慢性胰腺炎PPT课件.ppt

1,CHRONICPANCREATITIS,.,2,A49-year-oldmanwasadmittedwithanine-monthhistoryofintermittentattacksofepigastricpain,jaundiceandfever.Theseattacksusuallylastuptoseveraldaysassociatedwithnauseaandvomiting.Hewaswellinbetweenattacksandhadnolossofweight,3,Whatisyournextstep?,.,4,LabResults,AP=1017GGT=269AST=103ALT=186TB=2(DB=1.1)Alb=3.2Lipase=33(upto244duringattacks)Amylase=44,Hb=12WBC=5.7Plts=223Na=141K=4.2Ur=15Cr=0.9Ca=8.9FBS:178,5,Whatarearrows?,6,Pancreaticcalcification,.,7,TransabdominalUS:NogallstonesormassinheadofpancreasCTscan:Theextrahepaticbileductwasmildlydilatedandgenerouspancreaswasnotedbuttherewasnomass.,8,EndoscopicUltrasoundDiffusehypoechoicenlargementofpancreas.Fineneedleaspirateofthepancreaswasnegativefortumor.,9,ERCPTherewasalongsegmentofextrahepaticbiliarystricture.Thepancreaticductwasnormalinsizebutirregular.Brushings,biopsiesandbileaspiratewerenegativefortumor,10,11,ThepatientunderwentWhipplesoperationHistologyofthepancreasshowedchronicpancreatitis,nomalignancy,.,12,Twopresentation:EpisodesofacuteinflammationinapreviouslyinjuredpancreasChronicdamagewithpersistentpainormalabsorptionEtiology:sameasacutepancreatitis“pancreatitisassociatedwithgallstonespredaminantlyacuteorrelapsing-acute”Moreidiopathictypes,13,Mostcommoncause:Inadults:alcoholintakeInchildren:cysticfibrosisIdiopathicchronicpancreatitisistheleadingcauseofnonalcoholicchronicpancreatitis,14,PATHOPHYSIOLOGY,TheeventsthatinitiateaninflamatoryprocessarestillnotwellunderstoodInthealcohol-induced:suggestedthattheprimarydefectmaybetheprecipitationofprotein(inspissatedenzyme)Infact,shownthatalcoholhasdirecttoxiceffectonthepancreas,15,Clinicalfeatures,abdominalpain:maybecontinuous,intermittentorabsentPatternisoftenatypicalRUQorLUQofthebackDiffusethroughoutupperabdomenMaybereferredtotheanteriorchestorflankTypicalform:Persistent,deep-seated,UnresponsivetoantacidsWorsenedbyalcoholintakeoraheavymeal(especiallyfattyfoods)Oftenneednarcotics,16,PancreaticinsufficiencyWeightlossFatmalabsorption:Steatorrhea:15%ofpatientspresentwithsteatorrheaandnopainPancreaticdiabetes:LikeDM1needsinsulin,butriskofhypoglycemiaismorethanit(becausealfacellsisalsoaffectedFat-solublevitamindeficiencyrare,17,Labdata,Amylaseandlipase:usuallynormalCBC,electrolytes,andliverfunctiontestsaretypicallynormalBilrubinandALPmaybeincreasedImpairedglucoseintoleranceandelevatedfastingbloodglucoseSudanstainingoffecesorquantitativetestforsteatorrheafecalelastase(Amongpancreaticfunctiontests,fecalelastasemeasurementisthemostsensitiveandspecific,especiallyintheearlyphasesofpancreaticinsufficiency),18,Cont,Classictriad“pancreaticcalcification,steatorrhea,anddiabetesmellitus“usuallyestablisheschronicpancreatitisClassictriad:foundinfewerthanone-thirdItisoftennecessarytoperformsecretinstimulationtest(abnormalwhen60%ormoreofpancreaticexocrinefunctionhasbeenlost)Adecreasedserumtrypsinogen(20ng/ml)orafecalelastaselevelof100ug/mgofstoolstronglysuggestsseverepancreaticinsufficiency,19,Imagingstudies,Plainfilms:Pancreaticcalcifications:%30mostcommonwithalcoholicpancreatitis,butisalsoseeninthehereditaryandtropicalformsofthedisorder;itisrareinidiopathicpancreatitis.,20,21,22,CT,MRI,US,calcificationsductaldilatationenlargementofthepancreasfluidcollections(eg,pseudocysts),23,24,25,ERCP,Choicewhencalcificationsarenotpresentandthereisnoevidenceofsteatorrhea.anormalstudyshouldnotruleoutthediagnosisofchronicpancreatitis,26,ERCP,MayprovideusefulinformationonthestatusofthepancreaticductalsystemAbnormalitiesinclude:1)luminalnarowing2)irregularitisintheductalsystemwithstenosis,dilation,saculation,andectasia3)blockageoftheductbycalciumdeposits,.,27,28,Endoscopicultrasonography,ThemostpredictiveendosonographicfeatureisthepresenceofstoneOthersuggestivefeaturesinclude:visiblesidebranchescystslobularityirregularmainpancreaticduct,hyperechoicfociandstrandsdilationofthemainpancreaticducthyperechoicmarginsofthemainpancreaticduct.,29,30,Complications,pseudocystformationbileductorduodenalobstructionpancreaticascitesorpleuraleffusionsplenicveinthrombosisPseudoaneurysmspancreaticcanceracuteattacksofpancreatitis(particularlyalcoholicswhocontinuedrinking),31,DIFFERENTIALDIAGNOSIS,Pancreaticcancer(mostimportant)olderageabsenceofahistoryofalcoholuseweightlossaprotractedflareofsymptomsonsetofsignificantconstitutionalsymptomspancreaticductstricturegreaterthan10mminlengthonERCPMarkerssuchasCA19-9andCEApepticulcerdiseasegallstonesirritablebowelsyndromeAcutepancreatitis,32,TREATMENT,.,33,PAINMANAGEMENT,stepwiseapproach:generalrecommendationspancreaticenzymesupplementationAnalgesicsinvasiveoptions,34,Generalrecommendations,EstablishasecurediagnosisCessationofalcoholintakeSmallmeals,35,Pancreaticenzymesupplements,notveryeffectiveresponsemaybebetterinyoungwomenwithsmallductdisease.MECHANISM:suppressionoffeedbackloopsintheduodenumthatregulatethereleaseofcholecystokinin(CCK),thehormonethatstimulatesdigestiveenzymesecretionfromtheexocrinepancreassixtabletsofViokasewhichcontains:16,000unitsoflipase30,000unitsofprotease30,000unitsofamylase.,36,Patientsshouldalsobetreatedwithacidsuppression(eitherwithanH2receptorblockeroraprotonpumpinhibitor)toreduceinactivationoftheenzymesfromgastricacid.,37,Analgesics,ifpancreaticenzymetherapyfailstocontrolpain.shortcourseofnarcoticscoupledwithlowdoseamitriptylineandanonsteroidalantiinflammatorySimultaneousshort-termhospitalization,withthepatientkeptNPOtominimizepancreaticstimulation,mayalsobeofbenefitinbreakingthepaincycle.Chronicnarcoticanalgesiamayberequiredinpatientswithpersistentsignificantpain.Long-actingagentssuchasMSContinorFentanylpatchesaregenerallymoreeffectivethanshortactingmedications,whichlastonlythreeorfourhours.,38,Othermedicalther