Heat stroke
General
- temp > 40 and cns dysfnctn
- often fatal, if survive probable brain damage
- results from thermoregulatory failure coupled with exaggerated acute phase response and proteins
- classic/ nonexertional- from exposure to heat
-nonclassic/ exertional- from strenous activity
- is hyperthermia with systemic inflmm response and multiorgan dysfnctn predominated with encephalopathy
- usually v young or elderly, poor or socially isolated, no access to air conditioning
- genetic factors may lead to susceptibility- genes involved in making heat shock proteins and those involved in adaptation to heat stress.
Definitions
Heat wave- 3 or more consecutive days temp>32.3
Heat Stress- perceived discomfort and physio stress esp during work
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