HEAT STROKE

VetSuite Veterinarians
Critical Care & Emergency Medicine

Heat stroke is a condition resulting from injury to multiple organ systems by the non-pyrogenic elevation of body temperature. In experimental models of heat stroke severe organ injury typically occurs when core temperatures exceed 43 C (109.4 F), but signs of heat stroke can occur at lower core temperatures when animals are not acclimated to higher environmental temperatures. Elevation of body temperature, which can produce organ injury and a syndrome very similar to heat stroke, can occur as a consequence of other disease processes (seizures, upper airway obstruction), but by definition, the term heat stroke should be applied to causes associated with high environmental temperatures.

DIAGNOSIS OF HEAT STROKE

ETIOLOGY AND RISK FACTORS

• Causes - Heat stroke is typically caused by exercise in a hot environment or by confinement in an environment where normal heat dissipation mechanisms are impaired (locked in hot car or building). At core temperatures over 109 degrees F, critical organ failure can develop.
• Risk factors
• Age - Puppies and kittens up to 6 months of age and geriatric animals are predisposed.
• Breed/genetics - Brachycephalic animals are at increased risk.
• Sex - No known risk
• Geographic/environmental - Heat stroke usually develops in dogs who are not acclimated to exercise in environments with high temperature and/or humidity, and in pets confined to hot environments where they cannot dissipate heat effectively (cars, buildings).
• Other medical disorders - Pets that are overweight or overexert during work or exercise; those that are ill or on certain medications; and those patients with current problems such as airway obstruction, fever, dehydration, heart disease and poor circulation are predisposed.

• Prevention - Heat stroke can be prevented by restricting exposure to high environment temperatures. Minimize activity on hot humid days, and limit sun exposure during the mid-day hours. Pets should be walked or exercised in the early morning or late evening during the coolest times of the day. Pets should be kept in a well-ventilated area. Animals should never be left in a car or confined in a small enclosed space with limited ventilation and no protection from high environmental temperatures for any reason at any time.

HISTORY AND CLINICAL SIGNS

• Species affected - Dogs and cats
• Presenting signs and historical problems - The most common symptoms of heat stoke include difficulty breathing or excessive panting, collapse, weakness, coma, vomiting or diarrhea, and an elevated body temperature.

PHYSICAL EXAMINATION FINDINGS

• General
• Attitude - Mental status can vary. Most animals are weak and lethargic, but some may be comatose or moribund.
• Body condition - Often normal
• Vital signs - Body temperature is usually elevated at least over 105 degrees Fahrenheit. In advanced cases or in excessively cooled patients, hypothermia may be present. Heart rate is often elevated and accompanied by weak/thready pulses. Excessive panting is typically present. Cardiac arrhythmias may be ausculted. Blood pressure is likely to be low in patients with shock.
• Mucous membranes - Often injected with rapid capillary refill time
• Hydration status - Often dehydrated
• Head and neck - Petechiae may be present
• Eyes - Scleral or conjunctival injection is often present. Petechiae may be seen.
• Oral cavity - Petechiae within the oral cavity may be present. Ptyalism is often found.
• Thorax (cardio-pulmonary) - Tachycardia is a common finding. Excessive panting is a hallmark of heat stroke and helps differentiate heat-related illness from fever. Lung sounds may be harsh if heat-induced pulmonary edema has occurred.
• Abdomen (gastrointestinal/urinary) - Bloody vomiting or diarrhea may be present. Abdominal discomfort or pain may be associated with such cases.
• Reproductive system - Unremarkable
• Lymph nodes - Unremarkable
• Integumentary system - Petechiae may be present
• Neurologic examination - The mental status can vary. In the early stages, the animal is often anxious and frantic. Eventually, if no treatment is sought, the animal progresses to coma and may present moribund. In severe cases, seizures may develop.
• Musculoskeletal examination - In advanced stages, weakness and difficulty in rising or moving may be noted.

DIAGNOSTIC STUDIES

• Special examination techniques - Blood gas evaluation may reveal severe metabolic acidosis accompanied by respiratory alkalosis (panting) or acidosis (moribund patient).
• Clinical laboratory tests
• CBC - The complete blood count may reveal hemoconcentration. Anemia and hypoproteinemia may be present if significant GI bleeding has occurred. The platelet count may be decreased, particularly if DIC is developing. A stress response in the leukogram is typically present, but severe leukopenia may be present if bacterial translocation from the GI tract has resulted in sepsis.
• Serum biochemical tests - Biochemical tests may reveal various abnormalities, depending on the stage of disease and which organ systems have been most affected. Abnormalities may be detected in the blood urea nitrogen, creatinine, glucose, sodium, potassium, chloride, creatine kinase, ALKP, ALT and AST.
• Urinalysis - Urinalysis may reveal glucosuria, proteinuria, myoglobinuria or casts if rhabdomyolysis or tubular injury has occurred.
• Coagulation profile - Tests of hemostatic function (activated clotting time or activated partial thromboplastin time, one-stage prothrombin time, fibrin degradation products, D-dimer or antithrombin III activity) should be evaluated to identify disseminated intravascular coagulopathy.
• Diagnostic imaging
• Radiographs (thoracic/abdominal) - Often not performed but are recommended if dyspnea is present.
• Electrodiagnostics
• ECG - Electrocardiogram is recommended if arrhythmias are ausculted.

DIAGNOSIS AND PROGNOSIS

• Differential diagnosis
• Activity
• Anxiety
• Drug intoxication (hyperactivity or seizures)
• Exercise
• Fever
• Hyperthyroidism
• Hypoglycemia with seizures
• Malignant hyperthermia (rare)
• Organic hypothalamic disease (rare)
• Seizure disorder
• Recommended tests - Complete blood count, biochemical and coagulation profiles and urinalysis.
• Summary of diagnostic criteria - Results may vary depending on the severity of the heat illness.
• Prognosis - If the body temperature is under 107 degrees Fahrenheit when treated, prognosis is good. If the body temperature is over 107 degrees, treatment is delayed, or the animal presents in a coma, prognosis is poor to grave.

TREATMENT OF HEAT STROKE

TREATMENT PRINCIPLES

Treatment of heat stroke must be individualized based on the severity of the condition and other factors.

INITIAL/HOSPITAL THERAPY

Treatment intensity is dependent upon the cause and magnitude of the heat illness. For pets with mild heat illness such as temperature increases less than 105 degrees F, therapy may include rest, a fan to enhance air circulation, fresh drinking water and careful observation. With temperatures over 105 degrees F, hospitalization and aggressive medical therapy are recommended.

One of the first priorities in treating hospitalized heat stroke patients is active cooling. External cooling in severely affected patients may interfere with ability to dissipate heat through convection by vasoconstricting peripheral tissues. Internal cooling by gastric lavage, enemas, peritoneal fluid administration or peritoneal dialysis is indicated in patients with core temperatures greater than 107. For patients with core temperatures between 105 and 107, external cooling methods such as cool water spray, fans to enhance air circulation, and careful placement of towel-wrapped ice packs over areas containing large blood vessels (neck, inguinal, axilla) should be instituted. Core temperature should be measured every 5 minutes to ensure that temperature is dropping appropriately. Cooling attempts should cease when core temperature drops to approximately 103 to prevent overcooling.

Fluids are administered concurrently with cooling therapy. Initially a rate of 90 ml/kg/hr (dogs) or 40 to 60 ml/kg/hr (cats) of crystalloid solution (Plasmalyte 148®, Normosol R®, Lactated Ringer's solution) should be administered by rapid infusion to effect (improvement of tachycardia, mucous membrane color, capillary refill time, pulse quality and blood pressure) via one or more large bore peripheral IV catheters placed in the cephalic vein. Low volume resuscitative strategies composed of synthetic colloids (hydroxyethyl starches or dextrans) may also be administered at a rate of 20 ml/kg/day (dogs) or 10 to 15 ml/kg/day (cats) by rapid IV infusion to effect. Hypertonic saline has also been utilized successfully in resuscitation, but the effect is short-lived unless combined with synthetic colloids. Following resuscitation, a fluid therapy plan that incorporates dehydration estimates, maintenance and ongoing losses should be calculated. Patients with significant myocardial dysfunction or remain hypotensive despite aggressive fluid resuscitation may require inotropic or vasopressor support.

Dexamethasone sodium phosphate or methylprednisolone sodium succinate have been recommended in the past, but there is no evidence to support any beneficial treatment effect.

Ventricular arrhythmias should be managed by ensuring that the factors contributing to the release of catecholamines are minimized (hypovolemia, hypoxia, pain, anxiety) and that aggressive potassium supplementation is performed to maintain high normal potassium concentration. Ventricular arrhythmias requiring treatment (R on T phenomenon, VPCs with multiple morphologies, accompanied by syncope, ventricular tachycardia present at a rate greater than 160 to 180 for more than 30 percent of observed rhythm) should be treated initially with up to 3 boluses of lidocaine (2mg/kg) within 3 to 5 minutes followed by a continuous intravenous infusion of 50 to 75 µg/kg/min. If the arrhythmia does not respond (either eliminated or maintained within the above parameters) then additional or alternate antiarrythmic drugs should be considered (procainamide, beta-blockers, magnesium).

If liver injury is severe, administration of fresh frozen plasma for active clotting factors may be helpful. Treatment for hepatic encephalopathy (oral lactulose and IV penicillin antibiotics) may be indicated if severe hepatic injury is present.

Acute renal failure is a relatively common complication. Urine output should be monitored closely. Patients with oliguria (<0.75 ml/kg/hr) or anuria (<0.25 ml/kg/hr) in the face of complete volume resuscitation and normal to elevated central venous pressures should be treated aggressively. Oliguric patients may benefit from administration of mannitol (0.25 to 2 g/kg IV) or furosemide (2 mg/kg IV (dogs) or 1 mg/kg IV (cats)). Mannitol should not be administered to anuric patients (unless as a final course of attempted therapy). Dopamine is no longer thought to have a significant therapeutic effect in the treatment of acute renal failure. Patients with increasing azotemia and/or declining urine production in the face of adequate fluid therapy and medical management outlined above have a grave prognosis and require dialysis as a rescue therapy.

Gastric ulceration may be treated with proton pump inhibitors and/or sucralfate. Intestinal mucosal breakdown allowing endotoxin and bacterial translocation contributes to the development of systemic inflammatory response syndrome (SIRS) and/or sepsis. Aggressive antibiotic coverage with broad spectrum antibiotics (cefoxitin, ampicillin and enrofloxacin, ampicillin/sulbactam) is warranted. Hypoglycemia should be treated with appropriate glucose supplementation. Cardiovascular complications of septic shock may be anticipated in severe cases.

Numerous neurological signs may be seen including seizures, cranial nerve abnormalities and altered consciousness. Widespread neuronal ischemia and intraparenchemal hemorrhage may contribute to these clinical signs. Control of seizure activity with anticonvulsants, control of intracranial pressure with mannitol, and supportive therapy (maintain perfusion, prevent hypotension, hypoxia, hypo/hyper-glycemia) are administered if needed.

Treatment of disseminated intravascular coagulopathy is controversial. Generally, supportive treatment with fresh frozen plasma is considered helpful (6 to 10 ml/kg over 4 hours given 2 to 3 times daily). Treatment with heparin is more controversial. Generally 75 to 100 IU unfractioned heparin SC every 8 hours is considered the appropriate dose if heparin is to be used.

LONG TERM/HOME THERAPY

If heat stroke is suspected, owners should be instructed to begin cooling measures at home. Spraying the dog with a cool water stream or placing a cool towel on the neck and inguinal area can help reduce body temperature. Ice should not be used since it may lower the body temperature excessively and may cause frostbite. Despite cooling at home, all affected animals should be examined.

FOLLOW-UP CARE

Re-evaluation is recommended in 3 to 7 days. For a sudden high temperature change, allow the pet to acclimate. Heat illness often occurs in the spring when the pet is not acclimated to the new temperatures. If traveling to a hotter climate, allow several days for the pet to become acclimated before attempting any vigorous exercise.