Heatstroke in dogs
Regardless of the climate where you live, dogs run the risk of developing heatstroke. It is important to note the difference between fever (pyrexia) and heatstroke: fever is the body’s response to bacterial or viral invasion and is necessary to the healing process. The hypothalamus in the brain controls thermoregulation by detecting when the animal needs to pant/seek shade or when they need to start shivering to create heat. There is an internal set-point in the hypothalamus at which these behaviours are triggered, and during a fever the set-point is increased. In cases of true fever, active cooling is discouraged. The animal will work to keep their temperature increased even in the face of our attempts to cool it.
Dogs normally dissipate heat through four main channels:
- Conduction – by lying on a cool surface
- Convection – air blows over their skin and cools the dog
- Radiation – they release heat into the atmosphere
- Evaporation – by panting they evaporate heat
Heatstroke in dogs occurs when they can no longer dissipate heat efficiently and their body becomes overwhelmed. As the dog’s body temperature rises, the mechanisms to actively cool require an increased metabolic rate. Panting, vasodilation, increased cardiac output, and increased mean arterial pressure are attempts to cool, but also create heat. As the body temperature rises, heatstroke occurs, and without intervention the dog will soon be in critical condition. In severe cases of heatstroke, every body system is affected and these patients need close monitoring and critical supportive care to survive.
Dogs experiencing heatstroke will have a history of heat exposure or extreme exercise in a warm environment, may have or are currently suffering from seizure activity, may be experiencing a laryngeal paralysis respiratory crisis, or experiencing increased muscle activity from hypocalcemia. These dogs will present to the hospital with a core body temperature greater than 40°C. Many of these patients will also experience mentation changes (dull, collapsed), will have hyperemic mucous membranes, thick saliva, vomiting, and diarrhea. Dogs more prone to heatstroke are the brachycephalic breeds, dogs with laryngeal paralysis, and those that have previously survived a heatstroke episode.
Treating a dog with heatstroke
Soak the dog in room temperature water or even warm (never cold) water and blow a fan over the dog. This will allow for evaporative and radiative cooling. Room temperature IV fluids should be administered which will help with cooling as well as begin to address the multiple other problems these patients incur due to thermal injury. The issue of using alcohol on the pads of heatstroke patients is often mentioned – but it is no longer a recommended treatment. Not only is the surface area of the paw pads so small, the vasodilation occurring in these patients can lead to increased absorption of alcohol into the bloodstream. It is important to stop active cooling once the dog’s temperature reaches 39.4°C, then dry the patient and closely monitor their temperature and start warming methods as needed.
Because all body systems are affected by thermal injury, the cooling process is only the beginning of treatment. The patient should be monitored for coagulation function and observed closely for changes in perfusion, mentation, comfort, and infection.
Neurologic system
The intense heat experienced by heatstroke patients can cause cell rupture. Cellular death leads to edema and cerebral edema manifests as mentation changes. Heatstroke patients often present collapsed, but they can be stumbling/ataxic, mentally inappropriate, or even present to the hospital with seizure activity.
Shock
During thermal injury the body peripherally vasodilates to bring as much blood to the surface as possible in an attempt to cool, and heatstroke patients can quickly experience hypovolemic shock. Evaporative cooling (panting) can dehydrate the dog. As the heat situation becomes more dire, cardiac output, blood pressure, and perfusion decrease. Every major organ system fails to receive appropriate blood flow and can suffer ischemic injury. As a result we will see the clinical signs of shock in these heatstroke patients. Tachycardia, poor pulses, hyperemic mucous membranes and brisk CRT (some may have progressed to pale mucous membranes), and poor perfusion signal shock. Fluid therapy remains the mainstay of treatment for shock. Crystalloids are administered to clinical endpoints (decreasing tachycardia and increasing blood pressure) with the nursing team providing continued monitoring for patient improvement.
GI system and sepsis
A combination of direct thermal injury to tissues and poor perfusion to the gut can cause GI ulceration and often vomiting and diarrhea. Breakdown of the gut mucosal barrier can lead to gut-derived sepsis. Broad-spectrum antibiotics should be considered in patients that present with severe heatstroke and hematochezia/hematemisis. Blood glucose levels should be monitored frequently and hypoglycemia addressed as needed.
Coagulopathy
Coagulopathy is common in heatstroke patients. Systemic inflammation can activate the clotting cascade and clotting factors are consumed. Hemorrhage can occur and can be catastrophic. Direct thermal injury to the endothelium and liver from extreme heat can also lead to inappropriate bleeding and the dog’s inability to appropriately replace clotting factors. Once this occurs it is common to see petechiation, ecchymosis, hematochezia, hematemisis, and bleeding from injection sites.
Hepatic system
In heatstroke, the liver often suffers direct thermal damage. These dogs cannot rebound from clotting factor losses due to this damage. Liver enzyme elevations are common and should be monitored. Some patients may become icteric as total bilirubin levels rise due to red blood cell breakdown.
Kidneys
As blood shifts from the dog’s core to the periphery in an attempt to cool, the kidneys can experience a decrease in perfusion. As the dog continues to lose water and experiences further and severe hypovolemic shock, the kidneys begin to experience damage, and azotemia is noted in lab work. Urine output is important to monitor in these patients, and measures should be taken to ensure that they are able to process the fluids they are receiving.
Cardiac system
Many heatstroke patients are at risk for arrhythmias (mainly ventricular). Hypovolemia, hypoxia, direct thermal injury, ischemia, and reperfusion injury are common. ECG monitoring should be a part of heatstroke patient management, and arrhythmias treated as they occur.
Nutrition
Because the GI tract can be severely affected, nutrition can be a challenge in these patients. Feeding the gut is an important part of the healing process and should be started early in the treatment process. If possible, trickle feeding through an NG/NE tube should be instituted as soon as the patient is not vomiting.
Pain
Pain management should not be neglected in the heatstroke patient. These patients should be treated with opioids as needed to keep them comfortable during their hospital stay.
Summary
Heatstroke is a syndrome that requires quick and knowledgeable action from both the owner and the veterinary team. Multiple organ systems can be affected and need close monitoring. Nursing care is extensive and requires considerable understanding of the systems and organs that can be affected. Excellent communication between veterinary and nursing teams is necessary. With excellent nursing and supportive care it is possible for these patients to completely recover.
Suggested Reading:
Creedon, Jamie M Burkitt, and Harold Davis. Advanced Monitoring and Procedures for Small Animal Emergency and Critical Care. Chichester, West Sussex: Wiley-Blackwell, 2012.
Johnson, Scott I, Maureen McMichael, and George White. "Heatstroke in Small Animal Medicine: A Clinical Practice Review." Journal of Veterinary Emergency and Critical Care 16.2;2006: 112-19.
Silverstein, Deborah C, and Kate Hopper. Small Animal Critical Care Medicine. St. Louis, MO: Saunders/Elsevier, 2009.
Wingfield, Wayne E, and Marc R Raffe. The Veterinary ICU Book. Jackson Hole, WY: Teton NewMedia, 2002.
This article is based on Ms. Brashear’s presentation at the Canadian Veterinary Medical Association Convention in Calgary, AB.CVT
