Deer inhabit almost every continent on the globe; there are around a half dozen species that are common in North America, as well as other subspecies and non-native species.Interbreeding between species also takes place on occasion. Some species of deer in North America have been introduced, largely for the purposes of game hunting.
The axis deer (Axis axis) is one species. Native to the Indian subcontinent, it is a moderately large, spotted deer that was introduced into the U.S. in the early 1900s. Axis deer prefer sparse, secondary forests that supply adequate drinking water and shade, and they tend to avoid rugged terrain. Their food consists largely of grasses.1,2
The chemical immobilization of Axis 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.
While Axis deer in the field are almost never subjected to extreme cold in their native range (India), they may experience dangerously low temperatures in the areas in which they have been introduced (e.g., Europe and the U.S.). Frostbite is a cold-related injury in which body tissues 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.
Blood vessels throughout the body constrict to preserve heat when subjected to cold, and the body biochemically prioritizes keeping its core warm over the extremities. In cases of 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.
With superficial frostbite, ice crystals begin to form within the skin as it freezes, which can cause permanent damage to the tissue affected. At this stage, the skin may appear white and fluid-filled blisters may form. This may be difficult to detect in wild Axis deer, as their bodies are covered with fur. 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:
In the prefreeze phase, the tissues cool with accompanying vasoconstriction and ischemia, but 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. With vascular stasis, 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.4
Frostbite injury is divided into four stages (degrees) which follow the classifications for thermal burn injury. These stages have been based on acute physical findings and advanced imaging after rewarming.
The early stages of frostbite are different than frostnip, which is a superficial nonfreezing cold injury associated with intense vasoconstriction on exposed skin. Frostnip may, however, precede frostbite. In these cases, ice crystals do not form within the tissue and tissue loss does not occur.5,6
A version favored by McIntosh, et. al., involves a 2-tier classification scheme:
Regardless of the injury classification used, it should be noted that the severity of frostbite may vary within a single extremity.
Frostbite injury in Axis deer 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.5Frostbite prevention is far better than treatment, since this complication is usually not significantly improved by treatment. Underlying medical problems and the chemical immobilization event itself can increase the risk of frostbite, so prevention must address both health-related and environmental aspects.
Some 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 a chemically-immobilized animal’s extremities can remain numb before developing frostbite cannot be reliably determined. Therefore, any extremity at risk for frostbite (typically indicated by pale color) should be warmed.3
If an Axis deer’s body part is frozen in the field, the frozen tissue should be protected from further cold damage.3,4 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 injuries typically thaw spontaneously and should be allowed to do so if rapid rewarming cannot be done.
Hypothermia frequently accompanies frostbite; this 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.6
1. Hydration
Appropriate hydration and the avoidance of hypovolemia are important for frostbite recovery, since vascular stasis can result from frostbite injury. Intravenous saline should be given to maintain normal urine output. Optimally, IV fluids should 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.5,6
2. Low Molecular Weight Dextran Treatment
Low molecular weight dextran (LMWD) administered IV decreases blood viscosity by preventing red blood cell aggregation and formation of microthrombi; this can be given in the field once the animal/extremity 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; it was also more beneficial if given early.3,6
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.4
3. Treatment With NSAIDS
The use of nonsteroidal anti-inflammatory drugs (NSAIDs) for the treatment of frostbite remains controversial, since these drugs block the arachidonic acid pathway and decrease production of prostaglandins and thromboxanes, which can lead to vasoconstriction, dermal ischemia, and further tissue damage.3 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.7 Ibuprofen may be a superior alternative to aspirin, according to the authors of the rabbit ear study.
1tsusinvasives.org.
2animalia.bio.
3McIntosh, S., et. al. Clinical Practice Guidelines for the Prevention and Treatment of Frostbite: 2019 Update. Wilderness Medical Society Clinical Practice Guidelines, Volume 30, Issue 4, Supplement S19-S32, December 01, 2019.
4McIntosh, S.E., et. al. Wilderness Medical Society practice guidelines for the prevention and treatment of frostbite: 2014 update.Wilderness Environ Med. 2014; 25: S43-S54
5Mazur P. Causes of injury in frozen and thawed cells. Fed Proc. 1965; 24: S175-S182
6Lange K., et. al. The functional pathology of frostbite and the prevention of gangrene in experimental animals and humans.Science. 1945; 102: 151-152.
7Cauchy E., et. al. Retrospective study of 70 cases of severe frostbite lesions: a proposed new classification scheme. Wilderness Environ Med. 2001; 12: 248-255.