【持续性肾脏替代治疗crrt英文精品课件】血液净化cbp (91p)

CBP Nephrology Diseasesofthekidneys CasePresentation 43yearoldgentlemanwithCrytogenicCirrhosisisadmittedtotheICUaftermassiveGIbleedsecondarytobleedingesophagealvarices Hisvariceshavebeensuccessfullybandedandheisadmittedpost procedure Hereceivedmultipleunitsofblood aswellasplateletstocorrecthisthrombocytopeniaandFFPtocorrecthiscoaglulopathy INR4 3 Healsoreceived6Lofcrystalloid Heisnowhemodynamicallystable however hisrespiratoryrequirementshaveincreased inkeepingwithhisCXRfindingsofacutepulmonaryedema PSV 12 5 FiO2 45HeiskeptintubatedovernightandgivenmultiplebolusesofLasix totalof200mg tohelpencouragediuresis Whenassessedinthemorning itisnotedthathehasbeenanuricovernight HisadmissionBUN Crwere11 87 andarenow23 192 HeisnowonPSV16 8andFiO2is 65 Hiselectrolytesreveal Na 128 K 5 3 Cl 97 tCO2 18 ABG 7 31 39 84 19 2 Question1 BrieflydescribeHepatorenalsyndromeandit spathophysiology Whataresomepredisposingfactors Federico HepatorenalSyndrome DEFINITIONHepatorenalsyndromeisaclinicalconditionthatusuallyoccursinpatientswithadvancedliverdiseaseandportalhypertensionthatischaracterizedby Renalfailure withcreatininelevelmorethan1 5mg dl MarkeddecreaseinGFRandrenalplasmaflow RPF intheabsenceofotheridentifiablecauseofrenalfailure Markedabnormalityinsystemichemodynamics Activationofendogenousvasoactivesystems HRSoccurspredominantlyinthesettingofcirrhosis butitmayalsodevelopinothertypesofseverechronicliverdiseases suchasalcoholichepatitis orinacuteliverfailure ThetheorythatbestfitswiththeobservedalterationsintherenalandcirculatoryfunctioninHRSisthevasodilationtheory whichproposesthatHRSistheresultoftheeffectofvasoconstrictorsystemsactingontherenalcirculationandactivatedasahomeostaticmechanismstoimprovetheextremeunderfillingofthearterialcirculation Thatleadstodecreasedrenalperfusionandglomerularfiltrationrate GFR buttubularfunctionispreserved Therearetwowell differentiatedclinicalpatternsofHRSType1HRSCharacterizedbyrapidandprogressiveimpairmentofrenalfunctiondefinedasadoublingoftheinitialserumcreatininetoalevelgreaterthan2 5mg dlora50 reductionoftheinitial24 hourcreatinineclearancetoalevellowerthan20ml mininlessthan2weeks Usuallyoccurinsevereliverfailure Jaundice encephalopathy andcoagulopathy Occurfrequentlyafterprecipitatingfactor e g GIbleeding Mediansurvivaltimeisonly2weeks Type2HRSCharacterizedbyalesssevereandnon progressivereductionofGFR Associatedwithrelativelypreservedliverfunction ThemainclinicalconsequenceofthistypeofHRSisrefractoryascites duetoalackofresponsetodiuretics Mediansurvivaltimeisabout6months TheInternationalAscitesClubhasdefinedcriteriaforthediagnosisofHRS Majorcriteria necessaryonlyforthediagnosis areasfollows LowGFR definedbyaserumcreatininegreaterthan1 5mg dLor24 hourclearancelowerthan40mL minAbsenceofshock ongoingbacterialinfection fluidlossesandcurrenttreatmentwithnephrotoxicdrugsNosustainedimprovementinrenalfunction decreaseinserumcreatinineto40mL min followingdiureticwithdrawalandplasmavolumeexpansionwithalbumin or1 5Lofisotonicsaline Proteinurialessthan500mg dAbsenceofanyevidenceofobstructiveuropathyorparenchymaldiseaseasshownbyultrasonography PrecipitatingfactorsBacterialinfectionsBleedingLargevolumeparacentesiswithoutplasmaexpansion Patientremainsanuricandisgivenafurtherbolusof100mgofLasix PatientremainsanuricdespitemostrecentdoseofLasix Question2 AnyroleforincreasingdosesofLasixinananuricpatient Anyharm Anybenefit Federico DiureticsinAKI Diureticscanincreaseurineoutputbuthavenotbeenfoundtohaveaconsistentimpactonmortality JAMA2002 288 2547 2553 DiureticsinAKI DiureticshavenotbeenfoundtoshortenthedurationofAKI reducetheneedforRRT orimproveoveralloutcomes ContribNephrol2001 158 170 DiureticsinAKI Regardinganincreasedappreciationforthepotentialdetrimentaldownstreameffectsofvolumeoverload itmaybereasonabletotrydiureticsforcontrolofvolumeoverload Theclinicianshould however becarefulnottodelayinitiationofRRTforvolumeoverloadinthecriticallyillpatientwithAKI Crit Care2010 vol38 n1 Question3 DefineAcuteKidneyInjury Federico RIFLECriteria TheAcuteDialysisQualityInitiativeGroupproposedtheRIFLEsystemclassifyingARFinto3severitygroupsand2clinicaloutcomecategories CBPNephrolology WhatistheincidenceofAKIintheICUandhowdoesitaffectpatientoutcomes Whataresometraditionalandnovelmethodsfordetectingacutekidneyinjury IncidenceofAKIintheICU AKIoccursin 7 ofallhospitalizedpatients whereasitoccursin36 67 ofcriticallyillpatients Onaverage 5 ofICUpatientswithAKIrequirerenalreplacementtherapy DennenP DouglasIS AndersonR Acutekidneyinjuryintheintensivecareunit anupdateandprimerfortheintensivist CritCareMed 2010Jan 38 1 261 75 AKIandmortality Inmoststudies mortalityratesriseproportionallywithseverityofAKI EvensmallincreasesinserumcreatininehavebeenassociatedwithincreasingmortalityinvariousICUpopulationsdespiteadjustingforseverityofillnessandcomorbidities InpatientswithAKIrequiringRRT mortalityratesreach50 to70 DennenP DouglasIS AndersonR Acutekidneyinjuryintheintensivecareunit anupdateandprimerfortheintensivist CritCareMed 2010Jan 38 1 261 75 AKIandotheroutcomes AKIisalsoassociatedwith IncreasedlengthofstayIncreasedincidenceofCKDandend stagekidneydiseaseIncreasedcostForexample anincreaseinSCrof0 5mg dl 38mmol L wasassociatedwitha 6 5 foldincreaseintheoddsofdeath3 5dayincreaseinLOSnearly 7500inexcesshospitalcosts DennenP DouglasIS AndersonR Acutekidneyinjuryintheintensivecareunit anupdateandprimerfortheintensivist CritCareMed 2010Jan 38 1 261 75 ChertowGM BurdickE HonourM BonventreJV BatesDW Acutekidneyinjury mortality lengthofstay andcostsinhospitalizedpatients JAmSocNephrol 2005Nov 16 11 3365 70 TraditionalmethodsfordetectingAKI Currentlyavailablemeasuresdonotdetectactualkidneyinjurythewaytroponindetectsmyocardialinjury CreatinineUreaUrineoutputRathertheyaremarkersofabnormalrenalfunction thatcanbeusedtopresumekidneyinuryhasoccurred BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare 2007Dec 13 6 638 44 Serumcreatinine UsedtoestimateGFRProsProducedatarelativelyconstantrateFreelyfilteredbyglomerulusNotreabsorbedormetabolizedbythekidney BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare 2007Dec 13 6 638 44 Serumcreatinine UsedtoestimateGFRCons10 40 issecretedbythetubulesRelativelyinsensitive mayneeda50 reductioninfunctionbeforeadetectableriseinSCrisseen Creatinineproductionvariesbasedonage sex musclemass dietCertaindiseasestatescanincreaseproduction rhabdo Certaindrugscandecreasesecretion cimetidine trimethoprim Certainfactorsmayaffectassay ketoacidosis cefoxitin flucytosine Doesnotreflectreal timechangesinGFR BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare 2007Dec 13 6 638 44 DelayinSCrrise WaikarSS BonventreJV Creatininekineticsandthedefinitionofacutekidneyinjury JAmSocNephrol 2009Mar 20 3 672 9 Urea RateofproductionisnotconstantIncreaseswithproteinintakeIncreasesincriticalillness burns sepsis trauma GIBleedSteroids40 50 ofureaisreabsorbedbythekidney evenmorewhendry BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare 2007Dec 13 6 638 44 Urineoutput ProsAdynamicgaugeofkidneyfunction MaybeabarometerforchangeinkidneyperfusionConsPoorsensitivityandspecificityCanhavesevereAKIwithnormalorincreasedurineoutput BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare 2007Dec 13 6 638 44 NovelmethodsfordetectingAKI SerumCystatinCKidneyinjurymolecule 1Neutrophilgelatinase associatedlipocalin NGAL UrinaryIL 18 Serumcystatinc AnendogenouscysteineproteinaseinhibitorSynthesizedatarelativelyconstantrateReleasedintoplasmabyallnucleatedcellsinthebody KnightEL VerhaveJC SpiegelmanD etal FactorsinfluencingserumcystatinClevelsotherthanrenalfunctionandtheimpactonrenalfunctionmeasure ment KidneyInt2004 65 1416 1421 Serumcystatinc Reportedlynotaffectedbypatientage sex musclemassordietHowever onelargestudyshowedthatage sex height weight smokingstatus andCRPlevelswereallassociatedwithcystatinclevels Alsofoundtobeaffectedbyabnormalthyroidfunction immunosuppression steroids andsystemicinflammation KnightEL VerhaveJC SpiegelmanD etal FactorsinfluencingserumcystatinClevelsotherthanrenalfunctionandtheimpactonrenalfunctionmeasure ment KidneyInt2004 65 1416 1421 Serumcystatinc Almost99 isfilteredbytheglomerulusNotsecretedorreabsorbedbythetubulesThereforeariseincystatincisagoodindicationofadecreaseinGFR BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Serumcystatinc CystatinC basedestimatesofGFRmayperformbetterinthosewithlowerSCrconcentrationssuchas ElderlypatientsChildrenRenaltransplantrecipientsCirrhoticsThosethataremalnourishedMaybemoresensitivetoearlyandmildchangesofkidneyfunctioncomparedwithcreatinine BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Kidneyinjurymolecule 1 Atransmembraneglycoproteinthatisnormallyminimallyexpressedinkidneytissue ShowsmarkedupregulationinproximalrenaltubularcellsinresponsetoischemicornephrotoxicAKIShedfromproximalcellsanddetectedintheurinebyimmunoassay BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Kidneyinjurymolecule 1 UrinarylevelsofKIM 1aresignificantlyhigherinestablishedAKIcomparedwithothercausesofAKI i e PRA contrast inducednephropathy orCKD Thus KIM 1mayrepresentanearly noninvasivebiomarkerforproximaltubularAKI Morestudiesneededtodefineitsrole BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Neutrophilgelatinase associatedlipocalin NGAL BelongstothelipocalinsuperfamilyMarkedlyupregulatedinresponsetokidneyischemicornephrotoxicinjuryMaybeanearlyandsensitiveurinarybiomarkerofischemicandnephrotoxicAKI EarlyelevationsinurinaryNGALafterkidneytransplan tationhavebeenshowntobepredictiveof delayedgraftfailureNeedforRRTduringthefirstweekfollowingtransplantation BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Interleukin 18 IL 18canbeinducedintheproximaltubuleanddetectedintheurineinischemicAKIIsincreasedintheurineofpatientswithestablishedAKIwhencomparedtothosewithprerenalfailure urinarytractinfection CKDorhealthycontrols ElevatedurinaryIL 18valueshavebeenshowntoprecededclinicalevidenceofovertAKI 50 increaseinSCr by24 48hincriticallyillpatientswithARDS UrinaryIL 18valuesofatleast100pg mlwereassociatedwithanestimated6 5increasedoddsofdevelopingAKIwithin24h BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Summaryofnovelmarkers BagshawSM BellomoR Earlydiagnosisofacutekidneyinjury CurrOpinCritCare13 638 644 Question5 Whataresometraditionalandnovelmethodsforearlydetectionofkidneyinjury Marios Patientcontinuestohaveincreasingventilationsupportrequirmentsandisnowon 85FiO2 HisK isnow5 6 HeisgivenroutinehyperK therapy HehasbeenstartedonvasopressorsbecauseofdecliningMAP Question6 7 WhataretheindicationsforCRRTvsIHD Isonebetter Whataretheirassociatedadvantagesanddisadvantages Neil WhenshouldRRTbeinitiated A E I O U CRRTreviewChest2007 AcuteRenalFailureLancetreview pdf Boumanetal TimingofCRRT CurrOpCritCare2007 pdf CRRTreviewChest2007 Lameireetal Lancet2005 IsOnebetter CRRTvsIHDCochrane2007 pdf Question8 DefinethedifferentmodesofCRRT Useadiagramtohighlightthedifferences Noemie ItisdecidedtostartthepatientonCRRTtherapy Whatkindofanticoagulationshouldhereceive Question9 Comparethedifferentmodesofanticoagulation Explaintheuseofcitrateandhowtodoseit Pleaseexplainthecalciumgap Noemie Anticoagulation HeparinCanbegivensystemicallyorthroughcircuitAimforPTT35 45secRegionalcitrate IntensiveCareMed2004 30 260 265 KidneyInternational2005 67 2361 2367 KidneyInternational2005 67 2361 2367 IntensiveCareMed2004 30 260 265 Anticoagulation CitrateCitrateinfusionpre filterLeadstocalciumchelationand clottingtimeAimingforpostfilteriCabtw0 25 0 35Post filtercalciuminfusiontorestoresystemicCaandclottingfunction Citrate Concerns PricyOperatortraining timeconsumingRepeatlabsq6h PostfilteriCa SystemiciCaandtotalCaRiskofhypocalcemia Calcium TotalplasmaCalcium 40 boundtoalbumin45 circulatesasionizedcalcium15 boundtoorganic inorganicanions CitrateandCalciumGap 50 ofcitrateclearedthroughdialyserRemainingcitratemetabolizedinthelivertoBicarbonateIfcitratesystemicdelivery pt sabilitytometabolizecitrateSystemicaccumulationofCalciumCitrate hypocalcemia Calciumgap Calciumgap Totalcalcium ionizedCaCitrateaccumulationcauses Totalcalciumand iCaPtwithacuterenalfailureandliverfailureareatincreasedriskofcitrateaccumulation TidbitsfromDodek Citratetoxicity onlyclinicallyrelevantif LeadstohypernatremiaLeadstometabolicacidosis whencitrateisnotmetabolized b citisanacid Metabolicacidosis becauseitisconvertedtoHCO3 Hypocalcemia butjustturnupyourCainfusion Inrelationtoabove calciumgapnotallthatrelevant Question10 Whatisanidealdialysisdose Todd Whatistheidealdialysisdose Idon tknow AndI mnottheonlyone Speakingofflashbacks 2recentstudiesaddressingtheissueof dose ofrenalreplacementtherapyThefirstincludedmultipleRRTmodalities IHD SLED CVVHDFPatientsenrolledhadATNrequiringdialysisandeithersepsisoroneadditionalnonrenalorganfailureExcludedpatientswithchronickidneydisease CVVHDFdosewas20cc kg hrinthelessintensivegroupand35cc kg hrintheintensivegroupIntheIHD SLEDpatients dosingwas3timesperweekor6timesperweek respectively Essentiallynodifference Mortality recoveryofrenalfunction ICU freedays organfailurescores ordischargehomewithoutdialysis Thesecondruleof citywide JournalClub CriticallyillpatientswithAKIrequiringdialysisExcludedifondialysispre admissionCVVHDF withpost filterreplacementfluid25cc kg hrvs40cc kg hrDialysate replacementfluid HmosolB0 1 1 Whatdoesthismean Thatthedoseisunimportant Thatthedosebeyonda notquitedetermined valueisnotimportant Arewelookingforthewrongoutcomes WhatboxshouldIcheck AtRCH 35cc kghr asopposedto45 Savesafewbucksondialysis replacementfluid Question11 Ittu