HEAT STROKE AND HEAT EXHAUS.PPT

8/9/2019 HEAT STROKE AND HEAT EXHAUS.PPT

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Heat Stroke and Heat Exhaustion

Sholihul Muhibbi


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Fever vs Hyperthermia

Fever

Elevation of body temperature above the normal range as the

result of a change in the thermoregulatory center located inthe anterior hypothalamus.

The elevation of the body’s normal set point occurs through

the release of pyrogenic cytokines including: I!"# T$F# IF$!

gamma# I!% and their effects in the hypothalamus.

Elevation in temperature results from either increased heat

production &shivering' or decreased loss &peripheral

vasoconstriction'.


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Fever vs Hyperthermia

(yperthermia

Elevation of body temperature above the

hypothalamic set point due to insufficient heatdissipation

The body’s metabolic heat production or

environmental heat load e)ceeds the body’s ability tolose heat or energy

$ot mediated by cytokines


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Hyperthermia Differential

(eat Stroke

*rug!induced hyperthermia

$euroleptic malignant syndrome

Malignant hyperthermia

Endocrinopathy


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Drug-induced hyperthermia

Sympathomimetic poisoning

cocaine# methamphetamines# and amphetamines

Effects produced by raising synaptic concentrations of $E#*opamine# and serotonin

+nticholinergic poisoning syndrome

+ntihistamines# atropine# diphenhydramine# etc

Effects result from blockade of muscarinic acetylcholine

receptors

,hysostigmine raises acetylcholine concentrations


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Neuroleptic Malignant Syndrome

*efinition!Idiosyncratic reaction to certain medicationscharacteri-ed by muscle rigidity# hyperthermia# autonomicinstability# and altered mental status

ause! appears to be caused by the inhibition of centraldopamine receptors in the hypothalamus# /hich increases heatgeneration and decreased heat loss

*rugs

,henothia-ines# haloperidol# thiothi)ene# T+# M+0 Treatment! Early recognition of $MS# immediate

discontinuation of suspected medications# supportive care#increasing dopaminergic activity &bromocroptine'


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Malignant hyperthermia

*efinition! 1are clinical syndrome characteri-ed by hyperthermia#muscle rigidity# and metabolic acidosis seen in individuals undergoinggeneral anesthesia.

,athophysiology! inherited abnormality of skeletal muscle S1 thatcauses rapid increase in intracellular calcium levels in response tocertain drugs.

*rugs

2eneral anesthetics! halothane# enflurane# isoflurane

Muscle rela)ants! succinylcholine Treatment

*antrolene! a direct skeletal muscle rela)ant

,rocainamide remains the *0 for cardiac dysrhythmias


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Endocrinopathy

Thyroto)icosis

,heochromocytoma


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Conductive heat loss

onduction! the direct transfer of heat from skin

to the surrounding air also occurs# but /ith

diminished efficiency as the ambient temp rises.


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adiant heat loss

1adiation! passive transfer of heat from a /armer to cooler ob3ect.

+ccounts for %45 of body heat loss undernormal conditions.

1adiant heat losses decrease as temperature of

the surrounding environment increases up to66.7 F at /hich point heat transfer reversesdirection.


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Heat dissipation

S/eat production and evaporation are the ma3ormechanisms of heat removal.

+t normal temps evaporation accounts for 8975of the body’s heat loss# but becomes the ma3ormechanism for heat loss at higher temps.

S/eat loss can be as much as 9.4 h /ithvigorous e)ertion at elevated temps.

imited as humidity increases.


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!mpairment of heat loss

2eneral health conditions!

obesity# generali-ed skin diseases# diminished

cutaneous blood flo/# dehydration# malnutrition#hypotension# reduced cardiac output.

Medications

Impair s/eating! +nticholinergics# antihistamines#T+# M+0# diuretics

1educe cutaneous blood flo/! vasoconstrictors# ;!adrenergic blocking agents


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Heat induced illness

(eat syncope

(eat cramps

(eat e)haustion

(eat stroke


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Heat syncope

oss of consciousness can result from

cutaneous vasodilation /ith conse


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Heat cramps

Slo/ painful muscle contractions =cramps>

resulting from fluid and electrolyte depletion

Typically involves muscles most heavily used

ramping results from salt depletion as s/eat

losses are replaced /ith /ater alone

Temperature usually normal

0ral fluid hydration


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Heat exhaustion

*efinition!heat illness characteri-ed by volume

depletion that occurs under conditions of heat stress.

?ater depletion! results from inade


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Heat exhaustion" diagnosis

@ague malaise# fatigue# headache# $@# cramps

Increased pulse# skin usually moist

ore temperature only mildly elevated# usually

less than &"7AF'

Tachycardia# orthostatic hypotension

Mental function essentially intact# no signs of

severe $S damage &e.g.# no coma or sei-ures'


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Heat exhaustion" treatment

1est

ool environment

+ssess volume status &orthostatic changes# ;B$#hematocrit# serum sodium'

Fluid replacement:

oral hydration is prefered in pts /ho are conscious# coherent#

and /ithout $@ or diarrhea.

$S to replete volume if orthostatic# replace free /ater deficits

slo/ly to avoid cerebral edema


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Heat stroke

ife threatening medical emergency resulting

from failure of the body’s normal

thermoregulatory mechanisms resulting inelevation of body temperature to e)treme levels

usually greater the &"7%F' producing

multisystem tissue damage and organdysfunction.


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#athophysiology

Specific cellular mechanism underlying the failure of

thermoregulatory homeostatis is not completely

understood. *amage is a function of both temperature and e)posure

time.

circulating concentrations of I+M"# endothelin# and

von ?illebrand factor!antigen are significantly increasedin heat stroke patients suggesting endothelial

activationin3ury.


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pathophysiology

Functional hypovolemia is avoided by compensatoryvasoconstriction of the splanchnic and renal vasculature /hich may e)plain the nausea# vomiting# and diarrhea.

erebral edema and cerebrovascular congestion thatoccur /ith hyperthermia produce elevated intracranialpressure# /hich coupled /ith a reduction in meanarterial pressure caused by failure of compensatorysplanchnic vasoconstriction# produces a fall in cerebralblood flo/ resulting in the ma3or $S dysfunction seenin heat stroke.


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Exertional heat stroke

Typically occurs in younger individuals involved

in strenuous activity at high ambient

temperatures andor humidity. &+thletes andmilitary recruits'

other/ise healthy people /hose heat dispelling

mechanisms are over/helmed by endogenousheat production.


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Classic heat stroke

@ictims are usually aged# often bedridden# personsconfined to poorly ventilated homes /ithout airconditioning during summer heat /aves

A%4 deaths in hicago "664 certified as heat related

@ictims of (S commonly suffer from chronic diseases#alcoholism# or mental illness that predispose to heatillness.

,atients are often taking anticholinergics#antiparkinsonian drugs# or diuretics that impair the abilityto tolerate heat stress and therefore increase risk


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Classic vs Exertional sx

lassic

S/eating often absent

+1F 451espiratory alkalosis

E)ertional

S/eating usually present

+1F 94!C75rhabdomyolysis

(ypoglycemia

oagulopathy

actic acidosis


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Signs and symptoms

*i--iness

+ltered mental status

?eakness $ausea

@omiting

;lurred vision onvulsions

diarrhea

Syncope

+nhidrosis

?eak pulse (ypotension

(yperthermia

onstricted pupils


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$a% findings

decreased $a# D# a# and ,0A

Increased ;B$

(yperuricemiaactic acidosis

eukocytosis

(emoconcentration

ThrombocytopeniaIncreased I$1

Fibrinolysis

onsumption coagulopathy

oncentrated urine

*ehydration proteinuria

Tubular casts

Myoglobinuria

Elevated +MI, ED2 changes

*** Elevated AST/ALT ***


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Hepatic damage

(epatic damage is so consistent a feature in

heat stroke that its absence should cast doubt

on the diagnosis,atients often have no permanent impairment of

liver function.


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Heat stroke- treatment

Secure the air/ay

1emove patient’s clothing

Monitor temp /ith rectal probe and B0 /ith Foley Immediate cooling /ith evaporative methods or

immersion &stop /hen body temp reaches "79.9 F'

+dminister o)ygen

+dminister I@F /ith *4 "9 $S or *4$S# or 1 heck glucose

;# M,# +MI,# lactate# coags# *I# +;2# B+


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!mmersion cooling

Fastest /hole!body cooling rates and lo/est mortalityrates have been observed /ith cool /ater immersion

Immersion in ice!/ater results in rapid reduction of coretemp to less than &"79.9 F' /ithin "7!A7 minutes.

complications from hypotension and shivering in addition tothe possibility of ventricular fibrillation and the need fordefibrillation /hile in the /ater.

@asoconstriction from ice!/ater immersion has provedbeneficial to hypotensive patients and may have benefits invictims /ith shock /ho have poor peripheral circulation.


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Evaporative cooling

1apid and effective and easily performed in most

E1 settings.

,atient’s clothing should be removed and theentire body sprayed /ith /ater &846 F' /hile

cooled or ambient air is passed across the

patients body /ith large fans.


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&ther cooling modalities

,referred

Evaporative cooling

Ice!/ater immersion +d3uncts

Ice packs

ooling blanket

1ectal lavage

2astric lavage

ardiopulmonary bypass


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antipyretics

+spirin and acetaminophen are not indicated due to the

differing pathophysiology of heat stroke and fever

SalicylatesIn large doses# may /orsen hyperthermia by uncoupling

o)idative phosphorylation and aggrevating bleeding

tendencies

+cetaminophenan result in further hepatic damage


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shivering

Shivering

2reater potential /ith immersion methods

hlorproma-ine 94!47 mg I@ &only if cooling isinade


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convulsions

onvulsions

*ia-epam 4!97 mg I@

,henobarbital "C7!9%7 mg initially I@


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'cute renal failure

Myoglobinuria

Deep urine output G 47 mh

Mannitol 7.94 mgkg or "9.4 gm I@ initially# then "9.4gm I@F

bicarbonate to alkalini-e the urine


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hypokalemia

Fre


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hypocalcemia

Treatment usually not necessary unless cardiac

manifestations are present.


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Disseminated intravascular

coagulation- D!C(ypofibrinogenemia

Elevated fibrin split products

,rolonged prothrombin time

Thrombocytopenia

(eparin for *I remains controversial. H477 B


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Coagulation distur%ances

May occur initially but commonly present on 9nd

and Crd days.

Initial treatment should be replacement /ithfresh fro-en plasma and platelets.


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#revention

+cclimati-ation

+chieved by scheduled regulated e)posure to hot

environments and gradually increasing duration ofe)posure and /ork load

;ody ad3usts by producing s/eat /ith lo/er saltconcentration in greater amounts at lo/er ambient

temperatures+lso accompanied by increased plasma volume#cardiac output# stroke volume# and slo/er heart rate.


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Measurement of Environmental

Stress- (et )lo%e *ul% !ndex ?;2T inde) &7.H T /b' J &7.9 Tg' J &7." Tdb'

@ery high risk: ?;2T above 9K &K9F'

(igh risk: ?;2T 9C!9K &HC!K9F'

Moderate risk: ?;2T "K!9C &%4!HCF'

o/ risk: ?;2T belo/ "K &%4F' Tdb air temp measured /ith a standard dry bulb thermometer not in

direct sunlight

T/b measured /ith a /ater!saturated cloth /ick over a dry bulbthermometer in direct sunlight &not immersed in /ater'

Tg measured by inserting dry bulb thermometer into a standard blackmetal globe in direct sunlight


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#revention

+voiding strenuous e)ercise if concurrent illness#respiratory infection# diarrhea# vomiting# or fever.

+de


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eferences

+rmstrong# E.# et al. (eat and old Illness *uring *istance1unning. Medicine and Science in Sports and E)ercise. "66% 9K&"9'

han# Theodore .# et al. *rug!induced (yperthermia. ritical are

linics "66H "C&A': HK4!K7K. Farci# et al. (arrisons ,rinciples of Internal Medicine. "Ath ed.# $e/

Lork: Mc2ra/!(ill ompanies# Inc.

1osen. Emergency Medicine: oncepts and linical ,ractice# Ath ed.Mosby!Lear ;ook# Inc. "66K.

Tierney# a/rencence r.# et al. urrent Medical *iagnosis andTreatment. A7th ed. $e/ Lork: Mc2ra/!(ill ompany# Inc. "4AC!"4A%.


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+he end

HEAT STROKE AND HEAT EXHAUS.PPT

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