31 Mar 2020
Lotfi El Bahri DVM, MSc, PhD recounts the instance of a three-year-old male poodle that had ingested bait package containing this rodenticide.
Lotfi El Bahri
Job Title
You are presented with a three-year-old male poodle weighing 8kg at your emergency veterinary clinic.
The dog’s owner found him ingesting a large quantity of chloralose bait package. The owner has noted unsteadiness, profuse salivation, hyperexcitability and muscle tremors.
Chloralose (glucochloral) is a mixture of two isomers – alpha (greater than or equal to 85%) and beta (less than or equal to 15%). It is a rodenticide used to kill house mice.
Immobilisation of mice occurs shortly after bait consumption. The products are for indoor use only. The bait is placed in plastic, tamper‑resistant bait boxes containing 2% (cake crumb/cereal preparations) or 4% chloralose (oatmeal-type particles).
It is not approved for the control of rats and its hypnotic-sedative properties are employed as an avicide to control depredating birds (for example, pigeons, sparrows and gulls). The majority of toxicities are accidental, but malicious poisoning can occur.
Chloralose has moderate oral toxicity. The oral median lethal doses (LD50s) of alphachloralose are 611mg/kg and 212mg/kg in male and female rats, respectively, and 400mg/kg in mice. In dogs, the LD50 is approximately 500mg/kg, and the toxic dose range reported is between 200mg/kg and 500mg/kg. Birds are more susceptible.
A secondary poisoning risk is considered negligible; mammal predators may catch a poisoned mouse, but with LD50 values no less than 100mg/kg for dogs. Chloralose has both potent depressive and stimulant actions on the CNS.
Alphachloralose is an acute depressant on the brain. It has been used as general anaesthetic in laboratory animals, due to its minimal effects on cardiovascular function.
At high concentrations, alphachloralose activates gamma-aminobutyric acid (GABA) receptors on GABAergic presynaptic nerve terminals in the CNS, leading to depression of the cortical centres in the brain. In the hypothalamus, the thermoregulation does not operate properly and unconscious animals die from hypothermia.
After ingestion, chloralose is hydrolysed in the stomach by gastric acidity to chloral, which is mainly metabolised by hepatic alcohol dehydrogenase, to trichloroethanol (TCE), an active metabolite. TCE is lipid soluble, easily crosses the blood-brain barriers and depresses the cortical centres of CNS. TCE may also sensitise the myocardium to circulating catecholamines, resulting in cardiac arrhythmias.
Betachloralose is a potent stimulant on spinal reflex, producing hyperreflexia particularly to sudden sounds, spontaneous myoclonic movements and generalised convulsions.
CNS excitation and depression are the main clinical features, which appear usually within one to two hours after ingestion. Two types of clinical signs may be seen concurrently:
In human patients, the electroencephalogram of chloralose poisoning is characteristic, involving slow delta waves two to three cycles per minute, and an aspect of degraded waves and numerous spikes.
No specific antidote exists.
An IV catheter should be placed. To control seizures, diazepam (0.5mg/kg to 2mg/kg IV bolus) should be administered and repeated if necessary within 20 minutes (serum half-life in dogs is 2.5 hours to 3.2 hours) up to three times in a 24-hour period, or 1mg/kg to 2mg/kg rectally. Do not give diazepam by IM. This is contraindicated in patients with severe liver disease, however.
Alternatively, administer lorazepam (long-acting benzodiazepine 0.2mg/kg IV bolus, because of its high affinity for benzodiazepine receptors in the CNS) or midazolam 0.2mg/kg to 0.4mg/kg IV may be repeated once. When IV access is not available, midazolam can be administered by IM because it is rapidly absorbed by this route.
Barbiturates are contraindicated (cause depressed respiration and hypothermia). Ketamine is contraindicated (seizure-like effects have been reported).
Valproic acid is not recommended (serum half-life in dogs is 1.5 hours to 2 hours). Alternatively, administer levetiracetam 20mg/kg IV slow bolus. In cases of refractory seizures, administer propofol (3mg/kg to 6mg/kg IV initial bolus), followed by 0.1mg/kg/min to 0.6mg/kg/min constant rate infusion (CRI).
Alternatively, 2% to 2.5% concentrations of isoflurane alone with oxygen can be used. For maintenance, use 1.5% to 1.8% concentrations of isoflurane in oxygen. Attention to airway, breathing and circulation are paramount. Intubate affected animals and provide artificial respiration with oxygen during convulsions.
Arrhythmias may be treated with β-blockers: propanolol 0.02mg/kg/IV slowly (up to a maximum of 0.1mg/kg). Alternatively, esmolol: an initial loading dose of 0.25mg/kg to 0.5mg/kg (250µg/kg to 500µg/kg) administered IV as slow bolus over one to two minutes, then followed by a CRI of 10µg/kg/min to 200µg/kg/min.
Hypothermia increases the risk of complications. Slowly rewarm the patient using warm IV fluids, a circulating warm water blanket under the patient, or forced-air warming systems.
Body temperature must be monitored while these devices are in place because they can increase the temperature rapidly.
Emesis should be induced only if the animal is asymptomatic. Administer apomorphine 0.03mg/kg IV, 0.04mg/kg IM or a 0.025mg tablet crushed and dissolved in physiological saline.
Instil in the conjunctival sac and rinse with water after emesis has occurred. Alternatively, use xylazine (1.1mg/kg SC or IM).
To prevent further absorption of chloralose from the intestinal tract, use activated charcoal (AC; 1g/kg to 4g/kg) mixed with water to make a 20% slurry (1g/5ml water) via a nasogastric tube as soon as possible postingestion, and after the airway is secured. AC admitted orally is contraindicated in convulsing or comatose animals. Maintain the patient on IV-balanced crystalloid fluids, such as lactated Ringer’s solution 40ml/kg/hour to 90ml/kg/hour.
Correction of metabolic acidosis (normal values in dogs: pH less than 7.33; standardised base excess less than -4mmol/L) by sodium bicarbonate 8.4% solution: 1ml/Lb to 2.5ml/Lb bodyweight CRI depending on the severity of the acidosis, over a four-hour period.
Maintain affected animals in a quiet environment. Noises/actions can restart seizures (cotton earplugs to prevent auditory stimulation). The patient should be monitored for a minimum of three days (the half‑life of chloralose in dogs is 48 hours). IV lipid emulsion therapy is contraindicated, because chloralose is not lipid soluble (log P values of 0.85).
Chloralose is potentially persistent or very persistent in a marine environment. It is very toxic to aquatic organisms. The lethal concentration 50 (LC50) after 96 hours in rainbow trout (Oncorhynchus mykiss) is 2.4mg/L. Avoid chloralose release to the environment.
Educate clients to keep pets away from chloralose bait products. A bitter-tasting agent – denatonium benzoate – has been added to discourage pets from ingesting it.
