Heatstroke: A Primary Peril of Late Summer Sports

It is a typical warm, sticky late summer afternoon when EMS arrives, transporting a 13-year-old boy to the emergency department (ED). The paramedics state they were called after he collapsed and had a syncopal episode with altered mentation while at football practice. On scene, he was found to be tachycardic with a heart rate between 180 to 200 beats/min. No other history was known. Thought to be in supraventricular tachycardia (SVT), adenosine 6 mg was given with no response. A repeat dose of 12 mg dose was given, also with no change. Cardioversion with 50 joules was then unsuccessful. The patient could not provide any further history as he was oriented to self only-mumbling but not conversive or appropriate. He was able to maintain his airway and subsequently transported to the ED.

Upon arrival, he was found to be persistently tachycardic (pulse, 180 to 190 beats/min), hypotensive (BP 99/72 mm Hg), and tachypneic (respiratory rate 32 to 36 breaths/min). Estimated weight was 100 kg. He was very slow to respond to questioning, able to say his name but little else. Gag reflex was intact. Glasgow coma scale (GCS) score was 15. His skin was cold and clammy and he was diaphoretic.

Adenosine was repeated and multiple attempts at cardioversion were unsuccessful. During cardiology evaluation, ECG revealed sinus tachycardia and the patient exhibited posturing of the upper extremities that progressed to a 2- to 3-minute generalized tonic clonic seizure. This resolves with 2 IV doses of lorazepam. He was given a loading dose of fosphenytoin (20 mg/kg). 

What is wrong with this young man?
 

The answer becomes clear as a temperature-sensing Foley catheter is placed and reveals a core temperature of 42°C (107°F).

As cooling attempts begin, the patient’s parents arrive. They say he is a sedentary type of guy who stayed indoors in the air conditioning most of the summer playing video games. Today was the first day of football practice and he wanted to really impress the coaches with his blazing speed and strength. As he starts to awaken, he recalls "how hot it was" and can state the date and his full name. As he is being transported to the PICU, the lab calls and reports an elevated creatine (2.2 mg/dL); creatinine phosphokinase, 1447 IU/L; and urine myoglobin, 4834 µg/L. Liver studies and PT/PTT are normal.

What is the prognosis for this patient?

Discussion
Hyperthermia and heat-related illnesses comprise a continuum of disorders ranging from minor  conditions like muscle cramps and heat edema to the most severe,  life threatening form-heat  stroke.^1-5 Body temperature is the net result of the interaction between heat production, absorption, and dissipation. The hypothalamus maintains a core body temperature in a narrow range between 36° and 37.5°C (96.8° and 99.5°F).^4,8 In contrast to fever, where increased metabolic activity and shivering result in a rise in this core temperature, the hyperthermia associated with heat related illness is caused by an imbalance between heat absorption from the environment and the body’s failure to dissipate it.³ Normal body temperature cannot be maintained due to excess heat production or decreased heat transfer.⁶ Heat stroke occurs when the body’s thermoregulatory mechanisms are overwhelmed to the point of failure. Normal heat transfer mechanisms are ineffective, core temperature rises quickly to extreme levels ^6,7 and direct injury to the cells occur.^3,6

The most important risk factor for heat related illness is dehydration.⁸ Chronic medical conditions associated with excessive water loss (eg, GI infection, diabetes), suboptimal sweating (spina bifida) or diminished  thirst (cystic fibrosis), and obesity elevate the risk for heat related illnesses.⁸

Heat stroke is defined as an elevated core temperature greater than 40°C (104°F).^1-4,6,9 It is a true medical emergency with associated mortality rates close to 12% in adult patients.^4-6 Mortality rates can be as high as 80% in untreated patients.⁴ It is associated with central nervous system dysfunction.^3,6,9 Lack of sweating is not an absolute diagnostic criterion.⁷ (See Table 1.) 

Heat stroke is a multisystem disease with multiple systemic manifestations. CNS and cardiovascular symptoms are the most profound and recognizable. Neurologic abnormalities include seizures, delirium, and coma in severe heat stroke but may present as headache, hallucinations, change in mentation, or ataxia. Tachycardia is typical as heat dissipation is maximized via convection. Hyperventillation, diarrhea and vomiting, oliguria, and either hot dry skin or profuse sweating are other signs of heat stroke. Hypotension is a late and ominous sign.^3,4,6 Laboratory anomalies are numerous and include hypo- or hypernatremia, hypokalemia, metabolic acidosis, and hypoglycemia. Elevated renal function reflects azotemia and elevated transaminase levels indicate hepatic injury. This can lead to prolonged bleeding times and thrombocytopenia that suggest disseminated intravascular coagulation (DIC). Elevated serum creatinine phosphokinase (CPK) and myoglobinuria can be seen, especially in exertional heat stroke. Leukocytosis related to a stress response is not uncommon.^3,6  (See Table 2)

Traditionally, heat stroke has been classified as non-exertional (classic) and exertional.^3,4,6,7 Extremes of age are most affected by classic heat stroke. The elderly as well as infants and small children are most at risk. They may not be able to independently seek fluids or alter their environment.^3,7 Children also have higher metabolic rates, less developed sweating mechanisms, and a blunted thirst response compared with adults, increasing susceptibility to dehydration.^4,8 

Classic heat stroke usually occurs during summer heat waves. Prolonged exposure to constant elevation of heat and humidity without relief can produce heat stroke in epidemic proportions.^4,8 Dehydration, hot dry skin, coma, and ultimately death is the usual sequence of events. Children left unattended in automobiles are a tragic example. Temperatures  can reach 145°F (62.8°C) in less than 40 minutes in a car exposed to the sun, even with the windows cracked open; heat stroke can occur quickly (within 30 minutes) in such a setting.^6,8 

Exertional heat stroke is more common in the adolescent or young adult. It can develop after strenuous physical activity in a hot, humid environment, though it also can occur in temperate climates. The highly motivated, poorly acclimated or unconditioned athlete is the typical victim. ^4,7,8 Among high school athletes, heat stroke is the third leading cause of mortality.^6,8  Drinking alcohol, illicit drug use (cocaine, amphetamines; more in Table 3), and decreased fluid intake while participating in physical activity are associated with an increased risk for heat-related illness.¹⁰

Management of acute heat related illness begins with moving the patient to a cool shaded area. Airway, breathing, and circulation must be immediately addressed. Definitive airway control via endotracheal intubation may be necessary. Avoid administering succinylcholine given the risk of malignant hyperthermia and myoglobinuria.³ IVF resuscitation with normal saline solution or lactated Ringer’s solution should be started. Management then focuses on aggressive measures to rapidly cool the patient in an effort to minimize end organ damage and prevent further injury. ^3,7,10 Effective heat dissipation depends on rapid heat transfer from the core to the skin and from skin to the external environment. The goal of external cooling techniques is to accelerate this heat transfer. ^3-5,7-10 Bystanders should: 
 
• Remove all clothing. 
• Place ice packs in the neck, groin, and axilla.
• Assist convective heat dissipation with misted tepid (not cold) water.
• Maximize evaporative heat loss by cooling with large fans, if available. 
• Use cooling blankets, if available; may be beneficial.

Successful cooling with ice water peritoneal and thoracic lavage has been anecdotally reported. Gastric and bladder lavage are of little added benefit.^4,10 Alcohol sponge baths should never be used as they may result in alcohol toxicity via skin absorption.^4,7,8

Antipyretics are not useful and may be harmful.^7,8 The goal of active body cooling is not normothermia but to lower the body temperature enough to restore effective body function. Target temperature is 102.2° F (39°C) and, once reached should signal the end of active cooling to prevent hypothermia. Clinical improvement should follow as core temperature returns to normal.³ Therapy is then supportive with the ultimate goal to protect the patient from additional injury caused by hypotension and organ dysfunction.⁶ After initial stabilization and cooling, admission to a PICU/ICU is warranted.⁷

Patients with heat stroke typically will recover fully once cooled and rehydrated. Severity of injury appears to depend on duration of hyperthermia and severity of temperature elevation. Those with mild heat stroke generally recover without sequelae. However, those who survive moderate to severe heat stroke have a much higher risk for permanent neurologic abnormalities including behavioral changes, visual and memory impairments, ataxia, and incoordination.⁶ Prognosis is poor and the risk for death higher when presenting temperature is greater than 42°C (107°F), hypotension exists, and consciousness is significantly altered (GCS <12).^6,10

Heat-related illness can be life threatening. Fortunately, it is almost always preventable.^1,3,9  Many platforms exist to remind parents not to leave a child unattended in a parked car. Athletes can learn to acclimate themselves to the heat and humidity. Drinking at regular intervals (ie, every 30 minutes), not only when thirsty, frequent cooling breaks, and the ability of a coach/trainer to recognize the signs and symptoms early and promptly manage them have proven to reduce the rate of heat related illness.¹ Environmental awareness can also reduce the risk and includes using theheat index as a guide for appropriate level of activity, scheduling outdoor activities during cooler times of the day, increased time in air conditioned environments, and reinforcing proper hydration.⁹

Case Conclusion
John was cooled to a temperature of 39°C (102°F) and spent several days being closely monitored in the PICU. His rhabdomyolysis and acute renal insufficiency resolved with aggressive fluid replacement. He never exhibited signs of coagulopathy. At time of discharge, he had returned to his baseline mentation. John, indeed, was a lucky boy!

Take-home points:
1. Heat related illnesses are common and preventable in the pediatric population
2. Symptoms can range from mild to catastrophic
3. Multiple risk factors exist that put kids at higher risk:
   • Greater ratio of body surface area to mass
   • Higher metabolic rate
   • Blunted thirst response
   • Lower sweat output
   • Chronic illness and obesity
   • Dependency on caregiver for rehydration and removal from dangerous environment
4. Dehydration is the most important risk factor for heat related illness
5. Acclimation to hot, humid environment must be gradual¹⁰:
   • Kids, 10 to 14 days     
   • Adults, 8 to 12 days
6. Prompt recognition, aggressive fluid resuscitation, and aggressive cooling are crucial to good outcome when managing heat stroke
7. Risk factors for poor prognosis:
   • Higher core temperature on presentation (> 42°C [107.6°F])
   • Hypotension
   • Altered mentation/CNS findings (GCS <12)

References:
1. Wagner C, Boyd K. Pediatric Heatstroke. Air Med J. 2008;27:118-122.
2. Chesney ML. Pediatric Exertional Heatstroke. Air Med J. 2003;22:6-8.
3. Grubenhoff JA, du Ford K, Roosevelt GE. Heat-related illness. Clin Pediatr Emerg Med. 2007;8:59- 64.
4. Lin J, Losey R, Prendergast HM. An evidence based approach to hyperthermia an dother heat-related emergencies. Pediatric Emergency Medicine Practice. EMMedicine.net. April 2009;6:4.
5. Mechem CC. Severe hyperthermia in adults: heat stroke and malignant hyperthermia. UpToDate.
6. Jardine DA. Heat Illness and Heat Stroke. Pediatrics in Review. 2007;28:249-258.
7. Clem K, Kim G, Mellick LB. Managing pediatric environmental injuries: hypothermia, frostbite, minor heat illnesses, heat exhaustion, and heat stroke. Pediatr Emerg Med Rep. 1996:95-103.
8. Palmer K. Heat Related Illnesses in Pediatric Emergency Medicine Secrets. 2nd Edition. Selbst SM, Cronan KM. Mosby, Philadelphia, PA. 2008;562-568.
9. Bouchama A, Knochel JP. Heat Stroke. N Engl J Med. 2002;346:1978-1988.
10. LoVecchio F, Pizon AF, Berrett C, Balls A. Outcomes after environmental hyperthermia. Am J Emerg Med. 2007;25:442-444.