Hyperthermia and Heat-Induced Illness

Chapter 14

Hyperthermia and Heat-Induced Illness

Hyperthermia, defined as a severe elevation body temperature from 40.5° to 43° C (104.9° to 109.4° F), can occur with exposure to elevated ambient temperatures and high ambient humidity, after strenuous activity, or as a normal physiologic process in response to endogenous or exogenous pyrogens. A fever differs from hyperthermia in that with a fever, or pyrogenic hyperthermia, the thermoregulatory center set point in the hypothalamus is elevated in response to infection and inflammation. Nonpyrogenic hyperthermia is abnormal and is secondary to an inability to dissipate heat. Animals that exercise or are allowed to work or exert themselves under conditions of high environmental temperatures can develop hyperthermia in as little as 30 minutes unless adequate access to shade, water, and rest period is available.


Core body temperature is controlled by a thermoregulatory center that is located in the hypothalamus. Heat balance occurs through the actions of heat-gaining and heat-dissipating mechanisms. Heat gain occurs through oxidative metabolic processes after eating, exercise or increased metabolic activity, and elevated environmental temperature. Heat-dissipating mechanisms mitigate heat gain and include changes in behavior such as seeking a cooler location, peripheral vasodilation, and evaporative cooling in the form of respiratory heat exchange, radiation, and convection. When environmental temperature increases and approaches body temperature, evaporative heat loss becomes important to maintain normothermia. Domestic animals such as dogs and cats that largely lack sweat glands depend primarily on the dissipation of heat in the form of evaporative cooling from the respiratory system during panting. Panting is an adaptive mechanism to help dissipate heat and prevent hyperthermia. As body temperature increases, the thermoregulatory center in the hypothalamus is activated, senses a change in temperature, and sends a relay of signals to the panting center. The animal responds by panting, increasing both dead space ventilation and evaporative cooling mechanisms in an attempt to dissipate heat. Evaporative cooling occurs as air comes in contact with the mucous membranes of the upper airways. Evaporative cooling mechanisms are not efficient if high ambient humidity is present, and the body’s core temperature continues to rise. Early, an increase in dead space ventilation occurs, with little effect on carbon dioxide elimination. As hyperthermia progresses, however, metabolic alkalosis can occur. With prolonged hyperthermia, the body’s normal adaptive mechanisms no longer compensate, and cerebrospinal fluid hypocapnia and alkalosis, factors that normally decrease panting, are no longer effective, and panting continues.

Convection is a second method of cooling by which heat is passively transferred from an overheated animal to a cooler surface. Peripheral vasodilation increases blood flow to the skin and periphery and helps to dissipate heat by convective mechanisms. Peripheral vasodilation causes a state of relative hypovolemia, and in order to maintain adequate blood pressure, splanchnic vessels constrict to maintain adequate circulating volume. Catecholamines are released, causing an increase in heart rate and cardiac output. Early in hyperthermia, there is an increase in cardiac output and decrease in peripheral vascular resistance. However, as hyperthermia progresses, blood pressure and cardiac output decrease when the body can no longer compensate. Perfusion to vital organs decreases and can result in widespread organ damage if left untreated.

Widespread thermal injury occurs to neuronal tissue, cardiac myocytes, hepatocytes, renal parenchymal and tubular cells, and the gastrointestinal tract. The combined effects of decreased organ perfusion, enzyme dysfunction, and uncoupling of oxidative phosphorylation are a decrease in aerobic glycolysis and an increase in tissue oxygen debt, both of which contribute to increased lactate production and lactic acidosis. Lactic acidosis can occur within 3 to 4 hours of initial heat-induced injury.

Direct thermal injury to renal tubular and parenchymal cells, decreased renal blood flow, and hypotension cause hypoxic damage to the tubular epithelium and cell death. As hyperthermia progresses, renal vessel thrombosis can occur with disseminated intravascular coagulation (DIC). Consistent findings in patients affected with severe hyperthermia are renal tubular casts and glycosuria on urinalysis in the presence of normoglycemia. Rhabdomyolysis can also be associated with severe myoglobinuria and pigment-associated damage to the renal tubular epithelium.

The gastrointestinal tract is a key factor in multiorgan failure associated with hyperthermia. Decreased mesenteric and gastrointestinal perfusion and thermal injury to enterocytes often result in a disruption of the gastrointestinal mucosal barrier, with subsequent bacterial translocation. Bacteremia and elevation of circulating bacterial endotoxin can lead to sepsis, systemic inflammatory response syndrome (SIRS), and multiorgan failure. Patients with severe hyperthermia can present with hematemesis and severe hematochezia, and often slough the lining of their gastrointestinal tract.

Thermal damage to the liver can result in decreased hepatic function, with elevations of hepatocellular enzyme activities and increased alanine transaminase (ALT), aspartate transaminase (AST), and total bilirubin. Necropsy findings in one retrospective study of 42 dogs with hyperthermia found centrilobular necrosis, widespread tissue congestion, hemorrhagic diathesis, and pulmonary infarction. Persistent hypoglycemia in affected patients may be associated with hepatocellular dysfunction and glycogen depletion. Decreased hepatic macrophage function and portal hypotension can also predispose the patient to sepsis, with associated bacteremia and SIRS.

Virchow’s triad (vascular endothelial injury, venous stasis, and a hypercoagulable state) develops during hyperthermia and heat-induced illness. Widespread endothelial damage with exposure of subendothelial collagen and tissue factor cause systemic platelet activation, consumption of clotting factors, and activation of the fibrinolytic pathway. Sluggish blood flow during periods of hypotension, decreased production of clotting factors, and loss of natural anticoagulants such as antithrombin from the gastrointestinal tract combine to predispose the patient to DIC. Massive global thrombosis associated with DIC can result in multiorgan dysfunction syndrome (MODS) and death.

Finally, hyperthermia can cause direct damage to neurons, neuronal death, and cerebral edema. Thrombosis or intracranial hemorrhage can also occur with DIC. Damage to the hypothalamic thermoregulatory center, localized intraparenchymal bleeding, infarction, and cellular necrosis can all lead to seizures. Altered levels of consciousness are among the most common clinical signs of heat-induced illness. As hyperthermia progresses, severe central nervous system depression, seizures, coma, and death may occur. The potential for reversal of cerebral edema is related to the duration of the neurons to heat exposure. Severe abnormalities in mentation are associated with a negative outcome in animals with hyperthermia. In one retrospective study of dogs, the only presenting clinical sign that was negatively associated with outcome was if the animal was comatose on presentation. A less favorable outcome was also associated with the development of stupor, coma, or seizures within 45 minutes of presentation.

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Hyperthermia and Heat-Induced Illness

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