Heat stroke: diagnosis and treatment

Article

Heat stroke is a life-threatening condition characterized by an elevated core body temperature and central nervous system dysfunction. Despite aggressive lowering of core body temperature and treatment, the pathophysiologic changes associated with heat stroke can lead to multi-organ dysfunction, which can be fatal.

Heat stroke is a life-threatening condition characterized by an elevated core body temperature and central nervous system dysfunction. Despite aggressive lowering of core body temperature and treatment, the pathophysiologic changes associated with heat stroke can lead to multi-organ dysfunction, which can be fatal.

Melissa Marshall

Recent research has shown that heat stroke results from thermoregulatory failure coupled with an exaggerated acute-phase response and altered expression of heat-shock proteins. This article will summarize the incidence, thermoregulation, predispositions, pathophysiology, treatment and outcome of heat stroke.

Definition and incidence

Hyperthermia in dogs can be pyrogenic or nonpyrogenic. Nonpyrogenic hyperthermia can result from exposure to high environmental temperature (non-exertional heat stroke) or from strenuous exercise (exertional heat stroke).

The classic definition of heat stroke is an elevated core body temperature

> 41 C in dogs, accompanied by central nervous system dysfunction. An alternative definition that might be more appropriate in veterinary patients is: a form of nonpyrogenic hyperthermia associated with a systemic inflammatory response, leading to a syndrome of multi-organ dysfunction.

Data on incidence of heat stroke in veterinary patients are lacking, but it is a commonly recognized condition in dogs, especially in hot, humid environments.

Quick cool-down: The author with a patient, providing treatment aimed at rapid cooling and support of body systems affected by heat.

Thermoregulation

Heat is generated by basal metabolism, muscular activity and oxidative metabolism.

The thermoregulatory center of the body is located in the hypothalamus and receives input from hypothalamic sensor cells that detect the temperature of the circulating blood and cutaneous sensor cells. A physiologic response is triggered when afferent sensors throughout the body converge in the hypothalamus and warm blood supplying the hypothalamus stimulates compensatory cooling mechanisms.

There are four modes of heat dissipation: evaporation, conduction, convection and radiation (see Figure 1).

Evaporative cooling involves the loss of water to the environment and cools the tissue/skin surface. Radiative cooling is the transfer of heat between the animal and the atmosphere. Convective cooling involves the movement of air across a surface carrying the heat away. Conductive cooling is the exchange of heat between two objects in direct contact with one another.

At ambient temperatures <32 C, convection, conduction and radiation maintain normothermia. Cutaneous vasodilation and increased cardiac output lead to increased cutaneous circulation, which promotes heat loss through radiation, conduction and convection.

Approximately 70 percent of the total body heat loss in dogs and cats is due to radiation and convection from the body surface. As environmental temperature increases, evaporative cooling is more important.

The initial compensatory mechanism is activation of the panting center in the brain as the nasal turbinates provide a large surface area for loss of water from the moist mucous membranes. Some heat loss occurs through sweating (foot pads) and excretion of feces and urine.

Nonpyrogenic hyperthermia occurs when heat production cannot be adequately dissipated by normal thermoregulatory mechanisms.

Predisposing factors

Predisposing factors for the development of heat stroke can be categorized into conditions decreasing heat dissipation and those increasing heat production.

Environmental conditions decreasing heat dissipation include increased ambient temperature, humidity, poor ventilation and water deprivation.

Patient factors include any condition or medication that impairs the ability of the normal homeostatic response mechanism, such as laryngeal disease, brachycephalic anatomy, cardiovascular disease, central or peripheral nervous system disease, obesity, hair coat, age and medications (diuretics, B blockers, phenothiazine derivatives). Excessive heat production can occur through extreme exercise, seizures, hormonal hyperthermia and drugs/toxicities.

Pathophysiology

Heat stroke causes an altered heat-shock response and an exaggerated acute-phase response that leads to the production of reactive oxygen species, increased vascular and intestinal permeability, culminating in direct cellular injury and enzyme destruction.

The central nervous system changes are characterized by cerebral edema, hemorrhage, infarction and cerebellar dysfunction. Experimental studies suggest that temperatures as low as 41 C may cause permanent brain damage, which may predispose patients to subsequent hyperthermic episodes.

The cardiovascular and pulmonary systems are compromised due to the peripheral vasodilation and decreased peripheral vascular resistance leading to hypovolemia. Excessive panting leads to hemoconcentration, sludging of blood flow and respiratory muscle fatigue.

Direct cardiac injury may cause myocardial hemorrhage and necrosis. Pulmonary edema may result from cardiac failure, damage to the vascular endothelium or hypoproteinemia. Damage to the gastrointestinal system is characterized by gut ischemia, which predisposes to bacterial translocation. Hepatic damage also has been seen and is described as hepatocellular vascular degeneration with centrilobular necrosis and cholestasis.

Acute renal failure due to tubular necrosis is a result of direct thermal injury, hypoxia and microthrombi. Hyperthermia induces the platelet activation and coagulation factors; combined with endothelial and platelet damage, this can lead to disseminated intravascular coagulation. Rhabdomyolysis occurs as a direct result of high temperature and may be increased in patients experiencing an exertional heat stroke.

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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