MODS标准教案正文.docx

MODS标准教案正文.docx

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MODS标准教案正文

Chapter11

MultipleOrganDysfunctionSyndrome（MODS）

MODSCourseObjects

Bytheendofthishour,thestudentswillbeableto

Understandthediagnosticcriteria,pathogenesis,preventionandtreatmentofMODS

Mastertheclinicmanifestation,diagnosis,preventionandtreatmentofAcuteRespiratoryDistressSyndrome.

Correctlyunderstandanduseofthefollowingterms:

SIRSCARSMODSMOFALIARDS

1.Introduction

1.1Definition

MultipleOrganDysfunctionSyndromehasbeencharacterizedasprogressivesequentialdysfunctionorfailureoftwoormoreorgansystems-ARDSARFDICSUetc.fromanrefractoryinflammatoryresponsetoSevereInjurySepsisorShock.

HistoricalPerspectiveofMODS

1.1ClinicalCharacteristics

•FunctionoforgansisnormalbeforeMODSoccurred&MODSbetakenbadwithstressresponseorSIRS

•GenerallyfailureorganNoprimaryinjuredorgan

•Severaldaysintervalbetweenprimaryinjury&removedorgandysfunctionusually>24h

•Thedegreeoforgansdysfunctionisinconsistentwithpathologicdamagedegreeoforgans

•Acuteonset,refractorywithconventionaltreatment（anti-shockanti-infection）&highmortality

•MODSisreversibleexceptterminal400,000$/pt.

1.3RiskFactorsofMODS

•MajorCauses

-Injuries（SeveretraumaBurn&Post-operation）

-Sepsis

-Shock

•PostCardiopulmonaryResucitation（CPR）

•Acutehemorrhagicnecrosispancreatitis

•Miscellaneous

-includeage（>65）,malnutrition,Immunologicdisorders,

bloodtransfusionandpreexistingchronicdiseasesuchas

cancerordiabetesetc.

1.4PathophysiologyofMODS

–Injuryorendotoxinrelease

–Vascularendothelialdamage

–Neuroendocrineresponse

–Releaseofinflammatorymediators

–Activationofcomplement,coagulation,kallikrein/kininsystems

–VascularChanges

–Maldistributionofsystemicandorganbloodflow

–Hypermetabolism

–Oxygensupply/demandimbalance

–Tissuehypoxia

–Organdysfunction

1.5PathogenesisofMODS

•UnbalancebetweenSIRSsystemicinflammatoryresponsesyndrome&CARScompenstoryanti-inflammatoryresponsesyndrome.

•Gutbacterialtranslocation

•Ischemia-reperfusioninjury

•Proinflammatorycytokines:

–TNF–alpha

–IL-1,IL–6,IL–8,IL–12

–Interferon–gamma

•Anti-inflammatorycytokines

–IL–4,IL–10,IL–13

–Transforminggrowthfactor（TGF）-beta

1.6MODSDeterminantsafteronset

•Somepatientsrecoverwithoutcomplicationswhileothersdevelopsepticshock

•Cause

–Differenceinthedegreeofinflammatoryresponsetotheinfection

•Tumornecrosisfactor-alpha（TNF-）-principalmediatorofsepticshock

•MortalityandhemodynamicderangementcloselycorrelatedwiththeTNF-level

Bacteriatranslocation

OrganIschemia-reperfusioninjury

1.7SpecificOrganResponsesofMODS

•Heart:

-MIDCardiacDysfunctionorheartfailure

•Lung:

V/QmismatchHypoxemia

–Increasedmicrovascularpermeability

•Interstitial/alveolaredema

–ARDS

•Gastrointestinal/Hepatic:

ImpairedGImotility

•Bacterialtranslocation>>MODS

–Stress-ulcerGIbleeding

–Hepaticdysfunction

•Kidney:

–Alteredrenalfunction

–ATN/acuterenalfailure

•Increasesmortalityrate

•Neurologic:

–Encephalopathy

–Peripheralpolyneuropathy

•68%-100%

•Hematologic:

–Leukocytosis/leukopenia

–Thrombocytopenia

–Coagulopathy

–DIC

•~15%-20%

MODSClinicalcategories

–PrimaryMODS:

earlyorgandysfunction

–SecondaryMODS:

laterorgandysfunction

•MostcommonmanifestationsofsevereMODS:

–ARDS,ARF,DIC,StressUlcer.

1.8MODSDiagnosis

•PrincipaldiagnosticcriterionsofMODS:

•-History

SevereSepsisTraumaShock

Postgreatorcomplexoperation

PostCPR

•-ClinicalmanifestationsofSIRS&CARS

•-Twoormoreorgansystemsdysfunction

SIRSDiagnosis

–Widespreadinflammatoryresponseinabsenceofdocumentedinfection

–Need2ormore:

•Temp>380C（100.40F）or<360C（96.80F）

•Heartrate>90bpm

•Respiratoryrate>20/minorPaCO2<32mmHg

•WBC>12,000cells/mm3,<4,000cells/mm3,or

>10%immature（band）form

MODSEarlyDiagnoses

•EarlyexactlyjudgementtoSIRS&organsystemicdysfunction

•AcquaintancetoRiskFactorsofMODS

•PathogenesisSIRS+organdysfuction

•ClinicalcharacteristicsofMODS

•Thinkmuchoforgandysfunctionthanorganfailure

•Payattentiontohepaticgasro-intestinalhematologicorgansystemicdysfunction

1.9MODSPrevention&Treatment

•CurrenttherapyofMODSisaimedatpreventionandsupportivecare.

•Threegeneralareasare:

-sourcecontrol

-restorationandmaintenanceofoxygentransport

-metabolicsupport.

•Functionalstateoforgansespeciallycirculation&respiration

•Prevent&controlinfection

•Earlymanagementoffirstoutbreakorgandysfunction

•Improvegeneralsituation&maintenanceinternalenvironmentstabilization

•IntensiveGastro-intestinalprotect

•Monitorsystems&organs

•immunotherapy

•Sourcecontrolisamajoremphasis,aspersistenceofasourceguaranteesahighmortalityriskfromMODS.

•MalnutritionisoneoftheprimarymanifestationsofMODS.

2.AcuteRespiratoryDistressSyndromeARDS

2.1ARDSHistoricalPerspectives

OriginalDefinition

•Acuterespiratorydistress

•Cyanosisrefractorytooxygentherapy

•Decreasedlungcompliance

•Diffuseinfiltratesonchestradiograph

•Difficulties:

–lacksspecificcriteria

–controversyoverincidenceandmortality

ARDS1994Consensus

•Acuteonset

–mayfollowcatastrophicevent

•Bilateralinfiltratesonchestradiograph

•PAWP≤18mmHgnoclinicalevidenceofleftheartfailure

•Twocategories:

–AcuteLungInjury-PaO2/FiO2ratio<300

–ARDS-PaO2/FiO2ratio<200

2.2Epidemiology

•Earliernumbersinadequate（vaguedefinition）

•Using1994criteria:

–17.9/100,000foracutelunginjury

–13.5/100,000forARDS

–Currentepidemiologicstudyunderway

•Inchildren:

approximately1%ofallPICUadmissions

2.3ARDSIncitingFactors

•Trauma

•Infections

•Shock&DIC

•ARF

•Acutehemorrhagicnecroticpancreatitis

•Bloodtransfusion

•AspirationofgastriccontentsorInhalationoftoxicgasesandfumes

•Drugsandpoisons

2.3ARDSPathogenesis

•Incitingevent

•Inflammatorymediators

–Damagetomicrovascularendothelium

•Damagetoalveolarepithelium

–Increasedalveolarpermeabilityresultsinalveolaredemafluidaccumulation

•Targetorganinjuryfromhost’sinflammatoryresponseanduncontrolledliberationofinflammatorymediators

•LocalizedmanifestationofSIRS

•Neutrophilsandmacrophagesplaymajorroles

•Complementactivation

•Cytokines:

TNF-a,IL-1b,IL-6

•PlateletactivationfactorPAF

•Eicosanoids:

prostacyclin,leukotrienes,thromboxane

•Freeradicals

•Nitricoxide

2.4ARDSStages

2.4.1Acute,exudativephase

–rapidonsetofrespiratoryfailureaftertrigger

–diffusealveolardamagewithinflammatorycellinfiltration

–hyalinemembraneformation

–capillaryinjury

–protein-richedemafluidinalveoli

–disruptionofalveolarepithelium

•Basementmembranedisruption

–TypeIpneumocytesdestroyed

–TypeIIpneumocytespreserved

•Surfactantdeficiency

–inhibitedbyfibrin

–decreasedtypeIIproduction

•Microatelectasis/alveolarcollapse

2.4.2ARDSProliferativePhase

•ProliferativePhase:

–persistenthypoxemia

–developmentofhypercarbia

–fibrosingalveolitis

–furtherdecreaseinpulmonarycompliance

–pulmonaryhypertension

•TypeIIpneumocyte

–proliferate

–differentiateintoTypeIcells

–relinealveolarwalls

•Fibroblastproliferation

–interstitial/alveolarfibrosis

NORMALALVEOLUS

2.4.3ARDSFibroticPhase

•Characterizedby:

–localfibrosis

–vascularobliteration

•Repairprocess:

–resolutionvsfibrosis

ARDS

2.4.4Recoveryphase

•Recoveryphase

（Recuperative/TerminalPhase）

–gradualresolutionofhypoxemia

–improvedlungcompliance

–resolutionofradiographicabnormalities

2.5ARDSClinicalFeatures

Acutedyspnea/tachypnea

–rales/rhonchi/wheezing

Resistanthypoxemia

–PaO2/FIO2<150–200mmHg

CXR

–diffuse,bilateralinfiltrates

NoevidenceofLVfailure

–（PAWP<18mmHg）

ARDSABNORMALITIESOFGASEXCHANGE

•Hypoxemia:

HALLMARKofARDS

–Increasedcapillarypermeability

–Interstitialandalveolarexudate

–Surfactantdamage

–DecreasedFRC

–Diffusiondefectandrighttoleftshunt

earlydiffusealveolardamage

withhyalinemembranedisease

•Mediumpowersection（40x）lungparenchyma

•Extensivethickeningofalveolarseptum（wall）

•Congestionoflungcapillaries;withendotheliumleakage

•Alveolaredema

•Intenselyeosinophilicnoncellularhyalinemembranematerialinalveolarairspace

ARDS

latediffusealveolardamagewithType-2pneumocytemigration（hi-mag）

•ThebluearrowspointtothetypeIIpneumocyteswhichareveryprominent;theirnucleiprotrudingintothealveolarspace.

•Thearrowshighlightthethickenedseptum（alveolarwall）.

•Theseptumcontainsexcesscollagen,fibroblasts,andlymphocytes.

•Hyalinemembranesarenotpresentatthisstage.

2.6ARDSDifferentialDiagnosis

•CARDIOGENICPULMONARYEDEMA

Bronchopneumonia

Hypersensitivitypneumonitis

•Pulmonaryhemorrhage

•Acuteinterstitialpneumonia（Hamman-RichSyndrome）

ARDSMortality

•40-60%

•Deathsdueto:

–multi-organfailure

–sepsis

•Mortalitymaybedecreasinginrecentyears

–betterventilatorystrategies

–earlierdiagnosisandtreatment

2.7ARDSMANAGEMENT

2.7.1Monitoring:

–Respiratory

–Hemodynamic

–Metabolic

–InfectionsShockTraumasepesis（sources）

–Fluids/electrolytes

2.7.2ARDSBasicPrinciplesintheVentilatory

•Accomplisheffectivegasexchange

•Avoidcomplications

–reducedcardiacoutput

–barotrauma

–oxygentoxicity

–ventilator-inducedlu