Heat stroke in dogs is a common disorder with life-threatening consequences. This article will review the causes of hyperthermia and the negative impact of high temperatures on organ function.
Causes of Hyperthermia in Dogs
Hyperthermia is an abnormally high body temperature, and in dogs, it is typically observed between 104.9F – 109.4F. There are two forms of hyperthermia: pyrogenic and non-pyrogenic.
- With pyrogenic hyperthermia, the body is presented with pyrogens (ex – substances produced from bacteria), and as a response, the temperature set point of the hypothalamus regulatory center is reset. This is what we think of as a fever.
- With non-pyrogenic hyperthermia, the body’s temperature set point remains the same, but the body is unable to dissipate heat because the mechanisms are either impaired or there is too much of a heat insult for the body to handle. This is classified as heat stroke. With heat stroke, there are conditions that decrease heat dissipation like high ambient temperature, high humidity, poor ventilation and water deprivation. There are also conditions that increase heat production like strenuous exercise, seizures, animals that have not become acclimated to conditions, and certain drugs/toxicities to name a few. Also at higher risk are dogs with underlying medication conditions such as laryngeal paralysis or brachycephalic syndrome.
The Impact of Heat Stroke in Dogs
Heat stroke results in systemic inflammation, which can lead to multi-organ dysfunction, including encephalopathies, gastrointestinal failure, acute kidney injury, and coagulopathies. Organ dysfunction occurs as a result of prolonged circulatory shock and cellular necrosis. The initial response to hyperthermia is to shift blood flow from the internal organs to the periphery via peripheral vasodilation. As heat continues to rise, vasodilation occurs within the internal organ vasculature resulting in global hypoperfusion and circulatory shock.
Hyperthermia also causes cellular necrosis as a result of thermal injury at the cellular level. Proteins, including many enzymes, are denatured at high temperatures, rendering them ineffective.
It is important to understand the systemic effects of heat stroke in order to guide treatment and to communicate effectively and prepare owners for potential adverse events. Many laypersons are under the assumption that simply cooling a pet will be therapeutic. In order to align client expectations, there should be an emphasis on possible complications and the effect on prognosis if organ dysfunction occurs.
Central Nervous System
Heat stroke can cause cerebral edema, hemorrhage, infarction, and/or cerebellar dysfunction. Frequently, these patients have an altered mentation ranging from mental stupor to being comatose. Seizures can occur as a sequela of these changes, but it is important to consider that seizures can also be the cause of hyperthermia. When hyperthermia occurs as a result of seizures, management of potential organ damage is just as critical as seizure-control.
Anti-epileptics are indicated for any patient having seizures. Hypoglycemia should be avoided to prevent further deprivation of cerebral tissues. If there is evidence of cerebral edema, mannitol or hypertonic saline should be considered. Signs of cerebral edema include absent pupillary light response, Cushing’s reflex, and a persistently altered mentation despite normalization of cardiovascular parameters.
During states of shock, including heat stroke, the gastrointestinal tract suffers severe ischemia as it takes the brunt of vasoconstriction as blood is shunted to other organs. As a result of ischemia, there is damage to the integrity of the GIT lining allowing for bacterial translocation and endotoxemia. Clinical signs include hematemesis, hematochezia, melena, and ileus.
Treatment should be tailored based on individual patient signs. Consideration should be given to use of gastroprotectants, especially if hematemesis or melena are present. Anti-nausea management (maropitant, ondansetron) is also frequently utilized to prevent vomiting and reduce the potential for aspiration pneumonia. In more mild cases, antibiotics may not be necessary. However, if there is concern for bacteremia, broad-spectrum antibiotics should be considered.
Heat stroke can lead to renal tubular necrosis as a result of hypoperfusion, direct heat injury, microthrombi, endotoxemia and myoglobinuria. Acute kidney injury is common with heat stroke and can lead to permanent kidney dysfunction. Patients with an increased creatinine 24 – 48 hours after the initial insult, or a creatinine greater than 1.5 mg/dL after 24 hours, have a worse prognosis. If acute kidney injury occurs, it is important to monitor urine output for evidence of oliguria or anuria, and urinary catheterization with a closed set is often necessary for monitoring. Normal urine output in dogs is 1-2 ml/kg/hour. If urine output is less than 0.5ml/kg/hr, this is consistent with oliguria.
Thermal injury to the vascular endothelium can cause activation of the coagulation and complement cascades, leading to disseminated intravascular coagulopathy (DIC). There is no single diagnostic for DIC, but common signs of DIC include thrombocytopenia (<150,000), prolonged clotting times (PT, aPTT), and clinical signs of hemorrhage (petechiae, ecchymoses, hematochezia, hematemesis, and/or hematuria).
Transfusion with fresh frozen plasma is often used to replace the consumed coagulation factors, however, no survival benefit has been documented. Disseminated intravascular coagulopathy is a negative prognostic indicator. If present in addition to AKI, the prognosis is grave.
Other Body Systems
Other organs that can be affected by heat stroke in dogs include:
- Liver: Hepatic vacuolar degeneration due to hypoperfusion to the liver
- Heart: Cardiac myocardial injury, cardiac arrhythmias, and/or possible cardiac failure
- Lungs: Pulmonary edema (non-cardiogenic) and/or Acute Respiratory Distress Syndrome (ARDS)
- Skeletal Muscle: Rhabdomyolysis, which can further complicate renal damage due to myoglobinuria
- Acid-Base: Metabolic acidosis can occur due to lactate accumulation and hypoglycemia and/or respiratory alkalosis from hyperventilation
Heat stroke can result in severe, multi-organ failure which can ultimately be fatal. Initial treatment is targeted at shock management (IV fluids, oxygen therapy) and cooling the patient. Once stabilized, additional treatments are dictated by the organs affected and clinical signs.
Additional Links that May be Useful About Canine Heat Stroke:
- Heat Stroke in Dogs (Client education article)
- Cooling Methods for Canine Heat Stroke
- Diseases that Can Lead to Heatstroke in Dogs