The chemical immobilization of antelope can require extended periods of immobility in the captured animal, particularly as regards antelope species in North America and other areas of the Northern Hemisphere. 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.
Frostbite is a freezing injury that may be divided into four overlapping pathologic 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.2
Frostbite is classified into four degrees of injury following classification schemes for thermal burn injury. These are based on acute physical findings and advanced imaging after rewarming. 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. In these cases, ice crystals do not form within the tissue and tissue loss does not occur. Numbness and pallor resolve quickly after warming the skin.3,4
One 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.
The preponderance of literature suggests that prevention is a far better methodology than treatment for frostbite, which is usually preventable but often not improved by 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 perfusion and minimize heat loss to prevent frostbite.3
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 is unknown. Obviously, since this cannot be determined in a chemically immobilized animal, an extremity at risk for frostbite (typically indicated by pale color) should be warmed.1
If an antelope’s body part is frozen in the field, the frozen tissue should be protected from further damage.1,2 A decision must be made whether 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.4
Vascular stasis can result from frostbite injury, thus 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 clinical dehydration.3,4
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.1,5
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.2
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.1 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 vs 0% in the control group.4 However, aspirin theoretically blocks production of certain prostaglandins that are beneficial to wound healing.5 The authors of the rabbit ear model study recommended the use of ibuprofen rather than aspirin.