Heat Stroke - Chapter 139 (Third Edition) PDF

139 Heat Stroke Kenneth J. Drobatz, DVM, MSCE, DACVIM, DACVECC KEY POINTS Heat stroke is the most serious of the heat-associated illnesses. Heat stroke can be classified as exertional (overheating while exercising) or nonexertional (classic heat stroke). Heat stroke is generally associated with mult...

139 Heat Stroke Kenneth J. Drobatz, DVM, MSCE, DACVIM, DACVECC KEY POINTS Heat stroke is the most serious of the heat-associated illnesses. Heat stroke can be classified as exertional (overheating while exercising) or nonexertional (classic heat stroke). Heat stroke is generally associated with multiorgan derangements, but central nervous system dysfunction (ranging from mild to moderate altered mentation to seizures or coma) is the hallmark of the condition. Every body system can be involved, but the major ones affected are the cardiovascular, central nervous, gastrointestinal, renal, and coagulation systems. Treatment involves cooling the patient and providing aggressive supportive care. INTRODUCTION Three syndromes of heat-associated illness that represent a continuum from the least to the most severe are described in humans. Heat cramp is characterized by muscle spasms resulting from sodium and chloride depletion. When signs such as fatigue, weakness, muscle tremors, vomiting, and diarrhea occur, heat prostration or heat exhaustion is the most likely diagnosis. The hallmark of heat stroke is severe central nervous system (CNS) disturbance, and it is often associated with multiple organ dysfunction. A more recent definition of heat stroke describes it as a form of “hyperthermia associated with a systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates.”1 This latter definition is more physiologically based and gives a more informative description of what is seen clinically in dogs with heat stroke. Generally, clients seek veterinary attention when their pets are demonstrating signs consistent with heat prostration, heat exhaustion, or heat stroke. This chapter focuses primarily on dogs with heat-associated illness because cats rarely experience heat stroke. PHYSIOLOGY, PATHOGENESIS, AND PATHOPHYSIOLOGY A hot environment or exercise in a hot environment does not equate to overheating and heat-associated illness. It is the increase in core body temperature that results in heat-associated illness (see Chapter 10, Hyperthermia and Fever). Therefore, the body has developed a relatively effective thermoregulation system to protect itself from overheating. Thermal homeostasis is maintained by a balance between heat load (environmental heat and heat generated through metabolism In human medicine and experimental dog models, no one cooling method has proved superior to others. A worse prognosis in dogs has been associated with hypoglycemia, decreased cholesterol level, increased bilirubin concentration, decreased albumin level, ventricular arrhythmias, increased creatinine values, longer delay from incident to treatment, obesity, seizures, prolonged prothrombin time and activated partial thromboplastin time, disseminated intravascular coagulation, and increased number of nucleated red blood cells. and exercise) and heat-dissipating mechanisms controlled by temperature-sensitive centers in the hypothalamus. Body temperature increases when heat load exceeds heat dissipation. Heat dissipation may occur via four mechanisms: convection, conduction, radiation, and evaporation. As the body temperature increases, 70% of heat loss in dogs and cats occurs by radiation and convection through the skin. Heat loss is facilitated by increased cutaneous circulation as a result of increased cardiac output and sympathetically mediated peripheral vasodilation.2 Shunting of blood to the periphery involves a trade-off with blood supply to the viscera (intestines and kidneys). Significant heat loss also occurs as a result of evaporation from the respiratory tract through panting, and this becomes the predominant mechanism of heat loss when ambient temperature is equal to or greater than body temperature. A warm, humid environment and exercise are the two most common heat loads experienced by dogs that may cause extreme hyperthermia, even in animals with functional heat-dissipating mechanisms. Respiratory evaporative heat loss may be diminished by humid climatic conditions, confinement in a closed space with poor ventilation, and obstructive upper respiratory tract abnormalities (e.g., brachycephalic conformation, laryngeal paralysis, airway masses, or collapsing trachea). Additionally, the work of breathing in these latter conditions can contribute substantially to the heat load in these animals. Diminished radiational and convective heat loss from the skin may occur as a result of hypovolemia from any cause, poor cardiac output, obesity, extremely thick hair coat, or lack of acclimatization to heat. Situations that combine high heat load and diminished heat dissipation may result in a rapid and extreme body temperature increase. Most dogs with heat-induced illness are brought to the veterinarian when the warm, humid weather begins, so the seasonal pattern differs depending on climatic conditions and year-to-year variations 817 818 PART XVI Environmental Emergencies in temperature and humidity. In some instances, despite progressively warmer days later in the summer, heat-associated illness becomes less frequent.3 This may be related to the time available for acclimatization to the change in environmental temperature. In humans, acclimatization to heat can take 2 weeks or longer and is associated with enhanced cardiac performance, salt conservation by the kidney and sweat glands through activation of the renin-angiotensin-aldosterone axis, an increased capacity to sweat, plasma volume expansion, increased glomerular filtration rate, and increased ability to resist exertional rhabdomyolysis.4 Increased body heat induces three protective mechanisms: thermoregulation (mentioned previously), an acute-phase response, and increased expression of intracellular heat shock proteins.1 The acute-phase response involves a variety of proinflammatory and antiinflammatory cytokines. Proinflammatory mediators induce leukocytosis, promote synthesis of acute-phase proteins, stimulate the hypothalamic-pituitaryadrenal axis, and activate endothelial cells and white blood cells. These mediators are protective for the body when balance is maintained between the proinflammatory and antiinflammatory response systems (see Chapter 7, SIRS, MODS and Sepsis). The heat shock proteins protect the cell and the body against further heat insults and prevent denaturation of intracellular proteins. They also help to regulate the baroreceptor response during heat stress, thus preventing hypotension and conferring cardiovascular protection.5 Heat stroke results from a failure of thermoregulation followed by an exaggerated acute-phase response and alteration of heat shock proteins.1 Additionally, absorption of endotoxin from the gastrointestinal (GI) tract may fuel the inflammatory response because intestinal mucosal permeability is increased during heat stress.6 It has been noted that many of the mediators involved in heat stroke are the same mediators associated with sepsis and the systemic inflammatory response syndrome (see Chapters 7 and 90, SIRS, MODS and Sepsis and Sepsis and Septic Shock, respectively).1 The suggested pathophysiologic sequence in heat stroke involves initial production and release of interleukin-1 and interleukin-6 from the muscles into the circulation and increased systemic levels of endotoxin from the GI tract.1 These substances mediate excessive activation of leukocytes and endothelial cells, which results in the release of numerous proinflammatory and antiinflammatory cytokines as well as activation of coagulation and inhibition of fibrinolysis. Direct endothelial cell injury due to the heat, combined with an initial hypercoagulable state, results in microthrombosis and progressive tissue injury. These proinflammatory and procoagulation processes, in addition to direct heat injury, can lead to multiple organ dysfunction syndrome. Because of the multisystemic problems in patients with heat stroke, these animals should be assessed and monitored for multiple organ failure, with particular attention to the respiratory, cardiovascular, renal, GI, and central nervous systems, as well as the coagulation system. PHYSICAL EXAMINATION The physical examination findings of dogs suffering from heatassociated illness vary with the intensity and duration of the increased body temperature and the individual pathophysiologic responses that are initiated. Temperature, Pulse, and Respiratory Rate The rectal temperature may be decreased, normal, or increased depending on tissue perfusion and whether cooling measures have already been implemented. The pulse rate is usually increased as a result of a compensatory sinus tachycardia. The respiratory rate is very rapid, usually in an attempt to improve heat dissipation rather than as a result of primary respiratory disease. Cardiovascular System Most dogs arrive for treatment in a hyperdynamic state. The mucous membranes are usually hyperemic and the capillary refill time is very short. The pulses are often weak because of hypovolemia secondary to evaporative fluid loss, vomiting, diarrhea, and vasodilation (causing a relative hypovolemia). Sinus tachycardia is common. Rarely, a dog will have intermittent ventricular arrhythmias, which have been associated with a worse outcome in clinical cases of heat-associated illness.3 Electrocardiographic evaluation and monitoring should be performed for all patients with severe heat-associated illness. Respiratory System Careful evaluation of the respiratory system is warranted because evaporation through the respiratory tract is a major mechanism for heat dissipation. Loud or noisy breathing that is heard without the stethoscope suggests an upper airway abnormality such as laryngeal paralysis, upper airway edema, obstruction (e.g., brachycephalic syndrome), or collapse. Careful auscultation for loud airway or adventitious lung sounds (e.g., pulmonary crackles) should be performed. Many dogs with heatassociated illness have been vomiting; therefore, aspiration pneumonia must be considered. Dogs suffering from disseminated intravascular coagulation (DIC; see Chapters 101 and 104, Hypercoagulable States and Coagulopathy in the ICU, respectively) may have pulmonary parenchymal hemorrhage resulting in crackles or loud airway sounds. However, in a retrospective study of clinical heat stroke cases, respiratory abnormalities were not common.3 More recently, a necropsy-based study of dogs that died due to heat stroke revealed that the majority had hyperemia, edema, and hemorrhage in the lungs.7 Central Nervous System Mentation may range from alert to comatose, with depression being the most common abnormality. The severely affected dog is comatose or stuporous at presentation. Pupil size may range from dilated to pinpoint, but pupils are usually responsive to light. Some dogs may be cortically blind when they are brought in, but this may resolve after several hours. Similarly, head bobbing or tremors occur transiently and resolve over hours. Ambulatory dogs may be ataxic. The causes of these neurologic abnormalities may include poor cerebral perfusion, direct thermal damage, cerebral edema, CNS hemorrhage, or metabolic abnormalities such as hypoglycemia or hepatoencephalopathy, although the latter has not been documented in clinical cases of dogs with heat stroke. Renal System Physical evaluation of the renal system is very limited. Palpation of bladder size and the change in size as fluid therapy ensues may be helpful in assessing urine production. Acute kidney injury is a potential complication of heat stroke, and evaluation of the urine for casts, monitoring urine production and monitoring for gross abnormalities (e.g., pigmenturia) are valuable tools (see Chapter 121, Acute Kidney Injury). Gastrointestinal System Many of the severely affected dogs have protracted vomiting and diarrhea. The diarrhea may range from watery to hemorrhagic with mucosal sloughing. This may occur secondary to DIC or poor visceral perfusion and reperfusion as volume resuscitation is provided. Gastric ulceration may occur as well, resulting in vomiting with or without blood and melena. CHAPTER 139 Heat Stroke Coagulation System DIC is a relatively common finding in dogs with heat-associated illness. The presence of petechiae and ecchymoses or blood in the urine, vomit, or stool suggests that DIC may be present (see Chapters 101 and 104, Hypercoagulable States and Coagulopathy in the ICU, respectively). LABORATORY EVALUATION An initial data set including a blood smear, packed cell volume, total solids, dipstick blood urea nitrogen (BUN) level, whole blood glucose concentration, and blood sodium and potassium levels should be obtained, if possible. The packed cell volume and total solids are often elevated because of hemoconcentration. The dipstick BUN value may be increased, likely because of poor renal perfusion, although GI hemorrhage or acute kidney injury must also be considered. The blood glucose concentration may be very low in severely affected patients secondary to increased utilization from hyperthermia and/or early sepsis. Sodium and potassium concentrations are generally normal in these patients on arrival but warrant evaluation, especially if vomiting and diarrhea have occurred or an acidosis or kidney injury is suspected. In addition, excessive panting may quickly lead to hypernatremia due to a loss of free water. An increased number of nucleated red blood cells (NRBCs) may be noted on a blood smear and is associated with a worse outcome.8 Urinalysis should be performed, preferably before fluid therapy is initiated, to assess renal function or damage; however, collection by cystocentesis should be avoided because of potential coagulation abnormalities. Urine specific gravity should be interpreted in light of the patient’s hydration and perfusion status. Urine assessment by dipstick often yields positive results for protein and hemoglobin. Glucosuria may be detected despite normal or even low blood glucose levels, which may suggest proximal tubular damage or recent hyperglycemia with glucosuria. Urine sediment examination may reveal red blood cells, which indicates renal damage or coagulation abnormalities. The presence of casts in the urine indicates renal damage and warrants close monitoring of urine output and renal function. More recently, in a prospective canine heat stroke study, renal urine biomarkers were found to be much more sensitive in detecting acute kidney injury than traditional renal function parameters such as BUN and creatinine.9 Further laboratory evaluation should include a complete blood count, serum chemistry screen, measurement of serum creatinine kinase activity, and coagulation evaluation. The most common complete blood count abnormality reported is an increased number of NRBCs;3 as noted earlier, this is associated with a worse prognosis. In one canine heat stroke study, a value of 18 or more NRBCs per 100 leukocytes at presentation had a sensitivity and specificity of 91% and 88%, respectively, for predicting death.8 The NRBC level typically decreases rapidly over the first 24 hours. Serum alanine aminotransferase and creatinine kinase levels are often elevated and usually peak within 24 to 48 hours. Serum bilirubin level may be increased and serum cholesterol level decreased in more severely affected dogs. Serum creatinine and BUN concentrations may be increased as well. These increases may be a result of dehydration and poor renal perfusion but warrant serial evaluations because renal damage may be present; serial increases in renal clinicopathologic parameters are associated with a worse prognosis.3 Activation of the coagulation cascade is initiated by direct thermal injury to the tissues and endothelium and may result in consumption of platelets and coagulation factors. If prothrombin time, partial thromboplastin time, and platelet count measurements cannot be performed, then activated clotting time should be determined, and a blood 819 smear may reveal red blood cell fragments (schistocytes) and allow for platelet count to be estimated. In general, there should be at least 8 to 15 platelets per 1003 oil immersion field on a well-executed blood smear (see Chapter 196, Blood Film Evaluation). In patients with DIC, the platelet count is often decreased secondary to increased consumption and/or loss. The finding of DIC was not found to be associated with mortality in one study. In this same comprehensive coagulation study in dogs with heat stroke, the number of abnormal coagulation parameters in the first 24 hours was associated with mortality.10 TREATMENT AND MONITORING Cooling Procedures Cooling measures involve taking advantage of the physics of heatdissipating mechanisms: evaporation, conduction, convection, and radiation. Evaporative methods include wetting the dog’s whole body with tepid water and blowing fans over the body. In humans, ice water is used in this method, but recommendations are to massage the muscles to maintain circulation because extreme cooling of the periphery may result in vasoconstriction and paradoxical inhibition of body cooling. Whole body alcohol bathing should be avoided because not only is this noxious to the animal, but it may present a significant fire hazard should defibrillation be required in dogs that experience cardiac arrest. Intuitively, wetting the footpads with alcohol seems like an ineffective cooling measure given the small surface area involved, although this technique has not been rigorously evaluated for efficacy. External conduction cooling techniques include application of ice packs over major vessels (e.g., jugular veins), tap water immersion, ice water immersion, and use of cooling blankets. Water immersion methods can be cumbersome, and ice water baths may be uncomfortable and produce peripheral vasoconstriction and thus diminish heat dissipation overall. Internal conduction techniques include iced gastric lavage, iced peritoneal lavage, and cold water enemas, although the latter may interfere with rectal temperature monitoring. These techniques are invasive and can result in serious complications (aspiration pneumonia, septic peritonitis). Pharmacologic techniques such as administration of dantrolene sodium have been evaluated experimentally and have not been effective.11 Cooling measures are the only therapies for heat stroke that have been thoroughly evaluated. Many of the techniques already mentioned have been evaluated rigorously, both clinically in humans and experimentally in dogs. No single technique has been proven superior to any other, and in experimental canine studies, rates of temperature decline ranged from 0.15°C to 0.23°C (0.27°F to 0.41°F) per minute.12,13 Not surprisingly, many owners recognize that their dogs are overheated and hose them down with water. This is very effective and often results in a normal body temperature (or even hypothermia) by the time of presentation to the veterinarian.3 Whole body wetting with water combined with muscle massage and blowing fans is commonly performed. Additionally, administration of room temperature intravenous fluids may be helpful. Rarely, whole body shaving is needed to facilitate cooling in dogs with very thick hair coats. Cooling measures should be discontinued when the rectal temperature reaches 39.4°C (103°F) to prevent rebound hypothermia. Despite this, it is not unusual for dogs to develop body temperatures between 35°C and 37.8°C (95°F and 100°F) within the first few hours of hospitalization.3 If hypothermia occurs, warm water bottles or blankets may be necessary to maintain normothermia. Cardiovascular System Severely affected dogs often are in hypovolemic shock at presentation. If cardiovascular disease is unlikely, balanced electrolyte fluids of up to 820 PART XVI Environmental Emergencies 90 ml/kg should be administered intravenously to dogs (up to 50 ml/ kg in cats); perfusion status should be assessed continuously and the rate and volume of fluids titrated to effect (see Chapter 68, Shock Fluid Therapy). Excessive volume administration should be avoided. If large doses of intravenous fluids do not improve tissue perfusion and blood pressure, administration of synthetic colloids should be considered, with or without positive inotropic or vasopressor agents (see Part VI, Fluid Therapy and Chapter 147, Catecholamines). Dogs that cannot maintain an adequate blood pressure without pressure support (for prolonged periods) have a poor prognosis. Blood pressure and physical parameters of tissue perfusion should be monitored continuously in severely affected dogs (see Chapter 181, Hemodynamic Monitoring). Respiratory System Oxygen should be administered at presentation and should be continued until it has been determined that the dog can maintain adequate arterial oxygenation (see Chapters 16, 15 and 184, Hypoxemia, Oxygen Therapy, and Oximetry Monitoring, respectively). Serial physical assessments of the respiratory system including thoracic auscultation, observation of respiratory rate and effort, and evaluation of mucous membrane color is warranted in dogs with heat illness. More objective assessments such as arterial blood gas analysis and pulse oximetry may be required, especially in dogs with physical evidence of respiratory compromise. Central Nervous System At presentation, a full neurologic examination, including assessment of mentation level and cranial nerve function, should be performed to establish baseline parameters. More severely affected dogs may be stuporous or comatose at presentation. Serum electrolyte levels, packed cell volume, total solids, and blood glucose measurements should be performed and abnormalities corrected as warranted. Hypoglycemia is not unusual in the severely compromised dog with heat illness. An intravenous bolus of 0.25 to 0.5 g/kg of body weight of a diluted dextrose solution should be administered if hypoglycemia is documented, and dextrose should be added to the intravenous fluids to make a 2.5% to 5% concentration if hypoglycemia is persistent (see Chapter 75, Hypoglycemia). Poor tissue perfusion should be corrected and mentation reevaluated after perfusion is improved. If mentation continues to be abnormal after these abnormalities are corrected, then cerebral edema may be present (see Chapter 85, Intracranial Hypertension). Administration of mannitol (0.5 to 1 g/kg of body weight intravenously over 20 to 30 minutes) should be considered. The head should be elevated 15 to 30 degrees above the horizontal plane of the body while avoiding compression of the jugular veins. Progression of neurologic abnormalities despite therapy carries a poor prognosis. Renal System A urinary catheter should be inserted at presentation for monitoring urine output in more severely affected dogs. Complete urinalysis should be performed initially and serially as treatment progresses to detect early signs of renal damage such as the presence of urinary casts. Urine output should be maintained at 2 ml/kg of body weight per hour or more, depending on the amount of fluid being administered. Mean arterial pressure ideally should be at least 80 mm Hg. If urine output remains insufficient despite adequate fluid replacement and blood pressure, then measures to manage oliguria or anuria should be instituted (see Chapter 121, Acute Kidney Injury). If urine output remains inadequate and renal parameters increase, hemodialysis may be necessary (see Chapter 178, Renal Replacement Therapies). Serum sodium and potassium concentrations, total solids, BUN, acid-base status, and creatinine should be monitored every 4 to 24 hours as indicated. Coagulation System Evaluation of the coagulation system, including measurement of prothrombin time, partial thromboplastin time, platelet count, and levels of D-dimers and fibrin split products, should be performed at presentation and as indicated during therapy. Prolonged coagulation times, decreased platelet count, and increased levels of fibrin split products or D-dimers suggest DIC (see Chapter 104, Coagulopathy in the ICU). Thromboelastography may also prove useful, if available (see Chapter 187, Viscoelastic Monitoring). Gastrointestinal System Direct thermal damage and poor visceral perfusion and/or reperfusion may result in GI mucosal sloughing and ulceration. This leads to vomiting and diarrhea that may or may not be bloody. Sucralfate (if vomiting is not present) and histamine-2 blockers can help manage gastric ulceration (see Chapters 153 and 154, Gastrointestinal Protectants and Anti-emetics and Prokinetics, respectively). Breakdown of the mucosal barrier may result in bacteremia or endotoxemia. Broad-spectrum antimicrobial therapy should be considered in severely affected animals with bloody diarrhea. There are anecdotal reports of the development of small intestinal intussusceptions in some dogs with heat stroke. PROGNOSIS The degree of compromise depends on the prior physical health of the dog and the degree and duration of the heat insult. An increasing number of NRBCs is associated with more severe injury and worse outcome, and a severity of disease scoring system has been developed for dogs but it requires further testing and refinement before it can be applied for research purposes and practical clinical use. Dogs with multiple organ dysfunction or severe CNS disturbances have a more guarded prognosis.3 However, many dogs with severe CNS disturbances, DIC, and other organ dysfunction live without any residual problems. Severe heat-associated illness is challenging to treat, but with aggressive medical therapy dogs may recover and do well. Because cats rarely develop heat stroke, there is little information regarding the prognosis and outcome in this species. REFERENCES 1. Bouchama A, Knochel JP: Heat stroke, N Engl J Med 346:1978, 2002. 2. Flourroy WS, Wohl JS, Macintire DK: Heatstroke in dogs: pathophysiology and predisposing factors, Comp Contin Educ Pract Vet 25:410, 2003. 3. Drobatz KJ, Macintire DK: Heat-induced illness in dogs: 42 cases (19761993), J Am Vet Med Assoc 209:1894, 1996. 4. Knochel JP: Catastrophic medical events with exhaustive exercise: “white collar rhabdomyolysis,” Kidney Int 38:709, 1990. 5. Moseley PL: Heat shock proteins in heat adaptation of the whole organism, J Appl Physiol 83:1413, 1997. 6. Shapiro Y, Alkan M, Epstein Y, et al: Increase in rat intestinal permeability to endotoxin during hyperthermia, Eur J Appl Physiol Occup Physiol 55:410, 1986. 7. Bruchim Y, Loeb E, Saragusty J, et al: Pathological findings in dogs with fatal heatstroke, J Comp Pathol 140(2/3):97-104, 2009. 8. 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 23(3):544-551, 2009. 9. Segev G, Daminet S, Meyer E, et al: Characterization of kidney damage using several renal biomarkers in dogs with naturally occurring heatstroke, Vet J 206(2):213-215, 2015. CHAPTER 139 Heat Stroke 10. Bruchim Y, Kelmer E, Cohen A, Codner C, Segev G, Aroch I: Hemostatic abnormalities in dogs with naturally occurring heatstroke, J Vet Emerg Crit Care 27(3):315-324, 2017. 11. Amsterdam JT, Syverud SA, Barker WJ, et al: Dantrolene sodium for the treatment of heatstroke victims: lack of efficacy in a canine model, Am J Med 4:399, 1986. 821 12. White JD, Kamath R, Nucci R, et al: Evaporative versus iced peritoneal lavage treatment of heatstroke: comparative efficacy in a canine model, Am J Emerg Med 11:1, 1993. 13. Hadad E, Rav-Acha M, Heled Y, et al: Heat stroke: a review of cooling methods, Sports Med 34:501, 2004.