Heatstroke is a common, highly fatal emergency that occurs when intrinsic and extrinsic heat production exceeds mechanisms of heat dissipation (see Take-Home Messages).5 Heatstroke in dogs has been defined as a core body temperature >105.8°F (41°C) with concurrent CNS dysfunction.5 However, depending on the amount of time elapsed since the thermal injury and whether the pet owner initiated cooling of the patient (as in Fido’s case), dogs with heatstroke are not always presented with hyperthermia.5 It is thus essential that a diagnosis of heatstroke not be determined exclusively by the presence of hyperthermia or neurologic abnormalities on admission; rather, diagnosis should be based on patient history, clinical signs, and laboratory data.5
Heatstroke can be classified as either classic or exertional.6 Classic heatstroke is associated with exposure to high environmental temperatures and/or humidity; exertional heatstroke is associated with strenuous physical activity.6 Predisposing risk factors for heatstroke in dogs include, but are not limited to, exposure to a hot (often highly humid) environment, obesity, lack of fitness, and lack of acclimation to heat stress. In addition, certain breeds (eg, brachycephalic and large-breed dogs) are more susceptible than others.5
Routine CBC, which should always include blood film analysis, is essential for identification of the characteristic inappropriate rubricytosis and neutrophil morphologic changes that together support the diagnosis of heatstroke. Inappropriate rubricytosis is defined as rubricytosis in the absence of reticulocytosis.2 As such, an increased concentration of metarubricytes (in this case, 63 nRBC/100 WBC), along with only occasional polychromatophils and no anemia, is consistent with inappropriate rubricytosis.7 Inappropriate rubricytosis with no history of lead toxicity has been reported in up to 90% of dogs with heatstroke.8 The degree of rubricytosis has been reported to negatively correlate with survivability, and >18 nRBC/100 WBC is associated with decreased survival rates.7
Botryoid and karyolitic neutrophils have been reported to be a consequence of heatstroke in dogs.1 Karyolitic neutrophils (ie, neutrophils that exhibit nuclear lysis/degradation) were not identified in this case, but botryoid neutrophils, the pathogenesis of which are not well understood, were frequent. Botryoid neutrophils may be misidentified as hypersegmented neutrophils,1 which are characterized by a linear arrangement of nuclear segments and are typically associated with age-related changes of the cell.1
Although not seen in this case, thrombocytopenia is common in heatstroke patients and is typically considered to be due to consumption as a consequence of disseminated intravascular coagulation (DIC) and heat-induced vasculitis, GI bleeding, and hyperthermia-induced platelet aggregation and destruction1; therefore, assessment of a coagulation panel is recommended.5 In this case, a coagulation panel was not performed because of financial constraints, the platelet concentration was within the reference interval on the CBC panel, and there was no clinical evidence of a bleeding disorder.
Heatstroke and its associated lesions are a consequence of primary thermal insult. Secondary deterioration occurs because of dehydration, shock, poor perfusion, and thromboembolic disease.9 Common secondary complications of heatstroke can include neurologic dysfunction (eg, disorientation, stupor, seizures, coma), acute respiratory distress, acute kidney injury, rhabdomyolysis, myocardial damage, systemic inflammatory response syndrome, DIC, sepsis, and shock. Prompt diagnosis and aggressive intervention are crucial to achieving a positive outcome.9
Rapidly initiated cooling is the most important part of treatment. Owners should be instructed to begin cooling the dog immediately and to continue cooling during travel to the hospital. Mortality rate is significantly decreased when dogs have been cooled before presentation.9 Soaking or spraying with lukewarm water with subsequent use of fans, wind, or other airflow mechanisms helps maximize heat loss.8 Owners should also be instructed not to use ice or cold water for rapid cooling because vasoconstriction can result and has been shown to worsen the condition and increase mortality.4
The airway should be checked for patency. If necessary, the patient should be intubated because heatstroke can be exacerbated by upper airway obstruction, as can be seen in brachycephalic breeds or dogs with a history of laryngeal paralysis.8 Oxygen therapy should be initiated, an IV catheter placed, and samples collected for CBC, serum chemistry profile, coagulation profile, and urinalysis.8 IV isotonic crystalloids should be administered in incremental 10 to 20 mL/kg bolus volumes over 10 to 15 minutes until hypovolemia resolves. The patient should be reassessed between boluses to guide the need for further administration.9,10 Fluids assist with internal cooling, restoration of organ perfusion, and reduction of secondary complications.8
Active cooling should continue until the rectal temperature is 103.5°F (39.7°C).8 Rapid, large volumes of crystalloid fluids alone should be avoided in dogs with altered mentation, as these patients are more prone to cerebral edema.4 Crystalloids and colloids can be used together to maximize cerebral perfusion and minimize tissue edema.4 Additional therapies in severe cases may include fresh frozen plasma, dextrose, GI protectants, mannitol, antiarrhythmic medications, and broad-spectrum antibiotics if sepsis is suspected.8 More detailed treatment and monitoring recommendations are beyond the scope of this article but can be found in the literature.4,8,10
Despite appropriate intensive treatment, the mortality rate of patients with heatstroke is high. Many variables make outcome difficult to predict, but published mortality rates range from 36% to 56%.4,10 Prognosis is thus guarded, with most deaths occurring in the first 24 hours.4