Podcasts

Cocaine toxicosis in dogs | VETgirl Veterinary CE Podcasts

In this VETgirl online veterinary CE podcast, we review cocaine toxicosis in dogs. Have you ever seen a patient with cocaine toxicosis in your practice? Do you know how to recognize one? What do you tell owners about prognosis with treatment?

Cocaine is an illicit drug that works by preventing the reuptake of serotonin, dopamine and norepinephrine into the presynaptic neurons, so more is available at the synaptic cleft. Clinical signs are generally related to the central nervous system and cardiac system. While a number of studies have looked at experimental replication of cocaine toxicosis in dogs to mimic effects in people, there are only a couple of case reports available of veterinary patients.

So, Thomas et al out of University of Pennsylvania wanted to evaluate this in a study called “Presumptive cocaine toxicosis in 19 dogs: 2004-2012” to characterize cocaine toxicity in dogs. They retrospectively evaluated cases over an 8 year period. Patients were included if they had a positive urine drug screen for cocaine along with two or more clinical signs of toxicosis. (The authors determined clinical signs of cocaine toxicosis to include hyperexcitability, muscle tremors, seizures, bilateral mydriasis, hypersalivation, ataxia, tachycardia, hyperthermia, hypertension and vomiting.) From 2004-2012, the authors identified 29 dogs with presumptive cocaine toxicosis, but 2 were excluded due to possible or partial positive results on the urine drug screen. 8 dogs were also positive for THC (marijuana) and were excluded. These exclusions left 19 dogs included in the study, for a prevalence of 0.03% as compared to hospital population.

In this study, toy breeds (10/19, 53%) were the most commonly affected, with a median weight of 3.9 kg for all dogs. (I guess people who snort cocaine have smaller dogs? Not sure.) Anyway, the median age in this study was 1 year 3 months. 2/19 dogs had a history of probably ingestion (one was seen eating it, the other vomited up a bag containing white powder) and 1 dog ate an unknown substance “while on a walk” before developing signs of toxicity. Most of the cases (16/19, 84%) had no mention of possible exposure (Most pet owners don’t want to admit to cocaine toxicosis). Following the positive screen, exposure was confirmed in 5/19 patients and “possible” in 4/19 patients.

In this study, the most common presenting complaint for dogs with cocaine toxicosis was neurologic abnormalities (17/19, 89%), including (in order of frequency) muscle tremors, ataxia, hyperesthesia/hyperexcitability, altered mentation, seizures, excessive licking, excessive vocalization, hypersalivation and nystagmus. Other non-neurologic signs included weakness, vomiting and lethargy. On physical exam, tachycardia was common, affecting 10/19 (53%) dogs. Hyperthermia was seen in 5 (26%) dogs. The most common neurologic abnormalities on physical examination included bilateral mydriasis (11/19, 58%), hyperexcitability/hyperesthesia (53%), ataxia (42%), and tremors (42%). 3 dogs had 1 or more seizures in the hospital.

Abnormalities in initial diagnostics included variable blood pressures (4/19 hypertensive, 3/19 hypotensive) and sinus tachycardia on ECG. Blood work abnormalities most commonly included hyperlactatemia (9/19) and hyperglycemia (4/19). 3 dogs were discharged without treatment (2 stable for outpatient treatment, 1 “against medical advice”), and the remaining 16 were hospitalized. Treatments included intravenous fluids in all dogs (2/19 were treated with a fluid bolus). Other treatments included diazepam (9/19 dogs), phenobarbital, propofol and mannitol for seizures (2 dogs), acepromazine (4/19 dogs) and chlorpromazine (1 dog). 1 dog required esmolol (e.g., beta-blocker) to treat sinus tachycardia (HR 190 bpm).

Thankfully, all of the dogs in this study survived to discharge. Median length of hospitalization was 15 hours, with 8 of the dogs normal at discharge and the remainder improved but with some mild neurologic or cardiovascular signs.

So, what can we take away from VETgirl podcast?

By preventing the reuptake of dopamine, serotonin and norepinephrine, cocaine primarily causes neurologic and cardiac signs in both people and dogs. Clinical signs and incidence may be less severe and less frequent in veterinary patients due to mostly oral rather than direct mucous membrane exposure (e.g., snorting it), and reluctance of owners to bring their pets in or report ingestion. Remember that less common clinical signs and/or sequelae of cocaine toxicosis in people include vomiting (likely due to gastric mucosal irritation) and acute kidney injury due to rhabdomyolysis or direct cytotoxic effects. If patients are ill and hospitalized, monitoring of renal values might be a good idea, especially if they are tremoring or seizuring. Common treatments for cocaine toxicity in this study included intravenous fluids and benzodiazepines for tremors or seizures. Other treatments to consider include activated charcoal (if the patient is neurologically appropriate), levetirecetam, and lipids.

This is the first study looking at cocaine toxicosis in a group of canine veterinary patients (rather than experimental dogs), and it does a nice job of characterizing the most common clinical signs and treatments. However, the limitation of this study was that it was retrospective in nature and relied on urine drug tests designed for humans that often have many false positives (For example, lidocaine exposure can result in a false positive for cocaine on these urine drug tests).

In conclusion, if you have a patient that presents with acute neurologic or cardiac signs, cocaine toxicosis should be on your radar! Most patients respond well to supportive care and benzodiazepines, although further treatment of seizures or tachycardia may be indicated in some patients. Patients (especially young, toy breed dogs) that presented with acute neurologic and cardiac signs should have a urine drug screen, and cocaine toxicity should be considered. If your patient tests positive, hospitalization is recommended and seizure control may be indicated in severely affected patients.

For more information on cocaine toxicosis, check out this blog by Dr. Justine Lee here.

References:
1. Thomas EK, Drobatz KJ, Mandell DC. Presumptive cocaine toxicosis in 19 dogs: 2004-2012. J Vet Emerg Crit Care 2014; 24(2):201-207.

Abbreviations:
EKG: electrocardiogram
THC: delta-9-tetrahydrocannabinol

cocaine

Photo by Steve Rotman // cc 

Only VETgirl members can leave comments. Sign In or Join VETgirl now!