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The study compared immobilisation of blesbok (

Etorphine–azaperone is the most commonly used drug combination for chemical immobilisation of free-ranging white rhinoceroses, but causes several profound physiological disturbances, including muscle tremors. The addition of benzodiazepine sedatives, such as midazolam, has been proposed to reduce the muscular rigidity and tremors in immobilised rhinoceroses. Twenty-three free-ranging, sub-adult white rhinoceros bulls were darted and captured using a combination of etorphine plus either azaperone or midazolam. Skeletal muscle tremors were visually evaluated and scored by an experienced veterinarian, and tremor scores and distance run were compared between groups using the Wilcoxon rank sum test. No statistical differences were observed in tremor scores ( p = 0.435) or distance run ( p = 0.711) between the two groups, and no correlation between these variables was detected ( r = –0.628; p = 0.807). Etorphine–midazolam was as effective as etorphine–azaperone at immobilising rhinoceroses, with animals running similar distances. Although the addition of midazolam to the etorphine did not reduce tremor scores compared to azaperone, it might have other beneficial immobilising effects in rhinoceroses, and further investigation is necessary to elucidate possible methods of reducing muscle tremoring during chemical immobilisation of rhinoceroses.

Chemical immobilisation is essential for veterinarians to perform medical procedures in wild African ungulates. Potent opioids combined with neuroleptic drugs are most often used for this purpose. The present study aimed at comparing the quality of immobilisation and effects on physiological variables between a high (high etorphine-azaperone [HE]: 0.09 mg kg-1) and low etorphine dose (low etorphine-azaperone [LE]: 0.05 mg kg-1), both combined with azaperone (0.35 mg kg-1), in 12 adult female boma-acclimatised blesbok. It was hypothesised that a reduction in etorphine's dose in combination with azaperone would result in less cardiorespiratory impairment but likely worsen the quality of immobilisation. Both treatments resulted in rapid induction and recovery times. Overall inter-treatment differences occurred in pulse rate (HE and LE: 52 ± 15 and 44 ± 11 beats minute-1, p < 0.0001), respiratory rate (HE and LE: 15 ± 4 and 17 ± 4 breaths minute-1, p < 0.006), partial pressure of exhaled carbon dioxide (HE and LE: 62.0 ± 5.0 and 60.0 ± 5.6 millimetre of mercury [mmHg], p < 0.028) and arterial carbon dioxide (HE and LE: 58.0 ± 4.5 and 55.0 ± 3.9 mmHg, p < 0.002). Both HE and LE led to bradycardia, hypertension and marked hypoxia to a similar extent. Furthermore, quality of induction, immobilisation and recovery were similar in both treatments. The role of azaperone in the development of cardiorespiratory compromise and gas exchange impairment that occurred when these combinations were used is still unclear. Further studies are recommended to elucidate drug- and dose-specific physiological effects in immobilised antelope.

Potent opioids are known to cause negative alterations to the physiology of immobilised antelope. How these effects differ between species has not been studied. This study aimed to compare time to recumbence and effects of opioid-based immobilisation on the physiology of impala (Aepyceros melampus) and blesbok (Damaliscus pygargus phillipsi). Eight animals of each species were immobilised, with 0.09 mg/kg etorphine and 0.09 mg/kg thiafentanil respectively, in a randomised two-way cross-over study. Variables measured and analysed by means of a linear mixed model included time to recumbence, heart rate, respiratory rate, arterial blood pressure, blood gases, lactate and glucose. In blesbok, mean time to recumbence was not significantly different with either drug (2.5 minutes and 2.2 min, respectively), but in impala thiafentanil achieved a shorter time to recumbence (2.0 min) than etorphine (3.9 min). Mean heart rates of immobilised impala were within reported physiological limits, but lower in immobilised blesbok when both opioids were used (35 beats/min to 44 beats/min vs. 104 ± 1.4 beats/min resting heart rate). Impala developed severe respiratory compromise and hypoxaemia from both opioids (overall mean PaO2 values ranged from 38 mmHg to 59 mmHg over 30 min). In contrast, blesbok developed only moderate compromise. Therefore, significantly different species-specific physiological responses to potent opioid drugs exist in blesbok and impala. Given that these different responses are clinically relevant, extrapolation of immobilising drug effects from one species of African ungulate to another is not recommended.

Opioid-induced immobilisation results in severe respiratory impairment in the white rhinoceros. It has therefore been attempted in the field to reverse this impairment with the use of opioid agonist-antagonists, such as nalorphine, nalbuphine, butorphanol and diprenorphine; however, the efficacy of some of these treatments has yet to be determined. The efficacy of butorphanol, either alone or in combination with diprenorphine both with and without oxygen insufflation, in alleviating opioid-induced respiratory impairment was evaluated. The study was performed in two parts: a boma trial and a field trial. Rhinoceroses were immobilised specifically for the study, according to a strict protocol to minimise confounding variables. A two-way analysis of variance was used to compare the physiological responses of the rhinoceroses to the different treatments and their effects over time. The intravenous administration of butorphanol (at 3.3 mg per mg etorphine) plus diprenorphine (at 0.4 mg per mg etorphine) did not offer any advantage over butorphanol (at 15 mg per mg etorphine) alone with regard to improving PaO2, PaCO2 and respiratory rates in etorphine-immobilised white rhinoceroses. Both butorphanol + diprenorphine + oxygen and butorphanol + oxygen, at the doses used, significantly improved the etorphine-induced hypoxaemia in both boma- and field-immobilised white rhinoceroses. Clinically acceptable oxygenation in field-immobilised white rhinoceroses can be achieved by using either treatment regimen, provided that it is combined with oxygen insufflation.

Impalas (Aepyceros melampus) are increasingly valuable in the South African wildlife industry, and there is a greater need to chemically immobilise them, ideally with minimal risk. This study aimed to compare the times to recumbency and physiological effects of thiafentanilmedetomidine versus etorphine-medetomidine immobilisation. A combination of thiafentanil (2 mg) + medetomidine (2.2 mg) and etorphine (2 mg) + medetomidine (2.2 mg) was administered (to nine impalas; crossover design) via a dart. After darting, a stopwatch was started to record times to recumbency (time from darting until recumbent without attempts to stand). If apnoea was present, the impalas received one or more boluses of butorphanol (1:1 potent opioid dose). Data collection included arterial blood gas analysis and the number of butorphanol boluses. Two-sample t-tests were used to compare differences between combinations. The time to recumbency for thiafentanil-medetomidine was 12.2 (± 6.8) min and no different from 14.5 (± 5.2) min for etorphine-medetomidine (p = 0.426). The thiafentanilmedetomidine combination required more butorphanol boluses (median: 2; interquartile range: 2–3) compared to etorphine-medetomidine (median: 0; interquartile range: 0–1) (p = 0.001). Despite butorphanol treatment and resolution of apnoea, all impalas suffered hypoxaemia (PaO2 ± 44.0 mmHg). Thiafentanil-medetomidine did not immobilise impalas more rapidly than etorphine-medetomidine, and resulted in more apnoea that required rescue butorphanol boluses. Marked hypoxaemia resulted from both combinations, mainly because of right-to-left intrapulmonary shunting and not because of hypoventilation. Butorphanol and oxygen supplementation should be considered as essential rescue interventions for all impalas immobilised with these potent opioid combinations.

Impalas (Aepyceros melampus) are increasingly valuable in the South African wildlife industry, and there is a greater need to chemically immobilise them, ideally with minimal risk. This study aimed to compare the times to recumbency and physiological effects of thiafentanilmedetomidine versus etorphine-medetomidine immobilisation. A combination of thiafentanil (2 mg) + medetomidine (2.2 mg) and etorphine (2 mg) + medetomidine (2.2 mg) was administered (to nine impalas; crossover design) via a dart. After darting, a stopwatch was started to record times to recumbency (time from darting until recumbent without attempts to stand). If apnoea was present, the impalas received one or more boluses of butorphanol (1:1 potent opioid dose). Data collection included arterial blood gas analysis and the number of butorphanol boluses. Two-sample t-tests were used to compare differences between combinations. The time to recumbency for thiafentanil-medetomidine was 12.2 (± 6.8) min and no different from 14.5 (± 5.2) min for etorphine-medetomidine (p = 0.426). The thiafentanilmedetomidine combination required more butorphanol boluses (median: 2; interquartile range: 2–3) compared to etorphine-medetomidine (median: 0; interquartile range: 0–1) (p = 0.001). Despite butorphanol treatment and resolution of apnoea, all impalas suffered hypoxaemia (PaO2 ± 44.0 mmHg). Thiafentanil-medetomidine did not immobilise impalas more rapidly than etorphine-medetomidine, and resulted in more apnoea that required rescue butorphanol boluses. Marked hypoxaemia resulted from both combinations, mainly because of right-to-left intrapulmonary shunting and not because of hypoventilation. Butorphanol and oxygen supplementation should be considered as essential rescue interventions for all impalas immobilised with these potent opioid combinations.

When immobilising wildlife, adverse side effects can include hypoxaemia, acidosis and hypertension. Pulmonary gas exchange and acid-base status were evaluated during immobilisation of 25 free-ranging and one boma-held black rhinoceros (Diceros bicornis) in Zimbabwe. The effect of different body positions on arterial oxygenation was evaluated. A combination of the following drugs was used: an opioid (etorphine or thiafentanil), azaperone and an a2 -adrenoceptor agonist (detomidine or xylazine). Respiratory and heart rates, rectal temperature and pulse oximetry-derived haemoglobin oxygen saturation were recorded. Serial arterial blood samples were analysed immediately in the field. Marked hypoxaemia and hypercapnia were recorded in immobilised free-ranging black rhinoceroses. Arterial oxygenation was higher during sternal compared to lateral recumbency. Most rhinoceroses developed acidaemia of respiratory and metabolic origin. Initially high lactate concentrations in free-ranging rhinoceroses decreased during immobilisation. Pulse oximetry was unreliable in the detection of hypoxaemia. Positioning in sternal recumbency and routine use of oxygen supplementation are recommended in the management of immobilised rhinoceroses as measures to improve arterial oxygenation.

Opioid-induced immobilisation results in severe respiratory compromise in the white rhinoceros (Ceratotherium simum). The effectiveness of oxygen insufflation combined with butorphanol in alleviating respiratory depression in free-ranging chemically immobilised white rhinoceroses was investigated. In this prospective intervention study 14 free-ranging white rhinoceroses were immobilised with a combination of etorphine, azaperone and hyaluronidase. Six minutes (min) after the animals became recumbent, intravenous butorphanol was administered and oxygen insufflation was initiated. Previous boma trial results were used for comparison, using repeated measures two-way analysis of variance. The initial immobilisation-induced hypoxaemia in free-ranging rhinoceroses (arterial partial pressure of oxygen [PaO2] 35.4 mmHg ± 6.6 mmHg) was similar to that observed in boma-confined rhinoceroses (PaO2 31 mmHg ± 6 mmHg, n = 8). Although the initial hypercapnia (PaCO2 63.0 mmHg ± 7.5 mmHg) was not as severe as that in animals in the boma trial (79 mmHg ± 7 mmHg), the field-immobilised rhinoceroses were more acidaemic (pH 7.10 ± 0.14) at the beginning of the immobilisation compared with boma-immobilised rhinoceroses (pH 7.28 ± 0.04). Compared with pre-intervention values, butorphanol with oxygen insufflation improved the PaO2 (81.2 mmHg ± 23.7 mmHg, p < 0.001, 5 min vs 20 min), arterial partial pressure of carbon dioxide (55.3 mmHg ± 5.2 mmHg, p < 0.01, 5 min vs 20 min), pH (7.17 ± 0.11, p < 0.001, 5 min vs 20 min), heart rate (78 breaths/min ± 20 breaths/min, p < 0.001, 5 min vs 20 min) and mean arterial blood pressure (105 mmHg ± 14 mmHg, p < 0.01, 5 min vs 20 min). Oxygen insufflation combined with a single intravenous dose of butorphanol improved oxygenation and reduced hypercapnia and acidaemia in immobilised free-ranging white rhinoceroses.

White rhinoceros anaesthetised with etorphine and azaperone combination develop adverse physiological changes including hypoxia, hypercapnia, acidosis, tachycardia and hypertension. These changes are more marked in field-anaesthetised rhinoceros. This study was designed to develop a technique to improve safety for field-anaesthetised white rhinoceros by tracheal intubation and oxygen insufflation. Twenty-five free-ranging white rhinoceros were anaesthetised with an etorphine and azaperone combination for translocation or placing microchips in their horns. Once anaesthetised the rhinoceros were monitored prior to crating for transportation or during microchip placement. Physiological measurements included heart and respiratory rate, blood pressure and arterial blood gas samples. Eighteen rhinoceros were intubated using an equine nasogastric tube passed nasally into the trachea and monitored before and after tracheal insufflation with oxygen. Seven rhinoceros were not intubated or insufflated with oxygen and served as controls. All anaesthetised rhinoceros were initially hypoxaemic (percentage arterial haemoglobin oxygen saturation (%O2Sa) = 49% +/- 16 (mean +/- SD) and PaO2 = 4.666 +/- 1.200 kPa (35 +/- 9 mm Hg)), hypercapnic (PaCO2 = 8.265 +/- 1.600 kPa (62 +/- 12 mm Hg)) and acidaemic (pHa = 7.171 +/- 0.073 ). Base excess was -6.7 +/- 3.9 mmol/l, indicating a mild to moderate metabolic acidosis. The rhinoceros were also hypertensive (systolic blood pressure = 21.861 +/- 5.465 kPa (164 +/- 41 mm Hg)) and tachycardic (HR = 107 +/- 31/min). Following nasal tracheal intubation and insufflation, the %O2Sa and PaO2 increased while blood pHa and PaCO2 remained unchanged. Tracheal intubation via the nose is not difficult, and when oxygen is insufflated, the PaO2 and the %O2Sa increases, markedly improving the safety of anaesthesia, but this technique does not correct the hypercapnoea or acidosis. After regaining their feet following reversal of the anaesthesia, the animals' blood gas values return towards normality.

The physiological effects on respiratory function of etorphine (M99, Logos Agvet) (30 µg/kg) administered intramuscularly were determined in boer goats. The goats were habituated to the experimental procedures so that respiratory function could be determined while the animals stood quietly at rest. This enabled the physiological changes induced by etorphine to be measured and compared with those obtained before administration of the immobilising drug. The effectiveness of diprenorphine (M5050, Logos Agvet) (3 mg/1 mg etorphine) as an antagonist of the physiological changes induced by the etorphine treatment was also determined. Etorphine depressed respiratory function, which resulted in a decrease in PaO2 and an increase in PaCO2. These changes were limited and occurred as a result of decreases in respiratory minute volume and alveolar minute ventilation caused by a decrease in respiratory rate. The physiological shunt fraction did not change significantly but there was a significant decrease in percentage physiological dead space ventilation. It was not possible to determine how effectively diprenorphine reversed the respiratory effects due to etorphine.

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.

Anaesthesia of 2 five-year-old femaleAfrican elephants (Loxodonta africana) was required for dental surgery. The animals were each premedicated with 120 mg of azaperone 60 min before transportation to the hospital. Before offloading, 1 mg etorphine was administered intramuscularly (i.m.) to each elephant to facilitate walking them to the equine induction / recovery room. For induction, 2 mg etorphine was administered i.m. to each animal. Induction was complete within 6 min. Surgical anaesthesia was induced with halothane-in-oxygen after intubation of the trunk. During surgery the mean heart rate was 61 and 45 beats / min respectively. Systolic blood pressures increased to 27.5 and 25.6 kPa respectively, and were treated with intravenous azaperone. Blood pressure decreased thereafter to a mean systolic pressure of 18.1 and 19.8 kPa, respectively. Rectal temperature was 35.6 and 33.9 oC at the onset of surgery, and decreased to 35.3 and 33.5 oC, respectively, at the end of anaesthesia. Etorphine anaesthesia was reversed with 5mg diprenorphine at the completion of 90 min of surgery.

Anaesthesia of 2 five-year-old female African elephants (Loxodonta africana) was required for dental surgery. The animals were each premedicated with 120 mg of azaperone 60 min before transportation to the hospital. Before offloading, 1 mg etorphine was administered intramuscularly (i.m.) to each elephant to facilitate walking them to the equine induction/recovery room. For induction, 2 mg etorphine was administered i.m. to each animal. Induction was complete within 6 min. Surgical anaesthesia was induced with halothane-in-oxygen after intubation of the trunk. During surgery the mean heart rate was 61 and 45 beats/min respectively. Systolic blood pressures increased to 27.5 and 25.6 kPa respectively, and were treated with intravenous azaperone. Blood pressure decreased thereafter to a mean systolic pressure of 18.1 and 19.8 kPa, respectively. Rectal temperature was 35.6 and 33.9 degrees C at the onset of surgery, and decreased to 35.3 and 33.5 degrees C, respectively, at the end of anaesthesia. Etorphine anaesthesia was reversed with 5 mg diprenorphine at the completion of 90 min of surgery.

Respiratory rate, heart rate, blood-gas tensions (PO2 and PCO2) and pH of arterial (a) and peripheral venous (v) blood, concentration of haemoglobin in arterial blood (Hb), saturation of arterial haemoglobin with oxygen and the end-expiratory concentration of oxygen were measured in 22 juvenile African elephants (Loxodonta africana) anaesthetised with etorphine and azaperone during a period of 35-65 minutes after they had assumed lateral recumbency. Based on these parameters the alveolar-arterial and arterial-peripheral venous differences of PO2 [P(A-a)O2 and P(a-v)O2 respectively] and oxygen content of arterial blood (CaO2) were calculated. Elephants with body mass ofor = 600 kg showed statistically significant changes in the following parameters, compared with elephants with a body mass of more than 600 kg (x +/- SD): PaO2 (64 +/- 11 versus 82 +/- 8 mmHg), P(a-v)O2 (9 +/- 5 versus 22 +/- 9 mmHg), P(A-a)O2(37 +/- 16 versus 15 +/- 8 mmHg) and Hb (148 +/- 20 versus 130 +/- 10 g/l) (p0.05). These findings suggested a tendency towards impaired oxygen exchange in the lungs, reduced peripheral extraction of oxygen and elevated oxygen-carrying capacity of arterial blood in smaller elephants. These changes were theoretically attributed to the respiratory-depressant and sympathomimetic effects of higher dosages of etorphine used in the smaller elephants to maintain a clinically acceptable anaesthetic plane. Individual elephants spent 35-150 minutes under anaesthesia and all recovered uneventfully after reversal of etorphine with diprenorphine.

Clinical and pharmacological analyses showed a full immobilizing action of etorphine in adult sheep +/- 7 min. after a deep i.m. injection of the drug at a dosage rate of 20 micrograms/kg. Neurochemical analyses of motoric CNS-structures done within 30 min. after i.m. injection of etorphine in an immobilizing dose, showed the following: A significant decrease of dopamine (DA) and homovanilic acid (HVA) concentrations in the corpus striatum, the frontal motor cortex, cerebellum and in the lumbo-sacral portion of the spinal cord. A decrease of DA-concentration with a simultaneous increase of HVA-concentration in the pons. A significant decrease of noradrenaline (NA) concentration in the cerebellum and lumbo-sacral portion of the spinal cord and an insignificant decrease of amine concentration in the pons. A significant increase of adrenaline (A) concentration in the frontal motor cortex. A significant decrease of 5-hydroxytryptamine (5-HT) concentration in the frontal motor cortex and cerebellum and an equally significant increase in its concentration in the pons.

The effects of chemical immobilisation on impala (Aepyceros melampus) were investigated. The results indicate that etorphine HCl or Carfentanil should not be used in isolation but that xylazine should be included in the immobilisation "cocktail". The highest dose possible, commensurate with safety, should be used in order to minimise time and distance to recumbency. Body temperature should be monitored and if cooling measures are not effective the animal should be aroused. Either diprenorphine HCl alone or in combination with yohimbine and 4-aminopyridine should be used as antidote/s.