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Veterinarian Technician April 2007 (Vol 28, No 4) Focus: Summer Issues

Heatstroke in Dogs

by Brandy Tabor, CVT, VTS (ECC)

    CETEST This course is approved for 0.5 CE credits

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    Key Points

    • Heatstroke can cause central nervous system damage, circulatory collapse, and even death.
    • Many factors, such as brachycephalic conformation, cardiac conditions, and obesity, increase a dog's risk of developing heatstroke.
    • Dogs that are cooled before arriving at the clinic have a much better chance of survival.

    Click here for Glossary.

    Heatstroke is a life-threatening emergency that can affect any breed of dog. This condition typically occurs during the spring and summer months, particularly in hot, humid climates. However, many dogs succumb to heatstroke after strenuous exercise or confinement in an enclosed space. One of the most common causes of heatstroke in dogs is being left in a parked car. Prompt recognition and treatment of heatstroke are crucial in saving the animal's life.

    Heatstroke is the most severe illness caused by the body's inability to cope with heat.1 Other heat-related illnesses (i.e., heat cramps, heat exhaustion, heat prostration) are classified based on the type and severity of clinical signs, which range from muscle cramps to tachycardia. Heatstroke affects the entire body. It can result in damage to the central nervous system (CNS), circulatory collapse, alteration of normal cellular and enzymatic function, and even death.1

    Physiology and Thermoregulation

    Dogs maintain their temperature within a range called the "set-point."1 The set-point is determined by the thermoregulatory center in the preoptic region of the anterior hypothalamus.1 When an animal's temperature rises or falls out of this range, the body reacts by increasing or decreasing the core temperature in an attempt to return to the set-point.1

    The body obtains heat from endogenous (metabolism or muscle activity, such as shivering or seizures) and exogenous (environmental) sources.1,2 It dissipates heat through four methods: conduction, radiation, convection, and evaporation.1 Animals typically use the first three methods when the environmental temperature is at or below 89.6°F (32°C).1 The fourth comes into play as the environmental temperature gets closer to body temperature.1

    Conduction occurs when the animal's body comes into contact with a cooler surface, such as a wooden floor or grass.1,2 Dogs often take advantage of this method by lying in a position such that their ventral abdomen comes in contact with the cool surface.1 Because the ventral abdomen has little or no hair, it allows for a greater transfer of heat.1

    Radiation and convection account for 70% of the body's dissipation of heat.1 Both methods work in a manner similar to conduction but dissipate heat directly into the environment rather than onto a contact surface. Convection occurs when the animal lies in an area where it can be exposed to cool, circulating air.2 As air moves over the body, heat is transferred from the body into the air.2 With radiation, the heat moves naturally into the environment and is not dependent on air movement.2

    The dissipation of heat through conduction, radiation, and convection is greatly increased by peripheral vasodilation.1 When the temperature of the blood increases by as little as 1.8°F (1°C), the heat receptors of the peripheral hypothalamus are activated. This in turn activates the thermoregulatory center,3 which responds by constricting the renal and visceral blood vessels and increasing cutaneous vasodilation.3 These reactions shunt blood to the periphery to increase cutaneous circulation and the rate of cooling.1 As this blood returns to the core, it cools the vital organs.

    When the environmental temperature approaches the body temperature of the dog, the panting center in the hypothalamus is triggered, causing the dog to pant and allowing heat loss through evaporation.1 During panting, air passes over the large surface area of the nasal turbinates and cools the blood in the small capillaries in this area. This cooled blood then circulates throughout the body. Panting also increases the rate of moisture evaporation on the mucous membranes and allows for an increase in the amount of cooling achieved.1

    Hyperthermia

    Hyperthermia occurs when body temperature becomes elevated. There are two types of hyperthermia: pyrogenic and nonpyrogenic. Pyrogenic hyperthermia is caused by infection or inflammation and is usually referred to as fever. During fever, the body's set-point is raised, and because the increased temperature is within the new set-point, the body does not try to cool itself.4 Attempting to lower the animal's temperature by administering chilled intravenous (IV) fluids or by placing ice packs in the animal's cage is ineffective and may do more harm than good because the animal's body will further increase its internal temperature to stay within the elevated set-point.

    Nonpyrogenic hyperthermia occurs when the animal's temperature rises above the set-point and the body is unable to compensate to maintain normothermia.4 Common causes include damage to the hypothalamus (e.g., tumor) or an alteration to the thermoregulatory center's ability to respond to an increase in temperature. The latter can be caused by medications (e.g., chlorpromazine, acepromazine, famotidine), seizures, eclampsia, anesthesia with halothane, or macadamia nut toxicity.1,4 Heatstroke is a form of nonpyrogenic hyperthermia. It is most commonly caused by environmental conditions that limit the body's ability to dissipate heat.4

    Types of Heatstroke

    There are two types of heatstroke: exertional and nonexertional.1 Exertional heatstroke occurs when a dog works or plays in an environment to which it is not acclimated.1 It is uncommon in working dogs with handlers who are aware of the importance of acclimation, hydration, and avoiding overexertion, especially during the hottest time of the day.1 For example, military dogs that work in the desert can normally withstand temperatures that may exceed 140°F (60°C).1 Also, racing greyhounds normally do not exhibit signs of heatstroke, even though they may demonstrate rectal temperatures as high as 107.6°F (42°C) after a race.1

    Nonexertional heatstroke is caused by impairment of the dog's ability to dissipate heat because of a decrease in airflow, lack of shade or water, or increase in temperature or humidity.1 In an enclosed area, such as an automobile, a dog cannot cool itself through convection or radiation.1 One study suggested that at a temperature of 84.2°F (29°C) and 90% humidity, the survival time of a dog locked in a car could be as short as 48 minutes.5 If a dog locked in a car tries to escape, it can suffer a combination of exertional and nonexertional heatstroke.2

    Dogs tethered outside or left free to roam without access to water or shade can also develop heatstroke.1 Roaming dogs that have access to water and shade are unlikely to develop heatstroke, even when temperatures and humidity are high, because they can find the coolest area in which to lie down or the area with the most airflow in order to take advantage of heat-dissipating mechanisms.1

    Predisposing Factors

    As humidity and temperature increase, the body's heat-loss mechanisms become less effective.1 The exact temperature at which this occurs varies by breed and individual dog.1,4 Dogs with conditions that obstruct airflow (e.g., laryngeal paralysis, tracheal collapse, lesions in the larynx or trachea, brachycephalic conformation) cannot take advantage of heat loss through evaporation as well as other dogs.3 Heart conditions that cause a decrease in cardiac output or cutaneous circulation also decrease a dog's ability to cool itself through conduction, convection, or radiation.3 Obese animals are less able to dissipate heat because of the insulation of body fat.3

    Neurologic diseases can also affect a dog's ability to thermoregulate.3 A change in respiratory function caused by a peripheral nerve disorder, such as botulism or tick paralysis, can impair physiologic cooling mechanisms.1 Central neurologic lesions, brain tumors, and other intracranial lesions that affect the hypothalamus may also reduce a dog's ability to thermoregulate.1

    Effects on Organ Systems

    Heatstroke affects organ systems throughout the body, including the cardiac and respiratory systems, the gastrointestinal (GI) tract, hematologic and coagulation systems, the CNS, and the musculoskeletal system.1,4 The body is also affected at the cellular level.1 An increase in core body temperature to 109°F (42.8°C) destabilizes cell membranes, alters mitochondrial functions, deactivates enzyme systems, and denatures proteins, causing cell death.1,3

    The cardiac system initially responds to hyperthermia by renal and splanchnic vasoconstriction, cutaneous vasodilation, and increasing cardiac output. These changes cause blood to move to the periphery to be cooled.1 As time passes, the body is unable to maintain renal and splanchnic vasoconstriction.1 The resultant systemic and visceral vasodilation leads to venous pooling and a decrease in the circulating plasma volume. This in turn causes a decrease in cardiac output and the failure of heat-loss mechanisms.1,2 As the core body temperature continues to rise, damage to cells increases.1,4 Myocardial ischemia can lead to ventricular arrhythmias, furthering cardiac dysfunction.1

    The pulmonary system develops increased vascular resis­tance and cellular injury, leading to damage of the pulmonary endothelium.1 This injury, if severe enough, causes noncardiogenic pulmonary edema and acute respiratory distress syndrome.1 Necropsies performed on dogs that ­succumbed to heatstroke revealed significant alveolar hemorrhage and edema as well as septal thickening and congestion.1 The damaged pulmonary tissue, combined with decreased cardiac output and perfusion, causes a decrease in oxygen uptake by the tissues. The resultant ischemia can worsen the damage already done to the myocardium, leading to the collapse of the entire cardiovascular system.1,4

    Dehydration and hypovolemia concentrate the blood, which enhances the formation of microthrombi and can result in packed cell volume (PCV) levels as high as 82%.1 Dehydration is most likely the result of fluid loss from the GI tract (through a damaged GI tract, vomiting, or diarrhea) and increased evaporative loss through respiration.1 As the blood becomes concentrated, delivery of oxygen to the tissues is further decreased, leading to widespread ischemia.1,4 At this point, the vital organs, including the liver and GI tract, can be damaged. Liver damage caused by hepatocellular vascular destruction and thermal injury to the hepatocytes can lead to a decrease in the production of clotting factors.1 If the wall of the GI tract becomes compromised, hemorrhage into the GI tract can result in hematochezia and melena.1,4 At the same time, endotoxins may be absorbed and bacteria translocated into the blood­stream.1,6 As the cycle continues, bacterial translocation, endotoxemia, bacteremia, and sepsis lead to septic shock, resulting in further ischemia throughout the body.1

    Microthrombi and decreased perfusion can also affect the capillary and venous endothelium. Damaged endothelium releases thromboplastic substances (e.g., factor XII, thromboplastin) that activate clotting cascades and cause systemic coagulation. Proinflammatory substances (e.g., thrombin, factor VIIa, factor Xa) initiate an inflammatory process that quickly consumes platelets and leukocytes as they adhere to the activated endothelium.1,2 This process, combined with the already reduced production of clotting factors, predisposes the animal to the development of disseminated vascular coagulation (DIC).1 Capillary permeability increases as the DIC progresses, permitting blood loss through the vascular endothelium.1 When this is combined with the blood loss secondary to hemorrhage in the GI tract, anemia can develop.

    Systemic cell death also causes CNS damage, which can lead to hemorrhage, cerebral edema, infarction, and CNS dysfunction.1,4 The hemorrhage and edema result in brain-tissue necrosis, disorientation, seizure-like activity, or coma.1 Core body temperatures as low as 105.8°F (41°C) can result in permanent brain damage.1 Damage to the thermoregulatory center can predispose animals to future episodes of heatstroke and hyperthermia.1,4

    Renal failure is initially caused by the decrease in cardiac output and renal vasoconstriction, which results in a decrease in renal perfusion.7 The resultant hypoxia, when combined with microthrombosis and thermal injury, leads to tubular necrosis.1 Damage to the renal tissue combined with dehydration can result in prerenal and renal azotemia.1

    Thermal injury of the muscle tissue causes necrosis and rhabdomyolysis.1 Rhabdomyolysis appears to be more common in patients suffering from exertional heatstroke because of their increased muscle activity.1 The myoglobin produced during rhabdomyolysis is nephrotoxic and can contribute to renal failure.1

    History and Physical Examination

    Patient history and initial assessment play large roles in diagnosing heatstroke. It is important to identify the reason for the heatstroke episode. Was the dog enclosed in an automobile? Was it tethered in the yard without access to water, shade, or ventilation?2,4 Does it have any contributory health problems, such as laryngeal paralysis, tracheal collapse, heart conditions, neurologic diseases, or a history of heatstroke?4 When obtaining a patient history, the technician should ask if the dog's current attitude is normal and inquire about any cooling efforts the owner may have attempted before presentation.4

    When examining a dog with possible heatstroke, it is also important to pay close attention to its conformation. Does it have any physical characteristics (e.g., thick coat, brachycephalic conformation) that may hinder its ability to dissipate heat?4

    During the initial assessment, the dog's temperature, heart rate, respiratory rate and effort, mucous membrane color, capillary refill time (CRT), pulse quality, and overall neurologic status and attitude should be determined.2 Dogs with heatstroke most commonly present with listlessness, collapse, hypersalivation, excessive panting, bloody diarrhea, or emesis.4

    With hyperthermia, a dog's rectal temperature can be as high as 104.9°F to 109.4°F (40.5°C to 43°C).4 However, the dog's body temperature during examination may be normal or even low if its owners tried to cool the animal before coming to the hospital or if the dog is in the later stages of shock.8

    In early heatstroke, increased cardiac output and peripheral vasodilation can cause a dog to become tachycardic, with hyperdynamic pulses.3 As the condition progresses, hypovolemia can result in weak or thready pulses.3,4,8 Pulse deficits may indicate a ventricular arrhythmia, which can be confirmed on electrocardiogram (ECG).3,4 In the later stages of heatstroke, signs of circulatory shock and impending collapse may be evident.3 Pulses may be weak; mucous membranes may be pale or cyanotic. Emesis, hematochezia, or melena may be seen.3,4

    The dog may be tachypneic and panting, with a labored respiratory effort.4,6 The mucous membranes may be dry and tacky from panting, hyperemic or darkened from vasodilation,8 or icteric from hepatic damage or massive hemolysis.8 Because blood is being shunted to the periphery to increase cooling, the CRT can be less than 1 second or undetectable.3 If DIC occurs, petechial hemorrhage or ecchymosis of the skin or mucous membranes may be present.8

    As respiratory efforts become more marked, the animal may begin to show signs of fatigue and to hypoventilate, which can lead to hypercapnia.3,9 Hypoventilation decreases alveolar ventilation, which in turn causes the oxygen content of the arterial blood to fall sharply.9 When alveolar ventilation decreases by 40%, hemoglobin saturation drops to 50% and the cardiorespiratory system may collapse.9 This may lead to seizures, coma, or death.3

    Neurologic signs of heatstroke include CNS depression, ataxia, cortical blindness, seizures, and coma.8 Cerebral edema may cause listlessness, tremors, or paddling; the patient may appear obtunded.8

    Diagnostic Testing

    A complete laboratory work-up should be conducted, including measurement of PCV, total protein, blood glucose, coagulation factors, and electrolytes; a full blood chemistry panel; blood gas analysis; a complete blood count; a blood smear; and urinalysis. Because IV fluids dilute values, blood should be drawn before initiating fluid therapy in order to obtain an accurate representation of body function. If abnormalities are noted after fluids are started, fluid choice can be changed accordingly.

    Dehydration and hemoconcentration often cause elevated PCV and total protein levels.4,8 Occasionally, anemia caused by fluid losses sustained through the GI tract or through vascular inflammation will cause the PCV and total protein to be low.4 These values often decrease as fluid resuscitation is started.

    The increased metabolic demand of heatstroke quickly depletes the body's store of glucose, and hepatic dysfunction can prevent further glucose production, causing the patient to become hypoglycemic.8 Sepsis can also cause a decrease in blood glucose because of increased use by tissues involved in the immune system and sepsis-induced enhancement of insulin production.3,8

    Because DIC can occur, coagulation testing should be conducted. DIC is indicated by one or more of the following: an increase in fibrin degradation products and a decrease in platelets or an increase in prothrombin time, activated partial thromboplastin time, or activated clotting time.3,4,8,10

    Results of blood gas analysis vary depending on the severity of the heatstroke.4 As the dog progresses toward heatstroke and the respiratory rate and effort increase, the levels of carbon dioxide in the blood increase. Vomiting or the presence of renal failure can contribute to blood gas abnormalities.3

    The complete blood count can show evidence of dehydration, thrombocytopenia, anemia, leukopenia, or a stress leukogram.6 The blood smear may exhibit schistocytes, which can indicate DIC, or nucleated red blood cells (thermal injury of the bone marrow causes premature release of red blood cells).2

    Electrolyte abnormalities may include hypophospha­temia, hypocalcemia, hypokalemia, hyperkalemia, hypernatremia, or hyperchloremia.8 Blood chemistry analysis can identify multiorgan dysfunction or failure.8 Acute tubular necrosis causes azotemia.3,4 Aspartate transaminase and creatine kinase, which are indicative of muscle breakdown, will be elevated if rhabdomyolysis is present.8 These values peak at 24 to 48 hours, then decline.8 Rhabdomyolysis is also indicated by the presence of myoglobinuria, which can worsen the tubular necrosis already in progress.3,4

    Treatment

    Cooling

    If heatstroke is suspected, treatment must be started as soon as possible to increase the dog's chance of survival.8,10 Cooling the patient is the most important aspect of the initial emergency treatment of heatstroke, and it must be done to stop any additional damage to the vital organs.8 This process should begin before the dog is brought to the hospital. The animal's owners can be instructed over the phone to spray the dog with cool (not cold) water and to drive to the hospital with the air conditioner on or with the windows open to generate a breeze.4,8 One study showed that dogs cooled by their owners before arriving at the clinic had a lower mortality rate compared with dogs not cooled before their arrival (19% and 49%, respectively).11 However, the use of cold water or ice is contraindicated because it can cause cutaneous vasoconstriction and shunt the blood to the vital organs. This can increase body temperature while impairing heat loss by preventing the blood from moving to the surface for cooling through convection and radiation.2,3,7,8 Applying ice can also cause discomfort to the animal.2

    Because heatstroke can damage the normal thermoregulatory mechanisms, decreasing the dog's ability to thermoregulate, it is critical to avoid cooling the dog too quickly or too much.3,4 The goal of cooling is to bring the animal's core temperature to 103°F (39.4°C) over 30 to 60 minutes.4,8 Once this temperature has been reached, active cooling should be stopped to avoid causing rebound hypothermia or shivering. These conditions require muscle activity and will cause the dog's temperature to increase.2,4 If the animal becomes hypothermic, it should be dried and wrapped in a towel or blanket.3

    Gentle massage can increase vasodilation and peripheral blood flow.3 Ice-water enemas and gastric lavage have been used for cooling, but these methods are controversial because they are time consuming and may require sedation. Cold-water enemas may also impair rectal temperature readings.2,8

    Initial Therapy and Monitoring

    When a dog presents with heatstroke, its airway should be evaluated and oxygen supplementation immediately initiated using an oxygen mask. If the dog cannot tolerate the mask, flow-by oxygen should be used.8 Oxygen supplementation improves tissue perfusion and decreases the risk of ischemia; therefore, it is beneficial even if the patient shows no signs of requiring oxygen.10 Oxygen cages are not recommended because they may exacerbate overheating.8 If the dog is hyperventilating, sedation, intubation, and mechanical ventilation may be required.2,8

    An IV catheter should be placed and room-temperature IV fluids started.7 Because the dog may be dehydrated and hemoconcentration may be present, it is important to begin aggressive cardiovascular support through volume expansion, which will decrease blood viscosity and improve blood flow.2,7 If the animal presents in the early stages of heatstroke, fluid loss may be minimal. Fluids should be administered carefully to avoid fluid overload.3,10 Fluid therapy in dogs should start with crystalloids (e.g., Normosol-R, Plasmalyte), which can be given in doses up to 90 ml/kg/hr for the first 1 to 2 hours.7

    If blood pressure does not satisfactorily increase after several boluses of crystalloids, colloids (e.g., hetastarch) can be administered.8 An initial hetastarch bolus of 5 ml/kg can be given, followed by a maintenance dose of 20 ml/kg/day. If necessary, a second bolus can be administered. The use of a colloid may reduce the crystalloid fluid rate by 40% to 60%.8 Colloids most benefit dogs that are hypoalbuminemic or that have a decreased colloid osmotic pressure.8 Administration of a colloid, such as hetastarch or plasma, can help prevent intravascular fluid from leaking into the interstitial space and decrease the risk of edema. Human serum albumina is also an option and may be advantageous because albumin has a longer retention time than synthetic colloids.7 Plasma and albumin can be expensive, so it may be more financially feasible to keep the patient on hetastarch until the albumin level is normal. If the patient is vomiting, metoclopramide can be added to fluids at a rate of 1 to 2 mg/kg/day.

    If signs of DIC are present, fresh-frozen plasma or fresh whole blood, both of which contain clotting factors, can be administered.7 If anemia is present and there is no evidence of DIC, packed red blood cells can be administered.7 The animal's respiratory rate and effort, heart rate, and temperature should be assessed every 15 minutes for the duration of the transfusion to detect any reactions as early as possible. If the patient is hypoglycemic, a 25% dextrose bolus of 0.5 g/kg may be given over 10 to 15 minutes, followed by the addition of 2.5% to 5% dextrose to the IV fluids, given as a constant-rate infusion.6

    Electrocardiography should be used to identify any possible arrhythmias. Lidocaine may be indicated for any arrhythmias not caused by electrolyte abnormalities or imbalances.8 An initial 2 mg/kg bolus of lidocaine is followed by a 40 to 80 mg/kg/min constant-rate infusion for the next 48 to 72 hours.8 The lidocaine may then be slowly tapered over 12 to 24 hours and discontinued if the arrhythmias do not return.

    Extended Therapy

    Once immediate treatment has been initiated and the patient is stable, long-term concerns (e.g., DIC, pulmonary edema, acid-base abnormalities) can be addressed. GI protectants, antibiotics, and appropriate antiinflammatories may be administered. Recommended GI medications include a histamine H2-receptor antagonist and a GI protectant. These agents should be administered prophylactically even if there is no evidence of GI damage (e.g., diarrhea, vomiting). Thermal injury to the GI tract can allow bacterial translocation; therefore, a broad-spectrum, nonnephrotoxic antibiotic should be initiated.3,10

    Antipyretic drugs are contraindicated because heatstroke is a nonpyrogenic hyperthermia,4 which means that the thermoregulatory set-point is normal. Antipyretic drugs change the set-point and therefore can induce hypothermia in patients with heatstroke.4 Corticosteroid use is controversial because these drugs may worsen any GI ulceration and kidney damage.4 Fresh-frozen plasma can be continued to treat DIC; however, it does not contain platelets. If thrombocytopenia is present, fresh whole blood or platelet-rich plasma should be used.12

    Unless the patient is actively hemorrhaging, subcutaneous heparin may be given to prevent microvascular thrombosis.4,8 However, this therapy is controversial because heparin, an anticoagulant, works by binding with antithrombin III, which helps regulate clotting. Patients with DIC may already have depleted levels of antithrombin III; therefore, heparin use in these patients may lead to increased hemorrhage. It is best to use heparin early in DIC while antithrombin III levels are still relatively high.13 Also, heparin will be inactivated if the patient is acidotic and so should not be used until acidosis has been corrected. To prevent rebound thrombosis, heparin should not be discontinued abruptly but should be tapered over 48 hours.13

    Acid-base and electrolyte abnormalities can often be corrected by improving perfusion and ventilation. If hypoglycemia persists, dextrose can be added to the fluids at 2.5% to 5%, depending on the severity of the hypoglycemia.8 Blood glucose should be monitored every 4 to 6 hours to ensure that the dog does not become hyperglycemic. Pulmonary edema should be treated aggressively, and the dog should be monitored closely for fluid overload.8

    Prognosis

    In patients with heatstroke, a poor prognosis is usually associated with the presence of advanced or nonresolving CNS signs, hypothermia, DIC, and electrolyte abnormalities or abnormal renal values that do not resolve with glucose or electrolyte supplementation or fluid therapy.

    Recovery depends on reducing the animal's temperature quickly and safely. The higher the temperature and the longer it stays elevated, the more damage the animal's vital organs sustain.8 One study of 42 dogs that presented with heatstroke found that patients that died from the condition did so within 24 hours after development of signs. Those that were able to survive longer than 48 hours lived.11 In the same study, all of the dogs that were hospitalized longer than 72 hours survived, despite evidence of multiorgan involvement.11

    Role of the Technician

    When treating patients for heatstroke, the technician plays a major role in monitoring patients closely for edema, changes in attitude, vomiting, diarrhea, changes in vital signs, and worsening CNS signs. This monitoring should continue for several days. Continuous ECG and blood pressure monitoring, measuring central venous pressures, and measuring urine output can be particularly valuable in assessing patients. A continuous ECG allows the technician to closely monitor the patient for any ventricular arrhythmias that can cause further hemodynamic compromise.8 If the animal suffers from ventricular tachycardia or other arrhythmias, a blood pressure reading should be conducted to determine if the arrhythmia is affecting the blood pressure.

    Urine output should be monitored for possible renal failure. Output decreases with hypovolemia, hypotension, and a decrease in cardiac output.7 The most effective method for monitoring urine output is placement of a urinary catheter connected to a closed-collection system. The output should be at least 1 to 2 ml/kg/hr. If it is less, the patient is oliguric.8 The fluid rate may be increased if the oliguria is due to hypovolemia. If renal function has decreased, a diuretic may be administered.8 Fluid input and urine output can also be compared to ensure that fluid therapy is adequate to meet urine production. The patient should also be monitored closely for diarrhea and sloughing of the intestinal tract.

    Neurologic function should be assessed each time the technician visits the patient, and even the most subtle change should be reported. Seizures can be seen in patients with hypoglycemia and cerebral edema or hemorrhage.8 Nervous tissue is very sensitive to thermal injury, and hemorrhage and edema often result, causing injury to the cerebral tissue in the form of thrombosis and infarction.3 If neuronal death occurs, brain damage may be permanent.3

    Educating pet owners is key to preventing heatstroke. Owners should understand the risk of leaving any species of pet locked in the car or of exercising a pet on a hot day. They should also be made aware of the importance of making sure that dogs have access to plenty of cold water and adequate shade when outside. When moving to a warmer or more humid climate, owners should slowly introduce their pet to the new environment and allow it to become acclimated.4 For some animals, this process can take up to 2 months.8 If a dog does suffer from heatstroke, the owner should be made aware of the possibility that it can easily succumb to high temperatures again.

    Conclusion

    Heatstroke is a life-threatening condition; however, early recognition and treatment can greatly increase a dog's chance of survival. A complete patient history, thorough physical examination, and comprehensive blood work will help determine the extent of the damage and the treatment options that should be pursued. Veterinary technicians play a large role in monitoring the patient and alerting the treatment team to any abnormalities or changes in the animal's status. By understanding the pathophysiology of heatstroke, the veterinary health care team will be able to provide the best treatment available and increase the likelihood of survival.

    Acknowledgment

    The author would like to thank Michelle Marsh-Ng, DVM, DACVIM, for her time in helping to edit and correct this article.

    aFor more information about human serum albumin, see "The Role of Albumin and Fluids in the Body" and "Use of Human Serum Albumin in Dogs" on pages 848 and 860, respectively, in our December 2005 issue.

    1. Flournoy WS, Whol JS, Macintire DK: Heatstroke in dogs: Pathophysiology and predisposing factors. Compend Contin Educ Pract Vet 25:410-418, 2003.

    2. Johnson SI, McMichael M, White G: Heatstroke in small animal medicine: A clinical practice review. J Vet Emerg Crit Care 16:112-119, 2006.

    3. Hackett TB: Heat stroke, in Wingfield WE (ed): Veterinary Emergency Medicine Secrets, ed 2. Philadelphia, Hanley and Belfus, 2001, pp 48-52.

    4. Walters MJ: Hyperthermia, in Wingfield WE, Raffe MR (eds): The Veterinary ICU Book. Jackson, WY, Teton New Media, 2002, pp 1130-1135.

    5. Gregory NG, Constantine E: Hyperthermia in dogs left in cars. Vet Rec 139:349-350, 1996.

    6. Marks SL: Heatstroke and hyperthermia, in Tilley LP, Smith FS (eds): The 5-Minute Veterinary Consult Canine and Feline, ed 3. Philadelphia, Williams & Wilkins, 2004, pp 540-541.

    7. Grooters AM: Fluid therapy in endocrine and metabolic disorders, in DiBartola SP (ed): Fluid Therapy in Small Animal Practice, ed 2. Philadelphia, WB Saunders, 2000, pp 383-384.

    8. Flournoy WS, Whol JS, Macintire DK: Heatstroke in dogs: Clinical signs, treatment, prognosis, and prevention. Compend Contin Educ Pract Vet 25:422-431, 2003.

    9. McDonnell W: Respiratory system, in Thurman JC, Tranquilli WJ, Benson GJ (eds): Lumb and Jones' Veterinary Anesthesia, ed 3. Baltimore, Williams & Wilkins, 1996, pp 124-125.

    10. Macintire DK, Drobatz KJ, Haskins SC, Saxon WD: Miscellaneous emergencies, in Manual of Small Animal Emergency and Critical Care Medicine. Philadelphia, Williams & Wilkins, 2005, pp 402-404.

    11. Drobatz KJ, Macintire DK: Heat-induced illness in dogs: 42 cases (1976-1993). JAVMA 209:1894-1899, 1996.

    12. Abrams-Ogg AC: Platelet and granulocyte transfusions, in Feldman BF, Zinkl JG, Jain NC (eds): Schalm's Veterinary Hematology, ed 5. Ames, IA, Blackwell Publishing, 2006, pp 844-845.

    13. Kirby R, Rudloff E: Acquired coagulopathy VI: Disseminated intravascular coagulation, in Feldman BF, Zinkl JG, Jain NC (eds): Schalm's Veterinary Hematology, ed 5. Ames, IA, Blackwell Publishing, 2006, pp 584-587.

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