The Signs Of Heat Stroke In Dogs

Heat stroke in dogs cannot be precisely defined as such however, should be taken into consideration when in an otherwise healthy animal, heat-induced acute onset of severe clinical signs of illness are displayed. As the environmental temperature goes up and approaches to body temperature, evaporation, primarily through panting, becomes more important in maintaining normothermia.

The nasal turbinates provide a large surface area for water loss from the moist mucous membranes and have an important role in the evaporative cooling mechanism. Hypersalivation improves evaporation efficiency. More than 70% of the total body heat loss in dogs is dissipated through radiation and convection from body surfaces. High environmental temperature and increased humidity (>35%) reduce evaporation efficiency, and when the humidity is >80%, evaporation will be negated.

The signs for all cases in the present study included presence of systemic clinical signs of an acute onset, along with a history of exposure to a warm environment, strenuous activity, or both, in otherwise healthy puppies, with no other concurrent disease. Normally, high environmental temperatures cause peripheral vessels to dilate, allowing more blood to flow to the skin and dissipate heat. The brain and muscles have a concurrent need for increased blood flow. If the vascular system cannot meet these demands, heat exhaustion occurs.

The signs of heat stroke are related to the primary thermal insult. However, secondary deterioration occurs because of dehydration, shock and a poor perfusion. Thus, early diagnosis and intervention are crucial to the prevention of further cerebral and renal deterioration and exacerbation of coagulation abnormalities. An outcome in most cases of heat stroke is Azotemia which results due to prerenal and renal mechanisms, such as severe hemoconcentration and direct renal tissue damage, leading to tubular necrosis. This probably occurs as a consequence of dehydration, a direct renal thermal injury, hypoxia, endotoxemia, release of cytokines and vasoactive mediators.

Aggressive fluid therapy over the first 24 hours of hospitalization probably eliminates the prerenal component. Hypoglycemia can result from increased utilization or decreased production of glucose. Increased glucose utilization results from increased ATP demand, associated with high body temperatures, seizures, and respiratory efforts. Hypoglycemia may be a risk factor for the development of central nervous system abnormalities in canine heat stroke.

This result exemplifies the importance of restoring and maintaining normoglycemia in dogs with heat stroke as part of the routine treatment. The case in this study had occurred in the month of May corresponding to early peak of the hot season, in which most cases are usually presented. As the average temperature of the particular region in the summer months is usually high, owners should be advised to avoid exposure of their dogs to such environmental conditions, and clinicians should be aware that the likelihood of heat stroke is higher.