Frostbite in Kudu Antelope During Chemical Immobilization
The chemical immobilization of antelope can require extended periods of immobility in the captured animal. Hypothermia is an inherent risk to any animal undergoing chemical immobilization regardless of ambient temperature, and frostbite is an even greater risk during the winter months or at higher, cooler elevations.
Frostbite is a freezing injury that may be divided into four overlapping pathologic phases: Prefreeze, freeze–thaw, vascular stasis and late ischemic.1 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 Classifications
Frostbite is classified into four degrees of injury. These follow classification schemes for thermal burn injury, and 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.2,3
- 1.First-degree frostbite causes numbness and erythema. A white or yellow, firm, and slightly raised plaque develops in the area of injury. There may be slight epidermal sloughing and mild edema is common.
- 2.Second-degree frostbite injury causes superficial skin vesiculation. A clear or milky fluid will be present in superficial blisters surrounded by erythema and edema.
- 3.Third-degree frostbite causes deeper hemorrhagic blisters, indicating that the injury has extended into the reticular dermis and beneath the dermal vascular plexus.
- 4.Fourth-degree frostbite extends completely through the dermis and involves the comparatively avascular subcutaneous tissues, with necrosis extending into muscle and bone.1
One variation favored by McIntosh, et. al., involves a 2-tier classification scheme:
- 1.Superficial—Minimal anticipated tissue loss, corresponding to first- and second-degree injury.
- 2.Deep—Anticipated tissue loss corresponding to third- and fourth-degree injury.1
It should be noted that the severity of frostbite may vary within a single extremity.
Characteristics of Kudu Antelope
The kudu is a large African antelope that consists of two subspecies: the greater kudu (Tragelaphus strepsiceros), and the lesser kudu (Tragelaphus imberbis). The greater kudu is second in size to the eland, Africa’s largest antelope. Both subspecies have stripes and spots on their bodies and a chevron of white hair between the eyes.4 The males have long, spiraling horns, with the horns of the greater kudu growing as long as six feet. The females of both subspecies are substantially smaller than the males.
The greater kudu inhabits the dense brush and forested areas of southern Africa, while the more elusive lesser kudu is common in the arid lowland thornbush of northeast and East Africa.5 For food, both kudus forage on a wide variety of trees, shrubs, vines, herbs, seedpods, fruits and grasses. Both species prefer the green growth along watercourses in dry seasons and disperse through deciduous woodlands during rainy seasons.4
Prevention of Frostbite in Kudu
The available literature suggests that frostbite prevention is a far better methodology than 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. 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:
- Maintaining adequate core temperature
- Maintaining adequate body hydration
- Minimizing the effects of any known diseases that might decrease perfusion
- Covering the body and head to insulate from the cold
- Minimizing any blood flow restriction
- Using supplemental oxygen in severely hypoxic conditions1,3
Measures should also be taken to minimize exposure of the animal’s tissues to cold, such as:
- Avoid environmental conditions that predispose to frostbite if possible (e.g., below -15°C, even with low wind speeds
- Protecting exposed skin from moisture, wind, and cold
- Avoiding perspiration or wet extremities
- Increasing insulation and skin protection
- Using chemical and/or electric warmers to maintain peripheral warmth (These should be close to body temperature before being activated and must not be placed directly against skin or constrict flow)
- Regularly checking the animal’s temperature
- Recognizing frostnip or superficial frostbite before it becomes more serious
- Minimizing duration of cold exposure1,3
Treatment of Frostbite in Kudu
The time that an animal’s extremities can remain numb before developing frostbite is unknown. Since this cannot be determined in a chemically immobilized antelope, any extremity that is 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 damage1,2 and 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.6
Hydration Following Frostbite
Vascular stasis can result from frostbite injury, thus appropriate hydration and avoidance of hypovolemia are important in 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.3,6
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.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
1McIntosh, 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.
2McIntosh, 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
3Mazur 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.
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