WSVMA Annual Conference

Toxicology

Spokane Convention CenterSpokane, Washington

October 1-3, 2010

Ahna Brutlag, DVMPet Poison Helpline and the University of

Minnesota, Bloomington, MN

Ahna Brutlag, DVM Assistant Director of Veterinary Services, Pet Poison Helpline

Bloomington, MN Biography: Dr. Ahna Brutlag is the Assistant Director of Veterinary Services at Pet Poison Helpline™ (PPH). She received her veterinary degree at the University of Minnesota in 2006 and is currently preparing for veterinary toxicology board certification. Dr. Brutlag has authored multiple textbook chapters and has lectured throughout the United States. The primary focus of her publications and presentations include rodenticide toxicity, toxic plants, common pharmaceutical poisonings and the safety of household products. Contact Email: abrutlag@petpoisonhelpline.com

Rodenticides – An Oldie But A Goodie Ahna Brutlag, DVM

Assistant Director of Veterinary Services Pet Poison Helpline

Key Points

• Do not assume all rodenticides are anti-coagulants. • The active ingredient of a rodenticide cannot be determined by the color or shape of the

product. • Due to better absorption and less chance of reaction, the oral administration of Vitamin

K1 is preferred over injectable unless the animal is coagulopathic. Long-acting anticoagulants (i.e. brodifacoum, bromadiolone, diphacinone, difenthiolone, chlorphacinone)

• Determine the risk of toxicosis understanding that there is significant difference between the LAACs.

• Decontaminate via emesis and consider activated charcoal if there is risk of toxicosis. • Vitamin K 1 is the antidote. Oral K1 is preferred unless the pet is coagulopathic. Treat for

3-4 weeks and then check a PT 48 hrs after the final dose to ensure sufficient duration of dosing. Give K1 with a fatty meal.

• Common signs of toxicity: lethargy, exercise intolerance, pallor, difficulty breathing, weakness. Bleeding is more often cavital (into abdominal or thoracic cavities) as opposed to serosal (gums, GI tract, bladder).

• Signs of toxicity appear within 2-5 days of ingestion. Cholecalciferol (Vitamin D3)

• Toxicity results in elevated hypercalcemia and hyperphosphatemia within 24-48 hours. • Hypercalcemia/hyperphosphatemia lead to soft tissue mineralization which results in

renal failure. Cardiac and neurologic effects are possible but rarely seen. • Multi-dose activated charcoal is indicated because the toxin re-circulates through the

liver/GIT. • Treatment needs to begin before calcium and phosphorus levels rise for best prognosis. • Basic treatments of hypercalcium: saline diuresis, Lasix (furosemide), prednisone (used

to decrease the body’s absorption of calcium and promote calciuresis). • Specific treatments: Aredia (pamidronate) or salmon calcitonin. Aredia is the treatment of

choice and only needs to be given once or twice. However, it is more expensive than calcitonin.

Bromethalin

• Results in cerebral edema (swelling of the brain). • Because of the risk of CNS effects, use caution when inducing vomiting. Do not induce

vomiting if the animal has any neurological abnormalities. Multiple doses of activated charcoal may be beneficial.

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• Common signs of toxicity: staggering, ataxia, hyperexcitability or CNS depression, tremors, and seizures.

• Very large ingestions result in signs within 4-6 hrs. Smaller ingestions can take up to 24 hrs to show signs.

• There is no specific antidote and treatment is focused on reducing cerebral edema (head elevation, mannitol, etc). Steroid use is considered controversial.

Phosphides (zinc, aluminum, calcium)

• Phosphine gas is released when this product contacts stomach acid and is the agent of toxicosis. The metal (i.e. zinc) does not contribute to toxicosis.

• To reduce the formation of phosphine gas, administration of an oral antacid should be done as quickly as possible (at home or in the clinic).

• Phosphine gas has a fishy or garlicky odor and may cause severe respiratory irritation in humans. Advise pet owners to roll down the car windows if the pet vomits and decontaminate these animals outdoors if possible.

• Decontamination via emesis or activated charcoal alone is often not sufficient and gastric lavage (with a 5% sodium bicarbonate solution) if often necessary.

• Common signs of toxicosis: vomiting, agitation, abdominal distention/ pain, dyspnea, collapse and shock. Signs often begin within 15-30 minutes of ingestion.

• The end result is multi-organ damage (renal and hepatic) or death from circulatory collapse.

• There is no antidote; provide supportive are as needed. Treatment is focused on decontamination due to the serious toxic effects.

Poison Control Resources For assistance managing a potentially poisoned patient, a number of resources are available. In the US and Canada, veterinarians or pet owners may call Pet Poison Helpline ($35/case) at (800) 213-6680 or the ASPCA’s Animal Poison Control Center ($65/case) at (888) 426-4435. Both of these services are available 24/7 and are staffed with experts in the field of veterinary toxicology. Pet Poison Helpline is also staffed with veterinary specialists in emergency and critical care and internal medicine, as well as PharmDs. In order to obtain the most accurate and current veterinary-specific clinical advice, the use of these services is highly recommended.

From the Planter to the Carpet: Toxic Plants and the Small Animal Patient Ahna Brutlag, DVM

Assistant Director of Veterinary Services Pet Poison Helpline

INTRODUCTION For curious dogs or cats, it’s difficult to resist the allure of plants. Pet Poison Helpline receives multiple calls on a daily basis from concerned pet owners and veterinarians about plant ingestions. While many plants are simple gastrointestinal irritants, some have the potential to cause life-threatening toxicity. Thus, it is helpful for technicians and veterinarians to be familiar with common plants that have the potential to cause severe toxicosis in small animals. PLANTS CAUSING SERIOUS SYSTEMIC DISEASE Plant name: Lily (Lilium spp. and Hemerocallis spp.) Other common name(s): Easter lily, tiger lily, Japanese show lily, stargazer lily, rubrum lily, day lily Species of concern: Cats Toxic dose: 1-2 leaves or petals Toxic portion of plant: All, even pollen Onset/duration of clinical signs: Hours/days Clinical signs: Early onset vomiting, depression, anorexia. Acute anuric renal failure in 1-3 days. Azotemia, epithelial cats (12-18 hrs post ingestion) proteinuria, and glucosuria. Treatment: Aggressive decontamination and IV fluid therapy x 48 hrs. Peritoneal or hemodialysis has been successful. Prognosis: Good if treated early and aggressively; poor if treatment is delayed 18-24 hr or anuria has developed.

Stargazer Lily (Lillium spp.) Plant name: Foxglove (Digitalis lannata and D. purpuea), Oleander (Nerium oleander), Lily of the Valley (Convallaria majalis), Kalanchoe (Kalanchoe spp.) Other common name(s): Yellow Oleander, Lucky Nut, Be-Still Tree Species of concern: All

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Toxic dose: 2-3 oleander leaves; 1.5 gm dried foxglove toxic to children Toxic portion of plant: All, even oleander nectar/honey (“mad honey”) Onset/duration of clinical signs: 45 min/4-5 days Clinical signs: These plants contain cardiac glycosides. Signs may include vomiting and abdominal pain within 45 min, hyperkalemia, bradycardia with 1st, 2nd or 3rd degree AV block, ventricular arrhythmias, and asystole. Kalanchoe may also cause neurological signs. Treatment: Early emesis and activated charcoal. ECG monitoring x 24 hrs. Atropine, beta-blockers, lidocaine, a temporary pacemaker and digoxin antibody fragments (Digibind®, 1-2 vials needed, $600/vial). Prognosis: Poor unless treated early and aggressively.

Foxglove (Digitalis purpuea Plant name: Rhododendrons and azaleas (Rhododendron spp.), Laurels (Kalmia spp.) Other common name(s): Mountain Laurel, Sheep Laurel Species of concern: All Toxic dose: >0.2 % of animal’s body weight. An adult human can eat 3 leaves/flowers without developing clinical signs. Toxic portion of plant: All. Onset/duration of clinical signs: As early as 1 hr, more typical 4-12 hrs/1-3 days Clinical signs: These plants contain grayanotoxin glycosides which bind to sodium channels causing a prolonged depolarization. This may lead to bradycardia or tachycardia, arrythymias, and hypotension. May also cause cholinergic signs such as vomiting, diarrhea, salivation, and dyspnea. Treatment: Aggressive decontamination, monitor an ECG and blood pressure, sodium channel blockers, atropine, aggressive IV fluids to maintain perfusion. Prognosis: Good with early intervention.

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Plant name: Cycad palm (Cycas spp., Macrozamia spp.) Other common name(s): Sago palm, leatherleaf palm, and Japanese fern palm. These are not true palms. Species of concern: Dogs Toxic dose: 1-2 seeds are fatal in a medium sized dog. A “few bites” can cause toxicity. Toxic portion of plant: All, especially the seeds. Onset/duration of clinical signs: Variable (hours to days) Clinical signs: Common: Vomiting and diarrhea (+/- blood), lethargy, depression, liver failure, death. CNS signs possible and often related to liver failure. Treatment: Aggressive decontamination with multiple doses of activated charcoal, supportive care for GI signs and liver failure. Liver protectants such as SAMe and/or silymarin. Prognosis: Good if treated prior to the onset of liver failure.

Plant name: Cyanobacteria or blue-green algae (Microcystis, Nodularia, Anabena, Aphanizomenon, Lyngbya, and Oscillatoria) Species of concern: All Toxic dose: A few mouthfuls of contaminated water. Toxic portion of plant: Most algae blooms are non-toxic but you cannot determine toxicity by visual examination. Onset/duration of clinical signs: Neurotoxin: Onset of 1-60 min. Hepatotoxin: Onset of 1-4 hours. Clinical signs: Two toxidromes: Acute CNS toxicity or hepatoxicity (rarely both). CNS: Cholinergic signs (SLUD), dyspnea, tremors, seizures, respiratory paralysis. Liver: Vomiting, diarrhea (+/- blood), weakness, pallor, acute hypovolemic shock secondary to hepatic hemorrhage. Treatment: Aggressive decontamination and activated charcoal, atropine, diazepam/phenobarbital for seizures, IV fluids, liver protectants such as SAMe and/or silymarin. Prognosis: Grave if symptomatic. Death is often seen within hours with the neurotoxin.

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Plant name: Castor bean (Ricinus communis) and Rosary Pea (Abrus precatorius) Other common name(s): Prayer bean, jequirty bean, percatory bean (all names for A. precatorious) Species of concern: All Toxic dose: 1 seed (hull needs to be cracked/chewed) Toxic portion of plant: Primarily the seeds but castor bean plants have some toxin in the leaves. Onset/duration of clinical signs: Onset is generally within 6 hours but may be delayed as beans digest/signs may persists many days, often until death. Clinical signs: The seeds contain toxalbumins (ricin and abrin) which inhibit cellular protein synthesis. Abdominal pain, vomiting, diarrhea (+/- blood), depression, seizures, cyanosis, shock, and death. Elevated liver enzymes, renal values, WBC count, albumin, and globulins. Treatment: Aggressive decontamination with activated charcoal, supportive care for GI signs and organ failure. Prognosis: Poor if signs have already developed.

Rosary Pea (Abrus precatorius) Plant name: Autumn Crocus (Colchicum autumanale) and Glory Lily (Gloriosa spp.) Species of concern: All Toxic dose: 1.5-2 gm of plant material, 2-3 seeds, ½ a flower Toxic portion of plant: All portions contain colchicine (inhibits cell division). Onset/duration of clinical signs: Onset = 2-12 hrs. Bone marrow suppression = 4-5 days. Clinical signs: Early onset anorexia, salivation, vomiting, diarrhea (+/- blood), abdominal pain, weakness, collapse, and ataxia. May progress to anemia or leukopenia. Treatment: Aggressive decontamination with activated charcoal, supportive care for GI signs and organ failure. Use of chochicine-specific Fab fragments have been successful in human beings. Filgastrim (Neupogen) may be helpful. Prognosis: Poor if multiple organ systems are affected.

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Autumn crocus (Colchicum autumanale). (Photo courtesy of Ron Mandsager, DVM, DACVA, Oregon State University College of Veterinary Medicine, Corvallis, OR.) Plant name: Yesterday, Today and Tomorrow (Brunfelsia spp.) Species of concern: Potentially, only the dog, rat and mouse. This remains to be verified. Toxic dose: Unknown. Toxic portion of plant: All, especially the juicy fruit. Onset/duration of clinical signs: Minutes-hours/days Clinical signs: Signs mimic strychnine toxicity. Salivation, vomiting, retching, agitation, nystagmus, decreased motor activity, tremors, extensor rigidity and seizures. Treatment: Emesis and activated charcoal. Reduce external stimuli. Prevent and control seizures with diazepam, barbiturates and/or short-acting anesthetics. Prognosis: Poor good with early and aggressive care.

Yesterday, Today and Tomorrow (Brunfelsia spp.) (Photo courtesy of Lynn R. Hovda, DVM, DACVIM, Pet Poison Helpline, Bloomington, MN)

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Poison Control Resources For assistance managing a potentially poisoned patient, a number of resources are available. In the US and Canada, veterinarians or pet owners may call Pet Poison Helpline ($35/case) at (800) 213-6680 or the ASPCA’s Animal Poison Control Center ($65/case) at (888) 426-4435. Both of these services are available 24/7 and are staffed with experts in the field of veterinary toxicology. Pet Poison Helpline is also staffed with veterinary specialists in emergency and critical care and internal medicine, as well as PharmDs. In order to obtain the most accurate and current veterinary-specific clinical advice, the use of these services is highly recommended.

Common Pharmaceutical Poisonings from Adderall to Zocor Ahna Brutlag, DVM

Assistant Director of Veterinary Services Pet Poison Helpline

Introduction Over 50% of the calls received by Pet Poison Helpline involve animal exposures to

human drugs. This lecture will cover the most common and potentially serious prescription pharmaceutical exposures in cats and dogs: antidepressants, sleep aids, ADD/ADHD drugs (amphetamines), baclofen, and blood pressure medications (calcium channel blockers, beta blockers and ACE inhibitors). Due to the complicated and intensive treatment of these cases, early consultation with an animal poison control center is strongly recommended. Antidepressants This category of drugs encompasses many drug classes, namely selective serotonin reuptake inhibitors (SSRI), selective serotonin and norepinepherine reuptake inhibitors (SSNRI), and cyclic antidepressants. A growing number of these drugs are used in veterinary medicine. Some veterinary specific products such as Reconcile® (fluoxetine) and Clomicalm® (clomipramine) come in chewable, meat flavored tablets. Table 1. Common prescription antidepressants with correlating doses of canine toxicity. Generic name Trade name Drug Class Minimum Canine Toxic Dose Fluoxetine Prozac, Reconcile SSRI 1 mg/kg Sertraline Zoloft SSRI 10-20 mg/kg Venlafaxine Effexor SSNRI 1 mg/kg Paroxetine Paxil SSRI 1mg/kg Bupropion Wellbutrin, Zyban Monocyclic 10 mg/kg Clomipramine Clomicalm Tricyclic 12 mg/kg The range of toxicity varies depending on the drug and species. Cats, overall, are more sensitive to the effects of antidepressants. This is especially true with clomipramine as cats may develop sedation, mydriasis, and urinary retention at therapeutic doses (0.25-1 mg/kg). Similar sensitivities are also seen with fluoxetine as the feline LD50 is half that of dogs (>100 mg/kg in dogs, 50 mg/kg in cats).

Small overdoses of SSRIs typically cause sedation and lethargy. Larger overdoses may cause salivation, agitation, ataxia, tremors, and seizures. Serotonin syndrome may occur with SSRI overdoses and is more often seen in dogs. Common signs of serotonin syndrome include GI distress, confusion, agitation, vocalization, muscle rigidity, increased reflexes tremors, seizures, hyptherthermia and transient blindness.

Treatment of SSRI overdoses is largely supportive and symptomatic. For seizures in the absence of serotonin syndrome, benzodiazepines are highly effective. In cases of serotonin syndrome however, benzodiazepines may exacerbate neurologic signs and should be avoided. Cyproheptadine, a serotonin antagonist, is useful in reducing the severity of toxicosis and can be given orally or crushed and administered rectally. Additional treatments include methocarbamol for tremors, IV fluids for thermal cooling and to maintain hydration, sedation with

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chlorpromazine or acepromazine, and beta blockers for tachycardia and hypertension (if this is not corrected following sedation).

Overdoses of SSNRIs such as venlafaxine (Effexor®) have the added element of increased pre-synaptic concentrations of norepinepherine. This may lead to signs such as tachycardia, hyptherthermia and hypertension. Treatment is similar to SSRI overdoses but more focus on sedation may be needed.

Cyclic antidepressant overdoses such as those of the common tricyclic agents amitriptyline and clomipramine may lead to profound cardiac toxicity in addition to neurologic signs. Cardiac failure and collapse is the major cause of death following tricyclic antidepressant overdoses. Sleep Aids

Sleep aids are typically short-acting benzodiazepines such as temazepam (Restoril®) or non-benzodiazepine hypnotic agents such as zolpidem (Ambien®) and eszopiclone (Lunesta®). Non-benzodiazepines are chemically unrelated to benzodiazepines but still potentiate gamma-aminobutyric acid(A)-mediated (GABA) neuronal inhibition.

Though the exact range of toxicity for these drugs is not well reported in veterinary medicine, the drugs have a fairly wide margin of safety. It is unlikely that the ingestion of 1-2 pills will lead to life-threatening toxicity in most healthy adult animals. However, larger ingestions may be highly problematic and aggressive care may be necessary.

Animals, especially dogs, develop one of two clinical syndromes when exposed to these medications, each occurring about 50% of the time. Animals will either become sedate, lethargic, dull and depressed or exhibit paradoxical CNS stimulation evidenced by agitation, vocalization, panting, hyperesthesia and hyperactivity. The reason for this remains unknown. Animals exhibiting CNS stimulation should not be treated with benzodiazepines.

This class of drugs is designed to be rapidly absorbed and rapidly excreted. Therefore, the onset of clinical signs is typically 15-60 minutes and resolution is typically seen within 12 hours. Because the onset of neurologic signs can appear so quickly, it is often unadvisable to have emesis induced at home. Activated charcoal may help decrease the amount of drug absorbed. ADD/ADHD Rx Drugs (amphetamines) Prescription CNS stimulants are often used for the treatment of Attention Deficit Disorder, narcolepsy and obesity in humans. Examples of amphetamine containing drugs include Adderall®, Dexedrine®, Desoxyn® and Vyvanse®. Methylphenidate (Ritalin® and Concerta®) and dexmethylphenidate (Focalin®) are also commonly prescribed CNS stimulants. Exposures to these drugs make up a large number of the prescription drug calls managed by Pet Poison Helpline. Unfortunately, these drugs have narrow margins of safety and signs of toxicity are frequently noted following exposure. Amphetamines are sympathomimetic compounds and, although structurally related to norepinephrine, amphetamines are more potent.

While the range of toxicity varies amongst these drugs, clinical signs are typically begin at the dose of 1 mg/kg. These drugs are rapidly absorbed and clinical signs often occur 20-30 minutes after ingestion. Sustained-release products and dermal patches (if swallowed whole) may result in a slower onset of action as well as a prolonged duration of clinical signs. Signs of toxicity involve CNS over stimulation and excessive sympathomimetic effects such as agitation,

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vocalization, hyperactivity, hypertension, head bobbing, hyperthermia, tachycardia, tremors, and seizures.

Treatment is primarily symptomatic and supportive. Emesis is not often recommended due to the rapid onset of clinical signs. Gastric lavage and activated charcoal may be helpful. Maintaining control of hyperthermia, tachycardia and tremors are key elements in these cases. Chlorpromazine (up to 10-18 mg/kg) has been successfully used in a number of cases. Benzodiazepines are typically avoided as they may increase CNS stimulation. Other commonly used interventions include injectable methocarbamol, injectable beta-blockers, and IV fluids. In severe cases, general anesthesia is necessary. Baclofen Baclofen is a centrally acting skeletal muscle relaxant (GABA-B receptor agonist) commonly used for the symptomatic relief of painful muscle spasms in patients with spinal cord injury, multiple sclerosis, Parkinson’s and Huntington’s disease. The range of toxicity for dogs and cats is quite small. In dogs, signs of toxicity in adult animals have been noted as low as 3 mg/kg with death resulting from doses of 8-16 mg/kg.

Baclofen is rapidly absorbed from the GIT and the onset of clinical signs may occur as early as 15 minutes following ingestion. Thus, the induction of vomiting at home is not often recommended due to the risk of aspiration. Decontamination should take place under the supervision of veterinary staff to reduce the risk of aspiration.

The most common initial clinical signs include vocalization, disorientation, vomiting, and ataxia. As toxicity progresses, life-threatening respiratory depression, hypotension, coma and seizures develop. It is common for clinical signs to last for several days. Fortunately, if treated appropriately, many animals survive without residual CNS effects. The prognosis is guarded for those animals with persistent seizures.

As no antidote exists specifically for baclofen toxicity, treatment is largely supportive and symptomatic. Seizures may be treated with benzodiazepines but long-acting barbiturates should be avoided as they may prolong CNS depression. Bradycardia may respond to atropine, while hypotension may respond to intravenous fluid therapy, volume resuscitation, or vasopressor support. IV fluids should be used to maintain hydration and tissue perfusion. In severe cases where the patient is hypoventilating or very sedate, endotracheal intubation and mechanical ventilation may be needed for several (5-7) days. The use of hemodialysis and Intravenous Fat Emulsion (IFE) therapy (the direct administration of intravenous intralipid) has been used successfully in a small number of cases.

Blood Pressure Medications (calcium channel blockers, beta blockers, ACE inhibitors) The primary agents of concern are calcium channel blockers (such as amlodipine, diltiazem and verapamil) and beta-adrenergic blockers (such as atenolol, propranolol and sotalol). The ability of these drugs to cause life-threatening toxicity is great and all overdoses should be regarded with concern. ACE inhibitors, such as benazepril and enalapril, do not typically lead to significant toxicity unless very large quantities are ingested or the animal has compromised health.

While the range and clinical manifestation of toxicity varies depending on the drug, the target organ of toxicity for these agents is the cardiovascular system. Bradycardia, hypotension, and heart block are common sequela of overdoses.

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Aggressive treatment is often necessary in overdose cases involving calcium channel and beta blockers. Animals that develop signs of toxicity often need 24 hour support for one or more days. Treatment is focused on cardiovascular support and may include aggressive intravenous fluid therapy, atropine and calcium supplementation. Vasopressors must be used with extreme caution. Frequent monitoring of blood pressure, heart rate and rhythm (via ECG), electrolytes, renal indices, and urinary output are necessary.

Emerging therapies such as High Dose Insulin (HDI) and Intravenous Fat Emulsion (IFE) are showing great promise for the treatment of specific anti-hypertensive agents. Poison Control Resources For assistance managing a potentially poisoned patient, a number of resources are available. In the US and Canada, veterinarians or pet owners may call Pet Poison Helpline ($35/case) at (800) 213-6680 or the ASPCA’s Animal Poison Control Center ($65/case) at (888) 426-4435. Both of these services are available 24/7 and are staffed with experts in the field of veterinary toxicology. Pet Poison Helpline is also staffed with veterinary specialists in emergency and critical care and internal medicine, as well as PharmDs. In order to obtain the most accurate and current veterinary-specific clinical advice, the use of these services is highly recommended.

It’s not just marijuana anymore: A review of illicit drugs. Ahna Brutlag, DVM

Assistant Director of Veterinary Services Pet Poison Helpline

Marijuana Marijuana (Cannabis sativa) is also known by the street names “grass,” “pot”, “weed,” and “Mary Jane.” It is the most commonly reported illicit drug exposure to Pet Poison Helpline. Often, pets are exposed by ingesting baked goods (brownies or cookies) containing marijuana. Occasionally, pets ingest the dried and prepared plant or are intentionally exposed by people blowing smoke into their faces. Depending on the route of administration, the onset of clinical signs may be 5-10 minutes (inhaling the smoke) or 30-60 minutes (ingestion). The signs of intoxication are similar to those seen in human beings. Most common are depression, a glassy eyed appearance, ataxia, mydriasis, disorientation, tremors, hypothermia and weakness. Despite its potent antiemetic effects, vomiting and salivation are common if the product was ingested. Additionally, bradycardia or tachycardia, vocalization, CNS stimulation, hyperactivity and seizures may occur.

The margin of safety for marijuana is very wide with the lethal dose being approximately 1000 times greater than the effective dose. The oral rat LD 50 is 666-1000 mg/kg. However, no deaths were reported in dogs ingesting 3-9 gm/kg of marijuana. Thus, rarely does toxicity lead to fatality in dogs and cats.

Treatment is primarily symptomatic and supportive. Decontamination may be performed if the ingestion was recent or large. Multiple doses of activated charcoal may decrease the half-life. Inducing emesis may be difficult due to the antiemetic properties of marijuana. Vital signs, especially body temperature, should be monitored and corrected as needed. CNS stimulation may be treated with diazepam. Recovery may take 24-72 hrs, depending on the dose. Amphetamines (including MDMA or “Ecstasy”)

Common street names for these agents include: “speed,” “dexies,” “dex,” and “uppers” for amphetamine; “glass” or “ice” for crystal methamphetamine; and “meth” or “crank” for powdered methamphetamine (may be dosed intravenously). MDMA or “ecstasy” is a popular club drug with similar physical structure to amphetamines and mescaline.

Illicit amphetamines, like their pharmaceutical counterparts, are sympathomimetic compounds. Common clinical signs are often related to CNS stimulation and may include agitation, hyperactivity, mydriasis, head bobbing, tremors, and seizures. Additional signs include salivation, vocalization, hyperthermia, tachycardia and hypertension. Occasionally, animals will present with weakness, bradycardia, and depression. Death may be due to disseminated intravascular coagulation secondary to severe hyperthermia and respiratory failure. Signs of toxicity may last for 8 hours or more.

The range of toxicity varies with the agent of exposure. However, for MDMA (“Ecstasy”), dogs will typically develop clinical signs of mydriasis and agitation at 3 mg/kg within 45 minutes of ingestion. Dogs dosed at 9 mg/kg may develop tachypnea, circling, and excessive salivation. For dogs, 15 mg/kg has proven fatal.

Treatment is primarily symptomatic and supportive. Emesis is not often recommended due to the rapid onset of clinical signs. Gastric lavage and activated charcoal may be helpful if

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performed very soon after ingestion. Controlling hyperthermia, tachycardia and tremors are key elements in these cases. Cocaine Cocaine, an alkaloid extract from Erythroxylon coca, is typically sold in two solid forms—powder or crystal. The white powdered product (cocaine HCl) is commonly called “coke,” “C” or “blow” and is usually insufflated (snorted) or dissolved and injected IV. Cocaine can be further processed into the free alkaloid form (“free base”) often referred to as “crack”. “Crack” is a purer, more potent form of cocaine and is typically smoked. Cocaine is a potent CNS stimulator and is well absorbed from many mucosal surfaces leading to a rapid onset of clinical signs. Though the half life of the drug is short and the effects last only 5-20 minutes in human beings, prolonged signs in animals may be due to organ damage. Additionally, animals may be used as “body packers,” thus harboring large amounts of drug in their GIT or peritoneum. Radiographs will aid in the diagnosis of “body packers.” Early signs of cocaine intoxication include CNS stimulation such as hyperactivity, hyperesthesia, mydriasis, twitches/tremors, seizures and death. Common cardiac signs include tachycardia, hypertension, and cardiac arrest (likely secondary to coronary artery vasospasm and hypoxia). Life-threatening hyperthermia is also common. Treatment is largely focused on the neurologic and cardiac systems while maintaining body temperature, electrolyte, and acid-base status. Many animals present too late for decontamination. Heroin Heroin is a synthetic derivative of morphine. In human beings, it is usually injected intravenously but may be snorted or smoked. Animals, especially dogs, may be used as “pack mules” for the illegal transport heroin. The dogs are either fed baggies filled with the drug or baggies are surgically implanted in the peritoneum. Death may occur from either the drug itself or secondary to infection following non-sterile surgical technique. Heroin (along with most opioids) is well absorbed from the GI tract and undergoes significant first-pass metabolism. Therefore, the amount absorbed orally will be significantly less as compared to the same amount delivered via injection or inhaled. Regardless, the amount of heroin needed to cause toxicity in a dog or cat is quite small and all exposures need to be managed aggressively. Clinical signs resulting from heroin intoxication may include early onset aggressive behavior (especially in dogs), vomiting, salivation, miosis, ataxia, CNS depression and unconsciousness. Life-threatening respiratory and cardiac depression is common. Respiratory depression and subsequent hypoxia are the leading cause of death. Seizures may also occur. The induction of emesis following ingestion is typically not advised due to the rapid onset of CNS signs. In cases where a baggie of heroin has been ingested, extreme care must be taken to avoid rupture. Gastric lavage may be helpful in cases of large ingestions.

Treatment is typically focused on the respiratory and CNS signs. Respiratory depression and coma may be reversed with naloxone. Naloxone has a short half-life and should be re-dosed as needed, as often as 30-90 minutes. Additionally, assisted ventilation may be necessary. Body temperature must be monitored closely as hypothermia is common. Though heroin is cleared more rapidly than morphine, symptoms may persist for many hours. Additionally, organ damage secondary to hypoxic injury may cause long-lasting or permanent effects.

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Club Drugs (GHB and flunitrazepam) Club drugs are synthetic drugs that have become popular over the past 10 years. MDMA (“Ecstasy”) is one of the most popular stimulant club drugs and is discussed in the amphetamines section. GHB (gamma hydroxybutanoic acid) and flunitrazepam, other common club drugs, are CNS depressants. Due to their rapid onset of action and sedative effects in human beings, they are also referred to as “date rape drugs.”

Street names for GHB include “Liquid X” or “liquid ecstasy,” “G,” and “grievous bodily harm.” GHB has a wide margin of safety with an LD50 in rats and rabbits ~2 g/kg. Though fatalities from ingesting these drugs are rare, the clinical impact may be dramatic. Signs of intoxication include sedation with possible bradycardia, hypothermia, respiratory depression and seizures. Seizures have been successfully treated with diazepam in human beings.

Flunitrazepam, a prescription benzodiazepine available in many countries, is not sold legally in the U.S. Street names include “roofies,” “Mexican Valium,” and “Roche.” In human beings, clinical signs are apparent within 20-30 minutes of ingestion. Less is known about animal toxicity; however, a similar onset of action is anticipated. Signs of intoxication may include sedation though, in dogs and cats, paradoxical CNS stimulation may occur. Hallucinogens Hallucinogenic agents include lysergic acid diethylamide (LSD); mescaline, the active ingredient in peyote; psilocybin or “magic mushrooms” from the Psilocybe spp.; seeds of the morning glory plant, Ipomoea violacea; leaves of the plant Salvia divinorum; and nutmeg (Myristica fragrans). Though not true hallucinogens, phencyclidine (PCP) and ketamine are two agents often discussed amongst hallucinogens. They are more properly termed dissociative anesthetics, as their principle effect is to cause dissociation from pain and the environment. Of these agents, LSD is the most potent hallucinogen. Clinical signs may appear rapidly following the ingestion of hallucinogens include a severely altered mental status, disorientation, ataxia, mydriasis, excitation, depression, bizarre posturing and movements, and vocalization. Signs may persist up to 8 hours or more. Long durations of action are most likely from LSD; other agents have a shorter duration action. Treatment is symptomatic and supportive. Emesis should not be performed in a symptomatic animal as the risk for aspiration or seizure induction is greater. In asymptomatic animals, decontamination may be considered. Reducing external stimuli by containing the animal in a dark, quiet space is helpful. Sedation may be achieved with diazepam. Though rare, hyperthermia and rhabdomyolysis may occur. Death is not common following intoxication from these substances. Poison Control Resources

For assistance managing a potentially poisoned patient, a number of resources are available. In the US and Canada, veterinarians or pet owners may call Pet Poison Helpline ($35/case) at (800) 213-6680 or the ASPCA’s Animal Poison Control Center ($65/case) at (888) 426-4435. Both of these services are available 24/7 and are staffed with experts in the field of veterinary toxicology. Pet Poison Helpline is also staffed with veterinary specialists in emergency and critical care and internal medicine, as well as PharmDs. In order to obtain the most accurate and current veterinary-specific clinical advice, the use of these services is highly recommended.