Evidence of a sudden increase in α-chloralose poisoning in dogs and cats in the Netherlands between 2018 and 2021.

BACKGROUND: After changes in European Union biocide legislation, the Dutch Poisons Information Center observed a strong increase in information requests concerning dogs and cats exposed to α-chloralose. To investigate whether α-chloralose-based rodenticides are safe for non-professional use, additional information regarding poisoning scenarios and clinical course was collected. METHODS: Veterinarians reporting α-chloralose exposure over a 2.5-year period were contacted by mail for follow-up information concerning exposure scenario, product formulation, clinical course and treatment, and outcome. In total, information was collected for 96 dogs and 41 cats. RESULTS: Fifty-three of 96 dogs and 17 of 19 cats known to have been exposed to α-chloralose-based rodenticides developed signs of central nervous system (CNS) depression or sensory-induced CNS excitation. Mortality in dogs and cats following exposure was 1% and 18%, respectively. An additional 22 cats presented with clinical signs suggestive of α-chloralose poisoning, with a mortality of 5%. LIMITATIONS: Exposure to α-chloralose was not confirmed by biochemical analyses. CONCLUSION: Dogs and especially cats were at risk of poisoning from α-chloralose. If criteria such as acute toxicity and risk of (secondary) poisoning are applied during the approval of α-chloralose-based rodenticides, similar to anticoagulant-based rodenticides, it can be concluded that α-chloralose is also not safe for non-professional use.

Comparing the Effects of Isoflurane and Alpha Chloralose upon Mouse Physiology.

Functional magnetic resonance imaging of mice requires that the physiology of the mouse (body temperature, respiration and heart rates, blood pH level) be maintained in order to prevent changes affecting the outcomes of functional scanning, namely blood oxygenation level dependent (BOLD) measures and cerebral blood flow (CBF). The anesthetic used to sedate mice for scanning can have major effects on physiology. While alpha chloralose has been commonly used for functional imaging of rats, its effects on physiology are not well characterized in the literature for any species. In this study, we anesthetized or sedated mice with isoflurane or alpha chloralose for up to two hours, and monitored physiological parameters and arterial blood gasses. We found that, when normal body temperature is maintained, breathing rates for both drugs decrease over the course of two hours. In addition, alpha chloralose causes a substantial drop in heart rate and blood pH with severe hypercapnia (elevated blood CO2) that is not seen in isoflurane-treated animals. We suggest that alpha chloralose does not maintain normal mouse physiology adequately for functional brain imaging outcome measures.

Successful treatment of capture myopathy in three wild greater sandhill cranes (Grus canadensis tabida).

Two adult and 1 juvenile free-flying greater sandhill cranes (Grus canadensis tabida) were diagnosed with capture myopathy after alpha-chloralose baiting and physical capture during a banding and feeding ecologic study. Blood samples were collected for serum biochemical analysis at the time of capture for the 2 adults, and at 24 hours postcapture, at various intervals during treatment, and at the time of release for all 3 birds. Concentrations of creatine kinase, aspartate transaminase, and lactate dehydrogenase were high within 1 hour of capture and peaked approximately 3 days after capture. By days 10-17 after capture, creatine kinase and lactate dehydrogenase concentrations both decreased to within the reference range measured for cranes at capture, but aspartate transaminase concentrations remained 2-5 times higher than the measured reference range. Treatment consisted of corticosteroids, selenium/vitamin E, parenteral fluids, and gavage feedings. Physical therapy consisted of assisting the cranes to stand and walk 2-8 times a day, massaging leg muscles, and moving limbs manually through the range of motion. The adults were released when they were able to stand up independently and were pacing in the pen. The juvenile was released 12 hours after it was able to stand independently but was returned to the pen when it fell and could not rise. It was treated supportively for an additional 3 days and then successfully released. Both adult cranes were observed on their territories with their original mates after release and returned to their territories for the subsequent 8 years, raising chicks most years. After release, the juvenile was observed in a flock of cranes near its natal territory for the next 2 days.

[Severe chloralose intoxication in a toddler]. / Intoxication sévère par le chloralose chez un nourrisson.

UNLABELLED: We report a case of an accidental intoxication in a 20-month-old boy resulting from the ingestion of a rodenticide containing alpha-chloralose. CASE REPORT: Three hours after initial admission to the pediatric emergency department for wheezing bronchitis, this patient was readmitted with a clinical presentation of respiratory insufficiency, a Glasgow coma score of 9 alternating with agitation, areflexia and unilateral mydriasis. Parental interview revealed he had episodes of shaking in the afternoon. Chest x-ray showed thoracic distension. Blood investigations, electrocardiogram, cardiac echography, brain CT scan and CSF were normal. Electroencephalography registered slow delta waves 2-3 cycles/min and an aspect of degraded waves and spikes. The patient was transferred to the intensive care unit where he fully recovered within 48 hours. A second parental interview and clinical presentation confirmed an intoxication with a rodenticide containing alpha-chloralose. The late clinical orientation did not allow us to perform a urinanalysis. DISCUSSION: Clinical association of coma, spontaneous or triggered myoclonias and bronchial hypersecretion are indicative of chloralose intoxication. Presence of specific abnormalities on electroencephalogram and a positive Fujiwara-Ross reaction in an urine sample are additional elements for the diagnosis. The prognosis is usually good after early management which combines gastric lavage, activated charcoal, sedation with benzodiazepines, tracheal intubation and artificial ventilation if required. Severe clinical cases described in voluntary intoxications in adults and teenagers occur very rarely in toddlers.

Fentanyl-fluanisone-midazolam combination results in more stable hemodynamics than does urethane alpha-chloralose and 2,2,2-tribromoethanol in mice.

Near-physiologic hemodynamic conditions for several hours were needed to study cardiovascular physiology in a murine model. We compared two commonly used anesthetic treatments, urethane alpha-chloralose (U-alphaCh; 968 mg U and 65 mg alphaCh/kg) and 2,2,2-tribromoethanol (TBE; 435 mg/kg) and fentanyl fluanisone midazolam (FFM; 3.313 mg fentanyl, 104.8 mg fluanisone, and 52.42 mg midazolam/kg) with respect to mean arterial blood pressure (MAP) and heart rate (HR) for 100 min at similar levels of surgical anesthesia. Assessed every 10 to 15 min, the U-alphaCh+TBE group maintained a significantly (P < 0.001) lower mean MAP (49 4 mmHg) than did the FFM group (78 5 mmHg). Mean HR in the U-alphaCh+TBE group significantly (P < 0.001) increased from 308 34 bpm at the beginning to 477 43 bpm at the end of the experiment. In comparison, the FFM group showed a stable HR of 431 37 bpm. The MAP and HR of the U-alphaCh+TBE group were extremely unstable, with sudden and unpredictable changes in MAP when examined at 1-min intervals. The results of our study show that U-alphaCh+TBE anesthesia should not be used in murine models in which stable, near-physiologic hemodynamics are needed for cardiovascular studies.

A review of laboratory animal anesthesia with chloral hydrate and chloralose.

Chloral hydrate (CH) and alpha-chloralose (CS) are often used to anesthetize laboratory animals although, to our knowledge, there have been no controlled studies of their anesthetic or analgesic effects. Induction of and recovery from anesthesia can be stressful, and anesthesia and analgesic quality have been questioned. Intraperitoneal (i.p.) administration of CH has resulted in adynamic ileus and peritonitis in rats, gastric ulcers in rats, and peritonitis in swine. Light anesthesia is induced in rats. In dogs, CH induces sedation to deep anesthesia when given intravenously. Gastric irritation in dogs can occur when CH is given orally. Chloral hydrate is considered a good sedative-hypnotic for farm animals. Intravenously administered CS anesthetizes dogs and cats for 5 to 10 hours, but the animals may require respiratory support. Chloralose appears to be a satisfactory anesthetic for dogs when stage III thiobarbiturate anesthesia is first induced. It is difficult to gauge the depth of anesthesia and analgesia with CS. In our clinical experience with swine and calves, CH given i.p. leads to adynamic ileus. We have found that CS given i.p. causes an inflammatory response in guinea pigs, rats, and calves. We observed that CS analgesia varies with the type of surgical procedure performed. Based on a literature review and our clinical experience, we suggest that CH or CS anesthesia should be preceded by administration of barbiturates, opioids, alpha-2 agonists, or phenothiazine tranquilizers. Chloral hydrate should only be used as a sedative or hypnotic for dogs; CS should not be used as a sole anesthetic agent. Neither drug should be used i.p. for survival surgery.

The electrophysiological effects of alpha-chloralose anesthesia in the intact dog: (1) alone and (2) in combination with verapamil.

The electrophysiological effects of alpha-chloralose anesthesia were determined in 13 chronically instrumented dogs and compared to baseline electrophysiological parameters in the conscious state. Alpha-chloralose anesthesia (75 mg/kg of a 4% solution in polyethylene glycol (PEG) delayed conduction and prolonged refractoriness of the AV node: (1) the P-R interval increased from 108 +/- 14 msec (mean +/- SD) in the conscious state to 125 +/- 23 msec (P less than 0.02); (2) the A-H from 98 +/- 12 msec to 108 +/- 16 msec (P less than 0.04); (3) the AV nodal effective refractory period from 136 +/- 16 to 153 +/- 29 msec (P = .05) and the AV nodal functional refractory period from 232 +/- 58 to 247 +/- 46 msec (P = 0.07); and (4) the AV block cycle length from 228 +/- 54 msec to 248 +/- 43 msec (P less than 0.04). Chloralose anesthesia also increased the ventricular refractory period from 139 +/- 13 msec to 161 +/- 22 msec (P less than .03) and the QTc interval from 273 +/- 22 to 306 +/- 32 msec (P less than 0.0002). To determine whether these effects on AV nodal conduction would influence experimental results, responses to verapamil were studied in the conscious state and during chloralose anesthesia. During chloralose anesthesia, (1) no relationship was detected between the sinus cycle length and verapamil concentrations; (2) a greater increment in AV conduction time was seen for a given verapamil concentration; and (3) AV block occurred at verapamil concentrations associated with 1:1 conduction in the conscious state. We conclude that chloralose anesthesia has significant electrophysiological effects and that these effects must be taken into consideration during the interpretation of experiments performed in animals during chloralose anesthesia.

Intravenous chloralose is a safe anesthetic for longitudinal use in beagle puppies.

Chloralose is an intravenous anesthetic which preserves vagal and central baroreceptor reflexes, thus rendering it useful for physiologic research. However, chloralose is recommended for terminal experiments only, due to concerns relating to long-term toxicity. We investigated the safety of chloralose in longitudinal pulmonary function studies in beagle puppies. Twelve puppies received chloralose anesthesia repeatedly (8-12 times per dog) between the ages of 80 and 300 days. Constant anesthetic depth was maintained reliably throughout the course of the experiments. Recovery lasted approximately 4 hours in each experiment and occurred in four definable stages. Following recovery, the puppies exhibited normal health and growth as compared with other colony animals. There was no biochemical evidence of acute renal, hepatic, pancreatic or cardiac toxicity prior to and immediately after anesthesia, and no evidence of chronic toxicity following completion of the study protocol, after a total cumulative dose of 1.18 g/kg chloralose. These studies demonstrate that intravenous chloralose is a safe anesthetic for longitudinal use.

Intensification of the metabolic acidosis induced under alpha-chloralose anaesthesia with graded increase in the dose.

Surgical anaesthesia between planes 2-3 with alpha-chloralose in dogs induced simultaneous depression of ventilation viz., low oxygen (PaO2) tension, high carbon dioxide (PaCO2) tension and H+ion homeostasis (high base deficit). The anaesthesia on the aforesaid planes could be achieved only by doses not below 100 mg/kg. The progressive increase in the administered dose between 100 and 200 mg/kg did not alter the acid-base profile. Further increase beyond 200 mg/kg dose was followed by a steep increase in the base deficit enhancing H+ion (cH+) concentration. However, the steep fall in PaO2 accompanied by steep rise in PaCO2 was observed only when the dose was above 250 mg/kg. The findings in the present study indicated that depression of H+ion homeostasis under chloralose anaesthesia was induced by neural mechanism independent of respiratory centres.

The effect of polyethylene glycol-200 on metabolic acidosis induced by chloralose anaesthesia.

Chloralose may be used in a 10% solution as an anaesthetic in dogs. The solubility of chloralose was found to be much higher in polyethylene glycol-200 (PEG-200) than in either warm (body temperature) or cold saline (0.9% NaCl). The intravenous (i.v.) administration of chloralose in warm saline solution induced acidosis as a result of the increase in the level of metabolic acids. The acidity generated by chloralose in almost neutral saline was probably the result of increase in the base deficit in the animal. The infusion of PEG-200 (almost neutral) significantly reduced the base deficit without disturbing the PaO2 or PaCO2 in the arterial blood. The base deficit value was significantly lower after administration of chloralose solution in PEG-200 (almost neutral) than after administration in saline. The use of PEG-200 as a solvent for chloralose was advantageous in two ways. Firstly, it prevented the production of acids in anaesthetic solution and neutralized the blood metabolic acids generated by chloralose administration in saline. Secondly, the solubility of chloralose (10% w/v solution) in PEG-200 was very much higher than in warm or cold saline.