Heatstroke

Author: Erik Zager, DVM, DACVECC (Head of Critical Care)
Philadelphia Animal Specialty & Emergency

Heat stroke is an emergency condition that is life threatening if not treated promptly and aggressively. Heat stroke develops when hyperthermia induces thermal tissue injury, coagulopathy, and changes to immune modulators. Coagulopathies result from the denaturing of coagulation proteins or tissue damage exposing tissue factor. Effects on immune modulation include release of cytokines or bacterial translocation from GI tract and endotoxemia. The combination of these insults will lead to a systemic inflammatory response syndrome (SIRS), which if not addressed with aggressive treatment, will lead to multi-organ failure and death.
 

Heat stroke occurs secondary to high body temperatures. The combination of the degree of hyperthermia and duration that dictates the degree of insult. Heat shock proteins will develop over time when exposed to heat to help protect the body from heat injury. However, if the degree of heat stress is too high, or a patient has not been acclimatized the body cannot compensate and there will be maladaptive cellular responses. Temperatures above 109 will cause necrosis resulting in even more inflammation and worse organ injury.
 

Early in heat stress, the body undergoes physiologic alterations for self-protection:

●       Cutaneous vascular dilation to increase heat dissipation

●       Splanchnic venous constriction to increase effective circulating blood volume

●       Cardiac output and efficiency increases

●       Metabolic rate reduces

●       Thirst increases

As heat stress worsens, maladaptive responses in the body start to take place:

• As cutaneous vascular beds continue to dilate, circulation to the gut decreases 

  • Tight junction breakdown allows for bacterial translocation

• Cerebral blood flow decreases

• Immune dysregulation occurs leading to SIRS

As cerebral blood flow decreases, cerebral hypoxia occurs. Inflammation in the brain results in edema and intracranial hypertension, reducing cerebral perfusion pressure. Cerebral oxygen demand also increases with heat stress, which leads to further severe brain injury.
 

Coagulopathy is also a hallmark of heat stroke. Thermal injury to the endothelium leads to platelet aggregation, fibrin deposition, microvascular thrombosis and perfusion injury. This contributes to DIC and multi-organ dysfunction.
 

Muscle injury releases myoglobin which is filtered in the kidneys and results in acute kidney injury.

Predisposing factors for heat stroke include patient dependent and patient independent factors. Patient dependent factors include:

• Brachycephalic conformation

• Obesity

• Pre-existing airway disease such as laryngeal paralysis

• Exercise or stress

• Thick furcoats
   

Patient independent factors include:

• External heat

• Humidity

• Access to water

• Poor ventilation

• Toxins causing seizures or muscle tremors

The history of heat stroke patients often includes an inciting factor, such as exercise, being stuck in a vehicle, seizures/tremors, breathing difficulties, etc. It is important as to any at-home cooling that may have occurred, as this may alter the body temperature at presentation. In some of these cases, body temperatures may have even returned to normal by the time of presentation. These cases still need to be treated for sequelae of heat stroke.

Physical Exam findings that are frequent with heat stroke:

• Body temperatures is high

  • In up to 14% of patients, body temperatures can be normal or low (due to owner cooling measures)^[1]

• Tachycardia is common with 25% of patient having other arrhythmias

  • Ventricular premature complexes (VPCs) common

• Disorientation, obtundation, stupor, or coma

• Petechiae or ecchymosis

• Vomiting with possible hematemesis

• Diarrhea with possible melena or hematochezia

• Tachypnea or dyspnea

Blood work and other point of care findings

• CBC may show anemia from hemorrhage, thrombocytopenia from DIC, elevated WBC counts from inflammation

  • Blood smear evaluation should be performed to confirm platelet count and to look for evidence of nucleated red blood cells which are common in heat stroke^[2]

• Coagulation testing can show prolongations of PT or aPTT

• Chemistry panel can show evidence of liver injury, acute kidney injury, high protein from hemoconcentration, hyperkalemia from kidney injury, or hypernatremia from fee water loss

Aggressive treatment is needed in heat stroke to avoid death or organ dysfunction. The most important parts of initial treatment includes active cooling. This can be done in multiple ways, but the safest and most effective way in veterinary medicine is evaporative cooling, using cool water applied to the patient along with fans to increase evaporation. If evaporative cooling is not enough to bring the body temperature down, there are invasive cooling methods, but they come with risks

• Cold water lavage of colon

  • Can interfere with rectal temperature taking, making it difficult to know when to stop active cooling

• Cold water infusion into stomach

  • Requires sedation and can result in aspiration

• Sterile saline infusion of peritoneam or bladder^[3]

  • Can result in infection, organ injury, bladder rupture

Respiratory support may be needed in patients with severe neurologic dysfunction, or patients with compromised airways such as brachycephalic patients, patients with laryngeal paralysis, or patients with laryngeal edema. Early intubation of these patients can be life-saving.

• Sedation with opioids, benzodiazepines and ketamine can facilitate intubation with minimal depression of cardiac output.

• Propofol or alfaxalone can be used cautiously with monitoring of blood pressure and ventilation

• Dexmedetomidine should be avoided due to large drops in cardiac output
   

Neurologic support includes control of seizure activity with anticonvulsants such as benzodiazepines, levetiracetam, or phenobarbital. Neurologic dysfunction may be in part secondary to hypoglycemia, which should also be corrected with IV dextrose boluses or CRIs. The body should be angled using flat boards to achieve head elevation of 15 degrees without kinking the neck. Mannitol or hypertonic saline may be beneficial for cerebral edema, but caution should be used to prevent hypernatremia, or hypovolemia from osmotic diuresis.
 

Summary of treatment goals:

• Manage body temperature with active cooling

• Manage hypovolemia with aggressive iv fluid therapy

• Monitor for coagulopathy and treat with fresh frozen plasma when indicated

• Monitor for acute kidney injury and treat with iv fluid therapy, or in severe cases, consider dialysis

• Manage neurologic injury with hyperosmotic agents such as mannitol and hypertonic saline in conjunction with fluid therapy. Give anticonvulsants if seizures are present.

The overall prognosis for heat stroke in dogs is 50% with most non-survivors dying within 24 hours.^[4]

^[1] Bruchim, Yaron, et al. "Heat stroke in dogs: a retrospective study of 54 cases (1999–2004) and analysis of risk factors for death." Journal of veterinary internal medicine 20.1 (2006): 38-46.

^[2] Aroch, I., et al. "Peripheral nucleated red blood cells as a prognostic indicator in heatstroke in dogs." Journal of veterinary internal medicine 23.3 (2009): 544-551.

^[3] Bynum, G., et al. "Peritoneal lavage cooling in an anesthetized dog heatstroke model." Aviation, space, and environmental medicine 49.6 (1978): 779-784.

^[4] Bruchim, Yaron, Michal Horowitz, and Itamar Aroch. "Pathophysiology of heatstroke in dogs–revisited." Temperature 4.4 (2017): 356-370.