Heat stroke
Introduction
- Cause: inadequate heat dissipation after exposure to excessively increased ambient temperature and/or overexertion.
- Signs: hyperdynamic state, panting, vomiting or diarrhea, CNS signs ranging from obtundation to coma, death.
- Diagnosis: supportive history, elevated body temperature (if not cooled prior to presentation), 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.
Age predisposition
- Any age.
- Very young kittens and geriatric patients have less efficient temperature control mechanisms.
Breed/Species predisposition
- Breeds with long coats and brachcephalic Brachycephalic airway obstruction breeds are likely to be at increased risk.
Cost considerations
- Development of multiple organ dysfunction Multiple organ dysfunction syndrome (MODS) is associated with significant costs and prolonged hospitalization.
- Development of acute kidney injury Kidney: acute renal failure requiring dialysis Kidney: advanced renal therapies may be cost prohibitive to many owners.
Pathogenesis
Etiology
- Imbalance between heat load (eg environmental heat or that from metabolism or exercise) and heat dissipation (controlled by the hypothalamus).
- Classic, non-exertional heat stroke is more likely to be recognized in cats.
- Heat dissipating mechanisms in cats initially occur by radiation and convection through skin. Panting in cats is rarely seen in the early stages of heat exhaustion. Grooming also plays a key role in thermoregulation via evaporation of saliva.
- Peripheral vasodilation occurs to increase heat loss and cardiac output increases.
- Cutaneous and splanchnic pooling along with reduced circulating volume from dehydration can eventually lead to hypotension. This reduces the efficacy of heat dissipating 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 liquifaction, 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 mass 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). Cats may be particularly predisposed.
- 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. The lungs are the shock organ in cats and therefore dyspnea may be more likely in comparison to dogs.
- Cardiovascular: cardiac arrythmias Heart: dysrhythmia secondary to hypoperfusion, direct thermal injury, biochemical 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 locked in a shed.
- Lack of acclimatization.
- Breed.
- Obesity.
- Cardiac disease/failure to increase cardiac output.
- Upper respiratory tract disease/abnormalities:
- Brachycephalic breeds.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed papers
- Recent references from PubMed and VetMedResource.
- Segev G, Bruchim Y, Berl N, Cohen A & Aroch I (2018) Effects of fenoldopam on kidney function parameters and its therapeutic efficacy in the management of acute kidney injury in dogs with heatstroke. JVIM 32(3), 1109-1115 PubMed.
- Bruchim Y, Kelmer E, Cohen A, Codner C, Segev G & Aroch I (2017) Hemostatic abnormalities in dogs with naturally occurring heatstroke. JVECC 27(3), 315-324 PubMed.
- Bruchim Y, Horowitz M & Aroch I (2017) Pathophysiology of heatstroke in dogs - revisited. Temperature 4(4), 356-370 PubMed.
- Bruchim Y, Segev G, Kelmer E, Codner C, Marisat A & Horowitz M (2016) Hospitalized dogs recovery from maturally occurring heatstroke; does serum heat shock protein 72 can provide prognostic biomarker? Cell Stress and Chaperones 21(1), 123-130 PubMed.
- Nielsen L K, Bracker K & Price L L (2015) Adminstration of fenoldopam in critically ill small animal patients with acute kidney injury: 28 dogs and 34 cats (2008-2012). JVECC 25(3), 396-404 PubMed.
Other sources of information
- Bruchim Y, Lemer E (2018) Canine heat stroke. In: Textbook of Small Animal Emergency Medicine. Drobatz K J et al (eds), Wiley and Sons.