Dr. Mazzaferro is a staff critical care specialist that has lectured at national and international veterinary conferences on the treatment of hyperthermia and heat-induced illness. She has authored a chapter on this subject in Ettinger's Textbook of Veterinary Internal Medicine.
Exertional heat stroke or hyperthermia can occur in as little as 30 minutes if animals are exercised in hot humid weather with little shade or opportunity to cool down and rest, leading to an impaired ability to dissipate heat. The most common form of hyperthermia is when an animal has been locked inside a vehicle on a hot day. Rapid early recognition of hyperthermia and prompt aggressive appropriate treatment are of utmost importance in having a favorable outcome.
Normally, heat balance occurs through the actions of heat gaining and heat dissipating mechanisms. Heat gain occurs through oxidative metabolism of foodstuffs, exercise and increased muscle or metabolic activity, and elevated environmental temperature. Heat dissipating mechanisms to prevent excessive heat gain include behavioral changes (i.e., seek a cooler location), peripheral vasodilation and changes in circulation, evaporative cooling primarily in the form of respiratory heat exchange, radiation, and convection. As environmental temperature approaches body temperature, evaporative heat loss becomes important to maintain body temperature. Animals, who lack sweat glands, depend primarily on heat dissipation and evaporative cooling from the respiratory system by panting. When body temperature rises, signals to the thermoregulatory center initiates a relay of signals to the panting center, creating a reflex to help dissipate heat and prevent hyperthermia. As air comes in contact with the mucous membranes of the upper airways, evaporative cooling occurs. Further accumulation of heat occurs as metabolic rate increases. A second method of cooling can occur by convection, in which an overheated animal lays on a cooler surface, and the body heat is transferred to the cooler surface. Risk factors for developing hyperthermia include high ambient humidity, upper airway obstruction, laryngeal paralysis, brachiocephalic airway syndrome, collapsing trachea, obesity, and previous history of hyperthermia. Lack of shade and a lack of a cool-down period after exercise can also predispose an animal to develop exertional hyperthermia. Any animal that works or exercises in a hot humid climate must be allowed time to rest in a cool, shady place with plenty of water every ½ hour to hour. Animals that have not acclimated to warm humid climates should not be worked as hard, as they may have an increased risk of developing hyperthermia. In one study of 42 cases of hyperthermia, Weimaraners, St. Bernards, Australian Shepards, and Bulldogs were overrepresented.
Nonpyrogenic hyperthermia results from the body's inability to adequately dissipate heat. Antipyretic agents are therefore often ineffective in reducing body temperature, and are actually contraindicated due to potentially adverse side effects of decreasing renal perfusion and increased chance of gastrointestinal ulceration. Differential diagnoses in patients with rectal temperatures greater than 104.9 degrees Fahrenheit include inflammatory diseases of the central nervous system including meningitis and encephalitis, and hypothalamic mass lesions affecting the thermoregulatory center. Other potential differential diagnoses include malignant hyperthermia in affected animals, particularly Labrador Retrievers or Collie-type dogs, and unwitnessed seizure activity.
The gastrointestinal tract is also a key player in multiorgan failure associated with hyperthermia. Decreased perfusion to the mesentery and thermal injury to enterocytes often results in a disruption of the gastrointestinal mucosal barrier and subsequent bacterial translocation. Bacteremia and elevation of circulating bacterial endotoxin can lead to sepsis, systemic inflammatory response (SIRS) and multiorgan failure. Patients with severe hyperthermia often present with hematemesis and severe hematochezia, often sloughing the lining of their intestinal tract. Thermal injury to hepatocytes can also result in decreased hepatic function, with elevation of hepatocellular and cholestatic enzyme activities. Persistent hypoglycemia in affected patients may be associated with hepatocellular dysfunction and depletion of glycogen stores. Hyperthermia also induces widespread endothelial damage, one of the key factors in the development of disseminated intravascular coagulation (DIC). Massive global thrombosis can result in multiorgan failure and death. Finally, hyperthermia can cause cellular neuronal damage, neuronal death, and cerebral edema. Thrombosis or intracranial hemorrhage and seizures can also occur. Altered levels of consciousness are among the most common clinical signs of heat-induced illness.
As hyperthermia progresses, central nervous system depression, seizures, coma, and death may occur. Severe mentation abnormalities including coma is associated with a negative outcome.
Patients with heat-induced illness or hyperthermia often present with a history of excessive panting, collapse, vomiting, ataxia, hypersalivation, seizures, or diarrhea. Listlessness, muscle tremors, loss of consciousness, altered level of consciousness, hematuria, cyanosis, epistaxis, swollen tongues, head tremors, vocalizing, stridor, and dilated pupils are also less frequently described. Clinical signs may not become apparent for several days after the inciting event. Changes in mentation, oliguria, vomiting, hematemesis, diarrhea, dyspnea, icterus, and petechiation can occur almost immediately after heat-induced illness, or can occur 3–5 days after the inciting event.
All patients with hyperthermia should have serial complete blood counts, biochemical analyses, coagulation profiles, arterial blood gases, venous lactates, and urinalyses performed. In many cases, prerenal and renal azotemia is present, with elevated BUN and creatinine concentration secondary to renal tubular necrosis. Alterations and elevations in hepatocellular enzyme function secondary to hepatocellular thermal injury or hepatic thrombosis are also demonstrated with elevated ALT, AST, and total bilirubin. Elevations in creatine kinase (CK) and AST are secondary to rhabdomyolysis. Blood glucose may be decreased, but this finding is inconsistent. Packed cell volume and total solids may be increased secondary to hypovolemia and dehydration with subsequent hemoconcentration. Thrombocytopenia, prolonged PT and APTT and elevated FDPs may be observed if DIC is present. In some cases, thrombocytopenia may not become apparent for several days after the initial insult. Arterial blood gas analyses can be variable, with a mixed respiratory alkalosis and metabolic acidosis secondary to increased lactate can be present. Urinalysis may reveal the presence of renal tubular casts or glucosuria, both indicators of renal tubular epithelial damage.
Treatment goals are to manage the hyperthermia, provide cardiovascular support, and to treat any complications associated with the hyperthermia. Cornerstones of therapy include restoration of circulating blood volume, improving glomerular filtration and renal blood flow, stabilizing electrolyte balance, and providing broad-spectrum antibiotics to minimize complications of bacterial translocation and sepsis. In the field, the animal should be moved to a cool area in the shade or indoors, away from direct sunlight. The animal should be sprayed with cool but not cold water. Cool packs can be placed in the axillary and inguinal regions. Air conditioning or cool fans can also help dissipate heat and improve convective cooling mechanisms. It is very important to cool the patient to 103 degrees within 30 to 60 minutes of initial presentation, but to avoid overcooling. Immersion in ice baths or cold water is absolutely contraindicated because this practice causes peripheral vasoconstriction. Vasoconstriction results in further elevation of core body temperature. Other methods of cooling that have been described, but offer no real advantage or improvement of clinical outcome include administration of cool intravenous fluids, gastric lavage, cold-water enemas, and cool peritoneal lavage.
Intravenous fluids should be administered judiciously during the early stages of hyperthermia and heat-induced illness, as early in the course of disease, fluid loss is not great, and oversupplementation of crystalloids can worsen cerebral edema and cause pulmonary fluid overload. A balanced electrolyte fluid such as Normosol-R, Plasmalyte-M, or lactated Ringer's can be administered, tailoring each patient's individual fluid needs based on central venous pressure, acid-base and electrolyte status, blood pressure, thoracic auscultation, and colloid oncotic pressure. If a free water deficit is present, as evidenced by hypernatremia, the clinician should calculate the free water deficit and replace it slowly over a period of 24 hours, to prevent further cerebral edema. Oxygen should be administered in animals with signs of upper airway obstruction. If laryngeal paralysis is present, sedative and anxiolytic agents such as acepromazine should be administered. In severe cases of upper airway obstruction and laryngeal edema, glucocorticoids can also be administered to decrease airway edema. The use of empiric glucocorticoids in patients without signs of airway obstruction is controversial, as they can further impair renal perfusion and predispose to gastrointestinal ulceration. Their empiric use is not justified and is not advised at this time. Broad-spectrum antibiotics such as the Unasyn, cefoxitin, ampicillin with enrofloxacin, and sometimes metronidazole should be administered to decrease bacteriemia.
Severe hyperthermia can result in widespread organ failure, and must be recognized and treated promptly. In most cases, prognosis is guarded to grave, depending on the presence of underlying diseases and complications. Mortality rates are directly associated with the duration and intensity of hyperthermia. Permanent damage to kidneys, liver and brain can occur, including permanent changes in the hypothalamic thermoregulatory center that can predispose the patient to further hyperthermic episodes. The clinician must give a guarded prognosis in most cases.
If death is going to occur, it usually happens within the first 24 hours of the incident. If an animal survives past 48 hours of hospitalization, the outcome is generally good. Animals who present with coma or hypothermia after a hyperthermic event generally have a very grave prognosis, even with extremely aggressive therapy.
References are available upon request.