Heat stroke: diagnosis and treatment - DVM
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Heat stroke: diagnosis and treatment
Quick response, proper cool-down techniques essential to favorable outcome


DVM360 MAGAZINE
Volume 39, Issue 8

Clinical presentation and laboratory findings

A complete physical examination and thorough history should be performed on all cases, because certain changes have been associated with a poor prognosis. The exam will help determine if the hyperthermia is nonpyrogenic in origin. These patients should not be excluded from the suspicion of heat stroke if the history and clinical signs fit.

The temperature is typically greater than 41 C (106 F), although some patients may have normal temperatures at the time of presentation if the owner has already begun external cooling. The heart rate and pulse quality are variable, depending on state of shock ranging from bounding to absent pulses and tachycardia to bradycardia. Arrythmmias may be ausculated.

Tachypnea is common, and the patient may or not be dyspneic with stertorous breathing. With extreme neurologic dysfunction, apnea may occur. The mucous membrane color and capillary refill time are variable.

Initially these patients are hyperemic or have darkened mucous membranes due to systemic vasodilation and increased cardiac output, but can progress to pale or cyanotic mucous membranes with an absent CRT. Icterus may be noticed due to hemolysis or hepatic dysfunction. Patients may have altered mentation, seizures, be blind or comatose. Integument exam may reveal petechial hemorrhages or ecchymosis.

Initial assessment of patients with clinical signs related to hyperthermia should include: PCV/ts, blood glucose, electrolytes and blood urea nitrogen and/or creatinine.

Thorough laboratory work should occur early during resuscitation and include complete blood count, coagulation testing, chemistry and urinalysis.Complete blood-count changes seen can include thrombocytopenia and hemoconcentration.

Chemistry: hypoproteinemia/hypoalbuminemia, hypoglycemia, elevated alanine aminotransferase, alkaline phosphatase and total bilirubin, increases in creatinine phosphokinase, which may peak 24 to 48 hours after the insult, elevations in blood urea nitrogen and creatinine.

Various electrolyte changes are seen, such as hypernatremia, hyperkalemia and respiratory alkalosis and/or metabolic acidosis. Urinalysis may reveal casts indicating tubular damage, proteinuria and myoglobinuria. Coagulation testing may show prolongation in clotting times and elevations in fibrinogen degradation products.

Treatment

The goal of emergency treatment is to safely lower core body temperature as soon as heat stroke is suspected. This includes instructing owners to begin the cooling process before the patient arrives at the hospital. This can be accomplished by tepid water baths/hosing and fans. The use of ice baths is discouraged because it can cause peripheral vasoconstriction, which will impair heat dissipation. Additionally, leaving a cool towel on a patient will impair radiative, conductive and convective cooling once the initial conductive cooling has occurred.

Additional cooling mechanisms in hospital include cool water enemas and intravenous fluids. Cooling should be stopped once the temperature reaches 39.5 C (103 F) to avoid hypothermia and shivering, because temperature will continue to fall once cooling measures have stopped.

If dyspnea or cyanosis are observed on exam, upper airway disease should be suspected and appropriate treatment instituted (e.g., tracheostomy, sedation and intubation and supplemental oxygen).

Once cooling measures have been instituted and the airway is secure, therapeutic goals include volume resuscitation with isotonic crystalloids at a shock dose of 60ml/kg for cats and 90ml/kg for dogs.

Colloid resuscitation is indicated in patients with hypoproteinemia. If colloid resuscitation is used, the dose of crystalloid should be reduced by approximately 40 percent. Crystalloid and colloid fluid therapy should be continued based on the patient's cardiovascular and hemodynamic status.

Other factors taken into account should include the patient's need for oncotic support, glucose supplementation, electrolyte and acid-base abnormalities. Additional therapy should be directed at the affected body systems. Seizures should be treated appropriately with anti-convulsants (diazepam, phenobarbital, propofol). Cerebral edema may be treated with mannitol or corticosteroids. Corticosteroids also would benefit a patient with upper airway edema.

The gastrointestinal tract should be protected and antibiotic therapy instituted if bacterial translocation is suspected. The patient should be closely watched for the development of pulmonary edema, and treatment should be based on underlying cause (cardiogenic vs. noncardiogenic).

Nonsteroidal anti-inflammatory agents should be avoided due to increased risk of gastrointestinal bleeding, decreased platelet function and impaired renal function. Cardiac output and perfusion should be maximized by treating any underlying cardiac condition with appropriate medications (anti-arrythmics, positive inotropes) and with vasopressors once adequate intravascular volume is obtained.

Serial examinations and lab work are of utmost importance to quickly identify any complications such as DIC and renal failure.

Outcome/prognosis

There are limited studies evaluating the prognosis and outcome for patients with heat stroke. The largest study identified an overall mortality rate of 50 percent. Risk factors for death in this study included hypoglycemia and prolonged PT and PTT at admission, elevated creatinine at 24 hours, delayed admission to the hospital of >90 minutes, seizures and obesity.

Heat stroke can result in multi-organ dysfunction that can be life-threatening.

The key to successful treatment includes rapid recognition and protocols aimed at rapid cooling and support of the affected body systems.

Collection of laboratory values helps determine the prognosis. Prevention of heat stroke relies on educating clients about the disease, especially for those patients deemed at risk.

Melissa Marshall, DVM, Dipl. ACVECC, received her veterinary degree from Tufts University in 1999. She completed a rotating internship in small-animal medicine and surgery at Animal Specialty Group and her residency in emergency and critical care at Angell Memorial Animal Hospital. She joined Red Bank Veterinary Hospital in 2005.


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