Article

Heatstroke in dogs: Clinical signs, treatment, prognosis, and prevention

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  • Department of Defense
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Abstract

Heatstroke is an acute, life-threatening emergency with a complex pathophysiology - the key clinical features of which Include metabolic acidosis, oliguric renal failure, coagulation abnormalities, and neurologic disturbances. Physical examination is marked by excessive panting, hyperemia, hypersalivation, tachycardia, and various neurologic signs. Common laboratory changes associated with heatstroke are hemoconcentration, elevated liver enzymes, electrolyte changes, prolonged clotting times, azotemia, and hypoglycemia. Rapid cooling of the core body and support of vital organs are essential factors in the management of heatstroke and prevention of further secondary sequelae. Prognosis worsens if severe neurologic signs develop and persist throughout the course of treatment. Owners of heatstroke animals can decrease mortality if the animal is cooled before being transported to the veterinarian. Prevention of heatstroke is achieved primarily by educating owners about proper acclimatization times, exercising during cooler periods of the day, and providing adequate shade and cool water for dogs confined outdoors.

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... This complex form of hyperthermia is characterized by body temperatures above 41°C and dysfunction of the central nervous system (Bruchim et al., 2009;Hemmelgarn and Gannon, 2013a). Typical for this condition is the direct lethal damage to organ systems as a result of a non-pyrogenic increase in body temperature (Flournoy et al., 2003). Heat stroke is associated with a systemic in-flammatory response, leading to progressive multiple organ failure and possibly resulting in death (Bruchim et al., 2009;Hemmelgarn and Gannon, 2013b). ...
... This condition has high mortality rates of 50% to 56%. To achieve an increased chance of survival, early detec-tion, elimination of the cause, aggressive therapy and critical monitoring are necessary (Flournoy et al., 2003;Hemmelgarn and Gannon, 2013a). ...
... Tachypnea, dyspnea, an abundant haircoat, body weight (84.5 kg) and BCS (6/9) are additional endogenous predisposing factors affecting heat dissipation (Johnson et al., 2006;Hemmelgarn and Gannon, 2013b). Predisposing factors should be eliminated to prevent subsequent episodes of heat stroke (Flournoy et al., 2003;Mazzaferro, 2009). ...
Article
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In this case report, a seven-year-old, male, castrated Landseer presented with chronic respiratory distress, occasional coughing, dysphonia and exercise intolerance is described. The stress caused by transportation and the physical examination rendered the dog severely dyspneic and cyanotic. At that moment, the core body temperature was increased up to 42.5 °C. Based on the clinical signs, laryngeal paralysis causing heat stroke was the most likely diagnosis. The dog was anesthetized and intensive temperature control methods, like active cooling and fluid therapy, were applied. As soon as the dog was cardiovascularly stable, emergency treatment for laryngeal paralysis was performed. As a result of timely intervention, the dog recovered completely without any persisting complications.
... However, dogs with moderate to severe heat injury usually have sustained rectal temperatures of 107°F or higher. [31][32][33] Most dogs develop heat injury due to heavy exertion in hot, humid environments, especially if inadequately acclimated. Rarely, dogs are treated for heat injury secondary to partial airway obstruction or inadvertent enclosure in vehicles. ...
... Heat injury in dogs is described as mild ("heat stress"), moderate ("heat exhaustion"), and severe ("heat stroke"). 31,32,34,35 MWD handlers are trained to recognize and treat heat injury in the field; thus, dogs may be hypothermic on arrival if treated before presentation. Dogs with moderate to severe heat injury frequently develop multi-organ complications and have a high case fatality rate. ...
... Dogs with moderate to severe heat injury frequently develop multi-organ complications and have a high case fatality rate. 32,34,35 Poorly managed or untreated, heat injury is a progressive process. This progression is well described. ...
Article
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There are about 2,500 war and military service dogs in service, with about 700 serving at any given time overseas. Military Working Dogs (MWDs) are critical assets for military police, special operations units, and others operating in today’s combat environment. The expectation, given the significant combat multiplier impact of these dogs and the intense bond between the handler and dog, is that injured working dogs will receive the same level of care as any injured U.S. military personnel. Veterinary care is available at multiple locations throughout theater, and the veterinary healthcare team is the MWD’s primary provider. Yet, human healthcare providers (HCPs) may be the only medical personnel available to MWDs that are gravely ill or injured. As most HCPs are unfamiliar with medical care of dogs, the Joint Trauma System published a Clinical Practice Guideline (CPG), a set of detailed clinical guidelines for managing life-threatening problems of MWDs encountered in combat operations. The CPG is available at the JTS website. This article is covers the most common urgent MWD care challenges HCPs may face.
... Da bei einem Großteil der Patienten ein hypovolämischer bzw. distributiver Schock vorliegt, sollte aufgrund der verminderten zellulären Sauerstoffversorgung unmittelbar Sauerstoff verabreicht werden (8,9). Dies kann durch "Flow by", über eine Sauerstoffmaske, Aufsetzen eines "Sauerstoffkragens" oder Legen einer Sauerstoffsonde geschehen. ...
... Dies kann durch "Flow by", über eine Sauerstoffmaske, Aufsetzen eines "Sauerstoffkragens" oder Legen einer Sauerstoffsonde geschehen. Sauerstoffboxen erweisen sich je nach Bauweise als ungeeignet, da eine adäquate Kühlung nicht möglich ist und sich Tiere teilweise noch weiter aufheizen (8). Bei Hyperventilation sollte das Tier, wenn nötig, sediert, intubiert und mechanisch beatmet werden (8,9). ...
... Sauerstoffboxen erweisen sich je nach Bauweise als ungeeignet, da eine adäquate Kühlung nicht möglich ist und sich Tiere teilweise noch weiter aufheizen (8). Bei Hyperventilation sollte das Tier, wenn nötig, sediert, intubiert und mechanisch beatmet werden (8,9). Ferner sollten diesen Schockpatienten Kristalloide (bis zu 90 ml/kg/h in den ersten 1-2 Stunden) (10) und wenn nötig auch kolloidale Lösungen intravenös infundiert werden. ...
Article
Objective: Heatstroke is a life-threating emergency in dogs. The aim of this retrospective study was to analyse the sources of heat stroke in dogs, predisposing and prognostic factors, results of physical examination and clinical pathology as well as the course of this condition and appropriate treatment. Material and methods: Patient histories of 12 dogs diagnosed with heat stroke over a 5.5-year period were analysed retrospectively. Normality was tested using the Kolmogrow-Smirnow Test and analysed using T-tests, the Chi-square test and the Mann-Whitney U-test. P-values < 0.05 were considered significant. Results: Heat stroke occurred most frequently during summer, particularly in the afternoon. The most common cause of heat stroke was heat exposition in a car. Brachycephalic breeds were overrepresented. The most common clinical signs were polypnoea, tachycardia, hyperthermia and depression to prostration as well as gastrointestinal and neurological symptoms. Clinical pathology results included haemoconcentration, thrombocytopenia, hyperkalemia, prolonged activated partial thromboplastin time and azotemia. Therapies employed included oxygen application, cooling, fluid therapy and administration of gastrointestinal protectants, antiemetics and antibiotics. Duration of hospitalization was 1-6 days. The overall mortality rate was 50%. Most of the non-survivors died or were euthanized within 24-48 hours after presentation. All animals remaining alive after 3 days survived and could be discharged from hospital. Clinical relevance: Heat stroke is a life-threating condition, which can lead to shock, sepsis, coagulation disorders and multiorgan failure. Early recognition and appropriate treatment are important factors for a positive outcome. Furthermore, intensive monitoring and rapid therapy adaption as required are pivotal.
... Heatstroke is an acute, rapidly progressive life-threatening condition, commonly recognized in dogs and characterized by a nonpyrogenic rise in core body temperature above 41°C (105.8°F) that causes direct hyperthermal injury to tissues, especially central nervous system, possibly leading to multiple organ dysfunction. 1 It results from an imbalance between heat-generating and heat-dissipating mechanisms, and requires prompt, aggressive therapeutic intervention and continuous critical-care monitoring to avoid serious secondary complications and death. [2][3][4] Heatstroke is the most severe form of heat-induced illness, which is classified on the basis of the type and severity of clinical signs in humans. [5][6][7] The least severe is heat cramps, characterized by extreme dehydration, muscle cramps, and sodium chloride depletion, but it is rarely recognized in veterinary patients. ...
... although it is important to underline that patients can also be normo-or even hypothermic on presentation, particularly if cooling measures are initiated by the owners or if they are in an advanced stage of shock. [1][2][3]5 Heatstroke can be classified as either classic (nonexertional) or exertional. Classic heatstroke results from the exposure to high environmental temperatures, typically occurring in summer, and is seen in dogs that are confined in an overheated enclosure (eg, an unventilated automobile) or chained outdoors and deprived of water and shade. ...
... Dovepress Dovepress suggested to play a major role in heatstroke-induced neurological dysfunctions. [1][2][3]5,10 In particular, hypoglycemia can be a consequence of increased utilization or decreased production of glucose as a result of a generalized increased demand for ATP due to the elevated body temperature, hepatic failure, or sepsis that can develop because of intestinal mucosal damage and reduced host defenses. 3,5 Other recorded complications of canine heatstroke include acute respiratory distress syndrome due to thermal and biochemical injury to pulmonary endothelium causing non-cardiogenic pulmonary edema, as well as pneumonia and pancreatitis. ...
Article
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Canine heatstroke is a life-threatening condition resulting from an imbalance between heat dissipation and production, and characterized by a nonpyrogenic elevation in core body temperature above 41°C (105.8°F). Several exogenous and endogenous factors may predispose dogs to the development of heatstroke; on the other hand, adaptive mechanisms also exists which allow organisms to combat the deleterious effects of heat stress, which are represented by the cellular heat-shock response and heat acclimatization. The pathophysiology and consequences of heatstroke share many similarities to those observable in sepsis and are related to the interaction between the direct cytotoxicity of heat, the acute physiological alterations associated with hyperthermia, such as increased metabolic demand, hypoxia, and circulatory failure, and the inflammatory and coagulation responses of the host to the widespread endothelial and tissue injuries, which may culminate in disseminated intravascular coagulation, systemic inflammatory response syndrome, and multiple organ dysfunction.
... Heat stroke is a medical emergency requiring rapid diagnosis and treatment. This potentially life-threatening condition occurs mostly when environmental temperatures are high and is characterized by hyperthermia, tachypnea, tachycardia and changes in mental status following heat exposure (9,12,19,20). The various forms of heat related illness represent a spectrum from the mildest form of heat stress to heat exhaustion and finally to heat stroke. ...
... By definition, the body core temperature is not elevated, and the only negative effect is that one's performance may be very well below normal (26,48). The clinical signs observed in our patients were consistent with the symptoms of heat stroke as reported by various authors for other species (9,12,19,20,26). Yet, as to our knowledge, there are no studies on the effects of heat stroke on Saanen goat kids. ...
Article
Objective: Description of clinical, biochemical and haematological changes in Saanen goat kids post-exposure to a naturally occurring heatstroke. Material and methods:The experimental group consisted of goats of different age (1-4 months) and sex (8 males, 12 females) with an average weight of 7.2 ± 3.1 kg.Twenty clinically healthy, three to four months old, Saanen goat kids (sex-ratio 1:1) were used as a control. The average body weight in this group was 9.4 ± 2.6 kg. Case history, clinical signs, and results of haematology and blood biochemistry were documented in all goat kids Results: Most common findings were hyperthermia, ataxia, muscle tremor and depression. Increased serum urea, creatinine, potassium and plasma lactate concentrations as well as an increase in aspartate aminotransferase and lactate dehydrogenase activity were observed in goats post-exposure to heat stroke when compared to the control group.Two goat kids died despite supportive treatment Physical and biochemical blood parameters improved following treatment. Conclusion: This is the first study on heat stroke in Saanen goat kids. Heatstroke may be fatal in Saanen goat kids, despite appropriate treatment, and may lead to secondary complications. Plasma lactate concentration seems to be a reliable indicator for the prognosis of heat stroke in goat kids.
... Surface areas of the nasal turbinates and effective ventilation provide the mechanism to enable evaporative heat loss through panting, thus brachycephalic dogs have reduced heat dissipation mechanisms [15,18,50,64]. ...
... Older animals are more likely to have pre-existing conditions that limit effective heat dissipation such as heart disease, or respiratory diseases e.g., laryngeal paralysis [64]. ...
Article
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Heat-related illness will affect increasing numbers of dogs as global temperatures rise unless effective mitigation strategies are implemented. This study aimed to identify the key triggers of heat-related illness in dogs and investigate canine risk factors for the most common triggers in UK dogs. Using the VetCompassTM programme, de-identified electronic patient records of 905,543 dogs under primary veterinary care in 2016 were reviewed to identify 1259 heat-related illness events from 1222 dogs. Exertional heat-related illness was the predominant trigger (74.2% of events), followed by environmental (12.9%) and vehicular confinement (5.2%). Canine and human risk factors appear similar; young male dogs had greater odds of exertional heat-related illness, older dogs and dogs with respiratory compromise had the greatest odds of environmental heat-related illness. Brachycephalic dogs had greater odds of all three types of heat-related illness compared with mesocephalic dogs. The odds of death following vehicular heat-related illness (OR 1.47, p = 0.492) was similar to that of exertional heat-related illness. In the UK, exertional heat-related illness affects more dogs, and kills more dogs, than confinement in a hot vehicle. Campaigns to raise public awareness about heat-related illness in dogs need to highlight that dogs don’t die just in hot cars.
... Many authors consider a rectal temperature ≥41.5°C to be a critical level for initiation of heat illness in dogs (11,54,58,66,67). During the current study, 45 greyhounds recorded a postrace rectal temperature >41.5°C which if not reduced, would place them at risk of heat illness. ...
Article
Full-text available
Heat strain is a potential risk factor for racing greyhounds in hot climates. However, there have been limited studies into the incidence of heat strain (when excess heat causes physiological or pathological effects) in racing greyhounds. The aim of this study was to determine if heat strain occurs in racing greyhounds, and, if so, whether environmental factors (e.g. ambient temperature and relative humidity) or dog-related factors (e.g. sex, bodyweight, color) are associated with the risk of heat strain. A total of 229 greyhounds were included in over 46 race meetings and seven different race venues in South Australia, Australia. Rectal temperatures of dogs were measured pre- and post-race and urine samples collected for analysis of myoglobinuria. Ambient temperature at race times ranged between 11.0oC to 40.8oC and relative humidity ranged from 17% to 92%. There was a mean increase in greyhound rectal temperature of 2.1oC (range 1.1oC to 3.1oC). A small but significant association was present between ambient temperature and increase in rectal temperature (r2=0.033, P=0.007). The mean ambient temperature at race time, of dogs with post-race rectal temperature of or exceeding 41.5°C , was significantly greater than at race time of dogs with a post-race rectal temperature ≤41.5oC (31.2oC vs 27.3oC, respectively, P=0.004). When the ambient temperature reached 38oC, over one third (39%) of dogs had a rectal temperature >41.5oC. Over half of post-race urine samples were positive by Dipstick reading for haemoglobin/myoglobin, and of 77 urine samples positive for Dipstick readings, 95% were positive for myoglobin. However, urinary myoglobin levels were not associated with ambient temperature or post-race rectal temperatures. The mean increase in rectal temperature was greater in dark (black, blue, brindle) than light (fawn and white) coloured greyhounds. The results suggest heat strain occurs in racing greyhounds, evidenced by post-race rectal temperatures over 41.5oC and post-race myoglobinuria. Risk of heat strain may be increased in higher ambient temperatures and in darker coloured greyhounds. Further research into the incidence of heat strain in racing greyhounds, and longer term physiological responses to heat strain, are warranted.
... These risks can be reduced by ensuring the water is not cold (Pinson 2020). In domestic dogs (Canis familiaris), cold water baths have associated risks of vasoconstriction, decreased cutaneous blood flow and capillary sludging, which induces disseminated intravascular coagulation (Flournoy et al. 2003). In effect, cold water can actually slow down cooling of the animal, though the extent of reduction would depend on animal size and posture due to the effect of different surface area to volume ratios (Rübsamen et al. 1984;Zhang et al. 2008). ...
Article
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Heat stress events in Australian flying-fox camps have resulted in significant numbers of flying-fox deaths. The frequency and intensity of such events have increased in recent decades, attributed to anthropogenic climate change. Evidence-based interventions are required to address this growing threat. Responders currently use different combinations of a range of intervention methods. We undertook a systematic review of heat stress interventions, which we classified as either 'camp-scale' or 'individual-scale'. Camp-scale interventions included manual and automated misting of roost vegetation, whereas individual-scale interventions included spraying individual animals or removing them for intensive cooling and rehydration procedures. Our study showed that to date, evaluation of the efficacy of heat stress interventions has been largely anecdotal rather than empirical. This highlights the need for dedicated rigorous studies to evaluate the effectiveness of all the intervention methods described here. It will be especially important to understand the relationship between camp temperature and humidity levels and their influence on flying-foxes' ability to regulate their body temperature, because high relative humidity reduces the ability of mammals to cool themselves using evaporative heat loss. The development of biophysiological measures such as temperature and humidity indices for different flying-fox species would enable meaningful interpretations of intervention trials under controlled conditions.
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Chapter
This chapter discusses care and management of dogs and cats with various environmental injuries. Specific injuries to be discussed include burns, cold-induced injury, heat-induced injury, nonsurgical management of open wounds and necrotic tissues, and presurgical care of open fractures. The chapter emphasizes the specialized nursing guidelines that are critical to improve the likelihood of successful outcome. Burn injuries are typically caused by environmental factors or iatrogenic factors. Cold-induced injuries include local or regional injuries and generalized hypothermia. The duration and severity of hypothermia, type of hypothermia, and the patient's ability to adapt directly affect which complications develop and how severe those complications become. Hypothermic patients must be warmed rapidly but carefully, and with anticipation for possible complications. Heat-induced injury, primarily seen in dogs, develops when there is an increase in core body temperature as a result of exertion, exposure to increased environmental temperature and humidity, or both.
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Chapter
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The striatum plays a pivotal role in modulating motor activity and higher cognitive function. We analyzed variation in striatal volume and neuron number in mice and initiated a complex trait analysis to discover polymorphic genes that modulate the structure of the basal ganglia. Brain weight, brain and striatal volume, neuron-packing density and number were estimated bilaterally using unbiased stereological procedures in five inbred strains (A/J, C57BL/6J, DBA/2J, BALB/cJ, and BXD5) and an F2 intercross between A/J and BXD5. Striatal volume ranged from 20 to 37 mm3. Neuron-packing density ranged from approximately 50,000 to 100,000 neurons/mm3, and the striatal neuron population ranged from 1.4 to 2.5 million. Inbred animals with larger brains had larger striata but lower neuron-packing density resulting in a narrow range of average neuron populations. In contrast, there was a strong positive correlation between volume and neuron number among intercross progeny. We mapped two quantitative trait loci (QTLs) with selective effects on striatal architecture. Bsc10a maps to the central region of Chr 10 (LRS of 17.5 near D10Mit186) and has intense effects on striatal volume and moderate effects on brain volume. Stnn19a maps to distal Chr 19 (LRS of 15 at D19Mit123) and is associated with differences of up to 400,000 neurons among animals. We have discovered remarkable numerical and volumetric variation in the mouse striatum, and we have been able to map two QTLs that modulate independent anatomic parameters.
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Physical training and heat acclimation are both commonly adopted tactics to improve performance and/or tolerance times when individuals must compete or work in the heat. Potential benefits include: (i) improved aerobic fitness and thus a greater cardiovascular reserve (probably seen mainly after training); (ii) a lower resting body temperature that allows greater heat storage (probably seen mainly after acclimation); (iii) a decreased energy cost of a given intensity of exercise (seen after acclimation and also as the learning component of training); (iv) an enhanced sweating response at a given percentage of maximal effort (probably developed by both treatments); (v) a slower increase in body temperature owing to (iii) and/or (iv) [seen after both treatments]; (vi) a reduced cardiovascular stress because of changes in the autonomic nervous system (probably realised mainly by training), expansion of blood volume (seen after both treatments) and/or a decreased peripheral pooling of blood (probably found after both treatments); and (vii) improved subjective tolerance reflecting a decrease in the relative intensity of a given activity (probably seen mainly after training), a reduction in the physiological strain (found after both treatments) and/or habituation to heat-exercise stress (probably developed by both treatments). Factors affecting improvements in physiological and psychological responses to a given set of conditions include: (i) the individual’s initial fitness and acclimatisation to heat; (ii) age, gender, hydration, sleep deprivation, circadian rhythms and in women the menstrual cycle; (iii) use of ergogenic aids such as fluid ingestion, carbohydrate and/or electrolyte replacement and blood doping; (iv) event or test conditions such as the mode of exercise, the severity of environmental heat stress and the type of clothing worn; and (v) treatment conditions such as the intensity, duration and frequency of exercise and/or heat exposure, the length of any rest intervals and cumulative depletion of body water and minerals.
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The early stages of heatstroke in 3 dogs were characterized by hyperthermia, hyperpnea, tachycardia, depression, vomiting, diarrhea, and dehydration. Laboratory signs of hepatocyte degeneration and necrosis were detected. Clinical and laboratory changes characteristic of acute primary renal failure developed several days after overheating. After symptomatic and supportive therapy, 2 of the dogs regained a sufficient degree of renal function to cause remission of signs of renal failure.
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The capability of stroma-free hemoglobin solutions to act as a plasmaexpander with oxygen and carbon dioxide transport properties has encouragedthe idea of their possible use in settings of massive blood loss. Using acanine hemorrhagic shock model (systolic arterial pressure < or = 50torr for 60 min), we evaluated the efficacy of an ultra-pure stroma-freebovine hemoglobin solution (PBHg) as a resuscitation fluid in hypovolemicand acidotic animals, using homologous blood (PRBC) and 10% human serumalbumin (HSA) as control solutions. Following volume replacement, dogs werestudied for 2 h under anesthesia and for 4 h subsequently while awake.Resuscitation with PBHg (30 +/- 3 ml/kg) was able to restore stablehemodynamics and correct acidosis to an extent comparable to that inanimals treated with PRBC. Additionally, oxygen transport was maintained ata higher level than that in dogs treated with HSA. Administration of PBHgin this shock model revealed no significant cardiopulmonary toxicity oradverse effects. These short-term results suggest that PBHg may be usefulfor effective resuscitation after major blood loss.
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Malignant hyperthermia (MH) is an anesthetic agent-induced hypermetabolic state. Human beings and several other animal species, including dogs, have been described to be genetically predisposed to development of MH. The halothane-triggered MH syndrome was characterized in genetically predisposed dogs, and in vitro contracture sensitivity of biopsied gracilis muscle exposed to halothane and caffeine was quantitated. Within 1 hour of halothane administration, each MH-susceptible dog developed rapid increases in CO2 production and rectal temperature. Reversal of the hypermetabolic state was achieved when halothane was discontinued and dantrolene sodium was given i.v. Biopsied gracilis muscle from MH-susceptible dogs had abnormal in vitro contracture responses to halothane and caffeine. These findings were consistent with those observed for MH-susceptible human beings and pigs in which a loss in regulation of muscle cell Ca(+)+ is believed to be the primary etiologic event for induction of MH.
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Heatstroke was induced experimentally in dogs, in order to clarify the mechanism of haemorrhage in that disorder. Controls were provided both by dogs subjected to maximal effort at normal ambient temperatures and by dogs exposed to high enviromental temperature without exercise. It was found that above a critical temperature (43.3° C), dogs show a typical clinical and laboratory picture of heatstroke, similar to that occurring in human beings. Quick value and platelets dropped markedly, as did most of the clotting factors including factor V, II, VII and X. Factor VIII was sometimes raised, but also fell terminally. Significant fibrinolysis and shortened half life of labelled fibrinogen were further strong indications of general defibrination. The post-mortem presence of thrombi, provided confirmatory evidence of diffuse intravascular clotting (consumption coagulopathy).
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A remarkably effective and efficient thermoregulatory apparatus enables humans to maintain a normal body temperature despite widely varying and changing environmental and internal thermal conditions. Nevertheless, extreme ambient cold or heat and exhaustive exercise stress can overwhelm these defenses, leading to dangerous hypothermia or hyperthermia, respectively.
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ExtractAdult dogs can survive in an environment in which there are wide variations of temperature because of their ability to regulate their internal temperature.(1)1. Armistead , W.W. and Catcou , E.J. 1979. Canine Medicine, 211–215. Santa Barbara: American Vet. Publications. Inc.. View all references The internal temperature, however, must be maintained within the range of 5°C above normal to 15°C below the normal temperature of blood to avoid cellular injury or death. Thermal homeostasis occurs when there is a balance between “heat load” and heat dissipation. Heat load is defined as the summation of environmental and metabolic heat.(2)2. Krum , S.H. and Osborne , C.A. 1977. Heat Stroke in the Dog: A Polysystemic Disorder. JAVMA, 170(5): 531–535. View all references Heat stroke occurs when heat load markedly exceeds the ability of the body compensatory mechanisms to promote heat loss. In man heat stroke is also due to ineffective thermoregulation. It is caused by the cessation of sweating, which is the main thermoregulatory mechanism. Heat stroke is characterised by hyperthermia (above 105°F), often complicated by alterations in many systems and organs such as acid-base balance, kidney, liver, cerebral oedema, and the blood clotting mechanism.