INTRODUCTION

Three syndromes of heat illness that represent a continuum from the least to the most severe form are described in humans. Heat cramp is characterized by muscle spasms resulting from sodium and chloride depletion. When signs such as fatigue, weakness, muscle tremors, vomiting, and diarrhea occur, heat prostration or exhaustion may be diagnosed. The hallmark of heat stroke is severe central nervous system (CNS) disturbance and is often associated with multiple organ dysfunction. A more recent definition of heat stroke describes it as a form of “hyperthermia associated with a systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates.”¹ This latter definition is more physiologically based and gives a much more informative description of what is seen clinically in dogs with heat stroke. Generally, clients seek veterinary attention when their pets are demonstrating signs consistent with heat prostration, heat exhaustion, or heat stroke. This chapter will focus primarily on dogs with heat-induced illness because cats rarely suffer from heat stroke.

PHYSIOLOGY, PATHOGENESIS, AND PATHOPHYSIOLOGY

A hot environment or exercise in a hot environment does not equate to overheating and heat-induced illness. It is the increase in core body temperature that results in heat-induced illness (see Chapter 5, Hyperthermia and Fever). Therefore the body has developed a relatively effective thermoregulation system to protect itself from overheating.

Thermal homeostasis is maintained by a balance between heat load (environmental heat and heat generated through metabolism and exercise) and heat-dissipating mechanisms controlled by temperature-sensitive centers in the hypothalamus. Body temperature increases when heat load exceeds heat dissipation. Heat dissipation may occur via four mechanisms: convection, conduction, radiation, and evaporation. As the body temperature increases, 70% of heat loss in dogs and cats occurs via radiation and convection through the skin. Heat loss is facilitated by increased cutaneous circulation as a result of increased cardiac output and sympathetic-mediated peripheral vasodilation.² Shunting of blood to the periphery is a trade-off with blood supply to the viscera (intestines and kidneys). Significant heat loss also occurs as a result of evaporation from the respiratory tract through panting, and this becomes the predominant mechanism of heat loss when ambient and body temperatures become equal.

A warm, humid environment and exercise are the two most common heat loads that dogs experience and may cause extreme hyperthermia, even in animals with functional heat dissipating mechanisms. Respiratory evaporative heat loss may be diminished by humid climatic conditions, closed confinement with poor ventilation, and upper respiratory abnormalities such as brachycephalic conformation, laryngeal paralysis or masses, or collapsing trachea. Additionally, the work of breathing in these latter conditions can contribute substantially to the heat load in these animals. Diminished radiation and convective heat loss from the skin may occur as a result of hypovolemia from any cause, poor cardiac output, obesity, extremely thick hair coat, or lack of acclimatization to heat. Situations that combine high heat load and diminished heat dissipation may result in a rapid and extreme body temperature increase.

Most dogs with heat illness present when the warm, humid weather begins, so the seasonal pattern varies depending on climatic conditions and year-to-year variations in temperature and humidity. In some instances, despite progressively warmer days later in the summer, heat-induced illness becomes less frequent.³ This may be related to the time available for acclimatization to the change in environmental temperature. In humans, acclimatization to heat can take 2 weeks or more and is associated with enhanced cardiac performance, salt conservation by the kidney and sweat glands through activation of the renin-angiotensin-aldosterone axis, an increased capacity to sweat, plasma volume expansion, increased glomerular filtration rate, and an increased ability to resist exertional rhabdomyolysis.⁴

Increased body heat induces three protective mechanisms, including thermoregulation (mentioned previously), an acute phase response, and intracellular heat shock proteins.¹ The acute phase response involves a variety of proinflammatory and antiinflammatory cytokines. Proinflammatory mediators induce leukocytosis, stimulate synthesis of acute phase proteins, stimulate the hypothalamic-pituitary-adrenal axis, and activate endothelial cells and white blood cells. These mediators are protective for the body when balance is maintained between the proinflammatory and antiinflammatory sides.

The heat shock proteins protect the cell and the body against further heat insults, likely as a result of protection against denaturation of intracellular proteins and regulation of the baroreceptor response during heat stress, preventing hypotension and conferring cardiovascular protection.⁵ Heat stroke results from a failure of thermoregulation followed by an exaggerated acute phase response and alteration of heat shock proteins.¹ Additionally, absorption of endotoxin from the gastrointestinal (GI) tract may fuel the inflammatory response, because intestinal mucosal permeability is increased during heat stress.⁶ It has been noted that many of the mediators involved in heat stroke are the same mediators associated with sepsis and the systemic inflammatory response syndrome (see Chapters 11 and 106, Systemic Inflammatory Response Syndrome and Sepsis, respectively).¹

The suggested pathophysiologic sequence in heat stroke involves initial production and release of interleukin-1 and interleukin-6 from the muscles into the circulation and increased systemic endotoxin from the intestines.¹ These factors mediate excessive activation of leukocytes and endothelial cells, resulting in release of numerous inflammatory and antiinflammatory cytokines, as well as activation of coagulation and inhibition of fibrinolysis. Direct endothelial cell injury due to the heat, combined with an initial hypercoagulable state, result in microthrombosis and progressive tissue injury. These proinflammatory and procoagulation processes and direct heat injury can lead to multiple organ dysfunction syndrome. Because of the multisystemic problems in patients with heat stroke, these animals should be assessed and monitored for multiple organ failure, particularly the respiratory, cardiovascular, renal, GI, and central nervous systems, as well as the coagulation system.

PHYSICAL EXAMINATION

The physical findings of dogs suffering from heat-induced illness vary with the intensity and duration of the increased body temperature and the individual pathophysiologic responses that are initiated.

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