ISSN 2398-2950      

Heat stroke

ffelis

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 obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to obtain ten tokens to view any ten Vetlexicon articles, images, sounds or videos, 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.

Can’t find what you’re looking for?

We have an ever growing content library on Vetlexicon so if you ever find we haven't covered something that you need please fill in the form below and let us know!