Frostbite in Dromedary Camels During Capture and Chemical Immobilization
The domestic one-humped dromedary camel (Camelus dromedarius) remains an important resource in its range across northern Africa, the Middle East and western Asia. The ancestors of modern camels originated in North America, later becoming extinct there. It is believed that one-humped camels diverged from their two-humped ancestors (which later became the two-humped species, the Bactrian camel, C. bactrianus and C. ferus) around 4.4 million years ago.1,2
Camels were used almost exclusively as pack animals on the Silk Road, the network of routes used by traders between Europe and Asia for more than 1,500 years2 because they could carry more weight than horses or donkeys, needed less water and were able to thrive on tough desert plants. Today, camels are still used for their wool, milk, meat and leather,3and are engaged extensively in the tourism industry.
The dromedary camel (also known as the Arabian camel) has not occurred in the wild for nearly 2,000 years, having been widely domesticated beginning approximately 3,500 years ago. Dromedary camels are herbivorous, with a diet consisting of foliage, dry grasses and thorny plants that are common in the desert. Their thick, split upper lips allow them to access and eat things that other desert animals cannot. When foraging, groups of dromedary camels tend to spread out over large areas eat sparingly from numerous plant sources.
While the dromedary camel’s hump consists of fat and fibrous tissue (rather than water) that are used for energy storage, these animals are uniquely adapted to maintain their internal homeostasis and hydration whether water is plentiful or scarce. When water is available, they can drink up to 30 gallons of water in less than 15 minutes.1-3
Dromedary camels are diurnal and generally timid, although they are quite social among themselves in groups or herds. In most cases, they can be found in groups of four to six. In family groups, the male is dominant and brings up the family from the rear, with the several females with which he mates taking turns leading the group.
In the 1840's, dromedary camels were introduced into Australia to assist in the exploration of the inland continent, which is similar to the dromedary camel’s native habitat. Today, there are over one million feral camels in the rangeland ecosystems of Australia. Unfortunately, these animals are negatively impacting the natural environment to a significant degree. As a result, radio-collared camels are being used in Australia to enhance population control programs.4 The procedures involved in their capture—including chemical immobilization—carry the risk of inducing a wide range of complications.
The Risk of Frostbite in Dromedary Camels
Dromedary camels in their normal arid environments are generally at low risk for frostbite during chemical immobilization events (as opposed to Bactrian camels, whose range includes far cooler geographic regions). However, in zoos, research scenarios and on the fringes of their home ranges, the risk for frostbite still exists in these animals.
Frostbite is a freezing injury that may be divided into four overlapping phases:
- Vascular stasis
- Late ischemic5
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.5
The chemical immobilization of dromedary camels 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.6,7
The normal temperature of healthy camels at rest varies from about 34°C to more than 40°C.6 Due to the harsh environments that dromedary camels occupy, they have evolved with a unique ability for thermoregulation. This is referred to as adaptive hypothermia, or an ability to cool their bodies to avoid hyperthermia.
When deprived of drinking water during the summer, the camel’s daytime body temperature variations may exceed 6°C, but in animals with access to water, the variations are similar to those found during other seasons.7 These wide variations in temperature are tolerated by the camel, whereas in other animals, if body temperatures exceed more than 2 to 3 degrees higher than lower than the norm during an immobilization event, there is serious cause for concern.
The Classifications of Frostbite
Frostbite is classified into four degrees of injury, and these follow the classification schemes for thermal burn injury. Early stages of frostbite are different than frostnip, which is a superficial nonfreezing cold injury associated with intense vasoconstriction on exposed skin. Frostnip may precede frostbite, however. 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.7
- 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.7
It should be noted that the severity of frostbite may vary within a single extremity.
Prevention of Frostbite in Dromedary Camels
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.7
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 conditions8
Steps should also be taken to minimize exposure of the camel’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 exposure7,8
Treatment of Frostbite in Dromedary Camels
If it has been determined that a camel’s body part has suffered a frostbite injury in the field, the frozen tissue should be protected from further damage.8 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.7Frostbite thaws spontaneously and should be allowed to do so if rapid rewarming cannot be 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.7,8
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.7
Low Molecular Weight Dextran (LMWD) 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.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.7,8
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.8 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.7 However, aspirin theoretically blocks production of certain prostaglandins that are beneficial to wound healing, which may or may not be of concern following a chemical immobilization event.
5Haskins, S.C. (1995). Thermoregulation, hypothermia, hyperthermia. In: SJ. Ettinger. & EC. Feldman (Eds), Veterinary internal medicine (4th edition) (pp. 26–30). Philadelphia. U.S.A. W.B Saunders Company.
6Schmidt-Nielsen, K., et. al. Body Temperature of the Camel and Its Relation to Water Economy. American Journal of Physiology. 31 Dec 1956.
7McIntosh, 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.
8McIntosh, 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
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