You have a new patient!
A 24-year-old man was brought to your Emergency Department by his football coach. His coach informed you that he started “behaving strangely” and responding inappropriately to questions a few hours ago during a practice session on the football field. His initial vital signs are BP 80/50 mmHg, HR 115 bpm, RR 24 bpm, T 41.5oC, and SpO2 98%. His GCS is 13 (E3V4M6).
What do you need to know?
Climate change is widely considered the greatest threat to human health globally in the coming decades [1]. According to the assessment of the Intergovernmental Panel on Climate Change (IPCC), the next decades might witness global warming above 1.5 °C, exceeding the goals of the Paris Agreement [2]. Concomitantly, heat-related mortality has developed as a growing public health concern. Populations with pre-existing chronic diseases are more sensitive to climate change, warranting closer attention and more effective interventions to manage heat-related health risks [3]. Therefore, a comprehensive medical understanding of heat-related illnesses is required as the world faces climate change [1].
Heat-related illnesses include a spectrum of diseases, ranging from mild and self-limiting conditions such as heat edema, heat cramps, and heat stress to the life-threatening condition known as heat stroke. These conditions occur when the body’s thermoregulatory mechanisms fail to keep body temperature within normal limits in a hot and humid environment [4].
The emergency physician needs to have a high index of suspicion for heat stroke because these patients can mistakenly be diagnosed with other conditions that may present similar to heat stroke. Some examples are sepsis, intracranial bleeding, stroke, thyroid storm, anticholinergic toxicity, or other conditions where patients may have high fevers or altered mental status, similar to heat stroke. The most critical initial intervention in heat stroke is rapid cooling to <39°C. A misdiagnosis can result in a delay in rapid cooling. Failing to implement this intervention results in higher mortality [5].
According to the World Health Organization, more than 166,000 people died due to extreme temperatures between 1997 and 2017. This includes 70,000 deaths in the 3-month European heatwave of 2003 and 53,000 deaths in the 44-day Russian heatwave of 2010 [5]. A 2003 prospective study from France reported a 28-day and 2-year mortality rate of 58% and 71%, respectively, for patients diagnosed with heat stroke [6].
Body temperature is controlled by the hypothalamus. The body gains heat from metabolism and the environment, and this heat must be dissipated to maintain core body temperature between 36°C and 38°C (96.8°F and 100.4°F). Thermoregulation relies on four primary mechanisms: dilatation of blood vessels, particularly in the skin, increased sweat production and subsequent evaporation, decreased heat production, and behavioral heat control. Vasodilation contributes to the orthostatic pooling of interstitial fluid in the lower extremities, as seen in heat edema. When these processes are overwhelmed, core temperature will rise and may result in heat stress [4].
Cellular injury can begin when the core body temperature exceeds 39oC, especially if the elevation in temperature is sustained [7]. As the body temperature rises to 40°C, an acute phase response is elicited from heat-stressed cells. This involves the release of cytokines and heat shock proteins, materials that can cause damage to organ systems and result in heat stroke [4,8]. The incremental damage to cells and organ systems as body temperature rises above 39oC exemplifies the importance of rapid cooling in a patient with hyperthermia.
Heat stroke due to high external temperature and humidity without much contribution from physical exertion is termed classical heat stroke (CHS). Heat stroke is due to increased heat generation from strenuous physical activity, usually under extreme heat conditions and in a poorly acclimatized and conditioned body, and is termed exertional heat stroke (EHS). For example, classical heat stroke may be seen in elderly individuals sitting in poorly cooled and ventilated homes during the summer; exertional heat stroke may be seen in athletes exercising hours in the sun during a prolonged sporting event or race. Another heat-related illness that may be encountered in the athlete patient is heat cramps. These cramps occur from relative deficiencies in electrolytes such as sodium, potassium, and magnesium brought about by replenishing lost fluids with hypotonic drinking solutions after vigorous physical activity. This leads to painful involuntary contractions of skeletal muscles, most commonly the calves [4].
The exercising body has thermoregulatory mechanisms it utilizes when exposed to prolonged heat. During exercise, blood vessels dilate to release heat, the heart rate increases, and stroke volume decreases. Sweat production and evaporation from the skin surface also assist in cooling the body during exercise. These mechanisms may be diminished in patients with underlying cardiovascular disease (e.g., congestive heart failure) or those taking certain medications (e.g., beta-blockers or anticholinergic medications). These patient groups are at increased risk of heat-related illnesses during exercise [9].
Medical History
Ask patients with heat edema about exposure to hot and humid environments. The presence of other symptoms, such as dyspnea, easy fatigability, orthopnea, paroxysmal nocturnal dyspnea, and oliguria, are red flags that may point to alternative causes of the edema, such as congestive heart failure or kidney failure [4].
For patients with heat cramps, verify recent participation in strenuous activities, such as sports events and practices, military exercise, or procession-like activities. Ask if the patient took fluid during exertional activities and, if so, what type of fluid was consumed. Drinking hypotonic solutions, such as plain water, puts patients at risk for relative deficiencies in electrolytes and subsequent heat cramps. Ask about vomiting, diarrhea, and medications, like diuretics or antihypertensives, which can also put the patient at risk for electrolyte disturbances [4].
Heat stress is a diagnosis of exclusion because patients usually come in febrile with non-specific symptoms such as nausea, headache, weakness, and dizziness [4]. Again, patients with a recent history of exposure to hot and humid environments are at increased risk of heat stress. Still, the emergency physician should be aware of other more dangerous conditions, such as sepsis, CNS infection, endocrine dysfunction, myocardial infarction, and drug overdose. Ask for recent history of dyspnea, cough, dysuria, and headache, which may point to infectious diseases such as pneumonia, urinary tract infection, and CNS infection.
To diagnose heat stroke, the patient must have both Central Nervous System (CNS) impairment and a core temperature greater than 40°C. The spectrum of neurological abnormalities ranges from mild confusion to coma with a GCS of 3. Situational awareness is a vital skill for emergency physicians, as one should be aware of days with high ambient temperatures and high humidity that can increase the risk of CHS. Usage of medications that impair sweating, like anticholinergic medications, is another risk factor for developing heat illnesses. Generally speaking, CHS is uncommon in geographical areas where the average temperature throughout the year is high, as communities living there will develop behavioral tactics to avoid the heat. Intense exercise, military training, sports competitions, or prolonged labor, on the other hand, puts patients at risk for EHS. Patients not trained in hot environments may not be physiologically acclimatized, increasing their risk for EHS [4].
Physical Examination
Whenever heat illnesses are considered in the differential diagnosis of a given patient, measuring a core body temperature (e.g., rectal temperature) is the most important physical assessment. Using the physical exam to evaluate for other causes of elevated body temperature is important. Physical signs of infection (e.g., cellulitis, abscess, drainage from wounds, asymmetric breath sounds), intoxication (e.g., dilated pupils), and endocrine dysfunction (e.g. goiter) should be assessed.
Obtaining an accurate and continuous core body temperature is a crucial part of the physical examination. Core temperature should be assessed and monitored using rectal, bladder, or esophageal probes. Peripheral temperature measurements, like oral, axillary, or temporal temperatures, are unreliable and may not reflect actual core temperatures. A common pitfall in measuring rectal temperature is not inserting the probe to a sufficient depth, rendering readings inaccurate, mainly if ice packs have been applied to the groin area for cooling. Rectal probes, in general, have to be inserted 15 cm inside the rectum to mitigate the effects mentioned above, but manufacturers may recommend different depths. Note that unlike heat stroke and heat stress, heat edema, and heat cramps will not have an increased core temperature [4]. Tachycardia and hypotension may be seen on examination as a response to thermoregulatory peripheral vasodilation. This phenomenon contributes to other heat illnesses, such as heat edema and heat syncope.
After vital signs, a head-to-toe physical exam should be conducted with special care in conducting a thorough neurological examination. A hallmark finding of heat stroke, other than a core temperature above 40°C, is an abnormal neurological exam. CNS effects might range from mild confusion to deep coma. Ataxia and slurred speech may also be seen. CNS effects help distinguish heat stress from heat stroke, as only heat stroke will have CNS changes [4].
Assess for neurologic signs such as nuchal rigidity, lateralizing spasticity, and pathologic reflexes (e.g. extensor toe reflex) to determine the possibility of a central neurologic etiology. Seizures, in general, are common in heat stroke and might be confused with shivering during cooling. Both seizures and shivering should be treated for neural protection and prevention of heat generation, respectively. Benzodiazepines are appropriate for treating both conditions.
Alternative Diagnoses
Minor heat illnesses, like heat cramps and heat edema, can be diagnosed clinically based on the history. Alternative diagnoses for heat edema include congestive heart failure, renal failure, and chronic hepatic disease. The presence of exertional dyspnea, orthopnea, or paroxysmal nocturnal dyspnea would suggest congestive heart failure. Progressively decreasing urine output and generalized edema would suggest renal failure. A jaundiced patient with progressively enlarging abdomen would indicate a chronic hepatic disease. Alternative diagnoses for heat cramps are infectious conditions and electrolyte derangements. Many viral syndromes, like influenza, COVID-19, or Dengue, can be associated with myalgias. Other conditions, like Leptospirosis, can also present with lower extremity myalgia and calf tenderness. However, the absence of decreasing urine output, fever, and jaundice would make this diagnosis unlikely.
Heat stroke, with its cardinal features of hyperpyrexia and altered sensorium, has numerous alternative diagnoses. Some important diagnoses to consider are sepsis, CNS infections, thyroid storm, sympathomimetic or anticholinergic toxidromes, serotonin syndrome, alcohol withdrawal, stroke, or status epilepticus. Investigate accordingly for a focus of infection for these patients. Thyroid storm patients may also present with atrial fibrillation, diarrhea, and a trigger (e.g., missed thyroid medications, infection, or surgery). The presence of signs and symptoms such as sudden-onset lateralizing weakness, slurring of speech, headache, nuchal rigidity, and recurrent seizures despite adequate cooling may suggest central neurologic etiology for the patient’s condition. It may require a more tailored neurologic work-up. Reported illicit substance or alcohol use, or lack thereof, would support intoxication or withdrawal. Epilepsy history, missed doses of antiepileptic medications, or active seizure activity during the exam would support status epilepticus as a diagnosis.
Acing Diagnostic Testing
Heat stroke and other heat illnesses are diagnoses made clinically. However, diagnostic testing can help rule out alternative diagnoses and evaluate for concurrent organ dysfunction and metabolic derangements.
Immediately test point-of-care glucose because hypoglycemia is a common and easily reversible cause of altered sensorium. Hypoglycemia also sometimes accompanies exertional heat stroke since glucose reserves may become depleted from physical activity. Blood work-ups can include a complete blood count to evaluate for infection, creatinine to rule out acute kidney injury, and metabolic profile to assess for electrolyte imbalance. Hypernatremia may be present in severe dehydration. Hyponatremia and hypercalcemia may be present in patients who are dehydrated with hypotonic solutions after extreme physical activity. Hyperkalemia may be associated with acute kidney injury.
Blood gas analysis may help differentiate classical and exertional heat stroke. Classical heat stroke usually presents with respiratory alkalosis from hyperventilation as a compensatory mechanism to extreme heat. In contrast, exertional heat stroke may present with lactic acidosis from repeated muscular contractions from physical exertion [4]. Moreover, elevation of liver enzymes is very common in both EHS and CHS, mainly due to direct thermal injury and hypoxia from splanchnic vascular redistribution. Hepatic damage is almost always mild and reversible despite rare reports of fulminant hepatic failure from heat stroke [4,10].
Concerns for a central neurologic etiology for the patient’s encephalopathy can be assessed with CT brain imaging and CSF analysis. These studies should be especially considered if focal neurologic deficits, slurring of speech, nuchal rigidity, or meningeal signs persist despite lowering the core temperature.
Risk Stratification
Minor heat illnesses are generally self-limited and have good outcomes. Heat stroke, on the other hand, is a life-threatening emergency. Mortality rate is correlated with the maximum core temperature and time to initiate cooling methods [4]. A study in 2018 also showed that the presence of disseminated intravascular coagulation is an independent prognostic factor for hospital mortality in patients with heat stroke [11]. Patients suffering from multiple organ injuries due to thermal injury also have poorer prognosis, so it is imperative to closely monitor renal, hepatic, and cardiovascular status of heat stroke patients [10,12].
Management
A core temperature above 40°C should prompt the clinician to consider heat stroke and initiate rapid cooling.
Heat stroke is a time-sensitive condition where cooling takes precedence over everything else, including confirmation of the diagnosis. Every patient should be approached with the ABCDE assessment to ensure that all critical decisions are made promptly. Heat stroke is not an exception to this role, as the disturbance in consciousness could result in significant airway complications. A complete airway assessment should be immediately performed when the patient arrives in the emergency department while cooling measures are being set up. Many heat stroke patients may have a depressed level of consciousness, but the decision to intubate is ultimately clinical and based on local resources. Airway protection is paramount and should take priority over any other diagnostic or therapeutic procedures. Peripheral blood pooling is a component of heat stroke pathology, so hypotension is common in these patients. Intravenous fluid administration should be judicious, as blood pressure usually picks up as the core temperature drops. Aliquots of 250cc of crystalloids should be used when fluids are needed, and repeated dosing should take place after volume status assessments.
In heat stroke, external cooling methods are the main pillar of therapy. Antipyretics, such as Paracetamol, have no proven benefit in such cases. The fastest way to cool patients is through conduction, the direct transfer of heat between molecules. Full body water immersion can do this, and although this is theoretically the best cooling method, it is clinically challenging. Immersion of the patient in water poses a risk of aspiration and renders the patient’s accessibility quite difficult. Alternatively, ice packs can be placed on the patient’s neck, axilla, and groin areas. Convection, heat loss due to gas movement around the body, combined with evaporation, can achieve a cooling speed similar to full-body immersion. This combination can be achieved by spraying the patient with lukewarm water followed by fanning with warm air. Mist fans are very convenient and have the added benefit of their ability to fan multiple patients at once.
One complication of these cooling maneuvers is shivering. Shivering needs to be controlled as it increases internal heat generation. This can be overcome by administering benzodiazepines. It should be noted that high ambient temperature and high humidity make convection and evaporation less effective. For this reason, if these patients are encountered in the prehospital setting, the first priority is to remove them from the hot and humid environment [4,7].
Internal cooling procedures, such as cold IV fluids and internal cold fluid lavages, do not have high quality to support their safety and efficacy in heat stroke patients [4]. Internal cooling with cardiopulmonary bypass can be considered in severe cases that do not respond to typical cooling methods. However, it is costly, resource-intensive, and unavailable in many contexts [4]. Rapid and aggressive external cooling with evaporative cooling, cold water immersion, and ice packs should be prioritized as the initial preferred cooling methods. Invasive measures, like thoracic, bladder, rectal, or peritoneal lavage, should only be used when other measures fail.
Special Patient Groups
Patients at extremes of age are at increased risk for heat-related illnesses and should be carefully considered for these conditions when presenting with fever [4].
Pediatrics
Classical heat stroke can occur in pediatric patients, but these patients are also at risk of another type of heat stroke known as confinement hyperpyrexia. This happens when a child is left inside a vehicle with poor ventilation during extreme heat. Pediatric patients are especially susceptible to heat stroke because they still lack adequate thermoregulatory mechanisms and the instinctive capacity to replace their fluid losses [4]. Child abuse should be considered, and necessary actions should be taken to protect the child from abuse or maltreatment.
Pregnant Patients
Pregnant individuals are particularly vulnerable to heat-related illnesses due to physiological changes that increase metabolic and cardiovascular demands. Conditions such as heat cramps, heat exhaustion, and heat stroke can arise from prolonged heat exposure, posing risks to both maternal and fetal health, including preterm birth and low birth weight. Management involves moving the patient to a cooler environment, ensuring hydration with non-caffeinated drinks or intravenous fluids if needed, applying cooling measures like wet cloths and fans, and monitoring vital signs closely. Preventive measures are crucial and include staying hydrated, wearing lightweight clothing, avoiding outdoor activities during peak heat, and utilizing air-conditioned spaces. Recognizing early symptoms, such as excessive sweating, dizziness, or confusion, and seeking immediate medical care when necessary are critical to preventing complications.
Geriatrics
Geriatric patients may have comorbidities or take daily medications that impair thermoregulation or mobility, making them prone to heat-related illnesses. This population has a higher heat stroke mortality rate and is more likely to experience complications of heat stroke [4]. Advocating for closer community ties, monitoring by family or peers, and improved socioeconomic support may help elderly patients evade health-related illnesses.
Mass Gatherings
Preparing for a mass gathering event should involve mitigation measures for a possible mass casualty incident of heat stroke and heat exhaustion patients, especially during hot or humid summer months. Public education should be employed to seek shade, drink enough fluids, and use umbrellas. Preparations should also include installing mist pipes, vent fans, and nearby cooling stops.
When to admit this patient
Patients with minor heat illness (e.g., heat edema, cramps, and stress) can generally be discharged home. They should be advised to refrain from strenuous activities during extreme heat conditions, drink plenty of fluids, and wear light and loose-fitting clothing. Those who suffer from heat cramps should be advised to avoid hypotonic solutions for fluid replacement to prevent relative electrolyte deficiencies [4].
Consider admission for patients with minor heat illness but have comorbidities, such as congestive heart failure and renal failure, and those with severe electrolyte abnormalities. Patients suffering from heat stroke must be admitted after resuscitation and rapid cooling in the emergency department. Heat stroke patients need admission to adequately monitor core temperature and possible occurrence of late complications, such as renal failure, hepatic injury, and electrolyte abnormalities. Patients who are intubated or unstable hemodynamically require ICU admission for closer monitoring [4].
Revisiting Your Patient
You immediately assess the patient’s ABCDEs as part of the primary survey. You assess the patient’s airway for the presence of stridor and pooling of oral secretions. The airway is normal. The patient is able to speak in sentences, albeit confused. He is tachypneic but has normal work of breathing and clear breath sounds. Again, you note that the patient is hypotensive at BP 80/50, tachycardic at HR 115, and hyperthermia at 41.5oC. You start infusing 500 mL of normal saline intravenously as a bolus. The patient was confused but did not exhibit lateralizing weakness, slurring of speech, or nuchal rigidity. Point-of-care glucose was done to rule out hypoglycemia, which revealed 146 mg/dL. You did not elicit any history of trauma, and you did not note any obvious abrasions, lacerations, or bleeding. After the IV bolus, reassessment was as follows: BP 90/60, HR 110, RR 24, T 41.5oC, SpO2 98%, and GCS 13 (E3V4M6)
On further history taking, you elicit that the patient has no allergies, no daily medications, no known comorbidities, and last ate 3 hours ago. You learn the patient was at football team practice for 2 hours at noon today when they noted that the patient had decreased verbal responses, responded inappropriately, and was extremely warm to touch. There was no vomiting, headache, lateralizing weakness, or trauma noted during the incident. There was no history of cough, dyspnea, and fever in the preceding days. The coach said the patient had only joined the football team 4 days prior. You insert a rectal thermometer and note a temperature of 42.0oC. With this information, you suspected that the patient may be suffering from an exertional heat stroke and decided that the goal was to decrease the core temperature to less than 39oC as soon as possible. You immediately remove the patient’s clothing while still maintaining modesty. You direct a vent fan to the patient by incorporating water sprays and placing ice packs on the patient’s neck, axillary, and groin areas.
After 30 minutes of cooling, you observe shivering. To decrease the internal heat production that shivering may cause, you administer diazepam 2.5 mg IV, and the shivering subsides. A cardiac monitor with pulse oximetry is connected, and blood samples are drawn to evaluate for organ dysfunction and possible sepsis. After reaching a rectal temperature of 39°C, you direct your team to dry cover the patient with a light bed sheet. Upon subsequent examination, the patient was conscious, alert, and oriented. Vitals are BP 110/60, HR 105, RR 22, T 38.5oC O2Sat 96% on room air. Laboratories are remarkable for metabolic acidosis and elevated liver enzymes. Complete blood count is unremarkable. You admit the patient to a general medical ward for further monitoring and management.
Authors
Patrick Joseph G. Tiglao
Dr. Patrick Joseph G. Tiglao, FPCEM is a practicing Emergency Medicine Physician at the University of the Philippines - Philippine General Hospital. He is also affiliated with DOH regional hospitals in the other parts of the Philippines namely, Corazon Locsin Montelibano Memorial Regional Hospital in Bacolod City, Negros Occidental and Eastern Visayas Medical Center in Tacloban City, Leyte Province.
Rhodney P. Canada
Dr. Rhodney P. Canada graduated, being the top of his class, Doctor of Medicine from the University of St. La Salle – Bacolod in 2018. He spent a year of post-graduate internship at the University of the Philippines Manila – Philippine General Hospital from 2018-2019. Currently, he is a senior 4th year and Chief Resident of the Department of Emergency Medicine in Corazon Locsin Montelibano Memorial Regional Hospital, Bacolod City, Negros Occidental, Philippines.
Emmanuel Luis S. Mangahas
Philippine General Hospital
Acknowledgement
The authors would like to express their utmost gratitude to Dr. Abdulaziz Al Mulaik, the author of this chapter in the previous edition.
Listen to the chapter
References
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- Tollefson J. Top climate scientists are sceptical that nations will rein in global warming. Nature. 2021; 599(7883):22-24.
- Yang J, Zhou M, Ren Z, et al. Projecting heat-related excess mortality under climate change scenarios in China. Nat Commun. 2021; 12 (1039)
- LoVecchio F. Heat Emergencies. In Tintinalli J, ed. Emergency Medicine A Comprehensive Study. 9th ed. USA: McGraw Hill; 2020: 1345-1350
- Heat and Health. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/climate-change-heat-and-health. Published June 2018. Accessed April 2023.
- Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heatstroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183
- Beltran G. Heat-related Illneses. In Cone D, ed. Emergency Medical Services Clinical Practice and Systems Oversight. 3rd ed. New Jersey, USA: John Wiley & Sons; 2021: 403-409
- Benedetto W. Heat Stroke. In Parsons P, Wiener-Kronish J, ed.Critical Care Secrets. 5th ed. Mosby; 2013: 541-544
- Hifumi T, Kondo Y, Shimizu K, Yasufumi M: Heat stroke. J Intens Care. 2018: 6(30)
- Grogan H, Hopkins PM. Heat stroke: implications for critical care and anaesthesia. BJA. 2002: 88(5):700–707
- Hifumi T, Kondo Y, Shimazaki J, et al. Prognostic significance of disseminated intravascular coagulation in patients with heat stroke in a nationwide registry. J Crit Care. 2018;44:306-311
- Liu S, Xing L, Wang J, et al. The Relationship Between 24-Hour Indicators and Mortality in Patients with Exertional Heat Stroke. Endocr Metab Immune Disord Drug Targets. 2022;22(2):241-246
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Reviewed and Edited By
Joseph Ciano, DO, MPH, MS
Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.
Arif Alper Cevik, MD, FEMAT, FIFEM
Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.
