Heatstroke is a life-threatening illness triggered in dogs and cats by a combination of increased heat production, environmental heat, and inadequate heat dissipation. The body’s thermoregulatory mechanisms fail, leading to cellular damage and death. In early stage hyperthermia, the pet experiences increased cardiac output and decreased peripheral vascular resistance. As hyperthermia advances, blood pressure and cardiac output decrease when the body can no longer compensate and without treatment, perfusion to vital organs decreases, resulting in widespread organ damage.
Thermal injury becomes widespread, involving neuronal tissue, cardiac myocytes, hepatocytes, renal parenchymal and tubular cells, and the gastrointestinal tract. Decreased organ perfusion, enzyme dysfunction, and severance of oxidative phosphorylation result in decreased aerobic glycolysis and an increased tissue-oxygen debt. The combination contributes to increased lactate production and lactic acidosis, which may occur as quickly as 3 to 4 hours after the initial heat-induced injury.
Hyperthermia may also lead to neuron damage, neuronal death, and cerebral edema; altered mentation is a common clinical sign. Severe central nervous system depression, seizures, coma, and death may be seen as the illness progresses.
During exposure to high ambient temperatures, the heat load increases faster than the animal can dissipate heat from the body.
Large- and giant-breed dogs are at increased risk for heatstroke, as well as animals that have predisposing conditions such as obesity, laryngeal paralysis, tracheal collapse, and thick coats, or are brachycephalic.
In human medicine, a continuum of heat illness ranging from the least to most severe occurs. Heat cramps characterized by muscle spasms that result from the depletion of sodium and chloride would be on one side of the continuum. Fatigue, weakness, muscle tremors, vomiting, and diarrhea are representative of heat exhaustion. Severe central nervous system (CNS) disturbance associated with multiple organ dysfunction is the result of heatstroke.
Heatstroke happens quickly, especially in poorly ventilated environments such as inside a car with the windows closed, even on a moderately hot day. Temperatures inside a closed car in direct sun may exceed 120° F (48° C) in less than 20 minutes and death may occur in less than one hour.
Therefore, time is of the essence and veterinary team members must be familiar with the clinical signs and treatment options so they can intervene quickly from the outset. Education should emphasize the importance of instituting cooling measures when the animal is found, before he or she is presented to the practice
It is important that team members are familiar with the clinical signs so they quickly recognize heatstroke and can begin cooling measures as soon as possible.
Patients with heatstroke or heat exhaustion often present with one or more of the following signs:
– Extreme panting
Physical examination findings in patients suffering from heat-induced illness vary with the intensity and duration of the increased body temperature and the individual pathophysiologic responses.
Rectal temperature may be decreased, normal, or increased dependent upon tissue perfusion and implementation of cooling measures. Pulse rate is often increased because of a compensatory sinus tachycardia. Respiratory rate is typically rapid.
Most patients arrive at the practice in a hyperdynamic state. Mucous membranes are frequently hyperemic with short capillary refill time. Hypovolemia secondary to evaporative fluid loss, vomiting, diarrhea, and vasodilation cause a weak pulse. Sinus tachycardia is common.
Evaporation through the respiratory tract, which provides heat dissipation, should be carefully evaluated. Loud, noisy breathing, especially if audible without a stethoscope suggests an upper airway abnormality (eg, tracheal collapse, laryngeal paralysis, edema) or obstruction (eg, brachycephalic syndrome). The healthcare team should always perform careful auscultation for loud airway sounds or pulmonary crackles and consider aspiration pneumonia if a patient is vomiting.
Veterinary team members should also be cognizant of less common signs, including lethargy, muscle or head tremors, an altered mental state, hematuria, cyanosis, epistaxis, swollen tongue, vocalization, stridor, and dilated pupils.
First, move the patient out of the heat into an air-conditioned facility or shaded area. Then, spray or cover the animal with cool, not cold water.
Managing hyperthermia includes the following:
– Instituting cooling measures
– Restoring circulating intravascular blood volume
– Improving glomerular filtration and renal blood flow
– Stabilizing electrolyte balance
– Reducing complications of bacterial translocation/sepsis.
At the Practice
When a heatstroke patient is presented at the practice, place cooling packs in the axillary and inguinal areas. Use fans to disperse heat. Increase the convective cooling mechanisms—cooling the patient to 103° F (39.4° C) within 30 to 60 minutes is ideal. Cooling blankets, iced gastric or peritoneal lavage, cold water enemas, and intravenous fluids are also effective.
Take care to not overcool the patient. Immersion in ice or cold water is currently discouraged, because it may cause peripheral vasoconstriction, lead to an increased core body temperature, and prevent vasodilation, an animal’s primary method of thermoregulation.
Heatstroke can result in widespread, permanent organ failure (eg, renal, hepatic, cerebral). A hyperthermia patient’s prognosis depends on the following:
– The time taken to implement cooling measures
– The presence of underlying diseases and/or complications
– The time and intensity of the condition.
Concomitant renal failure, obesity, and disseminated intravascular coagulation (DIC) increase the risk of death associated with hyperthermia. As well as organ failure, the patient’s hypothalamic thermoregulatory center may also suffer permanent damage, predisposing the patient to additional hyperthermic or heatstroke episodes.
Death from heatstroke typically occurs within 24 hours, but patients that survive 48 hours usually have a favorable outcome. Thus, early recognition and quick treatment implementation are of the essence.