Heat illness (heat exhaustion and heat stroke)

Heat exhaustion and heat stroke — the AU general practice approach

Heat exhaustion (core 38–40 °C, sweating intact, orientation intact) and heat stroke (core above 40 °C with CNS dysfunction) form a dangerous spectrum. Mortality approaches 50% when cooling is delayed beyond two hours.

Cool immediately — cold-water immersion for exertional heat stroke, evaporative cooling (water spray, fan, ice packs to neck and groin) for frail elderly. Cold IV fluids for all. Do not give paracetamol or NSAIDs — the mechanism is environmental, not cytokine-driven.

Review heat-modifying medications (anticholinergics, diuretics, antipsychotics, lithium) before each summer in vulnerable patients.

Heat illness in Australia — the clinical stakes

Heat kills more Australians than any other natural hazard — more than bushfires, floods, cyclones, and storms combined. Bureau of Meteorology data document approximately 50–200 heat-related deaths nationally in a typical year, with sharp event spikes: the January 2009 heatwave that preceded Black Saturday killed 374 Victorians from heat alone, more than the fires themselves. Climate change projections (Vardoulakis Lancet 2014) indicate that heat-related mortality will approximately double by 2050 without mitigation.

General practice is on the front line. Vulnerable patients — elderly, frail, socially isolated, chronically ill, on heat-modifying medications — often have the GP as their first contact before a heatwave escalates. Two presentations demand different responses: heat exhaustion, where mental state is preserved and the situation is reversible with basic cooling and hydration; and heat stroke, a life-threatening emergency requiring immediate aggressive cooling and category-1 transfer.

The single most important clinical principle is time. Mortality from heat stroke approaches 50% when core temperature remains above 40 °C for more than two hours. It falls below 1% when core temperature is brought below 39 °C within 30 minutes (Demartini Wilderness Environ Med 2015; Casa Curr Sports Med Rep 2015). This gap defines the GP’s task.

A. Core clinical — the AU general-practice framework

The spectrum

Therapeutic Guidelines (eTG) and Bouchama NEJM 2022 define three stages:

Heat cramps — painful muscle cramping during exertion in heat from sodium and water loss. Temperature is normal or mildly elevated; mental state is fully intact. Treatment: rest, shade, oral electrolyte replacement (Gastrolyte). Does not mandate hospitalisation.

Heat exhaustion — core temperature 38–40 °C, profuse sweating, fatigue, malaise, headache, nausea, tachycardia, orthostatic hypotension. Mental state remains intact — the patient is oriented and able to follow commands. Reverses with rest, moving to a cool environment, and oral or IV rehydration. Warrants close observation because the clinical boundary with heat stroke is not always sharp.

Heat stroke — core temperature above 40 °C with CNS dysfunction (confusion, ataxia, dysarthria, seizure, or coma). This is the emergency. Two phenotypes:

  • Classical (non-exertional) heat stroke — heatwave-driven, slow onset over hours to days in sedentary elderly patients with multimorbidity and limited access to air conditioning. Sweating is often absent (anhidrosis) at presentation.
  • Exertional heat stroke (EHS) — rapid onset (minutes to hours) during prolonged exertion in heat in young athletes, labourers, military trainees, and hikers. Sweating is typically preserved.

History to take

  • Heat exposure — duration, ambient temperature, humidity, air-conditioning access
  • Exertional vs sedentary onset
  • Mental state changes — bystander-observed timeline is important
  • Substance use — MDMA, cocaine, amphetamines (endogenous heat generation), alcohol (vasodilation, impaired judgement, diuresis)
  • Full medication list: anticholinergics (tricyclic antidepressants, older antihistamines, antipsychotics, oxybutynin), diuretics, beta-blockers, SSRIs/SNRIs, antipsychotics, lithium, stimulants
  • Comorbidities — cardiovascular disease, COPD, chronic kidney disease, neurological conditions (dementia, Parkinson’s), psychiatric illness, diabetes, thyroid disease
  • Last fluid intake, last urine output, sweating status
  • Acclimatisation — recently arrived from a cooler climate, first days of an outdoor labour season

Examination

  • Rectal core temperature — peripheral readings (oral, axillary, tympanic) are unreliable at extremes; rectal temperature is the clinical standard; oesophageal probe if intubated
  • Vital signs — HR, BP (orthostatics if tolerated), RR, SpO₂, GCS
  • Mental state — orientation, command-following, gait, dysarthria
  • Skin — sweat status (anhidrosis = classical phenotype; sweating preserved = exertional), heat rash (miliaria), contact burns
  • Neurological — cerebellar signs, reflexes, focal weakness, pupil responses

Workup in the GP setting

  • Rectal temperature — the priority step before other investigations
  • Capillary blood glucose — exclude hypoglycaemia as a co-existing or confounding problem
  • ECG — sinus tachycardia, repolarisation changes, ischaemia, hyperkalaemia changes from rhabdomyolysis
  • Urinalysis — brown urine positive for blood without red cells on microscopy indicates myoglobinuria from rhabdomyolysis

The critical principle: do not delay cooling to investigate. Initiate aggressive cooling immediately on clinical recognition. Investigations are performed in parallel or after, never before.

Initial management — cool early, cool fast

The management sequence aligns with eTG, ACSM 2007 position stand, Casa 2015, and Wilderness Medical Society 2024 guidelines:

  1. Recognise — core above 40 °C with altered mental state is heat stroke until proven otherwise.
  2. Move to a cool environment — air-conditioned room, shaded area, out of direct sun and exertion.
  3. Remove all clothing — reduces convective and radiative heat retention.
  4. Cool the body:
    • Cold-water immersion (CWI) — gold standard for exertional heat stroke when a tub of ice water is accessible (sports facilities, pool change rooms, GP clinics with bathing facilities). Immerse to neck level, monitor rectal temperature continuously, remove at 38.5–39 °C to avoid overshoot hypothermia. Cooling rate approximately 0.16 °C/min; mortality below 1% if core temperature reaches below 39 °C within 30 minutes (Demartini 2015).
    • Evaporative + ice-pack cooling — preferred for frail elderly patients with classical heat stroke where immersion is impractical. Continuous tepid water spray plus electric fan plus ice packs to the neck, axillae, and groin. Cooling rate ~0.04–0.06 °C/min — slower than CWI but feasible in any setting including residential aged-care facilities.
  5. Cold IV fluids — Hartmann’s solution or 0.9% sodium chloride, 500–1000 mL bolus then approximately 1 L/hour. Refrigerated bags accelerate internal cooling.
  6. Airway and breathing — supplemental oxygen; intubate if GCS below 8 or airway at risk.
  7. Seizures — midazolam 5 mg IV/IM/buccal or lorazepam 2–4 mg IV; benzodiazepines also suppress shivering (which generates heat and counteracts cooling).
  8. Do not give antipyretics — paracetamol and NSAIDs are ineffective and harmful in heat stroke (see FAQ). Per Bouchama Crit Care Med 2007 and Casa 2015, these agents are explicitly contraindicated.
  9. No dantrolene — outside confirmed malignant hyperthermia. The mechanism of environmental heat stroke is different; RCTs show no benefit (Bouchama 2007).
  10. Category-1 ambulance transfer (000) — pre-alert the receiving ED. Continue active cooling throughout transport — cold water spray plus fan is the most accessible ambulance option. Continue IV fluids en route.

B. Cooling evidence — what supports each method

The core clinical question is which cooling method to deploy, and this depends primarily on patient phenotype and setting.

Cold-water immersion for exertional heat stroke. Multiple observational and cohort series support CWI as the most effective cooling method for EHS. The ACSM 2007 position stand and Demartini Wilderness Environ Med 2015 review both demonstrate mortality below 1% when EHS is treated with CWI to bring core temperature below 39 °C within 30 minutes. The “cool first, transport second” (CFTS) doctrine — endorsed by ACSM and WMS — recommends beginning immersion at the point of collapse rather than delaying for ambulance arrival. Concerns about cardiac arrhythmia from cold-water shock have not been substantiated in published series involving otherwise healthy young athletes and labourers.

Evaporative cooling for classical heat stroke in the elderly. Continuous tepid water spray plus a fan plus ice packs to major vascular regions (neck, axillae, groin) achieves meaningful cooling and is well tolerated by frail patients. This approach is recommended by Bouchama Crit Care Med 2007 and WMS 2024 guidelines for the classical phenotype. The slower cooling rate compared to CWI is partly offset by the typically slower onset of classical heat stroke.

Antipyretics — do not reach for them. Paracetamol and NSAIDs reset the hypothalamic temperature set-point by blocking the cytokine cascade that drives it upward in infection. Environmental heat stroke does not involve a cytokine-mediated set-point elevation — it is direct thermal injury and circulatory failure. Antipyretics are mechanistically inactive. Paracetamol worsens heat-induced hepatic injury; NSAIDs worsen acute kidney injury and disseminated intravascular coagulation (DIC) (Bouchama 2007).

Dantrolene — not indicated. Dantrolene blocks sarcoplasmic calcium release — the mechanism of malignant hyperthermia (an anaesthetic-triggered reaction) — and is not the pathway in classical or exertional heat stroke. RCTs and meta-analyses show no benefit (Bouchama 2007).

C. Prevention and the Australian heatwave landscape

Australian heat mortality data from AIHW and climate projections make heatwave preparedness a core element of chronic-disease management and preventive care in Australian general practice.

Medication review before summer. The RACGP polypharmacy framework supports applying a STOPP/START lens to heat-modifying medications at the beginning of the warm season. Anticholinergics impair sweating; diuretics and ACE inhibitors/ARBs reduce circulatory reserve; beta-blockers blunt the tachycardic heat response; antipsychotics disrupt central thermoregulation; lithium has a narrow therapeutic window that narrows further with dehydration. Temporary dose reduction or suspension during heatwave alerts — discussed with patients and their relevant specialists — is a practical risk-reduction intervention per the AMH.

Heatwave alerts. The Bureau of Meteorology Heatwave Service issues three-tier alerts (low, severe, extreme). GP practices can register at-risk patients and make proactive phone calls during severe or extreme alerts. This intervention has mortality benefit in community-level heatwave-plan evaluations.

Cooling access. Many heatwave deaths in elderly patients occur in poorly ventilated apartments without air conditioning. LGA cooling centres (libraries, community centres, shopping centres) are a practical resource. Document cooling-centre locations in care plans and advise families and carers. NSW Health — Beat the Heat and VIC Department of Health — Heat Health maintain state-specific cooling-centre directories.

Occupational heat safety. Safe Work Australia’s working in heat guidance mandates Wet Bulb Globe Temperature monitoring and work-rest cycles in at-risk industries (construction, mining, agriculture, emergency services). GPs supporting workers in these sectors can advise on heat acclimatisation (a 10–14 day graduated heat-exposure program reduces EHS incidence approximately 70%), conduct fitness-to-work assessments, and write supporting letters for staged warm-season return-to-work.

ATSI remote communities. The Top End and remote communities face the highest per-capita heat-mortality burden in Australia, compounded by limited cooling-centre access, water-security gaps, and under-resourced health infrastructure. Heat-vulnerability review should be integrated into MBS item 715/10987 ATSI health assessment cycles, with NACCHO-endorsed frameworks and Aboriginal Health Worker liaison.

D. Australian operations

MBS items. Initial acute assessment: Level B/C/D consults (23 / 36 / 44). Post-discharge chronic-disease review: GPMP 965 / 967; 75+ comprehensive health assessment 705 / 707 with a heat-vulnerability module. ATSI health assessment: 715 / 10987. Telehealth post-discharge follow-up: 91790 / 92029. Mental Health Care Plan for climate distress or heat anxiety: 2715 / 2717.

Notification. Heat-related death is not directly notifiable to public health authorities but warrants coronial referral when heat is the attributable cause during a heatwave. Occupational heat illness causing more than seven days of lost time is notifiable to the relevant state SafeWork authority under the Work Health and Safety Act.

PBS-relevant prescribing. IV fluids (Hartmann’s, 0.9% sodium chloride) are hospital supply. Oral electrolyte solution (Gastrolyte) is over-the-counter and appropriate for heat cramps and recovery. Benzodiazepines (midazolam, diazepam) for seizure management are PBS general. Paracetamol and NSAIDs are PBS-listed but explicitly contraindicated in heat stroke.

E. Special populations

Elderly and frail. The classical phenotype — slow-onset heatwave heat stroke in elderly multimorbid patients, often anhidrotic — accounts for the majority of Australian heat deaths. These patients are frequently on multiple heat-modifying medications. Evaporative cooling is preferred over immersion. Proactive pre-summer medication review and heatwave alert registration are the primary preventive interventions.

ATSI remote communities. Environmental, socioeconomic, and geographic factors compound heat risk substantially. Aboriginal Health Worker-led prevention and community cooling access are priority interventions. Integrate heat-risk flagging into 715 health assessment cycles, care plans, and chronic-disease management plans.

Pregnant women in the third trimester. Thermoregulation is impaired in late pregnancy — the placenta generates heat, and expanded blood volume plus reduced peripheral vascular resistance limit adaptive heat dissipation. Advise avoiding outdoor activity during peak heat (11:00–16:00), staying in cool environments, increasing fluid intake, and presenting promptly with any reduced foetal movement, contractions, or systemic illness during heatwaves.

Young athletes and labourers. EHS is the dominant phenotype in this group. The “cool first, transport second” doctrine applies: if a teammate or co-worker becomes confused, stops sweating, collapses, or shows ataxia in the heat — strip gear, cold-water immersion if accessible, ice packs to neck and groin, water spray plus fan — and call 000 while continuing cooling.

Infants. Impaired sweating capacity and inability to self-thermoregulate or communicate distress. Avoid leaving infants in parked vehicles. Evaporative cooling methods and urgent paediatric ED review if any reduced consciousness.

Patients with mental illness. Antipsychotics and tricyclic antidepressants directly impair central thermoregulation and peripheral sweating. Patients with severe mental illness may lack insight into overheating symptoms. Community outreach during heatwaves for this group has population-level mortality benefit.

When to escalate

Transfer via category-1 ambulance (000) immediately for:

  • Core temperature above 40 °C
  • Any CNS dysfunction — confusion, ataxia, seizure, coma
  • Persistent tachycardia and hypotension after initial fluid resuscitation
  • Anuria or oliguria below 0.5 mL/kg/hour
  • Tea-coloured urine or clinical features of rhabdomyolysis (severe muscle pain, CK rise)
  • Bleeding from cannula sites or petechiae (DIC)
  • Cardiac arrhythmia or ischaemic ECG changes

Continue active cooling throughout transport. Pre-alert the receiving ED — ICU pre-notification and cooling-equipment readiness improves outcome.

What this article is and is not

This is general health information drawn from Australian general practice guidelines — Therapeutic Guidelines, RACGP, Australian Medicines Handbook, NPS MedicineWise, and peer-reviewed emergency medicine literature — for educational purposes. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about medication changes during heatwaves, or any acute clinical management, are made with your own GP and treating team.

For Australian consumer resources on heat safety: NSW Health — Beat the Heat · VIC Department of Health — Heat Health · BOM Heatwave Service · HealthDirect — Heat Stroke.

For emergency heat illness: call 000 immediately for any person with confusion, seizure, or collapse in the heat.


Sources cited

  1. Bouchama A. Classical and Exertional Heat Stroke. NEJM 2022;387:1252–1262
  2. Bouchama A et al. Cooling and hemodynamic management in heatstroke. Crit Care Med 2007;35:2479–2483
  3. Casa DJ et al. Exertional Heat Stroke: New Concepts Regarding Cause and Care. Curr Sports Med Rep 2015;14:206–215
  4. Demartini JK et al. Effectiveness of Cold-Water Immersion in Exertional Heat Stroke. Wilderness Environ Med 2015;26:559–566
  5. ACSM Position Stand — Exertional Heat Illness during Training and Competition 2007
  6. Wilderness Medical Society — Heat Illness Practice Guideline 2024
  7. Vardoulakis S et al. Effects of climate change on heat and cold-related mortality. Lancet 2014;383:e22
  8. Therapeutic Guidelines (eTG complete) — Heat-related illness
  9. RACGP — Clinical resources
  10. Australian Medicines Handbook (AMH)
  11. NPS MedicineWise
  12. Bureau of Meteorology — Heatwave Service
  13. Safe Work Australia — Working in heat guide 2022
  14. NSW Health — Beat the Heat
  15. VIC Department of Health — Heat Health
  16. NACCHO — National Aboriginal Community Controlled Health Organisation
  17. AIHW — Environmental health and heat-related mortality
  18. Climate and Health Alliance — Heat & Health
  19. HealthDirect — Heat stroke

Frequently asked questions

  • What is the difference between heat exhaustion and heat stroke?

    Heat exhaustion (core 38–40 °C) features profuse sweating, fatigue, headache, nausea, tachycardia, and orthostatic hypotension — but mental state remains fully intact. The patient is oriented and can follow commands. It reverses with rest, cooling, and oral or IV rehydration. Heat stroke (core above 40 °C) adds CNS dysfunction — confusion, ataxia, dysarthria, seizure, or coma. That neurological change is the clinical red flag that transforms an uncomfortable medical situation into a life-threatening emergency requiring immediate aggressive cooling and category-1 ambulance transfer.

  • Why should I not give paracetamol or ibuprofen for heat stroke?

    Paracetamol and NSAIDs lower fever by resetting the hypothalamic set-point when it has been driven up by cytokines — during infection, for example. Heat stroke is mechanically different: the core temperature rises because of environmental heat load and circulatory failure, not because of a cytokine cascade. There is no set-point to reset. The drugs are simply ineffective for cooling. Worse, paracetamol worsens the heat-induced hepatic injury that occurs in severe heat stroke (AST/ALT often exceed 1000 in severe cases), and NSAIDs worsen the acute kidney injury and DIC that commonly complicate it.

  • Which medications make heat illness more dangerous?

    Several drug classes impair thermoregulation or circulatory reserve. Anticholinergics (tricyclic antidepressants, older antihistamines, antipsychotics, oxybutynin, hyoscine) block sweating. Diuretics and ACE inhibitors/ARBs reduce volume reserve. Beta-blockers blunt the tachycardic response to heat stress. SSRIs and SNRIs impair central thermoregulation and can contribute to serotonin syndrome overlap. Antipsychotics disrupt central temperature regulation. Lithium has a narrow therapeutic window that narrows further with dehydration — confusion from lithium toxicity can mimic and compound heat stroke. Stimulants (amphetamines, MDMA, cocaine) generate endogenous heat and impair perception of overheating.

  • How should I rapidly cool someone who has collapsed in the heat?

    Remove them from the heat source, strip all clothing, and begin active cooling immediately. For a young athlete or labourer with exertional heat stroke, cold-water immersion (tub of ice water to neck level, monitor rectal temperature, remove at 38.5–39 °C) achieves the fastest cooling — mortality falls below 1% when core temperature is brought below 39 °C within 30 minutes. For a frail elderly patient who cannot tolerate immersion, use continuous tepid water spray plus a fan plus ice packs to the neck, axillae, and groin. Cold IV fluids (500–1000 mL bolus, then approximately 1 L/hour) add internal cooling. Continue cooling throughout the ambulance transfer.

  • How can I reduce my at-risk patients' heat illness risk before summer?

    Conduct a STOPP/START-lens medication review at the start of the warm season, focusing on anticholinergics, diuretics, antipsychotics, and lithium — consider temporary dose reduction or suspension during extreme heatwave alerts, in discussion with the relevant specialists. Register at-risk patients for Bureau of Meteorology heatwave alerts. Document their access to a cool environment — if they have no air conditioning, identify the nearest LGA cooling centre (library, shopping centre). For frail elderly patients without family check-in, proactive phone calls during extreme heat alerts have population-level mortality benefit.

Source quality

Sources grouped by evidence tier. AU primary tier first; international where AU is silent or lagging; named-author reconstruction where guidelines have not yet caught up. How tiers work.