Comparative Physiologic Effects of Thiafentanil-Azaperone and Thiafentanil-Medetomidine-Ketamine in Free-Ranging Uganda Kob (Kobus kob thomasi)
American Association of Zoo Veterinarians Conference 2006

Nigel Caulkett1, DVM, MVetSc, DACVA; Jessica Paterson1, DVM; Jerry C. Haigh2, BVMS, MSc, FRCVS, DACZM; Ludwig Siefert3, DVM, PGCert, TropVetMed, MSciAgr

1Department of Small Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada; 2Department of Large Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan, Saskatoon, SK, Canada; 3WARM Department, Faculty of Veterinary Medicine, Makerere University, Kampala, Uganda


Thiafentanil is a potent μ-opioid agonist drug, that is slightly less potent than carfentanil, and has a shorter duration of action than carfentanil or etorphine.5 Thiafentanil administration will rapidly induce anesthesia, but when used as the sole agent, it can induce muscle rigidity.2 Thiafentanil can be effectively antagonized with naltrexone.1,2 Potent opioids are often combined with tranquilizers or sedatives to improve muscle relaxation and decrease opioid requirements.1-3 A combination of thiafentanil (Wildlife Pharmaceuticals, Inc., Karino, South Africa), medetomidine (Wildlife Pharmaceuticals, Inc., Fort Collins, CO), and ketamine (Produlab Pharma, Ruams-donksveer, Netherlands) has been evaluated for anesthesia in gemsbok2 and roan1 antelope. The combination induced a good quality of anesthesia with minimal disturbance of physiologic parameters.1,2 One objective of this study was to evaluate the efficacy and physiologic effects of a similar combination (TMK) in Uganda kob. A mixture of thiafentanil and azaperone (Stresnil,™ Janssen Pharmaceutica, Beerse, Belgium) (TA) had been used in 2003 and 2004 to capture kob for blood sampling as part of an ongoing study to determine the incidence of brucellosis in this population. A further objective was to evaluate the efficacy and physiologic effects of thiafentanil-azaperone in kob.

This study was performed in Queen Elizabeth National Park, Uganda, from February 18–23, 2005. The ambient temperature for this period ranged from 17–38°C. Male kob were approached by vehicle on their mating grounds. A Bushnell 400® laser rangefinder (Bushnell Corporation, Overland Park, KS) was used to determine range and the animal was darted in the hindquarters with either a Pneudart® 193 projector (Pneudart Inc. Williamsport, PA) or a Dan-inject® JM rifle (Dan-Inject, Børkop, Denmark). Induction time was taken as the time from dart placement to sternal recumbency, while down time was taken as time from sternal recumbency until time of antagonist administration. Recovery time was taken as time from antagonist administration to standing. The kob were maintained in sternal recumbency, and an arterial sample was obtained from the auricular or femoral artery. This sample was used for blood gas analysis, performed in the field with an I-STAT® blood gas analyzer (I-STAT Corp. East Windsor, NJ). Heart rate, respiratory rate, and body temperature were measured and recorded at five-minute intervals. The kob were weighed, and body weight was used to determine the actual dose of drugs administered. Naltrexone (Wildlife Pharmaceuticals, Inc., Fort Collins, CO) (N) was used to antagonize thiafentanil in both groups. It was administered half IV and half IM at a ratio of 50 (N):1 (T) in the TMK group and 40 (N):1 (T) in the TA group. Atipamezole (Antisedan,™ Orion Pharmaceuticals, Espoo, Finland) was administered at three times the medetomidine dose by IM injection in the TMK group. Comparisons of induction and recovery characteristics and blood gas data were performed between groups with a students t-test. A significance level of p<0.05 was used.

Data were obtained from eight animals in the TMK group. These animals received an actual dosage (mean±SD) of 15.16±3.3 μg/kg of medetomidine, 15.16±3.3 μg/kg of thiafentanil, and 0.99±0.04 mg/kg of ketamine. Data were obtained from nine animals in the TA group. These animals received an actual dosage (mean±SD) of 57.3 µg/kg of thiafentanil and 0.46 mg/kg of azaperone. Induction and recovery characteristics are summarized in Table 1. HR, RR, and rectal temperature are summarized in Table 2. This table illustrates the mean values of the first reading obtained from the animal and the final reading before reversal. Table 3 illustrates blood gas values.

Table 1. Induction times, down times, and recovery times in Uganda kob
receiving thiafentanil-medetomidine-ketamine (TMK) or thiafentanil-azaperone (TA)


TMK n=8

TA n=9

Induction time (mean±SD)a

3.7±1.8 m

2.1±0.71 m


1.1–7.1 m

0.42–2.9 m

Down time (mean±SD)a

21.6±6.8 m

14.3±2 m


15–35 m

12–17 m

Recovery time (mean±SD)a

6.2±3.4 m

1.1±0.2 m


2–11 m

0.72–1.3 m

aDenotes a significant difference between treatment groups p≤0.05.

Table 2. First and last reading of heart rate (HR), respiratory rate (RR), and rectal temperature (TEMP)
in Uganda kob receiving thiafentanil-medetomidine-ketamine (TMK) or thiafentanil-azaperone (TA)


TMK n=8

TA n=9

First HR (beats/min) mean/range



Last HR (beats/min) mean/range



First RR (breath/min) mean/range



Last RR (breath/min) mean/range



First TEMP (OC) mean/rangea



Last TEMP (OC) mean/rangea



aAll kob were routinely cooled with water.

Table 3. Arterial blood gas values from Uganda kob receiving
thiafentanil-medetomidine-ketamine (TMK) or thiafentanil-azaperone (TA)


TMK n=8

TA n=9

PaCO2 mm Hg (mean±SD)



PaO2 mm Hg (mean±SD)a



Ph (mean±SD)



Base excess (mean±SD)



aDenotes a significant difference between treatment groups p≤0.05.

Rolling during induction of anesthesia accompanied by regurgitation were the major complications noted in the TA group. Three of nine animals anesthetized with TA regurgitated. None of the eight animals anesthetized with TMK regurgitated. The TA animals that regurgitated had recently returned from water and this probably contributed to regurgitation.

Quality of anesthesia was superior with TMK. Animals in this group had good muscle relaxation and no movement. Animals anesthetized with TA had more spontaneous movement. Quality of recovery was superior with TA. Antagonism of thiafentanil resulted in a rapid and complete reversal of anesthesia. Recovery was slow from TMK and was characterized by stumbling and ataxia. Animals recovering from TMK needed to be closely watched to protect them from other kob and predators. Since both medetomidine and thiafentanil had been antagonized, the narcosis and ataxia probably resulted from residual ketamine.

Hypoxemia was a major complication with TMK, probably related to the addition of an alpha-2 agonist drug.4 Two animals in the TMK group developed profound hypoxemia (PaO2<25 mm Hg). This was accompanied by tachypnea and tachycardia, indicative of hypoxic stress.

Thermoregulation was good with both treatments and was somewhat surprising given the fact that ambient temperature approached 40°C.

Induction times were surprisingly fast with TA. The most rapid induction occurred in 25 seconds. The longest induction was still less than three minutes in duration. This characteristic is highly desirable in the anesthesia of free-ranging animals.

Based on these results TA proved to be the superior combination in this situation. The induction and recovery characteristics were ideal in this potentially hazardous environment, and the cardiopulmonary stability should decrease the risk of complications from hypoxemia. The quality of anesthesia produced by TA may be improved with the addition of a benzodiazepine drug, or a low dose of an alpha-2 agonist. TMK may be more useful in a captive situation, where induction and recovery can be closely controlled. Supplemental oxygen should be available to offset hypoxemia during anesthesia with TMK. It is possible that recovery characteristics may be improved if this mixture is used without ketamine.


The authors thank the students of the 2005 Africa experience rotation for their assistance, these included final-year students from the Western College of Veterinary Medicine and graduate students from Makerere University. We also thank the Uganda Wildlife Authority for their support of this research. Funding assistance was also provided by the 2005 Africa experience rotation and the WCVM research fund.

Literature Cited

1.  Citino SB, Bush M, Grobler D, Lance W. Anaesthesia of roan antelope (Hippotragus equinus) with a combination of A3080, medetomidine, and ketamine. J S Afr Vet Assoc. 2001;72:29–32.

2.  Grobler D, Bush M, Jessup D, Lance W. Anaesthesia of gemsbok (Oryx gazelle) with a combination of A3080, medetomidine, and ketamine. J S Afr Vet Assoc. 2001;72:81–83.

3.  Haigh JC. Opioids in zoological medicine. J Zoo Wildl Med. 1990;21:391–413.

4.  Read MR. A review of alpha-2 adrenoceptor agonists and the development of hypoxemia in domestic and wild ruminants. J Zoo Wildl Med. 2003.

5.  Stanley TH, McJames S, Kimball J, Port JD, Pace NL. Immobilization of elk with A3080. J Wildl Man. 1988;52:577–581.


Speaker Information
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Nigel Caulkett, DVM, MVetSc, DACVA
Department of Small Animal Clinical Sciences
Western College of Veterinary Medicine
University of Saskatchewan
Saskatoon, SK, Canada

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