to rapid onset of signs, decontamination should be performed only within the first 30 minutes following ingestion. Other treatment is symptomatic and supportive and includes fluid diuresis, thermoregulation, and correction of acidosis and hypoglycemia.


Most alkaline dry cell batteries use potassium hydroxide or sodium hydroxide to generate current, and disc, nickel-cadmium, and silver batteries are generally of the alkaline type. The alkaline gel within a battery causes liquefactive necrosis of tissue, resulting in burns that can penetrate deeply into the local tissue. Lithium disc batteries tend to lodge in the esophagus, increasing the risk of esophageal ulceration. In addition, batteries casings may result in respiratory or gastrointestinal obstruction if inhaled or swallowed. When batteries are chewed and the contents released, alkaline burns result. Signs of foreign body obstruction (vomiting, anorexia, tenesmus, etc.) may occur when casings are swallowed; disc batteries may be inhaled, resulting in acute dyspnea and cyanosis. Treatment of battery exposures is as for exposure to any alkaline product (see Treatment of Corrosives above). Radiography to determine the location of the battery casing should be performed in cases where the casing is missing. The decision to remove a battery present in the stomach depends on the size of the animal, battery size, and evidence of battery puncture.


Mothballs may be composed of either 100% naphthalene or 99% paradichlorobenzene. Naphthalene-based mothballs are more dangerous than paradichlorobenzene. Naphthalene causes Heinz bodies, hemolysis, and, occasionally, methemoglobinemia in dogs with doses of 411 mg/kg or more (one 2.7 g mothball contains 2700 mg of naphthalene). Signs of ingestion of naphthalene mothballs include emesis (early), weakness, icterus, lethargy, icterus, brown-colored mucous membranes, and collapse. Rarely, hepatitis has been reported 3-5 days post-ingestion. Treatment of mothball ingestion includes early emesis, activated charcoal, and cathartic. Treatment for hemolysis or methemoglobinemia (blood replacement therapy, methylene blue, etc.) may be necessary.


Of the existing US coins currently in circulation, only pennies pose a significant toxicity hazard. Pennies minted from 1982 on contain 97.5% zinc and 2.5% copper. Other potential sources of zinc include hardware such as screws, bolts, nuts, etc., all of which may contain varying amounts of zinc. In the stomach, gastric acids leach the zinc from its source, and the ionized zinc is readily absorbed into the circulation, where it causes intravascular hemolysis. The most common clinical signs of penny ingestion are vomiting, depression, anorexia, hemoglobinuria, diarrhea, weakness, collapse and icterus. Secondarily, acute renal failure may develop. Clinical laboratory abnormalities will be suggestive of hemolysis (elevated bilirubin, hemoglobinemia, hemoglobinuria, regenerative anemia) and may also indicate the development of kidney failure. Radiography of the abdomen may reveal the presence of coins or other "hardware" within the stomach. Treatment for recently ingested pennies would include induction of vomiting. Activated charcoal is not indicated, as it is of little benefit in binding metals. Removal of zinc-containing foreign bodies via endoscopy or gastrotomy/enterotomy may be required. The patient should be radiographed following removal to ensure that coins or coin fragments were not missed. Treatment for symptomatic animals should include blood replacement therapy as needed, intravenous fluids, and other supportive care. The use of chelators is generally not required as zinc blood levels should drop rapidly as soon as the source is removed.


Paintballs are used in recreation "war" games. They contain different types and colors of paint inside a gelatin capsule. Ingestion of large numbers of paintballs has been associated with acid/base imbalances, electrolyte disorders (most frequently hypernatremia), neurologic signs (ataxia, seizures), and occasional deaths in dogs. The mechanism of action is thought to be due to osmotic shifts of body water. Ingredients found in paintballs, such as polyethylene glycol, glycerol, and sorbitol are osmotically active agents capable of causing fluid shifts from the vasculature into the bowel lumen with a resultant increase in plasma osmolality and hypernatremia. Management should include emesis, in asymptomatic patients, if large numbers of paintballs are ingested. Activated charcoal is contraindicated as it will pull more fluids into the GI tract. Monitor electrolytes carefully and correct any imbalances. Warm water enemas may help stimulate movement of paintballs through the GI tract and will help correct hypernatremia. In symptomatic animals, monitor electrolytes and acid-base values every 2-4 hours until clinical signs resolve and values normalize. In hypernatremic patients, administer low sodium IV fluids (D5W, 2.5% dextrose + 0.45% NaCl) and repeat enemas until serum sodium levels return to normal. Fluid rates may need to be quite high due to compensate for loss of fluids into the GI tract.


There are a wide variety of chocolate and cocoa products to which pets may be exposed, including candies, cakes, cookies, brownies, and cocoa bean mulches. The active (toxic) agents in chocolate are methylxanthines, specifically theobromine and caffeine. Methylxanthines stimulate the CNS, act on the kidney to stimulate diuresis, and increase the contractility of cardiac and skeletal muscle. The relative amounts of theobromine and caffeine will vary with the form of the chocolate. Milk chocolates contain approximately 64 mg of methylxanthines per oz, semisweet/dark chocolates ~150mg/oz, baker's chocolate ~450 mg/oz and dry cocoa powder ~800 mg/oz. The LD50 for theobromine and caffeine are 100-300 mg/kg, but severe and life threatening clinical signs may be seen at levels far below these doses. Based on APCC experience, mild signs have been seen with methylxanthine levels of 20 mg/kg, cardiotoxic effects have been seen at 40-50 mg/kg, and seizures have occurred at 60 mg/kg. Accordingly, less than 2 ounces of milk chocolate per kg is potentially lethal to dogs. Clinical signs occur within 6-12 hours of ingestion. Initial signs include polydipsia, bloating, vomiting, diarrhea, and restlessness. Signs progress to hyperactivity, polyuria, ataxia, tremors, seizures, tachycardia, PVC's, tachypnea, cyanosis, hypertension, hyperthermia, and coma. Death is generally due to cardiac arrhythmias or respiratory failure. Hypokalemia may occur later in the course of the toxicosis. Because of the high fat content of many chocolate products, pancreatitis is a potential sequela. Management of chocolate ingestion includes decontamination via emesis followed by gastric lavage. Repeated doses of activated charcoal are usually of benefit in symptomatic animals. Intravenous fluids at twice maintenance levels will help maintain diuresis and enhance urinary excretion. Because caffeine can be reabsorbed from the bladder, placement of a urinary catheter is recommended. Cardiac status should be monitored via EKG and arrhythmias treated as needed; propranolol reportedly delays renal excretion of methylxanthines, so metoprolol is the beta-blocker of choice. Seizures may be controlled with diazepam or a barbiturate. In severe cases, clinical signs may persist up to 72 hours.

Moldy food (tremorgenic mycotoxins)

Tremorgenic mycotoxins produced by molds on foods are a relatively common, and possibly under-diagnosed, cause of tremors and seizures in pet animals. These molds, primarily Penicillium spp., grow on practically any food, including dairy products, grains, nuts, and legumes; compost piles may also provide a source of tremorgens. Tremorgens cause the development of muscle tremors and convulsions. Clinical signs include fine muscle tremors that may rapidly progress to more severe tremors and convulsions. Death generally occurs in the first 2 to 4 hours and is usually secondary to respiratory compromise, metabolic acidosis or hyperthermia. Other signs that may be seen include vomiting (common), hyperactivity, depression, coma, behavior alterations, tachycardia, and pulmonary edema. Asymptomatic animals exposed to moldy foods should be decontaminated via emesis or lavage followed by activated charcoal and cathartic. In symptomatic animals, control of severe tremors or seizures has priority over decontamination. Seizures may respond to diazepam, however others have had better success with methocarbamol (Robaxin; 55-220 mg/kg IV to effect), especially in seizuring animals. Barbiturates may be used in animals that are unresponsive to other anticonvulsants. Supportive care should include intravenous fluids, thermoregulation, and correction of electrolyte and acid-base abnormalities. In severe cases, signs may persist for several days, and residual fine muscle tremors may take a week or more to fully resolve. Testing of stomach content, suspect foods, or vomitus for tremorgens is available through the Animal Health Diagnostic Laboratory, Michigan State University (517-355-0281).

Grapes & raisins

The ingestion of raisins or grapes by dogs, cats, or ferrets has been associated with acute renal failure. The minimum toxic dose in dogs for grapes and raisins was 0.11 oz/kg and 0.7 oz/kg, respectively. Grapes have included those purchased from stores, home-grown grapes fresh off of the vine, and grape pressings left over from wine making, while the raisins have included a variety of brands of commercial raisins. To date the toxic principle is unknown. Analysis of grapes or raisins involved in some of these cases has been negative for heavy metals, pesticides, and known mycotoxins. In all cases, dogs have shown vomiting, usually within 6 hours of ingestion; grapes/raisins are often seen in the vomitus. Other signs reported in the first 24-36 hours were diarrhea (± blood), anorexia, lethargy, and abdominal pain. Most dogs have elevated serum creatinine and BUN upon presentation to the veterinarian. Some dogs also have elevations in serum calcium, phosphorus, glucose, liver enzymes, amylase or lipase. Many of the dogs will develop anuric or oliguric renal failure within 36-72 hours of ingestion of grapes or raisins. In one study, 47% of the dogs either died or were euthanized due to poor response to treatment for renal failure. One dog with anuric renal failure recovered following peritoneal dialysis.

Dogs, cats, or ferrets that have ingested grapes or raisins, especially in large quantities, should be managed aggressively. Early decontamination via emesis or lavage followed by activated charcoal is recommended. Fluid diuresis (two times maintenance) for 48 hours should be instituted, and serial serum chemistries should monitored for at least 72 hours post ingestion. Use of diuretics to maintain adequate urine flow is essential in cases of oliguria or anuria. If available, peritoneal dialysis or hemodialysis may be considered in cases of refractory anuria/oliguria. Symptomatic care for vomiting, diarrhea, or other signs may be required. Animals developing severe oliguria or anuria have a poor prognosis.


Xylitol is a sugar alcohol used in sugar-free products such as gums and candies as well as for baking. It doesn't cause significant increases in blood glucose or insulin levels in humans. However, in dogs, xylitol causes a rapid, dose-dependant insulin release followed by potentially significant hypoglycemia. Signs can include vomiting, weakness, ataxia, depression, hypokalemia, seizures, and coma. Some dogs have developed elevated liver enzymes following ingestion of xylitol. Some of these dogs have gone on to develop severely elevated liver enzymes, bilirubinemia, and coagulation abnormalities.

Treatment of xylitol ingestion by dogs should include emesis, provided that emesis can be performed very soon after ingestion—before clinical signs develop. A dog can show signs of hypoglycemia in as few as 30 minutes. Emesis performed after signs develop increase the risk of complications associated with vomiting such as aspiration. The efficacy of activated charcoal towards xylitol has not been determined. Frequent small meals or oral sugar supplementation may be used to manage dogs not showing signs. If clinical signs of hypoglycemia develop, a bolus of IV dextrose followed by dextrose CRI should be used to control moderate to severe hypoglycemia. Hypokalemia, likely secondary to insulin-induced movement of potassium into cells, should be treated if significant. Treatment should continue until blood glucose normalizes which may take 24 hours or longer. The use of liver protectants such as SamE may be helpful. Prognosis is generally good; however if elevated liver enzymes, bilirubinemia, and coagulation abnormalities develop, the prognosis is guarded.

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