In The Wild | Mixlab Blog

Respiratory Depression in Barasingha Deer During Capture and Chemical Immobilization

Written by Admin | June 23, 2023

The barasingha deer (Rucervus duvaucelii) is one of the most widely-recognized deer of the Indian subcontinent. Also called the swamp deer, it is found mostly in damp areas such as reed beds and marshes. The barasingha deer’s name is derived from the Hindi words for “twelve ends”, referencing this deer’s antlers, which can have from 12 to 20 tines. The name “swamp deer” refers to the habitat preferred by this deer, which encompasses swampland and a variety of forest types ranging from dry to moist deciduous to evergreen.1,2

The barasingha is a large, long-legged deer, with a short head and long, broad ears. Larger stags may have an overall length of up to 71 inches (180 cm) and weigh up to 620 lbs (280 kg). Their coats are a yellowish-brown color, which darkens during the winter months. Some individuals have yellowish spots scattered over their coats. In some individuals, the hair around the deer’s neck is longer, forming a shaggy mane.2

In its native India, there are three subspecies of barasingha deer:

  1. Wetland barasingha (Rucervus duvaucelii duvacelii)
  2. Hard-ground barasingha (Rucervus duvaucelii branderi)
  3. Eastern barasingha (Rucervus duvaucelii ranjitsinhii)3

The barasingha deer is extinct in both Bangladesh and Pakistan, where it once existed in large numbers. In the late 1960s, the numbers of these deer in India decreased drastically due to hunting, habitat loss and disease. It was brought back from the verge of extinction over several decades through successful breeding programs and conservation practices.1 Today, their populations are no longer in danger, and the barasingha has been introduced to many areas as a game animal, including the United States.

In their native range, barasingha deer have a number of natural predators including the tiger; thus, they have developed an apprehensive, nervous manner and are always on high alert. They have a loud, barking call that they use to signal danger which is said to be similar to the alarm call of the roe deer. Barasingha deer feed by day, but can also be found resting during the hottest times of the day. In the winter, large herds form, which dissipate during the summer into smaller herds composed chiefly of females and their fawns. During the summer, males live separately from females in small bachelor groups.1,2

Female barasingha deer are monoestrous, and usually have a single fawn after eight months of gestation. Fawns are weaned at around six months, and the female is ready to breed again about a year after giving birth. Stags reach puberty at two years of age, and females reach puberty at 18 to 24 months.2

Barasingha Deer and Capture Protocols

The management of wild and captive barasingha deer sometimes requires the capture of individual animals, and chemical immobilization is the safest and most effective method of capture.4 The reasons for capture typically include research, translocating nuisance animals, or for the treatment of injured or sick animals.

For research and wildlife management purposes, many techniques have been used to capture barasingha deer and other hoofstock, including live traps, drop nets, drive nets and rocket nets. Since these methods tend to limit the ability to select specific animals for capture, chemical immobilization using a remotely-delivered anesthetic agent has become the preferred capture technique. This is because this method is not only selective, but it reduces the stress of manual capture on animals.

With increased scientific and physiological knowledge and the refinement of immobilizing drugs, numerous chemical agents and drug formulations are now available. Still, chemical immobilization does cause physiological stress to deer. Anesthetized animals will be at risk of complications such as cardiovascular or respiratory depression and disruption of the thermoregulatory system. These effects can require supportive treatment by the attending veterinarian or support staff or the initiation of anesthetic reversal prior to completion of the procedure.4,5

Remote drug delivery systems are typically used for the purpose of chemical immobilization; this usually involves the use of a dart gun or blowpipe. Drugs are injected by means of a dart syringe which is fired from the dart gun at a distance. Since dart volume can be a limiting factor, immobilizing drugs must be highly potent and concentrated. They must also have a high therapeutic index and wide safety margin since animals cannot be examined and weighed prior to immobilization.4 The ideal drugs will also be fast-acting to limit stress and the likelihood of escape following darting. They should also be reversible, since animals are often released back into the wild immediately after the capture event.

In zoos, deer farms, breeding facilities and even in free-ranging situations, chemical immobilization is usually carried out from the ground. In some circumstances however, animals have to be located and darted from a helicopter.5 All of the above methods of capture can cause significant stress and trauma to these animals, potentially giving rise to complications.

Respiratory Depression Risks in Barasingha Deer

While chemical immobilization is a superior capture method for barasingha deer and other wildlife, it is still associated with risks. In many cases, animals cannot be examined with regards to their health status beforehand and they often cannot receive adequate supportive treatment during immobilization in the field. Additionally, they are often highly-stressed and can run long distances before they are immobilized.

Most of the drugs used for the chemical immobilization of wildlife have side effects. They not only cause sedation by influencing the central nervous system, but also influence cardiovascular, respiratory and thermoregulatory functions.1The most common problems encountered during wildlife immobilization include respiratory depression, cardiovascular disturbances, bloat, impaired thermoregulation, hypoxia and capture myopathy.4-6

Opioids are often used for the chemical immobilization of barasingha deer and other wild herbivores. A disadvantage of using these drugs is that they can cause clinically significant respiratory depression (due to their potent effect on mu-opioid receptors).5 Activation of mu-opioid receptors in the respiratory centers of animals depresses neurons that generate the normal respiratory rhythm. At the same time, activation of these receptors activate other receptors in the brain stem, on the aortic arch and carotid bodies, which depresses normal respiratory function.

The above processes lead to a reduction of the respiratory frequency and tidal volume, as well as pulmonary vasoconstriction which decreases pulmonary perfusion.6 Alpha-2 agonists such as guanabenz, clonidine, medetomidine, and dexmedetomidine cause reflex bradycardia and hypotension, which can lead to hypoxemia and tissue hypoxia. Hypoxia can cause capture myopathy, which can ultimately lead to cardiac arrest and death.4

Treating Respiratory Depression in Barasingha Deer

There are a number of approaches available to reduce the risk of opioid-induced respiratory depression in barasingha deer undergoing chemical immobilization. Assisted ventilation and oxygen insufflation can combat hypoxia,6 while agents such as opioid antagonists or partial antagonists can be used. Unfortunately, the latter also reduce desirable effects, such as the degree of immobilization, sedation and analgesia. Respiration can also be improved during chemical immobilization events via respiratory stimulants which act on non-opioid receptor systems such as potassium channel blockers, ampakines and serotonin receptor agonists.7

The administration of oxygen is recommended during the chemical immobilization of barasingha deer. This can be combined with a partial opioid reversal to better alleviate hypoxia.5 Naltrexone is frequently used to fully reverse opioid-based immobilization after capture, especially if the animal needs to be released back into the field and must be fully alert. If residual analgesic or sedative effects are required, partial opioid antagonists or mixed agonists/antagonists are used for the reversal of opioids such as diprenorphine, nalorphine or butorphanol.4,8 Signs of recovery after naltrexone administration typically consist of increased respiratory depth, followed by ear twitching, eye movement and lifting of the head.4

Partial mu-receptor antagonists like butorphanol can be used to reduce respiratory depression caused by strong mu-agonistic immobilization drugs.3,5 Some of these may also reduce the immobilization effects of opioids, however. Potassium channel blockers such as doxapram can also be used to stimulate breathing. Doxapram is widely used as a respiratory stimulant by veterinarians. It has been shown to increase the minute ventilation in large herbivores immobilized with etorphine.4 It should be noted that the respiratory effects of doxapram are usually short-lived.

Many safe and effective drug combinations for darting can now be purchased as highly-concentrated drug formulations in pre-mixed solutions from compounding pharmacies. These formulations are often species-specific, reliable and are less likely to bring about complications such as respiratory depression in barasingha deer than the drugs and combinations used in the past.


1worlddeer.org.
2animalia.bio.
3animaldiversity.org.
4Walsh VP, Wilson PR. Sedation and chemical restraint of deer. N Z Vet J. 2002 Dec;50(6):228-36. doi: 10.1080/00480169.2002.36318. PMID: 16032278.
5Arnemo, J. Kreeger, T. (2018). Handbook of Wildlife Chemical Immobilization 5th Ed. Sunquest Publishing, 2007.
6Arnemo, J., et. al. Field Emergencies and Complications. In: G. West, D. Heard, & N. Caulkett, eds. Zoo Animal and Wildlife Immobilization and Anaesthesia. Oxford: Wiley Blackwell, pp. 139–147.
7Bailey, P.L., et. al. (1985) The ED50 of carfentanil for elk immobilization with and without the Tranquilizer R51703. The Journal of Wildlife Management, 49(4), pp.931–934.
8Van der Schier, R., et. al. (2014) Opioid-induced respiratory depression: reversal by non-opioid drugs. F1000 Prime Reports, 6, pp.1–8.