SECTION 18 Toxicology
Acetaminophen Toxicosis
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
Acetaminophen is a non-aspirin pain reliever found in more than 200 formulations. The most recognized trade name is Tylenol. Acetaminophen is often found in combination with other drugs, such as antihistamines and decongestants.
Causes and Toxicity
Cats are most sensitive to the effects of acetaminophen, although dogs can also be poisoned. Cats lack an enzyme necessary to detoxify acetaminophen, so it can accumulate quickly. The ability of the blood to carry oxygen is most commonly affected in cats. The blood turns a brown or gray color and is unable to transport oxygen to body tissues. This condition is called methemoglobinemia. Dogs generally require higher doses to be poisoned, and the liver tends to be the most affected organ.
Clinical Signs
Within 2-4 hours after exposure, cats may develop a purplish-brown or gray discoloration to the gums, accompanied by weakness, rapid heart rate, and rapid breathing. In some cases, cats drool, vomit, or develop swelling of the face or paws. The blood may appear brown, gray, or black, and the urine may be discolored. Clinical signs of anemia and decreased urine production from kidney failure are also possible.
In dogs, vomiting and jaundice (yellow discoloration to the whites of the eyes and gums) may occur with liver toxicity. Dogs may also develop a reduction in the ability of the blood to carry oxygen, but at higher doses than those that cause liver failure. Occasionally, dogs develop dry eye (keratoconjunctivitis sicca) from decreased production of tears.
Diagnostic Tests
A tentative diagnosis is based on a history of exposure to acetaminophen, consistent clinical signs, and characteristic discoloration of the blood or urine. Laboratory tests often indicate an anemia in cats and liver damage in dogs. Specialized blood tests to detect methemoglobinemia or to measure acetaminophen levels can be performed by an outside laboratory. Other laboratory tests, x-rays, an abdominal ultrasound, and liver biopsy (in dogs) may be needed to rule out other diseases that cause similar clinical signs.
TREATMENT AND FOLLOW-UP
Treatment Options
Induction of vomiting may be recommended if the exposure was recent (within 1 hour). Vomiting should be induced only under the direction of a veterinarian. Activated charcoal may also be administered by mouth to help bind acetaminophen in the gut and prevent its absorption into the body. In many cases, hospitalization is required for intensive treatment and monitoring. Several medications (such as acetylcysteine, ascorbic acid, or cimetidine) may be administered to counter the effects of the acetaminophen by assisting the body in metabolizing and removing the acetaminophen. Supportive measures are usually needed and may include intravenous fluids, oxygen therapy, whole blood transfusions, and agents to assist the liver.
Follow-up Care
Laboratory tests are used to monitor for methemoglobinemia, anemia, jaundice, and liver and kidney function. Intensive monitoring may be required initially if liver or kidney failure occurs and may be continued for some time as the animal recovers. In dogs, tear production may also be monitored for several days. Keep all products containing acetaminophen out of the reach of pets.
Prognosis
For minor toxicoses, prognosis is good with prompt, aggressive treatment. For cases with prolonged or severe methemoglobinemia, anemia, liver damage, or kidney failure, prognosis is guarded (uncertain). The first 3-4 days following intoxication are critical, and animals that start to improve within that period have a higher chance of recovery.
Amitraz Toxicosis
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
Amitraz is used to control ticks, mites, and lice on dogs. It is available as a dip (Mitaban) and a collar (Preventic) and is an ingredient in a topical preparation (Promeris).
Causes and Toxicity
Clinical signs may develop following labeled use of the topical products on pets or from ingestion of the collars. Amitraz should not be used on cats. In general, toy and small-breed dogs are more susceptible to the adverse effects of amitraz even with appropriate use.
Clinical Signs
Signs usually begin within 2-4 hours but can be delayed as long as 12 hours following exposure. Signs can include vomiting, sedation, disorientation, unsteady gait, decreased gut movement (motility), slow heart rate, coma, and seizures. In severe cases, death may occur. Amitraz may also increase blood glucose levels, so care must be taken when using it on dogs that are diabetic.
Diagnostic Tests
Diagnosis is based on a history of exposure and the presence of consistent clinical signs. Analysis of amitraz may be performed on urine, plasma, skin, blood, or stomach contents. Such analyses cannot be performed at the veterinary hospital or clinic but require the use of an outside laboratory. Laboratory and other tests may be recommended to rule out other conditions that cause similar clinical signs.
TREATMENT AND FOLLOW-UP
Treatment Options
For topical exposures following use of a dip or topical formulation, the animal is bathed in a liquid dish detergent. Dogs that have ingested a collar may benefit from induction of vomiting under the guidance of a veterinarian. In some cases, retrieval of collar fragments from the stomach or intestines through endoscopy (use of a flexible viewing scope passed into the stomach through the mouth) or surgery (abdominal incision) may be warranted.
Treatment is symptomatic for the patient exhibiting clinical signs. The veterinarian may use a reversal agent, such as yohimbine or atipamezole, to hasten recovery. Animals exhibiting clinical signs usually require hospitalization for treatment and supportive care, such as intravenous fluids and anticonvulsants. Close monitoring is also required until the animal recovers.
Follow-up Care
Sedation following amitraz dips usually lasts about 24 hours but can persist up to 72 hours. If amitraz poisoning is diagnosed quickly and reversal agents are administered, recovery can occur within 24 hours in many animals. Recovery may be prolonged (several days) if treatment is delayed or ingested material is not removed from the gut. No residual effects are expected following recovery.
Antifreeze Poisoning
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
Antifreeze products can contain ethylene glycol, propylene glycol, methanol, or a combination of these agents. Most automotive antifreeze liquids contain ethylene glycol and pose the greatest hazard to pets; they are often dyed a fluorescent green. Some relatively safe antifreeze products are available that contain propylene glycol, and they are dyed a blue or green color. Propylene glycol is considered a GRAS (generally recognized as safe) substance and is found in many food and pharmaceutical products, such as toothpaste and cosmetics. When ingested in large amounts, however, it can still cause illness. Methanol is present in windshield washer fluids as well as gasoline antifreezes.
Causes and Toxicity
All three compounds (ethylene glycol, propylene glycol, and methanol) are metabolized in the body to acids. Therefore, animals can develop a serious metabolic condition known as acidosis after drinking these fluids. In addition, all of these compounds can depress the brain and cause “drunken” behavior, mental depression, and coma.
Of the three compounds, ethylene glycol is of the most serious concern for pets. It is said to have a “sweet” taste that is attractive to dogs and cats. When it is metabolized by the body, crystals form that are deposited in the kidneys. It is not uncommon for this crystal formation to be so severe that kidney failure and subsequent death occurs.
Clinical Signs
Signs can occur within 1 hour after ingestion. Animals may appear “drunk” and wobbly. Vomiting and increased urination may occur initially. In many instances, mild, early signs are overlooked by animal caretakers, delaying life-saving treatment.
With ethylene glycol ingestion, dogs may appear to recover for a brief period, but cats often remain mentally depressed. Within 4-6 hours, more serious changes can develop, such as acidosis, rapid breathing, serious vomiting, decreased body temperature, heart arrhythmias (irregular heart rhythms), and severe depression or coma. Anywhere from 12-36 hours after ingestion, kidney failure may develop with decreased urine production. The kidney damage is often irreversible and fatal.
Diagnostic Tests
Diagnosis is based on a history of exposure and appropriate clinical signs. Because many ethylene glycol formulations contain a fluorescent dye, muzzles, paws, urine, and vomitus may fluoresce (glow) under ultraviolet (UV) light. Initial laboratory tests may show nonspecific changes or evidence of early metabolic and kidney abnormalities. Test kits are available that measure the concentration of ethylene glycol in the blood. In the absence of a commercial ethylene glycol test kit, a human hospital laboratory may be able to perform this analysis.
Later in the clinical course, laboratory tests may show severe abnormalities in kidney function. An ultrasound and/or biopsy of the kidney may be recommended to search for changes compatible with ethylene glycol poisoning. More tests may be indicated to rule out other diseases and toxins that can cause similar clinical signs.
TREATMENT AND FOLLOW-UP
Treatment Options
Because antifreeze products are rapidly absorbed, vomiting is induced only if no clinical signs are present and should be performed only under the direction of your veterinarian. Activated charcoal does not bind antifreeze well, so it is not usually indicated. Animals that exhibit signs of inebriation or have a positive ethylene glycol test are often hospitalized for monitoring of body temperature, breathing, heart rate and rhythm, and urine production. For propylene glycol and methanol ingestions, supportive care generally results in full recovery with no residual effects.
Because every moment that passes means further metabolism of ethylene glycol, all ethylene glycol exposures are considered to be medical emergencies. Animals are hospitalized for administration of intravenous fluids to protect the kidneys. Medications to prevent further metabolism of ethylene glycol (into products that harm the kidney) may be given, such as ethanol (grain alcohol) or fomepizole (Antizol-Vet). Fomepizole is approved for use only in dogs but has shown some success in cats as well. Intensive supportive treatment is usually needed for several days, especially if acute kidney failure develops. In severe cases, your veterinarian may recommend referral to a specialty facility for dialysis treatment, if it is available.
Follow-up CareAvermectin Toxicosis
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
Avermectins are a group of antiparasite agents (parasiticides) used in the prevention of heartworm (Dirofilaria immitis) disease and in the treatment of infestations by mites such as scabies (sarcoptic mange), demodicosis (Demodex mites), and ear mites (Otodectes mites). Certain members of the avermectins can also be found in ant and roach baits. Some common avermectins are ivermectin (Heartgard, Ivomec, Tri-Heart), selamectin (Revolution), moxidectin (Proheart), milbemycin (Interceptor), and abamectin (Avomec, Raid, Hot Shot MaxAttrax).
Causes and Toxicity
The avermectins exert their effect by mimicking inhibitory neurotransmitters in the central nervous system (brain and spinal cord), which results in depression of brain activity and death of the parasite. Avermectins can have the same effect in animals. Most animals are quite resistant to the effects of these compounds, because they do not accumulate in the brains of animals. However, dogs with a deficiency in P-glycoprotein, an enzyme that helps remove avermectins from the brain, are exquisitely sensitive to these compounds. The avermectins accumulate and exert their inhibitory effect on the brain, and this action is reflected by the clinical signs.
In general, certain herding breeds of dogs are more likely to have the MRD1 genetic mutation that causes a deficiency in P-glycoprotein. Such breeds include the collie, Australian shepherd, Shetland sheepdog, and border collie. Individuals of other breeds, such as the Old English sheepdog, German shepherd dog, long-haired whippet, and a variety of mixed-breed dogs, may also have the MRD1 mutation and exhibit sensitivity to avermectins.
Most cases of avermectin toxicosis have resulted from administration of high doses of the drug (often of the oral livestock product) or from ingestion of horse dewormer paste by farm dogs. In some cases, the avermectin compound was injected subcutaneously as a treatment for mange.
Clinical Signs
Signs can occur within several hours after exposure. Initial signs include lethargy, pupil dilation, and staggered gait. These signs may be followed by apparent blindness (which is often reversible with time), tremors, decreased body temperature, slow heart rate, coma, and death. Seizures may also occur. Signs may persist for days or even weeks in severe cases.
Diagnostic Tests
Diagnosis is based on a history of exposure to an avermectin-containing product and consistent clinical signs. Breed predisposition also increases the likelihood of the diagnosis. There are no rapid tests for the avermectins that can be done in the veterinary clinic. Analyses may be performed on various body tissues by outside laboratories. Laboratory and other tests may be recommended to rule out other causes of similar clinical signs. A genetic test for the MDR1 gene mutation is available on a cheek swab sample from a dog with suspected P-glycoprotein deficiency.
TREATMENT AND FOLLOW-UP
Treatment Options
Your veterinarian may induce vomiting in the animal if an avermectin-containing product has been ingested and the pet is not exhibiting clinical signs. This is followed by administration of activated charcoal to decrease absorption of the compound into the body. Administration of activated charcoal also hastens elimination of the avermectin.
If the dog is exhibiting clinical signs, treatment is directed at controlling those signs and may include assisting breathing (placing the animal on a ventilator), administering intravenous fluids, maintaining body temperature, and providing nutrition. In severe cases, the animal may be in a coma-like state for weeks and will require good nursing care to prevent the formation of bedsores.
Follow-up CareBread Dough Poisoning
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
The ingestion of raw dough used for baking bread or pizza crusts can pose a hazard to dogs.
Causes and Toxicity
Dough containing yeast rises in the warm, humid environment of the stomach. Expanding dough can compromise blood flow to the stomach wall and decrease blood return to the heart. Yeast fermentation releases ethanol, an alcohol, which can make a dog act “drunk” or intoxicated.
Clinical Signs
Dogs may go through the motions of vomiting or retching without bringing up any stomach contents. The abdomen may become enlarged and distended. The dog may become mentally subdued and wobbly when walking, due to the production of ethanol. In severe cases, the dog may collapse and become comatose.
Diagnostic Tests
Diagnosis is based on evidence of ingestion of uncooked yeast dough and compatible clinical signs. X-rays of the abdomen may reveal foreign material in the stomach and help to rule out bloating and twisting of the stomach from other causes. Laboratory tests may be recommended to assess the effects on other organs and to rule out other causes of mental depression and collapse.
TREATMENT AND FOLLOW-UP
Treatment Options
Your veterinarian may recommend that vomiting be induced if the ingestion was recent (within 1-2 hours). This should be done only under the direction of a veterinarian. In severe cases, the animal may require hospitalization for fluid therapy and supportive care. The stomach may be pumped or surgery may be performed to remove the dough, if a large quantity was ingested.
Follow-up CareChocolate and Methylxanthine Toxicosis
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
Chocolate contains caffeine and theobromine, both of which are members of the methylxanthine group of compounds. Another member of this class is theophylline. The methylxanthines occur naturally in several plants, such as the leaves of Thea sinensis (used to make tea), the seeds of Theobroma cacao (used to make chocolate), and the fruit of Coffea arabica (used to make coffee). Theophylline is present in tea and some medications. Caffeine is found in coffee, tea, chocolate, colas, the herb guarana, and some human stimulant drugs. Theobromine is present in chocolate, cocoa beans, cocoa bean hulls (cocoa bean mulch), colas, and tea.
Causes and Toxicity
Methylxanthines as a group act as central nervous system stimulants. They are rapidly absorbed from the gastrointestinal tract. The most common cause of poisoning in small animals is eating (ingestion of) chocolate, although toxicity has occurred following ingestion of coffee grounds, tea bags, or human medications. In addition to their stimulant effects, many chocolate products contain high levels of fat that may cause gastrointestinal upset and pancreatitis. Cocoa powder contains the highest amounts of caffeine and theobromine, followed by unsweetened baker’s chocolate, semisweet chocolate, and milk chocolate. White chocolate contains negligible amounts of methylxanthines but can still pose a risk of gastrointestinal upset and pancreatitis.
Clinical Signs
The most common signs are restlessness and hyperactivity, vomiting, diarrhea, increased drinking and urinating, and a rapid heart rate. Animals may begin pacing and are unable to sit still. They may pant and appear anxious. Hyperactivity may progress to tremors and seizures if large amounts are ingested.
Diagnostic Tests
Diagnosis is based on a history of recent ingestion along with consistent clinical signs. The vomitus may contain evidence of the substance ingested. Various body tissues can be analyzed for methylxanthines; however, this test cannot be performed at the veterinary hospital or clinic, and samples must be sent to an outside laboratory. Laboratory and other tests may be recommended to rule out other causes of similar clinical signs.
TREATMENT AND FOLLOW-UP
Treatment Options
In some cases, your veterinarian may recommend that you induce vomiting at home. This should be done only under the direction of your veterinarian. Depending on the amount ingested and signs the animal is exhibiting, activated charcoal may be administered. Activated charcoal helps prevent absorption of the methylxanthine agent from the gut. Clinical signs are treated symptomatically and may require intravenous fluids, as well as medications to control hyperactivity, seizures, vomiting, and a rapid heart rate.
Follow-up CareCholecalciferol Rodenticide Poisoning
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
Cholecalciferol is also known as vitamin D3. It is formulated into rat and mouse baits and marketed under brand names such as Rampage, Quintox, Rat-B-Gon, and Mouse-B-Gon. Ingestion of (eating) these baits can result in life-threatening illness and even death in pets.
In most cases, the cholecalciferol found in vitamin supplements is not considered a serious risk for companion animals, even when massive ingestion has occurred.
Causes and Toxicity
Cholecalciferol is converted in the liver and kidneys to its active form. The active form causes calcium and phosphorus levels in the blood to rise through a series of interactions in the intestines, kidneys, and bone. Severe elevations in calcium and phosphorus can result in mineralization (deposition of calcium or calcification) within soft tissues such as the kidneys, gut, tendons, heart, and blood vessels. As little as ½ tablespoon of cholecalciferol bait can be enough to cause signs in a 20-pound (9.5-kg) dog.
Clinical Signs
Lethargy, vomiting, diarrhea (sometimes bloody), lack of appetite, and possibly an increase in drinking and urination are usually seen within 36-48 hours but can appear as soon as 12 hours after ingestion of the bait. Acute kidney failure with inability to produce urine may occur by 24-48 hours following large ingestions. Sudden death may occur, in an animal that previously appeared to recover, due to soft tissue mineralization and rupture of a calcified blood vessel such as the aorta.
Diagnostic Tests
Diagnosis is based on a history of exposure, consistent clinical signs, and laboratory findings. After the ingestion, there is a rapid (within 12-72 hours) and moderate increase in the blood phosphorus level, followed in a few hours by a more severe increase in calcium. Soft tissue mineralization may occur at this time and may sometimes be detected with x-rays or an ultrasound. Measurement of the active component of cholecalciferol may be done at certain laboratories. Other tests may be recommended to rule out other causes of elevated calcium, elevated phosphorus, and acute kidney failure.
TREATMENT AND FOLLOW-UP
Treatment Options
Treatment is aimed at removal of the poison (known as decontamination), reduction of calcium and phosphorus levels, and treatment of any kidney failure. If the ingestion occurred recently, vomiting may be induced to remove all the poison in the stomach, and activated charcoal may be given to prevent the poison from entering the bloodstream.
Intravenous administration of saline is used to lower blood calcium and may be given for several days or until calcium returns to normal. Other drugs, such as diuretics (furosemide) and steroids (prednisone), may also be tried to lower the calcium level. Drugs that bind phosphorus may be given if phosphorus remains high. Sometimes blood calcium does not respond to these therapies, and more aggressive measures may be considered. (See also the handout on Acute Kidney Failure.)
Follow-up CareGrape and Raisin Toxicosis in Dogs
Petra A. Volmer, DVM, MS, DABVT, DABT
BASIC INFORMATION
Description
A syndrome of kidney failure in dogs is associated with eating (ingestion of) commercially available grapes and raisins. Any type of grape or raisin, as well as pulp from wine pressings, can pose a hazard. Only dogs are affected.
Causes and Toxicity
All breeds of dogs are susceptible. Ingestion of as few as 4-5 raisins can cause the disease.
Clinical Signs
Dogs may develop vomiting, with or without diarrhea, within the first 6-8 hours following ingestion. Vomiting is closely followed by a decrease in activity and lack of appetite. Affected dogs may drink and urinate more. As the disease progresses, the kidneys may stop producing urine, and death can result.
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