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A Review of Heat Stroke and Its Complications in the Canine Renee L

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A Review of Heat Stroke and Its Complications in the Canine Renee L Volume 45 | Issue 1 Article 1 1983 A Review of Heat Stroke and Its Complications in the Canine Renee L. Larson Iowa State University Robert W. Carithers Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Small or Companion Animal Medicine Commons, and the Veterinary Physiology Commons Recommended Citation Larson, Renee L. and Carithers, Robert W. (1983) "A Review of Heat Stroke and Its Complications in the Canine," Iowa State University Veterinarian: Vol. 45 : Iss. 1 , Article 1. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol45/iss1/1 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. A Review of Heat Stroke and Its Complications in the Canine Renee L. Larson, BS * Robert W. Carithers, DVM, MS, PhD** SUMMARY most obvious prerequisite is a high en­ A review of heat stroke and its complications vironmental temperature. When the ambient is presented. The etiology, physiology, clinical temperature increases above 86°F, a rise in in­ signs, secondary complications, diagnosis, ternal body temperature results. Dogs can treatment, necropsy results and prevention of tolerate rising environmental temperature heat stroke are discussed. A clinical case is quite well. However, when the body tempera­ then presented to illustrate the disorder of heat ture exceeds 104°F a breakdown of the stroke. animal's thermal equilibrium begins. At 106°F the brain becomes involved and perma­ INTRODUCTION nent damage may develop.3 Adult dogs can survive in an environment in Inadequate ventilation is one of the most which there are wide variations oftemperature critical factors in heat stress development. because of their ability to regulate their inter­ Greater than 70 % of the total body heat loss in nal temperature. I The internal temperature, dogs and cats is due to radiation and convec­ however, must be maintained within the range tion from the body surface.3 Static air around of SoC above normal to 15°C below the nor­ the body is soon elevated to body temperature, mal temperature of blood to avoid cellular in­ and surface heat loss is blocked. Animals jury or death. Thermal homeostasis occurs placed in an enclosed environment with no air when there is a balance between "heat load" flow, such as an automobile, can develop seri­ and heat dissipation. Heat load is defined as ous problems. the summation of environmental and metabol­ Dogs that are confined by chain outdoors ic heat. 2 Heat stroke occurs when 'heat load have been known to develop heat stroke. Often markedly exceeds the ability of body compen­ these dogs are unable to get into the shade or satory mechanisms to promote heat loss. In have no drinking water available. In these man heat stroke is also due to ineffective ther­ cases, excitement and exercise associated with moregulation. It is caused by the cessation of animal fights appear to have precipitated heat sweating, which is the main thermoregulatory stroke. 4 Although exercise and excitement can mechanism. Heat stroke is characterized by significantly contribute to the induction of heat hyperthermia (above 105°F), often com­ stroke in confined dogs, heat stroke is rare in plicated by alterations in many systems and dogs that run free., regardless of exercise and organs such as acid-base balance, kidney, air temperature. liver, cerebral edema, and the blood clotting In contrast to human heat stress, humidity mechanism. has less of art effect on canine heat stress, primarily due to the poor development of ETIOLOGY canine sweat glands.3 However, high humidi­ Several factors are necessary for, or con­ ty may contribute to the likelihood of heat tribute to, the induction of heat stroke. The stroke because evaporation of water from the oral and nasal cavities is reduced in spite of maximal panting.4 • Ms. Larson is a fourth-year student in the College of Other predisposing factors include lack of Veterinary Medicine, Iowa State University. •• Dr. Carithers is a professor in Veterinary Clinical available water, brachycephalic anatomy, Sciences at Iowa State University. length of hair coat, obesity, specific dynamic 4 Iowa State Veterinarian action of food, and decreased heat tolerance tory centers occur. Tissue edema and hypoxia associated with young and old age. can develop which are most serious in such areas as the lungs and brain. The kidney can PHYSIOLOGY also be affected by shock-induced ischemia. Signals from temperature-sensitive organs Tissue enzyme systems operate effectively in skin, viscera, and central nervous system over a narrow range of temperature. When converge in the caudal hypothalamus7 (Fig. this range is exceeded, widespread cellular 1). The central effector signal is mediated damage and death of various tissues occurs. through the endocrines, the autonomic ner­ Central nervous system destruction, especially vous system, and by neuromuscular activity.s of Purkinje cells, and heart muscle destruction The initial compensatory response to in­ have been shown with heat stroke.9 Renal creased ambient temperature is panting.4 The tubular damage is probably a direct result of panting mechanism may be initiated reflexive­ heat injury in cases not associated with shock. ly and centrally, by an increase in body tem­ The liver is very susceptible, as heat itself perature or external temperature and by local causes liver cell death. warming of the anterior hypothalamus. This .mechanism of dissipating heat is efficient and CLINICAL SIGNS, SECONDARY involves a partial circle system of air passing COMPLICATIONS, AND DIAGNOSIS into the nasal cavity and out the oral cavity.6 The onset of heat stroke in three-fourths of This unidirectional flow maximizes evapora­ the cases is acute, with clinical signs develop­ tion and heat loss because of the greater ing fairly rapidly. The physical findings in evaporative surface area of the nasal tur­ dogs with heat stroke depend on duration and binates to which the air is exposed. Increased severity of the disease. Initial findings include salivation during panting greatly increases the panting, tachycardia, bright red oral mucosa evaporative cooling. Even though the animal and hyperthermia. The pulse is rapid and becomes dehydrated by 6-10%, salivation weak. 3 As the disease progresses the dog continues at the same rate, resulting in a becomes stuporous due to the development of decreased plasma volume and flow. Panting, cerebral edema. The extremities become hot however, is not without drawbacks. and dry to the touch. The bright red oral Hyperventilation occurs which may cause mucosa becomes pale, due to either peripheral respiratory alkalosis as carbon dioxide is vasoconstnctlOn or decreased circulatory blown off. The respiratory alkalosis induced in volume or both.4 Massive diarrhea and pentobarbital-anesthetized dogs subjected to vomiting may occur at this later stage. If the high temperature, however, is eventually diarrhea becomes bloody, disseminated in­ modified by metabolic acidosis presumably travascular coagulation (DIC) may be a com­ due to muscle activity associated with' pant­ plication. Progression of cerebral edema to ter­ ing.4 The acid-base status of the individual pa­ minal stages leads to coma and respiratory tient can be determined only if blood gas arrest. analysis is done. Survival from heat stroke depends heavily Sympathetic vasoconstrictor nerves control upon maintainence of a cardiac output the cutaneous vasomotor reactions to sufficient to meet the elevated circulatory de­ temperature changes. Inhibition of the sym­ mand. Complications attributable to cir­ pathetic vasoconstrictor tone causes peripheral culatory failure are myocardial damage and vasodilation, which increases heat loss. marked increase of pulmonary vascular However, when external temperature exceeds resistance. That direct thermal injury is at 31 DC, heat is no longer lost by cutaneous least partly responsible for myocardial damage vasodilation. This inhibition is mediated by an is suggested by widespread tissue injury in this increase in hypothalamic temperature or condition. 10 Elevated pulmonary vascular reflexively through thermoreceptors in the resistance is suggested by vascular congestion skin. 8 As blood is shunted to the peripheral and pulmonary edema, as well as right-sided vessels (capillaries), there is a large decrease in dilation of the heart at necropsy. 11 Ar­ circulatory blood volume. Eventually, if there rhythmias progressing from premature con­ is no compensatory increase in blood volume, traction and bradycardia to ventricular dilation of the heart and impaired cardiac fibrillation and heart block may occur if efficiency, and finally impairment of respira- hyperkalemia is present. Vol. 45, No. 1 5 HEAT LOSS MECHANISMS SKIN VASODILATATION '--_________SWEATING AND PANTING ...J" NEURO-MUSCULAR COLD HYPERTHERMIA EXTERNAL COLD DEFENSIVE MECHANISMS PERIPHERAL COLD THERMOREGULATORY -­ SKIN VASOCONSTRICTION "CENTER" RECEPTORS SHIVERING -+ HORMONAL COLD DEFENSE MECHANISMS SECR. OF NOREPINEPHRINE EPINEPHRINE THYROXINE + HEAT LOSS MECHANISMS SKIN VASODILATATION SWEATING AND PANTING + // L..--____----I~ , NEURO-MUSCULAR COLD 'r-----------------~ EXTERNAL HEAT HYPOTHERMIA DEFENSIVE MECHANISMS THERMOREGULATORY SKIN VASOCONSTRICTION - PERIPHERAL
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