Page 111 - JSOM Summer 2019

“When pestilence stalks the streets, men are on the fearful Thermoregulation
watch for its approach and are prepared, at least for a time, Body heat is produced by physiological and behavioral pro-
to combat the destroyer; if they fall, it is with a broken sword, cesses (e.g., metabolism and exercise) and can be absorbed by
and with their armor pierced. But sunstroke strikes down its the body from the environment. Heat dissipation depends on
victim with his full armor on. Youth, health, and strength the body’s physiological mechanisms (e.g., sweating, radiation,
oppose no obstacle to its power; nay, it would seem in some circulation) and environmental conditions (e.g., temperature,
instances, to seek out such as these, as if boldly to flaunt its humidity, solar radiation). When the balance is upset and heat
power, and in the very glare of day to deal its final blow. . . . production exceeds heat dissipation, a rise in body tempera-
I know of no other place other than the field of battle where ture will occur.
such sudden destruction of human life occurs.” 8
Body temperature is maintained by a complex series of inde-
The purpose of this report is to present the pathophysiology, pendent temperature sensitive loops involving ion channels
epidemiology, diagnosis, treatment, and prevention of EHS. and neurons, but the hypothalamus is considered a major
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Because of the limitations of the literature, it will sometimes thermoregulatory center in the body. The anterior hypothala-
be necessary to refer to the broader concept that includes both mus regulates body temperature at or near a “balance point”
classic heat stroke and EHS, but these cases will be noted. temperature of 37°C (99°F) via specialized neurons. These
neurons monitor the temperature of the blood perfusing the
anterior hypothalamus. An increase in blood temperature of
Definitions of EHS
<1°C will initiate a series of adjustments aimed at returning
Several definitions of EHS have been proposed that differ the body temperature to near 37°C (99°F). Peripheral (skin)
slightly, but share common characteristics. Anderson et al. thermal receptors (free nerve endings) also relay informa-
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defined EHS as a body core temperature >40.6°C (105°F), tion about heat to the hypothalamus. Heat can be dissipated
profound central nervous system dysfunction (disorientation, through radiation, conduction, convection, or evaporation,
delirium or coma), and moist skin experienced during heavy but evaporation through sweating is the major defense mech-
physical activity in the heat. Common complications cited in- anism against overheating. Sweating is initiated by the hypo-
cluded rhabdomyolysis, acute renal failure, and DIC. Bouch- thalamus in response to blood heating. There are 2–4 million
ama and Knochel characterized heat stroke as severe illness sweat glands distributed across the body surface and they
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characterized by core temperature >40°C (104°F) and central secrete a hypotonic solution (0.2–0.4% NaCl) that, when in
nervous system abnormalities such as delirium, convulsions, contact with heated skin, evaporate causing a cooling effect.
or coma resulting from exposure to environmental heat and Assuming low humidity (i.e., that the air around the body is
strenuous physical exercise. They noted that heat stroke it is as- not saturated with moisture) each 1L of evaporated sweat
sociated with systemic inflammation leading to multiorgan dys- transfers about 600kcal of heat to the environment. Water
function in which brain damage predominates. Yeo described lost through sweat can induce dehydration and impair ther-
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heat stroke as a “systemic inflammatory response with a core moregulation if not replaced. In addition to sweating, sym-
temperature of >40.6°C (105°F), most often accompanied by pathetic cutaneous vasodilation increases the blood flow to
mental status changes (anxiety, confusion, bizarre behavior, loss the skin up to 8L/min. This moves heat from the body core
of coordination, hallucinations, agitation, seizures, and often to the body surface where it can be dissipated. This periph-
coma) and varying degrees of organ dysfunction (acute renal eral vasodilation is complimented by a vasoconstriction in the
failure, liver failure, brain injury, respiratory failure, ischemic internal organs, especially the kidneys and gut. Loss of water
bowel injury, pancreatitis, gastrointestinal bleeding, thrombo- and electrolytes coupled with blood flow shunted to the skin
cytopenia, and disseminated intravascular coagulation).” The can deprive the central organs, especially the intestines and
Japanese Association for Acute Medicine (JAAM) has collected kidneys. Elevated body temperature also has other cardiovas-
data on heat-related illness from a nationwide registry since cular effects including tachycardia, increased cardiac output,
2006. They developed criteria for heat stroke in 2014, which and increased ventilation. Heat shock proteins are produced
they revised in 2016. The 2016 criteria included exposure to in virtually all cells during early exposure to heat and these
high environmental temperature with at least one of the fol- provide some protection against the denaturing of proteins,
lowing: 1) a Glasgow Coma Scale score ≤14, 2) creatinine arterial hypotension, and cerebral ischemia. 5,6,10,15,16
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or total bilirubin ≥ 1.2mg/dL, and 3) a JAAM DIC score ≥4.
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The DIC score is based on several criteria including platelet Heat Stroke Pathophysiology
count, prothrombin time, fibrin/fibrinogen degradation, and a The current understanding of EHS is that it is triggered and ex-
systemic inflammatory response syndrome (based on tempera- acerbated by high environmental temperatures and/or physical
ture, heart and respiratory rate, white cell count). What is activity, but the major pathological effects are due to septice-
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common to many of these definitions is 1) a core temperature mia and the resulting inflammation and blood coagulation. As
>40°C (104°F), 2) mental status changes (coma, confusion, be- noted above, when the body experiences heat stress blood is
havior changes), 3) inflammation, 4) multiorgan failure, and 5) shunted to the skin to aid in cooling but blood flow to the gut
DIC (i.e., small blood clots throughout the bloodstream). is reduced. The reduction is gut blood flow is proportional to
exercise intensity but can be >80%. This reduced blood flow
results in hypoxia, free radical production, acidosis, and other
Thermoregulation and EHS Pathophysiology
cellular dysfunctions that induce an increase in the permeabil-
To understand the pathophysiology of EHS, it is useful to ity in the gastrointestinal mucosa. This increased permeabil-
review the normal physiological processes involved in ther- ity results in excessive leakage of endotoxins into the portal
moregulation. These processes can be overwhelmed in some circulation (i.e., circulation from the intestines to the liver).
individuals who produce and/or absorb heat at a rate that ex- These endotoxins (primarily lipopolysaccharides) are nor-
ceeds the body’s ability to dissipate it. mally sequestered in bacteria in the gut space where they are

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