Author: Esteban Davila
Peer Editor: Alec Feuerbach
The Case
You’re having a relatively quiet morning when you hear EMS bringing in a patient. The patient is an 18-year-old male who collapsed on the route of a half marathon. You reflect that this day is particularly warm and humid. EMS reports that they have not been able to obtain any collateral history, and the patient has been unresponsive to noxious stimuli. They placed a non-rebreather oxygen mask on the patient.
As EMS wheels the patient to the stretcher, you glance at the portable monitor and see a heart rate of 170/min and a blood pressure of 120/70 mmHg. You note a young male with diaphoresis, respiratory distress, and tachypnea. The respiratory rate is 40/min, and the oxygen saturation is 91% on 15L of O2. There is a patent airway, clear lungs, and equal pulses. The patient’s GCS is 3. As peripheral venous access is established and the patient is placed on the monitor, the core temperature is measured at 107 degrees Fahrenheit. You realize you’re dealing with heat stroke. Let’s take a dive into the literature. Prior articles on this topic can be found here.
Exertional Heat Stroke
The terminology behind heat-related injuries can be confusing. Exertional heat illness is an umbrella term for heat exhaustion, heat injury, and heat stroke, which by itself can be separated into exertional and classic heat stroke. For simplicity, we will refer to exertional heat stroke when symptoms are related to vigorous physical activity in hot or humid environments. Exertional heat stroke (EHS) typically occurs in athletes, outdoor workers, and military personnel with risk factors including dehydration, aging, obesity, and previous infections.[1] The term ‘stroke’ in heat stroke refers to symptoms of central nervous system (CNS) dysfunction such as delirium, convulsions, and coma in addition to organ and tissue damage that may occur with hyperthermia.
Recognition
Though classically described as a core temperature > 40 degrees Celsius,[2] there is growing evidence that this threshold for diagnosis may be inaccurate.[3] Focusing on pathological symptoms such as CNS dysfunction with appropriate clinical context is likely to be more accurate than an arbitrary number.[1] The combination of varying terminology and inaccuracy of recommended temperature criteria makes measuring the incidence of exertional heat stroke difficult.
Pathophysiology
Though there is no one accepted underlying pathophysiology of EHS, there appears to be a complex interplay between cardiovascular and thermoregulatory failure leading to increased intestinal permeability (referred to as the “leaky gut theory”) and resulting systemic inflammation and coagulopathy. During exercise, skeletal muscles generate large amounts of heat. The majority of this heat is transferred to the blood and then circulates to the core.
Thermoregulation, primarily through evaporation (by sweating), convection, conduction, and radiation, allows for most heat dissipation. Sweat evaporation depends on both a vapor pressure and temperature gradient between the skin and the air, meaning that even in humid conditions evaporation can still occur as long as the air is cooler than the skin.[4] Convection, conduction, and radiation rely on cutaneous vasodilation to allow blood flow to the skin, shifting blood away from splanchnic and renal circulation.[5]
Under intense heat, and as heat production of the skeletal muscles increases, the ability to dissipate heat decreases, and the temperature gradient between the body and the outside environment narrows and then reverses. This causes decreased sweat production and reversal of heat transfer, as conduction, convection, and radiation now transfer heat internally, resulting in a rise in core body temperature.[6] Thermoregulatory failure combined with hypovolemia from sweat production, tachypnea, and cutaneous blood flow diversion compromise blood flow to skin, muscle, and brain, and circulatory collapse ensues.[3,6]
Presentation and Complications
Common presenting symptoms of EHS include loss of consciousness, delirium, confusion, agitation, convulsions, and coma. Physical exam findings include warm skin with or without diaphoresis, tachycardia, tachypnea, and hypotension. There is no cut-off temperature for tissue damage, though prior studies show that the severity of damage is related to the degree and duration of hyperthermia, with both the brain and liver being the most commonly affected organs.[7,8]
Common complications include thrombocytopenia, impaired coagulation, liver damage, acute kidney injury, lactic acidosis, cardiovascular dysfunction, and rhabdomyolysis. There is elevated hemoglobin and hematocrit from dehydration, decreased platelet count, and leukocytosis, likely from stress response.[9] Hyperkalemia is commonly present, usually from acute kidney injury.
Elevations in AST, ALT, and LDH are common early, and rhabdomyolysis is often demonstrated with CK levels > 1,000 U/L. Coagulation dysfunction is more commonly seen on the second or third day of admission. There is metabolic (lactic) acidosis and respiratory alkalosis.[9] Myocardial injury may occur in patients with heat stroke, demonstrated by ECG ST- deviation, elevated cardiac enzymes, and/or regional wall motion abnormalities, though limited data suggests this is from a supply-demand mismatch.[6] An early elevation in troponin appears to be an independent risk factor for 30-day mortality in patients with heat stroke.[10] Additionally, patients with heat stroke are at increased risk of dysrhythmia and cardiac arrest.
Back to the Patient
Given the patient’s hypoxemia, respiratory distress, and poor mental status, you pre-oxygenate and intubate the patient. You remove the soaked clothing of the patient and obtain this ECG:
You note sinus tachycardia, possible prolonged QTc, and peaked T waves. You have important management steps to perform. In Part 2, we will take a dive back into the evidence.
Take Home Points:
- Exertional heat stroke is a time-sensitive diagnosis
- The core body temperature threshold of > 40 degrees Celsius may be inaccurate. More attention should be focused on pathological symptoms in the right clinical context
- Anticipate common complications including thrombocytopenia, coagulopathy, liver damage, acute kidney injury, lactic acidosis, cardiovascular dysfunction, and rhabdomyolysis
- 1. Garcia CK, Renteria LI, Leite-Santos G, Leon LR, Laitano O. Exertional heat stroke: pathophysiology and risk factors. BMJ Med. 2022;1(1):e000239. Published 2022 Oct 11. doi:10.1136/bmjmed-2022-000239
- 2. Bouchama A, Knochel JP. Heat stroke. N Engl J Med. Jun 20 2002;346(25):1978-88. doi:10.1056/NEJMra011089
- 3. Laitano O, Leon LR, Roberts WO, Sawka MN. Controversies in exertional heat stroke diagnosis, prevention, and treatment. J Appl Physiol (1985). 2019;127(5):1338-1348. doi:10.1152/japplphysiol.00452.2019
- 4. Havenith G. Heat balance when wearing protective clothing. Ann Occup Hyg. 1999;43(5):289-296.
- 5. Epstein Y, Yanovich R. Heatstroke. N Engl J Med. 2019;380(25):2449-2459. doi:10.1056/NEJMra1810762
- 6. Marchand M, Gin K. The Cardiovascular System in Heat Stroke. CJC Open. 2021;4(2):158-163. Published 2021 Oct 12. doi:10.1016/j.cjco.2021.10.002
- 7. Savioli G, Zanza C, Longhitano Y, et al. Heat-Related Illness in Emergency and Critical Care: Recommendations for Recognition and Management with Medico-Legal Considerations. Biomedicines. 2022;10(10):2542. Published 2022 Oct 12. doi:10.3390/biomedicines10102542
- 8. Atha WF. Heat-related illness. Emerg Med Clin North Am. 2013;31(4):1097-1108. doi:10.1016/j.emc.2013.07.012
- 9. People’s Liberation Army Professional Committee of Critical Care Medicine. Expert consensus on standardized diagnosis and treatment for heat stroke. Mil Med Res. 2016;3:1. Published 2016 Jan 6. doi:10.1186/s40779-015-0056-z
- 10. Tang Y, Yuan D, Gu T, Zhang H, Shen W, Liu F. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2023;35(7):730-735. doi:10.3760/cma.j.cn121430-20221028-00948
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