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Canine Heat Stroke

Written by: Victoria T.


Introduction

Heat stroke, or hyperthermia, is defined as a severe elevation in body temperature from 104.9 to 109.4 ˚F and is considered the most serious of the heat-induced illnesses. Heat stroke can occur rapidly, especially in situations where there is little ventilation or in environments that have high ambient temperatures and humidity. It has been shown that temperatures inside a closed car exposed to sun may exceed 120 ˚F in less than 20 minutes when the outside temperature is only 75 ˚F. Death can occur in an hour, especially in animals that are predisposed. Working dogs can develop hyperthermia in as little as 30 minutes unless adequate shade, water, and rest is available. Heat stroke is a relatively common condition in dogs; therefore, it is important for veterinarians to understand the pathophysiology, diagnosis, treatment, prevention, and prognosis.

Pathophysiology

In order to maintain normal cellular and bodily function, a body will activate the respiratory system, induce heat shock proteins and the acute phase response, and increase cardiac output in response to heat stress. Heat is produced by the dog’s normal metabolism and activity, which in turn activates the thermoregulatory center in the hypothalamus. The thermoregulatory center goes on to activate panting to maximize evaporation and support cooling. Because dogs do not have sweat glands, they depend on the dissipation of heat from evaporation within the respiratory system during panting. When an increase in air flow contacts the mucous membranes of the upper respiratory tract, evaporative cooling mechanisms rise, however this is not efficient if there is a high environmental humidity present. Humidity levels of greater than 35% can threaten a dog’s evaporative losses and it has been shown that humidity over 80% can actually negate evaporative losses.

The thermoregulatory center also activates heat shock proteins and the acute phase response to try and shield cells from heat damage. Heat shock proteins help maintain cellular function under periods of extreme heat stress by protecting against the denaturation of intracellular proteins. Heat shock proteins also have a role in the baroreceptor response which prevents hypotension and confers cardiovascular protection. Animals that have acclimated to high temperatures normally display a high level of heat shock proteins. When they are re-exposed to these extreme temperatures, these proteins are readily available to take action. From experimental models, it can take 10-20 days up to months for a dog to acclimate to their surrounding climate, so it is important to remind owners of high risk dogs to slowly get them used to being in the heat. The acute phase response is an innate body defense seen during acute illnesses and involves the increased production of certain blood proteins termed acute phase proteins. Many of the heatstroke complications and symptoms are mediated by an out of control acute phase inflammatory response.

An overheated body will also attempt to cool itself by increasing cardiac output. The baroreceptor response first mediates peripheral vasodilation. This is an attempt by the body to dissipate heat via radiation where heat is passively transferred away from an overheated animal. Peripheral vasodilation leads to relative hypovolemia. To maintain adequate blood pressure, vessels constrict and catecholamines are released to increase heart rate and cardiac output. As hyperthermia progresses, blood pressure and cardiac output decrease when the body can no longer compensate.

Heat stroke results from failure of thermoregulation followed by an exaggerated acute phase response, alteration of heat shock proteins, and complications with the cardiovascular system. This leads to the production of reactive oxygen species, increased vascular and intestinal permeability, resulting in direct cellular injury and enzyme destruction. Perfusion to organs decreases, ultimately leading to organ damage and failure as a result of decreased blood pressure and cardiac output. Because hyperthermia becomes a systemic illness, almost every body system is involved and has its own specific signs.

Hyperthermia can lead to all the components of Virchow’s triad which includes vascular endothelial injury, venous stasis, and a hypercoagulable state. Widespread endothelial damage exposes subendothelial collagen and tissue factor which systemically activates platelets. A drastic increase in activated platelets during heat stress leads to the consumption of clotting factors and the activation of the fibrinolytic pathway. The combination of sluggish blood, decreased clotting factors, and the loss of anticoagulants from the permeable gastrointestinal tract result in disseminated intravascular coagulation or DIC. There is massive systemic thrombosis associated with DIC which also contributes to multi-organ dysfunction and eventually death.

The cardiovascular and pulmonary systems are compromised due to the peripheral vasodilation and hypovolemia. Excessive panting can cause hemoconcentration and respiratory muscle fatigue. Direct cardiac injury may cause myocardial hemorrhage and necrosis. Pulmonary edema may result from heart failure, damage to the vascular endothelium, or hypoproteinemia. In one retrospective case study, all 54 dogs necropsied after a heat stroke had pulmonary edema and/or hemorrhage.

Acute renal failure and hepatic failure is a result of direct thermal injury, hypoxia, and microthrombi from DIC. Rhabdomyolysis occurs as a direct result of high temperature and may be increased in patients experiencing an exertional heat stroke.
Severely affected dogs can have vomiting and diarrhea that may range from watery to hemorrhagic. DIC and/or poor visceral perfusion can cause a disruption of the gastrointestinal mucosal barrier which leads to translocation of gut bacteria, sepsis, gastric ulcerations, and sloughing of the intestinal lining. Patients with severe hyperthermia often present with hematemesis and hematochezia.

The hallmark sign of heat stress is severe central nervous system disturbance and it is often associated with multiple organ dysfunction. The combination of poor perfusion, direct thermal damage, cerebral edema, and hemorrhage all contribute to the central nervous system symptoms. CNS disturbances may include depression, tremors, ataxia, coma, and seizures.

Presentation and Physical Exam

Dogs with an increased risk of developing heat stroke include older dogs, dogs suffering from obesity, brachycephalic breeds, large breeds, and breeds with extremely thick hair coats. Any disease process that inhibits the dog’s normal ability to efficiently pant such as laryngeal paralysis, airway masses, and collapsed trachea also increase the risk of developing hyperthermia. Dogs who exercise, work, or live outside in hot, humid climates are also at a higher risk.

Owners often bring their dog to a veterinarian after noting external signs of heat stroke. Owners may observe and describe any combination of the following: excessive panting, hypersalivation, listlessness, muscle tremors, vomiting, diarrhea, ataxia, collapse, loss of consciousness and seizures. Usually owners are able to connect heat as a cause of the dog’s symptoms, but it is important to obtain a complete history to rule out any other diagnoses or causes. There are other causes of heat stress that do not relate to heat and humidity such as malignant hyperthermia; secondary to airway obstructions, cardiac or pulmonary disease; illnesses with pyrogenic origins; ingestion of toxins; and complications of halothane anesthesia.

On physical exam, a dog with heat stroke will have an elevated body temperature (>104.9 ˚F) upon entry. Initially the mucous membranes will appear congested with a short capillary refill time (CRT), but can progress to pale or cyanotic mucous membranes with an absent CRT. Icterus may be noticed due to hemolysis or hepatic dysfunction. The dog will be rapidly panting in an attempt to improve heat dissipation. Tachycardia is usually present as a result of compensatory mechanisms, systemic inflammation, and myocardial hypoxemia. If DIC is present, there may be cutaneous petechial hemorrhages and crackles in the lungs due to edema and/or pulmonary parenchymal hemorrhage. At this point, it is important to rapidly begin treatment and obtain laboratory results as described in the following sections.

Laboratory Findings

Immediate assessment of patients with physical exam findings and history related to hyperthermia should include: packed cell volume (PCV), total protein (TP), blood glucose, and blood lactate. PCV and TP will be elevated due to hemoconcentration. Glucose is often low due to hepatocellular dysfunction and glycogen depletion. Lactate is high and is produced from a decrease in aerobic glycolysis and a depletion of oxygen.

Thorough laboratory work should occur early during resuscitation efforts and include complete blood count, coagulation testing, chemistry, and urinalysis. Complete blood count changes may include thrombocytopenia and hemoconcentration. Chemistry findings may include hypoproteinemia, hypoglycemia, elevated alanine aminotransferase (ALT), alkaline phosphatase (ALP) and total bilirubin, increases in creatinine phosphokinase (CK), elevations in blood urea nitrogen (BUN) and creatinine. Studies have shown that the presence of nucleated red blood cells, hypocholesterolemia, hypoalbuminemia, and hypoproteinemia are associated with a less favorable outcome.

Various electrolyte changes are also seen, such as hypernatremia and hyperkalemia. Urinalysis may reveal casts indicating tubular damage, proteinuria and myoglobinuria. Coagulation testing may show prolongation in clotting times and elevations in fibrinogen degradation products. If a combination of prolonged clotting factors, low platelets, and elevated fibrinogen degradation products are found during diagnostics, it is likely the patient is currently undergoing DIC. The prognosis for patients with acute DIC is grave. If heat stroke can be eliminated and DIC is appropriately treated, patients can recover. However, severe organ failure or thrombosis is common and often life-threatening.

Treatment and Prognosis

The immediate treatment plan for a hyperthermic dog is to treat the hyperthermia and then treat the associated complications. The severely hyperthermic patient must first undergo immediate body cooling to prevent further organ damage. One can use fans, towel-covered ice packs, and alcohol placed on paw pads to encourage total body cooling. It has been shown that placing a dog in ice water is actually contraindicated. Ice water immediately causes vasoconstriction which reduces radiant heat loss. This can cause the animal’s internal body temperature to continue rising rather than help with cooling. The cooling process should be discontinued when body temperature approaches approximately 103 ˚F to prevent iatrogenic hypothermia.

Once cooling measures have begun and the airway is determined to be functional, therapeutic goals include volume resuscitation with shock dose fluids. This is best accomplished by administering intravenous fluid therapy. Fluid therapy should be continued based on the patient's status and their cardiovascular and hemodynamic systems should be closely monitored.

There are many steps to help treat the complications associated with hyperthermia. Oxygen should be administered in animals with heat stroke, especially in dogs that have signs of upper airway obstruction or brain injury. Broad-spectrum antibiotics such as cephalosporin, ampicillin, enrofloxacin, and/or metronidazole should be given to decrease bacteremia. If the hyperthermic animal has evidence of cerebral edema or increased intracranial pressure, give hypertonic saline or mannitol. Seizures should be treated appropriately with anti-convulsants such as diazepam or phenobarbital. Many of the heatstroke sequelae are mediated by an out of control acute phase inflammatory response. A low dose lidocaine constant rate infusion can be potentially helpful to lessen inflammation, scavenge oxygen free radicals, and improve endothelial cell function.

Antipyretic agents are not effective at decreasing temperature in a dog with an unbalanced hypothalamic thermoregulatory center, such as in cases of heat stroke. High doses of anti-prostaglandin drugs decrease renal perfusion and can complicate gastrointestinal issues associated with hyperthermia.

The prognosis with dogs diagnosed with heat stroke is guarded to poor. Death generally occurs within the first 24 hours and usually occurs due to multi-organ failure and DIC. One study found an overall mortality rate of 50%. Factors that increased the risk of death in this study included hypoglycemia and prolonged clotting factors at admission, elevated serum creatinine at 24 hours after admission, delayed admission to the hospital of >90 minutes, seizures, and obesity. Successful treatment depends on swift diagnosis and procedures aimed at rapid cooling and support of the different heat stroke complications.


References:

  • Aroch, I., Segev, G., Loeb, E., & Bruchim, Y. (2009). Peripheral Nucleated Red Blood
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  • Bonagura, J. D., & Twedt, D. C. (2014). Kirk’s Current Veterinary Therapy XV. St. Louis,
  • MO: Elsevier Saunders.
  • Bruchim, Y., Loeb, E., Saragusty, J., & Aroch, I. (2009). Pathological Findings in Dogs
  • with Fatal Heatstroke. Journal of Comparative Pathology, 140(2-3), 97-104.
  • Bruchim, Y., Segev, G., Kelmer, E., Codner, C., Marisat, A., & Horowitz, M. (2015).
  • Hospitalized dogs recovery from naturally occurring heatstroke; does serum heat shock protein 72 can provide prognostic biomarker? Cell Stress and Chaperones, 21(1), 123-130.
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