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HEAT STROKE
Shoshana J. Herzig, MD
July 17,2005
Introduction
Heat stroke is defined as severe illness with predominant CNS symptoms and a core temperature greater
than 40.5 degrees centigrade (105 degrees F) in the setting of a large environmental heat load that cannot be
dissipated. There are two types of heat stroke:
 Classic (nonexertional) heat stroke: Affects individuals with underlying chronic medical
conditions that either impair thermoregulation or prevent removal from a hot environment (ex –
cardiovascular disease, neurologic or psychiatric disorders, obesity, anhidrosis, extremes of age,
and drugs such as anticholinergics or diuretics).
 Exertional heat stroke: Generally occurs in young, otherwise healthy individuals who have
engaged in strenuous exercise in high temperature and humidity.
In a 2002 review in the NEJM, the definition was expanded to include an understanding of the
pathophysiology of this condition. The authors call heat stroke “a form of hyperthermia associated with a
systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy
predominates.” The high body temperature and CNS findings can cause a sepsis-like syndrome with
distributive shock, coagulopathy, and ultimately multisystem organ failure. In the United States, this
phenomenon is usually observed in the very young, the very old, the mentally ill, and the poor without
access to air conditioning.
Pathophysiology
The progression from heat exhaustion to heat stroke is caused by failure of thermoregulation, exaggeration
of the acute phase response, and alteration in heat shock response. It is unclear why some people have only
mild exhaustion while others progress to the systemic inflammatory response of heat stroke. Genetic
alterations in heat shock proteins, coagulation factors, and cytokines are postulated to play a role.
 Thermoregulation: In the normal host, a rise in blood temperature activates hypothalamic heat
receptors, which respond by activating mechanisms which increase delivery of heat to the surface
of the body. These mechanisms include:
1. Vasodilitation: Active sympathetic cutaneous vasodilitation increases blood flow to the
skin, leading to heat loss into the atmosphere. Keep in mind that as blood is shunted to
the skin, visceral perfusion is reduced, and, if severe enough, contributes to the
aforementioned organ dysfunction.
2. Sweating: If the air surrounding the surface of the body is not saturated with water,
sweat will vaporize and cool the body surface. This is why a humid environment,
saturated with water, predisposes to heat stroke. The act of sweating consumes a great
deal of salt and water from the body, and accordingly, thermoregulation is impaired in
those who are dehydrated, or salt-depleted.
3. Increased cardiac output: Cardiac output increases with heat exposure to up to 20L/min.
This output is shunted peripherally by the hypothalamus through peripheral vasodilation
and splanchnic vasoconstriction to increase heat loss.
Thus, people taking medicines that limit the myocardium’s ability to increase cardiac output,
diuretic induced salt and water depletion, and heart disease all interfere with cardiac
regulation of heat.
 Acute phase exaggeration: Based mainly on animal models, the splanchnic hypoperfusion that
accompanies high temperature works to decrease the immunologic barrier of the intestine,
allowing translocation of endotoxins. This may be the mechanism for the sepsis syndrome that
accompanies heat stroke. IL-6 and TNF levels correlate to severity of heat stroke. TNF and IL-1
are felt to play a role in the development of cerebral edema and to decrease cerebral perfusion.
These responses also change the hypothalamus’ ability to thermorgulate. Endothelial damage also
leads to increased vascular permeability and coagulation abnormalities leading to DIC.
 Heat shock protein attenuation: With high temperature, heat shock transcriptions factors are
activated that promote the production of heat shock proteins. These proteins (specifically HSP 72)
function to protect partially folded or incorrectly folded proteins from ongoing heat-induced
denaturation. Poor acclimatization to heat, old age, and some genetic polymorphisms may
attenuate the heat shock response.
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Clinical Presentation
Heat stroke is on the severe end of the spectrum of non-medication induced hyperthermic syndromes that
includes heat cramps and heat exhaustion (prostration). CNS dysfunction, a necessary criterion for heat
stroke, may range from mild confusion to frank coma. Headache, inappropriate behavior, slurred speech,
confusion, seizures, and hallucinations have all been described. Focal “hard” neurologic findings should be
absent.
Physical exam in classic heat stroke should reveal:
 Rectal temperature greater than 40.5 degrees centigrade
 Tachycardia
 Possible hypotension (25% of patients)
 Hyperventilation
 Flaccid muscles
 Lethargy, stupor, or coma
 Of note, the skin may be moist or dry depending on the underlying medical conditions, the speed
with which the heat stroke developed, and hydration status.
Lab abnormalities are initially more prominent in exertional heat stroke and include:
 Hemoconcentration
 Hypernatremia
 LFT elevation
 Rhabdomyolysis
 Hypercalcemia, hypophosphatemia, and hyokalemia. With exertional heat stroke, however, after
complete cooling one can see the opposite: hypocalcemia, hyperphosphatemia, and hyperkalemia.
 Respiratory alkalosis in classic variant
 Mixed respiratory alkalosis with lactic acidosis in exert ional
Both exertional and classic heat stroke may lead to multisystem organ failure, sepsis-like syndrome, ARDS,
seizures, coma, and disseminated intravascular coagulation. The kidneys, liver, pancreas, and intestine may
all be damaged during the acute phase of heat stroke. Though patients may survive these insults with
proper supportive care, about 20% of them go on to having permanent neurologic sequelae. The presence
of shock, DIC, and respiratory failure all portend a poor outcome. The speed at which heat stroke is
identified and treated impacts prognosis.
Treatment
Obviously, the mainstay of therapy is cooling. This is accomplished by applying cold water or ice to the
skin to decrease temperature while fanning the patient to utilize convection. Rectal and skin temperature
should be monitored. Peritoneal, gastric, and rectal lavages with cold water have also been described as
treatments. Caution must be taken with cooling techniques, as reduction of skin temperature to below 30
degrees centigrade can evoke cutaneous vasoconstriction and shivering, both of which increase body
temperature. Therefore, once the skin temperature drops to 30 degrees C, the patient should be massaged,
sprayed with 40 degree centigrade water, or blown with hot moving air. These heating techniques may be
applied alternating or along with cooling measures. Along with cooling, oxygen and crystalloid are the
mainstays of therapy. Seizures are treated with benzodiazepines; respiratory failure is managed with
intubation; hypotension is treated with fluids and pressors. Rhabdomyolysis is treated with hydration, fluid
expansion, diuretics, and bicarbonate. In general, normal ICU care is provided along with cooling
measures. Future therapies include activated protein c and perhaps NSAIDs (increase transcription of heat
shock proteins). More novel anti-inflammatories are also being studied.
Prevention
For both classic and exertional heat stroke prevention, the following advice should be given to patients:
 Build up outdoor activity slowly to help acclimatization
 Schedule activities at cooler times of day, or reduce level of activity
 Drink H20
 Eat salty food
 Use air conditioning or go to air conditioned space
 If no air conditioning, take multiple cold/cool showers or baths
 Do not leave children or elderly in cars unattended
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Bibliography
Bouchama, A et al. Heat Stroke. NEJM. June 20, 2002. Vol 346, No 25. 1978-88
Dematte, JE et al. Near-Fatal Heat Stroke during the 1995 Heat Wave in Chicago. Ann Internal Med.
August 1, 1998; 129:173-181
Harrison’s Principles of Internal Medicine.
Beth Israel Deaconess Medical Center Residents’ Report