Abstract
OBJECTIVE
This study aimed to evaluate the safety and feasibility of intranasal administration of dexmedetomidine as a premedication for preventing hypotension and hypothermia in canine patients undergoing MRI examinations.
ANIMALS
Dogs undergoing MRI examinations for neurological disorders were enrolled in this study. The dogs were randomly assigned: 15 to the N-Dex group (without premedication) and 13 to the Dex group (125 μg/m2 of dexmedetomidine, intranasally, as a premedication).
METHODS
During the examination, pulse rate, systolic blood pressure, diastolic blood pressure, and mean arterial blood pressure were recorded every 5 minutes for the first 30 minutes. Body temperature was measured before and after the examination. Any adverse events during the procedure were documented.
RESULTS
Significant changes in pulse rate during the examination were not distinguishable. Although blood pressure and body temperature decreased in both groups under anesthesia, dogs in the Dex group had a significantly smaller drop in blood pressure and body temperature and fewer hypotension events than those in the N-Dex group MRI examinations of 1 hour’s duration. Two dogs in the Dex group exhibited bradycardia at 45 and 60 minutes of MRI examination, which resolved after receiving atipamezole.
CLINICAL RELEVANCE
Our results indicate that intranasal administration of 125 μg/m2 of dexmedetomidine as premedication is safe and can potentially mitigate hypothermia and hypotension in dogs with neurological disorders during MRI examinations.
Introduction
Although the interest in using MRI to diagnose neurological disorders in dogs is increasing, the cold examination environment and prohibition of commercial active heating instruments during the procedure contribute to hypothermia. Additionally, anesthesia is commonly administered, further lowering the body temperature, causing concurrent hypotension,1–3 and impairing metabolism, immune function, circulation, and coagulation.4–6 Furthermore, the side effects of anesthesia may worsen illness in dogs with neurological disorders.7 Therefore, minimizing the risk of hypotension and hypothermia during this procedure is essential.
Previous studies8,9 have demonstrated that using an insulation device could reduce the decrease in body temperature during short-term MRI examinations. However, even with insulation, a considerable decrease in body temperature has been noted during long-term MRI examinations. Furthermore, hypotension remains a concern, particularly under anesthesia. While fluids and catecholamines are often used to manage hypotension, their use may be limited in certain cases due to potential risks such as hemodilution, hypoproteinemia, decreased oxygen transport,10 increased intracranial pressure,11,12 and increased oxygen consumption in the myocardium.13
Dexmedetomidine is a highly selective α2-adrenoreceptor agonist with sedative, anxiolytic, and analgesic effects.14 It can preserve blood pressure during inhalation anesthesia,15 reduce the minimum alveolar concentration of the inhalation anesthetic,16,17 maintain body temperature through peripheral vasoconstriction, reduce blood vessel dilation caused by isoflurane, and stabilize intracranial pressure.18–21 However, its IV and IM administration can lead to side effects such as profound bradycardia, hypertension, and hypotension due to the stimulation of the arterial baroreceptor response.22–24 Recent studies25,26 reveal that intranasal administration of dexmedetomidine in dogs is easy to operate and reduces pain during injection, preparation time, and the side effects mentioned. The nasal mucosa has a richer microvascular contact area than muscle, resulting in better drug absorption efficiency than IM administration. Furthermore, the drug acts on the CNS through the neural foramen, where the olfactory nerve enters, and affects blood distribution as well.27–29
In a previous study,26 intranasal administration of dexmedetomidine reduced the drop in body temperature in human infants during MRI examinations. Similarly, dexmedetomidine has been reported to reduce the decrease in body temperature during MRI examinations in dogs.18 However, the intranasal administration of dexmedetomidine as a preanesthetic medication for MRI examinations in dogs with neurological disorders has not been studied. Therefore, this study aimed to evaluate the safety and feasibility of the intranasal administration of dexmedetomidine to prevent hypothermia and hypotension in canine patients undergoing MRI examinations. The results of this study will broaden our knowledge of maintaining blood pressure and reducing body temperature loss during MRI examinations in dogs as well as ensure a safer process overall.
Methods
Animals
Twenty-eight dogs that underwent MRI for neurological disorders including brain or spinal cord disorders between July 2020 and February 2021 were included in the study. The inclusion criteria additionally required anesthesia risks graded as 1 to 2 on the American Society of Anesthesiologists (ASA) physical status score and no apparent abnormalities in CBC and biochemical profile. Dogs with heart disease and related clinical signs, diabetes mellitus, and intranasal masses were excluded, as were vicious dogs. This study was approved by the IACUC of National Pingtung University of Science and Technology (NPUST-110-039). Study-specific informed consent was obtained via the general client consent form at the hospital.
Procedures
The dogs were divided into 2 groups via a simple computer-generated randomization tool (Excel 2019; Microsoft Corp): those without premedication (N-Dex group) and those that received premedication with dexmedetomidine intranasally (Dex group). Of the 28 dogs, 15 and 13 were assigned to the N-Dex and Dex groups, respectively. The procedures used in this study are summarized (Figure 1). All dogs were allowed to stay in the anesthetic room next to the MRI room for at least 20 minutes before the procedure. A noninvasive oscillometric method was used to measure blood pressure throughout the study. Baseline pulse rate and systolic, diastolic, and mean arterial blood pressures were recorded using an all-in-one physiological monitor (iMEC8 Vet; Shenzhen Mindray Biomedical Electronics Co Ltd). In addition, the baseline body temperature was simultaneously measured using an electronic thermometer (Onbo Electronic; Shenzhen Co Ltd).
Summarized procedures applied in this study. A—The study procedure of the N-Dex group. B—The study procedure of the Dex group.
Citation: Journal of the American Veterinary Medical Association 262, 2; 10.2460/javma.23.06.0322
The hospital room temperature was controlled with a central air-conditioner system. The temperature in the anesthesia and recovery rooms was set between 23 and 24 °C and in the MRI room at 21 °C. No heat-preserving cover or heating device was applied to the dogs during the procedure.
A 20- or 24-gauge catheter was inserted aseptically into the cephalic vein. Dogs assigned to the Dex group were premedicated with intranasal administration of 125 μg/m2 of dexmedetomidine (Dexdomitor; Orion Corp), which was delivered through a mucosal atomization device (MAD 300; Wolfe Tory Medical Inc) connected to a 1-mL Luer lock syringe. Generally, dexmedetomidine was injected unilaterally into the nostrils within 2 seconds (Figure 2). If the total amount of the drug was more than 0.5 mL, the drug was equally divided and delivered into 2 nostrils. To prevent the dog’s head from shaking, the nostril was held briefly during administration. Sneezing or drug leakage from the nose within 5 minutes was recorded. Anesthesia was induced after 10 minutes.
Intranasal administration of dexmedetomidine using a mucosal atomization device.
Citation: Journal of the American Veterinary Medical Association 262, 2; 10.2460/javma.23.06.0322
The same anesthesia procedure for induction and maintenance was used for all dogs. Induction was started with 2-mg/kg loading boluses of propofol (Anesvan; Chi Sheng Pharma & Biotech Co Ltd), IV, followed by 1 to 2 mg/kg of propofol every 1 minute until jaw tone and laryngeal reflexes were absent. Subsequently, an experienced veterinarian performed the orotracheal intubation. A circular anesthetic rebreathing system (Aestiva/5 anesthesia machine; GE Healthcare) with intermittent positive-pressure ventilation was used to maintain end-tidal CO2 in the range of 35 to 45 mm Hg. Anesthesia was maintained with isoflurane (Terrell; Piramal Critical Care Inc) vaporized in 100% oxygen with a flow rate of 1 L/min delivered to effect. The concentration of isoflurane was managed according to the vaporizer dial setting. Initially, it was set at 2% for most dogs. The concentration of isoflurane was adjusted and maintained between 1.5% and 2.5% at the discretion of the anesthetist during the course of the MRI examination. Given the challenges of evaluating eyeball position and reflexes when the animal was wrapped with an MRI coil in the tunnel, especially during image acquisition, anesthesia depth was assessed primarily based on blood pressure, pulse rate, and body movement. If hypotension was observed, lightening anesthesia depth was recommended. Conversely, if the animal exhibited movement and increasing heart rate or blood pressure, insufficient anesthesia depth was suspected. For the safety of the anesthesia, an unblinded study design was implemented, allowing the anesthetists to be aware of all medications administered. If severe adverse events could not be reversed using conventional interventions, the duration of the imaging procedures was shortened, allowing the dogs to recover from anesthesia. Alternatively, administration of the antidote atipamezole (Antisedan; Orion Corp) would be considered.
An isotonic fluid solution (Ringer solution; Tai Yu Chemical & Pharmaceutical Co Ltd) was administered at a flow rate of 3 to 5 mL/kg/h. The dogs were then sent to the MRI room for examination 5 minutes after intubation. Owing to the varying duration of MRI examinations for each clinical case, the pulse rate and blood pressure were recorded using an all-in-one physiological monitor (Maglife Serenity; Minogue Medical Inc) every 5 minutes for the first 30 minutes (T5, T10, T15, T20, T25, and T30) in the MRI room.
The duration of each MRI examination was recorded. After the MRI examination, the dogs were sent to the recovery room, and their body temperature was measured within 5 minutes. Additionally, the duration in the MRI room was recorded as well. Then, atipamezole was administered IM to the dogs in the Dex group with the same volume as the dexmedetomidine delivered previously. Extubation was performed until the jaw tone was restored, and the extubation time was recorded from the end of isoflurane delivery to extubation. Recovery from anesthesia was closely monitored until the dogs were fully awake. Any adverse events that occurred during procedures were recorded.
Statistical analysis
All numerical data were recorded using a computer spreadsheet (Excel 2019; Microsoft Corp) and imported into Prism, version 7 (GraphPad Software Inc), for statistical analysis. All data were checked for normality of distribution using the Shapiro-Wilk test. Data are expressed as the median (range) when nonnormally distributed or mean ± SD if normally distributed. Demographic data, including patient sex, age, body weight, and body temperature, were compared via the Student t test. Between different time points and baselines in each group, pulse rate and blood pressure were analyzed using ordinary 1-way repeated ANOVA and the Kruskal-Wallis test for normally and nonnormally distributed data, respectively. An unpaired t test was used for normally distributed data and the Mann-Whitney U test for nonnormally distributed data to compare each time point between the N-Dex and Dex groups. Differences in body temperature were further compared between the dogs that underwent MRI examinations of < 1 hour and those that underwent MRI examinations of > 1 hour using an unpaired t test for normally distributed data and Mann-Whitney U test for nonnormally distributed data. The difference in body temperature between the baseline and final time points was compared via a paired t test. Values of P < 0.05 were considered significant in all analyses.
Results
Animals
Demographic data, including age, sex, body weight, body temperature, and ASA grade, were not significantly different between the groups (Table 1).
Demographic data, physical condition, disease, and baseline body temperature in the N-Dex and Dex groups.
| N-Dex group | Dex group | |
|---|---|---|
| n | 15 | 13 |
| Age (y) | 9.6 ± 3.0 | 7.6 ± 4.6 |
| Sex (n) | Male (7); female (8) | Male (4); female (9) |
| BW (kg) | 5.5 (3.0–14.7) | 8.5 (2.8–20.7) |
| BT (°C) | 38.3 ± 0.59 | 38.5 ± 0.57 |
| Breed (n) | ||
| Dachshund (5) | Dachshund (2) | |
| Maltese (3) | Crossbreed (2) | |
| Shiba Inu (1) | Pomeranian (1) | |
| Poodle (1) | Japanese Chin (1) | |
| Boston Terrier (1) | Maltese (2) | |
| Crossbreed (2) | Shiba Inu (2) | |
| Chihuahua (1) | Beagle (1) | |
| French Bulldog (1) | Corgi (1) | |
| Siberian Husky (1) | ||
| Disease (n) | ||
| Brain | Brain | |
| Inflammation (3) | Tumor (2) | |
| Idiopathic seizure (2) | Degeneration (2) | |
| Tumor (2) | Inflammation (2) | |
| Hemorrhage (1) | ||
| Idiopathic seizure (1) | ||
| Spinal | Spinal | |
| Disc (7) | Inflammation (2) | |
| Inflammation (1) | Disc (2) | |
| Tumor (1) | ||
Normally distributed data are presented as mean ± SD, and nonnormally distributed data are presented as median (range).
BT = Body temperature. BW = Body weight.
Anesthesia
Although the sedation score was not evaluated in this study, dogs that received premedication with intranasal dexmedetomidine showed no obvious changes in behavior in response to light sedation. The delivered dose of propofol for induction was 10.0 mg/kg (range, 4.8 to 14.3 mg/kg) in the N-Dex group and 9.6 mg/kg (range, 6.7 to 21.4 mg/kg) in the Dex group. There was no significant difference in the delivered dose of propofol between groups (P = .9728). The dogs stayed in the MRI examination room for 66.1 ± 21.0 minutes in the N-Dex group and 58.3 ± 18.1 minutes in the Dex group. The extubation time was 16.6 ± 10.4 minutes in the N-Dex group and 16.8 ± 7.1 minutes in the Dex group. There were no significant differences in the time the dogs stayed in the MRI examination room (P = .3042) or in the extubation time (P = .9604) between the groups.
Pulse rate, blood pressure, and body temperatures
Physiological data are presented (Table 2). Compared with the baseline, there were no significant differences in the N-Dex group’s pulse rate at different time points. In contrast, the pulse rate significantly decreased at T25 and T30 in the Dex group. Among the different time points within the group, the pulse rate was significantly higher in the N-Dex group at T5.
Physiological variables over time in the Dex and N-Dex groups.
| Variable | Group | Time points | ||||||
|---|---|---|---|---|---|---|---|---|
| TB | T5 | T10 | T15 | T20 | T25 | T30 | ||
| Pulse rate (bpm) | N-Dex | 106 ± 26.9 | 116 ± 33.4* | 104 ± 28.7 | 93 ± 25.5 | 92 ± 23.7 | 92 ± 22.5 | 93 ± 25.3 |
| Dex | 103 ± 17.2 | 87 ± 27.7* | 84 ± 24.0 | 83 ± 23.3 | 83 ± 20.5 | 79 ± 19.8† | 80 ± 20.1† | |
| MAP | N-Dex (mm Hg) | 119 ± 28.3 | 63 ± 19.0*† | 64 ± 18.8*† | 59 ± 14.2*† | 59 ± 17.7*† | 60 ± 15.9*† | 60 ± 12.2*† |
| Dex | 108 ± 14.1 | 85 ± 15.4*† | 81 ± 12.3*† | 80 ± 14.0*† | 84 ± 11.0*† | 82 ± 13.3*† | 83 ± 13.5*† | |
| Sys BP (mm Hg) | N-Dex | 146 (100–212) | 99 (59–123)*† | 105 (59–124)† | 92 (60–105)*† | 85 (62–125)*† | 91 (62–111)*† | 89 (66–107)*† |
| Dex | 140 (118–203) | 117 (74–203)*† | 106 (76–127)† | 110 (90–124)*† | 106 (89–125)*† | 104 (90–124)*† | 102 (86–127)*† | |
| Dia BP (mm Hg) | N-Dex | 100 ± 33.9 | 41 ± 14.9*† | 42 ± 16.7*† | 41 ± 14.5*† | 40 ± 13.6*† | 41 ± 12.7*† | 41 ± 12.2*† |
| Dex | 92 ± 20.1 | 66 ± 13.5*† | 61 ± 14.6*† | 62 ± 13.8*† | 63 ± 15.6*† | 67 ± 11.6*† | 65 ± 13.7*† | |
Normally distributed data are presented as mean ± SD, and nonnormally distributed data are presented as median (range).
*Significant difference between groups (P < .05). †Significant difference compared to the baseline value (P < .05). bpm = Beats per minute. Dia BP = Diastolic blood pressure. T5 = 5 minutes after the dogs were presented in the MRI room. T10 = 10 minutes after the dogs were presented in the MRI room. T15 = 15 minutes after the dogs were presented in the MRI room. T20 = 20 minutes after the dogs were presented in the MRI room. T25 = 25 minutes after the dogs were presented in the MRI room. T30 = 30 minutes after the dogs were presented in the MRI room. MAP = Mean arterial pressure. Sys BP = Systolic blood pressure. TB = Baseline.
Systolic blood pressure was significantly higher in the Dex group than in the N-Dex group at T5, T15, T20, T25, and T30. Diastolic and mean blood pressures were significantly higher in the Dex group at all time points. Compared with baseline, systolic, diastolic, and mean blood pressures significantly decreased at all time points in both groups.
The body temperature in N-Dex and Dex groups dropped significantly when the MRI examination ended (36.3 ± 0.8 °C [P < .0001]; 36.9 ± 1.1 °C [P = .0011]), but there was no significant difference between groups (P = .1202). Five and 7 dogs in the N-Dex and Dex groups, respectively, underwent MRI within 1 hour. After MRI examination, the dogs in the Dex group had significantly higher body temperatures (36.9 ± 0.5 °C) than the dogs in the N-Dex group (36.2 ± 0.5 °C; P = .0354). In contrast, no significant difference in body temperature was observed in dogs with an examination time > 1 hour (P = .7411). Nevertheless, at the end of the examination, the body temperature was significantly lower than the baseline in all groups (Figure 3).
Changes in body temperature of the N-Dex and Dex groups. The plots show the mean ± SD of the value range at scalar time points in the N-Dex group (●) and Dex group (▽). A—Compared N-Dex and Dex groups in < 1 hour. B—Compared N-Dex and Dex groups in over 1 hour. *Significant difference between groups (P < .05). †Significant difference compared to the baseline value (P < .05).
Citation: Journal of the American Veterinary Medical Association 262, 2; 10.2460/javma.23.06.0322
Adverse events
None of the dogs experienced severe adverse anesthesia events during data acquisition. The recruited dogs generally were all amenable to the procedure of intranasal administration. No instances of sneezing were observed during the procedures. Although some dogs exhibited mild scratching of the nose with their front paw after drug administration, no evidence of drug leakage from the nose was observed.
A total of 37 hypotension (mean arterial pressure < 60 mm Hg) events were noted in 90 measurements in the N-Dex group, while there was only 1 hypotension event in 78 measurements in the Dex group during the first 30 minutes. Typically, reducing the concentration of isoflurane and increasing the fluid rate would be attempted to restore the blood pressure. However, 2 dogs in the Dex group exhibited notable bradycardia, with pulse rates of 49 and 46 beats/min at 45 and 60 minutes, respectively, after intranasal administration of dexmedetomidine. Following the administration of atipamezole, the pulse rate returned to 60 to 70 beats/min within 5 minutes, and the MRI examination was completed without further complications. All dogs enrolled in this study were discharged on the same day as the examination. After the MRI examination, no unexpected symptoms of discomfort were reported in any dog.
Discussion
This study evaluated the effects of intranasal dexmedetomidine as premedication in dogs with neurological disorders during MRI examination. The cold environment and conventional anesthesia schedule impaired thermoregulation and lowered blood pressure in the dogs during the examination. However, the dogs that received intranasal dexmedetomidine were better able to preserve their body temperature and blood pressure. Intranasal administration was well tolerated by the selected dogs and was easy to perform. This study highlights the potential clinical advantages and safety of intranasal dexmedetomidine in canine patients undergoing MRI examinations.
Previous studies have shown that nasal blood flow is affected by factors such as inflammation, trauma, and humidity.30 Therefore, dogs with nasal diseases may have altered absorption rates following intranasal administration. In addition, intranasal administration is not recommended for dogs with nasal tumors. The administration technique requires holding the dog’s snout, which makes it unsuitable for fierce, nervous, or aggressive dogs. Restraints that immobilize the head and neck are not suitable for certain dogs, and in those cases this method may not be applicable. Additionally, this study found that it was challenging to administer medication through the intranasal route to short-muzzled dogs because of the difficulties in placing the mucosal atomization device into their nostrils, potentially leading to delivery failure of the drug into the nasal cavity.
Intranasal administration of dexmedetomidine doses used in this study was calculated according to the body surface area method rather than the body weight. Body surface area is a more accurate method of drug calculation that can reduce the risk of insufficiency or overdose and improve the metabolic rate of drugs in the body.31,32 A dose of 125 μg/m2 of dexmedetomidine was used in this study, which could be converted to the median dose by 0.006 mg/kg (range, 0.005 to 0.008 mg/kg). This dosage was notably lower than a previous study24 that used a dose of 0.02 mg/kg in dogs, which demonstrated an effective sedation effect. Although the sedative effects were barely observed at the dose of 125 μg/m2, the effects on blood pressure and body temperature were present. Furthermore, a low dose of dexmedetomidine could minimize the potential anesthesia risks in dogs with underlying diseases. Considering the protocols of this study revealed its effectiveness and safety, it is believed the dose of 125 μg/m2 is adequate for clinical use on dogs with neurological diseases that underwent MRI examination.
One study33 found that dexmedetomidine when administered intramuscularly as premedication, either alone or in combination with midazolam or methadone, had a significant propofol-sparing effect during induction. However, this effect was not observed when dexmedetomidine was delivered intranasally in this study. A recent study34 reported that administering dexmedetomidine at a dose of 5 μg/kg intranasally resulted in a mild sedative effect within approximately 10 minutes, and the sedation effect was found to be at its highest level at 30 minutes after administration. The induction procedure was initiated 10 minutes after the administration of dexmedetomidine in this study. However, this timing might have been insufficient to provide an adequate propofol-sparing effect. In addition, the isoflurane-sparing effect was not evaluated because the isoflurane concentration was adjusted based on the vaporizer scale, which may not have accurately reflected the actual concentration in the breathing circuit.
Protocols involving the use of propofol and isoflurane for general anesthesia in dogs can cause dose-dependent vasodilator effects and easily decrease myocardial contractility, leading to hypotension and increased heart rate.35 Hypothermia during MRI examinations can increase catecholamine secretion, causing vasoconstriction and a decreased heart rate.36 The opposite effects may neutralize changes in the heart rate of dogs without the application of intranasal dexmedetomidine during premedication. This may explain why a significant difference in heart rate between the groups was observed in only the first 5 minutes, after which the effect of propofol diminished. Although bradycardia is a common side effect of IM or IV dexmedetomidine administration, the decrease in pulse rate from baseline was seen only in dogs with intranasal dexmedetomidine 25 minutes after MRI examination, while there were no significant differences with the dogs without dexmedetomidine administration. The results indicated that intranasal dexmedetomidine had a low impact on the pulse rate. This can be attributed to the limited systemic distribution of the drug via the intranasal administration route, which results in fewer α2 adrenoreceptor agonist effects.24
The study reported here showed a significant decrease in blood pressure in both groups of dogs during MRI examination. However, dogs premedicated with intranasal dexmedetomidine exhibited higher blood pressure and were less likely to experience hypotensive episodes (mean arterial pressure < 60 mm Hg) in the first 30 minutes. Hypotension during anesthesia can lead to various complications, such as cerebral edema, increased intracranial pressure, ischemia of the liver and kidney, spinal cord ischemia, and hypoxia, which should be avoided. Previous studies have shown that systolic and diastolic blood pressures in dogs can be elevated by vasoconstriction after IV administration of dexmedetomidine and decrease over time.14 In contrast, intranasal administration of dexmedetomidine can result in more stable blood pressure variation.37 Therefore, using intranasal dexmedetomidine as a premedication can reduce the likelihood of hypotension when anesthesia protocols are administered with propofol and isoflurane during an MRI examination.
A significant decrease in body temperature from the baseline was noted in both groups of dogs. However, dogs administered intranasal dexmedetomidine showed a higher body temperature when the MRI examination ended within 1 hour. It is believed that this was due to the peripheral vasoconstriction effect of dexmedetomidine, which reduced the decrease in body temperature.18 Significant heat loss under general anesthesia can be observed in the first hour (rapid phase) from heat redistribution, followed by a linear phase of heat evaporation.8 Although intranasal administration of dexmedetomidine can help prevent heat loss, it is not entirely effective in maintaining body temperature, particularly during MRI examinations lasting longer than 1 hour. Furthermore, although the effect of dexmedetomidine has been reported to last for up to 2 hours,22 a cold environment could still accelerate heat loss and reduce the benefits of the medication. A previous report8 indicated that insulating materials could significantly prevent hypothermia during MRI examinations in dogs and cats. Therefore, combining insulating materials with intranasal dexmedetomidine administration may provide a synergistic effect for heat preservation.
During the MRI examination, 2 dogs with brain-associated disorders experienced bradycardia at 45 and 60 minutes, which resolved after the IM administration of atipamezole. The causes of bradycardia may include hypothermia, intracranial pressure increase, the cardiovascular inhibitory effect of isoflurane, or side effects of dexmedetomidine.35,38 As the heart rates of these 2 dogs significantly improved within 5 minutes of atipamezole administration, it was believed that the main cause of bradycardia was the administration of dexmedetomidine. In addition, none of the dogs died or had extended extubation and recovery time from anesthesia after the intranasal administration of dexmedetomidine. This indicated that the intranasal administration of 125 μg/m2 of dexmedetomidine in dogs with neurological disorders undergoing MRI examination was adequate and safe.
This study had several limitations. First, only dogs with a low ASA grade were included, so the safety and efficacy of intranasal dexmedetomidine administration in dogs with higher ASA grades or specific neurological diseases remain unknown. Second, the study did not compare the efficacy of different doses of dexmedetomidine or investigate its analgesic effects. Third, the study’s unblinded design could potentially give rise to subjective bias, particularly concerning the adjustment of isoflurane concentration during MRI procedures. Fourthly, the comparison of blood pressure and heart rate was limited to the initial 30 minutes, despite the potential for the effects of intranasally administered dexmedetomidine over the duration of the procedure, potentially leading to diminishing impact as time progresses. Therefore, dexmedetomidine’s ability to maintain blood pressure for more than 30 minutes in a constant cold environment is not yet established. Finally, this clinical trial had a small sample size, highlighting the need for larger studies to validate these findings. Despite these limitations, valuable practical information was obtained through the evaluation of clinical cases in this study.
In conclusion, the results of this study indicated that intranasal administration of 125 μg/m2 of dexmedetomidine as premedication for MRI examination is a technique with low difficulty and high safety in dogs with neurological disorders. This procedure can help maintain blood pressure and reduce body temperature loss when propofol and isoflurane are used in anesthesia protocols. No conventional side effects of dexmedetomidine, such as bradycardia or hypertension, were observed. However, physiological parameters should be closely monitored during anesthesia, and atipamezole can be used to antagonize the potential side effects.
Acknowledgments
The authors thank the UniCore Animal Hospital, Taipei City, Taiwan.
Disclosures
The authors have nothing to disclose. No AI-assisted technologies were used in the generation of this manuscript.
Funding
The authors have nothing to disclose.
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