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Pemicu 2B

Kegawatdaruratan

Clara Petrisiela

405100063


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SHOCK (INTRODUCTION)


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Shockis the clinical syndrome that resultsfrom inadequate tissue erfusion!

"he hyoerfusion#induced im$alance

$etween the deli%ery of and requirementsfor o&ygen and su$strate leads to cellulardysfunction!

'eads to a vicious cycle (((

Harrison's principles of internal


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Harrison's principles of internal


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Pathogenesis ) *rgan+esonses

1! ,icrocirculation

2! Cellular resonses

3! -euroendocrine resonses

4! Cardio%ascular resonses

5! Pulmonary resonses

6! +enal resonses

.! ,eta$olic dearangements

/! namatory resonses


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"reatment Principle

Monitoring

+equire care in an C

ssessment of the hysiologic status

,onitoring arterial ressure indwelling line7ulse7 and resiratory rate !

8oley catheter urin ow

,ental status assessment

9edated atients should $e awa:en daily;drug holiday;assess neurologic status )to shorten duration of %entilator suort!


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HYPOO!"MIC SHOCK


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Nor#%l p&ysiologic response

,aintain erfusion of the $rain and heartto restorean e@ecti%e circulating $lood %olume!

9igns=

symathetic acti%ity A

hyer%entilation7

collase of %enous caacitance %essels7

stress hormones A

an attemt to relace the loss of intra%ascular%olume

recruitment of interstitial and intracellular uid

$y reduction of urine outut!


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iagnosis


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Plasma losses hemoconcentration

8ree water loss hyernatremia

+educed cardiac outut Comensatory symathetic

tachycardia ) ele%ated systemic

%ascular resistance!


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"reatments

nitial resuscitation7 !D line

"he raid infusion of either isotonic saline7 or

Balanced salt solution = +ingerEs lactate

nfusion of 2F3 ' of salt solution o%er 20F30min!

cute $lood loss ' 10g>d'initiate $lood transfusion!

dds! fresh#froGen lasma 88P and lateletsaroaching a 1=1 ratio of P+BC>88P imro%e sur%i%al!


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Inotropic suort noreinehrine7%asoressin7 or doamine maintainadequate %entricular erformance but only

after $lood %olume has $een restored7 toa%oid tissue loss and organ failure!

9ulemental o&ygen (

Hndotracheal intu$ation to maintainarterial o&ygenation!


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N"URO'"NIC SHOCK


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-eurogenic 9hoc:

nterrution of symathetic %asomotorinut!

H!c>

high cer%ical sinal cord inIury

inad%ertent cehalad migration of sinalanesthesia

de%astating head inIury


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rteriolar dilation ) %enodilation

ooling in the %enous system%enousreturn and cardiac outut J!

T&e etre#ities %re o$ten %r#7 incontrast to the usual symathetic

%asoconstriction#induced coolness inhyo%olemic > cardiogenic shoc:!


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"reatment

9imultaneous aroach to therelati%e hyo%olemia and to the lossof %asomotor tone!

H&cessi%e %olumes of uid!

+ule out hemorragenoreinehrineor a ure #adrenergic agenthenylehrineto maintain ,P!


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C*RDIO'"NIC SHOCK


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eidemiology

,ost causes= ,#'osing a large amount of myocardium $ynecrosis

2!L= unsta$le angina ectoris

2!1L= non#9" ele%ation ,

"he median time to rogression of shoc:= .6#4hours7 4/ hours commonest

,ore often seen as a comlication of , with 9"ele%ation than other tyes of acute coronarysyndromes


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deMnition

isrution caused $y a decrease in cardiac oututsystemic intra%ascular %olume sucientcondition7 and can lead to tissue hyo&ia!

Primary diagnosis of systemic hyotension 9ystolic $lood ressure N0 mm


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"he clinical manifestationsfound signs of systemichyoerfusion include mental status changes7 colds:in7 and oliguria

Cardiogenic shoc:

#systolic BP N0 mm


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comonents cardiogenicshoc:

maired %entricular function

H%idence of organ failure due toreduced tissue erfusion

"he a$sence of hyo%olemia or othercauses


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etiology

cute myocardial infarction

Dentricular setal ruture

+uture or aillary muscledysfunction

myocardial ruture

+ight %entricular myocardialinfarction or without left %entriculardysfunction


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+is: factors

,yocardial ischemia >infarction

nemia= tachycardia >$radycardia

nfections=endocarditis7myocarditis7 or heartinfections outside

ulmonary em$olism

H&cess uid or salt

,yocardialsuressi%e drugssuch as $eta $loc:ers

*ther= regnancy7thyroto&icosis7anemia7 stresshysical or

emotional7 acutehyertension


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iagnosis of cardiogenicshoc:

,ain comlaint Cardiogenic 9hoc:

*liguric urine N20 m' > hour!

"here may $e a relationshi with ,acute myocardial infarction!

9u$sternal ain as ,!


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iagnosis of cardiogenicshoc:

mortant 9igns =

"ension dros N/0#0mm


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H&amination

HC?

Chest rays

Hchocardiograhy hemodynamic monitoring

o&ygen saturation


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TR*UM*TIC SHOCK


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9hoc: following trauma due tohemorrhage!

H%en when hemorrhage has $een controlled7

atients can continue to su@er loss of lasma%olume into the interstitium of inIured tissues!

na$ility of the atient to maintain a systolic

$lood ressure 0 mm


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"hese uid losses inIury#inducedinammatory resonses contri$ute tothe secondary microcirculatory inIury!

Proinammatory mediators are induced $y,Ps released from inIured tissue recogniGed $y the highly conser%edmem$rane recetors of the "'+ family!


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+ecetors on cells= the circulatingmonocyte7 tissue#M&ed macrohage7 anddendritic cell otent acti%ators of an

e&cessi%e roinammatory henotye inresonse to cellular inIury =

causes secondary tissue inIury andmaldistri$ution of $lood ow7

intensifying tissue ischemia

leading to multile organ system failure!


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"reatment

"he initial management = ;BCs; ofresuscitation

Control of ongoing hemorrhage

Harly sta$iliGation of fractures

e$ridement of de%italiGed orcontaminated tissues

H%acuation of hematomas 9ulementation of deleted

endogenous antio&idants


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S"PTIC SHOCK


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Sepsis

9+9 that has a ro%en or susectedmicro$ial etiology


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Syste#ic in+%##%toryresponse syn,ro#e (SIRS)

"wo or more of the following conditions=

1fe%er oral temerature O3/SC

or hyothermia N36SC

2 tachynea O24 $reaths>min

3 tachycardia heart rate O0 $eats>min

4 leu:ocytosis O127000>'7 leucoenia

N47000>'or O10L $ands may ha%e a noninfectiousetiology!


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Septic s&oc-

9esis with hyotension arterial $loodressure N0 mm


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9etic shoc: causes three maIor e@ects thatmust $e addressed during resuscitation=

hyo%olemia7

cardio%ascular deression7 induction of systemic inammation!

causes a$solute hyo%olemia fromgastrointestinal %olume losses7 tachynea7sweating7 and decreased a$ility to drin:during de%eloment of the illness!


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Htiology

n fact7 $lood cultures yield $acteria orfungi in only F20F40L of cases of se%eresesis and 40F.0L of cases of setic

shoc:! ndi%idual gram#negati%e or gram#ositi%e

$acteria account for F.0L of theseisolates the remainder are fungi or a

mi&ture of microorganisms


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Pathohysiology

,ost cases of se%ere sesis are triggered$y $acteria or fungi that do not ordinarilycause systemic disease in

immunocometent hosts ! "o sur%i%e within the human $ody7 these

micro$es often e&loit deMciencies in hostdefenses7 indwelling catheters or other

foreign matter7 or o$structed uiddrainage conduits!


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,icro$ial athogens7 in contrast7 cancircum%ent innate defenses $ecause they=

1 lac: molecules that can $e recogniGed

$y host recetors see $elow or 2 ela$orate to&ins or other %irulencefactors!

9o the $ody can mount a %igorousinammatory reaction se%ere sesis yetfails to :ill the in%aders!!


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Clinical ,anifestations


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Cellulitis7 ustules7 $ullae7 or hemorrhagiclesionshematogenous $acteria or fungi!

Bacterial to&ins distri$uted hematogenouslyand elicit di@use cutaneous reactions!

cutaneous etechiae or ururainfection N.meningitidisor7 less commonly7 H. inuenzae

etechial lesions and +oc:y ,ountain sotted

fe%er $itten $y a tic: while in an endemicarea!


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ecthyma gangrenosum7 almost e&clusi%elyin neutroenic atients caused $y P.aeruginosa!

?eneraliGed erythroderma in a seticatient suggests the to&ic shoc: syndromedue to S. aureusor S. pyogenes!


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?astrointestinal manifestations = nausea7%omiting7 diarrhea7 and ileus

Cholestatic Iaundice= ele%ated le%els of

serum $iliru$in and al:aline hoshatase Blood lactate le%els rise early increased

glycolysis as well as imaired clearance ofthe resulting lactate and yru%ate $y the

li%er and :idneys $lood glucose concentration often

increases!


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iagnosis

fe%er or hyothermia7 tachynea7tachycardia7 and leu:ocytosis or leu:oenia

acutely altered mental status7throm$ocytoenia7 an ele%ated $lood lactate

le%el7 or hyotension $lood cultures

?ramEs staining and culture of material fromthe rimary site of infection or from infected

cutaneous lesions PC+ dentiMcation of micro$ial - in

eriheral#$lood

Rosen's Emergency Medicine: Concepts and Clinical Practice, 6th ed


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"reatments


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+emo%al or drainage of a focal source ofinfection

dequate organ erfusion

nitial management of hyotension administration of D uids with 1F2 ' ofnormal saline o%er 1F2 h!

Patients w>setic shoc:7 lasma%asoressin le%els increase transiently $utthen decrease dramatically!


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Dentilator for rogressi%e hyo&emia7hyercania7 neurologic deterioration7 orresiratory muscle failure!

Hrythrocyte transfusion recommendedfor $lood d'7 with a targetle%el of g>d' in adults!

Bicar$onate for se%ere meta$olicacidosis arterial < N.!2!

C should $e treated with transfusionof fresh#froGen lasma and latelets!


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*n%p&yl%ctic S&oc-

+esults from an gH#mediated systemicresonse to an allergen!

"he mast cella central role!

gH causes mast cells to release histamine7which results in %ascular smooth musclerela&ation7 $ronchial smooth muscleconstriction7 and caillary lea: of lasma

into interstitial saces!


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Plateletssecreting latelet#acti%atingfactor P87 deri%ed from mem$ranehosholiid!

P8 eriheral %asodilation7

$ronchial constriction7

ulmonary arterial and coronary%asoconstriction!


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ntagonists to P8 can re%erse thenegati%e inotroy and %asodilation !

s such7 P8 may $e an imortant

mediator of anahyla&is that is refractoryto antihistamine treatments!


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"heray

ggressi%e %olume resuscitation withisotonic uid

Hinehrine e@ecti%ely counteracts the%asoderession7 $ronchoconstriction7 uid

transudation7 and reduced cardiac functionin anahyla&is!


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"pinep&rine intra%enously in atientswith hyotension7 e%en in the resence ofcoronary artery disease!

nitially7 1 m' of 1=107000 einehrine100 #g can $e inIected slowly and theresonse monitored!

fterward7 5 mg of einehrine can $e

diluted in 500 m' of saline7 with a startinginfusion rate of 10 m'>hr a$out 0!02 #g>:g>mintitrated to maintain erfusion!


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Corticosteroi,s are integral to arrestingsynthesis and release of anahyla&ismediators!

inhi$it hosholiase 2 and decreaserostanoid7 leu:otriene7 and P8 synthesis7quench "#cell and mast cell triggering andreduce late#hase $ronchial inammation!

:g !D ormethylrednisolone 1!5#2 mg>:g !D


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Hist%#ine receptor %nt%gonists (H.%n, H/)re%ent urticaria7 aid in reducing$ronchoconstriction7 reduce uid transudation7and may imro%e myocardial function!

ihenhydramine 0!5 mg>:g D and cimetidine2#5 mg>:g D

Ne0uli1e, p/2%gonists hel reduce

$ronchosasm!

Ket%#ineis a logical agent to use for sedationduring raid sequence intu$ation withsuccinylcholine!


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Whipple's triad

1 symtoms consistent withhyoglycemia7 2 a low lasmaglucose concentration measured with

a recise method not a glucosemonitor

3 relief of those symtoms after the

lasma glucose le%el is raised!


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Clinical ,anifestations

-euroglycoenic symtoms C-9 glucosederi%ation= $eha%ioral changes7 confusion7 fatigue7seiGure7 loss of consciousness7 and death!

-eurogenic or autonomic symtomsthe ercetion

of hysiologic changes caused $y the C-9#mediatedsymathoadrenal discharge =

drenergic syms= alitations7 tremor7 and an&iety!

Colinergic syms = sweating7 hunger7 andaresthesias!

iahoresis and allor


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Con%entional +is: 8actors

1 insulin or insulin secretagogue doses aree&cessi%e7 ill#timed7 or of the wrong tye

2 the inu& of e&ogenous glucose is reducede!g!7 during an o%ernight fast or following missed

meals or snac:s 3 insulin#indeendent glucose utiliGation is

increased e!g!7 during e&ercise


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4 sensiti%ity to insulin is increased e!g!7 withimro%ed glycemic control7 in the middle of thenight7 late after e&ercise7 or with increased Mtnessor weight loss

5 endogenous glucose roduction is reduced e!g!7following alcohol ingestion and

6 insulin clearance is reduced e!g!7 in renalfailure!


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rgent "reatment

*ral treatment with glucose ta$lets orglucose#containing uids7 candy7 or food!

initial dose is 20 g of glucose!

-euroglycoenia ntra%enous glucose 25 g ) followed $y a

glucose infusion guided $y serial lasmaglucose measurements!

su$cutaneous or intramuscular glucagon1!0 mg in adults

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