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Inflammation Sepsis and Shock.pdf

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Department
Nursing
Course
NURSING 2LA2
Professor
Nancy Matthew- Maich
Semester
Fall

Description
Inflammation:Sepsis and Shock November-13-11 11:21 PM Moduleoutline: -inflammation -mortalityratesforsepsisandhospitalcosts -continuumofdiseasefromsepsistosepticshock -otherformsofdistributiveshock -neurogenic -anaphylactic -othertypesofshock -hypovolemic -cardiogenic -pancreatitis Inflammation -an attemptbythebody toeliminateinjuriesstimuliandpromotehealing -anon-specificreactiontostimuli,suchastissuedamageorinfectedorganisms -non-specificmeansthatdifferenttypesofinsultswillemploythesamearsenalofprotectivecellsand molecules -theinflammatoryresponseispartoftheinnateimmunesystemthatreactsrapidlywhentissueinjuryis detected -youmay wishtoreviewtheinflammationandimmunitymodulefromN2N04toremindyourselfofthe processesthatoccurand the"keyplayers"ininflammation -theprocessesofsepsis,septicshockandothertypesofnon-bacterialshockareduetodysregulationof immuneprocessesthatwillbedescribed -can overreactorunderreact; Statistics -firstlargescalesepsisstudyin2001 -Cdn'study,outofthe morethan30,500 patientshospitalizedforsepsis,morethan9.300patientsdiedin 2008-2009 -overallmortality: -sepsisis30% -MI is 9.1% -Strokeis18% -Severesepsisis39.4% SepsisCosts -costhigherthenotherillness' -patientswithsepsisusuallyrequiregreaterhospitalresources,duetonecessarilyaggressivetreatmentand longerhospitalstays:12daysvs 3days (w/hospitalisation) -averaged75% longerstaysinUS hospitals -inaddition,thoseadmittedwithsepsiswhereinvolvedinmorecostlyassessments(ICU) -about45% ofsepsispatientsrequireastayintheICUduringhospitalcare -ageis afactorinsepsisascan be seeninthechart; veryyoungandveryold -ageis afactorinsepsisascan be seeninthechart; veryyoungandveryold -<1 and >60 -sepsisratesarehigherintheelderlyandthosewhoareimmunocompromised -thisiswhydevelopmentisnecessaryandresearchisbeingdoneheavilyinthisarea MortalityforSepsis -inadditiontoageand severityofsepsisinsepsismortality,otherimportantfactorsinclude: -co-morbidities:mortalityratesincreasewiththenumberofotherphysiologicalderangements(atleast halfpatientshad) -diabetesanddifferenttypesofcancers -gender;womenwere8%morelikelytodiefromsepsisthanmales,everythingelsebeingequal -onsetofsepsis;patientswhosesepsisoccurredafterhospitaladmissionhad56%higheroddsofdying; nosocomialinfectionshaveahighermortalityrate SIRS -systemicinflammatoryresponsesyndrome;indicateaninflammatoryresponsethatissystemicratherthan localized: -higherorlowerbodytemperature:>38C or< 36C -heartrate >90 beats/minute -respiratoryrate>20/minute(orPaCo2of <32 mmHg) -whitebloodcellcount>12,000 mm3 or<4,000 mm3 -bands>10% : indicatesbodywideinflammation;isinhigherproductionofWBC,immatureWBC's ProgressiontoSepticShock -theSIRisdetectedthroughtheappearanceofapatientinatleasttwoof the:rapidheartbeatorincreased breathing,anincreaseordecreasein WBCcount, and an increaseordecreaseinbodytemperature -theidentificationofthesesymptomswhenaninfectionisconfirmedorsuspectedprovidesevidenceforthe diagnosisofsepsis -progressionofthecondition,insuchthatorgansystemsstartto faildueto lackof perfusion,causesa deteriorationtoseveresepsis -organ dysfunctioncanbedetectedbysignsofalteredmentationsuchas: confusionoragitation,oliguriaor increasedurineproduction,orincreasedlactatelevelswhichareevidenceofinsufficientoxygendeliverytocells -whenthesyndromeworsenssuchthathypertensionoccursdespiteadministrationofresuscitationfluids,the patientisconsideredtobesufferingfromsepticshock patientisconsideredtobesufferingfromsepticshock -theorgan systemthatmalfunctionsinsepticshockisthe heartandthe entirecardiovascularsystem -theheartfailsto pumpsufficientbloodtosupplyorgansandtissueswithoxygenandnutrients -theoxygenthatisdelivered,isnottransferredtocellsefficientlydueto decreasedsystemicvascular resistancethatresultsinalackofadequatepressuretodrivetheoxygenacrossthecellmembranes -thisgivesrisetoanaerobicmetabolism,whichisnotonlyinefficientinATPproduction,butalsoleadsto lactic acidosis -ATPis requiredtofuelthesodium-potassiumpumpandmaintainthecorrectiondistributioninsideand outsideofthecell -withinsufficientenergytomaintaintheelectrochemicalgradient,sodiumandchloridebuildupinsidethecell andcauseswellingaswaterflowsintoodilutetheseions -watermovingfromtheextracellularspaceorinterstitialandintocellscauseswatertoflowoutofthe vasculaturetoreplaceit,aprocesscalledthirdspacing;thislowerstheintravascularvolumeandfurtherimpairs organand tissueperfusion -inadditiontothedefinitions;thegroupofexpertscametotheconsensuson sepsis,severe-sepsis,andseptic- shock -thesesyndromesexistasacontinuumanditiseasyforapatienttoprogressfromoneconditiontothenext, unlesstheyaretreatedaggressivelytopreventthephysiologicaldownwardspiralthatoccurswhenthe inflammatoryresponsedamagesendothelialcellsanddilatesthevesselssothatitinterfereswithpropertissue perfusion Hypoperfusion -dysfunctionatthecellularlevel -consequenceof:vasodilationandcapillaryleakduetoinflammatorymediatorsinsepsisandseversepsis,and additionallyfailuretodeliversufficientbloodtothecardiovascularsysteminsepticshock -aerobicmetabolismrequiresoxygen,withoutoxygencellsmustproduceenergyanaerobically -aerobicmetabolismisabout19xmoreefficientthananaerobic,producingcloseto38moleculesofATP,per moleculeofglucosevsonly2producedbyglycolysis,whichdoesnotrequireoxygen -thereducedamountofenergyproducedanaerobicallyisnotenoughtosustainallcellularprocess;as metabolicimpairmentcontinuesorgandysfunctionoccursasthenumberoffailingorgansystemsincreaseso doestheriskformortality -thecentralissueinsepsisorshockisthe lackof perfusion,whichleadstotissuehypoxiaandeventuallycell death -cellsdeprivedofoxygenandnutrientscannotproducesufficientATPtomaintaincellularmetabolism -dysfunctionoccursinorgansinwhichperfusionisinsufficient;organfailureistheusualcauseofdeathin sepsisandshock(seeinformationonMultipleOrganDysfunctionSyndrome[MODS]intheMultiple-Interacting Disordersmodule) Hypoxia-inducedMetabolicChanges Hypoxia-inducedMetabolicChanges -describesthechangesincellularmetabolismwhenthereishypoxia,orlackofoxygen -withoutoxygen,glycolysiscanproceedinthecytoplasmofthecellbutitsproductpyruvatecannotenterthe CACwithinthemitochondria -pyruvatemustthenbethenconvertedtolactateto allowenergyproductiontocontinue -farfewerATPmoleculesareproducedthiswayandcellularprocess,suchasthe sodium-potassiumpump,are negativelyimpacted;failureofthis pumpallowssodiumtoflowintothecellandpotassiumtoleavethecell, upsettingtheelectrochemicalgradient -thisgradientisrequiredforaction-potentials,suchasneuronsandmusclecells,sothateffectswillbeevident inthenervoussystemandthemyocardiumveryquickly -inadditiontointerference;waterflowsintothecell,leadingtoswelling,cellularmembranedysfunction,and releaseoflysosomalcontents -theseeventsinitiatepositivefeedbackloopsthatcausegreaterdeteriorationofthecellandimpairmentof perfusion -meanwhiletheongoinganaerobicmetabolismresultsinadropinpH, dueto lacticacid build-upanddepletion ofglycogenstores,becauseofreducednutrientdeliveryandincreasedmetabolicdemands -proteinsynthesisisreducedanduseofintracellularandplasmaproteinsfuelmayensueasthenutrientstores runout;the cellularresponsetothismetabolicstressmayexacerbatetheinflammatoryresponse OrganDysfunctioninSevereSepsis -cellularimpairmentfromhypoxia, influxofwaterandmetabolicby-productbuildup,instigatesprogression fromsepsistosever-sepsisinwhichorgansystemsbegintofail -mostpatientswithseversepsiswhereaffectedbyfailureofonlyoneorgansystem,butthosewho experiencedmultipleorgansystemfailurehadgreatlyincreasedratesofmortalitythatrosewiththenumberof systemfailures -therespiratorysystemisthatwhichfailsmostoften -thekidneyshavethenexthighestrateoffailurefollowedbythecardio-vascularsystemwhichresultsinseptic shock shock -ofnote;liverfailureisthe leastcommonbuthas the highestrate of mortality,highlighteningtheimportant effectivenessofthisorgan -thehepaticsystemisresponsibleforsynthesisofmostofthebloodproteins,detoxificationofammoniavia theureacycleandmaintenanceofbloodsugarlevelsthrough glycogenolysisandgluconeogenesis SepsisandSepticShock -sepsiswaspreviouslythoughttobeonlycausedbygram-negativebacteria,itisnoknowntobecausednot onlybygram-positiveorganismstoo,butaswellbyfungi,virusesandparasitesaswell -onceany oftheseinvadersaredetected,inflammatorymediatorsarereleasedbytheinnateimmunesystem andimpairthefunctionofthemicro-circulationthroughvasodilationandanincreaseincapillarypermeability -systemicinflammatoryresponseindicatorsbecomeobservableasthebodytriestocompensateforthe followingcirculatoryvolume,andinthepresenceofasuspectedorconfirmedinfection, therearetwoormore serioussymptoms,sepsisisdiagnosed -ifthepatientisnottreatedand orthecompensatorymechanismsfail,organsbecomedysfunctionalandthe patientprogressestoseveresepsis -continually,fluidenterstheextra-vascularspaceandincreaseneedforoxygenbythehearttryingto compensatefortheloweredbloodvolumemayresultin cardiovasculardysfunctionandprogressiontoseptic shock -inabilityofthehearttodeliveradequatebloodtooxygenatetissuesoccursinsepticshockevenoncefluids areadministered -specializeddetectorsorpatternrecognitionreceptors,calledtoll-likereceptors,areresponsibleforsensing invadingorganismsthroughpathogenassociatedmolecularpatterns,orPAMPs -thereareseveral;differenttoll-likereceptors,eachrecognizingadifferentPAMP -Example;TLR4;detectslipopolysaccharides(LPS-acomponentofgramnegativebacterialcellswalls [endotoxin])andbeginacascadeofinflammatoryprocesses;LPS(pink)shownattachedtolipopolysaccharide- binding-protein(Pink[TLR])andanothermolecularpatternisdoublestrandedRNA(detectedbyTLR-3) -onceboundto apatternrecognitionreceptor,PAMPscauseanintracellularsignallingcascade,suchas intrakit-1,thatresultsintheexpressionininflammatorymediatorstocytokines -NFkB;isa transcriptionfactorthatis activatedbyPAMPsthroughthispathwayand can illicittheexpressionof inflammatorymediators -microvascularchangesininflammation;cytokinesreleasedinresponsetobindingofPAMPstotoll-like receptorsleadtoendothelialcelldamageandincreasedpermeabilityinthecapillaries -leakageoffluidfromcapillariesintotheextravasculaturecapillariesresultsinlessbloodinthevasculature, leadingtotissuehypoxia -cytokinesanddamagedendothelialcellsalsoinitiatethecoagulationcascade,generatingsmallfibrinclots withinthemicrovasculature withinthemicrovasculature -organdysfunction;themostcommonorgan systemtofailinseversepsisisthe pulmonarysystem -endothelialdysfunctioninthecapillariesofthelungsalongwithextravagationoffluid,causesedemaofthe lungsandimpairsgasexchange;lesssurfactantisproducedandimmunecellsinfiltratelungtissueandcause furtherdamage -lossofaerationleadstohypoxiaandimpairedperfusioninotherorgansaswellasthelungs,where acute respiratorydistresssyndrome,orARDS,may occur;necessitatingmechanicalventilation TreatmentforSepsis -ithas beenshownthatearlyrecognitionandtreatmentarethemosteffectivewayindealingwiththis syndrome -theearliertreatmentbeginsthebetterthechancesareofrestoringhomeostasisandhaltingtheprogression ofsepticshock,organfailureanddeath -protocolisdevisedtoadministertreatmentsuchasfluidresuscitation,andmonitorthepatientforresults -treatinguntilthegoalshavebeenobtainedforcentralvenouspressure,orCVP,meanarterialpressure,or MAP,andcentralvenousoxygenation,orSv02 -goldenhour;insavingthelifeofthepatient -controland sourceofinfection+antibiotics(viacultures) -constantmonitoringisnecessarytoconfirmthatthetargetbloodpressureandO2saturationaremaintained -ifvasopressersorionotropic;epinephrine,norepinephrine,dobutamine,dopamine,milrinonearerequiredto increasebloodpressureorheartcontractility,thesewouldbeadministeredthroughtheICU,intravenouslyand preferablythroughacentralline preferablythroughacentralline ConsequencesofEarlyTreatment -16% absolutereductioninriskmortalitywiththeearlytreatmentprotocol -someofthesubsequentstudiesshowedevenmoredramaticresults,someachievinga50%orgreater reductioninmortalitywhenthetreatmentbundleswhereinstituted -studieshaveshownthatuseofthisprotocolinthefirst6 hoursafterrecognitionofseveresepsisresultsin lowermortalityrates -theCIHI reportedonsuccessatSt.Joseph'sHealthcareHamiltonintheir2009publication -sincethecreationofateamconsistingofacriticalcare nurseandphysicianaswellasa respiratory therapistwassetuptorespondquicklytodeterioratingpatientsinregularhospitalbeds,therehavebeen fewerpatientsgoingtotheICUwithsepsisandfewer"codeblue"calls Continued -aggressivefluidresuscitationandantibioticadministrationisatreatmentprotocolthatifstartedearlyand adheredtohasahighchance ofsuccessin preventingtheprogressionofsepsistoseveresepsisandseptic shock -theonlyactualpharmacologicalagentapprovedforsepsis isrecombinanthumanactivatedproteinC (rhAPC, alsoknownasDrotecoginalphaand Xigris);onlysignificantonetoprovesuccessful -an absolutemortalityriskreductionof6%wasseeninaclinicaltrialbutthistreatmentisindicatedonlyfor thosewithseveresepsisatahighriskfordeath- $10,000/dose - mustbetargeted -sideeffect;increaseinbleedingepisodes,naturallyoccurringanticoagulant -administeredIVovera96hrtimeperiodintheICU,orconstantmonitoringofthepatientcantakeplaceto includecoagulationstatus MechanismsofAPC(activatedproteinC) -inflammationandcoagulationareinterconnectedprocessinsepsis -tissuefactor;theinitiatorofcoagulationisactivatedbycytokines(suchasTNF-alpha)andIL-1beta,expressed byimmunecellsinresponsetothedetectionofinfectionagents -thrombinisproducedduringthecoagulationcascadeandactivatesinhibitorsoffibrinolysis,suchas thrombin activatedfibrinolysisinhibitor,or TAFI, andplasminogenactivator inhibitor,orPAI-1, as wellascleaving fibrinogentoformfibrinclots fibrinogentoformfibrinclots -activatedprotein-c;orAP-c, isthenatural inhibitorsoffactorsVaand VIIIaofthecoagulationcascade -thrombinisdiminishedthroughinhibitionofthecoagulationcascadethrough AP-candsoitsanti-fibrinolytic effectsaredecreased -AP-calso inhibitstheproductionofcytokinesbymonocytesanddownregulatestheexpressionofselectins amongthesurfaceoftheendothelium -selectinsattachtoneutrophilsandmonocytes,allowingthemtorolealongthevesselwallbeforeadhering andextravacatingintotissues,itisthoughtthatexogenousAP-cisto be administeredinseveresepsisbecause itsproductionisimpaired -survivorswithseveresepsishadhigherlevelsofbase AP-cthendidnonesurvivors -alsonoted;an anti-apopticactivityfrommonocytesofAP-caswelltheanticoagulantandanti-inflammatory profibrinolyticcapability MechanismsinSepsis -sepsisisacomplexsyndromethatw
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