HYPERTHERMIA SYNDROMES-2: HEAT STROKE

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HEAT STROKE is caused when thermoregulatory mechanism fails to dissipate heat in response to thermal stress.

It was first described by Roman in 84 BC, but only in 1940, it was recognized that heat stroke can result in multiorgan failure.

Heat stroke is defined as a core body temperature usually in excess of 40ºC (104ºF) with associated central nervous system dysfunction in the setting of prolong environmental heat exposure.

During high environmental heat exposure, blood flow to the skin increases many fold. However, when the ambient temperature is higher than the body’s core temperature, heat dissipating mechanism (conduction, convection and radiation) becomes ineffective.

Environmental conditions also effect evaporative cooling. A water vapor pressure gradient is basic requisite to sweat; to evaporate and release heat, into the environment. In high humidity (relative humidity >75 percent), evaporation becomes ineffective for transferring heat and may result in minimal or absent sweating.

Heat stroke can be divided into classical heat stroke and exertional heat stroke.  

CLASSICAL HEAT STOKE occurs in sustained environmental heat exposure. It affects more commonly elderly individuals (over 70 years) with underlying comorbidities that impair, mobility to escape a hot environment, ability to access hydration or attempts at cooling. Several physiologic mechanisms to cope with an increased environmental heat waves, are impaired in elderly patients. This includes reduced ability to deliver heat to the skin, reduced epidermal area available for heat transfer, and impaired vasodilation of the skin. Use of anticholinergic drugs, for various indication in elderly population, further increases the risk of heat stroke.

EXERTIONAL HEAT STROKE occurs in young, healthy individuals, who engage in strenuous physical activity, for prolong period in hot and humid environment. Typical patients are athletes and military recruits in basic training. During physical exertion, increased metabolic demand and decreased intravascular volume (dehydration) further complicates the heat dissipating mechanism, resulting in failure of the thermoregulatory system. 

Risk factors for exertional heat stroke are strenuous physical activity, lack of acclimatization, obesity, poor physical heath and dehydration. Drugs like anticholinergics, antihistaminics, decongestants, diuretics, tricyclic antidepressants, antiepileptics increase the risk of exertional heat stroke.

Heat stroke has high mortality, ranging from 21 to 63 percent. It correlates with degree of temperature elevation, time to initiation of cooling measures, and the number of organ failure. Studies have revealed that the risk of death increases substantially in patients with coma, hypotension and anuria.

Management starts with ensuring airway protection and optimizing breathing and circulation. Endotracheal intubation and mechanical ventilation should not be delayed, if required. 

Rapid fluid resuscitation with cold isotonic saline is the answer, to optimize intravascular volume and organ perfusion. Vasopressors (alpha adrenergic agonist) may be required, but should be avoided, as the resulting vasoconstriction decreases heat dissipation. 

Therefore intravascular volume should be optimized before starting vasopressors. Minimally invasive cardiac output monitoring (flow trac, volume view, PiCCO, EDM) would be very helpful in management.

Cooling measures should be started immediately, guided by continuous core temperature monitoring with esophageal or rectal probe. Cooling measures should be stopped, once core temperature decreases to 38 -39˚C, to avoid iatrogenic hypothermia.

Cooling employing evaporation, like spraying lukewarm water to moist skin, and blowing air with fans, is an easy, effective, non-invasive method and does not interferes with other simultaneous intervention in ICU.

Other method like applying ice back to neck, axilla and groin is also an efficient method, but poorly tolerated as may lead to shivering and paradoxically increase body temperature.

Immersion in ice cold water is a rapid method of cooling, but often not practical, in mechanically ventilated patient in ICU.

To prevent shivering by any of the cooling method, patient should be optimally sedated, and intermittent neuromuscular blocker agents should be used.

Cold saline should be used for resuscitation, as an adjunct to cooling method, as is cooling blankets and cool environment.

Gastric, thoracic and peritoneal lavage with cold saline is invasive method of cooling, and ensure rapid cooling, but have their inherent complications.

Antipyretics like acetaminophen is not effective in reducing temperature and may aggravate hepatic dysfunction, therefore should be avoided.

Early diagnosis and management of other complication like seizures, electrolyte disturbances, ARDS, arrhythmia, cardiac dysfunction, acute kidney injury, hepatic dysfunction, rhabdomyolysis and DIC is important to decreased mortality.