Standing sedation in captive zebra (Equus grevyi and Equus burchellii)

Nine Grevy's zebras (Equus grevyi) and three Burchell's zebras (Equus burchellii) were immobilized in a standing position a total of 70 times for minor, nonpainful procedures over a 9-yr period. Standing sedation was successfully obtained with a combination of detomidine and butorphanol on 47 occasions (67.1%). Detomidine i.m. (median 0.10 mg/kg; range: 0.07-0.21) was administered by dart, followed 10 min later by butorphanol i.m. (median 0.13 mg/kg; range 0.04-0.24). The dosages were varied depending on the initial demeanor of the animal. On 23 occasions (32.9%), small amounts of etorphine (median 2.5 microg/kg; range 1.1-12.3 microg/kg) plus acepromazine (median 10 microg/kg; range 4.4-50 microg/kg) (as in Large Animal-Immobilon) had to be administered i.m. to gain sufficient sedation. In these latter cases, the animals were either excited or known for their aggressive character. The zebras were sufficiently immobilized for the length of most procedures (<45 min) without supplementation. At the end of the procedure, the animals were given atipamezole (2 mg per 1 mg detomidine used) and naltrexone (0.1 mg/kg) to reverse the sedative effects, irrespective of whether etorphine was used or not. Standing sedation, using the combination of the alpha-2 agonist detomidine and the partial agonist-antagonist opioid butorphanol (in some cases supplemented with etorphine + acepromazine), proved to be a very efficacious and safe method to be used in zebras under zoo conditions for short-lasting, nonpainful procedures.     

Atipamezole in the management of detomidine overdose in a pony

OBSERVATIONS: A pony undergoing elective castration accidentally received an overdose of IV detomidine (200 microg kg(-1)) before anaesthesia was induced with ketamine and midazolam. A further 100 microg kg(-1) IV dose of detomidine was administered during anaesthesia. The mistake was recognized only when the animal failed to recover from anaesthesia in the expected time. The overdose (300 microg kg(-1) in total) was treated successfully with atipamezole, initially given IV and subsequently IM and titrated to effect to a total dose of 1100 microg kg(-1). The pony regained the standing position. A further injection of atipamezole (76 microg kg(-1) IM) was given 5 hours later to counteract slight signs of re-sedation. CONCLUSIONS: Atipamezole proved an effective antagonist for detomidine in a pony at an initial dose 3.65 x and a final total dose 3.9 x greater than the alpha2 agonist.     

Rectal prolapse associated with a healed pelvic fracture in a pregnant free-ranging African black rhinoceros (Diceros bicornis). Part 1: anaesthesia

Anaesthesia was required in a heavily-pregnant, adult, free-ranging African black rhinoceros Diceros bicornis with a rectal prolapse for examination and possible treatment. The animal was immobilised with 4.5 mg etorphine and 60 mg azaperone. For continued observation, the immobilised animal was transported to a boma. Additional etorphine and azaperone were administered to keep the animal anaesthetised during treatment and transport. In addition, 15 mg nalorphine was administered during this time to improve ventilation and reduce muscle rigidity. Sixty hours later, in preparation for surgery, 2.5 mg etorphine and 40 mg azaperone were administered, followed by endotracheal intubation and halothane anaesthesia. During anaesthesia, a decrease in tidal volume was observed. Venous blood-gas analysis indicated a decrease in the oxygen partial pressure, and a mixed respiratory and metabolic acidosis. Cardiac arrest was preceded by an increase in heart rate and tidal volume after 80 min of inhalation anaesthesia.     

Cardiopulmonary effects of romifidine and detomidine used as premedicants for ketamine/halothane anaesthesia in ponies

The cardiopulmonary effects of romifidine at 80 microg/kg (R80) or 120 pg/kg (R120), and detomidine at 20 pg/kg (D20) when used as premedicants for ketamine/halothane anaesthesia were investigated in six ponies. Using a blinded crossover design, acepromazine (0-04 mg/kg) was administered followed by the alpha-2 agonist. Anaesthesia was induced with ketamine at 2.2 mg/kg and maintained with halothane (expired concentration 1.0 per cent) in oxygen for three hours. During anaesthesia, arterial blood pressure, cardiac index, PaO2 and PmvO2 decreased, and systemic vascular resistance and PaCO2 increased. The cardiac indices for R80, R120 and D20 were, respectively, 39, 39 and 32 ml/kg/minute at 30 minutes and 29, 29 and 26 ml/kg/minute at 180 minutes. The alpha-2 agonists had similar cardiovascular effects, but PaO2 was significantly lower with R120. The quality of anaesthesia was similar in all three groups.     

Comparison of etorphine-detomidine and medetomidine-ketamine anesthesia in captive addax (Addax nasomaculatus).

Thirty-five anesthetic events involving 15 captive addax (Addax nasonzaculatus) were performed between August 1998 and February 2002 using a combination of etorphine (33.7 +/- 7.9 microg/kg) and detomidine (21.9 +/- 4.6 microg/ kg) or a combination of medetomidine (57.4 +/- 8.6 microg/kg) and ketamine (1.22 +/- 0.3 microg/kg), with or without supplemental injectable or inhalant anesthetic agents. Etorphine-detomidine anesthesia was antagonized with diprenorphine (107.1 +/- 16.4 microg/kg) and atipamezole (100.9 +/- 42.4 microg/kg). Medetomidine-ketamine anesthesia was antagonized with atipamezole (245.3 +/- 63.4 microg/kg). Animals became recumbent within 5 min when the combination of etorphine and detomidine was used and within 11 min when the combination of medetomidine and ketamine was used. Both drug combinations were suitable for use as primary immobilizing agents producing short-duration restraint and analgesia. Bradycardia was noted with both combinations. Further investigation of the cardiopulmonary effects of both combinations is warranted.     

Repeated chemical immobilization of a captive greater one-horned rhinoceros (Rhinoceros unicornis), using combinations of etorphine, detomidine, and ketamine.

An adult, 23 yr-old, male greater one-horned rhinoceros (Rhinoceros unicornis) was repeatedly immobilized with combinations of etorphine, detomidine, and ketamine to provide medical and surgical care to chronic, bilateral, soft tissue lesions on the hind feet and to collect semen by electroejaculation. The rhinoceros was successfully immobilized on 24 occasions over a 55 mo period at approximately 8-10 wk intervals, 17 times with a combination of etorphine and detomidine (M99-D, i.m.) by projectile dart and seven times with a combination of etorphine, ketamine, and detomidine (M99-K-D, i.m.) by pole syringe. The combination of etorphine, detomidine, and ketamine repeatedly and safely induced prolonged anesthesia, and a suitable drug combination includes 3.5-3.8 mg etorphine, 14 mg detomidine, and 400 mg ketamine (M99-K-D) administered i.m. into the neck.     

Evaluation of combinations of nalbuphine with acepromazine or detomidine for sedation in ponies

The effect of combinations of nalbuphine (0.3 mg/kg) with either detomidine (10 μg/kg) or acepromazine (50 μg/kg) was investigated in ponies. Nalbuphine enhanced the degree of sedation produced by both sedatives; sedation with detomidine and nalbuphine was profound. Cardiovascular and respiratory effects were mild and could usually be attributed to the effect of the sedative itself. Side effects were minimal and gave no cause for concern. It was concluded that nalbuphine, in combination with acepromazine or detomidine, is a safe and effective sedative for use in ponies.     

Stress responses during total intravenous anaesthesia in ponies with detomidine - guaiphenesin - ketamine

Six ponies were anaesthetised for two hours with intermittent injections of a combination of guaiphenesin (72 mg/kg/hr), ketamine (1.4 mg/kg/hr) and detomidine (0.015 mg/kg/hr) after premedication with detomidine 0.01 mg/kg and induction of anaesthesia with guaiphenesin 50 mg/kg and ketamine 2 mg/kg. Induction of anaesthesia was smooth, the ponies were easily intubated and after intubation breathed 100% oxygen spontaneously. During anaesthesia mean pulse rate ranged between 31–44 beats per minute and mean respiratory rate between 12–23 breaths per minute. Mean arterial blood pressure remained between 110–130 mm Hg, mean arterial carbon dioxide tension between 6.1–6.9 kPa and pH between 737–7.42. Arterial oxygen tension was over 23 kPa throughout anaesthesia. Plasma glucose increased to more than 25 mmol per litre during anaesthesia; there was no change in lactate or ACTH concentration and plasma cortisol concentration decreased. Recovery was rapid and smooth. A guaiphenesin, ketamine and detomidine combination appeared to offer potential as a total intravenous technique for maintenance of anaesthesia in horses.     

Cardiorespiratory, endocrine and metabolic changes in ponies undergoing intravenous or inhalation anaesthesia

Six Welsh gelding ponies (weight 246 ± 6 kg) were premedicated with 0.03 mg/kg of acepromazine intravenously (i.v.) followed by 0.02 mg/kg of detomidine i.v. Anaesthesia was induced with 2 mg/kg of ketamine i.v. Ponies were intubated and lay in left lateral recumbency. On one occasion anaesthesia was maintained for 2 h using 1.2% halothane in oxygen. The same group of ponies were anaesthetized 1 month later using the same induction regime and anaesthesia was maintained with a combination of detomidine, ketamine and guaiphenesin, while the ponies breathed oxygen-enriched air. Electrocardiogram, heart rate, mean arterial blood pressure, cardiac output, respiratory rate, blood gases, temperature, haematocrit, glucose, lactate and cortisol were measured and cardiac index and systemic vascular resistance were calculated in both groups. Beta-endorphin, met-enkephalin, dynorphin, arginine vasopressin (AVP), adrenocorticotrophic hormone (ACTH) and catecholamines were measured in the halothane anaesthesia group only and 11-deoxycortisol during total intravenous anaesthesia (TIVA) only. Cardiorespiratory depression was more marked during halothane anaesthesia. Hyperglycaemia developed in both groups. Lactate and AVP increased during halothane anaesthesia. Cortisol increased during halothane and decreased during TIVA. There were no changes in the other hormones during anaesthesia. Recovery was smooth in both groups. TIVA produced better cardiorespiratory performance and suppressed the endocrine stress response observed during halothane anaesthesia.     

Surgical management of rectal prolapse in an Indian rhinoceros (Rhinoceros unicornis).

An acute rectal mucosal prolapse in a 26-yr-old Indian rhinoceros (Rhinoceros unicornis) was repaired surgically by mucosal resection. Two days postoperatively, suture line dehiscence accompanied by substantial hemorrhage was managed by ligation and hemostasis during a second immobilization. Medical management with nonsteroidal anti-inflammatory drugs and diuretics reduced the mucosal edema and prevented recurrence of the prolapse. A combination of butorphanol and detomidine provided excellent reversible chemical restraint for this animal.     

Comparison of two combinations of sedatives before anaesthetising pigs with halothane and nitrous oxide

Two groups of 21 three-month-old Landrace x Large White pigs were sedated with either azaperone (2 mg/kg), butorphanol (0.2 mg/kg) and ketamine (5 mg/kg) (group A), or detomidine (100 microg/kg), butorphanol (0.2 mg/kg) and ketamine (5 mg/kg) (group D) administered intramuscularly, before being anaesthetised with halothane, oxygen and nitrous oxide for a bilateral stifle arthrotomy. The pigs' heart rate, respiratory rate, mean arterial blood pressure, electrocardiogram, arterial oxygen saturation, arterial blood gases, and oesophageal and rectal temperature were measured while they were anaesthetised and five minutes after they were disconnected, and their recovery times and any complications were recorded. Both groups were well sedated. Their heart rate was unchanged during the period of anaesthesia but increased when they recovered. The respiratory rate, mean arterial blood pressure and rectal temperature were lower in group A than in group D (P<0.05). Mild respiratory acidosis developed during anaesthesia in both groups. Both groups recovered equally rapidly and complications were generally minor, though two pigs in group D appeared to develop malignant hyperthermia.     

Electroencephalographic and cardiovascular variables as nociceptive indicators in isoflurane-anaesthetized horses

OBJECTIVE: To evaluate Fourier-transformed electroencephalographic (EEG) variables, mean arterial blood pressure (MAP) and pulse rate as nociceptive indicators in isoflurane-anaesthetized horses. ANIMALS: Five standardbred and three Norwegian cold-blooded trotter stallions undergoing castration, aged 2-4 years, mass 378-538 kg. MATERIALS AND METHODS: All horses received intravenous (IV) detomidine (10 microg kg(-1) IV) and butorphanol (0.01 mg kg(-1) IV). Additional detomidine (4 microg kg(-1) IV) was administered in the induction area. Anaesthesia was induced with ketamine (2.5 mg kg(-1) IV) and diazepam (40 microg kg(-1) IV), and maintained for 30 minutes with isoflurane (end-tidal concentration of 1.4%) vaporized in oxygen. The electroencephalogram, MAP and pulse rate were recorded for 15 minutes, beginning 5 minutes before skin incision. Differences between the mean values of recordings taken before, and during surgery were calculated and tested for significant differences using a two-sided Student's t-test. RESULTS: A significant rise in MAP and a fall in pulse rate were found. No significant change was found in any EEG variable. CONCLUSION/CLINICAL relevance Of the variables evaluated, MAP seems to be the most sensitive and reliable indicator of nociception in isoflurane-anaesthetized horses.     

The Stress Responses Involved in General Anaesthesia in Cattle

Anaesthesia was induced in four adult Friesian cows with intravenous thiopentone (10 mg/kg) after either intramuscular saline (2ml), acepromazine (0.05mg/kg) or xylazine pre- medication (0.05 mg/kg). At least 4 weeks was allowed to alapse between each anaesthetic in each cow. The stress involved in induction of and recovery from anaesthesia was assessed by measuring pulse and respiration rates, plasma cortisol and glucose concentrations, total plasma protein concentration and haematocrit at 10–15 minute intervals from 60 min prior to premedication to the time when the animals stood after anaesthesia. Recovery from anaesthesia was associated with an increase in cortisol concentration. This response was significantly attenuated by premedication with xylazine but not acepromazine. Xylazine produced a marked hyperglycaemia in comparison to the other premedicants. Anaesthesia was associated a marked increase in pulse rate and slight increase in haematocrit, but these changes were not markedly affected by the premedication given. Recovery from anaesthesia was deemed to be the most stressful period of short-term general anaesthesia.     

The effects of xylazine,detomidine, acepromazine and butorphanol on equine solid phase gastric emptying rate

The aim of this study was to measure the effects of specific commonly used sedative protocols on equine solid phase gastric emptying rate, using the 13C-octanoic acid breath test (13C-OABT). The gastric emptying of a standard 13C-labelled test meal was measured once weekly in 8 mature horses over two 4 week treatment periods. Each horse acted as its own control. In treatment Period 1, saline (2 ml i.v.), xylazine (0.5 mg/kg i.v.), detomidine (0.01 mg/kg i.v.) or detomidine/butorphanol combination (0.01/0.02 mg/kg i.v.) was administered in randomised order after ingestion of the test meal. During treatment Period 2, test meal consumption was followed by saline, xylazine (1.0 mg/kg i.v.), or detomidine (0.03 mg/kg i.v.) administration, or preceded by acepromazine (0.05 mg/kg i.m.) in randomised order. The 13C:12C ratio of sequential expiratory breath samples was determined by isotope ratio mass spectrometry, and used to measure the gastric half-emptying time, t 1/2, and duration of the lag phase, t lag, for each of the 64 tests. In treatment Period 1, detomidine/butorphanol prolonged both t 1/2 and t lag with respect to xylazine 0.5 mg/kg and the saline control (P < 0.05). In Period 2, detomidine 0.03 mg/kg delayed each parameter with respect to saline, acepromazine and xylazine 1.0 mg/kg (P < 0.001). Xylazine 1.0 mg/kg also lengthened t lag relative to the saline control (P = 0.0004), but did not cause a significant change in t 1/2. Comparison of treatment periods showed that the inhibitory effect of detomidine on gastric emptying rate was dose related (P<0.05). These findings may have clinical significance for case selection when these agents are used for purposes of sedation and/or analgesia.     

The effects of detomidine, romifidine or acepromazine on echocardiographic measurements and cardiac function in normal horses

OBJECTIVE: To evaluate by echo- and electrocardiography the cardiac effects of sedation with detomidine hydrochloride, romifidine hydrochloride or acepromazine maleate in horses. STUDY DESIGN: An experimental study using a cross-over design without randomization. ANIMALS: Eight clinically normal Standardbred trotters. MATERIALS AND METHODS: Echocardiographic examinations (two-dimensional, guided M-mode and colour Doppler) were recorded on five different days. Heart rate (HR) and standard limb lead electrocardiograms were also obtained. Subsequently, horses were sedated with detomidine (0.01 mg kg(-1)), romifidine (0.04 mg kg(-1)) or acepromazine (0.1 mg kg(-1)) administered intravenously and all examinations repeated. RESULTS: Heart rate before treatment with the three drugs did not differ significantly (p = 0.98). Both detomidine and romifidine induced a significant decrease (p < 0.001) in HR during the first 25 minutes after sedation; while acepromazine had a varying effect on HR. For detomidine, there was a significant increase in LVIDd (left ventricular internal diameter in diastole; p = 0.034) and LVIDs (left ventricular internal diameter in systole; p < 0.001). In addition, a significant decrease was found in IVSs (the interventricular septum in systole; p < 0.001), LVFWs (the left ventricular free wall in systole; p = 0.002) and FS% (fractional shortening; p < 0.001). The frequency of pulmonary regurgitation was increased significantly (p < 0.001). Romifidine induced a significant increase in LVIDs (p < 0.001) and a significant decrease in IVSs (p < 0.001) and FS% (p = 0.002). Acepromazine had no significant effect upon any of the measured values. CONCLUSIONS: and clinical relevance The results indicate that sedation of horses with detomidine and to a lesser extent romifidine at the doses given in this study has a significant effect on heart function, echocardiographic measurements of heart dimensions and the occurrence of valvular regurgitation. Although the clinical significance of these results may be minimal, the potential effects of sedative drugs should be taken into account when echocardiographic variables are interpreted in clinical cases.     

Cardiovascular effects of medetomidine, detomidine and xylazine in horses

The cardiovascular effects of medetomidine, detomidine, and xylazine in horses were studied. Fifteen horses, whose right carotid arteries had previously been surgically raised to a subcutaneous position during general anesthesia were used. Five horses each were given the following 8 treatments: an intravenous injection of 4 doses of medetomidine (3, 5, 7.5, and 10 microg/kg), 3 doses of detomidine (10, 20, and 40 microg/kg), and one dose of xylazine (1 mg/kg). Heart rate decreased, but not statistically significant. Atrio-ventricular block was observed following all treatments and prolonged with detomidine. Cardiac index (CI) and stroke volume (SV) were decreased with all treatments. The CI decreased to about 50% of baseline values for 5 min after 7.5 and 10 microg/kg medetomidine and 1 mg/kg xylazine, for 20 min after 20 microg/kg detomidine, and for 50 min after 40 microg/kg detomidine. All treatments produced an initial hypertension within 2 min of drug administration followed by a significant decrease in arterial blood pressure (ABP) in horses administered 3 to 7.5 microg/kg medetomidine and 1 mg/kg xylazine. Hypertension was significantly prolonged in 20 and 40 microg/kg detomidine. The hypotensive phase was not observed in 10 microg/kg medetomidine or detomidine. The changes in ABP were associated with an increase in peripheral vascular resistance. Respiratory rate was decreased for 40 to 120 min in 5, 7.5, and 10 microg/kg medetomidine and detomidine. The partial pressure of arterial oxygen decreased significantly in 10 microg/kg medetomidine and detomidine, while the partial pressure of arterial carbon dioxide did not change significantly. Medetomidine induced dose-dependent cardiovascular depression similar to detomidine. The cardiovascular effects of medetomidine and xylazine were not as prolonged as that of detomidine. KEY WORDS: cardiovascular effect, detomidine, equine, medetomidine, xylazine.     

Neuroleptanalgesia in wild Asian elephants (Elephas maximus maximus)

OBJECTIVE: To evaluate the suitability of etorphine with acepromazine for producing prolonged neuroleptanalgesia in wild Asian elephants. ANIMALS: Ten adult wild elephants (four males, six females), free-roaming in the jungles of the north-western province of Sri Lanka. MATERIALS AND METHODS: Ten wild elephants were tranquilized for attachment of radio transmitter collars from September to November 1997, using Large-Animal Immobilon (C-Vet Veterinary Products, Leyland, UK), which is a combination of etorphine (2.45 mg mL(-1)) and acepromazine (10 mg mL(-1)). This was injected using projectile syringes fired from a Cap-Chur gun (Palmer Chemical Co. Inc., Atlanta, USA). A volume of 3.3 (2.5-4.5) mL Immobilon (6.12-11.02 mg of etorphine and 25-45 mg acepromazine) was injected intramuscularly after body mass estimation of individual elephants. RESULTS: The body condition of all darted elephants was good, and the mean (minimum-maximum) shoulder height was 225 (180-310) cm. The average approximate distance to elephants at firing was 26 (15-50) m. The average time to recumbency after injection was 18 (15-45) minutes. Nine out of 10 elephants remained in lateral recumbency (and did not require additional dosing) for a period of 42 (28-61) minutes. The respiratory and heart rates during anaesthesia were 7 (4-10) breaths and 52 (40-60) beats minute(-1), respectively. An equal volume (8.15-14.67 mg) of diprenorphine hydrochloride (Revivon, 3.26 mg mL(-1) diprenorphine; C-Veterinary Products, Leyland, UK) was given intravenously when the procedure was completed. Recovery (return to standing position) occurred in 6 (2-12) minutes after diprenorphine injection. Immediately afterwards, all elephants slowly retreated into the jungle without complications. Continuous radio tracking of the animals involved in this study indicated no post-operative mortality for several months after restraint. CONCLUSIONS/CLINICAL RELEVANCE: Etorphine-acepromazine combinations can be used safely in healthy wild Asian elephants for periods of restraint lasting up to 1 hour.     

Anaesthesia of nyala (Tragelaphus angasi) with a combination of thiafentanil (A3080), medetomidine and ketamine

A combination of thiafentanil (A3080), medetomidine hydrochloride (MED) and ketamine hydrochloride (KET) was evaluated in 19 boma-habituated (12 female and 7 males) and 9 free-ranging nyala (7 male and 2 females) (Tragelaphus angasi) to develop a safe and reliable anaesthesia protocol. Wide dosages were used safely during this study with ranges for A3080 of 45 +/- 8 microg/kg with MED of 69 +/- 19 microg/kg and KET of 3.7 +/- 1.0 mg/kg (200 mg/ animal). The dosages developed on boma-habituated nyala proved to be equally effective in 9 adult free-ranging nyala (7 males and 2 females). The optimum dosage for nyala was a combination of A3080 (40-50 microg/kg), MED (60-80 microg/kg) plus 200 mg of KET/animal. The anaesthesia was characterised by a short induction, good muscle relaxation and mild hypoxaemia during monitoring the anaesthesia was rapidly and completely reversed by naltrexone hydrochloride (30 mg/mg of A3080) and atipamezole hydrochloride (5 mg/mg of MED) given intramuscularly. There was no mortality or morbidity associated with this protocol.     

Does the induction agent affect the course of halothane anaesthesia in horses?

Four hundred and ninety horses were anaesthetised with halothane for clinical surgical or diagnostic procedures following induction with either detomidine/keta-mine, detomidine/thiopentone, xylazine/ketamine or guaiphenesin/thiopentone. Routine clinical monitoring was performed during anaesthesia. All horses developed hypotension (mean arterial pressures below 80 mm Hg) and respiratory depression (significant fall in respiratory rate and arterial carbon dioxide tension above 7 kPa (53 mm Hg)) consistent with the recognised effects of halothane. All anaesthetic procedures incorporating xylazine or detomidine resulted in lower pulse rates (28–35 per min) than after guaiphenesin/thiopentone (36–44 per min) and there was greater respiratory depression after techniques employing thiopentone rather than keta-mine. Development of hypotension was delayed after techniques using the α₂ adrenoceptor agonist agents (xylazine and detomidine), particularly detomidine. Prernedication with acepromazine did not affect any of the physiological variables measured after techniques employing detomidine. Recovery to standing was fastest after xylazine/ketamine (31±1 min) and slowest after detomidine/thiopentone (53±2 min). Recovery quality was best after detomidine/thiopentone and all techniques employing an α₂ adrenoceptor agonist agent resulted in smoother recovery than after guaiphenesin/thiopentone. This study demonstrates that most of the physiological effects of individual induction agents are overridden by the cardiovascular and respiratory depressant effects of halothane. The study also shows that detomidine is an acceptable sedative for use before general anaesthesia with halothane in horses.