Heat Stroke
When animals are exposed to high ambient temperatures, intense solar radiation, and/or high humidity so that heat load increases at a rate faster than heat can be dissipated, heat stroke may develop.
Heat stroke is more common in ruminants because of their inability to sweat and thus their diminished evaporative ability for heat loss. Sheep with fleece and large dense cattle are especially prone to heat stroke when denied access to shade or adequate water and/or when physical activity is imposed on them. Rectal temperature will often exceed 107° F (41.5° C), and central body temperature may exceed 112° F (44.5° C). Heat stress is a recognized condition of llamas and alpacas that are exposed to high ambient temperature and high humid- ity.19 Normal camelids dissipate heat through evaporation of water through the respiratory system and sweat. In camelids, sweat glands are concentrated in the fleece-free areas of the axillary and inguinal regions. Camelids exposed to extreme heat conditions will seek out cool areas, decrease unnecessary physical activities, and stand or lie in a more upright position
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to improve sweating efficiency. They can also increase their respiratory rate and open-mouth breathe to help with heat loss through the respiratory system. Risk factors that can predispose animals to develop heat stroke include primary disorders that will render an animal weak or recumbent and obesity.20 With the peracute form of heat stroke, clinical findings include hyperthermia (often >105° F); tachycardia and/or tachyarrhythmia; recumbency; edema of the ventrum, perineum, and legs; and signs of respiratory distress including open-mouth breathing.20 Thoracic auscultation typically reveals increased bronchovesicular sounds and crackles suggestive of pulmonary edema.20 A frothy, blood-tinged oral or nasal discharge can be observed secondary to diffuse vasculitis.20 Affected animals are likely to die of multiple organ failure if rapid and aggressive treatment is not undertaken.20 With the more common subacute form (heat stress), affected animals are bright and alert but refuse to stand or have difficulties standing for long periods of time.20 With this form, the hyperthermia may be only present briefly or intermittently, and affected camelids typically maintain a normal appetite and organ function.
A neurologic examination may be difficult to interpret, and clinicians may often rely on the results of ancillary tests to rule out CNS disorders. A
Ieukogram is typically nonspecific and reflective of stress response. Biochemistry will usually reveal increased muscle enzymes, azotemia, hypoproteinemia, hyperlactemia, and 19 20 metabolic acidosis.19 20
Horses continuously exercised in high heat and humidity may also develop heat stroke. Evaporative heat loss from sweating is the most important means of heat loss as metabolic heat production increases during exercise, especially as ambient temperature and humidity increase.21 Efficiency of evaporative heat loss diminishes when temperature and humidity are high and there is a significant radiation component resulting from strong sunshine.22 Horses' susceptibility to heat stroke is enhanced if dehydration and electrolyte imbalances occur because of large losses of sweat (see also Exhaustion in Endurance Horses, Chapter 42). Adrenaline and noradrenaline may play a role in the adaptation of horses to thermal stress.23
As rectal temperature increases above 107° F (41.5° C), the homeostatic mechanisms of temperature regulation fail; peripheral vasoconstriction, decreased blood pressure, and decreased cardiac output occur. The animals are lethargic and have weak, flaccid muscles; prostration and shock occur rapidly. Disseminated intravascular coagulation, liver damage, renal failure, and myocardial necrosis are frequent complications.
The cornerstones of treatment of heat stroke are 1) to decrease the body temperature to normal levels and 2) to support the animal through its convalescent period.20 First, the animal should be removed from the extreme condition and brought to a cool, shady, and well-ventilated environment. For animals with fleece or heavy hair coat, clipping away the fleece is helpful. Pools of water (such as down cow float tanks or water troughs) are useful in rapidly cooling down camelids and small ruminants.
Topical alcohol and water (alcohol baths) are often ineffective at reducing body temperature as they may cause cutaneous vasoconstriction and can inhibit water evaporation from the skin. Administration of cool intravenous fluids may help with both decreasing body temperature and correcting hypovolemia and electrolyte losses. The rate of administration of intravenous fluids should be monitored closely, as animals with heat stroke (particularly camelids) can be prone to developing pulmonary edema. Other methods include administration of chilled water into the stomach or rectum and strategic placement of ice packs over areas with large vessels (neck, axilla, and inguinal regions). The administration of nonsteroidal antiinflammatory drugs is often useless at decreasing body temperature, as it is not a prostaglandin-mediated fever,20 and may even be harmful to the kidneys of a severely dehydrated animal. Attempts should be made at diagnosing and treating primary disorders that may have predisposed the animal to developing heat stroke, such as a neurologic condition. It is not uncommon for camelids or small ruminants that have survived the acute phase of heat stroke to remain recumbent for an extended period of time following the acute stage of the disease. Basic supportive and nursing care is important for those animals in order to avoid pressure sores and limb contracture.