Heat stroke: Difference between revisions

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==General==
==Background==
*Severe end of heat-related illness spectrum characterized by severe hyperthermia and neurologic dysfunction
*True emergency - universally fatal if left untreated
**Mortality approaches 30% even with treatment<ref name="Gaudio">Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. J Emerg Med. 2015 Oct 31.</ref>, and is directly associated with the duration of elevated core temperature
*Hallmark is multisystem organ dysfunction from heat-induced damage resulting in systemic inflammatory response


===Types===
*Classic (nonexertional) - insidious development over days
**Seen in children and elderly
**During the time of [[heat wave]]
*Exertional - rapid onset during exercise or other exertion
**Seen in otherwise young, healthy individuals


- temp > 40 and cns dysfnctn
==Clinical Features==
*Symptoms<ref name="Becker">Becker JA, Stewart LK. Heat-related illness. Am Fam Physician. 2011 Jun 1;83(11):1325-30.</ref>
**Elevated temperature >40°C (104°F) '''PLUS'''
**CNS neurologic abnormalities (e.g. inappropriate behavior, [[Confusion]], [[dysarthria|slurred speech]], [[Delirium]], [[Ataxia]], [[Coma]], [[Seizures]])
*Anhidrosis is frequently present; however, its absence does NOT rule out heat stroke
*May have massive [[rectal bleeding|hematochezia]] secondary to decreased intestinal perfusion and ischemia<ref>Lambert GP. Intestinal barrier dysfunction, endotoxemia, and gastrointestinal  symptoms: the 'canary in the coal mine' during exercise-heat stress? Med Sport Sci. 2008;53:61-73.</ref>


- often fatal, if survive probable brain damage
==Differential Diagnosis==
{{Template:Heat Emergencies}}


- results from thermoregulatory failure coupled with exaggerated acute phase response and proteins
===Non-Environmental===
*Infectious
**[[Sepsis (Main)|Sepsis]]
**[[Meningitis]]
**[[Encephalitis]]
**[[Malaria]]
**[[Typhoid]]
**[[Tetanus]]
*Endocrine
**[[Thyroid storm]]
**[[Pheochromocytoma]]
**[[Diabetic ketoacidosis|DKA]]
*Neurologic
**Hypothalamic [[ICH|bleeding]] or [[stroke|infarct]]
**[[Stroke (main)|CVA]]
**[[Status epilepticus]]
*Toxicologic
**[[Anticholinergic toxicity|Anticholinergic toxidrome]]
**[[Sympathomimetic toxicity]]
**[[Salicylate toxicity]]
**[[Serotonin syndrome]]
**[[Malignant hyperthermia]]
**[[Neuroleptic malignant syndrome]]
**Withdrawal (e.g. [[ETOH withdrawal|ETOH]], [[benzodiazepine withdrawal|benzodiazepines]])


- classic/ nonexertional- from exposure to heat
{{AMS and fever DDX}}


-nonclassic/ exertional- from strenous activity
==Evaluation==
===Workup===
*[[ECG]]<ref>Mimish L. Electrocardiographic findings in heat stroke and exhaustion: A study on Makkah pilgrims. J Saudi Heart Assoc. 2012 Jan; 24(1): 35–39.</ref>
**Most often sinus tachycardia, self-limited
**Less frequently ischemic changes including ST depressions, TWIs
*Core temperature (continuous monitoring is ideal, e.g. with bladder temperature monitor)
*Blood glucose
*CBC
*Metabolic panel
*[[LFTs]]
*Blood gas
*[[Lactate]]
*Coagulation studies ([[DIC (Disseminated Intravascular Coagulation)|DIC]])
*Creatine phosphokinase and myoglobin ([[Rhabdomyolysis]])
*[[Urinalysis]]
*[[CXR]]
*[[CT brain]] (± [[LP]]), if indicated (Cerebral Edema)


- is hyperthermia with systemic inflmm response and multiorgan dysfnctn predominated with encephalopathy
===Evaluation===
*Clinical diagnosis
*Exposure to hot environment and high index of suspicion.


- usually v young or elderly, poor or socially isolated, no access to air conditioning
==Management==
*Address ABCs
*Rapid cooling (see below) - mainstay of treatment
**Reduces morbidity/mortality, should be started in prehospital setting if no other life-threats exist<ref name="Becker" />
*Remove from environment
*[[IVF]] (for renal protection and avoiding rhabdomyolysis)
**Bolus if hypotensive
**Infusion titrated to UOP (goal 2-3ml/kg/hr)


- genetic factors may lead to susceptibility- genes involved in making heat shock proteins and those involved in adaptation to heat stress.
===Rapid Cooling===
*Cooling end point should be ~39°C (102.2°F) - no good data for this goal<ref name="Gaudio" />
*No role for: antipyretics or dantrolene
*Combination of methods, or adjuncts such as cool IVF may increase efficacy of individual methods
====Techniques====
*Cool water immersion - treatment of choice<ref name="Becker" /><ref name="Pryor" />
**Immersion of body to level of torso or neck in cool or ice-water
**Best for exertional heat stroke in young/healthy patients, but benefit shown in elderly patients as well
**Diffuse application of ice or cold packs to entire body may provide similar benefit (but less data)
***Applying ice packs only to neck, axillae, groin provides only minimal cooling<ref name="Gaudio" />
**Benefits: most rapid decrease in temperature, some studies have shown 100% survival (esp when started within 30 minutes of collapse)<ref name="Gaudio" /><ref name="Becker" /><ref name="Pryor">Pryor RR, Roth RN, Suyama J, Hostler D. Exertional heat illness: emerging concepts and advances in prehospital care. Prehosp Disaster Med. 2015 Jun;30(3):297-305.</ref>
**Disadvantages: requires special equipment (may not be immediately available), poorly tolerated, unable to provide defibrillation or many other resuscitative measures
*Evaporative/Convective Cooling
**Spray cool water (15°C / 59°F) on patient while directing fans at patient
**Benefits: Easier to apply in ED and while performing other interventions
**Disadvantages: Slower cooling (than immersion) with slightly higher morbidity/mortality
*Invasive Techniques (limited data <ref name="Gaudio" />)
**Bladder Lavage
**Gastric Lavage
**Thoracic Lavage with chest tubes
**Cardiopulmonary bypass/ECMO


==Complications==
*[[Hypotension]]
**Usually responds to small fluid bolus (500cc) and body cooling
**If no response to fluids → consider [[vasopressors]] (dopamine or dobutamine)
***Avoid peripheral vasoconstriction (e.g. norepinephrine), which may redirect blood flow away from skin and diminish cooling
*[[Electrolyte abnormalities]]
**Variable: [[hypokalemia]] and [[hypernatremia|hyper]] or [[hyponatremia]] may be seen
*Hematologic - [[DIC]] or abnormal bleeding
*[[hepatic failure|Hepatic injury]] - almost always reversible
*[[Renal failure]]
*[[ARDS]]
*[[Seizure]] - treat with [[Benzodiazepines]]
*[[focal neuro deficits|Neurologic deficit]]
**Persistent in 20%, associated with high mortality


==Definitions==
==Disposition==
*All patients require admission


==See Also==
*[[Heat emergencies]]
*[[Heat exhaustion]]
*[[Acute fever]]


Heat wave- 3 or more consecutive days temp>32.3
==References==
<references/>


Heat Stress- perceived discomfort and physio stress esp during work
[[Category:Environmental]]
 
Heat Stroke- temp >40 and cns dz
 
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)
 
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 17:01, 5 May 2022

Background

  • Severe end of heat-related illness spectrum characterized by severe hyperthermia and neurologic dysfunction
  • True emergency - universally fatal if left untreated
    • Mortality approaches 30% even with treatment[1], and is directly associated with the duration of elevated core temperature
  • Hallmark is multisystem organ dysfunction from heat-induced damage resulting in systemic inflammatory response

Types

  • Classic (nonexertional) - insidious development over days
    • Seen in children and elderly
    • During the time of heat wave
  • Exertional - rapid onset during exercise or other exertion
    • Seen in otherwise young, healthy individuals

Clinical Features

  • Symptoms[2]
  • Anhidrosis is frequently present; however, its absence does NOT rule out heat stroke
  • May have massive hematochezia secondary to decreased intestinal perfusion and ischemia[3]

Differential Diagnosis

Environmental heat diagnoses

Non-Environmental

Altered mental status and fever

Evaluation

Workup

  • ECG[4]
    • Most often sinus tachycardia, self-limited
    • Less frequently ischemic changes including ST depressions, TWIs
  • Core temperature (continuous monitoring is ideal, e.g. with bladder temperature monitor)
  • Blood glucose
  • CBC
  • Metabolic panel
  • LFTs
  • Blood gas
  • Lactate
  • Coagulation studies (DIC)
  • Creatine phosphokinase and myoglobin (Rhabdomyolysis)
  • Urinalysis
  • CXR
  • CT brain (± LP), if indicated (Cerebral Edema)

Evaluation

  • Clinical diagnosis
  • Exposure to hot environment and high index of suspicion.

Management

  • Address ABCs
  • Rapid cooling (see below) - mainstay of treatment
    • Reduces morbidity/mortality, should be started in prehospital setting if no other life-threats exist[2]
  • Remove from environment
  • IVF (for renal protection and avoiding rhabdomyolysis)
    • Bolus if hypotensive
    • Infusion titrated to UOP (goal 2-3ml/kg/hr)

Rapid Cooling

  • Cooling end point should be ~39°C (102.2°F) - no good data for this goal[1]
  • No role for: antipyretics or dantrolene
  • Combination of methods, or adjuncts such as cool IVF may increase efficacy of individual methods

Techniques

  • Cool water immersion - treatment of choice[2][5]
    • Immersion of body to level of torso or neck in cool or ice-water
    • Best for exertional heat stroke in young/healthy patients, but benefit shown in elderly patients as well
    • Diffuse application of ice or cold packs to entire body may provide similar benefit (but less data)
      • Applying ice packs only to neck, axillae, groin provides only minimal cooling[1]
    • Benefits: most rapid decrease in temperature, some studies have shown 100% survival (esp when started within 30 minutes of collapse)[1][2][5]
    • Disadvantages: requires special equipment (may not be immediately available), poorly tolerated, unable to provide defibrillation or many other resuscitative measures
  • Evaporative/Convective Cooling
    • Spray cool water (15°C / 59°F) on patient while directing fans at patient
    • Benefits: Easier to apply in ED and while performing other interventions
    • Disadvantages: Slower cooling (than immersion) with slightly higher morbidity/mortality
  • Invasive Techniques (limited data [1])
    • Bladder Lavage
    • Gastric Lavage
    • Thoracic Lavage with chest tubes
    • Cardiopulmonary bypass/ECMO

Complications

Disposition

  • All patients require admission

See Also

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. J Emerg Med. 2015 Oct 31.
  2. ↑ 2.0 2.1 2.2 2.3 Becker JA, Stewart LK. Heat-related illness. Am Fam Physician. 2011 Jun 1;83(11):1325-30.
  3. ↑ Lambert GP. Intestinal barrier dysfunction, endotoxemia, and gastrointestinal symptoms: the 'canary in the coal mine' during exercise-heat stress? Med Sport Sci. 2008;53:61-73.
  4. ↑ Mimish L. Electrocardiographic findings in heat stroke and exhaustion: A study on Makkah pilgrims. J Saudi Heart Assoc. 2012 Jan; 24(1): 35–39.
  5. ↑ 5.0 5.1 Pryor RR, Roth RN, Suyama J, Hostler D. Exertional heat illness: emerging concepts and advances in prehospital care. Prehosp Disaster Med. 2015 Jun;30(3):297-305.
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