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Chemical immobilization of free-ranging moose.

ABSTRACT: A wide range of drugs and drug combinations have been used to capture free-ranging moose (Alces alces). Currently, potent opioids are considered the drugs of choice for capture of free-ranging moose. Recommended doses are carfentanil at 0.01 mg/kg or etorphine at 7.5 mg/adult. Combining an opioid with a sedative drug like xylazine will increase the risk of bloat, regurgitation, and aspiration of rumen contents. Extreme toxicity for humans and lost darts are major concerns when using potent opioids under field conditions. The best non-opioid alternative is medetomidine at 40-50 mg/adult combined with ketamine at 600 mg/adult. Carfentanil, etorphine, and medetomidine-ketamine have wide safety margins in moose and the risk of severe anesthetic side effects in healthy animals is minimal. Chemical immobilization from a helicopter in winter is considered the best capture method for moose. Due to animal welfare considerations and a low therapeutic index, neuromuscular blocking agents should not be used in moose. A mortality rate greater than 2% during immobilization and a one month post capture period is not acceptable for routine moose captures.

Key words: Alces alces, anesthesia, capture, carfentanil, etorphine, immobilization, ketamine, medetomidine, xylazine


Free-ranging moose (Alces alces) are chemically immobilized for various research and management purposes: radiotransmitter deployment, collection of biological materials, morphometry, health examination, and translocation. Most moose are approached with a helicopter or occasionally by snowmobile, all-terrain vehicle, car, boat, or on foot, and drugs are administered by projectile darts fired from a dart gun. The first chemical immobilization of free-ranging moose was carried out in Alaska in 1957-58 with nicotine, a neuromuscular blocking (NMB) agent (Rausch and Ritcey 1961). Since then a wide range of drugs and drug combinations have been used to capture free-ranging moose in North America and Europe, including other NMB agents, tranquilizers, sedatives, and anesthetics. Franzmann (1982, 1998) has published excellent reviews of moose chemical immobilization. Here we present an update on recommended drugs, doses, and methods for chemical capture of free-ranging moose.


Although helicopter net-gunning has been successfully used on moose, with an immediate capture mortality rate of less than 1% (Carpenter and Innes 1995), mortality rates as high as 14% have been reported from other projects using this method (Olterman et al. 1994). There is no doubt that helicopter net-gunning is a useful method for capture of free-ranging ungulates, and in some species it is even considered to be better than chemical immobilization (Kock et al. 1987a,b,c). In moose, however, we are not aware of a single publication on stress physiology or possible long-term negative effects (e.g., exertional myopathy, increased risk of predation, reduced calving success, and reduced survival of offspring) after capture by helicopter net-gunning. Whether net-gunning is an acceptable method for moose capture remains to be documented.


There are three major groups of drugs currently used for wildlife capture: Alpha-2 adrenoceptor agonists, opioid agonists, and cyclohexanes (Kreeger et al. 2002). The NMB agents are a fourth group that was extensively used during the pioneer days of chemical immobilization. NMB drugs cause muscular paralysis but the animal is conscious, aware of its surroundings and fully sensory, and can feel pain and experience psychogenic stress. Due to a very narrow range between effective immobilizing doses and lethal doses, mortality rates as high as 70% have occurred with NMB agents (Kreeger et al. 2002). Although inferior to modern immobilizing drugs, the NMB agent succinylcholine has been used for moose capture in recent years (Delvaux et al. 1999). However, the reported mortality rate due to respiratory paralysis was 7% and only 63% of the immobilization attempts were successful. Due to animal welfare considerations and the low therapeutic index (effective dose:lethal dose), succinyl-choline or other NMB agents should not be used for moose immobilization.

Alpha-2 adrenoceptor agonists include xylazine, romifidine, detomidine, and medetomidine. These agents induce dose-dependent sedation and analgesia and they have anxiolytic and muscle relaxing properties. The difference in potency between the alpha-2 agonists is species dependent, but no controlled studies have been done in moose or other wildlife species. In sheep, the equipotent sedative doses (mg/kg) for xylazine, romifidine, detomidine, and medetomidine are 0.15, 0.05, 0.03, and 0.01, respectively (Kreeger et al. 2002). Although these drugs may induce deep sedation and immobilization in large doses, sudden arousal may occur. In highly excited animals, induction times are usually prolonged and immobilization may be impossible regardless of the dose administered. Alpha-2 agonists should therefore never be used as the sole agent for capture of free-ranging moose. They are, however, very useful in combination with opioids or cyclohexanes. Alpha-2 agonists have the ability to potentiate other CNS-drugs; e.g., if ketamine is combined with medetomidine the effective anesthetic dose of ketamine is reduced by as much as 75% in some species (Jalanka and Roken 1990). The effects of alpha-2 agonists can be rapidly and permanently reversed by atipamezole, a potent and specific alpha-2 adrenoceptor antagonist (Kreeger et al. 2002). Other less specific reversal agents, such as yohimbine and tolazoline, can be used to antagonize xylazine, the least potent of the alpha-2 agonists.

Opioid agonists used for wildlife immobilization include carfentanil, etorphine, fentanyl, and, to some extent, thiafentanil and sufentanil (Kreeger et al. 2002). In moose and other cervids, carfentanil (North America) and etorphine (Europe) have been the primary opioids, either alone or in combination with xylazine (Kreeger et al. 2002). Carfentanil and etorphine both have high therapeutic indices in moose; i.e., the same dose can be used in most adults regardless of body weight. Underdosing with opioids may cause excitement and hyperthermia and overdosing is therefore considered to be better than underdosing. Although not a "new" agent for wildlife captures (Stanley et al. 1988, 1989), thiafentanil (formerly identified as A-3080) is still an investigational drug for wild animal capture (Citino et al. 2001, Grobler et al. 2001, Kreeger et al. 2001, Citino et al. 2002). The relative potencies of carfentanil, etorphine, and thiafentanil in moose are approximately 2:1:1 (McJames et al. 1994, Kreeger et al. 2002). The effects of opioids can be reversed by several opioid antagonists. Naltrexone is the preferred agent due to its potency and long duration (i.e., less risk of renarcotization). Other opioid antagonists include naloxone, nalmefene, nalbuphine, and diprenorphine.

Cyclohexanes (also known as NMDA antagonists) include ketamine and tiletamine. These drugs are general anesthetics; i.e., they induce unconsciousness and amnesia. However, due to severe side effects like muscle rigidity, frequent convulsions, and rough recoveries, these agents should only be used in combination with an alpha-2 agonist or another tranquilizing or sedative drug (Kreeger et al. 2002). The relative potency between tiletamine and ketamine is approximately 2.5:1 and the duration of action of tiletamine is about three times longer than with ketamine. Tiletamine is not available as a single product and is marketed in a 1:1 combination with the benzodiazepine agonist zolazepam. There is no reversal agent to the cyclohexane drugs. Too early administration of an alpha2 antagonist in animals immobilized with an alpha-2 agonist in combination with ketamine or tiletamine, may uncover residual side effects of the cyclohexane component and can cause uncontrolled recoveries, hyperthermia, trauma, and even death (Kreeger et al. 2002).

In general, antagonists should be administered intramuscularly. Intravenous injection of the reversal agent will cause complete recovery in less than one minute in animals immobilized with opioids alone. Such rapid recoveries may be stressful to the animals and may jeopardize the safety of both animals and people. Intravenous administration of reversal agents should therefore only be considered in an emergency situation.


A large number of free-ranging moose have been immobilized with either carfentanil alone or carfentanil combined with xylazine (Franzmann 1982, 1998; Roffe et al. 2001; Kreeger et al. 2002). Recommended doses of carfentanil alone are 0.01 mg/kg or 3-6 rag/adult. Carfentanil is marketed as a 3 rag/ml solution (Wildnil[R], Wildlife Pharmaceuticals Inc., Ft. Collins, Colorado, USA) and the dose for an adult moose will fit into a standard dart of most remote drug delivery systems. For reversal, naltrexone at 100 mg per mg carfentanil should be administered (Kreeger et al. 2002).

In several studies carfentanil at 3-4 mg/ adult has been used in combination with xylazine (e.g., Cervizine[R] 10 mg/ml, Wildlife Pharmaceuticals Inc.) at 25-175 mg/ adult to improve muscle relaxation and to potentiate the effect of carfentanil so that the opioid part of the combination can be reduced. However, moose immobilized with carfentanil-xylazine are usually not able to support sternal recumbency and may be more susceptible to aspiration pneumonia (Kreeger 2000). Unless there are overriding considerations, the addition of xylazine to opioids in moose is not recommended (Kreeger et al. 2002). If carfentanil is combined with xylazine, the effects of xylazine should be antagonized by either atipamezole (Antisedan[R] 5 mg/ml, Orion Pharma Animal Health, Turku, Finland) at 1 mg per 10 mg xylazine, yohimbine (Antagonil[R] 5 mg/ml, Wildlife Pharmaceuticals Inc.) at 1 mg per mg xylazine, or tolazoline (Tolazoline[R] 100 mg/ml, Lloyd Laboratories, Shenandoa, Iowa, USA) at 15 mg per mg xylazine (Roffe et al. 2001, Kreeger et al. 2002, Plumb 2002).


Etorphine, alone or in combination with xylazine, has been the drug of choice for moose capture in Scandinavia (Sandegren et al. 1987, Arnemo et al. 2001). Standard doses are 7.5 mg etorphine/adult (Etorphine HCl[R] 9.8 mg/ml, Vericore Veterinary Products, Novartis Animal Health UK Ltd., Litlington, UK) or 2.25 mg etorphine + 10 mg acepromazine/adult (Large Animal Immobilon[R] 2.25 mg/ml, Vericore Veterinary Products, Novartis Animal Health UK Ltd.) combined with 100 mg xylazine/adult (Rompun[R] Dry Substance, Bayer AG, Leverkusen, Germany). These doses fit into a standard dart of most remote drug delivery systems. Data from 1,464 immobilizations carried out over a 19-year period in Norway (Arnemo et al. 2001; J. M. Arnemo, unpublished data) show that ethorphine alone is an extremely safe and effective drug in moose and there is no indication for combining etorphine with an alpha-2 agonist. Due to the potentiating effect and muscle relaxing properties of alpha-2 agonists, moose immobilized with etorphine-xylazine or etorphine-medetomidine are usually not able to maintain sternal recumency and regurgitation of rumen contents are frequently seen (J. M. Arnemo, unpublished data). Diprenorphine is a specific antagonist for etorphine and is marketed in the same package as etorphine at a concentration of 1.2 times the concentration of etorphine (Diprenorphine HCl[R] 12 mg/ml and Large Animal Revivon[R] 3 mg/ml, Vericore Veterinary Products, Novartis Animal Health UK Ltd.). For reversal of etorphine effects in moose, the volume of diprenorphine should be equivalent to the total volume of etorphine administered. If etorphine is combined with xylazine or medetomidine, the effects of the alpha-2 agonist should be reversed by atipamezole (Antisedan[R] 5 mg/ml, Orion Pharma Animal Health, Turku, Finland) at 1 mg per 10 mg xylazine or 5 mg per mg medetomidine (Kreeger et al. 2002).


We are aware of only two reports on the use of thiafentanil for immobilization of free-ranging moose. In one study average down time in moose (n = 18) darted with a standard dose of 10 mg thiafentanil was 1.5 rain compared to 4.5 min in moose (n > 100) injected with a standard dose of 4.5 mg carfentanil (Stanley et al. 1989). Reversals of immobilization were achieved with either nalmefene or diprenorphine (no data on antagonist doses was provided). Renarcotization in animals immobilized with thiafentanil was not observed and the authors state that the elimination half-life of thiafentanil is only half as long as the elimination time of carfentanil. Later, McJames et al. (1994) reported that a standard dose of 10 mg thiafentanil was used to immobilize moose from a helicopter in winter. The mean induction time in 59 moose immobilized after one injection was 3.6 min. The 10 mg dose was effective for large bulls and safe for calves. Three animals required a second dart to become immobilized and received a total dose of 20 mg thiafentanil. Reversals after different doses of nalmefene (50 and 300 mg) and naltrexone (50 and 100 mg) were rapid and complete with no residual ataxia. Mean standing times ranged from 1.9 to 2.4 min after intramuscular administration of the antagonist in all groups. Renarcotization was not seen and no deaths occurred. Although more studies on its efficacy and safety are required, there are strong indications that thiafentanil may be a very useful drug for immobilization of moose in the future: small volume (1 ml), induction time is rapid, duration of action is short, no major clinical side effects have been reported, and renarcotization has not been observed. This view is supported by several studies on thiafentanil in other artiodactylid species (Stanley et al. 1988, Janssen et al. 1993, McJames et al. 1993, Citino et al. 2001, Grobler et al. 2001, Kreeger et al. 2001, Citino et al. 2002). Currently, thiafentanil is only available for investigational purposes (A3080[R] 10 mg/ ml, Wildlife Pharmaceuticals Inc.).


Studies on medetomidine (MED), ketamine (KET), and atipamezole (ATI) in free-ranging moose were performed in Norway and Finland from 1992 to 1997. Although some of the data from these studies
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Author:Arnemo, Jon M.; Kreeger, Terry J.; Soveri, Timo
Date:Jan 1, 2003
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