Frostbite in Deer During Capture and Chemical Immobilization

Frostbite is a cold-related injury in which body tissues begin to freeze. Frostbite 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; this means that the body biochemically prioritizes keeping its core warm over the extremities. This is why they 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 Risks in Deer

In North America, deer are among the most well-known of the large wildlife species, and are popular with hunters and wildlife enthusiasts alike. Deer belong to the order Artiodactyla, a group of animals also known as cervids. Deer live on 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.^1,2

The chemical immobilization of deer can require extended periods of immobility in the captured animal, particularly as regards deer species in North America. 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 divided into four overlapping phases:

• Prefreeze
• Freeze–thaw
• Vascular stasis
• Late ischemic³

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.⁴

Classifications of Frostbite in Deer

Frostbite is classified into four degrees of injury that follow the 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. As indicated earlier, frostnip may, however, precede frostbite. In these cases, ice crystals do not form within the tissue and tissue loss does not occur.^5,6

• 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.
• Second-degree frostbite injury causes superficial skin vesiculation. A clear or milky fluid will be present in superficial blisters surrounded by erythema and edema.
• Third-degree frostbite causes deeper hemorrhagic blisters, indicating that the injury has extended into the reticular dermis and beneath the dermal vascular plexus.
• Fourth-degree frostbite extends completely through the dermis and involves the comparatively avascular subcutaneous tissues, with necrosis extending into muscle and bone.³

A variation favored by McIntosh, et. al., involves a 2-tier classification scheme:

• Superficial—Minimal anticipated tissue loss, corresponding to first- and second-degree injury.
• Deep—Anticipated tissue loss corresponding to third- and fourth-degree injury.³

It should be noted that the severity of frostbite may vary within a single extremity.

Prevention of Frostbite in Deer

Prevention is a far better methodology than treatment for frostbite, which is usually 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 tissue perfusion and minimize heat loss to prevent frostbite.⁵

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 conditions^3,6

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 exposure^3,6

Treatment of Frostbite in Deer

Since the time that an animal’s extremity can remain numb before developing frostbite cannot be determined in a chemically immobilized animal, any extremity at risk for frostbite (typically indicated by pale color) should be warmed.³

If a deer’s body part is frozen in the field, the frozen tissue should be protected from further 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 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

Treatment Modalities for Frostbite

1. Hydration

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.5,6

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.^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

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.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 vs 0% in the control group.⁶ However, aspirin theoretically blocks production of certain prostaglandins that are beneficial to wound healing.⁷ The authors of the rabbit ear model study recommended the use of ibuprofen rather than aspirin.