{"id":596,"date":"2014-09-01T15:23:24","date_gmt":"2014-09-01T15:23:24","guid":{"rendered":"http:\/\/phosdev.com\/todaysveterinarypractice\/?p=596"},"modified":"2022-07-05T14:05:55","modified_gmt":"2022-07-05T14:05:55","slug":"todays-technician-heatstroke-in-dogs","status":"publish","type":"post","link":"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/emergency-medicine-critical-care\/todays-technician-heatstroke-in-dogs\/","title":{"rendered":"Heatstroke in Dogs"},"content":{"rendered":"<p><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2016\/06\/T1409C05.pdf\"><img decoding=\"async\" class=\"alignnone size-full wp-image-9886\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2011\/07\/pdf_button.png\" alt=\"pdf_button\" width=\"110\" height=\"27\" \/><\/a><\/p>\n<hr \/>\n<p>Heatstroke is a common problem in pets during the summer months, especially in hot, humid climates. This life-threatening condition can affect dogs of any age, breed, or gender.<\/p>\n<p>Heatstroke in dogs is defined as a\u00a0<span class=\"italic\">nonpyrogenic increased body temperature above 104\u00b0F (40\u00b0C), with a spectrum of systemic signs<\/span>.<sup>1<\/sup>\u00a0The ability to rapidly recognize and begin treatment of heatstroke is vital to maximize the chances of saving the animal&#8217;s life.<\/p>\n<h2><strong><span class=\"font_purple\">HYPERTHERMIA<br \/>\n<\/span><\/strong><\/h2>\n<p>Maintenance of normal body temperature is an important aspect of preserving homeostasis and preventing interruption of normal metabolism.<\/p>\n<p>The thermoregulatory center, located in the anterior hypothalamus, maintains body temperature within a narrow range, or<span class=\"italic\">\u00a0set point. A pyrogenic hyperthermia, or fever, may be induced by an increase in the set point in response to disease.<\/span><\/p>\n<p>Differentiating between pyrogenic and nonpyrogenic hyperthermia is important, due to the variation in pathophysiology and treatment of each disease process.<\/p>\n<h3><strong>Pyrogenic Hyperthermia<\/strong><\/h3>\n<p>If a dog develops pyrogenic hyperthermia, the underlying cause guides treatment. Active cooling of a patient with pyrogenic hyperthermia causes metabolic stress and physical discomfort.<sup>2<\/sup><\/p>\n<p>In one human study, pyrogenic hyperthermia was induced via an injection of IL-2, a pyrogenic cytokine; then subjects were actively cooled, resulting in an increase in oxygen consumption and reported physical discomfort. Within that study, pyrogenic hyperthermia subjects exposed to forced air warming were most comfortable.<sup>2<\/sup><\/p>\n<h3><strong><span class=\"aquabold\">Nonpyrogenic Hyperthermia<\/span><\/strong><\/h3>\n<p><span style=\"line-height: 1.5\">A nonpyrogenic hyperthermia, such as heatstroke, is not due to a change in the hypothalamic thermoregulatory set point, which allows us to perform active cooling without the consequences previously mentioned.<\/span><\/p>\n<table border=\"1\" width=\"500\" cellspacing=\"0\" cellpadding=\"10\">\n<tbody>\n<tr>\n<td>\n<p class=\"arial\"><strong><span class=\"font_purple\">THERMOREGULATION<\/span><\/strong><br \/>\nThe body uses several methods to cool itself, which are described in\u00a0<strong>Table 1<\/strong>.<\/p>\n<table border=\"1\" width=\"500\" cellspacing=\"0\" cellpadding=\"1\">\n<tbody>\n<tr>\n<td align=\"center\"><strong><span class=\"GreenAqua\">Table 1. Methods of Cooling<\/span><\/strong><\/td>\n<\/tr>\n<tr>\n<td><strong><span class=\"aquabold\">EVAPORATION<\/span><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td>\n<ul>\n<li><span class=\"arial\">Occurs through panting, which dispels heat via evaporation of water from the surface of the tongue, and is one of the most important ways a dog thermoregulates<\/span><\/li>\n<li><span class=\"arial\">Most effective when the ambient temperature reaches 89.6\u00b0F (32\u00b0C);1 less efficient with high ambient humidity, which increases the risk for heatstroke<br \/>\n<\/span><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr>\n<td class=\"arial\"><strong><span class=\"aquabold\">CONDUCTION<\/span><\/strong><\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td>\n<ul>\n<li><span class=\"arial\">Occurs through transfer of heat from one object to another<\/span><\/li>\n<li><span class=\"arial\">In dogs, commonly achieved by lying with their sparsely haired abdomen in contact with a cool surface, allowing transfer of heat to this surface<br \/>\n<\/span><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr>\n<td><strong><span class=\"aquabold\">CONVECTION<\/span><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td>\n<ul>\n<li><span class=\"arial\">Occurs by movement of air over the body to disperse heat, such as wind or air from a fan<\/span><\/li>\n<li><span class=\"arial\">Plays an important role in treating heatstroke<br \/>\n<\/span><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr>\n<td><strong><span class=\"aquabold\">RADIATION<\/span><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td align=\"left\">\n<ul>\n<li><span class=\"arial\">Occurs when heat from the body dissipates into the environment<\/span><\/li>\n<li><span class=\"arial\">Less effective when ambient temperature reaches body temperature<\/span><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>A minimum nonpyrogenic body temperature elevation of 1.8\u00b0F (1\u00b0C) can activate heat receptors found in the periphery, triggering the thermoregulatory center, which in turn induces constriction of renal and splanchnic vessels, tachycardia, and cutaneous vasodilation. These processes result in increased blood flow to the skin, where it can be cooled.<sup>1<\/sup><\/p>\n<p>The hypothalamus also stimulates tachypnea and panting to assist with cooling.<sup>1<\/sup><\/p>\n<hr \/>\n<p><strong>Heat-related illness can vary in severity and, in humans, is classified based on that severity.<\/strong><\/p>\n<p><strong><span class=\"aquabold\">Heat stress<\/span><\/strong>\u00a0is rarely recognized in veterinary patients. It includes some discomfort and physiologic strain. The core body temperature will be normal.<sup>3<\/sup><\/p>\n<p><strong><span class=\"aquabold\">Heat cramps<\/span><\/strong>\u00a0are rarely recognized in veterinary patients. Muscle cramps occur secondary to the depletion of sodium and water. The core body temperature will be normal.<sup>3,4<\/sup><\/p>\n<p><strong><span class=\"aquabold\">Heat exhaustion<\/span><\/strong>\u00a0includes weakness, ataxia, fainting, and an inability to continue the work the person was performing. The core body temperature will be normal or slightly increased.<sup>3,4<\/sup><\/p>\n<p><strong><span class=\"aquabold\">Heat stroke<\/span><\/strong>\u00a0includes dysfunction of the central nervous system, hypovolemia, and cellular dysfunction. The core body temperature will be elevated.<sup>3,4<\/sup><\/p>\n<hr \/>\n<h2><strong><span class=\"font_purple\">TYPES OF HEATSTROKE<br \/>\n<\/span><\/strong><\/h2>\n<p>Heatstroke is classified as\u00a0<span class=\"italic\">exertional<\/span>\u00a0or\u00a0<span class=\"italic\">nonexertional<\/span>\u00a0(classical).<\/p>\n<h3><strong><span class=\"aquabold\">Exertional Heatstroke<\/span><\/strong><\/h3>\n<p>Exertional heatstroke occurs during exercise and is more common in dogs that have not been acclimated to their environment. If a period of temperature acclimation is allowed, dogs become less susceptible to heatstroke. Acclimation can take up to 60 days, although the animal is partially acclimated within 10 to 20 days.<sup>3<\/sup><\/p>\n<p>While exertional heatstroke can occur in working dogs, it is less common because handlers are typically more knowledgeable. For example, it is possible for military dogs to work in environmental temperatures reaching 140\u00b0F (60\u00b0C) without adverse effects. After racing, greyhounds can transiently have rectal temperatures as high as 107.6\u00b0F (42\u00b0C) without showing signs of heatstroke.<sup>4<\/sup><\/p>\n<h3><strong><span class=\"aquabold\">Nonexertional Heatstroke<\/span><\/strong><\/h3>\n<p>Nonexertional heatstroke results from exposure to increased environmental temperature in the absence of adequate means of cooling. This may be seen when a dog is enclosed in a parked car or left in a yard without shade and water.<\/p>\n<h2><strong><span class=\"font_purple\">RISK FACTORS<br \/>\n<\/span><\/strong><\/h2>\n<p>Several predisposing factors may decrease a dog&#8217;s ability to cool itself; therefore, increasing its risk for developing heatstroke. These factors are listed in\u00a0<strong><span class=\"bold\">Table 2<\/span><\/strong>. Dogs that have a history of heatstroke are more susceptible to developing it again.<sup>4<\/sup><\/p>\n<table border=\"1\" width=\"200\" cellspacing=\"0\" cellpadding=\"1\">\n<tbody>\n<tr>\n<td align=\"center\"><strong><span class=\"GreenAqua\">Table 2. Examples of Factors That Predispose Dogs to Heatstroke<\/span><\/strong><\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td>\n<ul>\n<li class=\"arial\">Brachycephalic syndrome<\/li>\n<li class=\"arial\">Cardiac disease<\/li>\n<li class=\"arial\">Laryngeal paralysis<\/li>\n<li class=\"arial\">Obesity<\/li>\n<li class=\"arial\">Tracheal collapse<\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<h2><strong><span class=\"font_purple\">PATHOPHYSIOLOGY<br \/>\n<\/span><\/strong><\/h2>\n<h3><strong><span class=\"aquabold\">Acute-Phase Response<\/span><\/strong><\/h3>\n<p>The acute-phase response is a coordinated cellular response that occurs in inflammatory events, such as infection, surgery, trauma, burns, immune-mediated diseases, and nonpyrogenic hyperthermia.<sup>3,5<\/sup>\u00a0During nonpyrogenic hyperthermia, this response is stimulated in an attempt to protect tissues from excessive heat and promote repair.<sup>3<\/sup><\/p>\n<p>Acute-phase proteins are divided into 2 categories:<\/p>\n<ol>\n<li><strong><span class=\"bold\">Negative acute-phase proteins<\/span><\/strong>\u00a0<span class=\"italic\">decrease<\/span>\u00a0by 25% during an acute-phase response.<sup>5,6<\/sup>In most species, albumin is a negative acute-phase protein, and levels may decrease during an acute-phase response due to gastrointestinal (GI) or renal loss or decreased production.<\/li>\n<li><strong><span class=\"bold\">Positive acute-phase proteins<\/span><\/strong>\u00a0<span class=\"italic\">increase<\/span>\u00a0by 25% during an acute-phase response.<sup>5,6<\/sup>In dogs, positive acute-phase proteins include C-reactive protein and serum amyloid A.\n<ul>\n<li>C-reactive protein activates the complement system, which promotes phagocytosis, and up- or down-regulates cytokine production and chemotaxis.<\/li>\n<li>Serum amyloid A causes chemotaxis of several types of white blood cells and inhibits inflammation.<sup>6<\/sup><\/li>\n<\/ul>\n<\/li>\n<\/ol>\n<p>Several other acute-phase proteins play important roles in the acute-phase response, including:<sup>6<\/sup><\/p>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li>Haptoglobin: Reduces oxidative damage<\/li>\n<li>Ceruloplasmin: Scavenges free radicals<\/li>\n<li>Fibrinogen: Plays a role in tissue repair.<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p>The acute-phase response also initiates production of heat shock proteins (HSPs).<sup>7<\/sup><\/p>\n<h3><strong><span class=\"aquabold\">Heat Shock Proteins<\/span><\/strong><\/h3>\n<p>When cells are exposed to an increased temperature, HSPs protect against protein denaturation.<sup>8<\/sup>\u00a0They prevent disaggregation of denatured proteins, refold denatured proteins, protect against endotoxin leakage across the intestines, and reduce cerebral ischemia.<sup>7<\/sup><\/p>\n<h3><strong><span class=\"aquabold\">Effects by Body System<\/span><\/strong><\/h3>\n<p>Heatstroke has multiple deleterious effects within the body (<strong><span class=\"bold\">Table 3<\/span><\/strong>). Direct cytotoxicity occurs at body temperatures ranging from 106.7\u00b0F to 107.6\u00b0F (41.5\u00b0C\u201442\u00b0C). At these temperatures enzymes and proteins are denatured.<sup>1<\/sup>\u00a0The severity of these effects depends on both degree of body temperature elevation and duration of time it is elevated.<\/p>\n<table border=\"1\" width=\"580\" cellspacing=\"0\" cellpadding=\"1\">\n<tbody>\n<tr align=\"center\">\n<td colspan=\"2\"><strong><span class=\"GreenAqua\">Table 3. Heatstroke Effects by Body System<\/span><\/strong><\/td>\n<\/tr>\n<tr class=\"aquabold\" align=\"center\">\n<td>BODY SYSTEM<\/td>\n<td>HEATSTROKE EFFECTS<\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td><span class=\"font_purple\">Central Nervous<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td>\n<ul>\n<li><span class=\"arial\">Susceptibility to cytotoxicity is increased, resulting in injury and death of neurons.<\/span><\/li>\n<li><span class=\"arial\">Cerebral edema, hemorrhage, and necrosis can occur.<sup>3<\/sup><\/span><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr bgcolor=\"#9ce8d6\">\n<td><span class=\"font_purple\">Coagulation<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td>\n<ul>\n<li><span class=\"arial\">Endothelial damage\u2014incited by direct cytotoxicity\u2014releases thromboplastin and factor XII, activating the coagulation cascade.<sup>3<\/sup><\/span><\/li>\n<li><span class=\"arial\">Disseminated intravascular coagulation may then occur (<strong>Figures 1 through 3<\/strong>).<\/span><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td><span class=\"font_purple\">Cardiovascular<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td>\n<ul>\n<li class=\"arial\">Initially, cardiac output, peripheral vasodilation, and central vasoconstriction are increased.<\/li>\n<li class=\"arial\">When these compensatory measures fail, venous blood pools, and central vasodilation leads to decreased circulating blood volume, hypotension, and shock.<sup>1<\/sup><\/li>\n<li class=\"arial\">Blood is unable to adequately circulate, resulting in electrolyte derangements, acidosis, and production of microthrombi.<\/li>\n<li class=\"arial\">Ventricular arrhythmias may occur due to ischemia of myocardium and exacerbate perfusion abnormalities.<sup>4<\/sup><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr bgcolor=\"#9ce8d6\">\n<td><span class=\"font_purple\">Pulmonary<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td>\n<ul>\n<li class=\"arial\">Direct injury to the pulmonary vascular endothelial cells can lead to pulmonary edema, increased pulmonary vascular resistance, and acute respiratory distress syndrome.<sup>4<\/sup><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr bgcolor=\"#bcefcf\">\n<td><span class=\"font_purple\">Gastrointestinal<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td>\n<ul>\n<li class=\"arial\">Direct cytotoxicity, prolonged hypotension, hypovolemia, and production of microthrombi cause decreased perfusion and ischemia, compromising the integrity of the GI tract.<sup>3<\/sup><\/li>\n<li class=\"arial\">Cellular hypoxia produces reactive oxygen and nitrogen species and stimulates inflammatory cells that further damage GI mucosa.<sup>9<\/sup><\/li>\n<li class=\"arial\">Increased permeability of GI mucosa can potentially result in translocation of bacteria and bacterial products, such as endotoxin.<\/li>\n<li class=\"arial\">Bacteremia, endotoxemia, and sepsis can cause further ischemia, cardiac dysfunction, shock, and eventually death.<sup>4<\/sup><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<tr bgcolor=\"#9ce8d6\">\n<td><span class=\"font_purple\">Renal<\/span><\/td>\n<td>\n<ul>\n<li class=\"arial\">Direct thermal injury and protein denaturation lead to tubular necrosis.<br \/>\nIndirect injury is secondary to vasoconstriction, dehydration, and myoglobinuria secondary to rhabdomyolysis.<sup>3,4<\/sup><\/li>\n<\/ul>\n<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<div id=\"attachment_1721\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke.jpg\"><img fetchpriority=\"high\" decoding=\"async\" aria-describedby=\"caption-attachment-1721\" class=\"wp-image-1721 size-medium\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke-300x223.jpg\" alt=\"figure 1A heatstroke\" width=\"300\" height=\"223\" srcset=\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke-300x223.jpg 300w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke-1024x761.jpg 1024w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke-768x570.jpg 768w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke-1536x1141.jpg 1536w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/figure-1A-heatstroke.jpg 2021w\" sizes=\"(max-width: 300px) 100vw, 300px\" \/><\/a><p id=\"caption-attachment-1721\" class=\"wp-caption-text\">Figure 1A. Petechial hemorrhage on (A) the abdominal wall, and (B) the ear pinna of a young pug with disseminated intravascular coagulation caused by heatstroke. Brachycephalic breeds are particularly at risk for heatstroke because of limited ability to thermoregulate as a result of partial upper airway obstruction.<\/p><\/div>\n<div id=\"attachment_1722\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke.jpg\"><img decoding=\"async\" aria-describedby=\"caption-attachment-1722\" class=\"wp-image-1722 size-medium\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke-300x225.jpg\" alt=\"Figure 1B heatstroke\" width=\"300\" height=\"225\" srcset=\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke-300x225.jpg 300w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke-1024x768.jpg 1024w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke-768x576.jpg 768w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke-1536x1152.jpg 1536w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-1B-heatstroke-2048x1536.jpg 2048w\" sizes=\"(max-width: 300px) 100vw, 300px\" \/><\/a><p id=\"caption-attachment-1722\" class=\"wp-caption-text\">Figure 1B. Petechial hemorrhage on (A) the abdominal wall, and (B) the ear pinna of a young pug with disseminated intravascular coagulation caused by heatstroke. Brachycephalic breeds are particularly at risk for heatstroke because of limited ability to thermoregulate as a result of partial upper airway obstruction.<\/p><\/div>\n<div id=\"attachment_1723\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke.jpg\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1723\" class=\"wp-image-1723 size-medium\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke-300x293.jpg\" alt=\"Figure 2 heatstroke\" width=\"300\" height=\"293\" srcset=\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke-300x293.jpg 300w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke-1024x1001.jpg 1024w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke-768x751.jpg 768w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke-1536x1501.jpg 1536w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-2-heatstroke.jpg 1777w\" sizes=\"(max-width: 300px) 100vw, 300px\" \/><\/a><p id=\"caption-attachment-1723\" class=\"wp-caption-text\">Figure 2. Bloody urine in a pug with heatstroke may reflect intravascular hemolysis or hemorrhage into the urinary tract due to coagulopathy<\/p><\/div>\n<div id=\"attachment_1724\" style=\"width: 310px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" aria-describedby=\"caption-attachment-1724\" class=\"wp-image-1724 size-medium\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-3-heatstroke1-300x175.jpg\" alt=\"Figure 3 heatstroke\" width=\"300\" height=\"175\" srcset=\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-3-heatstroke1-300x175.jpg 300w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-3-heatstroke1-1024x597.jpg 1024w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-3-heatstroke1-768x448.jpg 768w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-3-heatstroke1-1536x896.jpg 1536w, https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/Figure-3-heatstroke1-2048x1194.jpg 2048w\" sizes=\"(max-width: 300px) 100vw, 300px\" \/><p id=\"caption-attachment-1724\" class=\"wp-caption-text\">Figure 3. Emergency resuscitation of this comatose pug with disseminated intravascular coagulation due to severe heatstroke included administration of a blood transfusion.<\/p><\/div>\n<p><em><span class=\"references\">Figures 1-3 courtesy of Dr. Lesley G. King<\/span><\/em><\/p>\n<h3><strong><span class=\"aquabold\">Pathology<\/span><\/strong><\/h3>\n<p>Pathologic findings in dogs with heatstroke are extensive and severe. Necropsy of 11 dogs with fatal heatstroke revealed severe pulmonary edema, splenomegaly, and hepatomegaly. Hemorrhage was observed within the myocardium, peritoneum, mesentery, and throughout the GI tract. The brains of 9 dogs had edema and necrosis. The kidneys in all 11 dogs revealed lesions, glomerular congestion, and tubular degeneration and necrosis. The small intestine of 2 dogs, large intestine of another, and liver of a third could not be examined due to autolysis.<sup>9<\/sup><\/p>\n<h2><strong><span class=\"font_purple\"> DIAGNOSIS<br \/>\n<\/span><\/strong><\/h2>\n<h3><strong><span class=\"aquabold\">History &amp; Clinical Signs<\/span><\/strong><\/h3>\n<p>History often includes recent exercise or confinement in an area without access to water or shade.<\/p>\n<p>The most common clinical signs in one study were collapse, tachypnea, shock, inappropriate mentation, and signs of coagulopathy,<sup>10<\/sup>\u00a0but may also include tachycardia, hyperemia, and hyperdynamic to nonexistent pulses. Concurrent central nervous system (CNS) signs can range from slight ataxia to seizures or coma.<\/p>\n<p>Damage to the GI tract quickly leads to severe diarrhea. The diarrhea is often bloody (hematochezia) when it comes from the lower GI tract, or it may be black (melena) if originating from the upper GI tract.<\/p>\n<p>Although hyperthermia is usually present, a patient with heatstroke may present normothermic or hypothermic due to cooling efforts prior to arrival at the hospital, a prolonged travel time to the hospital, or secondary to shock.<\/p>\n<h3><strong><span class=\"font_purple\">Common Diagnostic Findings<\/span><\/strong><\/h3>\n<p>Upon presentation, perform a urinalysis and blood analysis, including:<\/p>\n<ul>\n<li>Serum biochemical profile, including electrolytes, blood glucose, and lactate<\/li>\n<li>Complete blood count and differential (manual)<\/li>\n<li>Coagulation panel, including prothrombin time (PT) and activated partial thromboplastin time (aPTT).<\/li>\n<\/ul>\n<p>Common findings in patients with heatstroke are listed in\u00a0<strong><span class=\"bold\">Table 4<\/span><\/strong>.<\/p>\n<table border=\"1\" width=\"580\" cellspacing=\"0\" cellpadding=\"1\">\n<tbody>\n<tr>\n<td colspan=\"3\"><strong><span class=\"GreenAqua\">Table 4. Clinicopathologic Findings: Heatstroke Patients<\/span><\/strong><\/td>\n<\/tr>\n<tr class=\"aquabold\">\n<td align=\"center\"><span class=\"aquabold\">COMPONENT<\/span><\/td>\n<td align=\"center\"><span class=\"aquabold\">RESULT<\/span><\/td>\n<td align=\"center\"><span class=\"aquabold\">CAUSE<\/span><\/td>\n<\/tr>\n<tr>\n<td colspan=\"3\"><span class=\"font_purple\">Serum Biochemical Profile<sup>10<\/sup><\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Alanine aminotransferase<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Hepatic injury<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Alkaline phosphatase<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Hepatic injury<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Aspartate aminotransferase<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Hepatic injury, rhabdomyolysis (due to direct thermal damage to muscle or increased muscular activity)<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Creatinine<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Renal (direct thermal damage, myoglobinuria due to rhabdomyolysis) and prerenal azotemia (dehydration, vasoconstriction)<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Creatinine kinase<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Rhabdomyolysis (due to direct thermal damage to muscle or increased muscular activity)<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Hypoglycemia<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be observed<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Increased use (due to increased ATP demand) or decreased production (due to hepatic damage) of blood glucose<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Lactate<\/strong><\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be increased<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Hypovolemia and decreased perfusion leading to tissue hypoxia<sup>10<\/sup><\/span><\/td>\n<\/tr>\n<tr>\n<td colspan=\"3\"><span class=\"font_purple\">Complete Blood Cell Count &amp; Differential<sup>10<\/sup><\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Thrombocytopenia<\/strong><br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Commonly observed<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Secondary to platelet consumption (caused by GI hemorrhage) and platelet aggregation (due to disseminated intravascular coagulation).<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Packed cell volume<\/strong><br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Commonly increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Dehydration<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Hemoglobin concentration<\/strong><br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Commonly increased<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Dehydration<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Nucleated red blood cells<\/strong><\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be observed<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Secondary to direct thermal damage to bone marrow causing premature release of cells<sup>10<\/sup><\/span><\/td>\n<\/tr>\n<tr>\n<td colspan=\"3\"><span class=\"font_purple\">Coagulation Panel<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Activated partial thromboplastin time<\/strong><br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be prolonged<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Direct thermal injury to endothelium and consumption of coagulation factors<sup>10<\/sup><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Prothrombin time<\/strong><\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">May be prolonged<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Direct thermal injury to endothelium and consumption of coagulation factors<\/span><\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<hr \/>\n<div class=\"orange-box\">\n<h2><strong><span class=\"font_purple\">What to AVOID During Treatment<\/span><\/strong><\/h2>\n<p><strong><span class=\"aquabold\">Avoid use of ice<\/span><\/strong>\u00a0as it causes peripheral vasoconstriction, preventing cooling of blood via shunting to the periphery.<sup>14<\/sup>\u00a0Ice may also damage the skin and make treatment uncomfortable for the patient.<\/p>\n<p><strong><span class=\"aquabold\">Avoid gastric lavage or cold water enemas<\/span><\/strong>, if possible. The risk of aspiration may outweigh the benefits of gastric lavage, and cold water enemas may further damage the already compromised GI tract.<sup>15<\/sup><\/p>\n<p><strong><span class=\"aquabold\">Avoid shivering in the patient<\/span><\/strong>; however, one human study states that shivering does not contribute to hyperthermia because the heat produced is minor relative to the amount of cooling achieved during emergency treatment for heatstroke.<sup>15<\/sup><\/p>\n<\/div>\n<p>The goal of active cooling is to return the dog to a normal body temperature, while avoiding further organ damage.<sup>12<\/sup>\u00a0An effective cooling method that combines evaporative and convective cooling is directing a fan toward the dog and applying cool or tepid water to the skin. Monitor the temperature every 5 minutes and, once body temperature reaches 103.5\u00b0F to 104\u00b0F (39.7\u00b0C\u201440\u00b0C), discontinue active cooling in order to avoid rebound hypothermia.<sup>1<\/sup><\/p>\n<hr \/>\n<h2><strong><span class=\"font_purple\">TREATMENT<br \/>\n<\/span><\/strong><\/h2>\n<p>Implementing treatment as soon as possible\u2014even before the patient reaches the hospital\u2014significantly improves the patient&#8217;s prognosis.<\/p>\n<h3><strong><span class=\"aquabold\">Cooling<\/span><\/strong><\/h3>\n<p>Active cooling is the most important aspect of treatment, although it may not prevent deleterious effects of heatstroke. If possible, instruct the owner to begin cooling his or her dog during travel to the hospital. One study revealed dogs actively cooled before arriving at the hospital had a lower mortality rate (19%) than dogs not cooled prior to arrival (49%).<sup>11<\/sup><\/p>\n<div class=\"orange-box\"><\/div>\n<h3><strong><span class=\"aquabold\">Respiration<\/span><\/strong><\/h3>\n<p>In addition to active cooling, evaluate the airway for patency and, if necessary, intubate the patient or perform an emergency tracheostomy. Provide supplemental oxygen via a mask or flow-by for dogs that are breathing unassisted. Note that older oxygen cages that do not have temperature and humidity controls may exacerbate hyperthermia.<sup>13<\/sup><\/p>\n<h3><strong><span class=\"aquabold\">Fluid Therapy<\/span><\/strong><\/h3>\n<p>Intravenous fluids are considered a cornerstone of heatstroke treatment.<\/p>\n<p>Upon arrival, establish IV access in the patient and administer room temperature crystalloids.<sup>1<\/sup>\u00a0A bolus of crystalloids is beneficial for hypovolemic and hemoconcentrated heatstroke patients. Crystalloids provide cardiovascular support by expanding intravascular volume, and increasing blood flow to the periphery, aiding with the cooling process. Once hospitalized, crystalloids should be continued to provide maintenance fluid therapy as well as replace continuous losses (seen with continued vomiting and diarrhea).<\/p>\n<p>If crystalloids do not adequately maintain intravascular volume, consider administering colloids.<sup>1<\/sup>\u00a0Colloids may also be considered if the patient is hypoalbuminemic.<sup>1,13,14<\/sup>\u00a0Fresh frozen plasma is recommended if the patient has prolonged PT and\/or aPTT.<\/p>\n<h3><strong><span class=\"aquabold\">Medical Therapy<\/span><\/strong><\/h3>\n<p><strong><span class=\"bold\">Antibiotics<\/span>.<\/strong> Due to the high risk of bacterial translocation secondary to GI damage, consider broad-spectrum antibiotics (<strong><span class=\"bold\">Table 5<\/span><\/strong>), while keeping the possibility of antibiotic resistance in mind.<sup>13<\/sup>\u00a0Once antibiotic therapy is initiated, continue until GI signs, such as hematochezia, melena, or hematemesis, resolve and the patient is eating.<sup>14<\/sup><\/p>\n<p><strong><em><span class=\"bold\">GI tract support<\/span>.<\/em><\/strong> Antiemetics (metoclopramide, dolasetron, maropitant) are beneficial when GI tract damage or CNS abnormalities cause nausea. Administer GI protectants because GI ulceration is likely to occur. Proton pump inhibitors (omeprazole, pantoprazole) are beneficial to prevent or treat gastric ulceration, while famotidine acts as an H2 receptor antagonist and also decreases the production of acid. Sucralfate is given orally and acts as a local protectant that binds to ulcers preventing further damage from acid, pepsin, or bile (<strong><span class=\"bold\">Table 5<\/span><\/strong>).<\/p>\n<p><strong><em><span class=\"bold\">CNS support<\/span>.<\/em><\/strong> CNS abnormalities are common in heatstroke patients. In some cases, these abnormalities may result from increased intracranial pressure.<\/p>\n<p>Mannitol<em>\u2014<\/em>an osmotic diuretic that expands intravascular volume, decreases blood viscosity and intracranial pressure, and improves cerebral microcirculation\u2014can be administered if the patient has neurologic signs (<strong><span class=\"bold\">Table 5<\/span><\/strong>).<sup>1<\/sup>\u00a0If mannitol is contraindicated (such as with dehydration, intracranial hemorrhage, pulmonary edema, or anuria secondary to renal disease) hypertonic saline (7.2%\u20147.5%) can be used instead. Hypertonic saline will increase cerebral, coronary, and microvascular blood flow as well as decrease intracranial pressure. As with mannitol, hypertonic saline is contraindicated with dehydration.<sup>1<\/sup><\/p>\n<p>Additional nursing management of patients with suspected cerebral edema may include elevation of the head and avoidance of compression of the jugular veins.<\/p>\n<p><strong><span class=\"bold\">Cardiac support<\/span>. <\/strong>Ventricular arrhythmias are common in patients presenting with heatstroke because cardiac cells are susceptible to thermal injury and ischemia. Damage to the myocardium causes defects in conduction leading to ventricular arrhythmias, which can be treated with lidocaine.<sup>4<\/sup><\/p>\n<table border=\"1\" width=\"580\" cellspacing=\"0\" cellpadding=\"1\">\n<tbody>\n<tr>\n<td colspan=\"4\"><strong><span class=\"GreenAqua\">Table 5. Medical Therapy for Canine Heatstroke Patients<\/span><\/strong><\/td>\n<\/tr>\n<tr>\n<td><span class=\"aquabold\">INDICATION<\/span><\/td>\n<td><span class=\"aquabold\">DRUG NAME<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td><span class=\"aquabold\">DRUG CLASS<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<td><span class=\"aquabold\">DOSAGE<\/span><span class=\"arial\"><br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td rowspan=\"4\" bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Bacterial Translocation<\/strong><\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Ampicillin<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Bactericidal aminopenicillin<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>20\u201340 mg\/kg<\/strong>\u00a0IV Q 8 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Cefazolin<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">First generation cephalosporin<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>22 mg\/kg<\/strong>\u00a0IV Q 8 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Enrofloxacin<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Bactericidal fluoroquinolone<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>5\u201320 mg\/kg<\/strong>\u00a0IV, IM, PO (once discharged) Q 24 H or divided Q 12 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Metronidazole<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Antibacterial and antiprotozoal<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>10\u201315 mg\/kg<\/strong>\u00a0IV, PO (once discharged) Q 12 H<\/span><\/td>\n<\/tr>\n<tr>\n<td rowspan=\"8\" bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Gastrointestinal Damage<\/strong><\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Dolasetron<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Antiemetic (5-HT3 antagonist)<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>1 mg\/kg<\/strong>\u00a0IV Q 24 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Famotidine<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">H2 antagonist<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>0.5 mg\/kg<\/strong> IV, IM, PO (once discharged) Q 12\u201324 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Maropitant<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Antiemetic (NK1 receptor agonist)<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>1 mg\/kg\/day<\/strong>\u00a0SC or IV,\u00a0<strong>2 mg\/kg\/day<\/strong>\u00a0PO (once discharged)<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Metoclopramide<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Antiemetic prokinetic<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>1\u20132 mg\/kg\/day<\/strong>\u00a0IV as a CRI<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Omeprazole<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Proton pump inhibitor<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>1 mg\/kg<\/strong>\u00a0PO (once discharged) Q 24 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Pantoprazole<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Proton pump inhibitor<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>1 mg\/kg<\/strong>\u00a0IV Q 24 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Ranitidine<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">H2 antagonist<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>0.5\u20132 mg\/kg<\/strong>\u00a0IV, IM, PO (once discharged) Q 8\u201412 H<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Sucralfate<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Gastric protectant<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Small dog:\u00a0<strong>0.25 g<\/strong>\u00a0PO Q 8 H<br \/>\nMedium dog:\u00a0<strong>0.5 g<\/strong>\u00a0PO Q 8 H<br \/>\nLarge dog:\u00a0<strong>1 g<\/strong>\u00a0PO Q 8 H<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Increased Intracranial Pressure<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Mannitol<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Osmotic diuretic<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>0.25\u20130.5 g\/kg<\/strong>\u00a0IV slowly over 20 minutes<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Ventricular Arrhythmias<\/strong><\/span><strong><span class=\"arial\"><br \/>\n<\/span><\/strong><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Lidocaine<br \/>\n<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Class 1B antiarrhythmic<br \/>\n<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>2 mg\/kg<\/strong>\u00a0bolus IV, then\u00a0<strong>40\u201380 mcg\/kg\/min<\/strong>\u00a0CRI<br \/>\n<\/span><\/td>\n<\/tr>\n<tr>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\"><strong>Cardiovascular Support<\/strong><\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\">Dopamine<\/span><\/td>\n<td bgcolor=\"#9ce8d6\"><span class=\"arial\">Catecholamine<\/span><\/td>\n<td bgcolor=\"#bcefcf\"><span class=\"arial\"><strong>3\u201315 mcg\/kg\/min<\/strong>\u00a0CRI\u00a0<\/span><\/td>\n<\/tr>\n<tr>\n<td class=\"references\" colspan=\"4\">Adapted from Plumb DC. Veterinary Drug Handbook, 4th ed. White Bear Lake, MN: PharmVet Publishing, 2002.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<h2><strong><span class=\"font_purple\">MONITORING<br \/>\n<\/span><\/strong><\/h2>\n<p>Initiate patient monitoring upon arrival, including:<\/p>\n<ul>\n<li>Baseline vital signs (heart rate, respiratory rate and effort, temperature, mucous membrane color, and capillary refill time)<\/li>\n<li>Blood pressure<\/li>\n<li>Electrocardiography (ECG)<\/li>\n<li>Pulse oximetry.<\/li>\n<\/ul>\n<p>Although unlikely to be seen on presentation, multiple organ dysfunction syndrome (MODS) may develop during hospitalization. MODS occurs when 2 or more systems are affected and begin to fail. Because heatstroke affects multiple organ systems, the risk for developing MODS is high, and the patient should be monitored closely during hospitalization.<\/p>\n<p>Placement of a urinary catheter and monitoring of urine production is beneficial in patients with renal insufficiency or failure.<sup>14<\/sup>\u00a0Normal urine output in a dog on IV fluids is at least 1 to 2 mL\/kg\/hour. A decrease in urine output may be due to renal failure, hypovolemia, or hypotension. If unable to place a urinary catheter, the patient&#8217;s urination should be monitored closely.<\/p>\n<p>Nutritional support is beneficial for the GI system. It improves the GI tract&#8217;s integrity and allows the patient to replace important proteins, electrolytes, and other nutrients. If the patient is not willing to eat, a nasoesophageal feeding tube can be placed to allow for trickle feeding.<sup>14<\/sup><\/p>\n<p>Serial monitoring during hospitalization should include:<\/p>\n<ul>\n<li>Neurologic status assessment<\/li>\n<li>Heart rate, pulse quality, respiratory rate and effort, blood pressure, and ECG<\/li>\n<li>PT and aPTT<\/li>\n<li>Packed cell volume and total protein<\/li>\n<li>Blood glucose and electrolytes<\/li>\n<li>Lactate and acid\u2014base balance<\/li>\n<li>Urine output.<\/li>\n<\/ul>\n<p>Response to therapy can be monitored, in part, with serial lactate tests because lactate clearance is associated with resolution of tissue hypoxia.<sup>1<\/sup><\/p>\n<h2><strong><span class=\"font_purple\">PROGNOSIS<\/span><\/strong><\/h2>\n<p>Prognosis is most dependent on length of time the patient was hyperthermic and highest body temperature experienced. When the body temperature reaches 109.4\u00b0F (43\u00b0C), marked organ damage and high mortality are seen. Cellular necrosis and destruction of all cellular structures occurs once body temperature has been maintained between 120.2\u00b0F to 122\u00b0F (49\u00b0C\u201450\u00b0C) for only 5 minutes.<sup>1<\/sup><\/p>\n<p>Probability of survival increases with decreased time period of hyperthermia; however, it is important to monitor the patient for MODS and coagulopathies.<sup>12<\/sup>\u00a0Negative indicators of prognosis associated with higher mortality include:<\/p>\n<ul>\n<li>Development of ventricular arrhythmias<sup>1<\/sup><\/li>\n<li>Severe coagulopathies<sup>10<\/sup><\/li>\n<li>Abnormal neurologic signs that do not resolve once body temperature normalizes.<\/li>\n<\/ul>\n<p>In humans, 20% of heatstroke victims suffer unresolved brain damage and CNS abnormalities, which have been linked to high mortality rates.<sup>12<\/sup>\u00a0Therefore, return of normal CNS function is considered a positive prognostic indicator for dogs that have suffered heatstroke.<\/p>\n<h2><strong><span class=\"font_purple\">PREVENTION<br \/>\n<\/span><\/strong><\/h2>\n<p>Prevention of heatstroke relies heavily on owner education. Owners can prevent heatstroke several ways:<\/p>\n<ul>\n<li>Ensure availability of adequate shade and drinking water outdoors<\/li>\n<li>Exercise dogs only during cooler periods of the day<\/li>\n<li>Never leave dogs alone in closed vehicles<\/li>\n<li>Acclimate dogs to warm temperatures for up to 2 months<\/li>\n<li>Surgically address upper airway obstructions, such as brachycephalic airway disease or laryngeal paralysis, to decrease risk in individual susceptible patients.<\/li>\n<\/ul>\n<p class=\"arial\">aPTT = activated partial thromboplastin time; CNS = central nervous system; ECG = electrocardiography; GI = gastrointestinal; HSP = heat shock protein; MODS = multiple organ dysfunction syndrome; PT = prothrombin time<\/p>\n<hr \/>\n<p><span class=\"author-bio\"><strong><a href=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/C05_b.jpg\"><img loading=\"lazy\" decoding=\"async\" class=\"alignleft size-full wp-image-6468\" src=\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2014\/09\/C05_b.jpg\" alt=\"C05_b\" width=\"100\" height=\"106\" \/><\/a>Brandy Tabor<\/strong>, CVT, VTS (ECC), is an emergency and critical care technician at Animal Emergency &amp; Specialty Center in Parker, Colorado. She is a board moderator for the Veterinary Support Personnel Network (VSPN). She has written over 25 book reviews and teaches continuing education courses for VetMedTeam. Ms. Tabor received her BS in equine science from Colorado State University.<\/span><\/p>\n","protected":false},"excerpt":{"rendered":"<p>This life-threatening condition can affect dogs of any age, breed, or gender.<\/p>\n","protected":false},"author":187,"featured_media":13414,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_acf_changed":false,"iawp_total_views":10950,"footnotes":""},"categories":[368],"tags":[13],"class_list":["post-596","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-september-october-2014","tag-peer-reviewed","clinical_topics-emergency-medicine-critical-care"],"acf":{"hide_sidebar":false,"hide_sidebar_ad":false,"hide_all_ads":false},"yoast_head":"<!-- This site is optimized with the Yoast SEO Premium plugin v24.7 (Yoast SEO v27.3) - https:\/\/yoast.com\/product\/yoast-seo-premium-wordpress\/ -->\n<title>Heatstroke in Dogs | Today&#039;s Veterinary 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