Comprised of several subspecies, the impala (Aepyceros melampus) is one of the most well-known and widespread of the African ungulates. Often known (and photographed) for their spectacular leaps, impala are most often found in Kenya, Zimbabwe, Uganda, Zambia, Botswana, and Southern Angola to northern South Africa.1
Impala are fawn-colored with white undersides and a black stripe that extends from the top of the rump down the back of each thigh.2 Impala males have lyre-shaped horns which reach a length of around 30 inches. The impala stands 28–36 inches high and weighs between 90–167 pounds. Impala males are around 20% heavier than females.
Impala are one of the top food consumers in their particular niche. On the savanna, they play a significant role in the local food chain, feeding upon shrubs and grasses. They are key prey items for predators such as lions, leopards and hyenas. Impala herds typically stay within a few miles of water sources.3 During the dry season when conditions are more harsh, impalas aggregate in mixed herds which can number from 100–200 individuals. During the wet season, males and females separate into different herds where males compete for dominance.
Impalas engage in a polygynous mating system. This means that each male mates with numerous females.3 From March through May, pregnant females live in isolation to give birth. Gestation lasts from 194 to 200 days, after which females give birth to a single calf. Shortly thereafter, the calf and its mother rejoin the herd.2
Although the risk of frostbite as a complication of chemical immobilization tends to be significantly lower for African species in the field (as opposed to those in the Northern Hemisphere), it still does present some risk. Chemically immobilizing impala often requires 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 cooler months, and at higher altitudes.
Frostbite is classified as a freezing injury which is divided into four phases:
Prefreeze involves tissue cooling 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 gives 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.4
In addition to the above phases, frostbite is further broken down into four degrees of injury which follow the classification schemes for thermal burn injury. The early stages of frostbite are to be differentiated from frostnip, which is a superficial nonfreezing cold injury associated with intense vasoconstriction on exposed skin. Frostnip may, however, precede frostbite.5,6
One variation offered by McIntosh, et. al., involves a 2-tier classification scheme:
Most of the available literature holds that prevention is a far better methodology than treatment for frostbite, since this injury is usually preventable but often not improved by treatment. Underlying medical problems and the anesthetic event itself can increase risk of frostbite, so prevention must address both health-related and environmental aspects.5
Preventive measures which help to ensure local tissue perfusion include:
Methods that can help to minimize exposure of the animal’s tissues to cold include:
In the event that an impala’s body part is frozen under field conditions, the frozen tissue should immediately be protected from further damage.3,4 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 can accompany 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 prior to treating frostbite injury.6
Frostbite injury can result in vascular stasis, so appropriate hydration and avoidance of hypovolemia 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 dehydration.5,6
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.3,7
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.4
Nonsteroidal anti-inflammatory drugs (NSAIDs) are useful in the treatment of frostbite in that they block the arachidonic acid pathway and decrease production of prostaglandins and thromboxanes. These can lead to vasoconstriction, dermal ischemia, and further tissue damage.3 One rabbit ear model study showed 23% tissue survival with aspirin vs 0% in the control group.6 However, aspirin can block the production of certain prostaglandins that are beneficial to wound healing.7 Ibuprofen is therefore recommended rather than aspirin in cases of frostbite in impala.
1ucsd.edu.