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Clinicalmanifestationsanddiagnosisofacutepancreatitis
OfficialreprintfromUpToDate
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Clinicalmanifestationsanddiagnosisofacutepancreatitis
Author
SanthiSwaroopVege,MD

SectionEditor
DavidCWhitcomb,MD,PhD

DeputyEditor
ShilpaGrover,MD,MPH

Alltopicsareupdatedasnewevidencebecomesavailableandourpeerreviewprocessiscomplete.
Literaturereviewcurrentthrough:May2016.|Thistopiclastupdated:Dec14,2015.
INTRODUCTIONAcutepancreatitisisanacuteinflammatoryprocessofthepancreas.Acutepancreatitisshould
besuspectedinpatientswithsevereacuteupperabdominalpainbutrequiresbiochemicalorradiologicevidenceto
establishthediagnosis.
Thistopicwillreviewtheclinicalmanifestationsanddiagnosisofacutepancreatitis.Theetiology,pathogenesis,
assessmentofseverity,andmanagementofacutepancreatitisarediscussedseparately.(See"Etiologyofacute
pancreatitis"and"Pathogenesisofacutepancreatitis"and"Predictingtheseverityofacutepancreatitis"and
"Managementofacutepancreatitis".)
CLASSIFICATIONAcutepancreatitisisdividedintothefollowing:
Mildacutepancreatitis,whichischaracterizedbytheabsenceoforganfailureandlocalorsystemic
complications
Moderatelysevereacutepancreatitis,whichischaracterizedbytransientorganfailure(resolveswithin48hours)
and/orlocalorsystemiccomplicationswithoutpersistentorganfailure(>48hours)
Severeacutepancreatitis,whichischaracterizedbypersistentorganfailurethatmayinvolveoneormultiple
organs
Thecomplicationsofacutepancreatitisarereviewedbelow.(See'Naturalhistoryandcomplications'below.)
Theclassificationandpredictorsofseverityarereviewedinmoredetailelsewhere.(See"Predictingtheseverityof
acutepancreatitis".)
CLINICALFEATURESMostpatientswithacutepancreatitishaveacuteonsetofpersistent,severeepigastric
abdominalpain[1].Insomepatients,thepainmaybeintherightupperquadrantor,rarely,confinedtotheleftside.
Inpatientswithgallstonepancreatitis,thepainiswelllocalizedandtheonsetofpainisrapid,reachingmaximum
intensityin10to20minutes.Incontrast,inpatientswithpancreatitisduetohereditaryormetaboliccausesoralcohol,
theonsetofpainmaybelessabruptandthepainmaybepoorlylocalized.Inapproximately50percentofpatients,the
painradiatestotheback[2].Thepainpersistsforseveralhourstodaysandmaybepartiallyrelievedbysittingupor
bendingforward.(See"Etiologyofacutepancreatitis".)
Approximately90percentofpatientshaveassociatednauseaandvomitingwhichmaypersistforseveralhours[3].
Patientswithsevereacutepancreatitismayhavedyspneaduetodiaphragmaticinflammationsecondaryto
pancreatitis,pleuraleffusions,oradultrespiratorydistresssyndrome.(See"Predictingtheseverityofacute
pancreatitis",sectionon'Classificationofacutepancreatitis'and"Acuterespiratorydistresssyndrome:Clinical
featuresanddiagnosisinadults",sectionon'Clinicalfeatures'.)
Approximately5to10percentofpatientswithacuteseverepancreatitismayhavepainlessdiseaseandhave
unexplainedhypotension(eg,postoperativeandcriticallyillpatients,patientsondialysis,organophosphatepoisoning,
andLegionnaire'sdisease)[46].(See"Sepsissyndromesinadults:Epidemiology,definitions,clinicalpresentation,
diagnosis,andprognosis"and"Definition,classification,etiology,andpathophysiologyofshockinadults"and
"Gastrointestinaldiseaseindialysispatients",sectionon'Pancreatitis'and"Organophosphateandcarbamate
poisoning"and"ClinicalmanifestationsanddiagnosisofLegionellainfection".)
PHYSICALEXAMINATIONPhysicalfindingsvarydependingupontheseverityofacutepancreatitis.Inpatients
withmildacutepancreatitis,theepigastriummaybeminimallytendertopalpation.Incontrast,inpatientswithsevere
pancreatitis,theremaybesignificanttendernesstopalpationintheepigastriumormorediffuselyovertheabdomen.
(See"Evaluationoftheadultwithabdominalpain".)
Patientsmayhaveabdominaldistentionandhypoactivebowelsoundsduetoanileussecondarytoinflammation
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(image1).
Patientsmayhavescleralicterusduetoobstructivejaundiceduetocholedocholithiasisoredemaoftheheadofthe
pancreas.(See"Diagnosticapproachtotheadultwithjaundiceorasymptomatichyperbilirubinemia"and
"Choledocholithiasis:Clinicalmanifestations,diagnosis,andmanagement",sectionon'Clinicalmanifestations'.)
Patientswithseverepancreatitismayhavefever,tachypnea,hypoxemia,andhypotension.In3percentofpatients
withacutepancreatitis,ecchymoticdiscolorationmaybeobservedintheperiumbilicalregion(Cullen'ssign)oralong
theflank(GreyTurnersign(image2))[7].Thesefindings,althoughnonspecific,suggestthepresenceofretroperitoneal
bleedinginthesettingofpancreaticnecrosis[8].(See"Evaluationoftheadultwithabdominalpainintheemergency
department",sectionon'Physicalexamination'and'Diseasecourse'below.)
Inrarecases,patientsmayhavesubcutaneousnodularfatnecrosisorpanniculitis(picture1)[9,10].Theselesionsare
tenderrednodulesthatfrequentlyoccuronthedistalextremitiesbutmayoccurelsewhere.(See"Panniculitis:
Recognitionanddiagnosis",sectionon'Enzymaticdestruction'.)
Patientmayalsohavefindingssuggestiveoftheunderlyingetiology(table1).Asexamples,hepatomegalymaybe
presentinpatientswithalcoholicpancreatitis,xanthomasinhyperlipidemicpancreatitis,andparotidswellingin
patientswithmumps(picture2andpicture3).(See"Etiologyofacutepancreatitis"and"Hypertriglyceridemiainduced
acutepancreatitis",sectionon'Clinicalfeatures'and"Epidemiology,clinicalmanifestations,diagnosis,and
managementofmumps",sectionon'Clinicalfeatures'.)
LABORATORYFINDINGS
PancreaticenzymesandproductsEarlyinthecourseofacutepancreatitis,thereisabreakdowninthesynthesis
secretioncouplingofpancreaticdigestiveenzymessynthesiscontinueswhilethereisablockadeofsecretion.Asa
result,digestiveenzymesleakoutofacinarcellsthroughthebasolateralmembranetotheinterstitialspaceandthen
enterthesystemiccirculation.(See"Pathogenesisofacutepancreatitis",sectionon'Intraacinaractivationof
proteolyticenzymes'.)
SerumamylaseSerumamylaseriseswithin6to12hoursoftheonsetofacutepancreatitis.Amylasehasa
shorthalflifeofapproximately10hoursandinuncomplicatedattacksreturnstonormalwithinthreetofivedays.
Serumamylaseelevationofgreaterthanthreetimestheupperlimitofnormalhasasensitivityforthediagnosisof
acutepancreatitisof67to83percentandaspecificityof85to98percent[11].
However,elevationsinserumamylasetomorethanthreetimestheupperlimitofnormalmaynotbeseenin
approximately20percentofpatientswithalcoholicpancreatitisduetotheinabilityoftheparenchymatoproduce
amylase,andin50percentofpatientswithhypertriglyceridemiaassociatedpancreatitisastriglyceridesinterferewith
theamylaseassay[12].Giventheshorthalflifeofamylase,thediagnosisofacutepancreatitismaybemissedin
patientswhopresent>24hoursaftertheonsetofpancreatitis.Inaddition,elevationsinserumamylasearenot
specificforacutepancreatitisandmaybeseeninotherconditions(table2).(See"Approachtothepatientwith
elevatedserumamylaseorlipase".)
SerumlipaseSerumlipasehasasensitivityandspecificityforacutepancreatitisrangingfrom82to100
percent[11].Serumlipaseriseswithinfourtoeighthoursoftheonsetofsymptoms,peaksat24hours,andreturnsto
normalwithin8to14days[13].
Lipaseelevationsoccurearlierandlastlongerascomparedwithelevationsinamylaseandarethereforeespecially
usefulinpatientswhopresent>24hoursaftertheonsetofpain[14].Serumlipaseisalsomoresensitiveascompared
withamylaseinpatientswithpancreatitissecondarytoalcohol.
However,nonspecificelevationsoflipasehavealsobeenreported(table3)[11,15].(See"Approachtothepatientwith
elevatedserumamylaseorlipase".)
OtherenzymesandproductsTrypsinogenactivationpeptide(TAP),afiveaminoacidpeptidethatiscleaved
fromtrypsinogentoproduceactivetrypsin,iselevatedinacutepancreatitis.Sinceactivationoftrypsinislikelyan
earlyeventinthepathogenesisofacutepancreatitis,TAPmaybeusefulindetectionofearlyacutepancreatitisandas
apredictoroftheseverityofacutepancreatitis[1619].(See"Predictingtheseverityofacutepancreatitis",sectionon
'Otherserummarkers'.)
Urinaryandserumtrypsinogen2levelsareelevatedinearlyacutepancreatitis.However,additionalstudiesare
neededtodeterminetheirroleinthediagnosisofacutepancreatitis[16,18,2023].(See"Postendoscopicretrograde
cholangiopancreatography(ERCP)pancreatitis",sectionon'Diagnosis'.)
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Otherpancreaticdigestiveenzymesthatleakintothesystemiccirculationandareelevatedinserumincludetrypsin,
phospholipase,carboxypeptidase,carboxylesterlipase,colipase,andpancreaticisoamylase.
MarkersofimmuneactivationActivationofgranulocytesandmacrophagesinacutepancreatitisresultsinrelease
ofanumberofcytokinesandinflammatorymediators.AcutepancreatitisisassociatedwithelevationsinCreactive
protein(CRP),interleukin(IL)6,IL8,IL10,tumornecrosisfactor(TNF),andPMNelastase[24].ACRPlevelabove
150mg/dLat48hoursisassociatedwithseverepancreatitis.(See"Predictingtheseverityofacutepancreatitis",
sectionon'Creactiveprotein'.)
OtherlaboratoryfindingsPatientswithpancreatitismayhaveleukocytosisandanelevatedhematocritfrom
hemoconcentrationduetoextravasationofintravascularfluidintothirdspaces.Metabolicabnormalitiesincluding
elevatedbloodureanitrogen(BUN),hypocalcemia,hyperglycemia,andhypoglycemiamayalsooccur.(See
"Pathogenesisofacutepancreatitis",sectionon'Systemicresponse'and"Hypoglycemiainadults:Clinical
manifestations,definition,andcauses",sectionon'Hypoglycemiaindiabetes'and"Diabeticketoacidosisand
hyperosmolarhyperglycemicstateinadults:Clinicalfeatures,evaluation,anddiagnosis",sectionon'Precipitating
factors'.)
IMAGINGSeveralfeaturesmaybeseenonimaginginpatientswithacutepancreatitis.
AbdominalandchestradiographsTheradiographicfindingsinacutepancreatitisrangefromunremarkableinmild
diseasetolocalizedileusofasegmentofsmallintestine(sentinelloop)orthecoloncutoffsigninmoreseveredisease
(image1).Thecoloncutoffsignreflectsapaucityofairinthecolondistaltothesplenicflexureduetofunctional
spasmofthedescendingcolonsecondarytopancreaticinflammation.Agroundglassappearancemayindicatethe
presenceofanacuteperipancreaticfluidcollection(table4).(See'Localcomplications'below.)
Approximatelyonethirdofpatientswithacutepancreatitishaveabnormalitiesvisibleonthechestroentgenogramsuch
aselevationofahemidiaphragm,pleuraleffusions,basalatelectasis,pulmonaryinfiltrates,oracuterespiratory
distresssyndrome[25].
AbdominalultrasoundInpatientswithacutepancreatitis,thepancreasappearsdiffuselyenlargedandhypoechoic
onabdominalultrasound.Gallstonesmaybevisualizedinthegallbladderorthebileduct(image3).(See
"Choledocholithiasis:Clinicalmanifestations,diagnosis,andmanagement",sectionon'Transabdominalultrasound'.)
Peripancreaticfluidappearsasananechoiccollectiononabdominalultrasound.Thesecollectionsmaydemonstrate
internalechoesinthesettingofpancreaticnecrosis(table4).(See'Localcomplications'below.)
However,inapproximately25to35percentofpatientswithacutepancreatitis,bowelgasduetoanileusprecludes
evaluationofthepancreasorbileduct[16].Inaddition,ultrasoundcannotclearlydelineateextrapancreaticspreadof
pancreaticinflammationoridentifynecrosiswithinthepancreas.
AbdominalcomputedtomographyContrastenhancedabdominalcomputedtomography(CT)scanfindingsof
acuteinterstitialedematouspancreatitis(image4)includefocalordiffuseenlargementofthepancreaswith
heterogeneousenhancementwithintravenouscontrast.
Necrosisofpancreatictissueisrecognizedaslackofenhancementafterintravenouscontrastadministration(image
5).
Ifperformedthreeormoredaysaftertheonsetofabdominalpain,contrastenhancedCTscancanreliablyestablish
thepresenceandextentofpancreaticnecrosisandlocalcomplicationsandpredicttheseverityofthedisease(table
4).(See'Localcomplications'belowand"Predictingtheseverityofacutepancreatitis",sectionon'CTscan'and
"Predictingtheseverityofacutepancreatitis",sectionon'CTseverityindex'.)
AcommonbileductstonemayoccasionallybevisualizedoncontrastenhancedabdominalCTscan.Apancreatic
massmaybeseeninpatientswithanunderlyingpancreaticcancer,anddiffusedilationofthepancreaticductora
cysticlesionmaybeseeninpatientswithanintraductalpapillarymucinousneoplasiaorcysticneoplasm.(See
"Etiologyofacutepancreatitis",sectionon'Mechanicalampullaryobstruction'and"Intraductalpapillarymucinous
neoplasmofthepancreas(IPMN):Pathophysiologyandclinicalmanifestations",sectionon'Clinicalpresentation'and
"Clinicalmanifestations,diagnosis,andstagingofexocrinepancreaticcancer",sectionon'Clinicalpresentation'.)
MagneticresonanceimagingOnMRT1weightedimageswithfatsuppression,diffuseorfocalenlargementofthe
pancreaticglandcanbeseeninpatientswithacutepancreatitisandthemarginsofthepancreasmaybeblurred.Due
topancreaticedema,thesignalintensityofthepancreaticparenchymamightbehypointenserelativetotheliveronT1
weightedimages,andhyperintenseonT2weightedimages.Oncontrastenhancedmagneticresonanceimaging(MRI),
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failureofthepancreaticparenchymatoenhanceindicatesthepresenceofpancreaticnecrosis.
MRIhasahighersensitivityforthediagnosisofearlyacutepancreatitisascomparedwithcontrastenhanced
abdominalCTscanandcanbettercharacterizethepancreaticandbileductsandcomplicationsofacutepancreatitis
[2628].Magneticresonancecholangiopancreatogram(MRCP)iscomparabletoendoscopicretrograde
cholangiopancreatogram(ERCP)forthedetectionofcholedocholithiasis[29].MRIhastheadvantageofnotrequiring
radiation,andgadoliniumhasalowerriskofnephrotoxicityascomparedwithiodinatedcontrast[28,30,31].Inaddition,
inpatientswithrenalfailure,anonenhancedMRIcanidentifypancreaticnecrosis.
However,MRIhasthedisadvantageofbeingoperatordependentwithconsequentvariabilityinqualityandtechnique
anditsuseislimitedbythepresenceoflocalexpertiseandavailability.Inaddition,MRIhasalongerscanningtimeas
comparedwithCTscan,makingitmoredifficulttoperformincriticallyillpatients.
(See"Endoscopicretrogradecholangiopancreatography:Indications,patientpreparation,andcomplications"and
"Magneticresonancecholangiopancreatography",sectionon'Clinicaluse'and"Choledocholithiasis:Clinical
manifestations,diagnosis,andmanagement",sectionon'Imagingtestcharacteristics'.)
DIAGNOSISThediagnosisofacutepancreatitisshouldbesuspectedinapatientwithacuteonsetofapersistent,
severe,epigastricpainwithtendernessonpalpationonphysicalexamination.
Thediagnosisofacutepancreatitisrequiresthepresenceoftwoofthefollowingthreecriteria:acuteonsetof
persistent,severe,epigastricpainoftenradiatingtotheback,elevationinserumlipaseoramylasetothreetimesor
greaterthantheupperlimitofnormal,andcharacteristicfindingsofacutepancreatitisonimaging(contrastenhanced
computedtomography[CT],magneticresonanceimaging[MRI],ortransabdominalultrasonography)[32].(See
'Imaging'above.)
Inpatientswithcharacteristicabdominalpainandelevationinserumlipaseoramylasetothreetimesorgreaterthan
theupperlimitofnormal,noimagingisrequiredtoestablishthediagnosisofacutepancreatitis.
Inpatientswithabdominalpainthatisnotcharacteristicforacutepancreatitisorserumamylaseorlipaselevelsthat
arelessthanthreetimestheupperlimitofnormal,orinwhomthediagnosisisuncertain,weperformabdominal
imagingwithacontrastenhancedabdominalCTscantoestablishthediagnosisofacutepancreatitisandtoexclude
othercausesofacuteabdominalpain.Inpatientswithseverecontrastallergyorrenalfailure,weperformanabdominal
MRIwithoutgadolinium.
Diagnosticevaluation
LaboratorystudiesElevationinserumlipaseoramylasetothreetimesorgreaterthantheupperlimitofnormal
issuggestiveofacutepancreatitis.Weevaluatelevelsofserumlipaseandamylase.Lipaseremainselevatedfora
longerperiodoftimeandhasahigherspecificityascomparedwithamylase.(See'Serumlipase'aboveand'Serum
amylase'above.)
Inaddition,acompletebloodcount,electrolytes,alanineaminotransferase(ALT),aspartateaminotransferase(AST),
bilirubin,calcium,andalbuminshouldbeobtainedtoruleoutothercausesofacuteabdominalpain.Apregnancytest
shouldbeperformedinallwomenofchildbearingage.(See'Differentialdiagnosis'below.)
ImagingThepresenceoffocalordiffuseenlargementofthepancreasoncontrastenhancedabdominalCTor
MRIissuggestiveofacutepancreatitis.(See'Abdominalcomputedtomography'aboveand'Magneticresonance
imaging'above.)
DIFFERENTIALDIAGNOSISThedifferentialdiagnosisofacutepancreatitisincludesothercausesofepigastric
abdominalpain.Acutepancreatitiscanbedistinguishedfromthesecausesbasedontheclinicalfeaturesand
laboratorystudies.However,insomecasesifthediagnosisofacutepancreatitisisstillindoubt,weperforma
contrastenhancedabdominalcomputedtomography(CT)scanforfurtherevaluation.(See'Clinicalfeatures'aboveand
'Physicalexamination'aboveand'Laboratorystudies'aboveand'Abdominalcomputedtomography'above.)
PepticulcerdiseasePatientsmayhaveahistoryoflongstandingepigastricpainthatisusuallyintermittent.
Thepaindoesnotradiatetotheback.Patientsmayhaveahistoryofnonsteroidalantiinflammatorydrug(NSAID)
useorpriorinfectionwithHelicobacterpylori.Onlaboratorytesting,patientswithpepticulcerdiseasehavea
normalamylaseandlipase.(See"Pepticulcerdisease:Clinicalmanifestationsanddiagnosis".)
CholedocholithiasisorcholangitisPatientswithcholedocholithiasisandcholangitismayhaveahistoryof
gallstonesorbiliarymanipulationsuchasendoscopicretrogradecholangiopancreatography(ERCP).Serum
alanineaminotransferase(ALT)andaspartateaminotransferase(AST)concentrationsaretypicallyelevatedearly
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inthecourseofbiliaryobstruction.Later,patientshaveelevationsinserumbilirubin,alkalinephosphatase,
exceedingtheelevationsinserumALTandAST.Serumamylaseandlipasearenormal.(See"Acutecholangitis",
sectionon'Clinicalmanifestations'and"Choledocholithiasis:Clinicalmanifestations,diagnosis,and
management",sectionon'Clinicalmanifestations'.)
CholecystitisPatientswithacutecholecystitistypicallycomplainofabdominalpain,mostcommonlyinthe
rightupperquadrantorepigastriumthatmayradiatetotherightshoulderorback.Unlikepatientswithacute
pancreatitis,patientswithacutecholecystitiscommonlyexperienceincreaseddiscomfortwhiletheareaaround
thegallbladderfossaispalpatedandmayhaveanassociatedinspiratoryarrest(Murphyssign).Mildelevations
inserumaminotransferasesandamylase,alongwithhyperbilirubinemiamaybeseenbutamylaseorlipase
elevationsofgreaterthanthreetimestheupperlimitofnormalarenotusuallyassociatedwithcholecystitis.An
abdominalCTscanshowsgallbladderwalledemaandpericholecysticstranding(image6).(See"Acute
cholecystitis:Pathogenesis,clinicalfeatures,anddiagnosis",sectionon'Clinicalmanifestations'and"Acute
cholecystitis:Pathogenesis,clinicalfeatures,anddiagnosis",sectionon'Diagnosis'.)
PerforatedviscusPatientswithaperforatedviscuspresentwithsuddenonsetabdominalpainandhave
peritonealsignswithguarding,rigidityandreboundtendernessthatarenotassociatedwithacutepancreatitis.
Patientsmayhaveanelevatedamylasebutelevationsareunlikelytobethreetimestheupperlimitofnormal.On
uprightchestfilmandabdominalfilmsandabdominalCTscan,freeaircanbeseen.Otherpossiblefindingson
abdominalCTincludefreefluid,phlegmon,andbowelwallpathologywithadjacentinflammation(image7and
image8).
IntestinalobstructionPatientswithintestinalobstructionhaveabdominalpainwithanorexia,emesis,
obstipation,orconstipationandelevationinserumamylaseandlipase.Thesepatientsmayhaveahistoryof
priorabdominalsurgeriesorCrohnsdisease.Onphysicalexamination,patientsmayhavepriorsurgicalscarsor
hernias.OnabdominalCTscaninadditiontodilatedloopsofbowelwithairfluidlevels,theetiologyandsiteof
obstruction(transitionpoint)maybeseen(image9).(See"Epidemiology,clinicalfeatures,anddiagnosisof
mechanicalsmallbowelobstructioninadults".)
MesentericischemiaInpatientswithmesentericischemia,thepainisoftenperiumbilicalandoutofproportion
tofindingsonphysicalexamination.Patientsmayhaveriskfactorsformesentericischemiaincludingadvanced
age,atherosclerosis,cardiacarrhythmias,severecardiacvalvulardisease,recentmyocardialinfarction,and
intraabdominalmalignancy.Althoughpatientsmayhaveelevationsinamylaseorlipasetheseareusuallyless
markedthanelevationsseeninacutepancreatitis.OnabdominalCTscantheremaybefocalorsegmentalbowel
wallthickeningorintestinalpneumatosiswithportalveingas(image10).Inaddition,arterialorvenous
thrombosisorhepaticorsplenicinfarctsmaybeseen.(See"Mesentericvenousthrombosisinadults",sectionon
'Clinicalpresentations'and"Nonocclusivemesentericischemia",sectionon'Clinicalfeatures'and"Acute
mesentericarterialocclusion",sectionon'Clinicalfeatures'and"Overviewofintestinalischemiainadults",
sectionon'Clinicalfeatures'.)
HepatitisPatientshaveacuterightupperquadrantpain,anorexia,andgeneralmalaise.Patientsmayalsonote
darkurine,acholicstool,jaundice,andpruritus.Onphysicalfindings,patientswithacutehepatitishavescleral
icterusandtenderhepatomegaly.Laboratorystudiesarenotableformarkedelevationsofserum
aminotransferases(usually>1000int.units/dL),serumtotalanddirectbilirubin,andalkalinephosphatasewith
normalamylaseandlipase.(See"OverviewofhepatitisAvirusinfectioninadults",sectionon'Clinical
evaluation'and"ClinicalmanifestationsandnaturalhistoryofhepatitisBvirusinfection",sectionon'Acute
hepatitis'.)
Inpatientswhopresentwithanelevatedamylaseorlipasewithoutabdominalpain,thedifferentialdiagnosisisbroad
(table2andtable3).Thistopicisdiscussedseparately.(See"Approachtothepatientwithelevatedserumamylaseor
lipase".)
ESTABLISHINGTHEETIOLOGYOncethediagnosisofacutepancreatitisisestablished,theunderlyingetiology
shouldbedetermined(table1).Anapproachtoidentifyingthecauseofacutepancreatitisisdiscussedindetail
separately.(See"Etiologyofacutepancreatitis",sectionon'Determiningtheetiologyofacutepancreatitis'.)
NATURALHISTORYANDCOMPLICATIONSPatientswithacutepancreatitisusuallypresentwithacuteonsetof
epigastricabdominalpainandelevatedserumamylaseandlipase.Withsupportivetreatment,mostpatientsrecover
withoutlocalorsystemiccomplicationsororganfailureanddonothaverecurrentattacks.However,asmallproportion
ofpatientswithacutepancreatitishavenecrosisofthepancreasorperipancreatictissueandcomplicationsdueto
pancreatitis.Thesepatientshaveahighoverallmortality.
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DiseasecourseApproximately85percentofpatientswithacutepancreatitishaveacuteinterstitialedematous
pancreatitischaracterizedbyanenlargementofthepancreasduetoinflammatoryedema[3].Approximately15percent
ofpatientshavenecrotizingpancreatitiswithnecrosisofthepancreaticparenchyma,theperipancreatictissue,orboth
(table4).
Inmostpatientswithacutepancreatitis,thediseaseismildinseverityandpatientsrecoverinthreetofivedays
withoutcomplicationsororganfailure.However,20percentofpatientshavemoderatelysevereorsevereacute
pancreatitiswithlocalorsystemiccomplicationsororganfailure.(See'Localcomplications'belowand'Systemic
complications'belowand'Organfailure'below.)
Theoverallmortalityinacutepancreatitisisapproximately5percentwithalowermortalityinpatientswithinterstitial
pancreatitisascomparedwiththosewithnecrotizingpancreatitis(3versus17percent)[3].
Patientswithacutepancreatitiscanhaverecurrentattacksofacutepancreatitisandcanalsodevelopchronic
pancreatitis[33,34].Inametaanalysisof14studies,whichincluded8492patientswithacutepancreatitis,thepooled
prevalenceofrecurrentacutepancreatitisandchronicpancreatitiswere22and10percent,respectively[34].The
prevalenceofchronicpancreatitisfollowingthefirstepisodeandwithrecurrentacutepancreatitiswere10and36
percent,respectively.However,therewassignificantvariabilityinthepooledprevalenceestimatesbasedonthe
designoftheprimarystudiesincludedintheanalysis.Insubgroupanalysis,theprevalenceofchronicpancreatitisin
individualswithahistoryofsmokingoralcoholusewere65and61percent,respectively.Theriskofprogressionfrom
acutetochronicpancreatitiswashigherinmenascomparedwithwomenaftercontrollingforageandtheseverityof
acutepancreatitis(oddsratiowomen0.12,95%CI0.020.2).
LocalcomplicationsLocalcomplicationsofacutepancreatitisincludeacuteperipancreaticfluidcollection(image
11),pancreaticpseudocyst,acutenecroticcollection(image12),andwalledoffnecrosis(table4).
Whileacuteperipancreaticfluidcollectionsandacutenecroticcollectionsmaydeveloplessthanfourweeksafterthe
onsetofpancreatitis,pancreaticpseudocystandwalledoffnecrosisusuallyoccurs>4weeksafteronsetofacute
pancreatitis.
Bothacutenecroticfluidcollectionsandwalledoffnecrosismaybecomeinfected.Themanagementofinfected
pancreaticnecrosis(image13)isdiscussedindetailseparately.(See"Pancreaticdebridement",sectionon'Infected
pancreaticnecrosis'.)
Portosplenomesentericvenousthrombosis(PSMVT)developsinapproximately50percentofpatientswithnecrotizing
acutepancreatitisandisrareintheabsenceofnecrosis[35,36].ComplicationsfromPSMVTarerareinpatientswith
acutepancreatitis.Inanotherstudythatincluded45patientswithsplanchnicvenousthrombosisinpatientswithacute
pancreatitisofwhom17(38percent)weretreatedwithanticoagulants,althoughtheuseofanticoagulantswasnot
associatedwithmajorbleeding,therewasalsonosignificantdifferenceintheratesofrecanalization[37].
SystemiccomplicationsAccordingtotherevisedAtlantaclassificationofacutepancreatitis,asystemic
complicationofacutepancreatitisisdefinedasanexacerbationofanunderlyingcomorbidity(eg,coronaryartery
diseaseorchroniclungdisease)[32].
OrganfailureIntheAtlantaclassification,organfailureisadistinctentityseparatefromasystemiccomplication
[32].Pancreaticinflammationresultsintheactivationofacytokinecascadethatmanifestsclinicallyasasystemic
inflammatoryresponsesyndrome(SIRS).PatientswithpersistentSIRSareatriskforfailureofoneormoreorgans.
Organfailure(acuterespiratoryfailure,shock,andrenalfailure)maybetransient,resolvingwithin48hoursinpatients
withmoderatelyseverepancreatitisorpersistentfor>48hoursinpatientswithsevereacutepancreatitis(table5).(See
"Sepsissyndromesinadults:Epidemiology,definitions,clinicalpresentation,diagnosis,andprognosis",sectionon
'Definitions'.)
INFORMATIONFORPATIENTSUpToDateofferstwotypesofpatienteducationmaterials,"TheBasics"and
"BeyondtheBasics."TheBasicspatienteducationpiecesarewritteninplainlanguage,atthe5thto6thgradereading
level,andtheyanswerthefourorfivekeyquestionsapatientmighthaveaboutagivencondition.Thesearticlesare
bestforpatientswhowantageneraloverviewandwhoprefershort,easytoreadmaterials.BeyondtheBasicspatient
educationpiecesarelonger,moresophisticated,andmoredetailed.Thesearticlesarewrittenatthe10thto12thgrade
readinglevelandarebestforpatientswhowantindepthinformationandarecomfortablewithsomemedicaljargon.
Herearethepatienteducationarticlesthatarerelevanttothistopic.Weencourageyoutoprintoremailthesetopics
toyourpatients.(Youcanalsolocatepatienteducationarticlesonavarietyofsubjectsbysearchingon"patientinfo"
andthekeyword(s)ofinterest.)
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Basicstopics(see"Patientinformation:Pancreatitis(TheBasics)")
BeyondtheBasicstopics(see"Patientinformation:Acutepancreatitis(BeyondtheBasics)")
SUMMARYANDRECOMMENDATIONS
Themajorityofpatientswithacutepancreatitishaveacuteonsetofsevereupperabdominalpain.Patientsmay
haveassociatednauseaandvomiting.Onphysicalexamination,patientshaveabdominaltendernessto
palpation.Patientswithsevereacutepancreatitismayhavefever,tachypnea,tachycardia,hypoxemia,and
hypotension.(See'Clinicalfeatures'aboveand'Physicalexamination'above.)
Earlyinthecourseofacutepancreatitis,pancreaticenzymesleakoutofacinarcellstotheinterstitialspaceand
thenthesystemiccirculation.Patientswithacutepancreatitismaythereforehaveacuteelevationsinserum
amylaseandlipaseinadditiontootherpancreaticenzymes,breakdownproducts,andinflammatorymediators.
(See'Laboratoryfindings'above.)
Thediagnosisofacutepancreatitisisdefinedbythepresenceoftwoofthefollowing:acuteonsetofpersistent,
severe,epigastricpainoftenradiatingtotheback,elevationinserumlipaseoramylasetothreetimesorgreater
thantheupperlimitofnormal,orcharacteristicfindingsofacutepancreatitisonimaging(contrastenhanced
computedtomography,magneticresonanceimaging,ortransabdominalultrasonography).(See'Diagnosis'
above.)
Serumlipasehasaslightlyhighersensitivityforacutepancreatitis,andelevationsoccurearlierandlastlongeras
comparedwithelevationsinamylase.Serumlipaseisthereforeespeciallyusefulinpatientswhopresentlateto
thephysician.Serumlipaseisalsomoresensitiveascomparedwithamylaseinpatientswithpancreatitis
secondarytoalcohol.(See'Serumlipase'aboveand"Approachtothepatientwithelevatedserumamylaseor
lipase".)
Inpatientswithcharacteristicabdominalpainandelevationinserumlipaseoramylasetothreetimesorgreater
thantheupperlimitofnormal,noimagingisrequiredtoestablishthediagnosisofacutepancreatitis.
Inpatientswithabdominalpainthatisnotcharacteristicforacutepancreatitisoraserumamylaseand/orlipase
activitythatislessthanthreetimestheupperlimitofnormal,weperformabdominalimagingwithacontrast
enhancedabdominalcomputedtomographyscantoestablishthediagnosisofacutepancreatitisandtoexclude
othercausesofacuteabdominalpain.(See'Abdominalcomputedtomography'aboveand'Differentialdiagnosis'
above.)
Approximately85percentofpatientswithacutepancreatitishaveacuteinterstitialedematouspancreatitis(image
4)characterizedbyanenlargementofthepancreasduetoinflammatoryedema.Approximately15percentof
patientshavenecrotizingpancreatitis(image5)withnecrosisofthepancreaticparenchyma,theperipancreatic
tissue,orboth.(See'Diseasecourse'above.)
Inmostpatientswithacutepancreatitis,thediseaseismildinseverityandpatientsrecoverinthreetofivedays
withoutcomplicationsororganfailure.However,20percentofpatientshavemoderatelysevereorsevereacute
pancreatitiswithlocalorsystemiccomplicationsororganfailure.(See'Naturalhistoryandcomplications'above.)
UseofUpToDateissubjecttotheSubscriptionandLicenseAgreement.
REFERENCES
1.SwaroopVS,ChariST,ClainJE.Severeacutepancreatitis.JAMA2004291:2865.
2.BanksPA.Acutepancreatitis:Diagnosis.In:Pancreatitis,LankischPG,BanksPA(Eds),SpringerVerlag,New
York1998.p.75.
3.BanksPA,FreemanML,PracticeParametersCommitteeoftheAmericanCollegeofGastroenterology.Practice
guidelinesinacutepancreatitis.AmJGastroenterol2006101:2379.
4.LankischPG,SchirrenCA,KunzeE.Undetectedfatalacutepancreatitis:whyisthediseasesofrequently
overlooked?AmJGastroenterol199186:322.
5.LankischPG,MllerCH,NiederstadtH,BrandA.Painlessacutepancreatitissubsequenttoanticholinesterase
insecticide(parathion)intoxication.AmJGastroenterol199085:872.
6.KesavanCR,PitchumoniCS,MarinoWD.AcutepainlesspancreatitisasararecomplicationinLegionnaires
disease.AmJGastroenterol199388:468.
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7.MookadamF,CikesM.Imagesinclinicalmedicine.Cullen'sandTurner'ssigns.NEnglJMed2005353:1386.
8.DicksonAP,ImrieCW.Theincidenceandprognosisofbodywallecchymosisinacutepancreatitis.Surg
GynecolObstet1984159:343.
9.DahlPR,SuWP,CullimoreKC,DickenCH.Pancreaticpanniculitis.JAmAcadDermatol199533:413.
10.BennettRG,PetrozziJW.Nodularsubcutaneousfatnecrosis.Amanifestationofsilentpancreatitis.Arch
Dermatol1975111:896.
11.YadavD,AgarwalN,PitchumoniCS.Acriticalevaluationoflaboratorytestsinacutepancreatitis.AmJ
Gastroenterol200297:1309.
12.FortsonMR,FreedmanSN,WebsterPD3rd.Clinicalassessmentofhyperlipidemicpancreatitis.AmJ
Gastroenterol199590:2134.
13.FrankB,GottliebK.Amylasenormal,lipaseelevated:isitpancreatitis?Acaseseriesandreviewofthe
literature.AmJGastroenterol199994:463.
14.GwozdzGP,SteinbergWM,WernerM,etal.Comparativeevaluationofthediagnosisofacutepancreatitis
basedonserumandurineenzymeassays.ClinChimActa1990187:243.
15.TreacyJ,WilliamsA,BaisR,etal.Evaluationofamylaseandlipaseinthediagnosisofacutepancreatitis.ANZ
JSurg200171:577.
16.DervenisC,JohnsonCD,BassiC,etal.Diagnosis,objectiveassessmentofseverity,andmanagementof
acutepancreatitis.Santoriniconsensusconference.IntJPancreatol199925:195.
17.TennerS,FernandezdelCastilloC,WarshawA,etal.Urinarytrypsinogenactivationpeptide(TAP)predicts
severityinpatientswithacutepancreatitis.IntJPancreatol199721:105.
18.HuangQL,QianZX,LiH.Acomparativestudyoftheurinarytrypsinogen2,trypsinogenactivationpeptide,and
thecomputedtomographyseverityindexasearlypredictorsoftheseverityofacutepancreatitis.
Hepatogastroenterology201057:1295.
19.KhanZ,VlodovJ,HorovitzJ,etal.Urinarytrypsinogenactivationpeptideismoreaccuratethanhematocritin
determiningseverityinpatientswithacutepancreatitis:aprospectivestudy.AmJGastroenterol200297:1973.
20.KylnpBckM,KemppainenE,PuolakkainenP,etal.Reliablescreeningforacutepancreatitiswithrapid
urinetrypsinogen2teststrip.BrJSurg200087:49.
21.MayumiT,InuiK,MaetaniI,etal.Validityoftheurinarytrypsinogen2testinthediagnosisofacutepancreatitis.
Pancreas201241:869.
22.KemppainenE,HedstrmJ,PuolakkainenP,etal.Increasedserumtrypsinogen2andtrypsin2alpha1
antitrypsincomplexvaluesidentifyendoscopicretrogradecholangiopancreatographyinducedpancreatitiswith
highaccuracy.Gut199741:690.
23.KemppainenE,HedstrmJ,PuolakkainenP,etal.Urinarytrypsinogen2teststripindetectingERCPinduced
pancreatitis.Endoscopy199729:247.
24.ToouliJ,BrookeSmithM,BassiC,etal.Guidelinesforthemanagementofacutepancreatitis.JGastroenterol
Hepatol200217Suppl:S15.
25.RansonJH,TurnerJW,RosesDF,etal.Respiratorycomplicationsinacutepancreatitis.AnnSurg1974
179:557.
26.LecesneR,TaourelP,BretPM,etal.Acutepancreatitis:interobserveragreementandcorrelationofCTandMR
cholangiopancreatographywithoutcome.Radiology1999211:727.
27.ArvanitakisM,DelhayeM,DeMaertelaereV,etal.Computedtomographyandmagneticresonanceimagingin
theassessmentofacutepancreatitis.Gastroenterology2004126:715.
28.StimacD,MiletiD,RadiM,etal.Theroleofnonenhancedmagneticresonanceimagingintheearly
assessmentofacutepancreatitis.AmJGastroenterol2007102:997.
29.TaylorAC,LittleAF,HennessyOF,etal.Prospectiveassessmentofmagneticresonance
cholangiopancreatographyfornoninvasiveimagingofthebiliarytree.GastrointestEndosc200255:17.
30.MorganDE,BaronTH,SmithJK,etal.Pancreaticfluidcollectionspriortointervention:evaluationwithMR
imagingcomparedwithCTandUS.Radiology1997203:773.
31.AmanoY,OishiT,TakahashiM,KumazakiT.Nonenhancedmagneticresonanceimagingofmildacute
pancreatitis.AbdomImaging200126:59.
32.BanksPA,BollenTL,DervenisC,etal.Classificationofacutepancreatitis2012:revisionoftheAtlanta
classificationanddefinitionsbyinternationalconsensus.Gut201362:102.
33.YadavD,O'ConnellM,PapachristouGI.Naturalhistoryfollowingthefirstattackofacutepancreatitis.AmJ
Gastroenterol2012107:1096.
34.SankaranSJ,XiaoAY,WuLM,etal.Frequencyofprogressionfromacutetochronicpancreatitisandrisk
factors:ametaanalysis.Gastroenterology2015149:1490.
35.EaslerJ,MuddanaV,FurlanA,etal.Portosplenomesentericvenousthrombosisinpatientswithacute
pancreatitisisassociatedwithpancreaticnecrosisandusuallyhasabenigncourse.ClinGastroenterolHepatol
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201412:854.
36.NadkarniNA,KhannaS,VegeSS.Splanchnicvenousthrombosisandpancreatitis.Pancreas201342:924.
37.HarrisS,NadkarniNA,NainaHV,VegeSS.Splanchnicveinthrombosisinacutepancreatitis:asinglecenter
experience.Pancreas201342:1251.
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GRAPHICS
Plainabdominalradiographdemonstratingileus

Plainfilmoftheabdomeninachildwithmalrotationillustratesa
nonspecificileuspattern.
ReproducedwithpermissionfromCarloBuonomo,MD,Children'sHospital
Boston.CopyrightCarloBuonomo,MD.
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GreyTurnersign

GreyTurnersignreferstoflankecchymosesthatresultfrombloodtracking
subcutaneouslyfromaretroperitonealorintraperitonealsource.
Reproducedfrom:MashaL,BernardS.GreyTurner'ssignsuggestingretroperitonealhaemorrhage.
Lancet2014383:1920.IllustrationusedwiththepermissionofElsevierInc.Allrightsreserved.
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Pancreaticpanniculitis

Inflammatorynodulesonthedistalleg.
Reproducedwithpermissionfrom:www.visualdx.com.CopyrightLogicalImages,Inc.
Graphic83789Version4.0

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Etiologyofacutepancreatitis
Mechanical

Gallstones,biliarysludge,ascariasis,periampullarydiverticulum,pancreaticor
periampullarycancer,ampullarystenosis,duodenalstrictureorobstruction

Toxic

Ethanol,methanol,scorpionvenom,organophosphatepoisoning

Metabolic

Hyperlipidemia(typesI,IV,V),hypercalcemia

Drugs

Didanosine,pentamidine,metronidazole,stibogluconate,tetracyclinefurosemide,
thiazides,sulphasalazine,5ASA,Lasparaginase,azathioprine,valproicacid,
sulindac,salicylates,calcium,estrogen

Infection

Virusesmumps,coxsackie,hepatitisB,CMV,varicellazoster,HSV,HIV
Bacteriamycoplasma,Legionella,Leptospira,salmonella
Fungiaspergillus
Parasitestoxoplasma,cryptosporidium,Ascaris

Trauma

Bluntorpenetratingabdominalinjury,iatrogenicinjuryduringsurgeryorERCP
(sphincterotomy)

Congenital

CholodochoceletypeV,?pancreasdivisum

Vascular

Ischemia,atheroembolism,vasculitis(polyarteritisnodosa,SLE)

Miscellaneous

PostERCP,pregnancy,renaltransplantation,alpha1antitrypsindeficiency

Genetic

CFTRandothergeneticmutations

5ASA:5aminosalicylicacidCMV:cytomegalovirusHSV:herpessimplexvirusHIV:human
immunodeficiencyvirusERCP:endoscopicretrogradecholangiopancreatographySLE:systemiclupus
erythematosusCFTR:cysticfibrosistransmembraneconductanceregulator.
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Eruptivexanthomata

Xanthomataareseenontheextensorsurfaceoftheforearmina
patientwithseverehypertriglyceridemia.
Reproducedwithpermissionfrom:DurringtonP.Dyslipidaemia.Lancet2003
362:717.Copyright2003Elsevier.
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Parotidglandswellinginayoungchild

Thereisswellingoftheparotidglandanteriorandinferiortotheauricle,obscuringtheangleofthemandible

ReprintedwithpermissionfromSalivaryGlandDisorders,June1,2014,Vol89,No11,AmericanFamilyPhysicianCopyrig
AmericanAcademyofFamilyphysicians.AllRightsReserved.
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Differentialdiagnosisofhyperamylasemia
Disease
Pancreaticdisease

Predominantamylaseisoform
Pancreatic

Acuteorchronicpancreatitis
PostERCP
Pseudocyst
Pancreaticascites

Acutecholecystitis

Pancreatic

Intestinaldiseases

Pancreatic

Parotitis
Trauma
Surgery
Radiation
Calculi
Obstruction
Infarction

Malignancywithectopicamylaseproduction

Salivary

Acidosisorketoacidosis

Salivaryorpancreatic

Renalfailure

Salivaryandpancreatic

Macroamylasemia

Macroamylase

Fallopiantubediseases

Salivary

Rupturedectopicpregnancy
Salpingitis

Miscellaneous

Salivaryand/orpancreatic

Alcoholism
Anorexianervosa/bulimia
Cirrhosis

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Conditionsassociatedwithahighserumlipase
Acutepancreatitis
Chronicpancreatitis
Renalfailure
Acutecholecystitis
Bowelobstructionorinfarction
Duodenalulceration
Pancreaticcalculus
Pancreatictumors
Diabeticketoacidosis
HIVdisease
Macrolipasemia
PostERCP/trauma
Celiacdisease
Idiopathic
Drugs
HIV:humanimmunodeficiencyvirusERCP:endoscopicretrogradecholangiopancreatography.
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Reviseddefinitionsofmorphologicalfeaturesofacutepancreatitis
1.Interstitialedematouspancreatitis
Acuteinflammationofthepancreaticparenchymaandperipancreatictissues,butwithout
recognizabletissuenecrosis
Contrastenhancedcomputedtomographycriteria:
Pancreaticparenchymaenhancementbyintravenouscontrastagent
Nofindingsofperipancreaticnecrosis

2.Necrotizingpancreatitis
Inflammationassociatedwithpancreaticparenchymalnecrosisand/orperipancreaticnecrosis
Contrastenhancedcomputedtomographycriteria:
Lackofpancreaticparenchymalenhancementbyintravenouscontrastagent,and/or
Presenceoffindingsofperipancreaticnecrosis(seebelowacuteperipancreaticfluidcollection
andwalledoffnecrosis)

3.Acuteperipancreaticfluidcollection(APFC)
Peripancreaticfluidassociatedwithinterstitialedematouspancreatitiswithnoassociated
peripancreaticnecrosis.Thistermappliesonlytoareasofperipancreaticfluidseenwithinthefirst
fourweeksafteronsetofinterstitialedematouspancreatitisandwithoutthefeaturesofa
pseudocyst.
Contrastenhancedcomputedtomographycriteria:
Occursinthesettingofinterstitialedematouspancreatitis
Homogeneouscollectionwithfluiddensity
Confinedbynormalperipancreaticfascialplanes
Nodefinablewallencapsulatingthecollection
Adjacenttopancreas(nointrapancreaticextension)

4.Pancreaticpseudocyst
Anencapsulatedcollectionoffluidwithawelldefinedinflammatorywallusuallyoutsidethepancreas
withminimalornonecrosis.Thisentityusuallyoccursmorethanfourweeksafteronsetof
interstitialedematouspancreatitistomature.
Contrastenhancedcomputedtomographycriteria:
Wellcircumscribed,usuallyroundoroval
Homogeneousfluiddensity
Nononliquidcomponent
Welldefinedwall(ie,completelyencapsulated)
Maturationusuallyrequires>4weeksafteronsetofacutepancreatitisoccursafterinterstitial
edematouspancreatitis

5.Acutenecroticcollection(ANC)
Acollectioncontainingvariableamountsofbothfluidandnecrosisassociatedwithnecrotizing
pancreatitisthenecrosiscaninvolvethepancreaticparenchymaand/ortheperipancreatictissues
Contrastenhancedcomputedtomographycriteria:
Occursonlyinthesettingofacutenecrotizingpancreatitis
Heterogeneousandnonliquiddensityofvaryingdegreesindifferentlocations(someappear
homogeneousearlyintheircourse)
Nodefinablewallencapsulatingthecollection
Locationintrapancreaticand/orextrapancreatic

6.Walledoffnecrosis(WON)
Amature,encapsulatedcollectionofpancreaticand/orperipancreaticnecrosisthathasdevelopeda
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welldefinedinflammatorywall.WONusuallyoccurs>4weeksafteronsetofnecrotizingpancreatitis.
Contrastenhancedcomputedtomographycriteria:
Heterogeneouswithliquidandnonliquiddensitywithvaryingdegreesofloculations(somemay
appearhomogeneous)
Welldefinedwall,thatis,completelyencapsulated
Locationintrapancreaticand/orextrapancreatic
Maturationusuallyrequiresfourweeksafteronsetofacutenecrotizingpancreatitis
Reproducedwithpermissionfrom:BanksPA,BollenTL,DervenisC,etal.Classificationofacutepancreatitis
2012:revisionsoftheAtlantaclassificationanddefinitionsbyinternationalconsensus.Gut201362:102.
BMJPublishingGroupLtd.Copyright2013.
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Cholelithiasis

Ultrasoundofthegallbladdershowsposterioracousticshadowing
(arrowhead)producedbyastoneinthelumenofthegallbladder
(arrow).Thereisnogallbladderwallthickening,afindingthatmaybe
seenwithcholecystitis.
CourtesyofJonathanKruskal,MD,PhD.
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CTscanofacuteinterstitialedematouspancreatitis

Thecomputedtomography(CT)scanina75yearoldmanwithacute
interstitialpancreatitisrevealsheterogeneousappearanceof
thepancreas(arrow)andperipancreaticfatstranding(arrowhead).
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CTscanofnecrotizingpancreatitiswithperipancreaticnecrosis

Computedtomography(CT)scanofa34yearoldmalewithacutepancreatitisrevealsthe
pancreasenhanceshomogeneously(arrow)butthereisevidenceofperipancreaticnecrosis
(arrowhead).
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Computedtomographic(CT)scanfromapatientwithacute
cholecystitis

TheCTscanshowsadistendedgallbladderwithanedematousandhyperemicwall(thick
arrow)andinflammatoryindurationinthefatsurroundingthegallbladder(arrowheads).A
calcifiedstoneisvisiblelyingdependentlyatthebaseofthegallbladder(thinarrow).
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Perforatedduodenalulcer

Computedtomographicscanshowingfreeairintheanteriorperitoneal
space(whitearrows),intheligamentumvenosum(blackarrow),and
inthehepatogastricligament(smallblackarrow)resultingfroma
perforationofaduodenalpepticulcer.
CourtesyofJonathanBKruskal,MD,PhD.
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Perforatedduodenalulcer

Decubituscomputedtomographicscanshowsmarkedthickeningand
inflammationoftheduodenalwall(whitearrows)withextraluminal
contrastmaterialandair(blackarrows)duetoaperforatedduodenal
ulcer.
CourtesyofJonathanBKruskal,MD,PhD.
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SmallbowelobstructionCT(coronalimages)

SmallbowelobstructionseenbyCTscan(coronalimages)showing
dilated,fluidfilledloopsofsmallintestine.
CourtesyofRichardAHodin,MD.
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CTscanofpneumatosiscoli

Computedtomography(CT)imagingoftheabdomenisfroma55yearoldfemalewho
presentedwithacuteabdominalpainanddistension.ImageAisascoutfilmofthe
abdomenandimageBisamagnifiedviewofthesmallbowelfromthescoutfilm.The
imagesrevealairwithinthewallofthedilatedloopsofsmallbowel,characteristicof
pneumatosisintestinalis.ThepaucityofgasinthecolonandrectumsuggestsSBOor
severeileus.ImageCiscoronalreformatthroughtheabdomenconfirmingthe
accumulationofbubblesofairwithinthewallofthesmallbowel(whitearrow).ImageD
isanaxialimagethroughtheaffectedsmallbowelloopthatshowsmoreextensive
accumulationofairwithinthewallofthethickenedsmallbowelwall.Associatedfindings
includedecompressedlargebowel(arrowheads),suggestingsmallbowelobstructionor
severeileus.Intheappropriateclinicalsetting,thefindingsarehighlysuggestiveof
acuteischemiaofthesmallbowelcausingasevereileusandfunctionalobstruction.
Lesslikelybutalsopossibleissmallbowelobstructionwithsecondaryischemia.
CT:computedtomographySBO:smallbowelobstruction.
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Clinicalmanifestationsanddiagnosisofacutepancreatitis

CTscanofacuteinterstitialpancreatitiswithacuteperipancreatic
fluidcollections

Computedtomography(CT)scanrevealsacuteinterstitialpancreatitiswithanacute
peripancreaticfluidcollections(APFC)aroundthebodyandtailofthepancreas
(arrowheads).Thereismildheterogeneityoftheenhancedpancreas(arrow).
Graphic88431Version2.0

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Clinicalmanifestationsanddiagnosisofacutepancreatitis

CTscanofacutenecroticcollection

Computedtomography(CT)scanrevealsanacutenecroticcollectionina20yearold
femalewithacutepancreatitis.TheaxialCTimageshowspancreaticnecrosiswith
anonenhancingregionintheneckandthebodyofthepancreas(betweenarrowheads).In
thesurroundinganteriorpararenalspace,thereisalargefluidaccumulationthatcontains
islandsofnecrosis(arrow).
Graphic88434Version1.0

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CTscanofacutenecrotizingpancreatitiscomplicatedby
infectedpancreaticnecrosis

Computedtomography(CT)scanrevealsgasbubbles(arrow)withinanareaof
pancreaticnecrosis.Thepresenceofgasbubblesisapathognomonicsignofinfection
ofthenecrosis.
Graphic88436Version1.0

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Clinicalmanifestationsanddiagnosisofacutepancreatitis

ModifiedMarshallscoringsystemfororgandysfunction
Score

Organsystem

>400

301400

201300

101200

101

(serumcreatinine,
micromol/L)

134

134169

170310

311439

>439

(serumcreatinine,

<1.4

1.41.8

1.93.6

3.64.9

>4.9

<90,fluid

<90,not

<90,pH

<90,pH

responsive

fluid

<7.3

<7.2

Respiratory
(PaO 2 /FiO 2 )
Renal*

mg/dL)
Cardiovascular(systolic

>90

bloodpressure,
mmHg)

responsive

Fornonventilatedpatients,theFiO 2 canbeestimatedfrombelow:
Supplemental
oxygen(L/min)

FiO 2 (percent)

Roomair

21

25

30

68

40

910

50

Ascoreof2ormoreinanysystemdefinesthepresenceoforganfailure.
*Ascoreforpatientswithpreexistingchronicrenalfailuredependsontheextentoffurtherdeteriorationof
baselinerenalfunction.Noformalcorrectionexistsforabaselineserumcreatinine134micromol/Lor1.4
mg/dL.
Offinotropicsupport.
Reproducedwithpermissionfrom:BanksPA,BollenTL,DervenisC,etal.Classificationofacutepancreatitis
2012:revisionsoftheAtlantaclassificationanddefinitionsbyinternationalconsensus.Gut201362:102.
BMJPublishingGroupLtd.Copyright2013.
Graphic87718Version2.0

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ContributorDisclosures
SanthiSwaroopVege,MDNothingtodisclose.DavidCWhitcomb,MD,PhDConsultant/AdvisoryBoards:AbbVie
[pancreaticexocrineinsufficiency(pancrelipase)].PatentHolder:SMARTMD[hereditarypancreatitis(genetictesting)].
EquityOwnership/StockOptions:SMARTMDAmbryGenetics[genetictesting].ShilpaGrover,MD,MPHNothingto
disclose.
Contributordisclosuresarereviewedforconflictsofinterestbytheeditorialgroup.Whenfound,theseareaddressed
byvettingthroughamultilevelreviewprocess,andthroughrequirementsforreferencestobeprovidedtosupportthe
content.AppropriatelyreferencedcontentisrequiredofallauthorsandmustconformtoUpToDatestandardsof
evidence.
Conflictofinterestpolicy

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