It’s getting hot in here: Heatstroke in dogs

Adrienne Felix, DVM
Massachusetts Veterinary Referral Hospital, Woburn, MA
Posted on 2017-06-13 in Emergency & critical care

Heat illnesses can be described as a range of syndromes from heat cramp to heatstroke. Heat cramp is when muscle spasms result from sodium and chloride depletion. Heat prostration/exhaustion can result in fatigue, weakness, muscle tremors, vomiting and diarrhea. Heatstroke is described as a form of “hyperthermia associated with systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates.” Heatstroke is frequently reported in dogs and is rarely reported in cats.

Heatstroke is characterized by a body temperature above 104oF with CNS dysfunction (delirium, convulsions, coma) and other varying degrees of organ dysfunction. Core temperature elevations associated with morbidity/mortality have not been defined in dogs. Temperatures as low as 105.8oF may cause permanent brain damage. Temperatures above 109.4oF cause severe organ damage and have a marked increase in mortality. Sustained temperatures of 120.2-122oF for 5 minutes or less result in destruction and necrosis of cellular structures. Although, to some degree, the canine brain appears to have an inherent resistance to temperature elevations.


The anterior portion of the hypothalamus is the main organ responsible for thermoregulation. Changes in temperature are detected by peripheral thermoreceptors and activate the hypothalamic thermoregulatory center. This causes constriction of renal and splanchnic blood vessels and peripheral vasodilation leading to shunting of heated core blood to the skin for heat dissipation.

There are four mechanisms of heat dissipation. Conduction occurs when the body comes into contact with a cooler surface like a metal table and heat is transferred. Radiation occurs when the body releases heat into the environment. Convection occurs when the heat is transferred to surrounding cool air as it passes. Evaporation occurs when fluid changes into vapor. Radiation and convection account for 70% of heat dissipation in dogs and cats.

There are several mechanisms by which animals adapt to hyperthermia. Through the action of aldosterone and antidiuretic hormone, water resorption is increased which results in increased cardiac output. This is also accomplished by additional mechanisms like tachycardia, salt conservation, increased GFR and an ability to resist exertional rhabdomyolysis. Without these mechanisms or if they fail, hypovolemia, dehydration and decreased cardiac output occur. This results in decreased tissue perfusion and resulting tissue hypoxia. This decompensation can result in hematochezia, coagulopathy, arrhythmias and renal injury. Acute renal failure is a common sequela due to severe dehydration, hypotension, hypoxia, and rhabdomyolysis. This results in glomerular damage and tubular necrosis. The acclimatization process takes roughly 60 days for complete acclimatization and 10-20 days for partial acclimatization.

Acute Phase Response (APR)

The APR is a systemic and coordinated reaction that is activated by inflammation, protects against tissue injury and promotes repair. It is initiated and modified by cytokines and cytokine modulators. The APR can be protective or destructive, inflammatory or anti-inflammatory or a combination. Generally, an exaggerated and inflammatory APR is involved in heatstroke.

Heat Shock Proteins (HSP)

The HSPs enhance the ability of enzymes to function during extreme heat. They are produced by cells in response to sudden increases in temperatures and act as “protein chaperones” or “molecular guardians.” They induce cellular tolerance to help maintain intracellular function and structural protein integrity. They facilitate protein repair, regulate and protect against apoptosis, maintain an antioxidant pool, protect against oxidative stress, decrease activation of NF-kB, and protect against arterial hypotension and cerebral ischemia.

The HSPs are also responsible for regulating the baroreceptor reflex during severe heat stress. They also confer cardiovascular protection by abating hypotension, bradycardia, and preventing protein denaturation. The use of NSAIDs has been reported to increase the upregulation of HSPs.

Risk Factors

Many factors have been associated with an increased risk for heatstroke.

  • Endogenous: Obesity, cardiovascular or neurologic disorder, hair coat, upper airway abnormalities
  • Exogenous: Lack of acclimatization, confinement with little shade or ventilation, water deprivation, medications (loop diuretics, beta blockers, phenothiazines)


Heatstroke can be broken down into two different types: classic and exertional, or a combination of both. Classic heatstroke occurs when an animal exposed to a high environmental temperature. Exertional heatstroke occurs when an animal undergoes strenuous exercise before acclimatization.

Heatstroke is described as hyperthermia associated with systemic inflammation which results in multiorgan dysfunction (MODS). MODS is the most serious complication of heatstroke. This may include circulatory collapse, encephalopathy, acute renal failure, disseminated intravascular coagulopathy, rhabdomyolysis, myocardial injury, hepatic failure, intestinal ischemia/infarct, acute respiratory distress syndrome and endothelial dysfunction.

Heatstroke associated MODS results from direct cytotoxicity, acute physiologic alterations associated with heat hyperthermia. These derangements include increased metabolic demand, circulatory shock, hypoxia, endotoxemia, release and activation of cytokines and chemokines, endothelial cell activation/damage, activation of coagulation and fibrinolysis, and activation and amplification of inflammation.

The effects from direct cytotoxicity are dependent on a critical thermal maximum. The critical thermal maximum quantifies the level and duration of heat necessary to initiate tissue injury. In primates, temperatures of 102.2-104.0F are reported to damage the gut wall allowing endotoxin to enter circulation. In experimental animal models, apoptosis in the liver, spleen, thymus, lymph nodes, small intestinal mucosa occurs after a few minutes in temperatures between 106.7-107.6F. At temperatures, greater than 109.4F oxidative phosphorylation is uncoupled and critical enzymes are denatured. Autopsy and necropsy findings show ultrastructural endothelial damage, widespread microthrombi, necrosis and/or hemorrhage into major organs – brain, kidney, liver, lungs and GI tract.

Heatstroke also has profound cardiovascular effects. It initially results in renal and splanchnic vasoconstriction and peripheral vasodilation. This results in the body maintaining or increasing cardiac output and in decreased systemic vascular resistance. This is the body’s attempt at protecting the core from an increased body temperature. As heatstroke and the cardiac effects progress, the splanchnic vasculature dilates and then results in venous pooling. This then results in a decrease in the circulating plasma volume (hypovolemia) and a decreased in cardiac output.

Heatstroke also commonly results in coagulation abnormalities. They result as a direct thermal injury to the endothelium, activation of the extrinsic coagulation pathway and monocyte/macrophage activation. Coagulation and fibrinolysis occur early. It results in elevations of thrombin-antithrombin, plasmin-anti-plasmin, D- dimer, decreased protein C and thrombocytopenia and prolonged prothrombin times. This leads to hemorrhagic diathesis, widespread microvasculature thrombi and results in DIC.

Physical Examination

On physical examination, there may be a variety of abnormalities noted. With heatstroke, rectal temperature can vary greatly depending on tissue perfusion and if cooling measures had been performed prior to presentation. The patient does not have to be hyperthermic on initial presentation to be a heatstroke suspect.

Generally, a sinus tachycardia is noted as the patient is likely in a hyperdynamic state. The mucous membranes are typically hyperemic, with a short CRT and weak femoral pulses. This is likely due to both primary and secondary hypovolemia. If a ventricular arrhythmia is noted, it has been correlated with a worse outcome.

The patient generally will present tachypneic in attempt to improve heat dissipation. If loud or noisy breathing is noted, that may indicate an upper airway abnormality (i.e.: laryngeal paralysis, laryngeal edema, upper airway obstruction, tracheal collapse). If previous vomiting was noted, there is a chance that aspiration pneumonia has developed. If there is a concern that DIC is developing, be sure to monitor for pulmonary hemorrhage. Generally, abnormal bronchovesicular sounds are not commonly noted on initial presentation. However, on necropsy, pulmonary hyperemia, edema and hemorrhage are noted frequently.

On neurologic evaluation, mentation changes are common. Typically, the PLRs are intact, however pupil size can vary. If there is an initial concern for cortical blindness, it may resolve after several hours. On gait evaluation, the patient may be ataxic. If during hospitalization, progressive neurologic signs are noted, it is associated with a worse prognosis. Neurologic signs can result from poor cerebral perfusion, direct thermal damage, cerebral edema, hemorrhage or metabolic derangements (like hypoglycemia or hepatic encephalopathy).

Heatstroke commonly affects the urinary system. Since acute renal failure is a common complication, be sure to monitor urine production and renal values carefully. Heatstroke commonly affects the gastrointestinal tract also. It results in vomiting and diarrhea. Specifically, hematochezia with mucosal sloughing. This is thought to be secondary to DIC or poor visceral perfusion and reperfusion injury. If a coagulopathy is developing, petechiation and ecchymoses will be present.

Laboratory Evaluation

When performing blood work, evidence of dehydration will be shown by an elevated PCV/TS. Hypovolemia will also be evident in azotemia as well. However, it may be due to a dehydration (pre-renal), although a renal insult is possible due to poor perfusion and developing AKI. The BUN may be elevated due to GI hemorrhage.

Hypoglycemia is a common finding in heatstroke patients. It is likely due to consumption of the blood glucose, but also may be due to the development of sepsis. The blood glucose level is significantly lower in non-survivors and persistent hypoglycemia is associated with an increased mortality.

When evaluating electrolytes, sodium and potassium may be normal initially. Changes in these electrolytes can develop due to GI losses (vomiting, diarrhea) and free water loss. Elevations in the lactate level are also very common. This can happen due to decreased global perfusion and decreased clearance. In sepsis, clearance of lactate is associated with resolving global tissue hypoxia and a decreased mortality rate.

Since the kidneys are a common site of damage during heatstroke, performing a urinalysis is very important. Ideally this is performed prior to performing fluid therapy to assess for renal damage/function. Always remember to interpret the USG in light of hydration and perfusion status. If proteinuria, hemoglobinuria, or glucosuria are noted, there is concern for tubular damage. If the urine sediment contains red blood cells, there is likely renal damage or a developing coagulopathy. If the sediment shows casts, then there is renal damage.

When evaluating a CBC, there are a few changes to look for. A leukocytosis can be seen and is likely due to an inflammatory response. If a leukopenia is present, it is possibly due to the direct cytotoxic injury, but may be due to impending or developing sepsis. Thrombocytopenia can also be noted. If noted, it is likely due to consumption from a variety of processes (i.e.: vasculitis, GI hemorrhage or hyperthermia induced aggregation). On evaluation of cell morphology, nucleated RBC is a common finding in heatstroke patients. It has been reported that an elevation is associated with a worse prognosis. The amount of nRBC decreases after the first 24 hours.

When evaluating organ function, a few abnormalities are likely to be seen. As previously mentioned, azotemia is a common abnormality. A serial increase in creatinine, has been associated with a worse prognosis. An elevated ALT is common and usually peaks within 24 to 48 hours. CK and total bilirubin may also be elevated.

It is also important to measure coagulation parameters. PT is often prolonged, potentially necessitating treatment. If able to measure, D-dimers and fibrin levels are also increased.


When a heatstroke patient presents, first begin active cooling as warranted based on their body temperature. There have been many methods evaluated, but no single technique has been proven superior. One easy way to take advantage of the natural ways of heat dissipation, is to spray the animal with water and then place them in front of a fan. However, since many owners realize their pet is overheated they will begin by cooling them off at home, so they are often normothermic on presentation. If you are performing active cooling, only cool to 103.5-104F as to prevent rebound hypothermia.

One of the mainstays of treating the emergent heatstroke patient is to provide fluid support. Administer crystalloid shock boluses (15-20 ml/kg) as indicated based on the patient’s perfusion status. Although, it is also important to avoid excessive volume administration. If the patient remains hypotensive despite being rehydrated, additional support like a synthetic colloid or a vasopressor agent may be indicated. If the patient is persistently hypotensive, there is a worse prognosis.

A urinary catheter will allow close monitoring of urine output (UOP). The UOP should be at least 2 ml/kg/hr. If the UOP is low despite being adequately hydrated and a normal blood pressure, then begin treatment for oliguria or anuria or consider hemodialysis or peritoneal dialysis.

The gastrointestinal tract is commonly injured in heatstroke patients. Administer antiemetics (maropitant and ondansetron) as needed to prevent further vomiting. Administer medications to help with any gastric ulcers that may have formed or are forming (sucralfate, omeprazole/pantoprazole, famotidine). Begin broad spectrum antibiotics as bacteremia/endotoxemia may result due to mucosal injury. Begin enteral feedings, as soon as the patient is able to tolerate it.

There are a variety of other treatments that may be indicated based on the patient’s clinical presentation. If the patient is hypoglycemic, administer a dextrose bolus, then start a 2.5-5% CRI. If there is concern for neurologic abnormalities or worsening urine output, a mannitol infusion is indicated. Mannitol will expand the IV volume, decrease blood viscosity, improve renal function, improve cerebral microcirculation, decrease ICP and acts as a reactive oxygen scavenger. However, if the patient is hyperosmolar, actively hemorrhaging, dehydrated, has pulmonary edema or in anuric renal failure, it is contraindicated. If the patient is having a ventricular arrhythmia, administer a lidocaine bolus (2 mg/kg) and then start a lidocaine CRI (50 mcg/kg/min). Lidocaine also acts a reactive oxygen species scavenger. If the patient is coagulopathic, administer fresh frozen plasma. If there is concern that arterial oxygenation is inadequate, administer oxygen support until oxygenation status is adequate.


Overall the prognosis for heatstroke is dependent on many things – duration of exposure, highest temperature, secondary complications, pre-existing conditions and length of time to treatment. There are a few parameters that are known to be unfavorable prognostic indicators: seizures, coma, hypothermia at presentation, progressive neurologic abnormalities, persistent hypoglycemia, progressive azotemia (creat > 1.5 mg/dl after 24 hours), oliguria, DIC, refractory hypotension, ventricular arrhythmias and pulmonary edema. Timing is also very important: if the patient is presented more than 90 minutes after the insult, it has strongly been correlated with a worse prognosis and death.

Further reading

  • Aroch I, Segev G, Loeb E, et al. Peripheral nucleated red blood cells as a prognostic indicator in heatstroke in dogs. J Vet Intern Med 2009; 23(3):544–551.
  • Bouchama A, Knochel JP. Heat stroke. N Engl J Med2002; 346 (25):1978–1988.
  • 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 Med2006; 20(1):38–46.
  • Bruchim Y, Loeb E, Saragusty J, et al. Pathological findings in dogs with fatal heatstroke. J Comp Pathol 2009; 140(2–3):97–104.
  • Drobatz KJ. Heat stroke, In: Silverstein DC, Hopper K. eds. Small Animal Critical Care Medicine, 2nd ed. St. Louis: Saunders; 2015, pp. 795–799.
  • Flournoy S, Macintire DK, Wohl J. Heatstroke in dogs: clinical signs, treatment, prognosis, and prevention. Comp Cont Educ Pract Vet 2003; 25 (9):422–431.
  • Flournoy S, Wohl J, Macintire DK. Heatstroke in dogs: pathophysiology and predisposing factors. Comp Cont Educ 2003; 25(6):410–417.
  • Holloway S. Heatstroke in dogs. Comp Cont Educ1992; 14 (12):1598–1604.
  • Johnson K. Pathophysiology of heatstroke. Comp Cont Educ 1982; 4 (2):141–144.
  • Johnson, S. I., McMichael, M. and White, G. (2006), Heatstroke in small animal medicine: a clinical practice review. Journal of Veterinary Emergency and Critical Care, 16: 112–119. 
  • Lu KC, Wang JY, Lin SH, et al. Role of circulating cytokines and chemokines in exertional heatstroke. Crit Care Med 2004; 32(2):399–403.
  • Segev, G., Aroch, I., Savoray, M., Kass, P. H. and Bruchim, Y. (2015), A novel severity scoring system for dogs with heatstroke. Journal of Veterinary Emergency and Critical Care, 25: 240–247.


About the author

Dr. Adrienne Felix completed her undergraduate training at the University of Arizona. She received her Doctor of Veterinary Medicine degree from the University of Wisconsin – Madison in 2015. She went on to complete a rotating small animal medicine and surgical internship at the Veterinary Specialty Hospital of the Carolina’s in Cary, NC. After completing her internship, she joined the emergency and critical care team at Massachusetts Veterinary Referral Hospital in July 2016.