Introduction

• Cause: inadequate heat dissipation after exposure to excessively increased ambient temperature and/or overexertion.
• Signs: hyperdynamic state (injected mucous membranes, hyperdynamic pulses, tachycardia), panting, vomiting or diarrhea, bleeding tendencies, CNS signs ranging from obtundation to coma and death.
• Diagnosis: supportive history, elevated body temperature (if not cooled prior to presentation or in shock), development of multiple organ dysfunction (including acute kidney injury (AKI) and disseminated intravascular coagulation (DIC) and encephalopathic state).
• Treatment: active cooling (generally to 39.4°C /103°F) and supportive therapies to prevent and treat systemic consequences.
• Prognosis: guarded if prolonged hyperthermia.
  Print off the owner factsheet Heat stroke Heat stroke to give to your client.

Pathogenesis

Etiology

• Imbalance between heat load (eg environmental heat or that from metabolism or exercise) and heat dissipation (controlled by the hypothalamus).
  • Both non-exertional (classic) and exertional heat stroke are recognized in dogs.
• Heat dissipating mechanisms in dogs and cats initially occur by radiation and convection through skin and evaporation through panting.
  • Peripheral vasodilation occurs to increase heat loss and cardiac output increases.
  • Cutaneous and splanchic pooling along with reduced circulating volume from severe dehydration can eventually lead to hypotension. This reduces the efficacy of heat disspitating mechanisms.
• Core body temperature rises if heat dissipating mechanisms are not sufficient.
  • Direct thermal damage results in cellular necrosis, protein and enzyme denaturation, lipid membrane disruption, mitochondrial damage and altered protein synthesis.
  • Thermal damage also results in the release of cytokines from muscle and increased absorption of endotoxin from the gastrointestinal tract.
  • Cytokines and endotoxins excessively activate leukocytes and endothelial cells.
  • This results in cytokine release resulting in activation of coagulation systems and inhibition of fibrinolysis.
  • This hypercoagulable state and endothelial injury results in microthombosis, leading to disseminated intravascular coagulation and multiple organ dysfunction.
• Protective mechanisms include production of acute phase proteins and increased expression of intracellular heat shock proteins which protect the cellular proteins against denaturation.
• Acclimatization can take weeks but include adaptive physiological and behavioral changes including increased blood volume, increased GFR and increased cardiac output.

Body systems affected by heat stroke

• Renal: acute kidney injury (AKI).
• Central nervous system: neuronal necrosis, cerebral edema, hemorrhage or multifocal vascular thrombosis and infarction.
• Respiratory: thermal and biochemical injury may lead to non-cardiogenic pulmonary edema Lung: pulmonary edema.
• Cardiovascular: cardiac arrythmias Heart: dysrhythmia secondary to hypoperfusion, direct thermal injury, metabolic abnormalities or DIC Disseminated intravascular coagulation.
• Gastrointestinal: intestinal ischemia may lead to intestinal permeability facilitating translocation of bacteria and endotoxin.

Predisposing factors

General

• High environmental temperature/humidity.
• Poor ventilation, ie dog locked in car.
• Lack of acclimatization.
• Breed.
• Obesity.
• Cardiac disease/failure to increase cardiac output.
• Upper respiratory tract disease/abnormalities:
  • Laryngeal paralysis Larynx: paralysis (reduced efficiency of panting).
  • Brachycephalic upper airway syndrome Brachycephalic airway obstruction syndrome.
  • Tracheal collapse Trachea: collapse.

Diagnosis

Treatment

Prevention

Outcomes