腹腔內(nèi)高壓與腹腔間隙綜合癥

Intra-AbdominalHypertension(IAH)&AbdominalCompartment

Syndrome(ACS)

Sillentkiller!

腹腔內(nèi)高壓與腹腔間隙綜合癥

Intra-Abdominal你關(guān)注過他們的腹內(nèi)壓是多少呢?你曾經(jīng)見過危重患者液體復蘇后越來越腫脹嗎？你見過ICU患者發(fā)生腎衰需要透析嗎？你曾經(jīng)見過患者發(fā)生多器官衰竭最后死亡嗎?你關(guān)注過他們的腹內(nèi)壓是多少呢?你曾經(jīng)見過危重患者液體復蘇后越病例1:膿毒癥兒童5歲女孩因膿毒癥入院治療:補液、血管活性藥物、抗生素24小時后癥狀加重：低血壓、無尿、低氧、高碳酸血癥。IAP=26腹腔減壓術(shù)迅速緩解了腎、肺和血流動力學不穩(wěn)定狀態(tài)7天后關(guān)腹、存活出院DeCou,JPedSurg2000病例1:膿毒癥兒童5歲女孩因膿毒癥入院DeCou,J病例2:肺栓塞46歲肺栓塞男性使用肝素抗凝后：迅速進展,需要血管活性藥物、大量補液、輸血（后腹膜血腫）無尿、血壓下降、通氣困難IAP50mmHg腹腔減壓后無尿、低血壓及呼吸機支持程度均好轉(zhuǎn)最后存活出院Dabney,IntensiveCareMed2001病例2:肺栓塞46歲肺栓塞男性使用肝素抗凝后：Dabney病例3:胸部和盆腔創(chuàng)傷54歲男性15英尺高墜落–肋骨、盆腔、腰椎骨折盆腔外固定、腰部制動2天后出現(xiàn)呼吸困難、插管機械通氣肺部癥狀進展，出現(xiàn)低血壓，需要大量補液及多巴胺和去甲腎上腺素肺動脈導管顯示前負荷正常，但是出現(xiàn)無尿膀胱壓力46cm減壓初期心肺功能迅速改善，但是后期惡化，9天后死于MSOF.Kopelman,JTrauma2000病例3:胸部和盆腔創(chuàng)傷54歲男性15英尺高墜落–肋骨、77歲男性臥床后誤吸.轉(zhuǎn)入ICU后插管，低血壓一晚上給與10升的靜脈補液,去甲腎1.0mg/kg/min.無尿(8小時35ml尿).血乳酸=4.6IAP=31mmHg.腹部平片–大小腸明顯腫脹，超聲未顯示腹腔積液.外科會診后予以剖腹減壓1小時后:IAP12mmHg,尿量210ml,去甲腎撤用Cheatham,WSACS2006病例4:誤吸患者77歲男性臥床后誤吸.轉(zhuǎn)入ICU后插管，低血壓Che由此可見創(chuàng)傷并不是ACS唯一病因:IAH

和ACS出現(xiàn)于多數(shù)ICU中(PICU,MICU,SICU,CVICU,NCC,OR,ER).臨床監(jiān)測IAP是必要的:

能有助于判定IAH是否會導致器官功能衰竭僅關(guān)注IAP升高到一定的值將會導致診斷的延誤:臨床出現(xiàn)明顯的ACS癥狀后才去測定IAP勢必會使亞急性的臨床事件變?yōu)榧卑Y.

IAP監(jiān)測能早期發(fā)現(xiàn)和早期干預

IAH，以免發(fā)生ACS.由此可見創(chuàng)傷并不是ACS唯一病因:定義–whatisit?病因病理生理流行病學對患者預后的影響監(jiān)測:經(jīng)膀胱測壓治療t猶他（Utah）大學的診療規(guī)范定義–whatisit?Whatiscompartmentsyndrome?Whatiscompartmentsyndrome?定義

WCACS,AntwerpBelgium2007腹腔內(nèi)壓Intra-abdominalPressure(IAP):

腹膜腔內(nèi)的壓力腹腔內(nèi)高壓Intra-abdominalHypertension(IAH):IAP持續(xù)>12mmHg(通常伴隨隱性缺血)，不伴明顯的器官功能障礙腹腔間隙綜合征AbdominalCompartmentSyndrome(ACS):IAH>20mmHg，并且至少1個器官功能衰竭定義

WCACS,AntwerpBelgium2007腹腔內(nèi)壓力水平是如何定義的?壓力(mmHg)

定義

0-5 正常

5-10 大多ICU患者常見

>12 (GradeI) 腹腔內(nèi)高壓

16-20 (GradeII) 危險的IAH-建議開始非創(chuàng)傷性的

干預

>21-25(GradeIII) 強烈提示ACS-剖腹減壓伴隨對腹腔內(nèi)壓力增高對器官功能的影響，對腹腔內(nèi)高壓的定義基準已經(jīng)下調(diào)WSACS.org腹腔內(nèi)壓力水平是如何定義的?壓力(mmHg) 生理改變/危重急癥組織缺血全身炎癥反應(SIRS)毛細血管滲漏組織水腫(包括腸壁和腸系膜)腹腔內(nèi)高壓（IAH）液體復蘇生理改變/危重急癥組織缺血全身炎癥反應(SIRS)毛細血IAP升高的原因嚴重的腹腔內(nèi)、腹膜后病變?nèi)毖淖?SIRS需要液體復蘇：24小時內(nèi)大量補液后正出的量超過5000ml這么多液體到哪里去了呢？IAP升高的原因嚴重的腹腔內(nèi)、腹膜后病變水在這兒呢!!水在這兒呢!!IAH

&

ACS病理生理改變IAH

&

ACS心血管系統(tǒng):

腹腔內(nèi)壓力增高導致:靜脈回心血流量減少導致大靜脈塌陷受壓胸腔內(nèi)壓力（ITP）增高后產(chǎn)生多種負性心肌效應結(jié)果:心臟輸出量減少全身血管阻力增加心臟負荷增加組織灌注降低,混合血血氧飽和度ScvO2降低CVP和PAWP升高，但并不能反應真正的右心室前負荷水平心臟供血不足心臟驟停

心血管系統(tǒng):PEEPPIP吸氣壓峰值腹內(nèi)壓胸廓順應性胸膜腔壓力肺順應性氣道阻力心臟內(nèi)壓力肺動脈導管心室順應性改變、瓣膜病變導管尖端的壓力

血管內(nèi)容量PEEPPIP吸氣壓峰值腹內(nèi)壓胸廓順應性胸膜腔壓力肺順應性氣CVP,PAOP&CIinthepresenceofIntra-abdominalHypertensionr=-0.33r=-0.33CVP,PAOP和心臟指數(shù)之間是無相關(guān)關(guān)系的Cheatham,Malbrain2005CVP,PAOP&CIinthepresenceRidings,etal1995Ridings,etal1995肺:

IAP增加導致:膈肌抬高導致肺容量減少,胸廓順應性變差，變得“僵硬”,肺泡充氣不良,組織間液增加(淋巴回流受阻)結(jié)果:胸內(nèi)壓增高氣道峰壓增加,潮氣量減少間質(zhì)水腫、肺充氣不良、低氧血癥、高碳酸血癥機械通氣相關(guān)性肺損傷/氣壓傷細胞因子釋放–前炎癥反應ARDS肺:病理生理改變:肺IAH正常ITP病理生理改變:肺IAH正常ITP胃腸道:腹內(nèi)壓增高導致:腸系膜靜脈和毛細血管受壓/充血心輸出到胃腸道血流量減少

結(jié)果:腸道灌注減少,水腫和滲出增加缺血、壞死、細胞因子釋放、中性粒細胞趨化聚集細菌易位SIRS發(fā)生發(fā)展腹腔內(nèi)液體進一步增加胃腸道:腎臟:腹腔內(nèi)壓力增加導致:腎靜脈和實質(zhì)受壓心臟輸出到腎臟血流量減少結(jié)果:腎血流量減少腎充血水腫腎小球濾過率降低(GFR)腎衰、少尿/無尿腎臟:正常腹部CT

下腔靜脈注意腹腔是橢圓的，而不是球形正常腎臟正常腹部CT

后腹膜血腫注意：腹腔是圓的，而不是橢圓形了！腎臟受壓，病人無尿Pickhardt,AJR1999ACS時異常的腹部–腎臟受壓變得扁平的下腔靜脈后腹膜血腫注意：腹腔是圓的，而不是橢圓形了！腎臟受壓，病人無中樞神經(jīng)系統(tǒng):腹腔內(nèi)壓力增高導致:胸內(nèi)壓增高上腔靜脈壓力增高導致回胸腔血流降低結(jié)果:中心靜脈壓增高顱內(nèi)壓增高大腦灌注壓降低腦水腫,腦缺氧,腦損傷—Maryland休克創(chuàng)傷中心對顱內(nèi)壓頑固升高的患者均常規(guī)實施開腹減壓手術(shù)中樞神經(jīng)系統(tǒng):病理生理改變腹腔內(nèi)壓力改變對其它壓力指標的影響:IAP增高會導致ICP（顱內(nèi)壓）,IJP（頸內(nèi)靜脈壓）andCVP(PAOP，肺動脈阻塞壓)增高15升袋置于腹壁(Citerio2001)病理生理改變腹腔內(nèi)壓力改變對其它壓力指標的影響:15升袋置IAHinneuropatientsJoseph2004:腹腔減壓治療頑固性顱內(nèi)高壓17位經(jīng)其它治療(其中14位實施開顱減壓手術(shù))后仍頑固性ICP增高患者-平均ICP30mmHg,平均IAP27mmHg17位均行剖腹減壓術(shù)100%ICP立即或數(shù)小時后下降-平均17mmHg11位ICP一直正常這11位均存活，并且無神經(jīng)系統(tǒng)后遺癥“goodneurologicoutcome”IAHinneuropatientsJoseph20缺血時間與細胞存活的關(guān)系不可逆的細胞凋亡或壞死Rivers–Earlygoaldirectedtherapyforsepsislecture細胞氧需量的基線無氧代謝有氧代謝缺血時間與細胞存活的關(guān)系不可逆的細胞凋亡或壞死Rivers時間緊迫的(黃金小時-分鐘為單位)心臟驟停(5min)

嚴重創(chuàng)傷(“Thegoldenhour”)急性心肌梗死(“timeismuscle”“90minDTB”)休克(“Brainattack”3hourtimewindow)嚴重的ICP升高(cranialcompartmentsyndrome)張力性氣胸、心包填塞(thoraciccompartsyndrome)時間緊急的(6小時-小時為單位)膿毒性休克(“Survivingsepsis”totalbodyischemia)IAH-ACS(“Survivingfluidresuscitation”totalbodyischemia)肢體缺血(栓塞,肢端間隔綜合征)腸系膜缺血(主動脈栓塞,IAH-ACS)時間緊迫的(黃金小時-分鐘為單位)CirclingtheDrainIntra-abdominalPressureMucosalBreakdown(Multi-SystemOrganFailure)Bacterialtranslocation,CellularApoptosis,NecrosisAcidosisDecreasedO2deliveryAnaerobicmetabolismCapillaryleakFreeradicalformationMSOFCirclingtheDrainIntra-abdomiICU患者ACS的發(fā)病率*?Malbrain,IntensiveCareMedicine(2004):Abdominalpressure:TotalPrevalenceMICUprevalenceSICUprevalenceIAP>1258.8%54.4%65%IAP>1528.9%29.8%27.5%IAP>20plus

organfailure8.2%10.5%5.0%*ThesedataareforALLICUpatients.MUCHhigherifyouuseaprotocoltoselecthighriskpatients.ICU患者ACS的發(fā)病率*?Malbrain,Intens膿毒癥患者的發(fā)病率*

Efstathiouetal,IntensiveCareMed

2005;31supp11:S183Abs703Abdominalpressure:TotalPrevalenceMedicalprevalenceSurgicalprevalenceIAP>1258%52.1%67%IAP>1529%27.6%25.2%IAP>20plus

organfailure6%9.3%4.1%*ThesedataareforALLsepsispatients.MUCHhigherifyoulookonlyatmajorfluidresuscitation.膿毒癥患者的發(fā)病率*

Efstathiouetal,I休克和液體復蘇患者的發(fā)病率？Requeira,2007:膿毒性休克患者ACS的發(fā)病率.51%incidenceofIAP>20mmHginsepticshock

Daugherty,2007:ACS常見于ICU中需要大量液體復蘇的患者.85%ofpatientswith5literspositivefluidbalancehadIAH30%hadIAP>20withorganfailure(abdominalcompartmentsyndrome)休克和液體復蘇患者的發(fā)病率？Requeira,2007

臨床判斷IAP升高的措施究竟有多少用處呢?隨機-雙盲的研究

結(jié)果:<50%時間臨床醫(yī)生能在IAP升高的時候第一時間發(fā)現(xiàn).“…研究發(fā)現(xiàn)需要一些更常規(guī)通用的方法如經(jīng)膀胱測壓…”Kirkpatrick,CanJSurg2000臨床判斷IAP升高的措施究竟有多少用處呢?隨機-雙盲的研IAH

能預測死亡IAH>12死亡率38.8%無IAH-死亡率:22.2%Malbrain,CritCareMed,2005內(nèi)外危重ICU患者IAH/ACS會影響患者結(jié)局嗎?IAH能預測死亡Malbrain,CritCareMAl-Bahrani,2008:重癥胰腺炎患者腹內(nèi)高壓的臨床相關(guān)性.18例重癥胰腺炎7(39%)例IAP<15mmHg:

14%死亡率 平均ICU住院時間4days11(61%)例IAP>15(均超過20)mmHg:

45%死亡率 平均ICU住院時間21daysIAH/ACS會影響患者結(jié)局嗎?Al-Bahrani,2008:重癥胰腺炎患者腹內(nèi)高壓的IAH干預會影響患者結(jié)局嗎?Ivatury,JTrauma,1998:損傷控制后的ACS.70例檢測IAP>18mmHg(25cmH2O)25例手術(shù)后立即關(guān)腹:52%IAP>18mmHg39%死亡-45例腹腔“開放”:

22%IAP>18mmHg10.6%死亡IAH干預會影響患者結(jié)局嗎?Ivatury,JTrSun,2006:爆發(fā)性胰腺炎持續(xù)腹腔引流與傳統(tǒng)治療.110例爆發(fā)性胰腺炎-RCT對照組:常規(guī)ICU治療實驗組:常規(guī)治療再加上IAP監(jiān)測(第一天平均21mmHg)持續(xù)腹腔內(nèi)引流(drain1800cconday1)結(jié)局:對照組- 20.7%死亡,28天住院時間

實驗組-10.0%死亡(p<0.01),15天住院時間IAH干預會影響患者結(jié)局嗎?Sun,2006:爆發(fā)性胰腺炎持續(xù)腹腔引流與傳統(tǒng)治療.Cheatham2007,積極管理IAH/ACS提高存活率嗎?ActaClinicaBelgica引入managementprotocolin2005前后的比較:開腹率

from28%to15%(medicalmanagement)如果開腹減壓,早期進行(不是發(fā)生ACS后)

關(guān)腹天數(shù)從平均21天降至6天初次成功關(guān)腹率從1/3to2/3機械通氣天數(shù)降低住院日從

28天到18天存活率從

51%到72%IAH干預會影響患者結(jié)局嗎?Cheatham2007,積極管理IAH/ACS提高DoesIAH/ACSaffectpatientoutcome?Points:IAH/ACSiscommonintheICUenvironment(includingyours).IAHandACSincreasemorbidity,mortalityandICUlengthofstay.Early,protocoldriveninterventionsimproveoutcomeswithoutincreasingcostofcare(shorterICUandhospitalLOS)However:ClinicalsignsofIAHareunreliableandonlyshowuplateintheclinicalcourse…..SO

Earlymonitoring(TRENDING)&detectionofIAHwithearlyinterventionisneededtoobtainoptimaloutcomes.DoesIAH/ACSaffectpatient

Intra-AbdominalPressureMonitoring

Intra-AbdominalPressure

Intra-AbdominalPressureMonitoring“ThereferencestandardforintermittentIAPmeasurementisviathebladderwithamaximalinstillationvolumeof25mlsterilesaline.”WSACS.org

Intra-AbdominalPressureMon“HomeMade”PressureTransducerTechniqueHome-madeassembly:Transducer2stopcocks160mlsyringe,1tubingwithsalinebagspike/luerconnector1tubingwithluerbothends1needle/angiocathClampforFoleyAssembledsterilely,usedinproperfashion!“HomeMade”PressureTransduce“HomeMade”PressureTransducerTechniquePROBLEMS:Home-made:

Nostandardization-confidenceproblemwithdataSterilityissues-CAUTInolongerreimbursedTimeconsuming*–thereforitsuseislateandinfrequentduetothehasslefactor(i.e.notmonitoring-waitingforACS)Datareproducibilityerrors-whatarethecosts/morbidityofinaccurateordelayedinformation?Other:Needlestick,Recurrentpenetrationofsterilesystem,Leaks,re-zeroingproblems,failuretotrend“HomeMade”PressureTransduceFluid-ColumnManometrySedrak2002Problems:FailuretopayextremeattentiontodetailmayleadtoerrorsSiphoneffectleadstofalseelevationsInadequatevolumeofinfusionwillleadtofalselylowmeasurementsCAUTIRisk-NeedtoinfuseurinebackintopatientFluid-ColumnManometrySedrak2BladderPressureMonitoring:HowtodoitCommerciallyavailabledevices:FoleyManometer–(Bladdermanometer)CiMon(Gastric)Spiegelberg(Gastric)AbViser–(Bladdertransduction)IAPmonitor–(Bladdertransduction)Advantages–Simple,Standardized,Reproducible,Timeefficient,SterileBladderPressureMonitoring:HAbViser:ReproducibilityStudy

Inter-observerScatterplot(r=0.95,p<0.001)

Kimball,IntCareMed2007

Nursingdrivenstudywith89differentnursesparticipating.Excellentintra-andinter-observerreproducibilityAbViser:ReproducibilityStudyCommonQuestions:Howmuchfluidshouldbeinfusedintobladder?Volumeofinfusion(ml)IAPMeasured(mmHg)Non-compliantbladder:

Measuredpressureincreasesasvolumesexceed50mlofinfusionCompliantbladder:

MeasuredpressurechangesverylittlewithhighervolumesoffluidinfusionWSACS:Maxvolume25ml,1ml/kginchildren.CommonQuestions:HowmuchflCommonQuestion:HowdoIrecognizeappropriateIAPtransductionontomymonitor?Propertransductionclues:Respiratoryvariationnoted(subtleatlowpressures)OscillationtestpositiveReproducibleoverseveralmeasurementsCommonQuestion:HowdoIrecConcern–UTIcancausesepsis.CAUTIisnotreimbursableInfectioncontrolstatements–“ClosedsystemisrequiredtoreduceUTIrisk,bladderpressuremonitoringviolatesclosedsystemconcept”Contraryconcern–EverythingismedicineisbasedonriskbenefitanalysisWhatistheriskofUTIversustheriskofmissingIAH/ACS?Howdoweresolvethis-Whatistheactualdata?CommonQuestions:WhatistheriskofUTIfromtransvesicularIAPmonitoring?Concern–UTIcancausesepsisCommonQuestions:WhatistheriskofUTIfromtransvesicularIAPmonitoring?Myth:

Breakingthe“closedsystem”increasesriskofUTIWong,GuidelinestopreventCAUTI,AmJInfControl1983ResearchData:

“Closedsealedsystems”versus“opensystems”demonstratenodifferenceinCAUTIrisk.Threeprospectiverandomizedcontrolledtrials(level1evidence),onenon-randomizedAllstudiescomparedopen(notconnected)vsclosed(pre-connected,tamperseal)drainsystemDeGroot,InfContHospEpid1988–203patients,RCT,CAUTIratesequalWille,JHospInf,1993–183patientsRCT,

CAUTIratesequalLeone,IntCareMed2003–311ICUpatients,RCT,

CAUTIratesequalLeone,IntCareMed2003–224ICUpatients,

CAUTIratesequalSowhatdoescauseCAUTI?CommonQuestions:WhatistheCommonQuestions:WhatistheriskofUTIfromtransvesicularIAPmonitoring?Maki,Engineeringouttheriskofinfectionwithurinarycatheters,EmergInfControl2001“Infectionsinwhichbiofilmdoesnotplayaroleareprobablycausedbymasstransportofintraluminalcontentsintothebladderbyretrograderefluxofmicrobeladenurinewhenacollectionsystemismanipulated.”(Loop)CommonQuestions:WhatistheCheatham,Intravesicularpressuremonitoringdoesnotcauseurinarytractinfection.IntCareMed2006ComparedICUpatientsgettingIAPmonitoringtothosewhodidnotgetIAPmonitoringCAUTIrate7.9versus6.5per1000cathdays(P=N.S.)despitehigheracuityandmortalityintheIAPgroup.CommonQuestions:WhatistheriskofUTIfromtransvesicularIAPmonitoring?Cheatham,IntravesicularpressConclusions:TransvesicularmonitoringofIAPprobablycarrieslittleriskofCAUTI.FailuretomonitoranddetectIAH/ACSdoescarryahighrisktopatientsoriskbenefitanalysissuggestsmonitoringneedstobedoneregardless.Closedsystemmythmayhavesomemerit(aseptictechnique),butisnotdefendedbyevidencebasedmedicineandisover-blown.Obviouslyweneedtobecareful,butnotparanoid.Manipulationoftheurinarydraintubewithrepeateddumpingofoldurinebackintothepatientsbladderisprobablyamodifiableriskwecanimpact.CommonQuestions:WhatistheriskofUTIfromtransvesicularIAPmonitoring?Conclusions:CommonQuestions:ManagementofIAHandACSManagementofIAHandACSIAH/ACSManagementRelativelyeasy,bedsidenursingcontrolinterventionsBedPosition(Binders–NO!)ConsiderfullyrecumbentwithreversetrendelenbergBalanceVAPissuesagainstIAHissues(riskbenefitanalysis)Sedation,PaincontrolOftenallthatisneededFluids–enoughbutnottoomuchBeawareofproblemswithhemodynamicdatainthefaceofIAHThinkaboutinfusionvolumes,concentratingsomeofthedripsAbdominalperfusionpressure(>50-60mmHg)

SimilartoCerebralperfusionpressureAPP=MAP-IAPNGT/Cathartics/Rectaltube/enemasParalysis-

Balanceriskvs.benefitIAH/ACSManagementRelativelyeIAH/ACSManagement:

PositioningVasquez,2007IAH/ACSManagement:

PositionIAH/ACSManagement:ParalysisDeWaele,CritCareMed2003UOPIAPIAH/ACSManagement:ParalysisDIAH/ACSManagement:ColloidsO’Mara,2005:ProspectiverandomizedevaluationofIAPwithcrystalloidandcolloidresuscitationinburns31caseswith>25%burnplusinhalationor>40%burnwithoutinhalationRandomizedtosalinevsplasmaResultspostresuscitation:CrystalloidIAPmean26.5mmHgPlasmaIAPmean10.6mmHgIAH/ACSManagement:ColloidsO’IAH/ACSManagement:HemofiltrationOda,2005:ManagementofIAHinpatientswithsevereacutepancreatitisusingcontinuoushemofiltration.17casesofseverepancreatitisandIAHTreatedwithhemofiltrationwhenIAP+15mm,PRIORtodevelopingrenalinsufficiency(maintainedadequateserumoncoticpressurewithalbumin)Results:Interleukin(IL-6)cytokinelevelscutinhalfReducedvascularpermeabilityandinterstitialedemaMeanIAPvaluedroppedfrom15mmtolessthan10mm16of17patientsdischargedalivewithoutcomplicationIAH/ACSManagement:HemofiltraIAH/ACSManagement:ParacentesisMultiplecaseseriesreportingsuccessfultreatmentofIAHandACS:Latenser2002:BurnpatientmanagementReckard2005:PeripancreaticfluidfilledmassSharp2002:PediatricblunttraumaEtzion2004:MalignantascitestherapySun2006:Pancreatitis(prospectiveRCT)Cutdeathsinhalf,cuthospitalLOSby13daysIAH/ACSManagement:ParacentesIAH/ACSManagementDecompressiveLaparotomy:ErronthesideofearlyvslateinterventionLessboweledemaorcelldamage,betterchanceofearlyclosureandearlyrecovery.BeawarethatdelayingcareuntilthiscomplicationoccursisVERYexpensive–moreexpensivethelongeryouwait:Vanderbiltcostsforopenabdomen(Vogel2007):Sameadmissionclosure-$150,000Failuretocloseoninitialadmission$250,000(estimatenearlyasmuchovernextyearbytimeventralherniafinallyrepaired).IAH/ACSManagementDecompressivIAH/ACSManagement:

DecompressiveLaparotomyRigidAbdomeninACS

Postdecompressivelaparotomy

IAH/ACSManagement:

DecompresDecompressiveLaparotomyDelayinabdominaldecompressionmayleadtointestinalischemiaDecompressEarly!DecompressiveLaparotomyDelayDecompressiveLaparotomyPost-operativedressingSeveraldayspost-opDecompressiveLaparotomyPost-oNosuchthingasan“OpenAbdomen”intheICU“OpenAbdomen”Vac-pacdressingplacedinOR.Now6hourspost-op:MAP=70HR=114IAP=24UOP<30cc/hour,PIP=60cmH2OLactate6.5AbdominaldressingfirmandbulgingVacuumpackisremoved,replacedwithsilo:DramaticboweleviscerationMAP=70HR=96IAP=12UOP>100cc/hourPIP=30cmH2ONosuchthingasan“OpenAbdoNosuchthingasan“OpenAbdomen”intheICU24hoursintoICUstay:WorsenedboweledemaHowever:MAP=79IAP=12Lactate=1.9NoteexpansionofvisceraNosuchthingasan“OpenAbdoSurgicalManagementofCompartmentSyndromesCompartmentCranium

ChestPericardiumLimbPathophysiologyICPelevationTensionpneumothoraxCardiactamponadeExtremitycompartmentsyndromeSurgicalManagement

Craniotomy,etc..ChesttubePericardiocentesisFasciotomySurgicalManagementofCompartCompartmentSyndromesversus

HypertensionAbdominalcompartmentsyndrome=EmergentSurgicalDisease.Intra-abdominalhypertension=UrgentMedicalDisease.CompartmentSyndromesversus

CostanalysisIsIAPmonitoringandinterventioncosteffective?CostanalysisIsIAPmonitoringCostanalysisCompartmentsyndromeriskcomparisonTheCranium:

Fall,hithead,LOC,vomitingbutalertIsitworththecostofaheadCT?(StandardofCare)Incidenceislessthan5%positiveLessthan0.5%needanyinterventionTheAbdomen:

ICUpatientwithmajorfluidresuscitation(5literspositiveat24hours)IsitworththecostofmeasuringtheirIAP?IncidenceofIAHis85%30%willhaveACSCostanalysisCompartmentsyndrCostanalysis:Timedependentcriticalcareinterventionsvs.livessavedNumberneededtotreattosaveonelife:IAH/ACSaggressiveprotocol: 3-10EGDTforsepsis: 6-8Lowvolumeventilation: 10Xigris–activatedproteinC: 16Thrombolyticsorcardiaccath: 37tPAforstroke: 100tPAinsteadofstreptokinase: 111Costanalysis:TimedependentCostanalysis:IAPmonitoringimpactonresourceutilization.SummaryofCheathamandSundata:Simplestandmostconservativecalculationis10to13daysreducedhospitalLOSwithfarhighersurvivalrate.Assumelowendof$1000-$2000/daysavings:Save$10,000-$20,000perpatientwithIAHwhohasearlymonitoringandprotocoldrivencare.OpenupICUbedsoonerIncreasesurvivalCostanalysis:IAPmonitoringCostanalysis:IAPmonitoringimpactonresourceutilization.OthermoredifficulttoquantifycostsOpportunitycosts(thinkwaitresswithatable)LongerICULOSleadstoinabilitytoadmitanotherpatienttothatbed.ICUchargesarefarhigherduringfirstfewdaysofadmission–sointermsofbusiness,longICULOSleadstolossesintermsofnewpatientbilling.MortalitycostsHigherdeathratewithouttreatmentleadstolossofthatpersonfromproductivelifeinsociety.Whatistheeconomicvalueofahumanlife?Whatisareasonablecosttosaveonelife?Costanalysis:IAPmonitoringSummary:IsIAPmonitoringandinterventioncosteffective?IAHisverycommoninfluidresuscitatedpatientsIAHcannotbeclinicallydetectedIAH/ACSoutcomeistimedependent.Delayeddetection/interventionconsumesmoreresourcesDelayeddetection/interventionresultsinhighermortality.Aggressiveinterventionleadstoreducedcostswithbetteroutcomes.So……………….Summary:IsIAPmonitoringandConclusion-IsIAPmonitoringandinterventioncosteffective?Thecostofmonitoringintra-abdominalpressure-earlyandoften-isfaroutweighedbythesavingsincliniciantime,organfunction,hospitaldaysandlivessaved.Conclusion-IsIAPmonitoringIAHmonitoringandinterventionprotocolIAHmonitoringandinterventioWSACSIAH/ACSGuidelines

2007AssessmentalgorithmManagementalgorithmWSACSIAH/ACSGuidelines

www.wIAPmonitoringalgorithmEntrycriteriadefinedintableNurseisempoweredtoenteranypatientfulfillingthesecriteriaIAPmonitoringalgorithmEntryIAPMonitoring&InterventionProtocolIAPmonitoringQ2hoursforfirst24-48hoursIAPconsistently<12mmHgIAP12to15mmHgIAP15-20mmHgwithnoevidenceoforgandysfunction/ischemia(ACS)IAP>20-25mmHgorevidenceoforgandysfunction/ischemia(ACS)CarefulfluidmanagementCorrectCVPforIAPAdjustbedposition?OptimizeAPP?ConcentratedripsSedateReduceIAPmeasurementstoQ4-6hoursfor24hours“SecondHit”pt.developsnewindicationforIAPmonitoringIAPremains<12mmHgdiscontinuemonitoring

MedicalManagementSedation/paincontrolEmptyGItractGastricsuction,catharticsRectaltube/enemasNeuromuscularblockadeColloids/diureticsParacentesis/PercutaneousdrainCVVHplusColloidsSurgicalconsult:ConsiderSurgicalDecompressionIAPMonitoring&InterventionFinalThoughtDoNOTwaitforsignsofACStobepresentbeforeyoudecidetocheckIAPBythenthepatienthasonefootinthegrave!YouhavelostyouropportunityformedicaltherapyThecostsofsavingthispatientarenowHUGEMonitorALLhighriskpatientsearlyandoften:TRENDIAPlikeavitalsignInterveneearly,beforecriticalpressuredevelopsFinalThoughtDoNOTwaitforsQuestions?IAHandACSEducationalWebsites:WSACS.orgMyemail:twolfe@ViaFerrataTridentina-ItalyQuestions?IAHandACSEducatioDoesIAHinterventionaffectpatientoutcome?Numberneededtotreattosaveonelife:Ivatury1998(majortrauma):3-4Sun2006(pancreatitis):10Cheatham2007(ACS):5Lengthofstayimpactofprotocoldrivencare:Sun2006(pancreatitis):13daymeanreductionCheatham2007(ACS):10daymeanreductionDoesIAHinterventionaffectp腹腔內(nèi)高壓與腹腔間隙綜合癥

Intra-AbdominalHypertension(IAH)&AbdominalCompartment

Syndrome(ACS)

Sillentkiller!

腹腔內(nèi)高壓與腹腔間隙綜合癥

Intra-Abdominal你關(guān)注過他們的腹內(nèi)壓是多少呢?你曾經(jīng)見過危重患者液體復蘇后越來越腫脹嗎？你見過ICU患者發(fā)生腎衰需要透析嗎？你曾經(jīng)見過患者發(fā)生多器官衰竭最后死亡嗎?你關(guān)注過他們的腹內(nèi)壓是多少呢?你曾經(jīng)見過危重患者液體復蘇后越病例1:膿毒癥兒童5歲女孩因膿毒癥入院治療:補液、血管活性藥物、抗生素24小時后癥狀加重：低血壓、無尿、低氧、高碳酸血癥。IAP=26腹腔減壓術(shù)迅速緩解了腎、肺和血流動力學不穩(wěn)定狀態(tài)7天后關(guān)腹、存活出院DeCou,JPedSurg2000病例1:膿毒癥兒童5歲女孩因膿毒癥入院DeCou,J病例2:肺栓塞46歲肺栓塞男性使用肝素抗凝后：迅速進展,需要血管活性藥物、大量補液、輸血（后腹膜血腫）無尿、血壓下降、通氣困難IAP50mmHg腹腔減壓后無尿、低血壓及呼吸機支持程度均好轉(zhuǎn)最后存活出院Dabney,IntensiveCareMed2001病例2:肺栓塞46歲肺栓塞男性使用肝素抗凝后：Dabney病例3:胸部和盆腔創(chuàng)傷54歲男性15英尺高墜落–肋骨、盆腔、腰椎骨折盆腔外固定、腰部制動2天后出現(xiàn)呼吸困難、插管機械通氣肺部癥狀進展，出現(xiàn)低血壓，需要大量補液及多巴胺和去甲腎上腺素肺動脈導管顯示前負荷正常，但是出現(xiàn)無尿膀胱壓力46cm減壓初期心肺功能迅速改善，但是后期惡化，9天后死于MSOF.Kopelman,JTrauma2000病例3:胸部和盆腔創(chuàng)傷54歲男性15英尺高墜落–肋骨、77歲男性臥床后誤吸.轉(zhuǎn)入ICU后插管，低血壓一晚上給與10升的靜脈補液,去甲腎1.0mg/kg/min.無尿(8小時35ml尿).血乳酸=4.6IAP=31mmHg.腹部平片–大小腸明顯腫脹，超聲未顯示腹腔積液.外科會診后予以剖腹減壓1小時后:IAP12mmHg,尿量210ml,去甲腎撤用Cheatham,WSACS2006病例4:誤吸患者77歲男性臥床后誤吸.轉(zhuǎn)入ICU后插管，低血壓Che由此可見創(chuàng)傷并不是ACS唯一病因:IAH

和ACS出現(xiàn)于多數(shù)ICU中(PICU,MICU,SICU,CVICU,NCC,OR,ER).臨床監(jiān)測IAP是必要的:

能有助于判定IAH是否會導致器官功能衰竭僅關(guān)注IAP升高到一定的值將會導致診斷的延誤:臨床出現(xiàn)明顯的ACS癥狀后才去測定IAP勢必會使亞急性的臨床事件變?yōu)榧卑Y.

IAP監(jiān)測能早期發(fā)現(xiàn)和早期干預

IAH，以免發(fā)生ACS.由此可見創(chuàng)傷并不是ACS唯一病因:定義–whatisit?病因病理生理流行病學對患者預后的影響監(jiān)測:經(jīng)膀胱測壓治療t猶他（Utah）大學的診療規(guī)范定義–whatisit?Whatiscompartmentsyndrome?Whatiscompartmentsyndrome?定義

WCACS,AntwerpBelgium2007腹腔內(nèi)壓Intra-abdominalPressure(IAP):

腹膜腔內(nèi)的壓力腹腔內(nèi)高壓Intra-abdominalHypertension(IAH):IAP持續(xù)>12mmHg(通常伴隨隱性缺血)，不伴明顯的器官功能障礙腹腔間隙綜合征AbdominalCompartmentSyndrome(ACS):IAH>20mmHg，并且至少1個器官功能衰竭定義

WCACS,AntwerpBelgium2007腹腔內(nèi)壓力水平是如何定義的?壓力(mmHg)

定義

0-5 正常

5-10 大多ICU患者常見

>12 (GradeI) 腹腔內(nèi)高壓

16-20 (GradeII) 危險的IAH-建議開始非創(chuàng)傷性的

干預

>21-25(GradeIII) 強烈提示ACS-剖腹減壓伴隨對腹腔內(nèi)壓力增高對器官功能的影響，對腹腔內(nèi)高壓的定義基準已經(jīng)下調(diào)WSACS.org腹腔內(nèi)壓力水平是如何定義的?壓力(mmHg) 生理改變/危重急癥組織缺血全身炎癥反應(SIRS)毛細血管滲漏組織水腫(包括腸壁和腸系膜)腹腔內(nèi)高壓（IAH）液體復蘇生理改變/危重急癥組織缺血全身炎癥反應(SIRS)毛細血IAP升高的原因嚴重的腹腔內(nèi)、腹膜后病變?nèi)毖淖?SIRS需要液體復蘇：24小時內(nèi)大量補液后正出的量超過5000ml這么多液體到哪里去了呢？IAP升高的原因嚴重的腹腔內(nèi)、腹膜后病變水在這兒呢!!水在這兒呢!!IAH

&

ACS病理生理改變IAH

&

ACS心血管系統(tǒng):

腹腔內(nèi)壓力增高導致:靜脈回心血流量減少導致大靜脈塌陷受壓胸腔內(nèi)壓力（ITP）增高后產(chǎn)生多種負性心肌效應結(jié)果:心臟輸出量減少全身血管阻力增加心臟負荷增加組織灌注降低,混合血血氧飽和度ScvO2降低CVP和PAWP升高，但并不能反應真正的右心室前負荷水平心臟供血不足心臟驟停

心血管系統(tǒng):PEEPPIP吸氣壓峰值腹內(nèi)壓胸廓順應性胸膜腔壓力肺順應性氣道阻力心臟內(nèi)壓力肺動脈導管心室順應性改變、瓣膜病變導管尖端的壓力

血管內(nèi)容量PEEPPIP吸氣壓峰值腹內(nèi)壓胸廓順應性胸膜腔壓力肺順應性氣CVP,PAOP&CIinthepresenceofIntra-abdominalHypertensionr=-0.33r=-0.33CVP,PAOP和心臟指數(shù)之間是無相關(guān)關(guān)系的Cheatham,Malbrain2005CVP,PAOP&CIinthepresenceRidings,etal1995Ridings,etal1995肺:

IAP增加導致:膈肌抬高導致肺容量減少,胸廓順應性變差，變得“僵硬”,肺泡充氣不良,組織間液增加(淋巴回流受阻)結(jié)果:胸內(nèi)壓增高氣道峰壓增加,潮氣量減少間質(zhì)水腫、肺充氣不良、低氧血癥、高碳酸血癥機械通氣相關(guān)性肺損傷/氣壓傷細胞因子釋放–前炎癥反應ARDS肺:病理生理改變:肺IAH正常ITP病理生理改變:肺IAH正常ITP胃腸道:腹內(nèi)壓增高導致:腸系膜靜脈和毛細血管受壓/充血心輸出到胃腸道血流量減少

結(jié)果:腸道灌注減少,水腫和滲出增加缺血、壞死、細胞因子釋放、中性粒細胞趨化聚集細菌易位SIRS發(fā)生發(fā)展腹腔內(nèi)液體進一步增加胃腸道:腎臟:腹腔內(nèi)壓力增加導致:腎靜脈和實質(zhì)受壓心臟輸出到腎臟血流量減少結(jié)果:腎血流量減少腎充血水腫腎小球濾過率降低(GFR)腎衰、少尿/無尿腎臟:正常腹部CT

下腔靜脈注意腹腔是橢圓的，而不是球形正常腎臟正常腹部CT

后腹膜血腫注意：腹腔是圓的，而不是橢圓形了！腎臟受壓，病人無尿Pickhardt,AJR1999ACS時異常的腹部–腎臟受壓變得扁平的下腔靜脈后腹膜血腫注意：腹腔是圓的，而不是橢圓形了！腎臟受壓，病人無中樞神經(jīng)系統(tǒng):腹腔內(nèi)壓力增高導致:胸內(nèi)壓增高上腔靜脈壓力增高導致回胸腔血流降低結(jié)果:中心靜脈壓增高顱內(nèi)壓增高大腦灌注壓降低腦水腫,腦缺氧,腦損傷—Maryland休克創(chuàng)傷中心對顱內(nèi)壓頑固升高的患者均常規(guī)實施開腹減壓手術(shù)中樞神經(jīng)系統(tǒng):病理生理改變腹腔內(nèi)壓力改變對其它壓力指標的影響:IAP增高會導致ICP（顱內(nèi)壓）,IJP（頸內(nèi)靜脈壓）andCVP(PAOP，肺動脈阻塞壓)增高15升袋置于腹壁(Citerio2001)病理生理改變腹腔內(nèi)壓力改變對其它壓力指標的影響:15升袋置IAHinneuropatientsJoseph2004:腹腔減壓治療頑固性顱內(nèi)高壓17位經(jīng)其它治療(其中14位實施開顱減壓手術(shù))后仍頑固性ICP增高患者-平均ICP30mmHg,平均IAP27mmHg17位均行剖腹減壓術(shù)100%ICP立即或數(shù)小時后下降-平均17mmHg11位ICP一直正常這11位均存活，并且無神經(jīng)系統(tǒng)后遺癥“goodneurologicoutcome”IAHinneuropatientsJoseph20缺血時間與細胞存活的關(guān)系不可逆的細胞凋亡或壞死Rivers–Earlygoaldirectedtherapyforsepsislecture細胞氧需量的基線無氧代謝有氧代謝缺血時間與細胞存活的關(guān)系不可逆的細胞凋亡或壞死Rivers時間緊迫的(黃金小時-分鐘為單位)心臟驟停(5min)

嚴重創(chuàng)傷(“Thegoldenhour”)急性心肌梗死(“timeismuscle”“90minDTB”)休克(“Brainattack”3hourtimewindow)嚴重的ICP升高(cranialcompartmentsyndrome)張力性氣胸、心