The chemical immobilization of large hoofstock such as deer can require extended periods of immobility in the captured animal. While hypothermia is an inherent risk to any animal undergoing chemical immobilization regardless of ambient temperature, frostbite is an even greater risk during the winter months, particularly as regards deer species in North America.
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 marshy, damp areas, such as reed beds and marshes in its native range. They occasionally dwell in open spaces, but usually remain very close to a source of water. The barasingha deer is one of several non-native species that has been introduced into the U.S. as a game animal, where they may be hunted on carefully-controlled ranches and reserves.
The barasingha deer is extinct in both Bangladesh and Pakistan, where it once had a wide range. Today, there are fragmented populations in central and northern India, as well as southwestern Nepal.2 The name “barasingha” is derived from the Hindi words for “twelve ends”; this references the deer’s antlers, which can have up to 20 tines.
The barasingha is a large, long-legged deer, with a short head and long, broad ears. Larger animals 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. The hair around the deer’s neck may be longer, forming a shaggy mane.2,3
In their native range, barasingha deer have several 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; this is said to be similar to the alarm call of the roe deer. Barasingha deer feed early and late in the day, and can often 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.
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.2,3
In the late 1960s, the numbers of barasingha 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. Habitat improvement and captive breeding led to a substantial increase in the population.3 Today, their populations are no longer considered to be in danger.
Frostbite is a cold-related injury in which the tissues of the body begin to freeze. It can affect any part of the body that is exposed to extreme cold for an extended period of time. This period of time is reduced as the relative (ambient) temperature drops. When subjected to cold, blood vessels throughout the body constrict to preserve heat, which reflects the body biochemically prioritizing keeping its core warm over its extremities. This is why the extremities are more at risk for frostbite.
With frostnip (early-stage frostbite or the near-freezing of tissues), the skin becomes red, cold to the touch and may begin to go numb. In these cases, if the skin is warmed soon enough after exposure, there is usually no permanent damage. Continued exposure to cold can result in superficial frostbite.
In superficial frostbite, ice crystals begin to form within the skin as it freezes. This can cause permanent damage to the tissue affected. At this stage, the skin may appear white and fluid-filled blisters can appear. Naturally, this may be difficult to detect in wild animals, as their bodies are covered with a fur coat. In cases of deep frostbite, large blisters form, and the tissue will often turn black and hard as it necrotizes.
Frostbite is divided into four overlapping phases:
Prefreeze consists of tissue cooling with accompanying vasoconstriction and ischemia and without ice crystal formation. The freeze–thaw phase is represented by the intracellular or extracellular formation of ice crystals. This can give rise to protein and lipid derangement, cellular electrolyte shifts, cellular dehydration, cell membrane lysis, and cell death. In the vascular stasis phase, vessels fluctuate between constriction and dilation, and blood may leak from vessels or coagulate within them. The late ischemic phase results from progressive tissue ischemia and infarction from a cascade of events, including inflammation, vasoconstriction and emboli.5
Frostbite is classified into four degrees of injury; these follow the classification schemes for thermal burn injury. They are based on acute physical findings and advanced imaging after rewarming. As indicated earlier, frostnip may precede frostbite. In these cases, ice crystals do not form within the tissue and tissue loss does not occur.6,7
A variation favored by McIntosh, et. al. involves a 2-tier classification scheme:
It should be noted that the severity of frostbite may vary within a single extremity.
Frostbite is usually not improved by treatment, so prevention is a better methodology than treatment. Underlying medical problems and the chemical immobilization event itself can increase risk of frostbite, so prevention must address both health-related and environmental aspects. Frostbite injury usually occurs when tissue heat loss exceeds the ability of local tissue perfusion to prevent freezing of soft tissues. The team in the field must ensure adequate tissue perfusion and minimize heat loss to prevent frostbite.6
Preventive measures to ensure local tissue perfusion include:
Measures should also be taken to minimize exposure of the animal’s tissues to cold, such as:
The time that an animal’s extremity can remain numb before developing frostbite cannot be determined in a chemically immobilized animal, so any extremity at risk for frostbite (typically indicated by pale color) should be warmed.4
If a barasingha deer’s body part is frozen in the field, the frozen tissue should be protected from further damage.4,5 Then, a decision must be made whether or not to thaw the tissue. If environmental conditions are such that thawed tissue could refreeze, it is safer to keep the affected part frozen until a thawed state can be maintained. Frostbite thaws spontaneously and should be allowed to do so if rapid rewarming cannot be easily achieved.
Hypothermia frequently accompanies frostbite and causes peripheral vasoconstriction that impairs blood flow to the extremities. Mild hypothermia may be treated concurrently with frostbite injury. Moderate and severe hypothermia should be treated effectively before treating frostbite injury.7
1. Hydration
Since vascular stasis can result from frostbite injury, appropriate hydration and avoidance of hypovolemic shock are important for frostbite recovery. Intravenous normal saline should be given to maintain normal urine output. IV fluids should optimally be warmed before infusion and infused in small, rapid boluses, as slow infusion can result in fluid cooling and even freezing as it passes through tubing. Fluid administration should be optimized to prevent clinical dehydration.6,7
2. Low Molecular Weight Dextran Treatment
Intravenous low molecular weight dextran (LMWD) decreases blood viscosity by preventing red blood cell aggregation and formation of microthrombi and can be given in the field once it has been warmed. In some animal studies, the extent of tissue necrosis was found to be significantly less than in control subjects when LMWD was used, and was more beneficial if given early.4,7
The use of LMWD has not been evaluated in combination with other treatments such as thrombolytics. LMWD should be given if the animal is not being considered for other systemic treatments, such as thrombolytic therapy.5
3. Treatment With NSAIDS
Nonsteroidal anti-inflammatory drugs (NSAIDs) block the arachidonic acid pathway and decrease production of prostaglandins and thromboxanes. These can lead to vasoconstriction, dermal ischemia, and further tissue damage.4 No studies have demonstrated that any particular anti-inflammatory agent or dosing is clearly related to outcome, however. One rabbit ear model study showed 23% tissue survival with aspirin versus 0% in the control group.6 However, aspirin theoretically blocks production of certain prostaglandins that are beneficial to wound healing,8 and the authors of the rabbit ear model study recommended the use of ibuprofen rather than aspirin.