Frostbite in Bongo Antelope During Chemical Immobilization

The bongo (Tragelaphus eurycerus) is a large forest-living African antelope. Bongo are found in montane rain forests with dense undergrowth. They thrive at the forest edge and in new growth areas that occur after disturbances. Eastern (or mountain) bongos are much less prevalent than the western bongo and are only found in a mountain forested region of central Kenya.

Bongo are one of the largest forest antelopes. At full maturity, they stand between 3.5 to 4.5 ft (1–1.4m) high at the shoulder, are 7-10 ft (2-3m) long, and weigh between 460 and 900 lbs (200-408kg), with males being heavier than females. Eastern bongos are larger than western bongos.¹

Bongo have a red-brown chestnut coat with 10-15 narrow vertical white stripes running over the back and down the sides and a single chest stripe. The front legs are dark brown to black with thick white stripes, and there is a white crescent above the hooves on all four legs. Males tend to be darker than females. The bongo’s face has a black muzzle with a white chevron under the eyes and there are one or two white cheek patches on either side of the face. The ears are large with some white spotting. Both sexes have lyre-shaped smooth horns with 1 to 1.5 turns; these can grow to be 2.5 ft long.¹

Bongo have developed many adaptations that help them survive in the wild. The markings on the sides and backs of a bongo camouflage them in forest shadows, and their large ears help them hear approaching predators. They are mainly nocturnal, but also graze during mornings and evenings.

Chemical Immobilization and Frostbite in Bongo Antelope

The chemical immobilization of bongo 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 also remains a risk, even in animals that live in subtropical regions such as bongo. The risk of frostbite in bongo during chemical immobilization may be increased during inclement weather, at higher altitudes, and in immature animals. Frostbite and ear tip loss have frequently been seen in antelope species at temperatures below 9° C (15° F).²

Frostbite is a freezing injury that may be 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

Injury Classifications of Frostbite

Frostbite is also classified into four degrees of potential 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.^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

One 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 Bongo

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. 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.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^3,7

Treatment of Frostbite in Bongo Antelope

The time that an animal’s extremities can remain numb before developing frostbite is unknown. Obviously, since this cannot be determined in a chemically immobilized bongo, an extremity at risk for frostbite (typically indicated by pale color) should be warmed.¹

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 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

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 versus 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.

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.^3,7

The use of LMWD has not been evaluated in combination with other treatments such as thrombolytics in bongo or other antelope. LMWD should be given if the animal is not being considered for other systemic treatments, such as thrombolytic therapy.⁴

¹awf.org.

²Wolfe, Barbara A.. Bovidae (Except Sheep and Goats) and Antilocapridae. Fowler's Zoo and Wild Animal Medicine, Volume 8 (2015): 626–645. doi:10.1016/B978-1-4557-7397-8.00063-3

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.

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