Heat stroke: diagnosis and treatment
Recent research has shown that heat stroke results from thermoregulatory failure coupled with an exaggerated acute-phase response and altered expression of heat-shock proteins. This article will summarize the incidence, thermoregulation, predispositions, pathophysiology, treatment and outcome of heat stroke.
Definition and incidenceHyperthermia in dogs can be pyrogenic or nonpyrogenic. Nonpyrogenic hyperthermia can result from exposure to high environmental temperature (non-exertional heat stroke) or from strenuous exercise (exertional heat stroke).
The classic definition of heat stroke is an elevated core body temperature
Heat is generated by basal metabolism, muscular activity and oxidative metabolism.
The thermoregulatory center of the body is located in the hypothalamus and receives input from hypothalamic sensor cells that detect the temperature of the circulating blood and cutaneous sensor cells. A physiologic response is triggered when afferent sensors throughout the body converge in the hypothalamus and warm blood supplying the hypothalamus stimulates compensatory cooling mechanisms.
There are four modes of heat dissipation: evaporation, conduction, convection and radiation (see Figure 1).
Evaporative cooling involves the loss of water to the environment and cools the tissue/skin surface. Radiative cooling is the transfer of heat between the animal and the atmosphere. Convective cooling involves the movement of air across a surface carrying the heat away. Conductive cooling is the exchange of heat between two objects in direct contact with one another.
At ambient temperatures <32 C, convection, conduction and radiation maintain normothermia. Cutaneous vasodilation and increased cardiac output lead to increased cutaneous circulation, which promotes heat loss through radiation, conduction and convection.
Approximately 70 percent of the total body heat loss in dogs and cats is due to radiation and convection from the body surface. As environmental temperature increases, evaporative cooling is more important.
The initial compensatory mechanism is activation of the panting center in the brain as the nasal turbinates provide a large surface area for loss of water from the moist mucous membranes. Some heat loss occurs through sweating (foot pads) and excretion of feces and urine.
Nonpyrogenic hyperthermia occurs when heat production cannot be adequately dissipated by normal thermoregulatory mechanisms.
Predisposing factors for the development of heat stroke can be categorized into conditions decreasing heat dissipation and those increasing heat production.
Environmental conditions decreasing heat dissipation include increased ambient temperature, humidity, poor ventilation and water deprivation.
Patient factors include any condition or medication that impairs the ability of the normal homeostatic response mechanism, such as laryngeal disease, brachycephalic anatomy, cardiovascular disease, central or peripheral nervous system disease, obesity, hair coat, age and medications (diuretics, B blockers, phenothiazine derivatives). Excessive heat production can occur through extreme exercise, seizures, hormonal hyperthermia and drugs/toxicities.
Heat stroke causes an altered heat-shock response and an exaggerated acute-phase response that leads to the production of reactive oxygen species, increased vascular and intestinal permeability, culminating in direct cellular injury and enzyme destruction.
The central nervous system changes are characterized by cerebral edema, hemorrhage, infarction and cerebellar dysfunction. Experimental studies suggest that temperatures as low as 41 C may cause permanent brain damage, which may predispose patients to subsequent hyperthermic episodes.
The cardiovascular and pulmonary systems are compromised due to the peripheral vasodilation and decreased peripheral vascular resistance leading to hypovolemia. Excessive panting leads to hemoconcentration, sludging of blood flow and respiratory muscle fatigue.
Direct cardiac injury may cause myocardial hemorrhage and necrosis. Pulmonary edema may result from cardiac failure, damage to the vascular endothelium or hypoproteinemia. Damage to the gastrointestinal system is characterized by gut ischemia, which predisposes to bacterial translocation. Hepatic damage also has been seen and is described as hepatocellular vascular degeneration with centrilobular necrosis and cholestasis.
Acute renal failure due to tubular necrosis is a result of direct thermal injury, hypoxia and microthrombi. Hyperthermia induces the platelet activation and coagulation factors; combined with endothelial and platelet damage, this can lead to disseminated intravascular coagulation. Rhabdomyolysis occurs as a direct result of high temperature and may be increased in patients experiencing an exertional heat stroke.