Heat stroke: Difference between revisions

(Created page with "==General== - temp > 40 and cns dysfnctn - often fatal, if survive probable brain damage - results from thermoregulatory failure coupled with exaggerated acute phase response...")
 
(Strip excess bold)
 
(60 intermediate revisions by 16 users not shown)
Line 1: Line 1:
==General==
==Background==
*Severe, life-threatening end of the [[heat emergencies|heat illness]] spectrum
*Defined as core temperature >40°C (104°F) with CNS dysfunction
*'''Universally fatal if untreated'''; mortality approaches '''30% even with treatment'''<ref>Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. ''J Emerg Med''. 2016;50(4):563-72. PMID 26525947</ref>
*Mortality directly correlates with duration and degree of elevated core temperature
*Hallmark is multisystem organ dysfunction from heat-induced systemic inflammatory response


===Types===
*Classic (nonexertional):
**Insidious development over days
**Seen in elderly, children, chronically ill, those on anticholinergic or diuretic medications
**During heat waves
*Exertional:
**Rapid onset during exercise or physical exertion
**Seen in otherwise young, healthy individuals (athletes, military, laborers)
**Typically faster presentation and higher CK levels


- temp > 40 and cns dysfnctn
==Clinical Features==
*Core temperature >40°C (104°F) PLUS
*CNS dysfunction<ref>Becker JA, Stewart LK. Heat-related illness. ''Am Fam Physician''. 2011;83(11):1325-30. PMID 21661715</ref>:
**Altered mental status, confusion, agitation, slurred speech
**Ataxia, [[seizures]], coma
**Inappropriate behavior may be earliest sign
*Anhidrosis is frequently present but its absence does NOT rule out heat stroke
**Sweating may still be present, especially in exertional heat stroke
*Tachycardia, [[hypotension]] (high-output state → eventual cardiovascular collapse)
*Tachypnea
*Massive hematochezia may occur from intestinal ischemia<ref>Lambert GP. Intestinal barrier dysfunction during exercise-heat stress. ''Med Sport Sci''. 2008;53:61-73. PMID 19208999</ref>
*Petechiae, purpura (DIC)


- often fatal, if survive probable brain damage
==Differential Diagnosis==
{{Altered mental status and fever DDX}}
{{Environmental heat illness DDX}}


- results from thermoregulatory failure coupled with exaggerated acute phase response and proteins
*Key diagnoses to consider:
**[[Sepsis]] / [[meningitis]] / [[encephalitis]]
**[[Thyroid storm]]
**[[Neuroleptic malignant syndrome]]
**[[Serotonin syndrome]]
**[[Malignant hyperthermia]]
**[[Anticholinergic toxicity]]
**Sympathomimetic toxicity ([[cocaine]], [[amphetamines]])
**[[Alcohol withdrawal]] / [[benzodiazepine withdrawal]]


- classic/ nonexertional- from exposure to heat
==Evaluation==
*Core temperature (rectal or bladder probe preferred; tympanic/temporal unreliable)
**Continuous monitoring essential (bladder temperature probe ideal)
*'''Blood glucose''' (POC immediately)
*ECG: most often sinus tachycardia; ischemic changes (ST depressions, TWI) may occur<ref>Mimish L. Electrocardiographic findings in heat stroke and exhaustion. ''J Saudi Heart Assoc''. 2012;24(1):35-39. PMID 23960068</ref>
*CBC: may show hemoconcentration initially; thrombocytopenia with DIC
*BMP: electrolyte abnormalities (variable hypo/hypernatremia, hypokalemia), [[AKI]]
*LFTs: transaminase elevation occurs in nearly all cases (peaks at 48-72h)
**AST/ALT >1000 suggests severe liver injury
*Coagulation studies: PT/INR, fibrinogen, D-dimer (DIC screening)
*CK and myoglobin: [[rhabdomyolysis]] (exertional >> classic)
*Lactate: marker of tissue hypoperfusion
*VBG/ABG: metabolic acidosis
*Urinalysis: myoglobinuria
*CT head ± LP: if concern for CNS infection or hemorrhage


-nonclassic/ exertional- from strenous activity
==Management==
===Immediate===
*Cooling is THE priority — every minute of delay increases mortality
*Remove from hot environment; remove clothing
*Address ABCs; intubate if necessary for airway protection
*Goal: reduce core temperature to 39°C (102.2°F) within 30 minutes
*Cooling rate target: 0.15-0.25°C/min


- is hyperthermia with systemic inflmm response and multiorgan dysfnctn predominated with encephalopathy
===Rapid Cooling Techniques===
====Cold Water Immersion (Treatment of Choice)====
*Most effective cooling method (cooling rate ~0.2°C/min)<ref>Pryor RR, et al. Exertional heat illness: emerging concepts and advances in prehospital care. ''Prehosp Disaster Med''. 2015;30(3):297-305. PMID 25959925</ref>
*Immerse body to torso or neck in cold/ice water (1-17°C)
*Best for exertional heat stroke in young/healthy patients
*Also beneficial in elderly patients
*Studies show up to 100% survival when initiated within 30 minutes of collapse<ref>Becker JA, Stewart LK. Heat-related illness. ''Am Fam Physician''. 2011;83(11):1325-30. PMID 21661715</ref>
*Disadvantage: limited access to resuscitative measures during immersion


- usually v young or elderly, poor or socially isolated, no access to air conditioning
====Evaporative/Convective Cooling====
*Spray lukewarm water (15°C / 59°F) continuously on patient while directing fans at exposed skin
*Easier to apply while performing other interventions in ED
*Slower cooling rate than immersion


- genetic factors may lead to susceptibility- genes involved in making heat shock proteins and those involved in adaptation to heat stress.
====Other Techniques====
*Cold IV fluids (4°C NS bolus) as adjunct (limited cooling on its own)
*Ice packs to entire body surface (better than just neck/axillae/groin)
**Ice packs only to neck, axillae, groin provides minimal cooling
*Invasive lavage (bladder, gastric, thoracic) — limited data, reserved for refractory cases
*ECMO — for refractory heat stroke


===What NOT to Do===
*NO antipyretics (acetaminophen, NSAIDs) — thermoregulatory set point is normal; these are ineffective and may worsen liver/renal injury
*NO dantrolene — not effective in heat stroke (heat stroke is not malignant hyperthermia)
*AVOID peripheral vasoconstrictors (norepinephrine) — may redirect blood from skin and impair cooling
*AVOID shivering (counterproductive) — treat with benzodiazepines if occurs during cooling


==Definitions==
===Supportive Care===
*IV fluid resuscitation:
**Bolus 500-1000 mL NS if hypotensive
**Titrate to UOP goal 1-2 mL/kg/hr (renal protection from rhabdomyolysis)
*Seizures: [[benzodiazepines]] (lorazepam 2-4 mg IV)
*Hypotension: small fluid boluses first; if refractory, consider dopamine or dobutamine
*Correct electrolyte abnormalities
*Treat [[DIC]] with blood products if clinically significant bleeding


==Complications==
*Hepatic injury: almost always present; usually reversible but can progress to fulminant failure
*[[Rhabdomyolysis]] → [[acute kidney injury]] (more common in exertional)
*[[DIC]] and abnormal bleeding
*[[ARDS]]
*Persistent neurologic deficits: present in ~20% of survivors, associated with high mortality
*Seizures
*Myocardial injury


Heat wave- 3 or more consecutive days temp>32.3
==Disposition==
*All patients require admission (most to ICU)
*Serial monitoring of core temperature, LFTs, coagulation studies, renal function, CK for 48-72h
*LFTs may worsen for 2-3 days after presentation — repeat at 24-48h


Heat Stress- perceived discomfort and physio stress esp during work
==See Also==
*[[Heat emergencies]]
*[[Heat exhaustion]]
*[[Rhabdomyolysis]]
*[[Malignant hyperthermia]]
*[[Neuroleptic malignant syndrome]]


Heat Stroke- temp >40 and cns dz
==References==
<references/>
*Hifumi T, et al. Heat stroke. ''J Intensive Care''. 2018;6:30. PMID 29850022
*Leon LR, Bouchama A. Heat stroke. ''Compr Physiol''. 2015;5(2):611-647. PMID 25880507


Heat Exhaustion- thirst, weakness, anxiety, dizzy, HA due to temp and water and salt depletion. Temp can be low, high or normal. (>37 but <40)
[[Category:Environmental]]
 
Hyperthermia- body temp above hypothal set point and heat dissapating mechs overwhelmed- either by internal or external factors
 
Multiorgan Dysfnc- changes occur after trauma, sepsis, heat stroke
 
 
==Pathogenesis==
 
 
-involves thermoregulation and acclimatization, acute phase response, and heat shock proteins
 
 
==Thermoregulation==
 
 
- body heat from metabolism and environment
 
- if blood temp rises 1C, peripheral and hypothalamic heat receptors triggered and warm blood shunted to periphery- sympathetic cutaneous vasodilatation- more blood to skin and muscles
 
- also get sweating- needs thermal gradient to work.
 
- increased blood temp causes increase cardiac output, tachycardia, increased minute ventilation.
 
- also get decreased splanchnic blood flow
 
- can lose 2L sweat per hour- need replenish with salt and water.
 
 
==Acclimatization==
 
 
- by successive increments- takes several weeks and enhances cardiovascular performance
 
- activete renin- angiotensin- aldosterone sys,
 
- salt conservation by sweat glands and kidneys
 
- increase in capacity for secrete sweat
 
- increase plasma vol
 
- increase ability to resist exertional rhabdo
 
 
==Acute Phase Response==
 
 
- protects against tissue inj and promotes repair
 
- onset of inflammation is local
 
- systemic progression of infl response secondary- similar to sepsis
 
 
==Heat Shock Response==
 
 
- all cells respond to heat by making heat shock or stress proteins- controlled at level of gene xcription
 
- increased level of intracellular heat shgck protein induce state of transient tolerance to second lethal heat stress
 
- heat shock protein acts as cellular chaperone that bind to partially folded or misfolded protein preventing irreversible denaturation
 
- other possibility is heat shock pro acts as central regulator of baroreceptor reflex response abating hypotnsn, bradycardia, and conferring cardiovascular protectn
 
 
==Progression from Heat Stress to Stroke==
 
 
- due to thermoreg failure, exagrtn of acute phase resp, and altertn of exprsn of heat shock protein
 
 
==Thermoreg Failure==
 
 
- normal cardiac adaption is to increase cardiac output and shift hot core blood to perifery
 
- may be unable to increase CO due to salt/ water balance, CAD, or med side effect.
 
- leads to heat stroke
 
 
==Exaggeration of Acute Phase Response==
 
 
- gi tract fuels response
 
- normally with exercise or hyperthermia, blood flows from gut to muscles- leads to intestinal ischemia and hyperpermeability
 
- gi hypoxia leads to free radical damage that increases mucosal injury
 
- with heat stress, endotoxin from gut enters circulation- leads to hemodynamic instab.
 
- if pretreat with anti- entox antibody- decrease response and improve outcome
 
- leakage of endotoxin leads to increased infl cytokines which lead to endothelial- cell activation- causes alteration of thermoregulatory set point, alters vasc tone and thereby precipitates hypotn, hyperthermia and heat stroke
 
 
==Alteration of Heat Shock Response==
 
 
- increased levels of heat shock proteins protect cells from damage from heat, ischemia, hypoxia, endotox and infl cytokines
 
- heat shock response is adaptive and protective
 
- less response and higher risk of going from heat stress to heat stroke in elderlly, lack of acclimitazation, genetics
 
 
==Pathophysiology==
 
 
Heat
 
- heat injures tissue/ cells
 
- thermal max is 41.6- 42C for 45 min to 8 hrs
 
 
Cytokines
 
- infl cytokines increase with heat but cooling does not suppress these factors
 
- lvls correlate to severity of heat stroke
 
- imbalance btwn infl and antiinfl cytokines leads to either infl induce injury or immune suppression
 
- incidence of infection in pt with heat stroke high
 
- IL-1 antagonist or steroids before heat stroke attenuates injury, sxs and improves survival
 
 
Coagulation Disorders and Endothelial Cell Injury
 
- heat stroke has microvasc thrombosis and endothelial cell damage- like DIC
 
- with heat get increased coagulation and fibrinolysis- but as cool, fibrinolysis stops but coagulation persists- as in sepsis
 
 
==Clinical and Metabolic Manifestations==
 
 
- heat stroke- hot and altered
 
- sz esp when cooling
 
- tachy and hyperventilation
 
- may have hypotn
 
- nonexertional heat stroke- have resp alk
 
- exertional- resp alk and lactic acidosis, also rhabdo and electrolyte abnormalities
 
- hypoglycemia rare
 
- can progress to multiorgan faillure
 
 
==TX==
 
 
- cool- by conduction, evaporaton, convection.
 
- but if lower skin temp <30, will get cutaneous vasoconstriction and shivering!
 
- avoid by spraying pt with warm water or hot moving air- gradually
 
- no drugs helpful
 
- dantrolene not effective
 
- antipyretics not studied yet
 
- cns recovery is a favorable sign- but 20% will have resid damage
 
 
==Prevention==
 
 
- is completely preventable
 
- acclimatize
 
- drink extra water
 
- eat more salt
 
- air conditioners
 
 
==Emerging Concepts==
 
 
- after heat stroke, cooling body may not stop infl, coagulation, multiorgan dysfnc
 
- so immune modulators- IL-1 recept antag, endotox antibody, steroids may be helpful but not proven yet
 
- consider tx c activated protein C- helps in sepsis
 
- ASA/ NSAIDS- activate transcription and translation of heat shock proteins and enhances tolerance of heat
 
 
==Source ==
 
 
6/06 MISTRY
 
 
 
 
[[Category:Environ]]

Latest revision as of 09:36, 22 March 2026

Background

  • Severe, life-threatening end of the heat illness spectrum
  • Defined as core temperature >40°C (104°F) with CNS dysfunction
  • Universally fatal if untreated; mortality approaches 30% even with treatment[1]
  • Mortality directly correlates with duration and degree of elevated core temperature
  • Hallmark is multisystem organ dysfunction from heat-induced systemic inflammatory response

Types

  • Classic (nonexertional):
    • Insidious development over days
    • Seen in elderly, children, chronically ill, those on anticholinergic or diuretic medications
    • During heat waves
  • Exertional:
    • Rapid onset during exercise or physical exertion
    • Seen in otherwise young, healthy individuals (athletes, military, laborers)
    • Typically faster presentation and higher CK levels

Clinical Features

  • Core temperature >40°C (104°F) PLUS
  • CNS dysfunction[2]:
    • Altered mental status, confusion, agitation, slurred speech
    • Ataxia, seizures, coma
    • Inappropriate behavior may be earliest sign
  • Anhidrosis is frequently present but its absence does NOT rule out heat stroke
    • Sweating may still be present, especially in exertional heat stroke
  • Tachycardia, hypotension (high-output state → eventual cardiovascular collapse)
  • Tachypnea
  • Massive hematochezia may occur from intestinal ischemia[3]
  • Petechiae, purpura (DIC)

Differential Diagnosis

Template:Altered mental status and fever DDX Template:Environmental heat illness DDX

Evaluation

  • Core temperature (rectal or bladder probe preferred; tympanic/temporal unreliable)
    • Continuous monitoring essential (bladder temperature probe ideal)
  • Blood glucose (POC immediately)
  • ECG: most often sinus tachycardia; ischemic changes (ST depressions, TWI) may occur[4]
  • CBC: may show hemoconcentration initially; thrombocytopenia with DIC
  • BMP: electrolyte abnormalities (variable hypo/hypernatremia, hypokalemia), AKI
  • LFTs: transaminase elevation occurs in nearly all cases (peaks at 48-72h)
    • AST/ALT >1000 suggests severe liver injury
  • Coagulation studies: PT/INR, fibrinogen, D-dimer (DIC screening)
  • CK and myoglobin: rhabdomyolysis (exertional >> classic)
  • Lactate: marker of tissue hypoperfusion
  • VBG/ABG: metabolic acidosis
  • Urinalysis: myoglobinuria
  • CT head ± LP: if concern for CNS infection or hemorrhage

Management

Immediate

  • Cooling is THE priority — every minute of delay increases mortality
  • Remove from hot environment; remove clothing
  • Address ABCs; intubate if necessary for airway protection
  • Goal: reduce core temperature to 39°C (102.2°F) within 30 minutes
  • Cooling rate target: 0.15-0.25°C/min

Rapid Cooling Techniques

Cold Water Immersion (Treatment of Choice)

  • Most effective cooling method (cooling rate ~0.2°C/min)[5]
  • Immerse body to torso or neck in cold/ice water (1-17°C)
  • Best for exertional heat stroke in young/healthy patients
  • Also beneficial in elderly patients
  • Studies show up to 100% survival when initiated within 30 minutes of collapse[6]
  • Disadvantage: limited access to resuscitative measures during immersion

Evaporative/Convective Cooling

  • Spray lukewarm water (15°C / 59°F) continuously on patient while directing fans at exposed skin
  • Easier to apply while performing other interventions in ED
  • Slower cooling rate than immersion

Other Techniques

  • Cold IV fluids (4°C NS bolus) as adjunct (limited cooling on its own)
  • Ice packs to entire body surface (better than just neck/axillae/groin)
    • Ice packs only to neck, axillae, groin provides minimal cooling
  • Invasive lavage (bladder, gastric, thoracic) — limited data, reserved for refractory cases
  • ECMO — for refractory heat stroke

What NOT to Do

  • NO antipyretics (acetaminophen, NSAIDs) — thermoregulatory set point is normal; these are ineffective and may worsen liver/renal injury
  • NO dantrolene — not effective in heat stroke (heat stroke is not malignant hyperthermia)
  • AVOID peripheral vasoconstrictors (norepinephrine) — may redirect blood from skin and impair cooling
  • AVOID shivering (counterproductive) — treat with benzodiazepines if occurs during cooling

Supportive Care

  • IV fluid resuscitation:
    • Bolus 500-1000 mL NS if hypotensive
    • Titrate to UOP goal 1-2 mL/kg/hr (renal protection from rhabdomyolysis)
  • Seizures: benzodiazepines (lorazepam 2-4 mg IV)
  • Hypotension: small fluid boluses first; if refractory, consider dopamine or dobutamine
  • Correct electrolyte abnormalities
  • Treat DIC with blood products if clinically significant bleeding

Complications

  • Hepatic injury: almost always present; usually reversible but can progress to fulminant failure
  • Rhabdomyolysis → acute kidney injury (more common in exertional)
  • DIC and abnormal bleeding
  • ARDS
  • Persistent neurologic deficits: present in ~20% of survivors, associated with high mortality
  • Seizures
  • Myocardial injury

Disposition

  • All patients require admission (most to ICU)
  • Serial monitoring of core temperature, LFTs, coagulation studies, renal function, CK for 48-72h
  • LFTs may worsen for 2-3 days after presentation — repeat at 24-48h

See Also

References

  1. ↑ Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. J Emerg Med. 2016;50(4):563-72. PMID 26525947
  2. ↑ Becker JA, Stewart LK. Heat-related illness. Am Fam Physician. 2011;83(11):1325-30. PMID 21661715
  3. ↑ Lambert GP. Intestinal barrier dysfunction during exercise-heat stress. Med Sport Sci. 2008;53:61-73. PMID 19208999
  4. ↑ Mimish L. Electrocardiographic findings in heat stroke and exhaustion. J Saudi Heart Assoc. 2012;24(1):35-39. PMID 23960068
  5. ↑ Pryor RR, et al. Exertional heat illness: emerging concepts and advances in prehospital care. Prehosp Disaster Med. 2015;30(3):297-305. PMID 25959925
  6. ↑ Becker JA, Stewart LK. Heat-related illness. Am Fam Physician. 2011;83(11):1325-30. PMID 21661715
  • Hifumi T, et al. Heat stroke. J Intensive Care. 2018;6:30. PMID 29850022
  • Leon LR, Bouchama A. Heat stroke. Compr Physiol. 2015;5(2):611-647. PMID 25880507
Retrieved from "https://www.wikem.org/w/index.php?title=Heat_stroke&oldid=389385"