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Hyperthermia and Heat Stroke – Diagnosis, Treatment, ICU

The Anesthesia Guide » Topics » Hyperthermia and Heat Stroke – Diagnosis, Treatment, ICU

Author:
Kai Knudsen



Updated:
30 August, 2025

Exogenous heat stroke is a life-threatening condition caused by external heat stress in combination with impaired thermoregulation. The condition is characterized by a core temperature ≥ 40 °C and neurological symptoms, and particularly affects individuals exposed to physical exertion, high humidity, or thermoregulatory-impairing medications. Prognosis is highly dependent on early diagnosis and the rapid initiation of active cooling, preferably within the first hour. Treatment aims to lower body temperature and prevent complications such as shock, coagulopathy, organ failure, and sepsis-like syndromes.

Content:
  1. Heat Stroke
  2. Definition of hyperthermia
  3. Effect of Heat Stress and Heat Stroke on Circulating Cytokines, Cytokine Receptors, Growth Factors, and Chemokines
  4. First line – Prehospital care
  5. Emergency department
  6. Intensive care – Acute and supportive management
  7. Treatment of hyperthermia in the ICU
  8. Available cooling methods for hyperthermia in the ICU

Heat Stroke

Introduction

Exogenous heat stroke is an acute, potentially life-threatening condition that occurs when the body’s thermoregulation is overwhelmed by external factors such as high ambient temperature, physical exertion and high humidity. It particularly affects risk populations—for example people performing heavy physical work in hot environments, military personnel, athletes, and patients under the influence of medications or toxic substances that impair thermoregulation. Heat stroke following intense physical exertion in a hot environment is referred to as exertional heat stroke.

The diagnostic hallmark is a core temperature ≥ 40 °C combined with neurological symptoms such as confusion, delirium, seizures or coma. Early recognition is essential, as prognosis largely depends on the rapid initiation of cooling. The first hour after onset—often called the “frozen hour”—is critical to prevent irreversible organ damage.

Treatment consists of immediate active cooling, with cold-water immersion or use of a cooling tunnel constituting the gold standard. In the emergency department and intensive care unit, evaluation and treatment of potential complications such as circulatory shock, coagulopathy, renal and hepatic failure, and sepsis-like syndromes are added. At the same time, differential diagnoses—including malignant neuroleptic syndrome—must be excluded.

Although exogenous heat stroke is rare in Nordic climates, it can rapidly develop into a catastrophic situation. Clinical success depends on preparedness, early diagnosis, and systematically applied interventions from prehospital care through intensive care.

Definition of hyperthermia

ConditionDefinition
Heat waveThree or more consecutive days with air temperature >32.2 °C.
Heat stressPerceived discomfort and physiological strain associated with exposure to a hot environment, especially during physical work.
Heat strokeSevere illness with core temperature >40 °C and central nervous system abnormalities (delirium, convulsions, coma). Caused by environmental heat (classic heat stroke) or strenuous exercise (exertional heat stroke).
Heat exhaustionMild-to-moderate illness due to water or salt depletion from exposure to heat or strenuous exercise. Symptoms include thirst, weakness, anxiety, dizziness, fainting, headache. Core temperature may be normal, low, or slightly elevated (>37 °C but <40 °C).
HyperthermiaRise in body temperature above hypothalamic set point when heat-dissipating mechanisms are impaired (drugs, disease) or overwhelmed (environmental, exertional).
Multiorgan-dysfunction syndromeContinuum of changes in more than one organ system after insults such as trauma, sepsis, or heat stroke.

Effect of Heat Stress and Heat Stroke on Circulating Cytokines, Cytokine Receptors, Growth Factors, and Chemokines

Cytokine or FactorHeat StressHeat StrokeReference
Exercise-inducedEnvironmentalTherapeutic †ClassicExertional
Tumor necrosis factor αIncreased or unchangedUnchangedIncreased or unchangedIncreased or unchangedIncreasedBouchama et al., Espersen et al., Robins et al., Camus et al., Ostrowski et al., Moldoveanu et al., Suzuki et al., Chang, Hammami et al.
Interleukin-1βIncreased or unchangedNAIncreasedIncreased or unchangedIncreasedCannon and Kluger, Robins et al., Ostrowski et al., Moldoveanu et al., Chang, Bouchama et al.
Interleukin-2Decreased or unchangedNAUnchangedNANAEspersen et al., Robins et al.
Interleukin-6IncreasedIncreasedIncreasedIncreasedIncreasedRobins et al., Moldoveanu et al., Suzuki et al., Hammami et al.
Interleukin-8IncreasedNAIncreasedNAIncreasedPedersen and Hoffman-Goetz, Robins et al., Suzuki et al., Bouchama et al.
Interleukin-10IncreasedIncreasedIncreasedNANAPedersen and Hoffman-Goetz, Robins et al., Suzuki et al.
Interleukin-12Increased or unchangedNAUnchangedNANAPedersen and Hoffman-Goetz, Robins et al., Suzuki et al., Akimoto et al.
Interleukin-1 receptor antagonistIncreasedNANANANAPedersen and Hoffman-Goetz, Ostrowski et al., Suzuki et al.
Soluble interleukin-2 receptorIncreasedNANANANAPedersen and Hoffman-Goetz, Ostrowski et al.
Soluble interleukin-6 receptorNAIncreasedNADecreasedNASuzuki et al., Hammami et al.
Soluble tumor necrosis factor receptors (p55 and p75)IncreasedIncreased or unchangedIncreasedIncreasedNAPedersen and Hoffman-Goetz, Hammami et al.
Interferon-γIncreased or unchangedNAUnchangedIncreasedNAPedersen and Hoffman-Goetz, Robins et al., Suzuki et al., Bouchama et al.
Interferon-αIncreased or unchangedNAUnchangedNANASuzuki et al., Viti et al.
Granulocyte colony-stimulating factorIncreasedNANANANAPedersen and Hoffman-Goetz, Robins et al., Suzuki et al.
Macrophage-inhibitor proteinsIncreasedNAUnchangedNANAPedersen and Hoffman-Goetz, Robins et al.

* Data are from studies in human subjects. NA denotes data not available.
† Whole-body hyperthermia may be induced in cancer therapy.

First line – Prehospital care

1. Identify the at-risk population

  • Heat exposure
  • Physical exertion
  • High humidity
  • Inappropriate clothing (construction workers, military personnel …)
  • Medications and toxic substances (neuroleptics, alcohol …)

2. Diagnose early

Diagnostic criteria:

  • Core temperature ≥ 40 °C
  • Neurological signs: confusion, delirium, seizures, coma
  • Identified risk factor (heat)

Warning:
Neurological symptoms in a heat-related context → measure core temperature.

3. Prioritize cooling

  • When? As soon as possible—no later than within the first hour = Frozen Hour.
  • How? Gold standard:
    • Cold-water immersion (15–25 °C)
    • Cooling tunnel (water-pouring stretcher)
  • Less effective:
    • Immersion in lukewarm water
    • Wet sheets
    • Showering, hosing
  • Cooling must continue during transport.
  • Do not use water that is too cold to avoid skin vasoconstriction and reduced therapeutic effect.
Illustration comparing cold-water immersion and a cooling tunnel

Emergency department

1. Active cooling

  • Continuous core temperature monitoring
  • Target: at most 0.1 °C decrease per minute until temperature < 38.5 °C
  • Methods:
    • Cold bath
    • Cooling tunnel
    • Other methods: cold infusions, lavage …

2. Evaluate organ injury

  • Arterial blood gases
  • Blood count
  • Electrolytes, urea, creatinine, myoglobin
  • Liver tests, haemostasis, D-dimer
  • Echocardiography

3. Exclude differential diagnoses

  • Lumbar puncture, imaging
  • Measurement of drug concentrations
  • Contexts: malignant neuroleptic syndrome

4. Reassess neurological status

  • Improvement after cooling?
  • If no: intubation, sedation and ventilation

Intensive care – Acute and supportive management

  • Shock: vasoplegic or hypovolaemic
  • Coagulopathy/DIC: sometimes very early—requires monitoring and transfusion strategy
  • Renal failure: rhabdomyolysis, need for extracorporeal renal replacement (dialysis)
  • Liver failure (within 24–48 hours):
    • Cytolysis, hepatocellular insufficiency
    • If liver failure: refer to specialist centre
    • Avoid hepatotoxic treatments
    • N-acetylcysteine may be administered
  • Sepsis-like syndrome

Important: Monitor for recurrent hyperthermia.

Treatment of hyperthermia in the ICU

1. Targets

  • Rapid active cooling to < 38.5–39 °C
  • Avoid decreases > 0.1 °C/min
  • Prevent rebound hyperthermia

2. Monitoring

  • Continuous core temperature (oesophageal/rectal/bladder)
  • ECG, blood pressure (arterial line), SpO2
  • Fluid status, urine output target: > 0.5 ml/kg/h

3. Active cooling – order of priority

  1. Highest-capacity available method:
    • Immersion in 15–25 °C water (gold standard for exertional heat stroke, when feasible)
    • Alternative: cooling tunnel
  2. Surface systems (ICU-friendly):
    • Water/gel-circulating cooling blankets/pads
    • Evaporative cooling: spray lukewarm water + strong fan
  3. Adjuncts:
    • Ice/cold packs in groins, axillae, neck
    • Cold IV infusions (30 ml/kg, 4 °C saline/Ringer’s)—short-lived effect
    • Gastric/vesical/peritoneal lavage
  4. Invasive:
    • Intravascular cooling catheter (rapid, controlled induction/maintenance)
    • ECMO for refractory shock/hypoxia with hyperthermia (specialist resource)

4. Shivering prophylaxis and treatment

  • Opioid: fentanyl/remifentanil infusion
  • Dexmedetomidine infusion (0.2–1.4 µg/kg/h)
  • Buspirone 30 mg PO/NG
  • Magnesium: correct to high-normal range
  • Skin counter-warming (warm hands/feet)
  • Propofol infusion if deeper sedation needed
  • Neuromuscular blockade (cisatracurium/rocuronium) for refractory shivering

5. Avoid

  • Antipyretics (ineffective and may be harmful in heat stroke)
  • Dantrolene (not indicated except in malignant hyperthermia)

6. Complication surveillance

  • Circulation: risk of vasoplegic/hypovolaemic shock
  • Coagulation: DIC—follow PT, aPTT, fibrinogen, D-dimer, platelets
  • Kidneys: risk of rhabdomyolysis/AKI—serum creatinine, myoglobin, K+
  • Liver: follow ALT, AST, INR—refer to liver centre if failure
  • Infection/sepsis-like syndrome

✅ Stop active cooling at 38.5 °C
✅ Continue frequent temperature checks due to rebound risk

Available cooling methods for hyperthermia in the ICU

1) External conductive cooling

  • Cold water (immersion / cooling tunnel): fastest cooling in heat stroke (especially exertional). Typical cooling rates 0.15–0.35 °C/min in experimental/clinical series; target 38.5–39 °C to avoid overshoot. Logistically challenging in ICU (airway/lines, hygiene), and often less well tolerated by frail elderly with classic heat stroke.
  • Ice/cold packs over major vessels (axillae, groins, neck): easy to apply but lower cooling capacity—adjunct, not a sole method.

2) External evaporative/convective cooling

  • Spray/shower with lukewarm–cold water + strong fanning: effective and often better tolerated than baths in older patients, but slower (~0.05–0.09 °C/min). Can be combined with ice/cold packs.

3) Surface medical devices

  • Water-circulating blankets/gel pads (e.g., Arctic Sun-type): provide controlled induction and high precision in maintenance; induction usually slower than immersion but very ICU-friendly.

4) Intravascular cooling

  • Closed cooling catheters in a central vein: rapid and very stable temperature control (induction ~1–1.5 °C/h) with good maintenance precision; requires central access and carries invasive risks. Useful when surface cooling is insufficient or impractical.

5) Internal (cavity) cooling

  • Cold IV infusions (bolus) and lavage (gastric/colonic/vesical/peritoneal): can provide temporary reduction/bridging while higher-capacity methods are established; evidence for whole-body effect is limited/mixed and invasiveness increases. Consider selectively and as an adjunct.

6) Extracorporeal systems (ECLS/ECMO)

  • VA/VV-ECMO: consider in refractory circulatory failure/hypoxia with hyperthermia (severe heat stroke with ongoing collapse) for perfusion support and controlled heat exchange; requires experienced ECMO resources.

Adjunctive measures in the ICU (improve cooling efficacy/safety)

  • Continuous core temperature measurement (rectal or oesophageal; bladder if adequate diuresis): stop active cooling around 38.5–39 °C to avoid overcooling and rebound.
  • Shivering control: multimodal approach—opioid analgesia, dexmedetomidine/propofol, buspirone, magnesium, skin counter-warming; neuromuscular blockade if needed.
  • Avoid antipyretics in heat stroke (ineffective and may worsen coagulopathy/hepatic injury); dantrolene has no role in classic/exogenous heat stroke (mandatory in malignant hyperthermia).

Practical ICU prioritization

  1. Rapid active cooling with the highest-capacity available method—in the ICU this is usually surface systems (gel/water-circulating pads) ± evaporative fanning, or an intravascular catheter when faster precision is required/if surface methods fail; immersion may be considered where logistics allow.
  2. Targeted control: continuous core temperature; stop at 38.5–39 °C and avoid overshoot; continue close monitoring due to rebound risk.
  3. Aggressive shivering control per protocol.
  4. Treat the cause (MH/NMS/infection/endocrine crisis) in parallel.

In summary: immersion cools fastest but is often logistically difficult in the ICU; surface systems and/or intravascular cooling offer the best controllability. Internal lavage/cold infusions are mainly adjuncts. In refractory circulatory failure, ECMO can be considered at experienced centres.

References

  1. Sorensen C, et al. Treatment and Prevention of Heat-Related Illness. N Engl J Med. 2022. https://doi.org/10.1056/NEJMcp2210623
  2. Bouchama A, Knochel JP. Heat Stroke. N Engl J Med. 2002. https://doi.org/10.1056/NEJMra011089
  3. Epstein Y, Yanovich R. Heatstroke. N Engl J Med. 2019. https://doi.org/10.1056/NEJMra1810762
  4. Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. J Emerg Med. 2016. https://doi.org/10.1016/j.jemermed.2015.09.014
  5. Casa DJ, et al. National Athletic Trainers’ Association Position Statement: Exertional Heat Illnesses. J Athl Train. 2015. https://doi.org/10.4085/1062-6050-50.9.07

Effect of Heat Stress and Heat Stroke on Circulating Cytokines, Cytokine Receptors, Growth Factors, and Chemokines

 

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