Illicit Drug Intoxications of Small Animals
Atlantic Coast Veterinary Conference 2001
Robert H. Poppenga, DVM, PhD
Chief, Toxicology Laboratory at the University of Pennsylvania
School of Veterinary Medicine


•  Be familiar with the major categories of illicit drugs that can intoxicate pets.

•  Understand the pathophysiologic effects of illicit drugs.

•  Be familiar with methods for confirming exposure/toxicosis

•  Be able to formulate effective case management strategies.

While the true incidence of pet intoxication due to illicit drugs such as marijuana, cocaine, heroin, amphetamines, among others, is unknown, their widespread availability and use undoubtedly leads to a number of poisonings. Often, a history of exposure is not forthcoming because owners may be unwilling to divulge such information. Two notable differences exist between human and animal exposure to illicit drugs. Exposure of pets is most likely via ingestion, whereas human exposure is often via the lungs or following intravenous administration. In addition, while adverse effects from chronic drug abuse are of concern in human medicine, single, acute exposures will be much more likely in pets. The rapidity of onset of clinical signs following toxic exposures makes the need for early intervention critical. Veterinarians should familiarize themselves with the most commonly abused illicit drugs in their area and their primary effects in order to recognize and appropriately manage intoxicated pets. The following discussion will focus on presenting clinical signs, decontamination procedures, symptomatic treatment and sample collection for confirmation of exposure.


The main active constituent in marijuana (Cannabis sativa) is the alkaloid, delta-9-tetra-hydrocannabinol (d-THC). Marijuana derivatives used as drugs are available as "grass" (1 to 5% d-THC), hashish (10% d-THC) and hash oil (> 50% d-THC). d-THC targets the brain, where it interacts with all major neurotransmitters such as norepinephrine, dopamine, serotonin, and acetylcholine and binds to specific receptors in the cerebellum and frontal cortex. A reported minimal lethal oral dose of d-THC in the dog is > 3 g although clinical signs of a "physiologic" effect occur at much lower doses.1 Thus, death following exposure to marijuana is unlikely. d-THC interacts with other commonly used drugs. It increases the depressant effects of CNS depressants such as alcohol, sedatives, hypnotics and opioids. Interactions with stimulants such as caffeine, nicotine, amphetamines and cocaine are complex and may be additive or antagonistic depending on dose and time interval between exposures. The effects of d-THC on dogs are similar to those in humans. Clinical signs include behavioral changes, ataxia, muscle weakness, conjunctival injection, mydriasis, depression, stupor, emesis, tachy- or bradycardia, hypotension, hypo- or hyperthermia, hyperesthesia, hyperactivity, tachypnea, tremors or seizures. Medical intervention in cases of marijuana intoxication is generally not necessary. If a large dose has been ingested recently (< 1 hr ago), induction of emesis may be indicated followed by the administration of activated charcoal (AC) + cathartic. In most cases, the administration of AC + cathartic followed by observation and monitoring is all that will be needed. d-THC undergoes enterohepatic recirculation. Therefore, repeated does of AC may be given, although a cathartic should be given only once.2 Monitoring should continue until signs resolve; this may take several days. If emesis is persistent or severe, intravenous fluids may be warranted. Supplemental heat should be provided if the animal is hypothermic. A quiet, darkened environment should also be provided.


Cocaine (benzoyl-methylecgonine) is an alkaloid derived from the cocoa plant (Erythroxylon coca and E. monogynum) which is processed into cocaine hydrochloride or sulfate powder. It is generally adulterated with one or more of the following: mannitol, sucrose, lactose, caffeine, talc, amphetamine, heroin, PCP, procaine, lidocaine, ergots or strychnine.3 "Free-base" or "crack" cocaine is the pure alkaloid. The purity of cocaine salts is variable (12% to 60%); the free-base form is > 90% pure. The intravenous LD100 of cocaine hydrochloride is reported to be ~ 12 to 20 mg/kg and 15 mg/kg for dogs and cats, respectively.1 The oral LD50 for dogs is ~ two to four times the i.v. LD50 (~ 13 mg/kg). Cocaine is rapidly absorbed from all sites and, once absorbed, has a relatively short-half life. Cocaine is an ester-type, tropane local anesthetic; it stabilizes axonal membranes and blocks nerve conduction when applied locally. CNS stimulation is one of the major systemic actions of cocaine. In humans, the CNS is stimulated in a rostral to caudal fashion with the cortex stimulated first followed by lower motor centers. This results initially in restlessness, excitement and increased motor activity followed by tonic-clonic seizures in more severe exposures. Its effect on the medulla results in an initial respiratory stimulation followed by respiratory depression and failure. The vomiting center is stimulated causing emesis. Bradycardia secondary to vagal stimulation is an early cardiovascular sign, which is followed quickly by tachycardia due to central sympathetic stimulation.3 Cocaine potentiates the excitatory responses of the sympathetic portion of the autonomic nervous system to epinephrine, norepinephrine and dopamine. Peripheral vasoconstriction and tachycardia lead to hypertension. Dogs given lethal i.v. injections exhibited ptyalism, hyperesthesia, tachycardia, pyrexia, seizures, increased mean arterial blood pressure and cardiac output, hypoglycemia and lactic acidosis.4 Just prior to death, severe hyperthermia, respiratory depression, coma and respiratory and cardiac arrest occurred. Decontamination of exposed animals is problematic due to the rapid absorption of the drug. If the ingestion is believed to be significant, multiple-dose activated charcoal should be considered along with a single administration of a cathartic. Correction of hypoglycemia and hypoxia is critical. Therefore, administration of dextrose in water and oxygen may be important symptomatic treatments. Diazepam is the drug of choice to achieve sedation or control seizures. If present, hyperthermia should be managed using a water bath with ice. In humans, control of central manifestations of intoxication often lead to a marked clinical improvement in cardiovascular signs.3 ECGs should be monitored for atrial or ventricular tachydysrhythmias; atrial tachydysrhythmias unresponsive to control of CNS stimulation and correction of hyperthermia often respond well to calcium channel blockers such as verapamil or diltiazem. Ventricular tachydysrhythmias often resolve following the administration of sodium bicarbonate; lidocaine should be avoided due to possible exacerbation of cardiac conduction abnormalities. Urine is the most appropriate sample to submit to a laboratory for detection of cocaine and its metabolites in order to confirm exposure.


Often the term "amphetamine" is used to refer to a large number of drug agents such as amphetamine, methamphetamine, phenmetrazine, mephentermine and so-called "designer" amphetamines such as 4-bromo-2,5 dimethoxyamphetamine (DOB), 4-methyl-2,5-dimethoxy-amphetamine (DOM) and 3,4-methylenedioxymethamphetamine (MDMA). Amphetamines are Class I or II controlled drugs legally prescribed for nacrolepsy, attention-deficit disorder and short-term weight reduction. The oral LD50 for rats and mice ranges from 10 to 30 mg/kg. Fortunately, there is a rather large difference between doses causing clinical signs of intoxication and those that are life-threatening. Amphetamines are rapidly absorbed following ingestion; sustained release formulations have prolonged absorption. Amphetamine has a human half-life ranging from 8 to 30 hours. The pharmacologic effects of amphetamines are complex and vary with the specific agent. They enhance the release and block the reuptake of catecholamines and they may have a direct effect on catecholamine receptors. Thus, both a and b-adrenergic receptors are stimulated. Amphetamine and methamphetamine have potent cardiovascular effects while DOB has potent hallucinogenic effects.5 Intoxications due to amphetamines, methylxanthines such as caffeine, and cocaine are clinically similar. Dogs given amphetamines experimentally show mydriasis, excitement, ptyalism, hyperthermia, hypertension, tachycardia, lactic acidosis and hypoglycemia. Seizures can occur. Rhabdomyolysis, a common sequela to agitation and hyperthermia in intoxicated humans, can result in acute renal failure. Decontamination procedures should be instituted when appropriate. Repeated doses of activated charcoal may be indicated in cases where a sustained-release preparation has been ingested. Diazepam is the drug of choice to control agitation and/or seizures. Hyperthermia is treated with ice water baths. Cardiovascular signs may improve once CNS signs and hyperthermia are treated. Urinary acidification can significantly increase the renal elimination of amphetamines. While this may be an appropriate way to decrease the t1/2 of such drugs, urinary acidification may increase the risk of renal damage due to precipitation of myoglobin within renal tubules. It is important to point out that street samples believed to contain amphetamines may actually contain substitutes such as caffeine, phenylpropanolamine, ephedrine, pseudoephedrine, lidocaine, and phencyclidine. In addition, a number of chemicals used in illicit methamphetamine production such as lead may be toxic. Exposure to an amphetamines can be confirmed by analysis of urine samples.


Opiates refers to those drugs derived from opium (morphine, codeine) semi-synthesized from opium (hydromorphone, heroin, oxymorphone and oxycodone) or totally synthetic (meperidine, methadone, pentazocine, butorphanol, and propoxyphene, paregoric, levorphanol and fentanyl). Opiates possess analgesic, sedative and hypnotic properties. The toxicity of opiates is variable as are their onset and duration of action. In the dog, 100 to 220 mg/kg of morphine given subcutaneously or i.v. is lethal. Opiates exert their principle pharmacologic actions on the CNS and intestines by binding to a number of opioid receptors. The mechanism by which opioids alter pain perception is unknown although it is believed that the permeability of cell membrane to K+ and Ca++ is altered. This affects central cholinergic, adrenergic, serotonergic and dopaminergic neurotransmitter systems. Dogs given toxic doses of morphine exhibit salivation, nausea, emesis, defecation, increased respiration and less commonly, urination early after administration. This is followed by respiratory and CNS depression, ataxia and bronchiolar constriction. Severely intoxicated animals exhibit stupor, coma, seizures and cyanosis with peripheral vasodilatation and hypoperfusion. Miosis is observed initially but mydriasis may ensue if hypoxia is severe. While opioids depress CNS function in dogs, they often cause CNS stimulation in cats. Hypothermia is observed in dogs while hyperthermia may be observed in cats. The clinical manifestations of intoxication following opioid exposure may vary somewhat due to differences in receptor binding of the individual drugs. Decontamination procedures should be instituted if soon after ingestion. Multiple doses of activated charcoal have been shown to hasten the elimination of propoxyphene and diphenoxylate and should be given in all cases of opioid ingestion. Due to delays in gastric motility and gastric emptying caused by opioids, decontamination procedures should be instituted even if there has been a delay in presentation. Maintenance of a patent airway and provision of adequate ventilation are perhaps the most important considerations in opioid intoxications due to their depressant effects on respiration. Naloxone is a specific opioid antagonist that is recommended for use in dogs and cats at 0.002 to 0.1 mg/kg given intravenously as needed. In cases where opioid ingestion is suspected, a trial bolus injection of naloxone may be useful for diagnostic purposes; rather prompt reversal of coma and cardiopulmonary depression is indicative of opioid intoxication. Several injections of naloxone may be needed before a response is noted. In human children, an initial dose of naloxone of 2 mg is given, if this does not result in clinical improvement, 2 to 4 mg doses are given at intervals up to a total dose of 10 to 20 mg. The effective dose of naloxone may have to be repeated at 20 to 60 minute intervals since opioids generally have a longer duration of action than naloxone. When a patient responds to a bolus injection of naloxone, an infusion may be established. In human medicine, a rule of thumb is that 2/3 of the initial bolus dose that caused a reversal of respiratory depression administered by continuous infusion each hour is adequate to prevent the recurrence of respiratory depression.6 However, the infusion dose should be increased if CNS or respiratory depression is noted.

Phencyclidine hydrochloride (PCP)

PCP was originally intended to be used as a human non-narcotic, non-barbiturate anesthetic but was removed from the market because of undesirable post-anesthetic reactions. It is considered a dissociative anesthetic. It is easily synthesized and therefore often abused. It is available in a variety of forms (powder, tablet, crystal and liquid) which vary considerably in purity (5% to 90%). Oral doses as low as 2.5 mg/kg are toxic to dogs while 1.1 mg/kg may be toxic for cats. The primary target organ system is the CNS; stimulation or depression may occur. Cardiovascular effects may also be seen. Dogs given PCP at 1 mg/kg i.v. showed increased motor activity, mydriasis, tonic-clonic seizures, hypersalivation, visual tracking, tremors, rigidity, nystagmus, stereotyped sniffing, jaw snapping, opisthotonus and death.7 Increases in heart rate, arterial blood pressure, cardiac output, body temperature and arterial pCO2 and decreases in total peripheral resistance, arterial pH, arterial pO2 and respiratory minute volume were noted. Death was believed to be due to respiratory failure. Early administration of activated charcoal + cathartic is important. Repeated doses of AC should be given since PCP undergoes extensive enterohepatic recirculation. Mild toxicosis should be managed by isolation in a cool, quiet area. Diazepam should be given if the animal is agitated. As with most suspected illicit drug intoxications, ensuring adequate respiration, circulation and thermoregulation is important. Most patients should rapidly regain a normal state within one to several hours of presentation.

Lysergic acid diethylamide (LSD) and other psychedelics: these constitute a large group of drugs that produce alterations in environmental awareness, although the individual (human at least) maintains the capacity to recognize that what is being experienced is not real. In humans, the use of psychedelics is often accompanied by physiologic changes that result in clinical signs. These physiologic responses in people may be directly related to an adrenergic response to a disturbing or enjoyable experience; whether animals would experience such responses is unknown. However, many psychedelics can cause a direct effect on the autonomic nervous system. Pharmacologic agents classified as psychedelics include ergot-based compounds, phenylethylamines (amphetamines), PCP, THC, opioids such as pentazocine and meperidine analogs, cocaine, anticholinergics, mushrooms and a number of miscellaneous plants.8 The mechanism of action of most psychedelics is unknown but is presumed to involve alterations in CNS neurotransmitters.

General treatment approaches include appropriate decontamination procedures, sedation with diazepam, and symptomatic treatment. Presence of hypertension, tachycardia, and hyperthermia may require more aggressive treatment. Psychedelic agents rarely cause life-threatening problems.


1.  Kisseberth, WC and Trammel, HL (1990): Illicit and abused drugs. The Veterinary Clinics of North America: Small Animal Practice 20:405-418.

2.  Dumonceaux, GA (1995): Illicit drug intoxications in dogs. In: Current Veterinary Therapy XII: Small Animal Practice, Bonagura, JD (ed.), pp: 250-252, W.B. Saunders, Philadelphia, PA

3.  Lewin, NA, Goldfrank, LR, and Hoffman RS (1994): Cocaine. In: Toxicologic Emergencies, Goldfrank, LR, Flomenbaum, NE, Lewin, NA, Weisman, RS, Howland, MA and Hoffman, RS (eds.), pp: 847-862, Appleton and Lange, Norwalk, CT.

4.  Catravas, JD, Waters, IW (1981): Acute cocaine intoxication in the conscious dog: studies on the mechanism of lethality. J Pharmacol Exp Ther 217:350-356.

5.  Chiang WK and Goldfrank, LR (1994): Amphetamines. In: Toxicologic Emergencies, Goldfrank, LR, Flomenbaum, NE, Lewin, NA, Weisman, RS, Howland, MA and Hoffman, RS (eds.), pp: 847-862, Appleton and Lange, Norwalk, CT.

6.  Goldfrank, LR and Weisman, RS (1994): Opioids. In: Toxicologic Emergencies, Goldfrank, LR, Flomenbaum, NE, Lewin, NA, Weisman, RS, Howland, MA and Hoffman, RS (eds.), pp: 847-862, Appleton and Lange, Norwalk, CT.

7.  Hackett, RB, Obrosky, KW, Borne, RF et al. (1981): Acute phencyclidine poisoning in the unanesthetized dog: pathophysiologic profile of acute lethality. Toxicology 19:11-20.

8.  Aaron, CK and Ferm, RP (1994): Lysergic acid diethylamide and other pyschedelics. In: Toxicologic Emergencies, Goldfrank, LR, Flomenbaum, NE, Lewin, NA, Weisman, RS, Howland, MA and Hoffman, RS (eds.), pp: 847-862, Appleton and Lange, Norwalk, CT.

Speaker Information
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Robert H Poppenga
Chief, Toxicology Laboratory at the University of Pennsylvania
School of Veterinary Medicine

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