Heat Stroke

Fig. 4.1

Extrinsic and intrinsic risk factors of exertional heat illness. (From Lopez and Jardine [2], with permission. Figure courtesy Douglas J. Casa, PhD and Miwako Suzuki, KSI Summer Fellow; Korey Stringer Institute)

../images/471692_1_En_4_Chapter/471692_1_En_4_Fig2_HTML.png — Fig. 4.2

Predisposing factors associated with fatal (n = 6) and nonfatal (n = 128) cases of exertional heat stroke. (From Rav-Acha et al. [3], with permission)

Typically, extrinsic risk factors (e.g., required clothing/protective equipment, environmental conditions, peer and/or organizational pressure, etc.) are non-modifiable in that these risk factors may not be avoidable during physical activity, particularly in hot environmental conditions. For example, in forward deployment in military operations or road construction work, it may not be possible to alter the amount of clothing worn or perform physical activity during cooler parts of the day depending on the objectives at hand. Intrinsic risk factors (e.g., acclimatization status, cardiorespiratory fitness, hydration status, etc.), on the other hand, are those that are typically modifiable in that these risk factors can be addressed to reduce overall risk. Implementation of a heat acclimatization protocol at the outset of athletic/military training and occupational work that allows progressive and gradual exposure to thermal stress to improve thermal tolerance is an example of one method to address one of the intrinsic risk factors associated with EHS. The latter example has been shown to be extremely effective in reducing EHI risk; data examining the incidence of EHI in secondary school athletics in the United States that have mandated heat acclimatization into preseason training has shown a 55% reduction in EHI risk, which provides compelling evidence on the effectiveness of such measures [4].

Pathophysiology

Homeostatic control of body temperature is tightly controlled by the preoptic portion of the anterior hypothalamus; afferent input from thermoreceptors in the skin via the spinal cord directs the appropriate efferent signals to the body to maintain the body’s set point of approximately 37 °C. During exercise, metabolic activity produces body heat (additional body heat is gained if environmental conditions exceed skin temperature), prompting the stimulation of sympathetic cutaneous vasodilation and visceral vasoconstriction which permits an increased skin blood flow, cardiac output, and sweating responses for evaporation of sweat from the skin’s surface to dissipate body heat [5, 6]. At the cellular level, the physiological response to thermal stress involves various cytokines (e.g., tumor necrosis factor (TNF) α, interleukin-1 (IL-1), and interleukin-6 (IL-6)), heat shock proteins (HSPs), endothelial cells, leukocytes, and epithelial cells that act to protect the body from injury, mediate the body’s inflammatory response, promote tissue repair, and mitigate the leakage of endotoxins across the intestinal barrier [7–14].

In EHS, there is a breakdown in the homeostatic control of internal body temperature , setting off a cascade of events leading to thermoregulatory failure (Fig. 4.3) that is triggered by endotoxemia originating in the gut [5, 6, 15–17]. The cardiovascular response to thermal stress, the redistribution of blood from the visceral organs to the skin, permits the hyperpermeability of the tight junctions of the endothelium in the intestines as a result of increased levels of hypoxia, thus allowing the infiltration of endotoxins into the systemic circulation [16, 18]. The ensuing systemic inflammatory response promotes a further increase in body temperature mediated by the increase in circulating cytokines and release of nitric oxide and endothelins [5, 6, 12]. Combined with the systemic inflammatory response and cytotoxicity, disseminated intravascular coagulation, a common occurrence in EHS, can contribute to prolonged tissue damage causing multi-organ failure and oftentimes death when prompt care is not provided [5, 6, 12, 19]. (This is similar to what occurs in sepsis and may be a clinical pearl for our medical readers.)

../images/471692_1_En_4_Chapter/471692_1_En_4_Fig3_HTML.png — Fig. 4.3

Pathophysiology of heat stroke. (From Vandermark et al. [17], with permission)

Recognition and Assessment

Timely recognition of EHS is of utmost importance, and is the first step, in ensuring survival and recovery from the condition [20]. Observation of altered mental status (e.g., combativeness, agitation, confusion, unresponsive, etc.) in anyone performing physical activity warrants prompt attention. If EHS is suspected (i.e., prolonged and intense exercise or physical activity in hot conditions, situations where heat dissipation may be impeded [e.g., warfighter wearing an impermeable chemical and biological warfare ensemble], etc.), confirmation of one’s internal body temperature is warranted in order to rule out other potential medical conditions causing altered mental status such as heat exhaustion (see Chap. 5, Heat Exhaustion), exertional hyponatremia, exertional sickling, head injury, cardiac event, respiratory event, or shock (Table 4.1) [21].

Table 4.1

Preventing sudden death in sport: a potentially complex overlap of signs and symptoms of common causes of death^a

	EHS	Heat cramp^b	Heat syncope^b	Exercise heat exhaustion^b	Exertional hyponatremia	Exertional sickling	Head injury	Cardiac^c	Respiratory^d	Shock
CNS dysfunction^e	X		X	X	X	X	X	X	X	X
Dizziness	X		X	X	X		X	X	X
Drowsiness	X				X		X			X
Fatigue	X	X	X	X	X	X	X	X	X	X
Headache	X		X		X		X
Light-headedness			X	X	X		X	X		X
Staggering	X		X	X	X	X	X	X	X
Syncope	X		X	X				X	X
Tunnel vision			X					X
Personality changes^f	X			X	X		X
Lethargy					X		X	X	X	X
Core body temperature usually <40 °C		X	X	X	X	X	X	X	X	X
Core body temperature usually >40 °C	X
Cool, clammy skin				X				X		X
Hot and wet or dry skin	X	X	X	X	X	X
Pale skin			X	X				X		X
Cerebral edema					X		X
Chills				X						X
Bradycardia			X					X	X	X
Decreased urine output	X			X	X
Dehydration	X	X	X	X
Diarrhea	X			X
Hyperventilation	X			X				X	X	X
Hypotension	X							X		X
Low blood sodium concentrations (<130 mEq Na+L-1)					X
Nausea/vomiting	X			X	X		X	X		X
Muscle cramps/pain		X				X
Pulmonary edema					X				X
Seizures	X				X
Swelling of hands and feet					X
Tachycardia (100–120 bpm)	X							X	X	X

From Casa et al. [21], with permission

bpm beats per minute, CNS central nervous system, EHS exertional heat stroke

^aThis table is not meant to be inclusive of all signs and symptoms of the conditions listed or of all conditions that could cause sudden death in sport. Nor is the table implying that all the signs and symptoms indicated for a particular condition would be present on each occasion

^bHeat cramps (i.e., exercise associated muscle cramps), heat syncope, and heat exhaustion are not life threatening but are included due to similarity of these conditions with other conditions that could cause sudden death and the potential for confusion with acute recognition

^cCardiac conditions could be heart attack, hypertrophic cardiomyopathy, commotio cordis, etc.

^dRespiratory could be asthma, pneumothorax, pulmonary edema, etc.

^eCNS dysfunction could include altered consciousness, coma, confusion, disorientation, collapse, etc.

^fPersonality changes could include hysteria, irrational behavior, combativeness, aggressiveness, irritability, apathy, decreased mental acuity, etc.

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