Heatstroke (Proceedings)


Heatstroke can be defined as severe hyperthermia resulting in thermal injury to tissues. Under normal circumstances, cats and dogs maintain their body temperature over a wide range of environmental temperature variations.

Heatstroke can be defined as severe hyperthermia resulting in thermal injury to tissues. Under normal circumstances, cats and dogs maintain their body temperature over a wide range of environmental temperature variations. In response to mild heat stress, reflex vasoactivity occurs and leads to the shunting of blood from muscles and visceral organs to the periphery, where cutaneous vasodilation allows heat loss by radiation and convection. During moderate heat stress, panting provides a means of heat loss by evaporation, as large volumes of air move across the mucosa of the oropharynx and tongue. Heat stroke occurs when these compensatory mechanisms fail or are overwhelmed and must be differentiated from pyrexia. Pyrexia leads to resetting of the thermoregulatory center in response to a pathological process such as infection or inflammation, while heatstroke occurs when the normal thermoregulatory system of the body is overwhelmed by exposure to extreme heat stress.

Predisposing factors

Factors predisposing to heatstroke include those causing either increased heat production or impaired heat loss. Endogenous factors include pre-existing respiratory or cardiac disease, which can cause an animal to become vulnerable to heat stroke by compromising heat dissipation. CNS abnormalities can impair the ability to thermoregulate. Extremes in age can also result in thermoregulatory problems, as infants do not acquire the ability to thermoregulate until they are 45 days old. Geriatric patients often have underlying cardiac or respiratory disease that decreases their ability to tolerate heat stress. Obese animals are predisposed to heatstroke because their tendency to retain heat, and abnormal upper airway conformation leads to difficulties with heat dissipation in brachycephalic breeds.

Exogenous factors include extreme exercise, high humidity, and confinement in poorly ventilated areas. Lack of acclimatization can predispose to heat stress, as can water deprivation. Drugs predisposing to heatstroke include phenothiazine derivatives and diuretics. Phenothiazines cause disturbances in thermoregulation by depressing the reticular activating system, whereas diuretics lead to depletion of fluid and electrolytes with subsequent dehydration.

Toxins predisposing to heatstroke include strychnine and organophosphates. Strychnine causes tetanic seizures induced by touch, noise, and bright light, which can lead to extreme heat production. Organophosphates are anticholinesterases and also cause heat production through muscle fasciculations and convulsions in severely affected animals.


The damaging effects of heatstroke are due to direct cellular injury and destruction of enzymes. The effect on organ systems is summarized below

Circulatory system

Peripheral vasodilation and decreased peripheral vascular resistance leads to hypovolemia. Hemoconcentration due to dehydration can predispose to red blood cell sludging and subsequent thrombosis. Red blood cell injury occurs and results in decreased survival time and hemolysis. The depletion of clotting factors through inactivation, DIC and decreased production from hepatic injury predisposes the heatstroke patient to hemorrhage. Hemorrhage also can occur as a result of platelet destruction, increases in vascular permeability due to damaged endothelium, and DIC.


Neuronal degeneration and necrosis results in cerebral edema. Signs include stupor, paddling behavior, and seizures and coma.


Thermal injury injury causes hepatocellular destruction, cholestasis, and dysfunction of the hepatic reticuloendothelial system. Such compromise of immune function along with bacterial translocation due to damaged GI mucosa predisposes the heatstroke patient to bacteremia and sepsis


Direct thermal injury along with hypoxia due to decreased circulating volume and increased metabolic demand for oxygen predisposes the kidneys to acute tubular nephrosis. Acute Renal Failure is a common complication of heatstroke, and can be worsened by thrombosis associated with DIC. Rhabdomyolysis resulting in myoglobinuria can also be a contributing factor.


Increased rectal temperature and excessive panting are the most obvious clinical signs. The presence of panting is important, as pyrexia caused by infection or inflammation will reset the hypothalamic thermoregulatory mechanism and panting will not be induced. Most animals present with injected mucous membranes, weakness, tachycardia, vomiting, and diarrhea. Body temperatures usually exceed 40.5C (105F). Stupor is an indication that the CNS has been affected. Convulsions or a state of coma can follow in severely affected animals. The presence of cyanosis should alert the clinician to the presence of concurrent upper airway disease or secondary upper airway obstruction from laryngeal edema. Differential diagnosis for heatstroke should include infection, neoplasia, and toxicosis.

Laboratory findings

The minimum data base of the heatstroke patient consists of a complete blood cell count, chemistry profile, urinalysis, and coagulation profile. An arterial blood gas is also useful. Increases in hematocrit and total solids are due to hemoconcentration, and hypoxia stimulates the release of nucleated red blood cells from the bone marrow. Azotemia and proteinuria indicate the presence of acute renal damage. Hepatocellular necrosis and cholestasis lead to increased levels of liver enzymes including alanine aminotransferase, serum alkaline phosphatase and total bilirubin. Elevated creatine phosphokinase and urine myoglobin levels suggest rhabdomyolysis. Electrolyte changes such as hypernatremia are due to dehydration. Initially, respiratory alkalosis from panting as well as vomiting can lead to hypokalemia. Over time, hyperkalemia predominates with the development of acute renal failure, metabolic acidosis from lactic acid production and rhabdomyolysis. A decreased platelet count with prolonged PT and PTT can occur with the development of DIC.


Emergency measures to normalize the body temperature must be initiated as soon as heatstroke is suspected. In human heatstroke patients, survival has been linked to the time until normalization of body temperature. Owners should be instructed to begin the cooling process before bringing their pet to the hospital. The use of hoses, cold water baths, wet towels, and fans can help with rapid cooling. Other cooling measures include cold water enemas and IV fluids with the lines cooled in an ice bath. The use of ice baths is discouraged as they can lead to peripheral vasoconstriction, which impairs heat dissipation, and shivering, which can increase heat production. Cooling measures should be stopped at 39.5C (103F) to avoid hypothermia, since temperatures continue to fall after cooling measures have been discontinued.

After cooling measures have been initiated, goals of therapy involve volume replacement, stabilization of cell membranes, and protection against infection. Fluid therapy is crucial as extreme dehydration is present. In addition, decreased cardiac output causes decreased effective circulating volume and consequently hypovolemia. Isotonic solutions such as 0.9% NaCl- or lactated Ringers solution should be initiated at a shock dose of 90 ml/kg/hr, and continued based on the cardiovascular and hemodynamic state of the patient.

Broad-spectrum antibiotic therapy should be initiated immediately, as the heatstroke patient is predisposed to infection and sepsis. Bacterial translocation occurs as the integrity of the intestinal mucosa becomes compromised, and decreased activity of the hepatic reticuloendothelial system also leads to general immunosuppression.

The use of corticosteroids has not been proven to be beneficial in the treatment of humans with heatstroke, but can be used to decrease cerebral edema if signs of CNS disturbances are present (dexamethasone sodium phosphate 1 mg/kg IV or prednisolone sodium succinate 5-11mg/kg IV). Mannitol should not be used initially, to avoid circulatory collapse of the cardiovascularly compromised patient.

Acepromazine (0.05-1.00 mg/kg IV) or diazepam (1 mg/kg IV) can be used if severe shivering occurs. Diazepam should be used as needed for seizures. The α-blocking effects of acepromazine can help counteract peripheral vasoconstriction associated with aggressive cooling measures. Hypotension associated with acepromazine use can be avoided with concurrent fluid therapy.

Antipyretics should be avoided since hyperthermia associated with heatstroke is not caused by resetting of the hypothalamic temperature regulating mechanism. NSAIDS should also not be used in the heatstroke patient due to the risk of causing GI bleeding, disturbed platelet function, and also because of the risk of impaired renal function.

If cyanosis, increased respiratory effort, and stridor are present, concurrent upper airway disease or laryngeal edema secondary to excessive panting should be suspected, and an emergency tracheostomy may be needed. Anti-arrhythmic therapy with lidocaine may be required if cardiac arrhythmias are severe enough to compromise perfusion. If DIC is present, blood products such as fresh frozen plasma or whole blood should be used as needed.

Prognosis for the heatstroke patient is guarded. If hyperthermia is corrected immediately, systemic thermal injury may be minimal and chances of recovery can be fair. Necropsy of dogs with fatal heatstroke support widespread systemic inflammation, disseminated intravascular coagulation and multiple organ failure. The development of acute renal failure, stupor or coma, and DIC can indicate a grave prognosis.


Bruchim Y, Loeb E, Saragusty J, Aroch I. Pathological findings in dogs with fatal heatstroke. J Comp Pathol 2000;140(2-3):97-104.

Bruchim Y, Klement E, Saragusty J, et al. Heat stroke in dogs : A retrospective study of 54 cases (1999-2004) and analysis of risk factors for death. J Vet Intern Med 2006;20(1):38-46.

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