Q. Please review heat-illness problems in dogs.
A. Dr. Kenneth J. Drobatz at the 2005 American College of Veterinary Internal Medicine Forum in Baltimore gave a lecture on pathophysiology and treatment of heat-induced illness. Some relevant points in this lecture are provided below.
Heat illness may represent a continuum from the least to the most severe form. 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/exhaustion may be diagnosed. The heatstroke is severe central nervous system disturbance and is often associated with multi-organ dysfunction. Generally, owners seek veterinary attention when their dogs demonstrate signs consistent with heat prostration/exhaustion or heatstroke.
Thermal homeostasis is maintained by a balance between heat load and heat-dissipating mechanisms controlled by temperature-sensitive centers in the hypothalamus. Environmental as well as metabolic heat are the major contributors to heat load. Body temperature increases when heat load exceeds heat dissipation. As the body temperature increases, heat loss via radiation and convection from the skin is facilitated by increased cutaneous circulation as a result of increased cardiac output and sympathetic mediated peripheral vasodilation. The shunting of blood to the periphery is 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.
A warm, humid environment and exercise are the most common heat loads that dogs experience and may cause extreme hyperthermia even in individuals with functional heat dissipating mechanisms. Respiratory evaporative heat loss may be diminished by humid climactic conditions, closed confinement with poor ventilation and upper respiratory abnormalities such as brachycephalic conformation, laryngeal paralysis or masses, or collapsing tracheobronchial tract. Diminished radiation and convective heat loss from the skin may occur as a result of hypovolemia due to any cause, poor cardiac output, obesity or lack of acclimatization to heat. Situations that combine high heat load and diminished heat dissipation may result in a rapid and extreme rise in body temperature.
Most heat illness in dogs usually presents during late spring or early summer when the warm humid weather begins. Despite progressively warmer days later in the summer, heat-induced illness becomes less frequent unless dogs are left in cars. This may be due to a lack of time for acclimatization to the change in environmental temperature. Acclimatization to heat can take two weeks or more 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 GFR and an increased ability to resist exertional rhabdomyolysis.
Heat stroke occurs due to a combination of events, which primarily include failure of thermoregulation, an exaggerated acute phase response, and alteration of heat-shock proteins. The reaction of the body during heat stroke involves many of the same mediators as sepsis.
The physical findings of dogs suffering from heat-induced illness vary with the intensity and duration of the increased body temperature. The rectal temperature may be decreased, normal or increased depending upon tissue perfusion and whether cooling measures have been implemented already. The pulse is often weak due to hypovolemia and fast as a result of compensatory sinus tachycardia. The respiratory rate is very rapid usually to improve heat dissipation rather than as a result of respiratory disease. Most dogs present in a hyperdynamic state. The mucous membranes are usually hyperemic, and the capillary refill time is short. The pulses are often weak due to hypovolemia secondary to evaporative fluid loss, vomiting, diarrhea and vasodilation. Sinus tachycardia is common. Some dogs have occasional ventricular arrhythmias. ECG evaluation should be performed on all dogs with severe heat-associated illness.
Evaluation of the respiratory system is warranted because evaporation through the respiratory tract is a major route for heat dissipation. Loud or noisy breathing that is heard without the stethoscope suggests an upper airway problem, such as laryngeal paralysis/edema, obstruction or tracheobronchial collapse. Many dogs with heat-induced illness have been vomiting, and aspiration pneumonia should be considered. Dogs suffering from disseminated intravascular coagulation may have pulmonary parenchymal hemorrhage resulting in crackles or harsh airway sounds.
Mentation may range from alert to comatose. Depression is the most common abnormality. The severely affected dog will be comatose or stuporous at presentation. Pupils can range from dilated to pinpoint but usually are responsive. Some dogs may be cortically blind at presentation. This may resolve after several hours. Ambulatory dogs may be ataxic. The cause of these neurologic abnormalities may be poor cerebral perfusion, direct thermal damage, cerebral edema, CNS hemorrhage or metabolic abnormalities such as hypoglycemia or hepatoencephalopathy.
Many of the severely affected dogs have protracted vomiting and diarrhea. The diarrhea may range from watery to hemorrhagic with mucosal sloughing. This may be secondary to disseminated intravascular coagulation or poor visceral perfusion. Gastric ulceration may occur as well, resulting in vomiting with or without blood. Disseminated intravascular coagulation is not an uncommon finding in dogs with heat-induced illness. The presence of petechiae and ecchymoses or blood in the urine, vomit or stool suggests that this may be occurring.
Many owners recognize that their dogs are overheated and hose them down with cool water. This is very effective and often results in a normal body temperature at presentation if the dog is brought in immediately. Wetting the dog with water and blowing a fan over it is quite effective. Ice packs over the large superficial vessels in inguinal and axillary areas may help as well. Administering cool intravenous fluids is helpful and cooling measures are stopped when the rectal temperature reaches 103 F to avoid rebound hypothermia. Despite this, it is not unusual for these dogs to develop body temperatures between 95 F-100 F within the first few hours of hospitalization. If hypothermia occurs, warm water bottles or blankets may be necessary to maintain normothermia.
The severely affected dog often presents in hypovolemic shock. If cardiovascular disease is unlikely, then we administer cool balanced electrolyte fluids intravenously at 90 ml/kg/hr and continuously assess perfusion status and then titrate the rate and volume of fluids. Central venous pressure monitoring will help guide fluid therapy if massive volumes are required. If large doses of intravenous fluids do not improve tissue perfusion and blood pressure, then administration of colloids (i.e., hetastarch) should be considered and/or use of positive inotropes or pressure agents (such as dobutamine, dopamine or epinephrine). Dogs that cannot maintain an adequate blood pressure without them (for prolonged periods of time) carry a poor prognosis. Blood pressure and physical parameters of tissue perfusion should be continuously monitored in severely affected dogs.
Oxygen should be administered at presentation and should be continued until it has been determined that the dog can maintain arterial oxygenation. Serial physical assessment of the respiratory system, such as auscultation, respiratory rate and effort, and mucous membrane color is warranted in the dogs suffering from heat illness. More objective assessments such as arterial blood gas analysis and pulse oximetry may be required.
At presentation, neurologic examination should be performed to establish a baseline for future reference during the animal's hospital stay. The more severely affected dogs may present stuporous or comatose.
Serum electrolytes, PCV, 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 ¼ to ½ gram per kilogram body weight of 25 percent dextrose should be administered and dextrose added to the intravenous fluids to a 2.5-percent to 5-percent concentration if hypoglycemia is present. Poor tissue perfusion should be corrected and mentation re-evaluated after perfusion is improved. If mentation continues to be abnormal after correcting these abnormalities, then cerebral edema may be present. Mannitol (0.5 grams/kg body weight slow IV) and/or anti-inflammatory doses of dexamethasone should be considered. The head should be slightly elevated (approximately 30 degrees above horizontal) to avoid occluding the jugular veins. Progression of neurologic abnormalities despite therapy carries a poor prognosis.
At presentation, a urinary catheter should be placed for monitoring urine output in the more severely affected dog. A complete urinalysis should be performed initially and serially as treatment progresses to detect early signs of renal damage, such as urinary casts. Urine output should be maintained at 2 ml/kg body weight or greater depending upon the amount of fluid being administered. Mean arterial pressure should ideally be at least 80 mmHg. If urine output remains insufficient despite adequate fluid replacement, then a combination of dopamine (3 micrograms/kg/min) and furosemide (2 mg/kg IV bolus followed by 1 mg/kg/hr infusion) should be considered, although the efficacy of dopamine in treating anuric/oliguric renal failure is questionable. Some veterinarians prefer to try 0.5 grams/kg IV of mannitol to induce diuresis. Serum sodium, potassium, total solids, BUN and creatinine should be monitored.
Coagulation evaluation including prothrombin time, partial thromboplastin time, platelet count and fibrin split products concentration should be obtained at presentation and as indicated during therapy. Prolonged coagulation tests, decreased platelet count and increased fibrin split products suggest disseminated intravascular coagulation. Therapy for disseminated intravascular coagulation is controversial. Removal of the underlying cause is essential. Symptomatic therapy may include fresh frozen plasma intravenously and low-dose heparin therapy (100 IU/kg q 4-6 hours) subcutaneously. Alternatively, 20 IU/kg body weight of heparin incubated with fresh frozen plasma may be administered.
Direct thermal damage and poor visceral perfusion may result in gastrointestinal mucosal sloughing and ulceration. This results in vomiting and diarrhea that may or may not be bloody. Sucralfate (if vomiting is not present) and H2 blockers will help treat gastric ulceration. Breakdown of the mucosal barrier may result in bacteremia or endotoxemia. Broad-spectrum antibiotics should be considered in severely affected animals with severe bloody diarrhea. Small intestinal intussusceptions may develop in some dogs with heat stroke.
The degree of compromise depends upon the prior physical health of the dog and the degree and duration of the heat insult. Dogs with multi-organ dysfunction or severe CNS disturbance warrant a more guarded prognosis. Alternatively, some dogs with severe CNS disturbance, disseminated intravascular coagulation and other organ dysfunction may live without any residual problems. Severe heat-induced illness is challenging to treat, but with aggressive medical therapy many dogs may respond and do well.
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Dr. Hoskins is owner of DocuTech Services. He is a diplomate of the American College of Veterinary Internal Medicine with specialities in small animal pediatrics. He can be reached at (225) 955-3252, fax: (214) 242-2200, or e-mail: