201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology

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.
http://emedicine.medscape.com/article/181364overview#a4 11/18
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.
http://emedicine.medscape.com/article/181364overview#a4 12/18
201767 AcutePancreatitis:PracticeEssentials,Background,Pathophysiology

ClinicalPresentation

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36.vanSantvoortHC,BesselinkMG,BakkerOJ,etal,fortheDutchPancreatitisStudyGroup.A
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37.WuBU,HwangJQ,GardnerTH,etal.LactatedRinger'ssolutionreducessystemic
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38.KimSB,KimTN,ChungHH,KimKH.Smallgallstonesizeanddelayedcholecystectomy
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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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