Danielle Berube, DVM, DACVECC
As we head into the warm summer months, we need to be prepared for an influx of patients suffering from heat stroke. It is important to remember that although brachycephalic breeds and dogs with laryngeal paralysis have an increased risk, any patient can suffer from heat stroke in the right conditions. It is also important to keep in mind that patients can present with a normal body temperature, especially if the owners have started active cooling.
Heat stroke (106-109 ͦF) occurs when the heat load exceeds the patient’s ability to dissipate heat and is defined as “hyperthermia associated with systemic inflammatory responds leading to a syndrome of multiple organ dysfunction in which encephalitis predominates.”
Dogs and cats have four ways to dissipate heat: radiation, conduction, convection, and evaporation. Radiation and convection occur through vasodilation and increased cardiac output. Conduction occurs through contact with cool surfaces, and evaporation occurs with heat loss from the respiratory tract during panting. Evaporation is the main mechanism of heat loss when the ambient temperature is equal to or greater than body temperature and explains why brachycephalic patients and patients with laryngeal paralysis are less tolerant of heat.
Physical Exam Findings and Clinical Signs:
Patients can present with normal physical exam parameters, especially if cooling methods were started before presentation. Common exam findings include increased, loud, or noisy breathing, vomiting, diarrhea (including hemorrhagic diarrhea or mucosal sloughing), compensatory tachycardia, ventricular arrhythmias, and bruising/ecchymosis. Patients can also have neurologic abnormalities, including cortical blindness and head bobbing/tremors, which can resolve with treatment.
Diagnostics should be performed and rechecked/monitored frequently.
Although hemoconcentration (dehydration) is frequently reported, the most common abnormality is the presence of nucleated red blood cells (NRBCs). This not only supports the diagnosis of heat stroke but can also be used as a predictor of death. A value of 18+ NRBCs per 100 leukocytes seen at presentation has a sensitivity of 91% and specificity of 88% for predicting death. The number of NRBCs typically decreases over the first 24 hours. Thrombocytopenia can also be seen and may indicate the presence of DIC.
Azotemia can be seen as a result of dehydration (prerenal) or direct renal injury (acute kidney injury) and should be interpreted in light of the urine-specific gravity. Hypoglycemia can be seen as a result of increased utilization or early sepsis. Hypernatremia is a result of free water loss (panting, vomiting, diarrhea). Additional values to be monitored include the ALT and creatinine kinase, which typically peak within 24 hours.
Urinalysis (not by cystocentesis due to potential DIC and before IV fluids):
A urinalysis is recommended to evaluate urine-specific gravity (prerenal vs. renal azotemia) and other signs of acute kidney injury. Proteinuria indicates renal damage, and the presence of glucose can indicate proximal renal tubular damage. Hemoglobinuria indicates muscle damage and can lead to further kidney injury, and the presence of RBC can indicate renal damage or a coagulopathy.
Coagulation testing identifies DIC (prolonged PT/PTT and thrombocytopenia), which is due to the consumption of clotting factors during the initial hypercoagulable state.
Treatment and Monitoring:
Patients are often in critical condition and require prolonged hospitalization with 24-hour aggressive supportive care, monitoring, and frequent reassessment.
Mechanisms of cooling take advantage of patient heat dissipating mechanisms and should be discontinued when body temperature reaches 103 ͦF to prevent rebound hypothermia. Wetting the patient’s entire body with cool water and using a fan appears to be the most effective cooling method. The use of ice packs or ice water should be avoided as they can cause peripheral vasoconstriction and decreased body cooling (unless frequent muscle massage is performed). The use of gastric lavage, enemas, peritoneal lavage, and whole-body alcohol baths all have risks of complication, and the wetting of the paw pads with alcohol has not been shown to decrease temperature.
Patients often present in hypovolemic shock. Balanced electrolyte fluid boluses up to 90 ml/kg should be given in 1/4 increments with frequent reassessment and titration to affect. If tissue perfusion and blood pressure do not improve, synthetic colloids (vetstarch, hetestarch), blood products (plasma), or vasopressors (norepinephrine, dopamine, dobutamine) may be needed.
Oxygen support should be provided until the patient can maintain normal arterial oxygenation. Monitoring of respiratory rate/effort, thoracic auscultation, arterial blood gas, and/or pulse oximetry should be performed frequently.
Monitoring of urine production (indwelling urinary catheter with urine measurement every 1-4 hours) and electrolytes/renal values (every 4-24 hours) should be performed. A urine production of at least 2 ml/kg/hr and a mean arterial pressure of 80 mmHg should be maintained. If renal values worsen or if patients progress to oliguric/anuric renal failure, then hemodialysis or peritoneal dialysis are likely needed.
The use of H2 blockers and sucralfate (if not vomiting) can help protect the intestinal tract from further damage. The use of broad-spectrum antibiotics in patients with hemorrhagic diarrhea is recommended to help prevent sepsis from bacterial translocation.
Central Nervous System:
The correction of hypoglycemia with a dilute dextrose bolus followed by a constant rate infusion of 2.5-5% dextrose should be administered. Poor perfusion/hypovolemia/hypotension should be corrected to improve CNS perfusion. If neurologic signs do not improve once perfusion parameters and hypoglycemia are corrected, mannitol (0.5-1 gram/kg IV over20-30 min) should be considered to treat cerebral edema.
Monitoring of PT/PT, platelet count, and D dimers should be monitored throughout treatment. The use of plasma products should be considered in patients with prolonged coagulation times
Mortality has been reported to be 36-50%. Findings that have been associated with a worse prognosis include:
• Decreased cholesterol
• Increased total bilirubin
• Decreased albumin
• Ventricular arrhythmias
• Increased creatinine
• Longer delay from incident to treatment
• Prolonged PT/PTT
• Disseminated intravascular coagulation (DIC)
• Increased number of nucleated red blood cells
– Danielle Berube, DVM, DACVEEC
Drobatz, Kenneth J. Chapter 149 Heat stroke. In: Small Animal Critical Care Medicine 2nd edition. Silverstein and Hopper; Saunders, an imprint of Elsevier Inc. 2015 Pages 795-799.
Powel, Lisa. Canine Heat Stroke. NAVC Clinician’s Brief. August 2008 Pages 13-16