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ICU TopicsEnvironmental emergencies

ICU · Environmental emergencies

Heat Stroke & Heat Illness

Also known as Heat stroke · Heat exhaustion · Heat illness · Exertional heat stroke · Classic heat stroke · Hyperthermia · Rapid cooling

The heat stroke — the core temperature above 40 degrees C with the CNS dysfunction (the confusion, the seizure, the coma). The two types (the classic — the elderly, the drugs; the exertional — the young, the athletes). The thermoregulatory failure → the multi-organ (the CNS, the cardiac, the liver, the renal, the DIC). The RAPID cooling (the priority — the ice-water immersion the fastest; the evaporative the practical). The NOT the antipyretics (the central set-point normal). The benzodiazepine for the shivering. The mortality 10 to 50 per cent.

medium7 referencesUpdated 2 July 2026
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Overview & definition

The heat stroke — the core temperature above 40 degrees C with the CNS dysfunction. The thermoregulatory failure → the multi-organ (the CNS, the cardiac, the liver, the renal, the DIC). The mortality 10 to 50 per cent (the delay → the higher). The RAPID cooling the priority.[1][1]

Cinematic ICU scene of a patient with cooling blankets and ice packs, IV fluid running, cardiac monitor tachycardia, thermometer suggesting high temperature, cool blue lighting suggesting active cooling
FigureThe heat stroke — the rapid cooling (the priority). The ice-water immersion (the fastest for the exertional); the evaporative (the practical for the ICU). The target below 39 degrees C as fast as possible. The NOT the antipyretics.

The two types

  • The classic (non-exertional) — the elderly, the comorbid, the drugs (the anticholinergics, the diuretics, the beta-blockers, the antipsychotics), the poor ventilation (the heatwave, the enclosed). The anhidrosis (the dry/hot skin).[1][2][1]
  • The exertional — the young, the athletes, the military, the labourers. The exertion in the heat → the thermogenesis exceeds the dissipation. The sweating (the skin may be wet). The rhabdomyolysis more common.[1][2]

The clinical

  • The hyperthermia (the core above 40).[1]
  • The CNS — the confusion, the agitation, the ataxia, the seizure, the coma (the hallmark — distinguishes from the heat exhaustion).[1][1]
  • The cardiovascular — the tachycardia, the hypotension, the distributive shock.[1][1]
  • The multi-organ — the AKI, the liver failure (the transaminitis, the coagulopathy), the rhabdomyolysis, the DIC.[1][1]

The management — rapid cooling

Downward-trending blue temperature line graph connected by an arrow to a water-droplet-and-fan evaporative cooling icon, on a white clinical-blue background
FigureThe rapid cooling — the priority. The target below 39 degrees C as fast as possible (the every the degree the minute the delay the increases the mortality). The fastest: the ice-water immersion. The practical ICU: the evaporative (the spray + the fan).
Heat stroke management pathway prioritising rapid cooling and multi-organ support
FigureCool first: immersion or evaporative methods to core below 39°C; benzos for shivering; fluids and organ support. Antipyretics and dantrolene do not work.

1. The rapid cooling (the priority).[1][2][1]

  • The ice-water immersion (the gold standard for the exertional — the fastest cooling rate, about 0.15 degrees C/min).[1]
  • The evaporative cooling (the practical ICU — the misting the body with the lukewarm the water + the continuous the fanning; about 0.1 degrees C/min).[1]
  • The cold IV fluids (the 30 mL/kg the balanced the crystalloid at the 4 degrees C).[1]
  • The cooling blankets (the gel pads, the Arctic Sun), the ice packs (the groin, the axillae, the neck).[1][1]
  • The target: below 39 degrees C, then the stop the active (the avoid the over-shoot the hypothermia).[1]

2. The NOT the antipyretics.[1]

  • The paracetamol / the NSAID the INEFFECTIVE (the central the hypothalamic the set-point is the normal in the heat stroke — the not the pyrogen-driven).[1]

3. The benzodiazepine.[1][1]

  • For the shivering (the shivering generates the heat — the defeats the cooling), the agitation, the seizures. The NOT the antipyretics; the NOT the dantrolene (the not the true the MH).[1][1]

4. The fluids.[1][1]

  • The aggressive (the shock, the dehydration, the rhabdomyolysis → the AKI). The balanced crystalloid. The titrate to the haemodynamics + the urine output.[1]

5. The multi-organ support.[1][1]

  • The vasopressor (the noradrenaline) for the shock. The lung-protective ventilation if the ARDS. The renal replacement if the AKI. The correction of the electrolyte (the potassium, the phosphate). The FFP / the cryoprecipitate for the DIC.[1][1]

Prognosis

The mortality 10 to 50 per cent (the delay → the higher). The multi-organ failure (the liver, the renal, the DIC) the worse. The prompt cooling (the within 30 min → the below 39) the reduces dramatically.[1][2][1]

The one-paragraph exam answer

The heat stroke — the core above 40 degrees C + the CNS dysfunction (the confusion, the seizure, the coma). The two types: the classic (the elderly, the drugs, the heatwave, the anhidrosis) and the exertional (the young, the athletes, the rhabdomyolysis). The multi-organ (the AKI, the liver, the DIC). The management: the RAPID cooling (the priority — the ice-water immersion the fastest for the exertional; the evaporative [the spray + the fan] the practical ICU; the cold IV fluids; the cooling blankets + the ice packs; the target below 39 then the stop). The NOT the antipyretics (the set-point the normal — the ineffective). The benzodiazepine for the shivering (the shivering generates the heat). The fluids (the shock, the rhabdomyolysis). The multi-organ support. The mortality 10 to 50 per cent.[1][2][1]

Red flags

The rapid cooling — the priority; the NOT the antipyretics

The rapid cooling (the ice-water immersion, the evaporative, the cold IV, the blankets) is the priority. The target below 39 degrees C as fast as possible. The paracetamol / the NSAID INEFFECTIVE (the hypothalamic set-point the normal — the not the pyrogen-driven).[1][1]

The shivering — the benzodiazepine (the shivering generates the heat)

The shivering during the cooling generates the heat → the defeats the purpose. The benzodiazepine (the diazepam, the lorazepam) to the suppress the shivering + the treat the agitation/seizures. The NOT the antipyretics. The NOT the dantrolene (the not the true the MH).[1][1]

The CNS dysfunction the hallmark — distinguishes from the heat exhaustion

The CNS dysfunction (the confusion, the agitation, the seizure, the coma) is the hallmark of the heat STROKE (distinguishes from the heat EXHAUSTION — which has the malaise, the nausea, the headache, the tachycardia, but the NORMAL the mental state). The heat exhaustion → the cooling + the fluids; the heat stroke → the rapid cooling + the ICU.[1][2]

The rhabdomyolysis + the DIC — the multi-organ

The exertional heat stroke → the rhabdomyolysis (the CK high, the myoglobinuria → the AKI). The coagulopathy / the DIC (the thermal the injury to the endothelium). The check the CK, the coagulation, the FBC, the LFTs, the renal. The fluids for the rhabdomyolysis; the blood products for the DIC.[1][1]

The classic vs the exertional — the two types in detail

The two subtypes of the heat stroke — the same endpoint (the core above 40 + the CNS dysfunction + the multi-organ), the different the mechanism + the patient + the prognosis.[1][3][4]

The classic (the non-exertional)

The classic — the elderly, the chronic the disease (the cardiopulmonary, the renal, the diabetes, the dementia), the drugs (the anticholinergics, the diuretics, the beta-blockers, the antipsychotics, the antihistamines), the poor the ventilation / the no air-conditioning, the social isolation, the enclosed (the upstairs the apartment, the locked-in the car). The epidemic during the heatwave (the 2003 the European the heatwave — the 70,000 the dead; the 1995 the Chicago; the 2022 the Europe). The thermoregulatory the FAILURE (the impaired the dissipation) → often the anhidrosis (the dry / the hot the skin). The insidious (the days). The mortality the HIGH (the 10 to 50 per cent).[3][4][6]

The drug the list — why the elderly the vulnerable. The anticholinergics (the tricyclics, the oxybutynin, the antihistamines) the block the sweating. The diuretics the dehydrate. The beta-blockers the reduce the cardiac the output + the blunt the tachycardic the response. The antipsychotics (the phenothiazines) the impair the hypothalamic the regulation + the block the sweating. The stimulants (the MDMA, the cocaine, the amphetamines) the increase the heat the production. The alcohol the vasodilates (the heat the loss) BUT the impairs the judgement + the dehydration.[1][4]

The exertional

The exertional — the young, the fit (the athletes, the military the recruits, the miners, the firefighters, the labourers). The intense the exertion in the hot / the humid → the heat the PRODUCTION exceeds the dissipation. The sporadic (the individual). The sudden (the hours). The sweating usually the PRESENT (the profuse — the skin the wet). The rhabdomyolysis, the DIC, the AKI, the lactic the acidosis the more the severe. The mortality the LOW (the below 5 per cent) IF the rapid the cooling.[1][3][5]

The 'sweating present' the pearl. The presence of the sweating + the wet the skin does NOT the exclude the heat stroke (the common the exam the trap). The exertional the heat stroke the typically the sweaty. The classic the often the dry (the anhidrosis). The anhidrosis is NOT the required for the diagnosis — the CNS the dysfunction + the core above 40 is the required.[3][4]

The classic vs the exertional — the exam the favourite

The featureThe classic (the non-exertional)The exertional
The patientThe elderly, the chronic the disease, the psychiatric the medsThe young, the fit (the athlete, the military, the miner)
The contextThe heatwave, the no air-conditioning, the poor the ventilationThe intense the exertion in the hot / the humid
The epidemiologyThe EPIDEMIC (the mass during the heatwave)The sporadic (the individual)
The onsetThe insidious (the days)The sudden (the hours) during / after the exertion
The mechanismThe impaired the DISSIPATION (the thermoregulatory the failure)The overwhelming the PRODUCTION the greater than the dissipation
The sweatingThe often the ABSENT (the anhidrosis — the dry)The usually the PRESENT (the profuse — the wet)
The temperatureThe 40 to 41 degrees CThe often the very the high (the above 42)
The rhabdomyolysisThe mild to moderateThe common + the SEVERE (the CK the above 10,000)
The DICThe variableThe common, the early
The AKIThe common (the dehydration + the comorbidity)The common (the rhabdo + the dehydration)
The lactic the acidosisThe variableThe severe (the exertion + the shock)
The hypoglycaemiaThe less the commonThe common (the glycogen the depletion)
The drugs the implicatedThe anticholinergics, the diuretics, the beta-blockers, the antipsychoticsThe ergogenic the aids, the stimulants (the ephedra, the MDMA)
The best the coolingThe evaporative (the mist + the fan) ± the ice the packsThe COLD-WATER the IMMERSION (the on-site)
The mortality (the treated)The 10 to 50 per cent (the worse with the age / the comorbidity)The below 5 per cent (with the rapid the cooling)
[1]

The pathophysiology — the heat as the toxin

The pathophysiology — the heat as the direct the toxin + the trigger of the SIRS-like the cascade. The core above 40 degrees C → the protein the denaturation + the membrane the lipid the peroxidation → the cell the death → the systemic the inflammatory the response (the cytokine the cascade — the IL-1, the IL-6, the TNF) → the endothelial the activation + the coagulation + the complement → the multi-organ the failure (the 'sepsis from the heat').[3][7]

The cascade in the steps

  1. The protein the denaturation — the heat (the above 41 to 42 degrees C) the denatures the enzymes + the structural the proteins → the cell the death. The time- + the temperature-dependent (the every the minute the above 40 the worse the injury).[3][7]
  2. The membrane the lipid the peroxidation — the heat the damages the cell the membranes → the increased the permeability → the leak → the oedema. The direct the cytotoxicity.[7]
  3. The SIRS-like the response — the cytokine the cascade (the IL-1, the IL-6, the TNF-alpha) → the endothelial the activation → the NO the release → the distributive the vasodilation + the capillary the leak. The picture the indistinguishable from the septic the shock (Bouchama + Knochel 2002).[3]
  4. The gut the translocation — the splanchnic the ischaemia → the bacteria / the endotoxin the leak → the amplifies the inflammatory the response (the positive the feedback the 'malignant' the cycle). The heat the kills the gut the barrier.[3][7]
  5. The coagulation the activation — the endothelial the damage → the tissue the factor the release → the DIC (the consumption + the bleeding + the microvascular the thrombosis).[3][7]
  6. The multi-organ the failure — the brain (the Purkinje the cells the heat-sensitive → the cerebellar the ataxia), the liver (the centrilobular the necrosis), the kidney (the ATN from the myoglobin + the hypoperfusion), the muscle (the rhabdomyolysis), the lung (the ARDS), the heart (the myocardial the dysfunction), the coagulation (the DIC).[1][3][4]

The organ-specific the injury

  • The brain — the Purkinje the cells (the cerebellum) the exquisitely the heat-sensitive → the cerebellar the ataxia (the may be the permanent). The diffuse the injury → the confusion, the coma. The cerebral the oedema. The later: the cognitive the impairment, the parkinsonism (the basal the ganglia), the seizures.[3][4]
  • The liver — the centrilobular the necrosis (the zone 3) → the transaminitis (the AST / the ALT the above 1000), the coagulopathy (the impaired the synthesis), the jaundice. The usually the recovers if the patient the survives.[3]
  • The kidney — the ATN from the myoglobin (the pigment the nephropathy) + the hypoperfusion (the pre-renal) + the DIC (the microvascular). The rhabdomyolysis the particularly the nephrotoxic.[1][7]
  • The muscle — the rhabdomyolysis → the CK the high (the above 10,000 in the exertional), the myoglobinuria (the dipstick the blood the positive + the no the RBCs), the hyperkalaemia, the hypocalcaemia (the early — do NOT the treat unless the symptomatic), the phosphate the high.[1][7]
  • The coagulation — the DIC → the PT / the aPTT the prolonged, the fibrinogen the low, the D-dimer the high, the platelets the low. The bleeding AND the thrombosis.[3]
  • The lung — the ARDS (the direct the heat the injury + the aspiration + the transfusion if the massive the transfusion).[1][1]
  • The heart — the myocardial the dysfunction (the stunned the myocardium), the tachycardia, the distributive the shock.[1][1]

The cooling methods in detail

The rapid the cooling — the #1 the priority. The target the below 39 degrees C as the fast as the possible (the every the minute the above 40 → the irreversible the protein the denaturation). The cooling the rate the target the at least 0.15 degrees C / the min. The do NOT the delay for the tests / the transport — the start at the point of the collapse.[1][3][5]

The cooling methods compared — the rate + the indication

The methodThe cooling the rateThe best forThe practical the notes
The cold-water the immersion (CWI) 2 to 15 degrees CThe FASTEST — 0.15 to 0.20 degrees C / minThe EXERTIONAL (the gold the standard)The on-site / the tub; the reduces the mortality the 50 per cent to the below 5 per cent; the remove at 38.5 to 39 degrees C
The evaporative (the warm the mist + the fan)~0.1 degrees C / minThe CLASSIC / the hospital (the ICU)The practical; the warm the water (the 15 to 25 degrees C) the mist — the NOT the ice the water (the vasoconstriction) + the continuous the fan
The ice the packs (the groin / the axilla / the neck)~0.05 degrees C / minThe adjunct / the no the other the methodThe slow the alone; the rotate the sites; the better with the massage
The cold the IV the crystalloid (4 degrees C)~1 to 1.5 degrees C per 2 LThe adjunct / the dehydratedThe 4 degrees C the saline the 30 mL / kg; the never the sole the method; the cool if the shocked
The intragastric / the bladder the lavageThe adjunctThe refractoryThe cool the saline the lavage via the NG / the urinary the catheter
The peritoneal the lavageThe moderate to fastThe refractoryThe cool the dialysate; the invasive
The intravascular the catheter (the closed the loop)The fastThe ICU (if the available)The heat the exchange; the precise the temp the control
The ECMO (VA)—The cardiac the arrest / the severe the shockThe last the resort — the supports the circulation while the cooling
[1]

The cold-water the immersion (CWI) — the gold the standard for the exertional

The CWI — the definitive the on-site the treatment for the exertional. The ice the bath / the tub at the 2 to 15 degrees C. The FASTEST the cooling (~0.15 to 0.20 degrees C / the min). The reduces the mortality from the ~50 per cent to the below 5 per cent. The large the athletic the surveillance → the 100 per cent the survival when the started the promptly (Casa 2015 NATA). The mantra: the 'cool the first, the transport the second' — the cool to the below 38.6 degrees C (101.5 F) before the moving the athlete.[5]

The technique. The immerse the athlete up to the neck / the shoulders in the tub of the ice the water. The stir the water (the maintains the convection). The monitor the core the temp the continuously. The REMOVE at the 38.5 to 39 degrees C to the avoid the overshoot. The myth the busted: the 'the CWI the causes the dangerous the vasoconstriction / the afterdrop' — the in the practice the high the thermal the gradient the overwhelms the vasoconstriction + the CWI the demonstrably the fastest the method.[3][5]

The evaporative the cooling — the practical the ICU the method

The evaporative — the spray the WARM / the TEPID the water the mist (the 15 to 25 degrees C) over the maximally the exposed the skin + the continuous the high-flow the fan. The WHY the warm the mist, the not the ice the water: the ice the water the causes the cutaneous the VASOCONSTRICTION → the shunts the blood the away from the skin → the REDUCES the heat the loss → the paradoxically the slows the cooling. The tepid the water the keeps the cutaneous the vessels the dilated → the sweat / the evaporation the removes the heat the efficiently. The rate ~0.1 degrees C / the min — the slightly the slower than the CWI BUT the practical in the ED / the ICU for the classic the heat stroke (the elderly, the can't the immerse). The combine with the ice the packs to the groin / the axilla / the neck + the cold the IV the fluids. The maximise the skin the exposure (the remove all the clothing) + the continuous the airflow.[1][1][4]

The ice the packs + the cold the IV the fluids

The ice the packs — to the groin, the axilla, the neck (the high-flow the vascular the areas). The slow the alone (~0.05 degrees C / the min) — the rotate the sites; the better with the massage. The adjunct the not the sole. The cold the IV the fluids — the 4 degrees C the saline the 30 mL / kg; the cools the ~1 to 1.5 degrees C per 2 L; the doubles as the resuscitation; the never the sole the method.[1][1]

The complications — the multi-organ

The complications — the 'sepsis from the heat' the multi-organ. The check + the treat the each.[1][3][7]

  • The rhabdomyolysis — the CK the high (the above 10,000 in the exertional), the myoglobinuria (the dipstick the blood the positive + the no the RBCs). The AGGRESSIVE the IV the fluids (the target the urine the output the 200 to 300 mL / the hr the once the perfusion the restored). The monitor the potassium (the hyperkalaemia — the cardiac the arrest), the calcium (the early the hypo — the do NOT the treat unless the symptomatic), the phosphate. The consider the RRT if the refractory the hyperkalaemia / the acidosis / the fluid the overload.[1][7]
  • The DIC — the monitor the PT / the INR / the aPTT / the fibrinogen / the D-dimer / the platelets. The transfuse the platelets / the FFP / the cryoprecipitate if the bleeding or the before the procedures. The heparin the generally the NOT the indicated (the consumption, the not the thrombosis — the unless the thrombosis the dominates).[3]
  • The ARDS — the lung-protective the ventilation (the VT the 6 mL / kg the PBW, the plateau the below 30 cmH2O, the PEEP the titrated).[1][1]
  • The AKI — the pre-renal (the dehydration) + the intrinsic (the ATN from the myoglobin / the hypoperfusion) + the pigment. The fluids; the RRT if the refractory.[1][1]
  • The hepatic the necrosis — the centrilobular (the zone 3). The transaminitis (the above 1000). The usually the recovers if the patient the survives. The do NOT the give the paracetamol (the worsens).[3]
  • The cardiac — the myocardial the dysfunction, the arrhythmias (the electrolyte, the acidosis). The noradrenaline for the shock; the correct the potassium / the magnesium.[1][1]

The NOT the antipyretics — why

The antipyretics (the paracetamol / the NSAID) the INEFFECTIVE + the potentially the harmful. The KEY the concept: the heat-stroke the hyperthermia is the NOT the fever. The in the fever, the hypothalamic the set-point is the RAISED by the prostaglandins (the PGE2) → the antipyretics (the paracetamol = the COX the inhibitor, the NSAID = the COX the inhibitor) the lower the set-point → the reduce the temperature. The in the heat stroke, the set-point is the NORMAL — the body is the simply the OVERWHELMED by the external / the exertional the heat the gain the exceeds the dissipation. The therefore the paracetamol / the NSAID the CANNOT the reduce the temperature (the no the abnormal the prostaglandin the signal to the block).[1][3][4]

The harm. The paracetamol the worsens the already-injured the liver (the hepatocyte the necrosis the hallmark). The NSAID the worsens the AKI + the bleeding the risk (the DIC). The do NOT the wait for the antipyretics — the start the external the cooling the immediately. The exam the pearl: 'the patient with the heat stroke the given the paracetamol — the no the response' → the confirms the set-point the normal; the switch to the physical the cooling.[1][4]

The dantrolene — the also the ineffective

The dantrolene the INEFFECTIVE — the heat stroke is the NOT the malignant the hyperthermia (the no the ryanodine-the-receptor the Ca2+ the leak in the skeletal the muscle). The randomised the trials the show the NO the benefit (the no the faster the cooling, the no the mortality the reduction). The do NOT the give (the wastes the time, the risk of the hepatotoxicity + the muscle the weakness). The exception the nuance: the dantrolene the occasionally the discussed if the concomitant the MH the suspected (the post-the-anaesthetic) BUT the do NOT the routine.[1][4]

The heat stroke vs the other the hyperthermia (the differential)

The featureThe heat strokeThe malignant the hyperthermia (MH)The neuroleptic the malignant (NMS)The serotonin the syndromeThe sepsis (with the fever)
The triggerThe heat / the exertionThe volatile the anaesthetics / the suxamethoniumThe antipsychotics (the dopamine the blockade)The serotonergic the drugsThe infection
The onsetThe minutes to hoursThe minutes to hours (the intra-op)The days to weeksThe hours (after the drug / the dose up)The hours to days
The set-pointThe NORMALThe normalThe normalThe normalThe RAISED (the fever — the PGE2)
The tempThe above 40The rapid the rise the above 40The 38 to 41The usually the below 41The 38 to 41 (the fever)
The muscleThe rhabdomyolysisThe sustained the rigidity (the 'rigor')The lead-the-pipe the rigidityThe clonus, the hyperreflexiaThe variable
The sweatingThe exertional: yes; the classic: noThe profuseThe variableThe diaphoresisThe variable
The antipyreticsThe INEFFECTIVEThe ineffectiveThe ineffectiveThe ineffectiveThe EFFECTIVE (the reduces the fever)
The dantroleneThe INEFFECTIVEThe DEFINITIVE the cureThe may the help (the adjunct)The not the indicatedThe not the indicated
The treatmentThe RAPID the COOLINGThe dantrolene + the stop the triggerThe stop the drug, the cooling, the bromocriptine / the dantroleneThe stop the drug, the cyproheptadine, the benzodiazepineThe antibiotics + the source the control
[1]

The management — the step-by-step

The management of the acute heat stroke

  1. THE RECOGNISE — the core the above 40 + the CNS the dysfunction = the HEAT STROKE — (a) The DIAGNOSIS (the triad): (i) the CORE the TEMPERATURE the above 40 (the use the rectal / the oesophageal / the bladder — the NOT the oral / the tympanic — the inaccurate at the extremes; the low-reading the thermometer the may the needed). (ii) The CNS the DYSFUNCTION — the confusion, the agitation, the delirium, the ataxia (the cerebellar), the seizure, the coma (the hot + the confused = the heat stroke the until the proven the otherwise). (iii) The HOT the skin — the exertional the often the WET (the sweating the persists); the classic the often the DRY (the anhidrosis). (b) The SUBTYPE: the EXERTIONAL (the young, the fit, the exertion) vs the CLASSIC (the elderly, the chronic, the heatwave, the anticholinergics). (c) The EXCLUDE the differentials: the sepsis (the bloods / the cultures / the lactate — the heat stroke the RESEMBLES the sepsis BUT the no the obvious the source), the MH (the anaesthetic the history), the NMS (the antipsychotic), the serotonin the syndrome (the serotonergic), the thyroid the storm, the neuroleptic, the stimulant the toxicity.[1][3][4]

  2. THE RAPID THE COOLING — the #1 the PRIORITY (the start IMMEDIATELY, the do NOT the delay for the tests / the transport) — (a) The PRINCIPLE: the every the minute the above 40 → the irreversible the PROTEIN the DENATURATION + the cell the death → the FASTER the cool, the better the outcome. The target: the reduce the core to the below 39 the within the 30 to 60 the min. The rate the target the at least 0.15 degrees C / the min. (b) The GOLD the STANDARD for the EXERTIONAL: the COLD-WATER the IMMERSION (CWI) — the ice the bath / the tub at the 2 to 15 degrees C. (i) The FASTEST (~0.15 to 0.20 degrees C / the min) + the REDUCES the MORTALITY the ~50 per cent to the below 5 per cent. (ii) The START the ON-SITE — the 'cool the first, the transport the second' (Casa 2015 NATA: the cool to the below 38.6 the before the moving). (iii) The REMOVE at the 38.5 to 39 to the avoid the overshoot. (c) For the CLASSIC / the ICU: the EVAPORATIVE (the warm the mist + the fan) — the spray the tepid (the 15 to 25 degrees C) the mist + the continuous the high-flow the fan; the WHY the warm (the not the ice): the ice → the vasoconstriction → the slows the cooling. (d) The ADJUNCT: the ice the packs (the groin / the axilla / the neck) + the cold the IV the fluids (4 degrees C the saline the 30 mL / kg). (e) The STOP at the 38.5 to 39 — the overshoot the hypothermia → the arrhythmia / the coagulopathy / the shivering. (f) The CONTROL the shivering (the generates the heat) — the counter-warming the extremities + the benzodiazepine (the midazolam) / the paralysis if the intubated + the severe.[1][3][5]

  3. THE AIRWAY + THE BREATHING + THE CIRCULATION (the supportive) — (a) The AIRWAY: the reduced the consciousness / the coma → the intubate (the RSI — the beware the heat-related the hypotension; the ketamine / the etomidate the cautiously; the avoid the propofol in the profound the shock). The seizure → the secure the airway. (b) The BREATHING: the oxygen for the hypoxaemia; the if the ARDS → the lung-protective (the VT the 6 mL / kg, the plateau the below 30, the PEEP). (c) The CIRCULATION: the heat stroke → the volume the depletion (the sweating / the insensible) + the vasodilation + the myocardial the dysfunction → the hypotension. (i) The IV the FLUIDS — the cool the balanced the crystalloid (the doubles as the cooling); the titrate to the MAP the above 65 + the urine the output the above 0.5 mL / kg / the hr; the avoid the over-the-resuscitation (the pulmonary the oedema). (ii) The VASOPRESSORS (the noradrenaline) if the refractory the shock.[1][1][1]

  4. THE TREAT the COMPLICATIONS (the 'sepsis from the heat') — (a) The RHABDOMYOLYSIS: the check the CK (the above 10,000), the urine the myoglobin (the dipstick the blood + the no the RBCs). The AGGRESSIVE the IV the fluids (the target the UO the 200 to 300 mL / the hr). The monitor the K+, the Ca2+ (the early the hypo — the do NOT the treat unless the symptomatic), the phosphate. The RRT if the refractory. (b) The DIC: the monitor the PT / the aPTT / the fibrinogen / the D-dimer / the platelets; the transfuse the platelets / the FFP / the cryoprecipitate if the bleeding; the heparin the generally the NOT. (c) The AKI: the fluids; the RRT. (d) The hepatic: the monitor the LFTs; the avoid the paracetamol. (e) The GLUCOSE: the check (the hypoglycaemia the common in the exertional — the glycogen the depletion). (f) The SEIZURES: the benzodiazepine (the lorazepam / the diazepam). (g) The VTE the prophylaxis (the immobilised).[1][1][7]

  5. THE NOT TO DO (the common the dangerous the errors) — (a) The ANTIPYRETICS (the paracetamol / the NSAID) the INEFFECTIVE + the harmful: the set-point the normal; the paracetamol the worsens the liver; the NSAID the worsens the AKI + the bleeding. (b) The DANTROLENE the INEFFECTIVE: the NOT the MH. (c) The do NOT the DELAY the cooling for the transport / the investigations. (d) The do NOT the use the ice the water the mist for the evaporative (the vasoconstriction). (e) The do NOT the cool the below 38.5 (the overshoot the hypothermia). (f) The do NOT the forget the shivering the control (the generates the heat).[1][3][4]

  6. THE PREVENTION (the population the intervention) — (a) The HEATWAVE the PLANNING (the classic): the early the warning, the cooling the centres, the check on the elderly / the vulnerable, the ensure the hydration + the air-conditioning, the reduce the anticholinergic / the diuretic the burden during the heatwaves. (b) The EXERTIONAL the prevention: the ACCLIMATISATION (the 7 to 14 the days the graded the heat the exposure → the up the plasma the volume, the up the sweat the rate, the down the sweat the sodium), the hydration (the beware the exertional the hyponatraemia), the schedule the exercise for the cooler the hours, the WBGT (the wet-the-bulb the globe the temperature) the monitoring, the cooling the stations, the gradual the intensity, the identify the high-the-risk (the sickle-the-cell the trait, the stimulant, the illness). (c) The DRUG the review: the stop / the reduce the anticholinergics, the diuretics, the antipsychotics in the elderly during the heatwaves.[1][3][5]

SAQ — Exertional heat stroke with rhabdomyolysis in a military recruit

10 minutes · 10 marks

A 22-year-old male military recruit collapses 8 km into a timed pack march on a humid summer day (wet-bulb globe temperature 31 degrees C). On arrival at the medical tent his core (rectal) temperature is 41.8 degrees C, GCS 12 (confused and combative), HR 152, BP 86/48, RR 34, SpO2 92 percent on room air. He is profusely diaphoretic with hot, wet skin and is trembling with rigors. Initial bloods: sodium 148, potassium 6.8, creatinine 180 (baseline 85), CK 28,400 IU/L, venous pH 7.18, lactate 7.2, INR 2.4, platelets 86, creatine kinase markedly elevated. Urine is dark tea-coloured and dipstick blood-positive with no red cells on microscopy. An ice-water immersion tub is available on-site.

[1]

SAQ — Classic (non-exertional) heat stroke in an elderly woman during a heatwave

10 minutes · 10 marks

An 82-year-old woman with dementia, hypertension and chronic kidney disease is brought by ambulance from her un-air-conditioned top-floor apartment during the third day of a city heatwave (ambient 43 degrees C). She was found unresponsive by a neighbour. On arrival: core (rectal) temperature 41.2 degrees C, GCS 8 (E2V2M4), HR 118 sinus, BP 82/46 (MAP 58), RR 28, SpO2 94 percent on room air. Her skin is hot and strikingly DRY (anhidrotic). Medications brought in by the family include furosemide 40 mg daily, amitriptyline 25 mg nocte, and temazepam. Bloods: sodium 156, creatinine 240 (baseline 120), lactate 4.6, INR 1.9, platelets 92, ALT 380. She has not urinated for the ambulance journey. The emergency department has no immersion tub but does have a cooling blanket, fans, and a high-flow misting device.

[1]

The clinical pearls

The high-yield the heat-stroke the points for the CICM / the FFICM / the EDIC the exam

  1. The core the above 40 + the CNS the dysfunction = the heat stroke. (1) The TRIAD: (a) the CORE the TEMPERATURE the above 40 (the some the above 40.5), (b) the CNS the DYSFUNCTION — the confusion, the agitation, the delirium, the ataxia, the seizure, the coma, (c) the HOT the skin (the exertional the wet; the classic the dry / the anhidrotic). (2) The CNS the involvement the DISTINGUISHES the heat the STROKE from the heat the EXHAUSTION (the malaise, the headache, the nausea, the tachycardia, the temp the below 40, the normal the mental). (3) The measure the CORE (the rectal / the oesophageal / the bladder) — the oral / the tympanic the underestimate. (4) The collapse + the confusion + the hot → the heat stroke the until the proven — the START the COOLING the immediately.[1][3][4]

  2. The classic vs the exertional — the exam the favourite. (1) The CLASSIC: the elderly, the chronic, the anticholinergic / the diuretic / the antipsychotic, the social the isolation, the no air-conditioning — the EPIDEMIC during the heatwave (the 2003 the European the 70,000 the dead). The thermoregulatory the FAILURE → the anhidrosis (the dry). The mortality the 10 to 50 per cent. (2) The EXERTIONAL: the young, the fit (the athletes, the military, the miners) — the intense the exertion the overwhelms the dissipation; the sweating the PRESENT; the rhabdo / the DIC / the AKI / the lactate the more the severe; the mortality the below 5 per cent IF the rapid the cool. (3) The pearl: the 'the sweating the present' → the exertional; the 'the dry' → the classic. (4) The 'the sweating the does NOT the exclude' the trap.[3][4][6]

  3. The 'the heat stroke the like the SEPSIS the from the heat' — the pathophysiology the unifier. (1) The above 40: (a) the PROTEIN the DENATURATION (the threshold ~41 to 42), (b) the membrane the LIPID the PEROXIDATION + the permeability, (c) the direct the cytotoxicity. (2) The SIRS: the cytokine (the IL-1, the IL-6, the TNF), the endothelial the activation, the complement + the coagulation, the leucocyte the margination. (3) The picture — the distributive the shock, the multi-organ, the DIC, the ARDS, the AKI — the INDISTINGUISHABLE from the septic the shock (Bouchama + Knochel 2002). (4) The GUT the translocation (the splanchnic the ischaemia → the bacteria / the endotoxin the leak) the amplifies — the true the positive-the-feedback the 'malignant' the cycle.[3][7]

  4. The RAPID the COOLING the #1 the priority — the every the minute the counts. (1) The time to the cooling the single the most the important the determinant of the survival + the neurological. The every the minute the above 40 → the irreversible the cell the death. (2) The TARGET: the below 39 the within the 30 to 60 the min; the rate the at least 0.15 degrees C / the min. (3) The do NOT the delay — the start at the point of the collapse. The 'COOL the FIRST, the TRANSPORT the SECOND' — the cool to the below 38.6 before the moving. (4) The single the highest-the-yield: the RAPID the COLD-WATER the IMMERSION the reduces the mortality the ~50 per cent to the below 5 per cent.[3][5]

  5. The cold-water the immersion (CWI) — the gold the standard for the exertional. (1) The WHY the BEST: the water the conducts the heat ~25x the faster than the air → the CWI the FASTEST (~0.15 to 0.20 degrees C / the min) — the 100 per cent the survival in the large the athletic the cohorts. (2) The Casa 2015 NATA: the immediate the CWI → the zero the exertional the heat-stroke the mortality the over the years. (3) The technique: the immerse the up to the neck / the shoulders; the stir; the monitor; the REMOVE at the 38.5 to 39. (4) The myth the busted: the 'the CWI the vasoconstriction / the afterdrop' — the high the gradient the overwhelms.[5]

  6. The evaporative the cooling — the practical the ICU the method. (1) The HOW: the warm the mist (the 15 to 25 degrees C) + the continuous the fan. (2) The WHY the WARM the not the ice: the ice → the cutaneous the VASOCONSTRICTION → the shunts the blood the away → the REDUCES the heat the loss. The tepid the keeps the vessels the dilated. (3) The rate ~0.1 degrees C / the min — the practical for the classic / the intubated. (4) The combine with the ice the packs + the cold the IV. (5) The maximise the skin the exposure + the continuous the airflow.[1][1][4]

  7. The antipyretics the INEFFECTIVE — the potentially the harmful. (1) The KEY: the heat-stroke the hyperthermia the NOT the fever. The fever → the set-point the RAISED (the PGE2) → the antipyretics (the COX the inhibitor) the lower → the reduce. The heat stroke → the set-point the NORMAL — the body the OVERWHELMED by the external / the exertional the heat. (2) The therefore the paracetamol / the NSAID the CANNOT the reduce (the no the prostaglandin the signal). (3) The HARM: the paracetamol the worsens the liver; the NSAID the worsens the AKI + the bleeding (the DIC). (4) The exam: the 'the paracetamol → the no the response' → the confirms the set-point the normal.[1][3][4]

  8. The dantrolene the INEFFECTIVE — the NOT the MH. (1) The MH = the intracellular the CALCIUM the dysregulation (the ryanodine the receptor → the uncontrolled the Ca2+ → the sustained the contraction → the massive the heat). The dantrolene the blocks → the DEFINITIVE. (2) The heat stroke the NO the ryanodine the leak — the heat the external / the exertional. (3) The RCTs the NO the benefit. (4) The do NOT the give (the time, the hepatotoxicity, the weakness). (5) The exception: the if the concomitant the MH the suspected (the post-the-anaesthetic).[1][4]

  9. The cerebellar the ataxia — the classic the permanent the sequela. (1) The PURKINJE the cells (the cerebellum) the EXQUISITELY the heat-sensitive — the first to the die. (2) The result: the CEREBELLAR the ATAXIA (the wide-based the gait, the dysmetria, the dysarthria, the intention the tremor, the nystagmus). (3) The may be the PERMANENT — the persists the long the after the temp the normal. (4) The exam the classic: the 'the recovery the from the heat stroke → the ataxia + the dysarthria — the cause?' → the cerebellar the Purkinje the injury. (5) The other: the cognitive, the parkinsonism (the basal the ganglia), the seizure, the coma.[3][4]

  10. The rhabdomyolysis + the DIC + the AKI — the multi-organ the triad. (1) The RHABDO: the heat + the exertion → the myoglobin, the CK, the K+ → the myoglobin the nephrotoxic (the casts the obstruct + the toxicity) → the ATN. The CK the above 10,000 (the exertional). The aggressive the IV (the target the UO the 200 to 300 mL / the hr), the treat the K+, the RRT. (2) The DIC: the heat the damages the ENDOTHELIUM → the tissue the factor → the consumption → the bleeding + the thrombosis. The component the therapy; the underlying the resolves the as the cools. (3) The AKI: the pre-renal (the dehydration) + the intrinsic (the ATN) + the pigment.[1][3][7]

  11. The shivering during the cooling — the counterproductive. (1) The WHY: the shivering = the involuntary the muscle the contraction → the HEAT → the opposes the cooling + the up the O2 / the CO2. (2) The WHEN: the common with the CWI + the aggressive. (3) The MANAGEMENT: (a) the COUNTER-WARMING (the warm the extremities the while the torso the cooled — the tricks the peripheral the warmth the sensors), (b) the BENZODIAZEPINE (the midazolam) — the suppress the central + the agitation / the seizure, (c) the if the intubated + the severe: the NEUROMUSCULAR the BLOCKADE (the vecuronium / the rocuronium) — the abolishes; the requires the sedation + the ventilation. (d) The AVOID the meperidine (the pethidine) as the sole.[1][1]

  12. The stop the cooling at the 38.5 to 39 — the avoid the overshoot. (1) The cooling the INERTIA — the peripheral the tissues the continue the cool the core the even the after the stopped. (2) The cool to the normal (the 37) or the below → the OVERSHOOT the HYPOTHERMIA → the arrhythmia, the coagulopathy (the worsens the DIC), the shivering (the re-warms), the impaired the immunity. (3) The RULE: the STOP the active the cooling at the 38.5 to 39 — the drifts the down the little the further, the settles the near the normal. (4) The monitor for the rebound (the rare if the trigger the removed).[1][3]

  13. The Argaud 2007 — the Lyon the heatwave the outcome (the prognosis the pearl). (1) The cohort of the 83 the classic the heat-stroke the patients the during the August 2003 the French the heatwave. (2) The 28-day the mortality the 58 per cent; the 2-year the 71 per cent — the MOST the die + the survivors the poor. (3) The INDEPENDENT the PREDICTORS (the admission): the institutional (the nursing the home) the HR 1.98; the long-term the ANTIHYPERTENSIVE the HR 2.17; the ANURIA the HR 5.24; the COMA the HR 2.95; the CARDIOVASCULAR the failure the HR 2.43. (4) The TAKE-HOME: the classic the heat stroke the NOT the benign — the aggressive + the honest the prognostication.[6]

  14. The prevention + the acclimatisation — the population the intervention. (1) The CLASSIC the public-the-health: the early-the-warning, the cooling the centres, the 'the check on the neighbour', the air-conditioning / the hydration for the elderly, the reduce the anticholinergic / the diuretic. The 2003 the European + the 1995 the Chicago the drove the policy. (2) The EXERTIONAL: (a) the ACCLIMATISATION (the 7 to 14 the days the graded → the up the plasma, the up the sweat, the down the sweat the sodium, the earlier the onset), (b) the HYDRATION (the beware the exertional the hyponatraemia — the weigh the before / the after), (c) the WBGT the monitoring + the work-the-rest the cycle, (d) the high-the-risk (the sickle-the-cell the trait, the stimulant, the illness, the no the acclimatisation).[1][3][5]

  15. The heat the exhaustion vs the heat the stroke — the threshold. (1) The heat the EXHAUSTION: the malaise, the headache, the nausea, the vomiting, the tachycardia, the diaphoresis, the temp the below 40, the NORMAL the mental. (2) The heat the STROKE: the same + the CNS the dysfunction (the confusion / the seizure / the coma) + the core the above 40. (3) The management: the exhaustion → the cooling + the fluids (the oral / the IV), the observe; the stroke → the rapid the cooling + the ICU. (4) The do NOT the wait for the lab — the clinical the diagnosis.[1][2]

  16. The heat the cramps + the heat the syncope — the minor the spectrum. (1) The CRAMPS: the painful the muscle (the legs / the abdomen) the during / the after the exertion; the sodium the depletion; the treat: the rest + the oral the electrolyte the replacement. (2) The SYNCOPE: the orthostatic the during the heat the exposure; the peripheral the vasodilation + the volume the depletion; the recover the supine; the exclude the other. (3) The hyponatraemia the exertional: the over-the-hydration → the dilutional; the CNS (the confusion, the seizure) — the distinguish the from the heat the stroke (the sodium the low, the temp the not the above 40); the hypertonic the saline if the severe.[2][5]

  17. The 'the sepsis the mimic' — the always the rule the out. (1) The heat stroke the INDISTINGUISHABLE from the sepsis (the fever, the tachycardia, the hypotension, the leukocytosis, the DIC, the multi-organ). (2) The ALWAYS the send the cultures + the lactate (the sepsis the co-the-exists or the primary). (3) The if the uncertain → the empirical the antibiotics (the cover the sepsis) the while the cooling. (4) The do NOT the attribute the altered the mental + the high the temp to the sepsis the alone if the heat the exposure / the exertion the present.[1][3]

  18. The lab the pattern — the recognise. (1) The CK the high (the above 10,000 in the exertional). (2) The AST / the ALT the high (the above 1000 — the hepatic the necrosis; the muscle the contribution). (3) The coagulopathy (the PT / the aPTT the up, the fibrinogen the down, the platelets the down — the DIC). (4) The creatinine the up (the AKI). (5) The potassium the up (the rhabdo). (6) The calcium the down the early (the do NOT the treat unless the symptomatic — the binds the damaged the muscle; the up the later). (7) The glucose the down (the exertional). (8) The lactate the up (the severe). (9) The leukocytosis + the transaminitis the do NOT the equal the sepsis / the hepatitis — the heat.[1][3][7]

The additional the red flags

The cold-water the immersion for the exertional — the on-site; the cool the first

The cold-water the immersion the reduces the exertional the heat-stroke the mortality from the ~50 per cent to the below 5 per cent. The start the ON-SITE; the do NOT the delay for the transport. The 'the cool the first, the transport the second' — the cool to the below 38.6 the before the moving. The every the minute the delay the worse the outcome.[3][5]

The evaporative the warm the mist — the NOT the ice the water (the vasoconstriction)

The evaporative the cooling the uses the WARM / the TEPID the mist (the 15 to 25 degrees C) + the fan. The ice the water the causes the cutaneous the VASOCONSTRICTION → the shunts the blood the away → the REDUCES the heat the loss → the paradoxically the slows the cooling. The warm the keeps the vessels the dilated.[1][1]

The antipyretics + the dantrolene — the both the ineffective

The paracetamol / the NSAID the INEFFECTIVE (the set-point the normal; the worsens the liver / the AKI / the bleeding). The dantrolene the INEFFECTIVE (the NOT the MH — the no the ryanodine the leak). The do NOT the wait; the physical the cooling the definitive.[1][1][3]

The stop the cooling at the 38.5 to 39 — the avoid the overshoot

The cooling the inertia → the core the continues the cool the after the stop. The cool the below 38.5 → the overshoot the hypothermia → the arrhythmia, the coagulopathy (the worsens the DIC), the shivering (the re-warms). The STOP the active at the 38.5 to 39.[1][3]

The rhabdomyolysis the hyperkalaemia — the cardiac the arrest

The rhabdomyolysis (the CK the above 10,000) → the hyperkalaemia → the cardiac the arrest. The monitor the K+; the aggressive the IV the fluids (the target the UO the 200 to 300 mL / the hr); the treat the hyperkalaemia (the calcium the gluconate, the insulin / the dextrose, the salbutamol); the RRT if the refractory.[1][7]

The cerebellar the ataxia — the permanent (the Purkinje the cells)

The Purkinje the cells (the cerebellum) the exquisitely the heat-sensitive → the cerebellar the ataxia the may be the PERMANENT. The persists the long the after the temp the normal. The other: the cognitive, the parkinsonism (the basal the ganglia), the seizure.[3][4]

The classic the heat stroke the mortality the 10 to 50 per cent (the Argaud 2007)

The classic the heat stroke the mortality the 10 to 50 per cent (the Argaud 2007 the Lyon — the 28-day the 58 per cent). The worse: the elderly, the institutional, the antihypertensive, the coma, the shock, the anuria. The honest the prognostication + the aggressive the cooling.[3][6]

The always the rule the out the sepsis (the mimic)

The heat stroke the INDISTINGUISHABLE from the sepsis. The ALWAYS the send the cultures + the lactate. The if the uncertain → the empirical the antibiotics the while the cooling. The do NOT the attribute the high the temp + the altered the mental to the sepsis the alone if the heat / the exertion.[1][3]

The landmark the trials + the guidelines

Casa 2015 — NATA the position the statement: the exertional the heat the illness (PMID 26381473)

Source

Journal of Athletic Training — the National Athletic Trainers' Association the position the statement

Authors

Casa DJ, DeMartini JK, Bergeron MF, et al.

Scope

The prevention, the recognition + the management of the exertional the heat the illness (the cramps, the exhaustion, the stroke)

The key the recommendation

The COLD-WATER the IMMERSION the definitive the on-site for the exertional the heat the stroke — the 'the cool the first, the transport the second'

The evidence

The large the athletic-the-programme the surveillance → the 100 per cent the survival when the CWI the started the promptly; the mortality the ~50 per cent to the below 5 per cent

The cooling the rate

The CWI ~0.15 to 0.20 degrees C / the min — the fastest the available

The clinical the bottom the line

The single the most the important the paper for the exertional the heat the stroke — the immediate the CWI the before the transport

[1]

Argaud 2007 — the Lyon 2003 the heatwave the cohort (PMID 17698677)

Source

Archives of Internal Medicine — the prospective the cohort

Authors

Argaud L, Ferry T, Le QH, et al.

Population

83 the patients with the classic (the non-the-exertional) the heat the stroke the admitted during the August 2003 the French the heatwave

28-day mortality

58 per cent

2-year mortality

71 per cent

Independent the predictors

The institutional the admission (HR 1.98), the antihypertensive (HR 2.17), the anuria (HR 5.24), the coma (HR 2.95), the cardiovascular the failure (HR 2.43)

The functional

The survivors the dramatic the functional the decline at the 1 + the 2 the years

The clinical the bottom the line

The classic the heat the stroke the NOT the benign — the very the poor the short- + the long-the-term; the aggressive + the honest the prognostication

[1]

Bouchama + Knochel 2002 — the Heat Stroke (NEJM) (PMID 12075060)

Source

New England Journal of Medicine — the definitive the review

Authors

Bouchama A, Knochel JP

The definition

The core the above 40 + the CNS the dysfunction + the multi-organ

The pathophysiology

The systemic the inflammatory the response the INDISTINGUISHABLE from the sepsis — the cytokine, the endothelial, the coagulation

The management

The RAPID the COOLING the definitive; the antipyretics + the dantrolene the ineffective

The mortality

The classic the 10 to 50 per cent; the exertional the below 5 per cent with the rapid the cooling

The clinical the bottom the line

The foundational the modern the reference — the heat stroke the 'the sepsis the from the heat'

[1]

Epstein + Yanovich 2019 — the Heatstroke (NEJM) (PMID 31216400)

Source

New England Journal of Medicine — the current-the-concepts the review

Authors

Epstein Y, Yanovich R

The scope

The updated the pathophysiology + the management of the classic + the exertional

The key the update

The reaffirms the rapid the physical the cooling; the antipyretics / the dantrolene the NO the benefit; the dantrolene the RCTs the negative

The subtype

The classic (the elderly, the drugs, the heatwave) vs the exertional (the young, the fit) — the different the mechanism, the same the endpoint

The clinical the bottom the line

The modern the companion the to the Bouchama 2002 — the same the message the reaffirmed

[1]

Leon + Bouchama 2015 — the Heat Stroke (Comprehensive Physiology) (PMID 25880507)

Source

Comprehensive Physiology — the mechanistic the review

Authors

Leon LR, Bouchama A

The scope

The detailed the molecular the pathophysiology — the heat the cytotoxicity, the SIRS, the organ the injury

The key the mechanism

The protein the denaturation (the above 41 to 42) + the lipid the peroxidation + the gut the translocation → the SIRS the indistinguishable the from the sepsis

The organ the injury

The brain (the Purkinje), the liver (the centrilobular), the kidney (the ATN), the muscle (the rhabdo), the coagulation (the DIC)

The clinical the bottom the line

The mechanistic the underpinning for the 'the sepsis the from the heat' + the multi-organ the management

[1]

The prognosis — the summary

The mortality the 10 to 50 per cent (the classic — the worse with the age / the comorbidity / the delay); the below 5 per cent the exertional with the rapid the cooling. The poor-the-prognosis the features: the prolonged the hyperthermia (the above 40 the for the above 1 to 2 the hr), the coma, the shock, the DIC, the AKI, the severe the acidosis, the elevated the lactate, the transaminitis the above 1000. The neurological the sequelae: the cerebellar the ataxia (the Purkinje — the permanent), the cognitive the impairment, the parkinsonism, the seizure — the may the persist the despite the full the systemic the recovery. The prompt the cooling (the within the 30 the min → the below 39) the reduces the dramatically.[1][3][6]

References

  1. [1]Lipman GS, et al. Management of Heat-Related Illness and Injury in the ICU: A Concise Definitive Review Crit Care Med, 2024.PMID 38240487
  2. [2]Pryor RR, et al. Heat-Related Illnesses Ann Intern Med, 2025.PMID 40569698
  3. [3]Bouchama A, Knochel JP Heat stroke N Engl J Med, 2002.PMID 12075060
  4. [4]Epstein Y, Yanovich R Heatstroke N Engl J Med, 2019.PMID 31216400
  5. [5]Casa DJ, et al. National Athletic Trainers' Association Position Statement: Exertional Heat Illnesses J Athl Train, 2015.PMID 26381473
  6. [6]Argaud L, et al. Short- and long-term outcomes of heatstroke following the 2003 heat wave in Lyon, France Arch Intern Med, 2007.PMID 17698677
  7. [7]Leon LR, Bouchama A Heat stroke Compr Physiol, 2015.PMID 25880507