How to Treat Heastroke in Dogs by Lexi Hansen, BS, LVT, RVT, VTS (ECC)
By Lexi Hansen, BS, LVT, RVT, VTS (ECC), ECC Veterinary Technician Manager, BluePearl Pet Hospital Cary, NC
In today’s VETgirl blog, guest veterinary technician blogger Lexi Hansen, BS, LVT, RVT, VTS (ECC) reviews all things heatstroke! While summer is coming to an end, apparently this climate change heat isn’t! In veterinary medicine, we’re often presented the dog with heatstroke during the summer and as temperatures increase. In this blog, learn how to recognize and treat it!
What is Heatstroke?
Heatstroke is defined as a non-pyrogenic elevation in core body temperature greater than 105.8⁰F/41⁰C along with central nervous system (CNS) dysfunction. In veterinary medicine, heatstroke can be broken into two categories: exertional and environmental. Exertional heatstroke is exercise induced or can be seen in dogs who are not acclimated to their environment. Environmental heatstroke is due to an increase in environmental temperatures and can be exacerbated by an absence of adequate cooling means such as water, or shade.
When a patient suspected of heatstroke shows up to your veterinary clinic, it is vital to get a thorough history and diagnostics. This will inevitably help direct the treatment plan, as treatment needs to be quick and aggressive for success. Patients will commonly present with a history of collapse, tachypnea, and ataxia or disorientation.
With heatstroke, we can see the following clinical signs:
• Injected mucous membranes
• Temperature > 103.5⁰F/39.7⁰C*
• Signs of coagulopathy (e.g., petechia, bruising, erythema)
• Cardiovascular collapse/shock (e.g., tachycardia, poor perfusion, weak pulses)
• CNS signs (e.g., dull mentation, coma, tremors, seizures).
*Often, we may not have an accurate peak patient temperature, as most often owners often try to actively cool their pet prior to presentation (e.g., cold water, fan, air conditioning, etc.).
The body has normal cooling methods to help maintain homeostasis, including evaporation, conduction, convection, and radiation. Evaporation is one of the most important ways that a dog can cool themselves. This occurs through panting and subsequently evaporation of water. This method of cooling is less effective in hot, humid environments. Conduction is the transfer of heat from one object to another. This is why you will often find dogs seeking a cool place to lay down, as contact with their lightly haired abdomens on a cool surface will cause a transfer of heat (Likewise, how patients become hypothermic lying on a cold, stainless steel gurney or surgical table in the hospital!). Convection is when the movement of air over the body allows the dissipation of heat into the environment. This is most often seen with wind or a fan. Radiation is when the body dissipates heat into the environment naturally. This is less effective as the environmental temperatures reaches that of a patient’s body temperature.
Under normal conditions, greater than half of a patient’s total body heat is dissipated through convection and radiation. Heatstroke can occur when the body is unable to dissipate the accumulated heat.
The body has a thermoregulatory center located in the anterior hypothalamus that maintains core body temperature between a very narrow set point. This thermoregulatory center in the brain is so sensitive that it can sense a non-pyrogenic change in core body temperature as little as 1⁰C. When an elevation is body temperature outside the normal set point occurs, it triggers a cascade of changes within the body to maintain hemostasis.
Pathophysiology of Heatstroke
Once a patient starts accumulating more heat than they can dissipate utilizing normal methods, the body will trigger compensatory pathways to aid in more aggressive cooling. The first step is to peripherally vasodilate to increase heat loss through the integument. The cardiovascular system aids in this by first increasing heart rate. This, along with the decreased systemic vascular resistance, will ensure maximum blood flow and subsequently maximum heat loss through the periphery.
If these initial compensatory methods are not effective, the body will continue to try and cool itself; however, deleterious side effects may be seen at this stage. Patients will start to exhibit splanchnic vascular dilation which can cause venous pooling and decreased circulating volume. The lack of forward blood flow significantly decreases heat dissipation through the integument and the venous pooling from splanchnic vasodilation leads to hypotension and inevitably circulatory shock.
As the body continues to decompensate secondary to global hypoperfusion, massive cellular destruction, thermal injury, and damage or failure of vital organs can occur. Multi-organ dysfunction syndrome (MODS), where body systems become affected secondary to heatstroke can occur; it is important to recognize how to monitor and support each system to create an effective treatment plan and monitor for decline.
Body System Complications From Heatstroke
Patients often present with some level of CNS dysfunction. They may present with mild CNS signs such as ataxia or dulled mentation, all the way up to seizures, coma, and even death. This can be due to the hypoperfusion of the brain, thrombi, cerebral edema, cerebral hemorrhage, increased intracranial pressure (ICP), or direct vascular damage. To support a patient’s CNS and treat cerebral edema, it is recommended to elevate their head, while avoiding compression of the jugular veins. The use of hypertonic saline or mannitol can be used to decrease ICP. Mannitol, an osmotic diuretic, may be contraindicated in patients with dehydration, hypotension, and concerns for intracranial hemorrhage.
We can see a multitude of dysfunctions affecting the cardiovascular system including cardiac arrhythmias (e.g., ventricular tachycardia, etc.). Appropriate monitoring with an electrocardiogram (ECG) is imperative in the critically ill heatstroke patient. Ventricular arrhythmias should be treated with an antiarrhythmic such as lidocaine if signs of altered perfusion (e.g., hypotension, pallor, etc.) or sustained tachycardia are seen (e.g., HR > 180 bpm). Secondary causes of arrhythmias, such as electrolyte abnormalities (e.g., hypokalemia, hyperkalemia, etc.), acid-base disturbances, or pain should be evaluated and treated if appropriate, to maintain cardiac function. There is also a concern for side effects secondary to hypoperfusion such as myocardial ischemia.
Vasculature such as arteries, capillaries, and venous structures are widely affected with heatstroke; increased vascular permeability can result in edema and hypoalbuminemia. The trauma to the endothelium causes the release of thromboplastin and factor XII which activate the coagulation cascade. With heatstroke, the global damage causes an exaggerated release and utilization of coagulation factors; prolonged PT/PTT and thrombocytopenia is commonly seen. At this point the body will start to exhibit signs of Systemic Inflammatory Response Syndrome (SIRS) and/or disseminated intravascular coagulopathy (DIC). DIC, which may not be seen immediately, presents as microthrombi in the vasculature, but also can present as spontaneous bleeding due to the severe overstimulation of the coagulation cascade. This can be seen on the skin as petechia or ecchymosis.
Clinical signs of DIC associated with heatstroke may include:
• Bleeding from intravenous catheter insertion sites
• Seizures (from bleeding into the CNS)
Once a patient is exhibiting signs of SIRS or DIC, treatment should focus on aggressive supportive care and transfusions with fresh frozen plasma (FFP) to try to replenish coagulation factors.
With heatstroke, the pulmonary system may not be able to appropriately perform oxygen exchange due to pulmonary embolism (from secondary coagulopathy), alveolar hemorrhage, and pulmonary edema. Even with rapid identification and treatment, a continued decline in a patient’s respiratory status may occur. Other pulmonary complications such as aspiration pneumonia and non-cardiogenic pulmonary edema (NCPE)/Acute Respiratory Distress Syndrome (ARDS) may be seen, with the latter having a poor prognosis. It is important to provide oxygen support and ventilatory support, if needed. Patients should have respiratory rate and effort closely monitored, including pulse oximetry and blood gas monitoring. It is ideal to get base line thorax radiographs to monitor any changes during hospitalization.
The renal system, which can be very sensitive to hypotension and acute injury, will need to be monitored closely. We often see azotemia and decreased urine production (e.g., oliguria and anuria) secondary to MODS. The secondary damage from heatstroke can send patients into acute kidney injury secondary to prolonged hypotension, SIRS, DIC, and renal tubular necrosis. Placing an indwelling urinary catheter and monitoring the ins and outs will be helpful in directing the treatment plan.
The hepatic system, which normally helps produce Vitamin-K dependent factors of the clotting cascade, is unable to do so with severe heatstroke. It is common to see thermal injury from prolonged hypoperfusion and splanchnic vasodilation. Microembolisms may start to form due to coagulopathy. Hypoglycemia can also be seen with heatstroke secondary to decreased hepatic function, bacterial translocation, sepsis, or an increased utilization of blood glucose with severely decreased production.
• Gastrointestinal tract (GIT)
The gastrointestinal tract, which is the shock organ in our canine patients, can be severely affected with heatstroke. Mucosal damage, leading to hyperpermeability and concern for bacterial translocation out of the GIT (leading to sepsis), may occur. Supportive care for the GI tract may include anti-emetics (to prevent secondary aspiration pneumonia), anti-diarrheals, antacids (e.g., H2 blockers such as famotidine, proton pump inhibitors such as pantoprazole, etc.), and judicious antibiotics, if appropriate.
Heatstroke can result in drastic injury to multiple organ systems. This critically ill population is at high risk for developing MODS (which is defined as a dysfunction of two or more organ systems). This disease process is known for having an increased morbidity and mortality rates, and significantly increases a patient’s ICU stay.
Treatment for Heatstroke
With the critically ill heatstroke patient, prompt stabilization is imperative. This may include oxygen therapy, establishing venous access with an IV catheter, checking a blood glucose, treating for hypoglycemia, volume resuscitating with crystalloids, and cooling measures/thermoregulation.
First, ensure that your patient has a secure, patent airway and is adequately oxygenating and ventilating. Flow-by oxygen is immediately warranted. Some patients, especially those at high risk of heatstroke (e.g., such as brachycephalic breeds, obese patients, black-furred or long-haired dogs, or patients with laryngeal paralysis) may need to be intubated or have a tracheostomy tube placed.
Next, you want to rapidly gain venous access to start fluid therapy. It is ideal to collect blood while placing your intravenous catheter. A stat blood glucose, along with PCV/TS should be immediately assessed. You will want to limit the number of times we phlebotomize these patients, especially when we are not aware of their coagulation status. You will be able to gain information about the patient’s status through running a chemistry, complete blood count (CBC), packed cell volume (PCV), electrolytes, blood gases, prothrombin time (PT), and partial thromboplastin time (PTT). Even if we do not see abnormalities in these values on presentation, it is very helpful to have a baseline so we can continue to monitor trends. Clinicopathologic changes seen with heatstroke may include increases in serum hepatic and renal values, hyperlactatemia, hypoglycemia, thrombocytopenia, hemoconcentration, and prolonged PT/PTT. Electrolyte abnormalities can also be seen with heatstroke, including hypernatremia, hyperkalemia or hypokalemia.
Fluid therapy is warranted with heatstroke patients. A balanced, isotonic crystalloid should be used. Dextrose supplementation (2.5-5%) may be warranted, depending on what the blood glucose levels are; these should be frequently checked and adjusted as appropriate. The use of colloids should be limited to severe hypoproteinemic patients. The use of plasma transfusions may be warranted if the patient is coagulopathic (e.g., prolonged PT/PTT, etc.).
Cooling the patient should be done so in a controlled manner. Using a fan, placing cold wet towels between the inguinal region, placing the patient on a cool treatment table, or utilizing room temperature intravenous fluids can help. We want to avoid submersion in any ice cold baths, or direct ice packs as these may cause peripheral vasoconstriction and lead to further damage by shunting all the patient’s warm blood to their vital organs. Temperature should be monitored at least every 5 minutes and active cooling efforts should stop once you reach a temperature of approximately 103.5⁰F/39.7⁰C. The body may continue to cool once active cooling is stopped, resulting in significant hypothermia.
Patients suffering from heatstroke require intensive nursing care and close monitoring. You should be continually assessing the patient’s perfusion, hydration status, blood glucose, lactate, blood gases, blood pressure, urine production, vitals, ECG, and mentation. Nursing care is a big part of managing these patients as they are often non-ambulatory and time intensive.
Patients suffering from heatstroke have a mortality rate of 40-50%. Unfortunately, even despite aggressive supportive care, the prognosis may be grave. Quick and aggressive care are imperative to achieve the best outcome. It is often the secondary complications such as SIRS, sepsis, MODs, and DIC that lead to death or euthanasia.
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