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AcutePancreatitis
Updated:Feb13,2017
Author:JeffreyCFTang,MDChiefEditor:BSAnand,MDmore...
OVERVIEW
PracticeEssentials
Recognizingpatientswithsevereacutepancreatitisassoonaspossibleiscriticalforachieving
optimaloutcomes.Managementdependslargelyonseverity.Medicaltreatmentofmildacute
pancreatitisisrelativelystraightforward.Treatmentofsevereacutepancreatitisinvolvesintensive
care.Surgicalintervention(openorminimallyinvasive)isindicatedinselectedcases.
Signsandsymptoms
Symptomsofacutepancreatitisincludethefollowing:
Abdominalpain(cardinalsymptom):Characteristicallydull,boring,andsteadyusually
suddeninonsetandgraduallybecomingmoresevereuntilreachingaconstantachemost
oftenlocatedintheupperabdomenandmayradiatedirectlythroughtotheback
Nauseaandvomiting,sometimeswithanorexia
Diarrhea
Patientsmayhaveahistoryofthefollowing:
Recentoperativeorotherinvasiveprocedures
Familyhistoryofhypertriglyceridemia
Previousbiliarycolicandbingealcoholconsumption(majorcausesofacutepancreatitis)
Thefollowingphysicalfindingsmaybenoted,varyingwiththeseverityofthedisease:
Fever(76%)andtachycardia(65%)hypotension
Abdominaltenderness,muscularguarding(68%),anddistention(65%)diminishedorabsent
bowelsounds
Jaundice(28%)
Dyspnea(10%)tachypneabasilarrales,especiallyintheleftlung
Inseverecases,hemodynamicinstability(10%)andhematemesisormelena(5%)pale,
diaphoretic,andlistlessappearance
Occasionally,extremitymuscularspasmssecondarytohypocalcemia
Thefollowinguncommonphysicalfindingsareassociatedwithseverenecrotizingpancreatitis:
Cullensign(bluishdiscolorationaroundtheumbilicusresultingfromhemoperitoneum)
GreyTurnersign(reddishbrowndiscolorationalongtheflanksresultingfromretroperitoneal
blooddissectingalongtissueplanes)morecommonly,patientsmayhavearuddyerythema
intheflankssecondarytoextravasatedpancreaticexudate
Erythematousskinnodules,usuallynolargerthan1cmandtypicallylocatedonextensor
skinsurfacespolyarthritis
SeeClinicalPresentationformoredetail.
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Diagnosis
Onceaworkingdiagnosisofacutepancreatitisisreached,laboratorytestsareobtainedtosupport
theclinicalimpression,suchasthefollowing:
Serumamylaseandlipase
Liverassociatedenzymes
Bloodureanitrogen(BUN),creatinine,andelectrolytes
Bloodglucose
Serumcholesterolandtriglyceride
Completebloodcount(CBC)andhematocritNLR
Creactiveprotein(CRP)
Arterialbloodgasvalues
Serumlacticdehydrogenase(LDH)andbicarbonate
ImmunoglobulinG4(IgG4)
Diagnosticimagingisunnecessaryinmostcasesbutmaybeobtainedwhenthediagnosisisin
doubt,whenpancreatitisissevere,orwhenagivenstudymightprovidespecificinformation
required.Modalitiesemployedincludethefollowing:
Abdominalradiography(limitedrole):Kidneysuretersbladder(KUB)radiographywiththe
patientuprightisprimarilyperformedtodetectfreeairintheabdomen
Abdominalultrasonography(mostusefulinitialtestindeterminingtheetiology,andisthe
techniqueofchoicefordetectinggallstones)
Endoscopicultrasonography(EUS)(usedmainlyfordetectionofmicrolithiasisand
periampullarylesionsnoteasilyrevealedbyothermethods)
Abdominalcomputedtomography(CT)scanning(generallynotindicatedforpatientswith
mildpancreatitisbutalwaysindicatedforthosewithsevereacutepancreatitis)
Endoscopicretrogradecholangiopancreatography(ERCP)tobeusedwithextremecaution
inthisdiseaseandneverasafirstlinediagnostictool[1]
Magneticresonancecholangiopancreatography(MRCP)(notassensitiveasERCPbutsafer
andnoninvasive)
Otherdiagnosticmodalitiesincludethefollowing:
CTguidedorEUSguidedaspirationanddrainage
Genetictesting
Acutepancreatitisisbroadlyclassifiedaseithermildorsevere.AccordingtotheAtlanta
classification,severeacutepancreatitisissignaledbythefollowing[2]:
Evidenceoforganfailure(eg,systolicbloodpressurebelow90mmHg,arterialpartial
pressureofoxygen[PaO2]60mmHgorlower,serumcreatininelevel2mg/dLorhigher,GI
bleedingamountingto500mLormorein24hours)
Localcomplications(eg,necrosis,abscess,pseudocyst)
Ransonscoreof3orhigherorAPACHEscoreof8orhigher
SeeWorkupformoredetail.
Management
Medicalmanagementofmildacutepancreatitisisrelativelystraightforwardhowever,patientswith
severeacutepancreatitisrequireintensivecare.
Initialsupportivecareincludesthefollowing:
Fluidresuscitation[3]
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Nutritionalsupport
Antibiotictherapyisemployedasfollows:
Antibiotics(usuallyoftheimipenemclass)shouldbeusedinanycaseofpancreatitis
complicatedbyinfectedpancreaticnecrosisbutshouldnotbegivenroutinelyforfever,
especiallyearlyinthepresentation
Antibioticprophylaxisinseverepancreatitisiscontroversialroutineuseofantibioticsas
prophylaxisagainstinfectioninsevereacutepancreatitisisnotcurrentlyrecommended
Surgicalintervention(openorminimallyinvasive)isindicatedwhenananatomiccomplication
amenabletoamechanicalsolutionispresent.Proceduresappropriateforspecificconditions
involvingpancreatitisincludethefollowing:
Gallstonepancreatitis:Cholecystectomy
Pancreaticductdisruption:Imageguidedpercutaneousplacementofadrainagetubeintothe
fluidcollection[4]stentortubeplacementviaERCPinrefractorycases,distal
pancreatectomyoraWhippleprocedure
Pseudocysts:Nonenecessaryinmostcasesforlargeorsymptomaticpseudocysts,
percutaneousaspiration,endoscopictranspapillaryortransmuraltechniques,orsurgical
management
Infectedpancreaticnecrosis:Imageguidedaspirationnecrosectomy
Pancreaticabscess:Percutaneouscatheterdrainageandantibioticsifnoresponse,surgical
debridementanddrainage
SeeTreatmentandMedicationformoredetail.
Background
Thisarticlefocusesontherecognitionandmanagementofacutepancreatitis.Pancreatitisisan
inflammatoryprocessinwhichpancreaticenzymesautodigestthegland.Theglandsometimes
healswithoutanyimpairmentoffunctionoranymorphologicchangesthisprocessisknownas
acutepancreatitis.Pancreatitiscanalsorecurintermittently,contributingtothefunctionaland
morphologiclossoftheglandrecurrentattacksarereferredtoaschronicpancreatitis.
Bothformsofpancreatitismaypresentintheemergencydepartment(ED)withacuteclinical
findings.Recognizingpatientswithsevereacutepancreatitisassoonaspossibleiscriticalfor
achievingoptimaloutcomes(seePresentation).
Onceaworkingdiagnosisofacutepancreatitisisreached,laboratorytestsareobtainedtosupport
theclinicalimpression,tohelpdefinetheetiology,andtolookforcomplications.Diagnostic
imagingisunnecessaryinmostcasesbutmaybeobtainedwhenthediagnosisisindoubt,when
severepancreatitisispresent,orwhenanimagingstudymightprovidespecificinformationneeded
toansweraclinicalquestion.Imageguidedaspirationmaybeuseful.Genetictestingmaybe
considered(seeWorkup).
Managementdependslargelyonseverity.Medicaltreatmentofmildacutepancreatitisisrelatively
straightforward.Treatmentofsevereacutepancreatitisinvolvesintensivecarethegoalsof
medicalmanagementaretoprovideaggressivesupportivecare,todecreaseinflammation,tolimit
infectionorsuperinfection,andtoidentifyandtreatcomplicationsasappropriate.Surgical
intervention(openorminimallyinvasive)isindicatedinselectedcases(seeTreatment).
Pathophysiology
Normalpancreaticfunction
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Thepancreasisaglandlocatedintheupperposteriorabdomen.Itisresponsibleforinsulin
production(endocrinepancreas)andthemanufactureandsecretionofdigestiveenzymes
(exocrinepancreas)leadingtocarbohydrate,fat,andproteinmetabolism.Approximately80%of
thegrossweightofthepancreassupportsexocrinefunction,andtheremaining20%isinvolved
withendocrinefunction.Thefocusofthisarticleisontheexocrinefunctionofthepancreas.
Thepancreasaccountsforonly0.1%oftotalbodyweightbuthas13timestheproteinproducing
capacityoftheliverandthereticuloendothelialsystemcombined,whichtogethermakeup4%of
totalbodyweight.Digestiveenzymesareproducedwithinthepancreaticacinarcells,packaged
intostoragevesiclescalledzymogens,andthenreleasedviathepancreaticductalcellsintothe
pancreaticduct,wheretheyaresecretedintothesmallintestinetobeginthemetabolicprocess.
Innormalpancreaticfunction,upto15differenttypesofdigestiveenzymesaremanufacturedin
theroughendoplasmicreticulum,targetedintheGolgiapparatusandpackagedintozymogensas
proenzymes.Whenamealisingested,thevagalnerves,vasoactiveintestinalpolypeptide(VIP),
gastrinreleasingpeptide(GRP),secretin,cholecystokinin(CCK),andencephalinsstimulate
releaseoftheseproenzymesintothepancreaticduct.
Theproenzymestraveltothebrushborderoftheduodenum,wheretrypsinogen,theproenzyme
fortrypsin,isactivatedviahydrolysisofanNterminalhexapeptidefragmentbythebrushborder
enzymeenterokinase.Trypsinthenfacilitatestheconversionoftheotherproenzymesintotheir
activeforms.
Afeedbackmechanismexiststolimitpancreaticenzymeactivationafterappropriatemetabolism
hasoccurred.Itishypothesizedthatelevatedlevelsoftrypsin,havingbecomeunboundfrom
digestingfood,leadtodecreasedCCKandsecretinlevels,thuslimitingfurtherpancreatic
secretion.
Becauseprematureactivationofpancreaticenzymeswithinthepancreasleadstoorganinjuryand
pancreatitis,severalmechanismsexisttolimitthisoccurrence.First,proteinsaretranslatedinto
theinactiveproenzymes.Later,posttranslationalmodificationoftheGolgicellsallowstheir
segregationintotheuniquesubcellularzymogencompartments.Theproenzymesarepackagedin
aparacrystallinearrangementwithproteaseinhibitors.
ZymogengranuleshaveanacidicpHandalowcalciumconcentration,whicharefactorsthat
guardagainstprematureactivationuntilaftersecretionhasoccurredandextracellularfactorshave
triggeredtheactivationcascade.Undervariousconditions,disruptionoftheseprotective
mechanismsmayoccur,resultinginintracellularenzymeactivationandpancreaticautodigestion
leadingtoacutepancreatitis.
Pathogenesisofacutepancreatitis
Acutepancreatitismayoccurwhenfactorsinvolvedinmaintainingcellularhomeostasisareoutof
balance.Theinitiatingeventmaybeanythingthatinjurestheacinarcellandimpairsthesecretion
ofzymogengranulesexamplesincludealcoholuse,gallstones,andcertaindrugs.
Atpresent,itisunclearexactlywhatpathophysiologiceventtriggerstheonsetofacute
pancreatitis.Itisbelieved,however,thatbothextracellularfactors(eg,neuralandvascular
response)andintracellularfactors(eg,intracellulardigestiveenzymeactivation,increasedcalcium
signaling,andheatshockproteinactivation)playarole.Inaddition,acutepancreatitiscandevelop
whenductalcellinjuryleadstodelayedorabsentenzymaticsecretion,asseeninpatientswiththe
CFTRgenemutation.
Onceacellularinjurypatternhasbeeninitiated,cellularmembranetraffickingbecomeschaotic,
withthefollowingdeleteriouseffects:
Lysosomalandzymogengranulecompartmentsfuse,enablingactivationoftrypsinogento
trypsin
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Intracellulartrypsintriggerstheentirezymogenactivationcascade
Secretoryvesiclesareextrudedacrossthebasolateralmembraneintotheinterstitium,where
molecularfragmentsactaschemoattractantsforinflammatorycells
Activatedneutrophilsthenexacerbatetheproblembyreleasingsuperoxide(therespiratoryburst)
orproteolyticenzymes(cathepsinsB,D,andGcollagenaseandelastase).Finally,macrophages
releasecytokinesthatfurthermediatelocal(and,inseverecases,systemic)inflammatory
responses.Theearlymediatorsdefinedtodatearetumornecrosisfactoralpha(TNF),
interleukin(IL)6,andIL8.
Thesemediatorsofinflammationcauseanincreasedpancreaticvascularpermeability,leadingto
hemorrhage,edema,andeventuallypancreaticnecrosis.Asthemediatorsareexcretedintothe
circulation,systemiccomplicationscanarise,suchasbacteremiaduetogutfloratranslocation,
acuterespiratorydistresssyndrome(ARDS),pleuraleffusions,gastrointestinal(GI)hemorrhage,
andrenalfailure.
Thesystemicinflammatoryresponsesyndrome(SIRS)canalsodevelop,leadingtothe
developmentofsystemicshock.Eventually,themediatorsofinflammationcanbecomeso
overwhelmingthathemodynamicinstabilityanddeathensue.
Inacutepancreatitis,parenchymaledemaandperipancreaticfatnecrosisoccurfirstthisisknown
asacuteedematouspancreatitis.Whennecrosisinvolvestheparenchyma,accompaniedby
hemorrhageanddysfunctionofthegland,theinflammationevolvesintohemorrhagicornecrotizing
pancreatitis.Pseudocystsandpancreaticabscessescanresultfromnecrotizingpancreatitis
becauseenzymescanbewalledoffbygranulationtissue(pseudocystformation)orviabacterial
seedingofpancreaticorperipancreatictissue(pancreaticabscessformation).
Lietalcompared2setofpatientswithsevereacutepancreatitisonewithacuterenalfailureand
theotherwithoutitanddeterminedthatahistoryofrenaldisease,hypoxemia,andabdominal
compartmentsyndromeweresignificantriskfactorsforacuterenalfailureinpatientswithsevere
acutepancreatitis.[5]Inaddition,patientswithacuterenalfailurewerefoundtohaveasignificantly
greateraveragelengthofstayinthehospitalandintheintensivecareunit(ICU),aswellashigher
ratesofpancreaticinfectionandmortality.
Etiology
Longstandingalcoholconsumptionandbiliarystonediseasecausemostcasesofacute
pancreatitis,butnumerousotheretiologiesareknown.In1030%ofcases,thecauseisunknown,
thoughstudieshavesuggestedthatasmanyas70%ofcasesofidiopathicpancreatitisare
secondarytobiliarymicrolithiasis.
Biliarytractdisease
Oneofthemostcommoncausesofacutepancreatitisinmostdevelopedcountries(accountingfor
approximately40%ofcases)isgallstonespassingintothebileductandtemporarilylodgingatthe
sphincterofOddi.Theriskofastonecausingpancreatitisisinverselyproportionaltoitssize.
Itisthoughtthatacinarcellinjuryoccurssecondarytoincreasingpancreaticductpressures
causedbyobstructivebiliarystonesattheampullaofVater,althoughthishasnotbeendefinitively
proveninhumans.Occultmicrolithiasisisprobablyresponsibleformostcasesofidiopathicacute
pancreatitis.
Alcohol
Alcoholuseisamajorcauseofacutepancreatitis(accountingforatleast35%ofcases[6]).Atthe
cellularlevel,ethanolleadstointracellularaccumulationofdigestiveenzymesandtheirpremature
activationandrelease.Attheductallevel,itincreasesthepermeabilityofductules,allowing
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enzymestoreachtheparenchymaandcausepancreaticdamage.Ethanolincreasestheprotein
contentofpancreaticjuiceanddecreasesbicarbonatelevelsandtrypsininhibitorconcentrations.
Thisleadstotheformationofproteinplugsthatblockpancreaticoutflow.
Mostcommonly,thediseasedevelopsinpatientswhosealcoholingestionishabitualover515
years.Alcoholicsareusuallyadmittedwithanacuteexacerbationofchronicpancreatitis.
Occasionally,however,pancreatitiscandevelopinapatientwithaweekendbinginghabit,and
severalcasereportshavedescribedasolelargealcoholloadprecipitatingafirstattack.
Nevertheless,thealcoholicwhoimbibesroutinelyremainstheruleratherthantheexceptionforthe
developmentofpancreatitis.
Currently,thereisnouniversallyacceptedexplanationforwhycertainalcoholicsaremore
predisposedtodevelopingacutepancreatitisthanotheralcoholicswhoingestsimilarquantities.
Endoscopicretrogradecholangiopancreatography
Pancreatitisoccurringafterendoscopicretrogradecholangiopancreatography(ERCP)isprobably
thethirdmostcommontype(accountingforapproximately4%ofcases).Whereasretrospective
surveysindicatethattheriskisonly1%,prospectivestudieshaveshowntherisktobeatleast5%.
TheriskofpostERCPacutepancreatitisisincreasediftheendoscopistisinexperienced,ifthe
patientisthoughttohavesphincterofOddidysfunction,orifmanometryisperformedonthe
sphincterofOddi.Aggressivepreinterventionintravenous(IV)hydrationhasbeendurablyshown
topreventpostERCPpancreatitisinrandomizedstudies.Morerecently,rectalindomethacinhas
beenemployedithasbeenshowntoreducetheincidenceofpostERCPpancreatitisandisnow
widelyacceptedatmostinstitutions.Theliteraturecontinuestodebatetheroleofrectal
indomethacin.[7]
Trauma
Abdominaltrauma(approximately1.5%)causesanelevationofamylaseandlipaselevelsin17%
ofcasesandclinicalpancreatitisin5%ofcases.Pancreaticinjuryoccursmoreofteninpenetrating
injuries(eg,fromknives,bullets)thaninbluntabdominaltrauma(eg,fromsteeringwheels,horses,
bicycles).Bluntinjurytotheabdomenorbackmaycrushtheglandacrossthespine,leadingtoa
ductalinjury.
Drugs
Consideringthesmallnumberofpatientswhodeveloppancreatitiscomparedtotherelativelylarge
numberwhoreceivepotentiallytoxicdrugs,druginducedpancreatitisisarelativelyrare
occurrence(accountingforapproximately2%ofcases)thatisprobablyrelatedtoanunknown
predisposition.Fortunately,druginducedpancreatitisisusuallymild.
Drugsdefinitelyassociatedwithacutepancreatitisincludethefollowing:
Azathioprine
Sulfonamides
Sulindac
Tetracycline
Valproicacid,
Didanosine
Methyldopa
Estrogens
Furosemide
6Mercaptopurine
Pentamidine
5aminosalicylicacidcompounds
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Corticosteroids
Octreotide
Drugsprobablyassociatedwithacutepancreatitisincludethefollowing:
Chlorothiazideandhydrochlorothiazide
Methandrostenolone(methandienone)
Metronidazole
Nitrofurantoin
Phenformin
Piroxicam
Procainamide
Colaspase
Chlorthalidone
Combinationcancerchemotherapydrugs(especiallyasparaginase)
Cimetidine
Cisplatin
Cytosinearabinoside
Diphenoxylate
Ethacrynicacid
Inaddition,therearemanydrugsthathavebeenreportedtocauseacutepancreatitisinisolatedor
sporadiccases.
Lesscommoncauses
Thefollowingcauseseachaccountforlessthan1%ofcasesofpancreatitis.
Infection
Severalinfectiousdiseasesmaycausepancreatitis,especiallyinchildren.Thesecasesofacute
pancreatitistendtobemilderthancasesofacutebiliaryoralcoholinducedpancreatitis.
Viralcausesincludemumpsvirus,coxsackievirus,cytomegalovirus(CMV),hepatitisvirus,Epstein
Barrvirus(EBV),echovirus,varicellazostervirus(VZV),measlesvirus,andrubellavirus.Bacterial
causesincludeMycoplasmapneumoniae,Salmonella,Campylobacter,andMycobacterium
tuberculosis.Worldwide,Ascarisisarecognizedcauseofpancreatitisresultingfromthemigration
ofwormsinandoutoftheduodenalpapillae.
PancreatitishasbeenassociatedwithAIDShowever,thismaybetheresultofopportunistic
infections,neoplasms,lipodystrophy,ordrugtherapies.
Hereditarypancreatitis
Hereditarypancreatitisisanautosomaldominantgainoffunctiondisorderrelatedtomutationsof
thecationictrypsinogengene(PRSS1),whichhasan80%penetrance.Mutationsinthisgene
causeprematureactivationoftrypsinogentotrypsin.
Inaddition,theCFTRmutationplaysaroleinpredisposingpatientstoacutepancreatitisby
causingabnormalitiesofductalsecretion.Atpresent,however,thephenotypicvariabilityof
patientswiththeCFTRmutationisnotwellunderstood.Certainly,patientshomozygousforthe
CFTRmutationareatriskforpancreaticdisease,butitisnotyetclearwhichofthemorethan800
mutationscarriesthemostsignificantrisk.Inaddition,theroleofCFTRheterozygotesin
pancreaticdiseaseisunknown.
MutationsintheSPINK1protein,whichblockstheactivebindingsiteoftrypsin,renderingit
inactive,alsoprobablyplayaroleincausingapredispositiontoacutepancreatitis.
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Thisprobablyexplainsthepredisposition,ratherthanthecause,ofacutepancreatitisinthese
patients.Ifenoughmutantenzymesbecomeactivatedintracellularly,theycanoverwhelmthefirst
lineofdefense(ie,pancreaticsecretorytrypsininhibitor)andresistbackupdefenses(ie,proteolytic
degradationbymesotrypsin,enzymeY,andtrypsinitself).Activatedmutantcationictrypsincan
thentriggertheentirezymogenactivationcascade.
Hypercalcemia
Hypercalcemiafromanycausecanleadtoacutepancreatitis.Causesinclude
hyperparathyroidism,excessivedosesofvitaminD,familialhypocalciurichypercalcemia,andtotal
parenteralnutrition(TPN).Routineuseofautomatedserumchemistrieshasallowedearlier
detectionandreducedthefrequencyofhypercalcemiamanifestingaspancreatitis.
Developmentalabnormalitiesofpancreas
Thepancreasdevelopsfrom2budsstemmingfromthealimentarytractofthedevelopingembryo.
Thereare2developmentalabnormalitiescommonlyassociatedwithpancreatitis:pancreas
divisumandannularpancreas.
Pancreasdivisumisafailureofthedorsalandventralpancreaticductstofuseduring
embryogenesis.Probablyavariantofnormalanatomy,itoccursinapproximately5%ofthe
population(seetheimagesbelow)inmostcases,itmayactuallyprotectagainstgallstone
pancreatitis.ItappearsthatthepresenceofstenoticminorpapillaeandanatreticductofSantorini
areadditionalriskfactorsthattogethercontributetothedevelopmentofacutepancreatitisthrough
anobstructivemechanism(althoughthisiscontroversial).
Pancreasdivisumassociatedwithminorpapillastenosiscausingrecurrentpancreatitis.Becausepancreas
divisumisrelativelycommoninthegeneralpopulation,itisbestregardedasvariantofnormalanatomyand
notnecessarilyascauseofpancreatitis.Inthiscase,notebulbouscontourofductadjacenttocannula.This
appearancehasbeentermedSantorinicele.Dorsalductoutflowobstructionisaprobablecauseofpancreatitis
whenSantoriniceleispresentandisassociatedwithaminorpapillathataccommodatesonlyaguidewire.
ViewMediaGallery
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Recurrentpancreatitisassociatedwithpancreasdivisuminanelderlyman.Pancreatogramofthedorsalduct
showsdistalstenosiswithupstreamchronicpancreatitis.Afterthestenosiswasdilatedandstented,pain
resolvedandthepatientimprovedclinicallyduring1yearofquarterlystentexchanges.FollowupCTscans
showedresolutionoftheinflammatorymass.Althoughductalbiopsiesandcytologywererepeatedlynegative,
painandpancreatitisreturnedwhenthestentswereremoved.Patientdevelopedduodenaloutflowobstruction
andwassenttosurgeryWhippleprocedurerevealedperiampullaryadenocarcinoma(ofminorpapilla).
ViewMediaGallery
Annularpancreasisanuncommoncongenitalanomalyinwhichabandofpancreatictissue
surroundsthesecondpartoftheduodenum.Usually,itdoesnotcausesymptomsuntillaterinlife.
Thisconditionisararecauseofacutepancreatitis,probablythroughanobstructivemechanism.
SphincterofOddidysfunctioncanleadtoacutepancreatitisbycausingincreasedpancreatic
ductalpressures.However,themechanismofpancreatitisinducedbysuchdysfunctioninpatients
withoutelevatedsphincterpressuresonmanometryremainscontroversial.
Hypertriglyceridemia
Clinicallysignificantpancreatitisusuallydoesnotoccuruntilapersonsserumtriglyceridelevel
reaches1000mg/dL.ItisassociatedwithtypeIandtypeVhyperlipidemia.Althoughthisviewis
somewhatcontroversial,mostauthoritiesbelievethattheassociationiscausedbytheunderlying
derangementinlipidmetabolismratherthanbypancreatitiscausinghyperlipidemia.Thistypeof
pancreatitistendstobemoreseverethanalcoholorgallstoneinduceddisease.
Tumors
Obstructionofthepancreaticductalsystembyapancreaticductalcarcinoma,ampullary
carcinoma,isletcelltumor,solidpseudotumorofthepancreas,sarcoma,lymphoma,
cholangiocarcinoma,ormetastatictumorcancauseacutepancreatitis.Thechancesofpancreatitis
occurringwhenatumorispresentareapproximately14%.Pancreaticcysticneoplasms,suchas
intraductalpapillarymucinousneoplasm(IPMN),mucinouscystadenoma,orserouscystadenoma,
canalsocausepancreatitis.
Toxins
Exposuretoorganophosphateinsecticidecancauseacutepancreatitis.Scorpionandsnakebites
mayalsobecausativeinTrinidad,thestingofthescorpionTityustrinitatisisthemostcommon
causeofacutepancreatitis.Hyperstimulationofpancreasexocrinesecretionappearstobethe
mechanismofactioninbothinstances.
Surgicalprocedures
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Acutepancreatitismayoccurinthepostoperativeperiodofvarioussurgicalprocedures(eg,
abdominalorcardiopulmonarybypasssurgery,whichmaydamagetheglandbycausing
ischemia).Postoperativeacutepancreatitisisoftenadifficultdiagnosistoconfirm,andithasa
highercomplicationratethanpancreatitisassociatedwithotheretiologies.Themechanismis
unclear.
Vascularabnormalities
Vascularfactors,suchasischemiaorvasculitis,canplayaroleincausingacutepancreatitis.
Vasculitiscanpredisposepatientstopancreaticischemia,especiallyinthosewithpolyarteritis
nodosaandsystemiclupuserythematosus.
Autoimmunepancreatitis
Autoimmunepancreatitis,arelativelynewlydescribedentity,isanextremelyrarecauseofacute
pancreatitis(prevalence,0.82per100,000individuals).Whenitdoescauseacutepancreatitis,itis
usuallyinyoungpeople(approximatelyage40years)whoalsosufferfrominflammatorybowel
disease.Thepathogenesisisunclear,butitispotentiallyrelatedtoimmunoglobulin(Ig)G4
autoimmunedisease.[8]
Epidemiology
UnitedStatesstatistics
Acutepancreatitishasanincidenceofapproximately40casesperyearper100,000adults.[9]In
2007,nearly220,000patientswithacutepancreatitisareexpectedtobeadmittedtononfederally
fundedhospitals.In1998,183,000patientswithacutepancreatitiswereadmitted.Thistrendin
risingincidencehasbeenrecognizedoverthepastseveraldecades.[10]
Internationalstatistics
Worldwide,theincidenceofacutepancreatitisrangesbetween5and80per100,000population,
withthehighestincidencerecordedintheUnitedStatesandFinland.[11]InLuneburg,Germany,
theincidenceis17.5casesper100,000people.InFinland,theincidenceis73.4casesper
100,000people.SimilarincidencerateshavebeenreportedinAustralia.Theincidenceofdisease
outsideNorthAmerica,Europe,andAustraliaislesswellknown.
InEuropeandotherdevelopednations,suchasHongKong,morepatientstendtohavegallstone
pancreatitis,whereasintheUnitedStates,alcoholicpancreatitisismostcommon.
Agerelateddemographics
Themedianageatonsetdependsontheetiology.[12]Thefollowingaremedianagesofonsetfor
variousetiologies:
Alcoholrelated39years
Biliarytractrelated69years
Traumarelated66years
Druginducedetiology42years
ERCPrelated58years
AIDSrelated31years
Vasculitisrelated36years
Hospitalizationratesincreasewithage.Forpeopleaged3575years,theratedoublesformales
andquadruplesforfemales.
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201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology
Sexrelateddemographics
Generally,acutepancreatitisaffectsmalesmoreoftenthanfemales.Inmales,theetiologyismore
oftenrelatedtoalcoholinfemales,itismoreoftenrelatedtobiliarytractdisease.Idiopathic
pancreatitishasnoclearpredilectionforeithersex.
Racerelateddemographics
Thehospitalizationratesofpatientswithacutepancreatitisper100,000populationare3times
higherforblacksthanwhites.Theseracialdifferencesaremorepronouncedformalesthan
females.TheriskforAfricanAmericansaged3564yearsis10timeshigherthanforanyother
group.AfricanAmericansareatahigherriskthanwhitesinthatsameagegroup.
TheannualincidenceofacutepancreatitisinNativeAmericansis4per100,000populationin
whites,5.7per100,000populationandinblacks,20.7per100,000population.[13]
Prognosis
Theoverallmortalityinpatientswithacutepancreatitisis1015%.Patientswithbiliarypancreatitis
tendtohaveahighermortalitythanpatientswithalcoholicpancreatitis.Thisratehasbeenfalling
overthelast2decadesasimprovementsinsupportivecarehavebeeninitiated.Type2diabetes
mellitushasalsobeenassociatedwithhigherseverityandmortalityinthesettingofacute
pancreatitis.[14]Inpatientswithseveredisease(organfailure),whoaccountforabout20%of
presentations,mortalityisapproximately30%.[15]Thisfigurehasnotdecreasedinthepast10
years.Inpatientswithpancreaticnecrosiswithoutorganfailure,themortalityapproacheszero.
Inthefirstweekofillness,mostdeathsresultfrommultiorgansystemfailure.Insubsequentweeks,
infectionplaysamoresignificantrole,butorganfailurestillconstitutesamajorcauseofmortality.
Acuterespiratorydistresssyndrome(ARDS),acuterenalfailure,cardiacdepression,hemorrhage,
andhypotensiveshockallmaybesystemicmanifestationsofacutepancreatitisinitsmostsevere
form.
Identifyingpatientsinthegreatestneedofaggressivemedicaltreatmentbydifferentiatingtheir
diseaseseverityasmildorsevereisrecommended.Inmilddisease,thepancreasexhibits
interstitialedema,aninflammatoryinfiltratewithouthemorrhageornecrosis,and,usually,minimal
ornoorgandysfunction.Inseveredisease,theinflammatoryinfiltrateissevere,associatedwith
necrosisoftheparenchyma,oftenaccompaniedbyevidenceofsevereglanddysfunction,andit
maybeassociatedwithmultiorgansystemfailure.
Differentstrategieshavebeenusedtoassesstheseverityofacutepancreatitisandpredict
outcome(seeWorkupandStaging).Severalclinicalscoringsystems(eg,Ransoncriteria,
Glasgow,Imrie)areavailable.TheAPACHEIIscoringsystem,thoughcumbersome,appearstobe
thebestvalidated(seetheAPACHEIIScoringSystemcalculator).Biologicalmarkershavealso
beenusedforthispurpose.Geneticmarkersarebeingstudiedandhavenotyetcomeintoclinical
use.
Peritoneallavagehasahighspecificity(93%)however,ithasalowsensitivity(54%).DynamicCT
scanningoftheabdomeniswidelyavailableandusefulinpredictingtheoutcomeofacute
pancreatitis.WhentheBalthazarcriteria(seeWorkupandComputedTomographyScanning)are
used,sensitivityis87%andspecificityis88%.
Suppiahetalexaminedtheprognosticvalueoftheneutrophillymphocyteratio(NLR)in146
consecutivepatientswithacutepancreatitis.[16]TheyfoundthatelevationoftheNLRduringthe
first48hoursofhospitaladmissionwassignificantlyassociatedwithsevereacutepancreatitisand
wasanindependentnegativeprognosticindicator.TheNLRiscalculatedfromthewhitecell
differentialandprovidesanindicationofinflammation.
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201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology
Inaretrospectivestudyofdatafrom822patientshospitalizedwithacutepancreatitis,Mikolasevic
etalfoundthatpatientswhohadnonalcoholicfattyliveratadmission(n=19824.1%)hada
statisicallyhigerincidenceofmoderatelysevere(35.4%vs14.6%)andsevereacutepancreatitis
(20.7%vs9.6%)thanthosewithoutnonalcoholicfattyliver.[17]Moreover,thesepatientshad
higher(1)Creactiveproteinlevelsnotonlyonthedayofadmissionbutalsoatday3,(2)APACHE
IIscoresatadmission,(3)CTscanseverityindex,and(4)occurrenceoforganfailureandlocal
complications.Althoughmortalitywasalsohigherinthenonalcoholicfattylivergroupcomparedto
thegroupwithoutthisdisease,thedifferencewasnotstatisticallysignificant.[17]
Complications
Acutefluidcollectionsmayoccur,typicallyearlyinthecourseofacutepancreatitis.Theseare
primarilydetectedbyimagingstudiesratherthanbyphysicalexamination.Becausetheylacka
definedwallandusuallyregressspontaneously,mostacutefluidcollectionsrequirenospecific
therapy.
Anacutepseudocystisacollectionofpancreaticfluidthatiswalledoffbygranulationtissueafter
anepisodeofacutepancreatitisitrequires4ormoreweekstodevelop.Althoughpseudocystsare
sometimespalpableonphysicalexamination,theyareusuallydetectedwithabdominal
ultrasonographyorcomputedtomography(CT).
Intraabdominalinfectioniscommon.Withinthefirst13weeks,fluidcollectionsorpancreatic
necrosiscanbecomeinfectedandjeopardizeclinicaloutcome.From3to6weeks,pseudocysts
maybecomeinfectedorapancreaticabscessmaydevelop.Apancreaticabscessisa
circumscribedintraabdominalcollectionofpus,withinorinproximitytothepancreas.Itisbelieved
toarisefromlocalizednecrosis,withsubsequentliquefactionthatbecomesinfected.
Theintestinalfloraisthepredominantsourceofbacteriacausingtheinfection.Theusualsuspects
areEscherichiacoli(26%),Pseudomonasspecies(16%),Staphylococcusspecies
(15%),Klebsiellaspecies(10%),Proteusspecies(10%),Streptococcusspecies
(4%),Enterobacterspecies(3%),andanaerobicorganisms(16%).Fungalsuperinfectionsmay
occurweeksormonthsintothecourseofseverenecrotizingpancreatitis.
Pancreaticnecrosisisanonviableareaofpancreaticparenchymathatisoftenassociatedwith
peripancreaticfatnecrosisandisprincipallydiagnosedwiththeaidofdynamicspiralCTscans.
Distinguishingbetweeninfectedandsterilepancreaticnecrosisisanongoingclinicalchallenge.
Sterilepancreaticnecrosisisusuallytreatedwithaggressivemedicalmanagement,whereas
almostallpatientswithinfectedpancreaticnecrosisrequiresurgicaldebridementorpercutaneous
drainageiftheyaretosurvive.
Hemorrhageintothegastrointestinal(GI)tract,retroperitoneum,ortheperitonealcavityispossible
becauseoferosionoflargevessels.Intestinalobstructionornecrosismayoccur.Commonbile
ductobstructionmaybecausedbyapancreaticabscess,pseudocyst,orbiliarystonethatcaused
thepancreatitis.Aninternalpancreaticfistulafrompancreaticductdisruptionoraleaking
pancreaticpseudocystmayoccur.
Intheweeks(tomonths)followingpresentation,thephysiciansattentionshiftstodevelopingsigns
ofintraabdominalinfection,pancreaticpseudocyst,intraabdominalhemorrhage,colon
perforation,obstructionorfistulization,andmultiorgansystemfailure.
PatientEducation
Educatepatientsaboutthedisease,andadvisethemtoavoidalcoholinbingeamountsandto
discontinueanyriskfactor,suchasfattymealsandabdominaltrauma.
Forpatienteducationresources,seetheCholesterolCenter,aswellasPancreatitisand
Gallstones.
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201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology
ClinicalPresentation
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MediaGallery
Suspectedacutepancreatitis.Etiologicfactorsandformsofacutepancreatitis.Ranson
criteria.
Mildpancreatitis.Favorableprognosticsignsforacutepancreatitis.Medicalmanagement
andstudiesusedforacutepancreatitis.
PrognosticindicatorsforseverepancreatitisandICUmanagement.
Diagnosisandtreatmentofnecrotizingpancreatitis.
Treatmentofandstudiesusedforpancreaticpseudocysts.
Idiopathicrecurrentpancreatitis.Etiologiesforacutepancreatitis.
Pancreaticabscess.Definitionofanabscess.
Thispatientwithacutegallstonepancreatitisunderwentendoscopicretrograde
cholangiopancreatography.Cholangiogramshowsnostonesincommonbileductand
multiplesmallstonesingallbladder.Pancreatogramshowsnarrowingofthepancreaticduct
inareaofgenu,resultingfromextrinsiccompressionofductalsystembyinflammatory
changesinthepancreas.
Pancreasdivisumassociatedwithminorpapillastenosiscausingrecurrentpancreatitis.
Becausepancreasdivisumisrelativelycommoninthegeneralpopulation,itisbestregarded
asvariantofnormalanatomyandnotnecessarilyascauseofpancreatitis.Inthiscase,note
bulbouscontourofductadjacenttocannula.Thisappearancehasbeentermed
Santorinicele.Dorsalductoutflowobstructionisaprobablecauseofpancreatitiswhen
Santoriniceleispresentandisassociatedwithaminorpapillathataccommodatesonlya
guidewire.
Normalappearingventralpancreasinapatientwithrecurrentacutepancreatitis.Dorsal
pancreas(notpictured)showedevidenceofchronicpancreatitis.
Endoscopicretrogradecholangiopancreatographyexcludedsuppurativecholangitisand
establishedthepresenceofanularpancreasdivisum.Dorsalpancreatogramshowed
extravasationintoretroperitoneum,andsphincterotomywasperformedonminorpapilla.
Pigtailnasopancreatictubewastheninsertedintodorsalductandoutintoretroperitoneal
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201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology
fluidcollection.Theotherendofthetubewasattachedtobulbsuctionandmonitoredevery
shift.
Althoughpercutaneousdrainsremoveloculatedfluidcollectionselsewhereintheabdomen,
nasopancreatictubeisdrainingtheretroperitonealfluidcollection.Oneweeklater,the
retroperitonealfluidcollectionismuchsmaller(imageisreversedinhorizontaldirection).By
thistime,patientisoffpressorsandisreadytobeextubated.
Recurrentpancreatitisassociatedwithpancreasdivisuminanelderlyman.Pancreatogram
ofthedorsalductshowsdistalstenosiswithupstreamchronicpancreatitis.Afterthestenosis
wasdilatedandstented,painresolvedandthepatientimprovedclinicallyduring1yearof
quarterlystentexchanges.FollowupCTscansshowedresolutionoftheinflammatorymass.
Althoughductalbiopsiesandcytologywererepeatedlynegative,painandpancreatitis
returnedwhenthestentswereremoved.Patientdevelopedduodenaloutflowobstructionand
wassenttosurgeryWhippleprocedurerevealedperiampullaryadenocarcinoma(ofminor
papilla).
of13
Tables
Table1.RiskFactorsforPostERCPPancreatitis.
Table1.RiskFactorsforPostERCPPancreatitis.
Acutepancreatitis(any)orahistoryofpostERCPpancreatitis
Youngerage
Femalesex
Absenceofbileductstones
Morethan10attemptstocannulatethepapillaofVater
Pancreaticductcannulation
Contrastmediuminjectionofthethepancreaticsystem
Pancreaticsphincterotomy
SphincterofOddidysfunction
BacktoList
ContributorInformationandDisclosures
Author
JeffreyCFTang,MDSeniorStaffGastroenterologist,HenryFordHealthSystem
JeffreyCFTang,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeof
http://emedicine.medscape.com/article/181364overview#a4 16/18
201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology
Gastroenterology,AmericanCollegeofPhysicians,AmericanMedicalAssociation,American
SocietyforGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.
Coauthor(s)
JohnathonTMarkus,MDFellow,DepartmentofGastroenterology,HenryFordHospital
JohnathonTMarkus,MDisamemberofthefollowingmedicalsocieties:AmericanAssociationfor
theStudyofLiverDiseases,AmericanGastroenterologicalAssociation,AmericanMedical
Association,AmericanSocietyforGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.
ChiefEditor
BSAnand,MDProfessor,DepartmentofInternalMedicine,DivisionofGastroenterology,Baylor
CollegeofMedicine
BSAnand,MDisamemberofthefollowingmedicalsocieties:AmericanAssociationfortheStudy
ofLiverDiseases,AmericanCollegeofGastroenterology,AmericanGastroenterological
Association,AmericanSocietyforGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.
AdditionalContributors
BrianSBerk,MDStLuke'sClinic
BrianSBerk,MDisamemberofthefollowingmedicalsocieties:AmericanAssociationforthe
StudyofLiverDiseases,AmericanCollegeofGastroenterology,AmericanGastroenterological
Association
Disclosure:Nothingtodisclose.
TimothyBGardner,MDAssistantProfessor,DepartmentofMedicine,DartmouthMedicalSchool
DirectorofPancreaticDisorders,SectionofGastroenterology,DartmouthHitchcockMedical
Center
TimothyBGardner,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeof
Gastroenterology,AmericanCollegeofPhysiciansAmericanSocietyofInternalMedicine,
AmericanGastroenterologicalAssociation,AmericanMedicalAssociation,AmericanPancreatic
Association,AmericanSocietyforGastrointestinalEndoscopy
Disclosure:Nothingtodisclose.
Acknowledgements
TusharPatel,MB,ChBProfessorofMedicine,OhioStateUniversityMedicalCenter
TusharPatel,MB,ChBisamemberofthefollowingmedicalsocieties:AmericanAssociationfor
theStudyofLiverDiseasesandAmericanGastroenterologicalAssociation
Disclosure:Nothingtodisclose.
FranciscoTalavera,PharmD,PhDAdjunctAssistantProfessor,UniversityofNebraskaMedical
CenterCollegeofPharmacyEditorinChief,MedscapeDrugReference
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201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology
Disclosure:MedscapeSalaryEmployment
NoelWilliams,MDProfessorEmeritus,DepartmentofMedicine,DalhousieUniversity,Halifax,
NovaScotia,CanadaProfessor,DepartmentofInternalMedicine,DivisionofGastroenterology,
UniversityofAlberta,Edmonton,Alberta,Canada
NoelWilliams,MDisamemberofthefollowingmedicalsocieties:RoyalCollegeofPhysiciansand
SurgeonsofCanada
Disclosure:Nothingtodisclose.
PaulYakshe,MDAssistantProfessorofMedicine,UniversityofMinnesota,MedicalDirectorof
PancreasandBiliaryClinic,DepartmentofMedicine,DivisionofGastroenterology,Hepatology,
andNutrition,FairviewUniversityMedicalCenter
PaulYakshe,MDisamemberofthefollowingmedicalsocieties:AmericanCollegeof
Gastroenterology,AmericanPancreaticAssociation,andAmericanSocietyforGastrointestinal
Endoscopy
Disclosure:Nothingtodisclose.
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