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[quote=Anonymous][quote=Anonymous]The necropsy on the dog failed to determine its CoD.  The dog did NOT suffer heatstroke.  hS in canine is easily detectable.

Eleven dogs with fatal heatstroke were examined grossly and histopathologically post mortem. All showed multi-organ haemorrhagic diathesis with coagulative necrosis. Hypaeremia and diffuse oedema were observed in the skin (eight dogs), lungs (11), brain (11) and bone marrow (one). Congestion of the splenic pulp (10 dogs) and hepatic sinusoids (nine) was also noted. Necrosis was observed in the mucosa of the small intestine (seven dogs), large intestine (eight), renal tubular epithelium (nine), hepatic parenchyma (eight) and brain neural tissue (four). The results showed that naturally occurring, fatal canine heatstroke induces acute multiple organ lesions affecting most body systems, and suggest that the more prevalent lesions include haemorrhagic diathesis, microthrombosis and coagulative necrosis. These are probable sequels of hyperthermia-induced disseminated intravascular coagulation and systemic inflammatory response syndrome, which lead to multi-organ dysfunction and death.[/quote]

Neurological dysfunction and abnormalities

Neurological abnormalities are invariably present in dogs with clinical heatstroke, including coma (40%), seizures (35%) and stupor (33%).30 Mild cases may show milder central nervous system (CNS) signs, such as disorientation or ‘delirium-like’ behavior. Extreme hyperthermia leads to cerebral hypoperfusion due to respiratory alkalosis and shock.72 This metabolic derangement is combined with the direct hyperthermic effects resulting in vascular damage, cerebral edema, hemorrhage and multifocal vascular thrombosis and infraction.72 Brain histopathology in fatal heatstroke cases in dogs has recorded cerebral edema, hemorrhage, hyperemia, and neuronal necrosis.34 The brain damage in heatstroke has been previously investigated in other mammals, including humans, and has been mainly attributed to a direct brain tissue thermal injury.73 Conversely, it has been shown that the canine brain has intrinsic thermal resistance, protecting it from direct thermal injury.72 It is therefore unlikely that direct thermal brain injury per se is the major factor in the pathogenesis of CNS lesions and abnormalities in dogs, although it might play a more minor part in the pathogenesis. The CNS abnormalities in dogs with heatstroke probably occur mostly secondary to shock and multi-organ dysfunction, including metabolic derangement, alkalosis or acidosis, hypoxia, hypoglycemia, bleeding and formation of microthrombi.34,72

Muscle damage and rhabdomyolysis

Rhabdomyolysis is a prominent feature of heatstroke in dogs, occurring during and following the heat insult, and is exacerbated during the first 24 hrs of hospitalization due to skeletal and cardiac muscular hypoperfusion, resulting from hypovolemic, distributive shock and microthromboses, secondary to developing DIC.37,74 Heatstroke in dogs is invariably reflected by increased muscle leakage enzymes activity.75 The severity of this increase reflects the extent of cellular muscular damage and the direct thermal injury to myocardial and skeletal muscle myocytes.74 In humans, rhabdomyolysis is confirmed through measurement of serum and urinary myoglobin concentration, however, in dogs, the human-based myoglobin immunoassays are insensitive, and currently no myoglobin immunoassay has been validated for use in dogs. Nevertheless, since oftentimes creatine kinase (CK) activity is markedly increased (median 17,000 U/L, >5 to 400-fold its upper reference limit) in dogs presented with heatstroke, it is reasonable to assume that rhabdomyolysis does occur in dogs with heatstroke, as described in humans victims of heatstroke.[/quote]

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