Felis ISSN 2398-2950

Heat stroke

Contributor(s): F A Mann, Poppy Gant, Stefano Cortellini

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.

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

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to purchase a 30 day trial, or Login

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.


ADDED