Signalment:
10-year-old female spayed mixed breed canine weighing 11.10 kg.
History:
The patient presented to GCVS Emergency at approximately 1:50 PM for ataxia and trembling. She had been at home alone since 8:00 AM, and the family determined that she had ingested an unknown amount of THC gummies and semi-sweet chocolate chips. The patient did not have any underlying heath conditions and was current on preventatives.
Vital Signs:
- Temp 99.6,
- HR 120
- RR 30 with normal RE
- mm pink, slightly tacky
- CRT 1-2 sec
Physical Exam:
Initially obtunded with menace intact OU, non-ambulatory; During triage the patient’s mentation quickly worsened (comatose) and she was not responsive with pinpoint pupils OU (direct/indirect PLR still intact OU), absent menace OU, vertical and slightly rotary nystagmus OU, and absent withdrawal reflexes in all limbs. Shortly after arrival, while still on the triage table, the patient suffered a grand mal seizure.
Initial Diagnostics:
- CBC: Thrombocytosis (493 K/uL)
- Chemistry: Hyperglycemia (157 mg/dL), rest WNL
- PT: 12s
- ASPCA Poison Control Consultation
Treatment plan Day #1:
- IVC placement x2
- Supplemental oxygen therapy via face mask while on triage table
- Phylyte 35 mL/hr
- Maropitant 1 mg/kg IV q24h
- Mannitol 1 g/kg IV once, continue as needed
- Diazepam 0.3 mg/kg IV once for agitation
- Levetiracetam 60 mg/kg IV loading dose
- Levetiracetam 40 mg/kg IV q8h for maintenance dose
- Midazolam 0.5 mg/kg IV as needed for seizure if patient is not lipemic
- Intralipid therapy
- Bolus 16.5 mL over 2-3 min IV once
- CRI 165 mL over 60 minutes IV once – repeat for an additional two doses (q4h) if patient is not lipemic
- Supportive care as needed
- Tachycardia – can be treated with propranolol
- Agitation – can be treated with acepromazine or benzodiazepines
- Muscle tremors, stiffness – can be treated with methocarbamol
- Continuous ECG monitoring
- Keep head elevated, recumbency care q4h
- Seizure watch
Overnight #1:
9:00 PM: mentation- very obtunded and non-responsive to any stimuli. Serum lipemic, additional intralipid not administered.
11:00 PM: Her eyes are now central, pupils miotic OU and palpebral present OU. She is more reactive when taking temperature, but not other stimuli; serum lipemic; additional intralipid not administered
1:00 AM: PCV/TP: 40%, 10.7 g/dl; serum lipemic; additional intralipid not administered.
5:00 AM: The patient was more responsive to vocal and touch stimulation. She would intermittently look around the room. Menace and palpebral present OU. Added lube eyes Q 4 hours
6:00 AM: PCV/TP (6am): 43%, 7.5 g/dl; serum lipemic; additional intralipid not administered
Day #2 Hospitalization:
- PE: mentation—sedate to obtunded. Euhydrated; Cranial nerves intact, non-ambulatory but does have motor in all 4 limbs. Too sedate to stand without assistance. Responds to both verbal and physical stimuli
- Treatment Plan:
- Phylyte @ 35 ml/hour
- Levetiracetam 440 mg (39.64 mg/kg) IV q8h
- Maropitant 11.1 mg (1 mg/kg) IV q24h
- Continuous ECG monitoring d/c 10:00 PM
- Lube eyes q4h, d/c 10:00 PM
- Keep head elevated, keep sternal, rotate hips q4h moving on her own as of 6:00 PM
- Heat support as needed d/c as of 6:00 PM
- Seizure monitoring with Midazolam 5.55 mg (0.5 mg/kg) IV on retainer
- Diagnostics:
- 4pm: PCV 41%, TP 7.0 g/dl, serum clear
Overnight #2:
The patient’s mentation steadily improved throughout day 2 and overnight. She ate a small amount of food at 2:00 AM and 6:00 AM. No treatment changes were made overnight.
Day #3 Hospitalization:
- PE: Much improved mentation. Standing, and walking on her own. No neurological deficits
- Treatment Plan:
- Phylyte @ 35 ml/hour, decrease to 17 ml/hour @ 12:00 PM
- Levetiracetam 440 mg (39.64 mg/kg) IV q8h, d/c after 2pm dose
- Monitor for seizures with Midazolam 5.55 mg (0.5 mg/kg) IV on retainer
- At 3:30 PM, the patient’s family visited her. She was still slightly sedate but responsive to her owner and ambulating well. The family elected to take the patient home after the visit and was warned that full recovery might take another few days as she continued to process the THC.
Case Discussion:
Increased legalization of THC use in the United States is accompanied by an increase in toxicosis in pets, mostly dogs. Cases of intoxication in family pets are increasing due to increased access, higher potency products, and client willingness to admit possible exposure. Any form of THC can cause toxicosis in pets (dried plant material, edibles, vapes, topicals, concentrates, and excreted human feces). Edibles have increased in popularity and are attractive to pets, but dogs are more likely to consume vs. cats. Edibles may also contain chocolate, which would need to be factored into the overall toxicity. Diagnostic testing is limited due to the small quantities of THC and metabolites excreted in urine compared to humans. Most OTC drug tests will give a false negative result for THC in dog urine. This is presumably because different metabolites are produced in dogs, and the test is specific for the human metabolite. Most true positive results are secondary to fecal ingestion (ingesting the metabolite). Diagnosis is usually based on clinical signs and known products in the environment if admitted by the client.
Clinical signs of THC ingestion can appear from 30 minutes to several hours after ingestion. Common clinical signs include:
- Dogs:
- Most common: hyperesthesia, lethargy, urine dribbling
- Less common: ataxia, disorientation, bradycardia, hypothermia, mydriasis, and tremors.
- Ingestion of high doses can lead to hypotension and a comatose state.
- Cats:
- Most common: ataxia, lethargy
- Less common: vomiting/nausea
Treatment is symptomatic and supportive and varies according to the time of exposure and severity of clinical signs. For patients with low exposure, many can be managed on an outpatient basis and monitored at home. Because THC has anti-emetic properties, emesis may not be successful but can be attempted if ingestion was <30 minutes. Activated charcoal is not normally recommended because most cases are mild.
For patients with more clinical signs, IV fluid therapy should be started, and patients should be monitored in the hospital for hypotension and hypothermia. Younger patients may benefit from blood glucose monitoring. Vomiting/nausea should be treated if indicated. For patients with agitation or tremors, low dose acepromazine or diazepam can be used.
For patients with hypotension despite fluids or mentation changes (obtunded/comatose), intralipid emulsion therapy (ILE)is beneficial, given that THC is lipid soluble. When using ILE, non-selective binding to therapeutic agents occurs (example: benzodiazepines). Other toxins in which ILE therapy may be used include baclofen, permethrins, ivermectin, and tremorgenic mycotoxins.
In this patient’s case, semi-sweet chocolate ingestion had to be factored into her treatment plan. We assume her agitation and seizures were secondary to the theobromine and caffeine within the chocolate. Treatment was instituted as needed for these symptoms.
Recovery in most patients occurs within 24 hours; however, in more severe cases like this patient’s, it may take 3-5 days to fully recover.
Case Update:
The patient’s family reported that she was back to her normal personality 2-3 days after discharge.
