A 15-year-old football player collapses during practice on a day when the heat index is 114 degrees F.
Bystanders move the patient to the shade and EMS is called. Upon arrival, paramedics jump in to assist the bystanders, who are removing the boy’s pads, uniform and equipment.
The transport of the patient to the hospital took 15 minutes. In the ED, the patient’s Glasgow coma scale was 5, and his rectal temperature was 107.3 degrees F. He is cooled with IV fluids and cool water misting.
The patient died on the fourth day of hospitalization as a combined consequence of the effects of an exertional heat stroke (EHS), including, hepatorenal failure, sepsis, coagulopathy, and cardiopulmonary collapse.1
Preventable & Treatable
Despite enumerable studies on the prevention and treatment of heat illness, EHS not only continues to be a leading cause of death among athletes in the United States, but disturbingly, the incidence is on the rise. According to the National Center for Catastrophic Sport Injury Research, there have been 146 EHS deaths from 1931-2015, with 54 of those EHS deaths occurring since 1996 in football alone.2
Active populations who exert themselves in the heat, such as soldiers, laborers, and athletes are at especially high risk for EHS. The rate in football (4.42 per 100,000 athlete exposures) is 11.4 times that in all other sports combined and is due to the combination of a variety of factors, including wearing heavy equipment, inadequately balancing hydration and sweating, and participating in high intensity workouts often during the day. In the military setting, the rate of death due to EHS increased from 2 cases per 100,000 soldiers in 1980 to 14 cases per 100,000 soldiers in 1999,3 while in U.S. high school athletes, exertional heat illness is also increasing with a current rate of 1.2 cases per 100,000 athlete exposures.2
In the U.S., the number of EHS cases between 2005-2009 was higher than any five-year period in the previous 35 years, and in football alone, there were 39 heat stroke deaths between 2004-2015.2,4
Given that heat-related deaths are entirely preventable, these numbers are unacceptable. When prompt, proper and aggressive treatment begins within 10 minutes of collapse, EHS is 100% survivable.5,6 The ongoing trend in the mortality related to EHS represents a gap between current evidence and practice patterns, both in the ED and at the site of collapse.
In EHS, like cardiac arrest, immediate, early action by bystanders and EMS is critical for survival. The National Athletic Trainers Association recommends, “Cool First, Transport Second” for the treatment of EHS patients.7
Currently, there’s no established, evidence-based EMS protocol to manage EHS in the prehospital setting. A review of the current prehospital literature and EMS training algorithms finds that practice patterns aren’t evidence-based and are likely contributing to the high mortality.
Possible barriers to the proper delivery of prehospital care include: the wide differential diagnosis in the collapsed athlete, longstanding myths on the treatment of EHS, and logistical issues involved with cold water immersion.
We aim to provide the evidence to support the establishment of a prehospital algorithm for the care of patients suffering from EHS. Furthermore, we recommend effective methods of cooling both in the resource limited setting and during transport by EMS.
Exertional heat stroke is a life threating condition characterized clinically by central nervous system (CNS) dysfunction with an elevated core temperature, often above 105 degrees F (40.5 degrees C); however, the important caveat is the CNS dysfunction as EHS can be present in patients below 105 degrees F.
The pathophysiology of EHS fundamentally differs from classic (non-exertional) heat stroke in that it occurs in individuals who are physically exerting themselves when the rate of heat gain (through skeletal muscle contraction and environmental factors) exceeds that of heat loss (e.g., evaporative heat loss). Conversely, classic heat stroke isn’t related to exertion and occurs typically during heat waves, when the ambient temperature increases. Classic heat stroke primarily affects sedentary elderly individuals, persons who are chronically ill, and very young persons, and is associated with a higher morbidity and mortality when compared to EHS.
At a cellular level, excess heat above a critical threshold (> 40.83 degrees C, or 105.5 degrees F) causes denaturation and liquefaction of membrane lipids, which leads to multi-organ dysfunction including encephalopathy, rhabdomyolysis, and hepatic and renal failure. This damage becomes irreversible and ultimately fatal if hyperthermia isn’t quickly corrected.8,9
Well-conditioned athletes may be able to tolerate core temperatures in excess of 105 degrees F due to the protective effect of heat acclimatization resulting in decreased cardiovascular strain and decreased rectal temperature.10-12
Pre-existing conditions, such as febrile or gastrointestinal illnesses, drug use (e.g., diuretics, certain psychiatric medications, asthma medications), and obesity, place individuals at greater risk of developing EHS.7
In compensated heat stress, the body is able to maintain a steady state internal temperature balancing heat gain and heat loss. When cooling mechanisms are overwhelmed by internal (metabolic) or external (environmental) heat such as with strenuous activity in a warm/humid environment, the athlete can no longer maintain a steady state temperature. An uncompensated rise in internal temperature leads to the development of EHS. During heat stress, cerebral blood flow decreases as internal temperature rises, contributing to the early pre-syncopal signs seen in EHS.13
Research suggests that multi-organ failure is due to the combined effects of heat cytotoxicity, coagulopathies, and an endotoxin mediated systemic inflammatory response.14
The initial cardiovascular response to hyperthermia is the dilation of peripheral blood vessels, increasing blood flow to the skin to maximize evaporative cooling. This is augmented by a decrease in splanchnic blood flow. This blood is shunted to the peripheral circulation to maintain systemic blood pressure and contributes to heat loss.
A prolonged decrease in splanchnic blood flow, however, results in an ischemic environment leading to nitrosative and oxidative stress to the gastrointestinal track that subsequently causes circulatory and intestinal barrier dysfunction. The intestine becomes increasingly permeable and gut bacteria leaks into the systemic circulation.15 This endotoxemia coupled with increased cytokine levels occur in both trained and untrained individuals during exertional heat stress and the inflammatory profile in those with EHS mirrors that of those seen during septic shock.12,16,17
As EHS progresses, disseminated intravascular coagulation sets in and a complex cascade of cellular responses activates coagulation pathways causing excessive fibrin deposition and platelet aggregation, leading to microvascular thrombi. These thrombi cause ischemic damage to peripheral tissues leading to end organ dysfunction, and eventually, failure.14
The rate of platelet and coagulation protein consumption eventually exceeds that of production, increasing the risk of excessive, prolonged bleeding.10,18 This explains the pleural, corneal, and mesenteric hemorrhage that’s been observed in fatal EHS.19
The direct thermal insult to the brain also leads to CNS abnormalities including an altered level of consciousness, loss of sweating mechanisms, and constricted pupils. Similar to the gastrointestinal system, the integrity of the blood brain barrier is lost and increasing permeability leads to cerebral edema, coma, and eventually, irreversible brain damage and death.10,20
These physiologic changes progress rapidly. With immediate cooling, the body is able to recover from this acute damage with almost no residual effect. However, prolonged hyperthermia above the cellular critical threshold of 105.5 degrees F could result in irreversible organ damage and/or death.
A thermistor which has a flexible probe can remain inside the
rectum while the patient is being cooled, allowing for constant internal
temperature monitoring and eliminating the need to repeatedly roll the patient.
Exertional heat stroke (EHS) victims may exhibit a range of CNS changes from syncope and altered level of consciousness to subtle behavioral changes such as aggression. Although not a fully comprehensive list, other neurophysiologic changes include sensory motor deficits, impaired concentration, visual disturbances and delirium.
For healthcare providers, both in the ED and in the prehospital setting, presentation of a patient with altered mental status or CNS dysfunction presents a diagnostic challenge due to the broad range of possible etiologies such as cardiac arrhythmia, drug overdose, hyper- or hypoglycemia, etc. Other signs and symptoms of EHS such as nausea and muscle cramping are non-specific and may be seen with less severe forms of exertional heat illness as well as with other conditions such as head trauma, electrolyte abnormalities, and exertional sickling.21
Frequently, individuals suffering from EHS will demonstrate a lucid interval which makes diagnosis more complicated.22-25 Multiple marathon runners with initial rectal temperatures of > 106 degrees F were observed to be conversant upon immersion in cold water baths, however soon lapsed into unconsciousness. Treated quickly, they recovered completely without incident.22
EHS must be considered in the young, active population, especially in high-risk populations such as football players, runners, military personnel, and emergency personnel who wear encapsulated suits.
A common misconception is that hot, dry skin is a necessary diagnostic feature of EHS. In EHS, however, the victim is most likely to be sweating just prior to collapse or might be wearing protective clothing that prevents the evaporation or identification of sweat, therefore, the presence of diaphoresis shouldn’t be used to exclude the diagnosis of EHS. Dismissing excessive sweating as a less severe form of heat illness may lead to delays in diagnosis and loss of critical cooling time.
The diagnosis of EHS can only be excluded after a rectal temperature is obtained. Other more convenient body temperature measurements such as temporal, tympanic, sublingual and axillary don’t accurately measure core body temperature in the exercising individual. These modalities can significantly underestimate internal body temperature and are subject to the effects of alterations in blood flow to the skin, the presence of moisture and sweat, and the effect of air temperature.26-29 These devices don’t provide accurate data and can steer the provider away from the correct diagnosis.
The best device for obtaining a rectal temperature is a thermistor, which has a flexible probe. This can remain inside the rectum while the patient is being cooled, allowing for constant internal temperature monitoring and eliminating the need to repeatedly roll the patient.
The perceived invasiveness of obtaining a rectal temperature shouldn’t deter athletic trainers, EMS personnel, or other healthcare providers, especially because obtaining such measurements are within the healthcare provider’s scope of practice.
Fears of legal repercussions from performing a rectal temperature on an individual, especially a minor, should be thoughtfully balanced against legal repercussions from withholding the standard of care from the patient suffering from heat stroke.
Combativeness related to CNS dysfunction and vehement protests from the individual should also not prevent obtaining a rectal temperature, even if such protests seem logical and understandable. Progression from a lucid interval to unresponsiveness is quick and can be mitigated by early diagnosis and initiation of treatment. If an individual is at risk for EHS and is suspected of having EHS, a rectal temperature must be obtained.
The most rapid cooling rates are achieved with cold water
immersion, making this the gold standard for treatment of exertional heat stroke.
Timely and rapid cooling is critical as adverse outcomes are related to both the severity, and more importantly, the duration of visceral organ hyperthermia above the critical cellular threshold of 105.5 degrees F.7
In animal models, increased mortality was related to the duration of hyperthermia rather than peak rectal temperature.30,31 Numerous case studies in high school and collegiate athletes, military settings and marathon runners have shown an increase in fatal outcomes related to delays in the proper identification of EHS, the lack of cooling, or delayed initiation of cooling, or the use of ineffective cooling methods.1,9,19
The goal of treatment is to reduce internal body temperature to ≤ 102 degrees F (38.9 degrees C) in less than 30 minutes from the onset of CNS symptoms, including syncope.5,32,33 To achieve this goal a minimum cooling rate of 0.1-0.2 degrees C per minute (32.18-32.36 degrees F per minute) is suggested if cooling is initiated immediately. If cooling is delayed, a rate of 0.15 degrees C per minute (32.27 degrees F per minute) is recommended. These cooling rates allow for patients with EHS to be cooled to normothermic temperatures in as quickly as 15 minutes.34
The most rapid cooling rates are achieved with cold water immersion (CWI), making this the gold standard for treatment and the recommended method by the National Athletic Trainers Association7 and the American College of Sports Medicine.23,35,36 Numerous studies and case reports of the use of CWI have demonstrated its efficacy,35 with the largest cohort conducted at the Falmouth Road Race in Cape Cod, Mass.34 In 274 cases of EHS observed over an 18-year period at the Falmouth Road Race, all were treated with CWI.
In these athletes, initial rectal temperatures averaged 41.44 degrees C (106.59 degrees F). Cold water immersion achieved an average cooling rate of 0.22 ± 0.11 degrees C per minute for patients with EHS. Despite high rectal temperatures, this method resulted in a 100% survival rate for all patients.34
Exertional heat stroke (EHS) victims should be placed in a large tub filled with cold water and ice, with maximal body surface area submerged. Stirring the water around the individual will further increase the rate of cooling.
In the absence of CWI, rotating cold, wet towels provides an effective but slower alternative with cooling rates of 0.11 degrees C per minute. Towels are soaked in ice water and laid on the skin of the patient. The towels should cover the maximal amount of body area, including the back, and be changed every few minutes.37
The cold towel method is also an alternative when space is an issue or during transport. A cooler filled with water, ice and 10-12 towels takes up minimal space making it portable and ideal in the resource-limited setting.
Given the space issues in an ambulance, this method could be used by EMS; however, in a setting where space and resources isn’t an issue, cold towels shouldn’t be chosen over CWI. Every possible effort should be made to have CWI available especially in controlled settings such as athletic events where EHS is a predictable injury.
Other cooling methods, such as aggressive cold water dousing and ice massage, also known as wet ice therapy (WIT), while not as effective as CWI, do achieve rapid cooling rates. In a small study of nine patients during the 2004-2008 Marine Corps Marathons, a cooling rate of 0.13±0.04 degrees C per minute was achieved with WIT, 70% as effective as CWI.38,39
Immediate cold water dousing is the protocol for the treatment of EHS in the Israeli Defense Forces and has been used with excellent outcomes.40 The downfall of this method is that it requires much of the same equipment as CWI while achieving suboptimal cooling rates. Alternatively, in the absence of both CWI and WIT, the use of cold showers with ice is recommended when these are available on scene.
Ineffective Cooling Methods
Numerous state EMS protocols recommend the use of ineffective cooling methods such as fanning patients, opening windows, and applying cold packs to the armpits, neck, and groin.41-44 Fanning relies on evaporation, which is limited with high ambient humidity. Using fans to blow warm air over the patient increases conductive heat gain.45
Chemical cold packs (CCPs) have substandard cooling rates and shouldn’t be used as a primary method of cooling.46,47 If CCPs are used to treat an EHS victim with an initial rectal temperature of 41.44 degrees C (106.59 degrees F)-the average seen at the Falmouth Road Race-it would take over 70 minutes to reach the target temperature of 38.9 degrees C (102 degrees F).
It should be noted that equivalent sized ice-filled packs offer significantly higher rates of cooling (2.5 degrees C change vs. < 0.05 degrees C change, respectively) and stay colder for longer periods of time when compared to CCPs.48
Hurdles to the adoption of more aggressive prehospital cooling protocols include concerns regarding risk of cardiovascular shock, cooling the patient too quickly or overcooling the patient, and inadequate access for other medical interventions.
Sudden immersion in cold water has been suggested to cause cardiac arrhythmias and cardiovascular shock due to a rapid sympathetic response resulting in sudden vasoconstriction. These hypotheses are based on two studies. 49,50
Cardiac arrhythmias, such as premature atrial and junctional complexes, supraventricular tachycardia, and premature ventricular complexes, were found in 12 healthy, normothermic individuals submerged in water at 5 and 10 degrees C.49
A second review paper hypothesized that the mammalian dive reflex seen when people are submerged in cold water would be seen in hyperthermic people immersed in cold water.50 However, hyperthermic patients weren’t found to experience these adverse effects (i.e., bradycardia, peripheral vasoconstriction, and core blood shunting) demonstrating the differing thermoregulatory responses of normothermic individuals when compared to hyperthermic individuals.21,50
The temperature of the water for immersion has been debated due to concerns that peripheral vasoconstriction (PVC) and shivering due to cold water submersion may paradoxically prolong hyperthermia, known as the Currie response.35 Described in 1798, normothermic patients responded to exposure to cold water by cutaneous vasoconstriction, reducing the area available for heat exchange at the skin-water interface.51 Cold water exposure also led to shivering, leading to heat production. It was hypothesized that since these mechanisms that protect the normothermic patient by heating them, these would lead to further pathology in the hyperthermic patient.35
In the normothermic individual, the Currie response will be observed due to normal thermoregulatory function; however, in the hyperthermic individual where thermoregulatory function has been disrupted, the Currie response isn’t observed.
Using CWI, one study found that the cooling rates in hyperthermic individuals were consistently reported to be about 0.16-0.2 degrees C per minute (0.29-0.36 degrees F) and increased to 0.35 degrees C (0.63 degrees F)
when multiple cooling modalities were utilized (e.g., circulating water, immersing the entire body except the head, etc.).37
Normothermic individuals who were placed in cold water showed no change or a slight increase in internal temperature.35,37 The rise in core body temperature seen when a normothermic patient is placed in cold water isn’t seen in the hyperthermic individual.35
Finally, inadequate access during CWI to manage other complications of hyperthermia is cited as a problem of this modality. Cardiac monitoring and IV fluid administration can be successfully done during CWI. The authors, experienced in using CWI, estimate the incidence of intubation at < 1%, vomiting < 10%, seizures < 5%, and combativeness 15-20%. Cooling must not be halted while managing these complications, as they are often due to the hyperthermic state.52
The majority of patients are tachycardic at the time of presentation, though not all are hypotensive, and vital signs typically normalize after resolution of hyperthermia. In the prehospital setting, IV access is almost never needed, and while heat stress potentiates dehydration and EHS patients may benefit from IV fluids, this is often required only in those patients requiring transport to the emergency department. Most patients are able to be directly released from onsite treatment after CWI.34,53
The National Athletic Trainers Association position statement on exertional heat illness recommends, “Cool First, Transport Second,” demonstrating the time sensitive nature of treatment. Cooling should be initiated by coaches, staff, and supervisors when medical staff is not present.7
EMS providers are trained to address immediate life-threatening conditions and to deliver patients to definitive care. However, in the case of EHS, immediate rapid cooling is the definitive care. Delays in that care, such as for transport, is detrimental to patient outcomes.
EHS Chain of Survival
In the confused or altered patient, initial assessment consists of obtaining vital signs, including a measurement of core temperature and blood glucose. Excess protective clothing and sporting equipment should be removed, preferably in concert with cooling.7
If the rectal temperature is > 105 degrees F (40.5 degrees C) with accompanying CNS dysfunction, on-scene CWI should be initiated immediately. If CWI isn’t available, alternative cooling modalities, including rotating cold, wet towels, ice massage and cold showers should commence. If effective methods of cooling are available onsite, cooling of the patient shouldn’t be stopped for transport to the hospital until the target rectal temperature of 102 degrees F (38.9 degrees C) is reached.
If a rectal thermistor/thermometer isn’t available and the clinical scenario strongly supports EHS, it’s recommended that CWI should be initiated. The endpoint of these efforts in the prehospital setting should be either the initiation of shivering or 15-20 minutes of cooling, as this timeframe results in sufficient cooling for the majority of patients.54
Relying on these measures should be done cautiously. Shivering occurs quickly in the normothermic patient, however, patients suffering from EHS generally don’t shiver due to a dysfunctional thermoregulatory system unless they are cooled too long, at which point hypothermia is a real concern.35
Additionally, estimating a time for immersion should be done conservatively. Utilizing recommended cooling rates stated above, it would take an individual with an internal temperature of 41 degrees C (105.8 degrees F) to cool to a temperature of 38.9 degrees C in < 10 minutes, resulting in hypothermia if the patient is immersed for 15 minutes.
On the other hand, an individual with an internal temperature of 44.5 degrees C (112.1 degrees F) would take over 25 minutes to cool to a safe temperature, meaning they would still be hyperthermic upon tub removal. Therefore, patients without a core temperature should be transported to the hospital for further care after this brief cooling period.
On-site cooling may not always be available, and EMS should carry equipment to treat EHS, especially in high-risk seasons, such as a cooler of ice water towels. This modality may also enable the provider to initiate other care such as establishing IV access.
As an adjunct, EMS providers may also administer cold IV saline once hyponatremia is ruled out.21 As with any other critical patient, the hospital should be alerted about the arrival of any potential EHS patient.
Immediate and rapid cooling is the cornerstone of treatment in EHS, making first responders and EMS a critical link in the chain of survival. Although a “scoop and run” approach may be appropriate for many conditions, EHS is a true medical emergency and when effective methods of prehospital cooling are available, it’s better to “stay and play.” On-scene CWI has been shown to be safe and effective with 100% survival.
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33. Casa DJ, Kenny GP, Taylor