A spectrum of severity is seen in dogs suffering from heat-induced illness in terms of both pathophysiological derangements and clinical consequences. It may therefore be more accurate to employ a gradation of severity from heat stress to heat exhaustion to heatstroke. Nevertheless, the general term ‘heatstroke’ will be used here.
Heatstroke results from severe hyperthermia, although a specific threshold above which heatstroke occurs has not been defined in dogs. Cellular injury may occur above 41°C and permanent brain damage is reportedly possible. Enzyme dysfunction, protein denaturation and severe organ damage may occur above 43°C and are associated with a significant increase in mortality. Further information regarding the prognosis in dogs with heatstroke is provided in Box 38.1.
Heatstroke may occur more readily in dogs suffering from a lack of acclimatization to warmer weather. The acute phase response and heat shock proteins may also be involved in the pathogenesis of heatstroke.
Heatstroke can be avoided in the majority of cases if appropriate preventative measures are employed. Preventative measures are especially important in dogs predisposed to heatstroke (e.g. brachycephalic breeds, dogs with laryngeal dysfunction, obese dogs) and include:
Heatstroke may be divided into two types. Classic heatstroke occurs due to exposure to high environmental temperature, for example being locked in a car with shut windows on a warm day, or being tied up outside without shade/water. Exertional heatstroke is the result of strenuous exercise. Many pathophysiological derangements are possible in heatstroke due to both direct heat-induced cytotoxicity and acute physiological changes due to hyperthermia. These are summarized in Box 38.3. Multiple organ dysfunction syndrome (MODS) (Box 38.4) is the most serious potential sequela of heatstroke.