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| ==General== | | ==Background== |
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| - temp > 40 and cns dysfnctn
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| - often fatal, if survive probable brain damage | | - often fatal, if survive probable brain damage |
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| - results from thermoregulatory failure coupled with exaggerated acute phase response and proteins
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| - classic/ nonexertional- from exposure to heat
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| -nonclassic/ exertional- from strenous activity
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| - is hyperthermia with systemic inflmm response and multiorgan dysfnctn predominated with encephalopathy
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| - usually v young or elderly, poor or socially isolated, no access to air conditioning | | - usually v young or elderly, poor or socially isolated, no access to air conditioning |
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| - genetic factors may lead to susceptibility- genes involved in making heat shock proteins and those involved in adaptation to heat stress. | | - heat stroke has microvasc thrombosis and endothelial cell damage- like DIC |
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| ==Definitions== | | ==Diagnosis== |
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| Heat wave- 3 or more consecutive days temp>32.3
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| Heat Stress- perceived discomfort and physio stress esp during work
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| Heat Stroke- temp >40 and cns dz | | Heat Stroke- temp >40 and CNS dz |
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| 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) | | 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) |
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| Hyperthermia- body temp above hypothal set point and heat dissapating mechs overwhelmed- either by internal or external factors
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| Multiorgan Dysfnc- changes occur after trauma, sepsis, heat stroke
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| ==Pathogenesis==
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| -involves thermoregulation and acclimatization, acute phase response, and heat shock proteins
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| ==Thermoregulation==
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| - body heat from metabolism and environment
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| - 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
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| - also get sweating- needs thermal gradient to work.
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| - increased blood temp causes increase cardiac output, tachycardia, increased minute ventilation.
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| - also get decreased splanchnic blood flow
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| - can lose 2L sweat per hour- need replenish with salt and water.
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| ==Acclimatization==
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| - by successive increments- takes several weeks and enhances cardiovascular performance
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| - activete renin- angiotensin- aldosterone sys,
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| - salt conservation by sweat glands and kidneys
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| - increase in capacity for secrete sweat
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| - increase plasma vol
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| - increase ability to resist exertional rhabdo
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| ==Acute Phase Response== | | ==Signs & Symptoms== |
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| - protects against tissue inj and promotes repair
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| - onset of inflammation is local
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| - systemic progression of infl response secondary- similar to sepsis
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| ==Heat Shock Response==
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| - all cells respond to heat by making heat shock or stress proteins- controlled at level of gene xcription
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| - increased level of intracellular heat shgck protein induce state of transient tolerance to second lethal heat stress
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| - heat shock protein acts as cellular chaperone that bind to partially folded or misfolded protein preventing irreversible denaturation
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| - other possibility is heat shock pro acts as central regulator of baroreceptor reflex response abating hypotnsn, bradycardia, and conferring cardiovascular protectn
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| ==Progression from Heat Stress to Stroke==
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| - due to thermoreg failure, exagrtn of acute phase resp, and altertn of exprsn of heat shock protein
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| ==Thermoreg Failure==
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| - normal cardiac adaption is to increase cardiac output and shift hot core blood to perifery
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| - may be unable to increase CO due to salt/ water balance, CAD, or med side effect.
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| - leads to heat stroke
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| ==Exaggeration of Acute Phase Response==
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| - gi tract fuels response
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| - normally with exercise or hyperthermia, blood flows from gut to muscles- leads to intestinal ischemia and hyperpermeability
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| - gi hypoxia leads to free radical damage that increases mucosal injury
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| - with heat stress, endotoxin from gut enters circulation- leads to hemodynamic instab.
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| - if pretreat with anti- entox antibody- decrease response and improve outcome
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| - 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
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| ==Alteration of Heat Shock Response==
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| - increased levels of heat shock proteins protect cells from damage from heat, ischemia, hypoxia, endotox and infl cytokines
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| - heat shock response is adaptive and protective
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| - less response and higher risk of going from heat stress to heat stroke in elderlly, lack of acclimitazation, genetics
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| ==Pathophysiology==
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| Heat
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| - heat injures tissue/ cells
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| - thermal max is 41.6- 42C for 45 min to 8 hrs
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| Cytokines
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| - infl cytokines increase with heat but cooling does not suppress these factors
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| - lvls correlate to severity of heat stroke
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| - imbalance btwn infl and antiinfl cytokines leads to either infl induce injury or immune suppression
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| - incidence of infection in pt with heat stroke high
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| - IL-1 antagonist or steroids before heat stroke attenuates injury, sxs and improves survival
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| Coagulation Disorders and Endothelial Cell Injury
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| - heat stroke has microvasc thrombosis and endothelial cell damage- like DIC
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| - with heat get increased coagulation and fibrinolysis- but as cool, fibrinolysis stops but coagulation persists- as in sepsis
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| ==Clinical and Metabolic Manifestations==
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| - heat stroke- hot and altered | | - heat stroke- hot and altered |
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| - sz esp when cooling
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| - tachy and hyperventilation | | - tachy and hyperventilation |
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| - exertional- resp alk and lactic acidosis, also rhabdo and electrolyte abnormalities | | - exertional- resp alk and lactic acidosis, also rhabdo and electrolyte abnormalities |
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| | - may have muscular rigidity |
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| - hypoglycemia rare | | - hypoglycemia rare |
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| ==TX== | | ==Treatment== |
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| - cool- by conduction, evaporaton, convection.
| | General |
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| - but if lower skin temp <30, will get cutaneous vasoconstriction and shivering!
| | 1) Rapid Cooling |
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| - avoid by spraying pt with warm water or hot moving air- gradually | | -by conduction, evaporaton, convection |
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| - no drugs helpful | | -continue only until the temperature drops to 38.5 or 39 C to avoid overshoot hypothermia |
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| - dantrolene not effective | | -evaporative cooling and iced gastric lavage recommended |
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| - antipyretics not studied yet | | -e.g. luke-warm water or wet towels + blowing air with a fan |
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| - cns recovery is a favorable sign- but 20% will have resid damage | | -may consider peritoneal and thoracic lavage |
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| | -cooling blankets may be effective for mild heatstroke |
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| | | -immersing or covering the patient in ice NOT recommended (causes vasoconstriction and shivering) |
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| ==Prevention==
| | *no drugs helpful (dantrolene not effective; antipyretics not studied) |
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| - is completely preventable | | Specific Co-Symptom |
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| - acclimatize
| | 1) Shivering |
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| - drink extra water | | -Treat with chlorpromazine, benzodiazepines, or thiopental |
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| - eat more salt
| | 2) Seizure |
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| - air conditioners | | -Treated with diazepam or thiopental (dilantin is ineffective) |
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| ==Emerging Concepts== | | ==Prognosis== |
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| | - cns recovery is a favorable sign- but 20% will have resid damage |
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| - after heat stroke, cooling body may not stop infl, coagulation, multiorgan dysfnc
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| - so immune modulators- IL-1 recept antag, endotox antibody, steroids may be helpful but not proven yet
| | ==See Also== |
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| - consider tx c activated protein C- helps in sepsis
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| - ASA/ NSAIDS- activate transcription and translation of heat shock proteins and enhances tolerance of heat
| | Environ: Heat Exhaustion |
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| 6/06 MISTRY
| | Mistry, KajiQuestions, Donaldson |
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Background
- often fatal, if survive probable brain damage
- usually v young or elderly, poor or socially isolated, no access to air conditioning
- heat stroke has microvasc thrombosis and endothelial cell damage- like DIC
Diagnosis
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)
Signs & Symptoms
- heat stroke- hot and altered
- tachy and hyperventilation
- may have hypotn
- nonexertional heat stroke- have resp alk
- exertional- resp alk and lactic acidosis, also rhabdo and electrolyte abnormalities
- may have muscular rigidity
- hypoglycemia rare
- can progress to multiorgan faillure
Treatment
General
1) Rapid Cooling
-by conduction, evaporaton, convection
-continue only until the temperature drops to 38.5 or 39 C to avoid overshoot hypothermia
-evaporative cooling and iced gastric lavage recommended
-e.g. luke-warm water or wet towels + blowing air with a fan
-may consider peritoneal and thoracic lavage
-cooling blankets may be effective for mild heatstroke
-immersing or covering the patient in ice NOT recommended (causes vasoconstriction and shivering)
- no drugs helpful (dantrolene not effective; antipyretics not studied)
Specific Co-Symptom
1) Shivering
-Treat with chlorpromazine, benzodiazepines, or thiopental
2) Seizure
-Treated with diazepam or thiopental (dilantin is ineffective)
Prognosis
- cns recovery is a favorable sign- but 20% will have resid damage
See Also
Environ: Heat Exhaustion
Source
Mistry, KajiQuestions, Donaldson
