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Heatstroke in dogs (Proceedings)
In people, there are four types of heat-induced illness described: heat cramps, heat exhaustion, heat prostration, and heatstroke.
In people, there are four types of heat-induced illness described: heat cramps, heat exhaustion, heat prostration, and heatstroke. Heat cramps are muscle cramps which occur secondary to sodium chloride depletion from excessive sweating. Because dogs do not sweat, this form of heat-induced illness does not occur in dogs. The other types of heat-induced illness represent a continuum from the least to the most severe form. Heat exhaustion is defined as lethargy and inability to perform work secondary to extreme heat. Heat prostration is accompanied by headache, vomiting, tachycardia, mental confusion, and hypotension. Heatstroke is a more severe form of heat prostration which is characterized by CNS signs ranging from fainting to coma.
Normal Physiologic Cooling
In dogs, the primary normal physiologic cooling mechanisms are evaporation and conduction rather than sweating. Evaporation occurs mainly through panting, as water is lost through the moist mucous membranes of the upper respiratory tract. Panting is an effective method of cooling but requires respiratory muscle activity that in itself generates heat. Panting can become ineffective in dissipating heat in conditions of high environmental humidity when evaporation is reduced or in conditions involving defects of the upper airway, thereby impairing breathing and increasing the work of respiration.
Heat loss through conduction is aided by the development of peripheral vasodilation in warm environments. Animals often lie down on cool surfaces allowing the relatively hairless skin surface of the ventral abdomen to lose heat through conduction. Heat is also lost through radiation and convection as warm blood is shunted from visceral organs to surface skin. Heat loss through reflex vasodilation can be impaired by conditions that result in poor perfusion, such as underlying cardiac disease, dehydration, or hypovolemia from any cause.
Heatstroke can be exertional or nonexertional. In one study of 42 cases of heatstroke in dogs, 45% of them had a history of physical activity prior to the onset of clinical signs. Exertional heatstroke is more likely to occur in late spring or early summer before dogs become acclimatized to the high environmental temperatures. Dogs with obesity, laryngeal paralysis, tracheal collapse, eversion of laryngeal saccules, elongation of the soft palate, or brachycephalic conformation are at risk for exertional hyperthermia. Heatstroke can also occur in working dogs that over-exert themselves in hot, humid environments.
Non-exertional heatstroke most commonly develops when dogs are confined in an overheated enclosure, such as an automobile, or chained outdoors in the hot sun, especially when they are deprived of water or shade.
Heatstroke is a polysystemic medical emergency which can occur when the body temperature exceeds 106°F (41°C). High body temperatures can cause generalized cellular necrosis through denaturization of proteins, inactivation of enzyme systems, destruction of cell membrane lipids, and mitochondrial dysfunction. Multiple organ system dysfunction can occur, primarily involving the respiratory, cardiovascular, gastrointestinal, renal, CNS, and coagulation systems.
The most common signs of heatstroke reported by dog owners include excessive panting and inability or unwillingness to rise. Other signs include vomiting and/or diarrhea, especially following attempts to drink large amounts of water. Dogs also may exhibit hypersalivation, ataxia, muscle tremors, loss of consciousness, and seizures.
On physical examination membranes are usually hyperemic with an immediate capillary refill time. Loud breathing sounds may be detected in dogs with underlying anatomical defects of the upper airway. Petechial hemorrhages may be seen on mucous membranes or axillary and inguinal regions. Tachycardia is usually present and pulse deficits can be detected if there are arrhythmias present. Some animals exhibit dementia and cortical blindness. Melena, bloody diarrhea, or mucosal sloughing may be detected on rectal examination.
Common laboratory abnormalities include hemoconcentration (elevated packed cell volume and total solids concentration) associated with dehydration. Hypernatremia can be seen because panting results in water loss in excess of sodium loss. Blood glucose is often decreased secondary to the hypermetabolic state or possibly as a result of sepsis. Sepsis can result from bacterial translocation across damaged GI mucosa. Blood urea nitrogen and creatinine may initially be elevated as a result of pre-renal azotemia from dehydration and poor perfusion. Heatstroke may also cause direct renal damage from thermal injury, renal ischemia from poor perfusion, or myoglobinuria. Urine sediment should be checked for casts, epithelial cells or hemorrhage, and urine output should be monitored closely. Oliguric acute renal failure can occur as a sequela to heatstroke.
Hepatocellular damage usually results in elevation of SALT concentration. Mild icterus may also occur. Muscle damage can cause very high levels of creatinine phosphokinase levels which peak at 24-48 hours and then decline.
Coagulation abnormalities are secondary to endothelial damage and capillary sludging. Heatstroke causes a hypercoagulable state which can result in bleeding tendencies if coagulation factors are consumed. Disseminated intravascular coagulation is characterized by thrombocytopenia, presence of shistocytes on a blood smear, decreased fibrinogen levels, and prolongation of prothrombin time, partial thromboplastin time, and activated clotting time.
Blood gas analysis may reveal respiratory alkalosis initially followed by metabolic acidosis. Electrolyte abnormalities are common and may include hypernatremia, hyperkalemia, and hypokalemia. Hypophosphatemia and hypocalcemia may occur 24-48 hours later.
A common hematologic finding in dogs with heatstroke is the presence of nucleated red blood cells on the bloodsmear. This finding is usually transient and disappears with effective treatment.
1.Cooling - If possible, dogs should be hosed down by the owner at home before transport to the veterinary hospital. Evaporation can be enhanced by driving with all windows open or placing the dog by the air conditioning vent.
2. Ensure patent airway - Intubation or tracheostomy may be necessary in dogs with upper airway problems. Always supply oxygen.
3. Place IV catheter and obtain minimum data base: PCV, TS, Azostick, dextrostick, electrolytes, blood gases, and urine analysis.
4. Begin IV fluid therapy: 40-90 ml/kg/hr of room temperature crystalloid balanced electrolyte solution (LRS or Normasol-R). If Na+ > 160 mEq/L, use 0.45% NaCl and 2.5% dextrose. Decrease fluid rate to 4.4 - 6.6 ml/kg/hr when PCV decreases to mid-forties.
5. Continue cooling by wetting dog and placing under fans. AVOID ICE BATHS as these cause peripheral vasoconstriction, shunting of warm blood internally, capillary sludging promoting DIC, and shivering which generates heat. Ice packs can be placed on the head and ventrum to hasten cooling. Cooling measures should be discontinued when the temperature reaches 103°F, as it may continue to drop precipitously.
6. Administer corticosteroids to prevent cerebral edema: Dexamethasone sodium phosphate 2 - 8 mg/kg IV or prednisolone sodium succinate 10 - 25 mg/kg IV.
7. Administer antibiotics to prevent sepsis from bacterial translocation and GI mucosal damage: Ampicillin 22 mg/kg q 8 h IV and Enrofloxacin 5 mg/kg diluted 50:50 in saline q 12 h IV.
8. Correct hypoglycemia if present by administering 0.5 g/kg glucose diluted to 10% as an IV bolus and adding 50-100 ml of 50% dextrose to each liter of fluids.
9. Protect the GI tract by administering 1 gram of sucralfate (mix into a slurry by diluting with 10 ml water) per os q 8 hr.
10. Prevent D.I.C. if possible by administering 100 - 200 U/kg heparin SC q 8 h. If evidence of clinical bleeding is present or coagulation tests are prolonged, heparin can be added to plasma (10-20 ml/kg) and incubated for 30 minutes and administered IV. Heparin should be continued SC q 8 h and tapered off after the dog improves.
11. Correct acid-base and electrolyte abnormalities and continue to monitor until normal.
12. Monitor ECG and if cardiac arrhythmias occur consider nasal oxygen supplementation (50 - 100 ml/kg/min) and lidocaine (4 -8 mg/kg slow IV bolus followed by 50 - 80 μg/kg/min constant rate infusion). Taper off lidocaine if arrhythmias improve after 72 hours or change to oral procainamide (10 - 20 mg/kg q 8 h) for long-term therapy if desired.
13. Monitor urine output and if it is < 1 ml/kg/hr after the patient is well hydrated, consider mannitol (0.5 - 1 g/kg IV), dopamine (3 μg/kg/min CRI), and furosemide (2 mg/kg IV bolus followed by 1 mg/kg/hr infusion). After urine flow is initiated, fluid therapy should be continued at 2 - 3 times maintenance levels and tapered off. Urine sediment, BUN, and creatinine should be monitored.
14. Monitor neurologic status and if it is deteriorating consider mannitol (1 g/kg IV) and repeat corticosteroids q 8 hr. Monitor and correct hypoglycemia. Control seizures with diazepam (2 - 10 mg IV PRN).
Most dogs recover within 1 - 5 days with aggressive supportive care. Non-survivors usually die during the initial 24 hours of treatment.