Medic 35 is dispatched to a local subdivision for an obese 62-year-old woman with syncope. The responding unit is a fire-based ALS unit staffed by two paramedics.
It’s approximately 2:30 p.m., with outside temperatures reaching 95 degrees F and the humidity is at 65%.The patient is lying in the grass next to a picnic blanket and paper plates with half eaten sandwiches. Her husband crouches over her. He says his wife started to complain she felt unwell, and then passed out.
Upon evaluation, she’s unresponsive to sternal rub. Her airway is patent. Her breaths are rapid and shallow with rales bilaterally. Her pulses are easily palpable. She’s flushed, but her skin is hot and dry. There’s no external evidence of trauma.
She’s placed on the monitor and vitals are as follows: respiratory rate (RR) of 24, heart rate (HR) of 132, blood pressure (BP) of 94/48, and oxygen saturation of 84% on room air. The paramedic initiates delivery of 100% oxygen via a non-rebreather (NRB) mask and she’s moved into the ambulance without difficulty.
Prehospital ECG demonstrates sinus tachycardia at 136 with a right bundle branch block (RBBB) and prolonged QTc interval. A 20-gauge IV is obtained in the left forearm and 1 L of normal saline is administered. The medication list provided by the husband includes sumatriptan, olanzapine and duloxetine. The patient is transported to the nearest hospital which is 10 minutes away with no change in condition.
On arrival, care is transferred to ED staff, who notes the patient has an HR of 140, a systolic BP of 95, and a pulse oximetry of 94% on NRB. She continues to be unresponsive to pain and is emergently intubated for airway protection. Secondary survey reveals no signs of trauma and normal rectal tone. There’s no muscular rigidity or clonus (i.e., rapid tensing and relaxing of muscles) noted.
The patient’s ECG reveals sinus tachycardia with prolonged QRS and prolonged QTc. Labs reveal an elevated creatinine indicative of acute kidney injury. Chest X-ray reveals pulmonary edema. A CT scan of the head demonstrates no sign of bleeding or abnormality.
A rectal temperature is noted to be critically high at 108 degrees F (42.2 degrees C). Evaporative cooling measures are undertaken, including mist spray bottle with fan along with a cooling blanket.
The patient is subsequently moved to the ICU with a rectal temperature of 102 degrees F (38.9 degrees C). With continued cooling, the patient improves rapidly and is extubated the following day. Her kidney function normalizes two days later. She’s discharged after six days in the hospital with no neurological deficits and a final diagnosis of environmental hyperthermia.
Hyperthermia is the elevation of core body temperature above 99.5 degrees F (37.5 degrees C), which is the generally accepted upper limit of normal.1 Environmental hyperthermia is an elevated core body temperature due to the body’s thermoregulatory capabilities being overwhelmed by environmental conditions.2,3 Heat exhaustion is usually defined as a core temperature between 100.4 degrees F (38.0 degrees C) and 104.0 degrees F (40 degrees C) and is accompanied by systemic symptoms including nausea, vomiting, malaise and lightheadedness.3 Physical signs include tachycardia, decreased urine output, and diaphoresis. There’s no associated neurologic dysfunction.3,4 If not treated, heat exhaustion will develop into heat stroke, which is defined as a core temperature above 104 degrees F (40 degrees C) with associated neurologic dysfunction. The physical exam may demonstrate tachycardia, tachypnea, flushing of the skin, pulmonary crackles, altered mental status, agitation, syncope, seizures or coma.3–5
Hypotension may develop due to cutaneous vasodilation, diaphoresis-induced hypovolemia or cardiac dysfunction.4,5 The patient eventually develops multi-organ failure with rhabdomyolysis, renal injury, cardiovascular collapse, respiratory failure and disseminated intravascular coagulation.3–7 Heat stroke carries an estimated mortality of 10%–63%.2–5,7,8 Elderly people with comorbidities such as coronary or pulmonary disease, patients with psychiatric disease, young children, and patients presenting with hypotension or somnolence have the highest mortality.2,6,7
The first step in managing environmental hyperthermia is recognizing it. This doesn’t require obtaining a core temperature, but EMS medical directors should consider protocols that include temperature checks when ambient temperatures surpass certain preset values. Rectal temperature is the most accurate,1 but this isn’t feasible in most prehospital settings.
Once hyperthermia is recognized, there’s a mortality benefit to rapid cooling, with a goal of 100.9 degrees F (38.3 degrees C) to prevent iatrogenic hypothermia.3,4,9 The patient should be moved out of the hot environment, preferably into an air-conditioned space, and their clothing should be removed.3,4 There are many different treatment modalities and protocols may include infusing small volumes (250 cc boluses) of cooled IV normal saline, placing ice packs or other similar equipment in the axilla, neck and groin,3–6 or use of a commercial cooling blanket.
Partial immersion in ice water has been shown to be effective, but is poorly tolerated and not feasible for general EMS operations. Evaporative cooling with convection is efficacious, well tolerated, and easy to perform by soaking a sheet in tepid sterile fluid (such as normal saline) and fanning this over the patient. However, there isn’t enough evidence to support one particular method as superior to another. There’s also no demonstrated benefit to antipyretics and their use isn’t recommended.3–6 Shivering can be controlled with IV fentanyl and if allowed by protocol.10
Patients may require airway management if their mental status declines or if they develop hypoxia. Prehospital providers should follow their local airway management protocols. If hypotension or tachycardia is present, small IV crystalloid boluses should be given.4,6 Large-volume boluses should be used with caution due to concern regarding development of pulmonary edema.9 Avoid vasopressors unless absolutely necessary, as there’s theoretical concern that any peripheral vasoconstriction could slow heat loss. Prehospital ECGs should be obtained to screen for cardiac dysfunction.3,5 Seizures should be managed with benzodiazepines.4
In addition to environmental hyperthermia, there’s a broad differential diagnosis to consider in the patient with an elevated core temperature, including sepsis, intracranial bleed, thyrotoxicosis, medication overdose (e.g. lithium, sympathomimetics), serotonin syndrome, neuroleptic malignant syndrome (NMS) and seizures. The prehospital provider should consider this list when presented with a patient with hyperthermia, and use the history and physical exam to help narrow the diagnoses. In this case, NMS and serotonin syndrome were both possibilities due to the patient’s medications and ECG findings; however, both were ruled out by the patient’s lack of muscular rigidity and her rapid improvement.
Despite concerns for another etiology, it’s recommended that treatment of possible environmental hyperthermia be initiated as early as possible given the mortality of the disease and the minimal risks of cooling. Furthermore, prompt patient recovery with cooling measures can be used as a diagnostic aid as it strongly suggests environmental hyperthermia.4
Environmental hyperthermia is a relatively uncommon chief complaint in the prehospital setting. Once recognized, it should be managed with rapid initiation of cooling according to protocol. Cardiopulmonary support may also be required. Although there are many other underlying etiologies that cause elevated temperatures, consideration of these shouldn’t delay treatment.
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2. LoVecchio F, Pizon AF, Berrett C, et al. Outcomes after environmental hyperthermia. Am J Emerg Med. 2007;25(4):442–444.
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8. Bouchama A, Debhi M, Mohaned G, et al. Prognostic factors in heat wave related deaths: A meta-analysis. Arch Intern Med. 2007;167(20):2170.
9. Vicario SJ, Okabajue R, Haltom T. Rapid cooling in classical heat stroke: Effect on mortality rates. Am J Emerg Med. 1986;4:394–398.
10. Choi HA, KoSB, Presciutti M, et al. Prevention of shivering during therapeutic temperature modulation: the Columbia anti-shivering protocol. Neurocrit care. 2011;14(3):389–394.