Acute pancreatitis SP

Pancreatitis is a dreaded condition associated with development of acute and sudden inflammation of the pancreas.

Pancreatic enzymes are released in the abdomen and cause inflammation by the damage from digestion of normal body structures, especially fat in the abdomen.

Mortality ranges from 3 percent in patients with interstitial edematous pancreatitis to 17 percent in patients who develop pancreatic necrosis.
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lethal condition care & cure
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DR SREEJOY PATNAIK

2. U&cvevFvTe DEFINITIONP
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•Pancreatitis is a condition associated with development of acute and
sudden inflammation of the pancreas.
•Pancreatic enzymes are released in the abdomen and cause
inflammation by the damage from digestion of normal body
structures, especially fat in the abdomen.
•Mortality ranges from 3 percent in patients with interstitial
edematous pancreatitis to 17 percent in patients who develop
pancreatic necrosis.
Acute Pancreatitis

3. SodgAoMpMoHgighgOiApsiMpaBsAAgHgashgOip
OHpsathop sialoshghgA Revised definitions and classification
of acute pancreatitisP
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•Definition of diagnosis of acute pancreatitis
•The diagnosis of acute pancreatitis requires two of the
following three features:
• (1) abdominal pain consistent with acute pancreatitis (acute
onset of a persistent, severe, epigastric pain often radiating to
the back)
•(2) serum lipase activity (or amylase activity) at least three
times greater than the upper limit of normal.
• (3) characteristic findings of acute pancreatitis on CECT and
less commonly MRI) or USG abdomen.
Acute Pancreatitis

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•The onset of AP is defined as the time of onset of abdominal pain (not the
time of admission to the hospital).
•The time interval between onset of abdominal pain and first admission to
the hospital should be noted.
•When patients with severe disease are transferred to a tertiary hospital,
the intervals between onset of symptoms, first admission and transfer
should be noted.
• Data recorded from a tertiary care hospital should be stratified to allow
separate consideration of the outcomes of patients who were admitted
directly and those admitted by transfer from another hospital.
Acute Pancreatitis

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•Acute pancreatitis (AP) is one of the most common disease of the gastrointestinal tract, leading to
tremendous emotional, physical, and financial human burden.
•Recent studies show the incidence of AP varies between 4.9 and 73.4 cases per 100,000 worldwide
•Mortality
–2-3% overall mortality from acute pancreatitis
•Tertiary centers report rates of 15- 30%
–Interstitial pancreatitis (1%)
–Necrotizing pancreatitis/organ failure (30%)
•Physician office visits
–911,000 per year

Hospitalizations
–230,000 in 2002
•Deaths
–2500 per year
Acute Pancreatitis

6. UoHgighgOipOHphu oApOHpsathop sialoshghgA Definition of types of acute pancreatitis
Acute PancreatitisPaaMl giUphMphNopPhSsihsp
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According to the Atlanta
classification, Acute Pancreatitis can
be divided into two broad categories +n viholAhghgsBpoMo,shOtApp sialoshghgAn
2npeoalOhgJgi'p sialoshghgAp
1.Interstitial edematous pancreatitis.
2. Necrotizing pancreatitis

7. viholAhghgsBpoMo,shOtAp sialoshghgA Interstitial edematous pancreatitis
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The majority of patients with AP have diffuse (or occasionally localised)
enlargement of the pancreas due to inflammatory oedema. (75-80% )
On CECT, the pancreatic parenchyma shows
relatively homogeneous enhancement, and the peripancreatic fat usually
shows some inflammatory changes of haziness or mild stranding.
There may also be some peripancreatic fluid .
The clinical symptoms of interstitial oedematous pancreatitis usually
resolve within the first week.

8. A 63-year-old man with acute interstitial oedematous pancreatitis.
Banks P A et al. Gut 2013;62:102-111
Copyright © BMJ Publishing Group Ltd & British Society of Gastroenterology. All rights reserved.

9. Acute PancreatitiseoalOhgAgi'p sialoshghgA
Necrotising pancreatitisPLOthp8=+;<pOHp shgoihApModoBO pioalOAgApOHphDop sialoshgap
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gidOBdgi'pLOhDphDop sialosApsiMp olg sialoshgaphgAAtoApsiMpBoAAp
aO,,OiBupsApioalOAgApOHpOiBuphDop olg sialoshgaphgAAto(psiMp
lsloBupOHphDop sialoshgap sloiaDu,spsBOion
About 5–10% of patients develop necrosis of the pancreatic
parenchyma, the peripancreatic tissue or both.
Necrotising pancreatitis most commonly manifests as necrosis
involving both the pancreas and peripancreatic tissues and less
commonly as necrosis of only the peripancreatic tissue, and
rarely of the pancreatic parenchyma alone.

10. (A) Acute necrotic collections (ANC) in a 44-year-old man with acute necrotising pancreatitis
involving only the peripancreatic tissues.
Banks P A et al. Gut 2013;62:102-111
Copyright © BMJ Publishing Group Ltd & British Society of Gastroenterology. All rights reserved.

11. viHoahoMp sialoshgapioalOAgA Infected pancreatic necrosisP
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• Necrosis is variable, may remain solid or liquefy, remain sterile or
become infected, persist, or disappear over time.
• occurs > the first week.
•Infected pancreatic necrosis is important because of the need for
antibiotic treatment and likely active intervention.
•The presence of infection - extraluminal gas in the pancreatic and/or
peripancreatic tissues on CECT or PFNA is positive for bacteria and/or
fungi on Gram stain and culture.
• There may be suppuration (pus) associated with the infected
pancreatic necrosis, leading to liquefaction – abscess
Acute Pancreatitis

12. A 47-year-old man with acute necrotising pancreatitis complicated by infected pancreatic
necrosis.
Banks P A et al. Gut 2013;62:102-111
Copyright © BMJ Publishing Group Ltd & British Society of Gastroenterology. All rights reserved.

13. cA4vUp3TAA&3FvTeEpvepPypS&BvE&UpPFAPeFPp
3APEEvcv3PFvTepIpvFEpveF&SB&eFvTe FLUID COLLECTIONS IN AP REVISED ATLANTA
CLASSIFICATION & ITS INTERVENTION
Acute Pancreatitis

14. Acute Pancreatitis

15. yDsAoApOHpsathop sialoshghg A Phases of acute pancreatitisEuAho,gapMgAhtlLsiaoAploAtBhpHlO,phDopDOAhploA OiAophOpBOasBp sialoshgapgi7tlunp
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Systemic disturbances result from the host response to local pancreatic injury.
Is usually over by the end of the 1st wk or extend to 2nd wk.
Cytokine cascades are activated by the pancreatic inflammation which manifest
clinically as the SIRS. An increased risk of developing OF.
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The determinant of the severity in this phase is primarily the presence and
duration of OF.
Transient OF -if the organ failure resolves within 48 h
 
Persistent OF - if organ failure persists for >48 h.
 
Multiple organ failure (MOF) – If OF affects > 1organ system.
Acute Pancreatitis&PSAGpyEPE&
EARLY PHASE

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•SIRS—defined by presence of two or more criteria:
• HR >90 beats/min
• Core temperature <36°C or >38°C
• WBC count <4000 or >12000/mm
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• Respiration >20/min or PCO
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<32 mm Hg
   
Acute Pancreatitis

17. VlpasOTlAa Late phaseP
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•The late phase is characterised by

-Persistence of systemic signs of inflammation or by the presence of local complications, --
occurs only in patients with moderately severe or severe acute pancreatitis.
•- Local complications evolve during the late phase.
•-It is important to distinguish the different morphologic characteristics of the local complications
by radiologic imaging.
•- Persistent OF, however, remains the main determinant of severity, so characterisation of AP in
the late phase requires both clinical and morphologic criteria.
•The SIRS of the early phase may be followed by a Compensatory anti-inflammatory response
syndrome (CARS) that may contribute to an increased risk of infection.
Acute Pancreatitis

18. 3APEEvcv3PFvTepP33TSUve5pFTpE&B&SvFG CLASSIFICATION ACCORDING TO SEVERITY
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1. Mild acute pancreatitis, which is characterized by the absence
of organ failure and local or systemic complications

2. Moderately severe acute pancreatitis, which is characterized
by no organ failure or transient organ failure (<48 hours) with
systemic or local complications

3. Severe acute pancreatitis, which is characterized by
persistent organ failure (>48 hours) that may involve single or
multiple organs

19. GoegAo pPhSsihspaSsAAgIgashgMip Revised Atlanta classification P
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•According to the revised Atlanta classification of AP is clinically defined by at
least the first two of three features:
• (a) abdominal pain (epigastric often radiating to the back),
• (b) serum amylase and lipase levels three or more times normal (imaging is
to be used if the elevated values are ,3 times normal)
• (c) characteristic findings on CT, magnetic resonance (MR) imaging, or
transabdominal ultrasonographic (US) studies.
•If AP is diagnosed on the basis of the first two criteria with no systemic sign of
severe SIRS or persistent OF , CECT may not be necessary for determining
patient care.
Acute Pancreatitis

20. 7(*5859: ETIOLOGY

22. Dsialoshgap*i;tl& Pancreatic InjuryPViMlLsSpDsialoshgapoi,&Lo
PahgeshgMipgiAg opsagislpaoSSAp
Abnormal Pancreatic enzyme
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<S&AMAMLoApgiAg opsagislpaoSSAp
Colonization of zymogen granules
&lysosomes inside acinar cells Dsialoshgapo oLs
Pancreatic edema
Auto-digestion of normal
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2&hM1gioApIlMLpsagislpaoSSA
Release of Pro-inflammatory
Cytokines from acinar cells(+6u=
TNF-α*8u,EJE<p>p IL-1,2,& 6 *8u,Hp<p*8u,p IL-10 & IL-1
(Anti inflammatory mediators) Pathophysiology
Pathophysiology

23. (NoAopLo gshMlApylMysUshophNoploAyMiAopSMasSS&p<p
A&AhoLgasSS&p? These mediators propagate the response locally &
systemically >(+6pE*8EpiothlMyNgSAp<pLsalMyNsUoApsloploSosAo pgihMp
hNopysialoshgapysloiaN&Lsp?ploSosAopMIpLMlop
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IsahMlAp<p8otaMhlgoioAT
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loAyMiAo?
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Severe cases- inflamm. Response > localised
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localised SIRGoAhp,H'upLsAAgeoploSosAopMIpgiISsLTpno gshMlApgihMp
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Rest 10%- massive release of inflam. Mediators into
systemic circulation > SIRS and OF.

24. 2SgigasSpLsigIoAhshgMiA0 Clinical manifestations:P
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•ABDOMINAL PAIN- ( cardinal symptom) characteristically dull,boring &
steady; sudden in onset ,gradually becomes severe > constant ache.
•Location- epigastric & or peri-umbilical that radiates to the back & is
constant
•NAUSEA & VOMITING – 90%- does not relieve pain. sometimes anorexia
/diarrhea
•Fever (76%),Tachycardia (65%), Hypotension ( 73%)
•Abdominal tenderness, muscle guarding (68%),distension (65%),diminished or
absent bowel sounds.
•Jaundice (28%),Dyspnea (10%),tachypnea, basal rales left lung.
• Severe cases- haemodynamic instability (10%),haematemesis or malena (5%);
pale, diaphoretic, & listless appearance.
• Occasionally, muscular spasm of extremities secondary to hypocalcemia.
Acute Pancreatitis

25. 2SgigasSpLsigIoAhshgMiA0 Clinical manifestations:P
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P
JT 9lo&u(tliolpAgUi uplo gANpVlMFip gAaMSMlshgMipsSMiUphNopISsi1AploAtShgiUpIlMLp
lohlMyolghMiosSpVSMM p gAAoahgiUpsSMiUphgAAtopySsioAEpLMlopaMLLMiS&pyshgoihApNseopsp
lt &pol&hNoLspgiphNopISsi1ApAoaMi sl&phMpoChlsesAsho pysialoshgapoCt shoT
P
7l&hNoLshMtApA1gipiM tSoAEp tAtsSS&pDp,paLEh&ygasSS&pSMasho pMipoChoiAMlpA1gip
AtlIsaoABpyMS&slhN lghgAn
P
DSotlsSpoIItAgMiApBIStg pgiphNopVsAoApMIphNopySotlsSpasegh&O
P
9lEiFsS pAgUip BsyyoslsiaopMIpoaaN&LMAgAEpSslUopVltgAoEpslMti phNoptLVgSgatAp tophMp
SMasSphMCgapSoAgMipMIphNopeoAAoSAO
P
FGlhoHApAgUip BysgipMlploAgAhsiaopgiphNop,MiopFNolophNopNos pMIpysialosApgApSMasho pBgip
oygUsAhlgtLEp>@cpaLpsVMeophNoptLVgSgatAOO
pppp p FsLoiaNg1HApAgUip BysgipFghNpyloAAtlopti olphNopCgyNMg pylMaoAAO
pppppp ns&MuGMVAMiHApAgUip BysgipFNgSopyloAAgiUpshphNophMypMIphNopsiUSopSsholsSphMphNop7loahMlp
AygisopLtAaSoApsi pVoSMFphNopSoIhp,JhNplgVpBSoIhpaMAhMeolhoVlsSpsiUSopB2IPOO
•Uncommon findings associated with severe necrotizing pancreatitis:
•1.Cullens sign- bluish discolouration around the umbilicus resulting from
haemoperitoneum.
•2.Grey-Turner sign- reddish brown discoloration along the flanks resulting from
retroperitoneal blood dissecting along tissue planes, more commonly patients have a
ruddy erythema in the flanks secondary to extravasated pancreatic exudate.
•Erythematous skin nodules, usually < 1 cm,typically located on extensor skin
surfaces; polyarthritis.
•Pleural effusions (fluid in the bases of the pleural cavity)
•Grünwald sign (appearance of ecchymosis, large bruise, around the umbilicus due to
local toxic lesion of the vessels)
•Körte's sign (pain or resistance in the zone where the head of pancreas is located (in
epigastrium, 6–7 cm above the umbilicus))
Kamenchik's sign (pain with pressure under the xiphoid process)
Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector
spinae muscles and below the left 12th rib (left costovertebral angle (CVA))

26. P/EP
n*8/p(5pn5/7GP(7p7D*9P4(G*2p(7+/7G+744
P
PJ/5n*+P8p/*4(7+4*5+
P
97+7GP8pG7J53+/p<pPJ/5n*+P8pG*9*/*(:
P
2.74(pG(Tp4*/7p@p/388+744p5+pD7G2344*5+p?pG(TpD873GP8p
76634*5+T
P
/72G7P47/pJG7P(.p453+/4p5+pG(p4*/7
•MILD TO MODERATE EPIGASTRIC TENDERNESS
•ABDOMINAL DISTENSION
•GENERAL REBOUND & ABDOMINAL RIGIDITY
•CHEST RT. SIDE – DULLNESS ON PERCUSSION > RT. PLEURAL
EFFUSION.
•DECREASED BREATH SOUNDS ON RT SIDE
Acute Pancreatitis

27. 3tBBoiLApAg'i Cullen’s sign
Acute Pancreatitis

28. 5lsupFtliolLA Gray Turner’s
Acute Pancreatitis

29. 3Avev3PApyS&Uv3FTSE CLINICAL PREDICTORSP
3BgigasBp7tM',oihp
P
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P
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P
EDOlhphg,opgiholdsBphOpAu, hO,pOiAoh
P
p TLoAghu
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P
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P
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P
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•Clinical judgment
•Older age
•Alcoholic pancreatitis
•Short time interval to symptom onset
• Obesity
•Organ failure
•LABORATORY AND RADIOLOGIC
PREDICTORS
•Hemoconcentration
•C-reactive protein
•Blood urea nitrogen
•Serum creatinine
•Other serum markers
•Chest radiographs
•CT scan
•MRI and MRCP
Acute PancreatitisE3TSve5pEGEF&)E
SsiAOiMApalgholgsp
FDopPyP3E&pvvpAaOlop
EvSEpAaOlo
KvEPypAaOlop
Esl,BoAApsathop sialoshghgApAaOlo
Tl'sipHsgBtlo9LsAoMpAaOloAp
3FpAodolghupgiMo?pKsBhDsJslpAaOlo
SCORING SYSTEMS
Ranson's criteria
The APACHE II score
SIRS score
BISAP score
Harmless acute pancreatitis score
Organ failure-based scores
CT severity index Balthazar score

30. *+I74(*9P(*5+4pupJ*52.7n*2P8 INVESTIGATIONS - BIOCHEMICALP
2J2psi pNoLshMalgh
P
PL& SsAopsi pSgysAo
P
86(pEp99(
P
4oltLpoSoahlMS&hoAEpJ3+EpaloshgigioEpUStaMAoEp8gyg pDlMIgSoT
P
2ulosahgeopylMhogi
P
5hNolphoAhA
P
u PJ9
P
u 8sahgap oN& lMUoisAopB8/.OEppsi p.25dpSoeoSA
P
u p*U9vppSoeoSA
P
u (l& yAgipsi pghApyloatlAMlphl&yAgiMUoiuJpgipVMhNphNoptlgiopsi phNop yolghMiosSp
IStg
•CBC and hematocrit
•Amylase and lipase
•LFT , GGT
•Serum electrolytes, BUN, creatinine, glucose, Lipid Profile.
•C-reactive protein
•Other tests
•-ABG
•-Lactic dehydrogenase (LDH), and HCO3 levels
•- IgG4 levels
•-Trypsin and its precursor trypsinogen-2 in both the urine and the peritoneal
fluid
Acute Pancreatitis

31. P
PL&SsAopMlpSgysAopSoeoSApshpSosAhp?pdphgLoApsVMeoppu gsUiMAhgapMIpPDT
P
4oltLpsL&SsAop oholLgishgMiApslopiMhpAyoagIgapIMlpPD
P
PL&SsAopDpSoeoSpgApLMlopAyoagIgaphMpysialoshgapyshNMSMU&
P
6sSAopKpgiupp4P*5EpLoAoiholgapgAaNoLgsEphtVMuMeslgsip gAosAoEploisSpgiAtIIgagoia&EpMlp
LsalMsL&SsAoLgsTp
P
(NopAoltLpNsSIuSgIopMIpsL&SsAopgApANMlhEpsi poSoeshgMiApUoiolsSS&plohtliphMploIoloiaop
lsiUoApFghNgipspIoFp s&A n
P
8gysAopNsApspASgUNhS&pSMiUolpNsSIuSgIopT
P
7Soesho pSgysAopSoeoSApslopLMlopAyoagIgaTp8gysAopSoeoSAploLsgipNgUNpIMlp,Jp s&A
P
p P8DEp4JEpP4(Epsi pP8(pSoeoSAphMpAoslaNpIMlpoeg oiaopMIpUsSSAhMiopysialoshghgATp
P
PipP8(pSoeoSpNgUNolphNsip,)Hp3-8pAtUUoAhApUsSSAhMiopysialoshghgApsi pspLMlop
ItSLgisihp gAosAopaMtlAoT •Amylase or lipase levels at least > 3 times above -diagnostic of AP.
•Serum amylase determinations are not specific for AP
•Amylase P level is more specific to pancreatic pathology
•False + in- SAIO, mesenteric ischemia, tubo-ovarian disease, renal insufficiency, or
macroamylasemia.
•The serum half-life of amylase is short, and elevations generally return to reference
ranges within a few days.
•Lipase has a slightly longer half-life .
•Elevated lipase levels are more specific. Lipase levels remain high for 12 days
• ALP, SB, AST, and ALT levels to search for evidence of gallstone pancreatitis.
•An ALT level higher than 150 U/L suggests gallstone pancreatitis and a more
fulminant disease course.
Acute Pancreatitis

32. P
PaPthopysilg AiBDBOttMtINL USEttt&DAVtMtBpTGpFApetviogGirvViFylopcrthd,HOtlpooBnt
P
JFtceGDBBDiFtVpGcAilrDAtucoyptTrpcAprtAVcFt'()t*tVcBt+ppFtvriviBpetcBtctBpFBDADupt
GpcByrpti,tGirptBpuprpteDBpcBp
P
t P*rpclADuptvriApDFthP-dOtucoyptlcFt+pti+AcDFpetN'*'.tViyrBtc,AprtvrpBpFAcADiFtAitvriuDept
BiGptDFeDlcADiFti,tvriTFiBDBnt
P
/DTVprtopupoBtVcupt+ppFtBVi&FtAitlirrpocApt&DAVtctvrivpFBDAgtAi&cretJ0tn
P
t 1tP-dtucoyptDFteiy+opt,DTyrpBthDpLt2tI tGTUeEOtBAriFTog tDFeDlcApBtBpuprptvcFlrpcADADBn
P
t P-dtDBtcFtclyAp*vVcBptrpclAcFAtAVcAtDBtFiAtBvplD,Dlt,irtvcFlrpcADADBn •CBC (leukocytosis) > 12,000/µL with > segmented polymorphonuclear (PMN) cells.
•On admission hematocrit value greater than 47% - has been proposed as a sensitive
measure of more severe disease
• C-reactive protein (CRP) value can be obtained 24-48 hours after presentation to provide
some indication of prognosis.
•Higher levels have been shown to correlate with a propensity toward OF .
• A CRP value in double figures (ie, ≥ 10 mg/dL) strongly indicates severe pancreatitis.
• CRP is an acute-phase reactant that is not specific for pancreatitis.
Acute Pancreatitis

33. P
3ucoycApt1a4tD,tctvcADpFAtDBtegBvFpDlnt
P
5VpAVprtAclVgvFpctDBteyptAitclyAptrpBvDrcAirgteDBArpBBtBgFeriGpth1-67Otirt
eDcvVrcTGcADltDrrDAcADiFtGyBAt+ptepAprGDFpen
P
E6/Lta8HLtcFet/PJ9topupoBtBViyoet+ptGpcByrpet+iAVtcAtceGDBBDiFtcFetcAt'.tViyrBt
DFtireprtAitVpovtepAprGDFptAVpt-cFBiFtlrDAprDct,irtByruDucon
P
:GGyFiToi+yoDFt4'th:T4'OtopupoBtlcFt+ptlVplspetAitpucoycApt,irtcyAiDGGyFpt
vcFlrpcADADB
P
;rg vBDFtcFetDABtvrplyrBirtArg vBDFiTpF*Nt*tDFt+iAVtAVptyrDFptcFetAVptvprDAiFpcot,oyDet
Vcupt+ppFtpucoycApetcBtviBBD+optGcrsprBt,irtclyAptvcFlrpcADADBthpBvplDcoogtviBA*
3-PdtvcFlrpcADADBn •Evaluate ABG if a patient is dyspneic.
•Whether tachypnea is due to acute respiratory distress syndrome (ARDS) or
diaphragmatic irritation must be determined.
•LDH, BUN, and HCO3 levels should be measured both at admission and at 48 hours
in order to help determine the Ranson criteria for survival.
•Immunoglobulin G4 (IgG4) levels can be checked to evaluate for autoimmune
pancreatitis
•Trypsin and its precursor trypsinogen-2 - in both the urine and the peritoneal fluid
have been evaluated as possible markers for acute pancreatitis (especially post-
ERCP pancreatitis.
Acute Pancreatitis

34. 1+eiGDFcot-ceDiTrcvVg Abdominal RadiographyP
1+eiGDFcotrceDiTrcvVBtVcuptctoDGDApet
rioptDFtclyAptvcFlrpcADADBnt
P
<8atrceDiTrcvVgtDFttyvrDTVAtviBDADiFtDBt
vrDGcrDog tvpr,irGpetAitepAplAt,rpptcDrtDFt
AVptc+eiGpFLtDFeDlcADFTtctvpr,ircApet
uDBlyBLtcBt&iyoet+ptAVptlcBptDFtct
vpFpArcADFTLtvpr,ircApeteyiepFcotyolprnt
P
:FtBiGptlcBpBLtAVptDF,ocGGcAirg tvrilpBBt
Gcg tecGcTptvprDvcFlrpcADltBArylAyrpBLt
rpByoADFTtDFtctlioiFtlyA*i,,tBDTFLtctBpFADFpot
oiivLtirtcFtDopyBnt
P
;VptvrpBpFlpti,tlcolD,DlcADiFBt&DAVDFtirt
criyFetAVptvcFlrpcBtGcg tDFeDlcAptlVriFDlt
vcFlrpcADADBn
•Abdominal radiographs have a limited
role in acute pancreatitis.
•KUB radiography in upright position is
primarily performed to detect free air in
the abdomen, indicating a perforated
viscus, as would be the case in a
penetrating, perforated duodenal ulcer.
•In some cases, the inflammatory process
may damage peripancreatic structures,
resulting in a colon cut-off sign, a sentinel
loop, or an ileus.
•The presence of calcifications within or
around the pancreas may indicate chronic
pancreatitis.
Acute Pancreatitis

35. 8oArcBiFiTrcvVg UltrasonographyP
874thtBlrppFDFTtOi,tAVptc+eiGpFtDBt
AVptGiBAtyBp,yotDFDADcotApBAtDFt
epAprGDFDFTtAVptpADioiTg ti,t
vcFlrpcADADBtcFetDBtAVptAplVFD=ypti,t
lViDlpt,irtepAplADFTtTcooBAiFpBn
P
t 7pFBDADuDAgtDBtrpeylpetAit( *. )n
htdcFlrpcADADBtO
P
t :FtceeDADiFLtAVptc+DoDAgtAitDepFAD,gt
lViopeilVioDAVDcBDBtDBtoDGDApentt
P
HiAtBvplD,DltD,tiuprog DFTtTcBt
BVcei&BtBpliFecrg tAit+i&pot
eDBApFADiFtcrptvrpBpFAnt
P
PcFFiAtGpcByrptAVptBpuprDAgti,t
eDBpcBpn
•USG ( screening )of the abdomen is
the most useful initial test in
determining the etiology of
pancreatitis and is the technique of
choice for detecting gallstones.
• Sensitivity is reduced to 70-80%.
( Pancreatitis )
• In addition, the ability to identify
choledocholithiasis is limited.
•Not specific if overlying gas
shadows secondary to bowel
distention are present.
•Cannot measure the severity of
disease.

36. 3FeiBlivDltyoArcBiFiTrcvVg*t387 Endoscopic ultrasonography- EUSP
t
P
*:BtcFtpFeiBlivDltvrilpeyrptAVcAtcooi&Btct
VDTV*,rp=ypFlg tyoArcBiyFetArcFBeylprtAit+pt
DFBprApetDFAitAVptTcBAriDFApBADFcoth4:OtArclAtAit
uDBycoD>ptAVptvcFlrpcBtcFetAVpt+DoDcrgtArclAn
P
:ABtvrDFlDvcotrioptDBtDFttepAplADiFti,t
GDlrioDAVDcBDBtcFetvprDcGvyoocrg topBDiFBn
P
1tBplrpADF*BADGyocApet387tBAyegt?
P
*Gcg trpupcotrpBDBAcFlptAiteylAcotiyA,oi&tcAt
AVptopupoti,tAVptvcvDoocLtt,irtpucoycADiFti,tt
rplyrrpFAtDeDivcAVDltvcFlrpcADADBn
•
•-Is an endoscopic procedure that allows a
high-frequency ultrasound transducer to be
inserted into the gastrointestinal (GI) tract to
visualize the pancreas and the biliary tract.
•Its principal role is in detection of
microlithiasis and periampullary lesions.
•A secretin-stimulated EUS study –
•-may reveal resistance to ductal outflow at
the level of the papilla, for evaluation of
recurrent idiopathic pancreatitis.
Acute Pancreatitis

37. PiGvyApet;iGiTrcvVg Computed TomographyP
1+eiGDFcottP;tDBttFiAtDFeDlcApet,irtvcADpFABt&DAVtGDoetvcFlrpcADADBnt
P
1o&cgBtDFeDlcApetDFtBpuprpt1dtcFetDBtAVptDGcTDFTtBAyeg ti,tlViDlpt,irtcBBpBBDFTt
liGvoDlcADiFBnt
P
7lcFBteiFptc,AprtMt(NtViyrBtc,AprtBgGvAiGtiFBpAtyFopBBtAVpteDcTFiBDBtDBt
yFlprAcDFLt+plcyBptDF,ocGGcAirgtlVcFTpBtcrpti,ApFtFiAtrceDiTrcvVDlcoog tvrpBpFAt
yFADotAVDBtADGpn
P
1+eiGDFcotP;tBlcFBtcoBitvriuDeptvriTFiBADltDF,irGcADiFt+cBpetiFtAVpt
,iooi&DFTtTrceDFTtBlcoptepupoivpet +gtacoAVc>crt@tlioopcTypBn
P
4rcept1t*tHirGcotvcFlrpcB
P
4rceptat*t0ilcotirteD,,yBptTocFetpFocrTpGpFAt
P
4rceptPt*t:FArDFBDltTocFetc+FirGcoDAg trpliTFD>pet+gtVc>DFpBBtiFtAVptBlcF
P
4rcept6t*t7DFToptDoo*ep,DFpetliooplADiFtirtvVopTGiF
P
4rcept3t*t;&itirtGirptDoo*ep,DFpetliooplADiFBtirtAVptvrpBpFlpti,tTcBtDFt
irtFpcr+gtAVptvcFlrpcB
•Abdominal CT is not indicated for patients with mild pancreatitis.
•Always indicated in severe AP and is the imaging study of choice for assessing
complications.
•Scans done after > 72 hours after symptom onset unless the diagnosis is
uncertain, because inflammatory changes are often not radiographically present
until this time.
•Abdominal CT scans also provide prognostic information based on the
following grading scale developed by Balthazar & colleagues.
•Grade A - Normal pancreas
•Grade B - Focal or diffuse gland enlargement
•Grade C - Intrinsic gland abnormality recognized by haziness on the scan
•Grade D - Single ill-defined collection or phlegmon
•Grade E - Two or more ill-defined collections or the presence of gas in
or nearby the pancreas
Acute Pancreatitis

38. Pat CT
Acute Pancreatitis

39. hoppysiltgAtPa Gallsone AP CT
Acute Pancreatitis

40. AlBDtOoiMBloIDMtNpLD Peri pancreatic fluid
Acute Pancreatitis

41. AoiMBloIDMtilMBsyDy Pancreatic necrosis
Acute Pancreatitis

42. UlMBsyDytStOBsEBlyyDsi Necrosis - progression
Acute Pancreatitis

43. P ;VptlVcFlpBti,tDF,plADiFtcFetepcAVtcrptuDrAycoogtFDotDFtTrcepBt1tcFetat
+yAtBApceDog tDFlrpcBptDFtTrcepBtPtAVriyTVt3nt
P dcADpFABt&DAVtTrcept3tvcFlrpcADADBtVcuptctA )tlVcFlpti,tepupoivDFTtcFt
DF,plADiFtcFetctIA)tlVcFlpti,tegDFTn •The chances of infection and death are virtually nil in grades A and B
but steadily increase in grades C through E.
•Patients with grade E pancreatitis have a 50% chance of developing an
infection and a 15% chance of dying.
Acute Pancreatitis

44. ,cTFpADlt-pBiFcFlptPViocFTDivcFlrpcAiTrcvVg
,-Pd Magnetic Resonance Cholangiopancreatography
MRCPP
pen t,-PdtVcBtcFtpGprTDFTtrioptDFtAVpteDcTFiBDBti,tByBvplApet+DoDcrg tcFetvcFlrpcADlt
eylAti+BArylADiFtDFtAVptBpAADFTti,tvcFlrpcADADBnt
P
,-PdtDBtFiAtcBtBpFBDADuptcBt3-PdtLtDAtDBtBc,prLtFiFDFucBDupLtcFet,cBALtcFetDAt
vriuDepBtDGcTpBtyBp,yotDFtTyDeDFTtloDFDlcotlcrpteplDBDiFBnt
P
,-PdtBViyoet+ptyBpetD,tlViopeilVioDAVDcBDBtDBtByBvplApet+yAtAVprptDBtliFlprFtAVcAt
vcFlrpcADADBtGDTVAt&irBpFtDB
P
:,t3-PdtDBtvpr,irGpen
•ed. MRCP has an emerging role in the diagnosis of suspected biliary and pancreatic
duct obstruction in the setting of pancreatitis.
•MRCP is not as sensitive as ERCP , it is safer, noninvasive, and fast, and it
provides images useful in guiding clinical care decisions.
•MRCP should be used if choledocholithiasis is suspected but there is concern that
pancreatitis might worsen is
•If ERCP is performed.
Acute Pancreatitis

45. &VPA ERCPP
3-PdtDBtcFtpFeiBlivDltvrilpeyrptyBpetAit
pucoycAptAVpt+DoDcrgtcFetvcFlrpcADlteylAcot
Bg BApGtcFetDBtDFeDlcApetDFtctBy+BpAti,tvcADpFABt
&DAVtclyAptvcFlrpcADADBn
P
t 3BArpGptlcyADiFtDFtvcADpFABt&DAVtclyApt
vcFlrpcADADBtcFetBViyoetFpuprt+ptyBpetcBtct,DrBA*
oDFpteDcTFiBADltAiiotDFtAVDBteDBpcBpn
P
:AtBViyoet+ptvpr,irGpetiFog tDFtAVpt,iooi&DFTt
BDAycADiFBC
P
:H6:P1;:JH7tC
P
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pBvprDpFlDFTt&irBpFDFTtDcyFeDlptcFetloDFDlcot
epAprDircADiFtepBvDAptGcBDGcotByvvirADupt
AVprcvgn
P
5VpFtliG+DFpet&DAVtBvVDFlApriAiGgtcFet
BAiFptpBArclADiFLt3-PdtGcg trpeylptAVptopFTAVt
i,tViBvDAcotBAcg LtAVptliGvoDlcADiFtrcApLtcFeLt
viBBD+ogLtGirAcoDAg n
•ERCP is an endoscopic procedure used to
evaluate the biliary and pancreatic ductal
system and is indicated in a subset of patients
with acute pancreatitis.
• Extreme caution in patients with acute
pancreatitis and should never be used as a first-
line diagnostic tool in this disease.
•It should be performed only in the following
situations:
•INDICATIONS :
•The patient has biliary pancreatitis and is
experiencing worsening jaundice and clinical
deterioration despite maximal supportive
therapy.
•When combined with sphincterotomy and
stone extraction, ERCP may reduce the length
of hospital stay, the complication rate, and,
possibly, mortality.
Acute Pancreatitis

46. PatTGoElShLD l tgyODBoIDsitoi tFBoDioEl CT Image-Guided Aspiration and DrainageP
P;*TyDepetFppeoptcBvDrcADiFtDBtyBpetAiteD,,prpFADcAptDF,plApetFplriBDBt,riGtBAprDopt
FplriBDBtDFtvcADpFABt&DAVtBpuprptFplriAD>DFTtvcFlrpcADADBnt
P
;VptFppeoptDBtvoclpetDFAitcFtcrpcti,toi&tcAApFycADiFtDFtirtcriyFetAVptvcFlrpcBti,tct
vcADpFAt&DAVt,puprtcFetAclVglcreDctirtiAVprtBDTFBti,tct7:-7tLtTpFprcoog t,iooi&DFTtAVpt
,DrBAt&ppsti,tBpuprptvcFlrpcADADBnt
P
;VptvrilpeyrptGcg t+ptrpvpcApet&ppsogtD,tloDFDlcoogtDFeDlcApen
P
;VptBvplDGpFtBViyoet+ptepoDuprpetAitAVptoc+ircAirg t&DAVDFtcFtViyrtcFetDFAprvrpApet
vriGvAogn
P
t
P
;VptBvplDGpFtBViyoetco&cgBt+ptpucoycApet,irt4rcGtBAcDFLtcFetPU7tBAyegnt
P
:,tAVpt4rcGtBAcDFtBVi&Bt+clAprDctirt,yFTDLtByrTDlcotep+rDepGpFAti,tAVptDF,plApet
FplriBDBtDBtTpFprcoog tDFeDlcApent
P
1FtpBlpvADiFt&iyoet+ptD,tAVptvcADpFAtliyoetFiAtAioprcAptByrTprg EtDFtAVDBtlcBpLtP;*
TyDepetlcAVpAprtercDFcTptGcgt+ptGirptp,,plADupn
•CT-guided needle aspiration is used to differentiate infected necrosis from sterile
necrosis in patients with severe necrotizing pancreatitis.
•The needle is placed into an area of low attenuation in or around the pancreas of a
patient with fever and tachycardia or other signs of a SIRS , generally following the
first week of severe pancreatitis.
•The procedure may be repeated weekly if clinically indicated.
•The specimen should be delivered to the laboratory within an hour and interpreted
promptly.
•
•The specimen should always be evaluated for Gram stain, and C/S study.
•If the Gram stain shows bacteria or fungi, surgical debridement of the infected
necrosis is generally indicated.
•An exception would be if the patient could not tolerate surgery; in this case, CT-
guided catheter drainage may be more effective.
Acute Pancreatitis

47. eDyIspsEDMopttvDi DiEy Histological FindingsP
;VptDF,DFDAptBvplAryGti,tvcFlrpcADADBtBpuprDAg tDBtyBycoogtBy+eDuDepetDFAitGDoet
cFetBpuprptlcApTirDpBtcBt,iooi&BC
P
,DoetvcFlrpcADADBt*t;VptTocFetpBVD+DABtDFAprBADADcotpepGctcFetcFtDF,ocGGcAirg t
DF,DoArcApt&DAViyAtVpGirrVcTptirtFplriBDBLtyBycoog t&DAVtGDFDGcotirtFitirTcFt
egB,yFlADiFt
P
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vcrpFlVgGctcrptvrpBpFALti,ApFtcBBilDcApet&DAVtBpuprptTocFeteg B,yFlADiFtcFet
GyoADtirTcFtt,cDoyrpn
•The infinite spectrum of pancreatitis severity is usually subdivided into mild
and severe categories as follows:
•Mild pancreatitis - The gland exhibits interstitial edema and an inflammatory
infiltrate without hemorrhage or necrosis, usually with minimal or no organ
dysfunction
•Severe pancreatitis - Extensive inflammation and necrosis of the pancreatic
parenchyma are present, often associated with severe gland dysfunction and
multi organ failure.
Acute Pancreatitis

48. Vo DoIDsitsNtOoDi Radiation of pain
Acute Pancreatitis

49. grr&rrc&Uatdvtr&,&VTaHtnraghTUhtdvtgJA ASSESSMENT OF SEVERITY –STAGING OF A.PP
Pathotpysoiltg
P
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p yOiB,pUiOaDltltOpLO&OLp41p,g5 (poipLovOiFp
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•Ranson Scoring
•Acute Physiology and Chronic Health Evaluation (APACHE) II,
•Glasgow
•BISAP Scoring
•Balthazar CTSI scoring systems.
•Each has advantages and disadvantages, and none is currently recognized as a
criterion standard.
Evidence of ORGAN FAILURE:
Systolic B.P below 90 mm Hg,
Arterial partial pressure of oxygen [Pa O2] 60 mm Hg or lower,
Serum Creatinine level -2 mg/dL or lower,
GI bleeding amounting to 500 mL or more in 24 hrs
•Local complications (eg, necrosis, abscess, pseudocyst)
•Ranson score of 3 or higher or
•APACHE score of 8 or higher
•
•.
Acute Pancreatitis

50. VoiysitrMsBl Ranson ScoreP
-cFBiFtlrDAprDctDBtctloDFDlcotvrpeDlADiFtryopt,irtvrpeDlADFTtAVptBpuprDAgti,t
clyAptvcFlrpcADADBnt:At&cBtDFArieylpetDFtIF('n
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P
/pGcAilrDAt,cootMI tGGioUo
P
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P
a8HtDFlrpcBpet+gtIn.tirtGirptGGioUEthAtirtGirptGTUeEOtc,Aprt:It,oyDet
VgercADiF
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•Ranson criteria is a clinical prediction rule for predicting the severity of
acute pancreatitis. It was introduced in 1974.
•At admission
•age in years > 55 years
•TLC > 16000 cells/mm3
•BG > 10 mmol/L (> 200 mg/dL)
•Serum AST > 250 IU/L
•Serum LDH > 350 IU/L
•At 48 hours
•Calcium (serum calcium < 2.0 mmol/L (< 8.0 mg/dL)
•Hematocrit fall >10 mmol/l
•Oxygen (hypoxemia PO2 < 60 mmHg)
•BUN increased by 1.8 or more mmol/L (5 or more mg/dL) after IV fluid
hydration
•Base deficit (negative base excess) > 4 mEq/L
•Sequestration of fluids > 6 L
Acute Pancreatitis

51. VoiysitrMsBl Ranson ScoreP
-cFBiFJBtBlirpti,t2t.t?J0tUtt7y+BAcFADcotvcFlrpcADltFplriBDBthcAtopcBAt
9 )tTocFeyocrtFplriBDBtcllireDFTtAitP3P;O
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t :,tAVptBlirpt2t9LtBpuprptvcFlrpcADADBtDBtoDspognt:,tAVptBlirptHt9LtBpuprpt
vcFlrpcADADBtDBtyFoDspogt
P
Jr
P
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•Ranson's score of ≥ 8 –OF / Substantial pancreatic necrosis (at least
30% glandular necrosis according to CECT)
•Interpretation
• If the score ≥ 3, severe pancreatitis is likely. If the score < 3, severe
pancreatitis is unlikely
•Or
•Score 0 to 2 : 2% mortality/ Score 3 to 4 : 15% mortality /Score 5 to
6 : 40% mortality/ Score 7 to 8 : 100% mortality
Acute Pancreatitis

52. gAgPe&tTTt
ugMLIltA'(yDspsE(tgi tP'BsiDMtelopI't&)opLoIDsiut APACHE II
"Acute Physiology And Chronic Health Evaluation" 1d1P/3*::tBlirpt+cBpetvcADpFAKBtcTpLtvrpuDiyBtVpcoAVtBAcAyBLtcFetINriyADFptvVgBDioiTDlt
GpcByrpGpFABLtTpFprcotGpcByrpti,tAVptBpuprDAg ti,teDBpcBpt.tirtVDTVprtep,DFpBtBpuprpt
vcFlrpcADADBnt8BpetiFtceGDBBDiFtcFetrpvpcApetcAtcFgtADGpntdiBDADuptvrpeDlADuptucoypti,t'9)t
cFetctFpTcADuptvrpeDlADuptucoypti,t.F)nt:AtDBtcFtiFoDFptlcolyocAirn
* 1d1P/3t::OtBlirptMt.tviDFABtvrpeDlABtII)tAitI.)tGirAcoDAg
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tttttt dJ
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tttttt 7pryGtlcolDyGtHtInF tGGioUEthH.n tGTUeEOtirtBpryGtco+yGDFtH99tTUEthH9nNnTUeEOM
APACHE-II score based patient’s age, previous health status, and 12routine physiologic
measurements, general measure of the severity of disease 8 or higher defines severe
pancreatitis. Used on admission and repeated at any time. Positive predictive value of 43%
and a negative predictive value of 89%. It is an online calculator.
(APACHE II) score > 8 points predicts 11% to 18% mortality

Hemorrhagic peritoneal fluid
•Obesity
Indicators of organ failure
•Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min
PO
2
<60 mmHg
•Oliguria (<50 mL/h) or increasing BUN and creatinine
Serum calcium < 1.90 mmol/L (<8.0 mg/dL) or serum albumin <33 g/L (<3.2.g/dL)>
Acute Pancreatitis

53. hpoyEs+tMBDIlBDo Glasgow criteriaP
;Vpt4ocBTi&tlrDAprDctDBtucoDet,irt+iAVtTcooBAiFptcFetcoliViotDFeylpetvcFlrpcADADBLt
&VprpcBtAVpt-cFBiFtBlirptDBtiFogt,irtcoliViotDFeylpetvcFlrpcADADBnt:,tctvcADpFAt
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•The Glasgow criteria is valid for both gallstone and alcohol induced pancreatitis,
whereas the Ranson score is only for alcohol induced pancreatitis. If a patient
scores 3 or more it indicates severe pancreatitis and the patient should be
transferred to ITU.
•It is scored through the mnemonic, PANCREAS:
•P - PaO2 <8kPa
•A - Age >55 years old
•N - Neutrophilia - WCC >15x10(9)/L
•C - Calcium <2 mmol/L
•R - Renal function, Urea >16 mmol/L
•E - Enzymes: LDH >600iu/L; AST >200iu/L
•A - Albumin <3.2g/L (serum)
•S - Sugar: blood glucose >10 mmol/L
Acute Pancreatitis

54. a:71dtBlirp
apeBDeptDFepBti,tBpuprDAgtDFt1d BISAP score
Bedside index of severity in APP
Ina8HtMtNA,4UeEt
P
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•1.BUN > 25MG/dL
•2. Impaired mental status ( GCS score < 15)
•3.SIRS score _>2
•4.Age > 60 yrs.
•5.Pleural effusion
Acute Pancreatitis

55. ,opI'o-oBtMBDIlBDot Balthazar criteria P
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TrceptviDFABC
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P
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+y++opBtDFtirtceDclpFAtAitvcFlrpcB tttttttttttttttttttttttttttttttttttttttttttttttttttttt
tttttttttttttt
•Developed in the early 1990s by Emil J. Balthazar et al. the Computed
Tomography Severity Index (CTSI) is a grading system used to determine the
severity of acute pancreatitis. The numerical CTSI has a maximum of ten
points, and is the sum of the Balthazar grade points and pancreatic necrosis
grade points:
•Balthazar GradeAppearance on CT CT Grade Points
•Grade A Normal CT 0 points
•Grade BFocal or diffuse enlargement of the pancreas 1 point
•Grade CPancreatic gland abnormalities and
• peripancreatic inflammation 2 points


•Grade DFluid collection in a single location 3 points
•Grade ETwo or more fluid collections and / or gas 4 points
bubbles in or adjacent to pancreas

Acute Pancreatitis

56. ,opI'o-oBtMBDIlBDot Balthazar criteria P
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tttttt
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•Necrosis Score
•Necrosis PercentagePoints
•No necrosis 0 points
•0 to 30% necrosis2 points
•30 to 50% necrosis4 points
•Over 50% necrosis6 points
•CTSI's staging of acute pancreatitis severity has been shown by a number of studies
to provide more accurate assessment than APACHE II, Ranson, and C-reactive
protein (CRP) level. However, a few studies indicate that CTSI is not significantly
associated with the prognosis of hospitalization in patients with pancreatic necrosis,
nor is it an accurate predictor of AP severity.

CTSI – 0-3 =mortality 3%, morbidity -8%
• CTSI- 4-6 = mortality 6%, morbidity -35%
• CTSI -7-10 = mortality 17%, morbidity- 92 %
Acute Pancreatitis

57. Acute PancreatitisPathopysoiltgoA
Normal Pancreas

58. PatvDi DiEy CT Findings
Acute Pancreatitis
Tail Indistinct
Intraperitoneal fluid
P
A
N
C
P
A
N
C
LIVERLIVER

59. PatvDi DiEy
rl)lBltAoiMBloIDIDy CT Findings
Severe Pancreatitis
Acute Pancreatitis
Peripancreatic edema
and inflammation
Unenhancing
Necrosis
P
A
N
C
P
A
N
C
LIVERLIVER
GBGB

60. sSAaoAA abscessE&Vi
wopnE&Vi
wopnE&Vi
wopnVAotT&aGAh
pseudocyst

61. dLIMsGly Outcomes
Acute Pancreatitis

62. Acute Pancreatitis

63. Acute Pancreatitis

64. Acute Pancreatitis

65. Acute Pancreatitis

66. Acute Pancreatitis

67. Acute Pancreatitis

68. Acute Pancreatitis

69. ImagingPathopystiltgostAhtgBDyhoOBaMtINaIhpaBaMtL ht
DhUhpBLstNStL htEoaIphoLBLBD&tDBaIhtBLtIoatVaOhphDLBgoLht
L htEphDhaIhtoaOtogNVaLtNStahIpNDBDT
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VaIhpLoBa&tNptBatIoDhtNStDVDEhILhOthopystINgEyBIoLBNaDt
DVI toDtEhpSNpoLBNatNptBDI hgBoT
An early CT may be misleading concerning the
severity of the pancreatitis, since it can underestimate
the presence and amount of necrosis.
Early CT is only recommended when the diagnosis is
uncertain, or in case of suspected early complications
such as perforation or ischemia.
golden rule

70. Interstitial
edematous
pancreatitis
Interstitial
edematous
pancreatitis
Acute peripancreatic
fluid collection
pancreatic
pseudocyst

71. Acute necrotizing
pancreatitis.
Acute necrotizing
pancreatitis
acute necrotic
collection
walled off cystic
necrosis

72. acute necrotizing
pancreatitis
acute necrotic
collection
Interstitial
edematous
pancreatitis
acute peripancreatic
fluid collection
d 0 to d 28

73. acute necrotizing
pan.
walled off necrosis
IEP
pancreatic
pseudocyst
after 28

74. yossilipgotAByothpDOoO Differential DiagnosisP
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•Mesenteric ischemia
•Perforated peptic ulcer
•Intestinal obstruction
•Biliary colic
•Inferior wall MI
•Ectopic pregnancy
Acute Pancreatitis

75. D/D OF A.P
Acute Pancreatitis

76. MtpthiaipgBdSiOgoDpO Management questionsP
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e hatONtrtNpOhptotiltDIoa,
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P
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SNptL htEoLBhaLtFBL tHPv,t
P
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EoaIphoLBLBDtVaOhpMNtBaLhpUhaLBNaDtLNtIyhoptL htAByhtOVIL,t
P
e oLtophtL htBaOBIoLBNaDtSNptDVpMhpstBatPvJtNELBgoytLBgBaMt
SNptBaLhpUhaLBNa&toaOtpNyhDtSNptyhDDtBaUoDBUhtoEEpNoI hDt
BaIyVOBaMtEhpIVLoahNVDtOpoBaoMhtoaOtyoEopNDINEs,
•When should patients admitted with AP be monitored in an
ICU or step-down unit?
•When do I order a CT scan?
•Should patients with SAP receive prophylactic abx?
•What is the optimal mode and timing of nutritional support
for the patient with SAP?
•Under what circumstances should patients with gallstone
pancreatitis undergo interventions to clear the bile duct?
•What are the indications for surgery in AP; optimal timing
for intervention, and roles for less invasive approaches
including percutaneous drainage and laparoscopy?
Acute Pancreatitis

77. ,NipByDBPBHltpOsilBgDBgNiBnpogBJ When Do I Transfer to the Unit ?P
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•Severe pancreatitis
•Multi-organ failure
–Pulmonary
–Renal
•Consider it if you are placing the patient on
antibiotics and/or ordering a CT to evaluate
non-improvement
Acute Pancreatitis

78. ui'iliBLtpIlitgogoO
rgAtpgtBIlogilot Severe Pancreatitis
Atlanta criteriaP
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•Organ Failure
–i.e. systolic blood pressure <90 mm Hg, PaO
2
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mg/dL, >500 mL/24 h GI bleeding OR
•Local Complications
–Necrosis
–Abscess
–Pseudocyst OR
•Unfavorable Early Prognostic Signs
–³ 3 Ranson's signs OR
–³ 8 APACHE-II points
Acute Pancreatitis

79. elhtpBvtoASli Organ FailureP
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•Cardiovascular
–Hypotension
–Septic physiology
•­ HR, CO and ¯ SVR
•Respiratory
–Hypoxemia
–Pleural effusions
•Renal
–ATN
–OliguriaP
.iatgDADhoI
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•Hematologic
–DIC
–Thrombocytosis
•Hepatic
–Encephalopathy
–­ T bili (3 mg/dl)
–­ AST/ALT 2X nl
•GI
–Stress ulcer
–Acalculous cholecystitis
Acute Pancreatitis

80. ,NipByDBPBel ilBrB*HJ When Do I Order A CT?P
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•If the patient has…..
–Signs of severe acute pancreatitis
–No signs of clinical improvement after several days
–Diagnostic dilemma
–Infection suspected
•T > 101
o
F
•Positive blood cultures
•What kind of CT?
–Dynamic with rapid bolus IV contrast
•What are you looking for?
–Necrosis: Lack of enhancement with contrast
–Fluid Collections
–Alternate diagnosis
Acute Pancreatitis

81. *HBvop ophO CT FindingsP
LtpIlitO
a
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a
yiIlitOi B ipOogVB SiBgDBi iat
a
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a
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vASo BIDAAiIgoDpOBtp BOgltp ophB ipOogoiO
a
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•Pancreas
–Pancreatic enlargement
–Decreased density due to edema
–Intrapancreatic fluid collections
–Blurring of gland margins due to inflammation
•Peripancreatic
–Fluid collections and stranding densities
–Thickening of retroperitoneal fat
Acute PancreatitisDBPgBatVBgtBiBSUBgDBE0NBsDlBopsAtaatgDlVBINtphiOBgDBEiIDaiBtUUtlipgBDpB*HBD
DBPgBatVBgtBiBSUBgDBE0NBsDlBopsAtaatgDlVBINtphiOBgDBEiIDaiBtUUtlipgBDpB*HBD
P
P
* It may take up to 72h for inflammatory changes to become apparent on CT ** It may take up to 72h for inflammatory changes to become apparent on CT *

82. Acute PancreatitisBBBBBBBBBBBBBBBB BBB
B
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athop
athop P PathopystilgoAslyByBD P
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POINTSPOINTS
GradeGrade of Acute Pancreatitis
A = Normal pancreas 0
B = Pancreatic enlargement 1
C = Pancreatic/peripancreatic
inflammation 2
D = Single peripancreatic fluid collection 3
E = Multiple fluid collections 4
Grade E = 50% chance of developing an infection and 15% chance of deathGrade E = 50% chance of developing an infection and 15% chance of death
DegreeDegree of Necrosis
No necrosis 0
Necrosis of one third of pancreas 2
Necrosis of one half of pancreas 4
Necrosis of more than one half 6

CT Severity Index = Grade + Degree of necrosis

83. H)GrHMG7H TREATMENT
Acute Pancreatitis

84. Mtpthiaipg
MoA (MD iltgi Management
Mild-ModerateP
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opgDBgNiBliglDUilogDpiSaBtp Bopglt(tE DaoptABtlitcBLlDaUgBP;BNV ltgoDpB
TogNopBgNiBsolOgB05BNDSlOcBGOUiIotAAVBopBgNiBitlAVBUNtOiBDsBgNiBoAApiOO/BthhliOOo'iB
sASo BliOSOIogtgoDpBoOBIlogoItAAVBoaUDlgtpg
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*ipgltAB'ipDSOBUliOOSli/BUSAaDptlVBtlgilVBTi hiBUliOOSli/Btp BSlopiB
DSgUSgB=2-c4Ba3FBhFN>BItpBEiBsDAADTi BSUBtOBatlBilOBDsBt idStgiB
NV ltgoDpc
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ugtlgBIAitlBAodSo OBTNipBUtopFtpDli<otBliODA'i
•NPO with IVF (crystalloids)
–Colloid (blood if Hct <25, albumin if serum alb <2)
–Patients with acute pancreatitis lose a large amount of fluids to third space
into the retroperitoneum and intra-abdominal area. Prompt IV hydration
within the first 24 hours. Especially in the early phase of the illness, aggressive
fluid resuscitation is critically important
•Central venous pressure, pulmonary artery wedge pressure, and urine
output (>0.5 mL/kg/h) can be followed up as markers of adequate
hydration.
•Generous narcotics
•NGT decompression
–if frequent emesis or evidence of ileus on plain films
•Start clear liquids when pain/anorexia resolve
Acute Pancreatitis

85. P
uVLpBLBNaoytDVEENpL
P
'ByOtVaINgEyBIoLhOtEoaIphoLBLBD&taNtAhahSBLtBDtNADhpUhOtSpNgtaVLpBLBNaoytDVEENpL&tt
Naystr(tOhnLpNDht)*tBatFoLhpt+,)e-tDVSSBIhDJtNpoytShhOBaMDtD NVyOtAhtBaBLBoLhOt
hopysT
P
'NOhpoLhdLNdDhUhphtEoaIphoLBLBD&tAhMBataVLpBLBNaoytDVEENpLthopystBatL htINVpDhtNSt
goaoMhghaL&toDtDNNatoDtDLoAByB.oLBNatNStSyVBOtoaOt hgNOsaogBItEopoghLhpDt
EhpgBLDJtNELBgoyys&taoDN/h/VaoytShhOBaMDtFBL totyNFdSoLtSNpgVyoLBNatD NVyOtAht
BaBLBoLhOT
P
lNLoytEophaLhpoytaVLpBLBNat+lvu-tgostAhtph0VBphOtF hatEoLBhaLDtIoaaNLtghhLtL hBpt
IoyNpBItahhODtFBL thaLhpoytaVLpBLBNatNptF hatoOh0VoLht/h/VaoytoIIhDDtIoaaNLtAht
goBaLoBahOJtL htlvutDNyVLBNatD NVyOtBaIyVOhtSoLthgVyDBNaDtBatogNVaLDtDVSSBIBhaLt
LNtEphUhaLthDDhaLBoytSoLLstoIBOtOhSBIBhaIs
P
rStDVpMhps tBDtph0VBphOtotShhOBaMt/h/VaNDLNgstoLtL htLBghtNStL htNEhpoLBNaJtVDhtot
yNFdSoLtSNpgVyot
P
1hMBatNpoytShhOBaMDtNaIhtoAONgBaoytEoBat oDtphDNyUhOtoaOtL htEoLBhaLtphMoBaDt
oEEhLBLhJtL htOBhLtD NVyOtAhtyNFtBatSoLtoaOtEpNLhBa •Nutritional support
•Mild uncomplicated pancreatitis, no benefit is observed from nutritional support,
only IV dextrose 5% in water (D5W) suffices; oral feedings should be initiated
early.
•Moderate-to-severe pancreatitis, begin nutritional support early in the course of
management, as soon as stabilization of fluid and hemodynamic parameters
permits; optimally, nasojejunal feedings with a low-fat formulation should be
initiated.
•Total parenteral nutrition (TPN) may be required when patients cannot meet their
caloric needs with enteral nutrition or when adequate jejunal access cannot be
maintained; the TPN solution should include fat emulsions in amounts sufficient
to prevent essential fatty acid deficiency
•If surgery is required a feeding jejunostomy at the time of the operation; use a
low-fat formula
•Begin oral feedings once abdominal pain has resolved and the patient regains
appetite; the diet should be low in fat and protein
Acute Pancreatitis

86. vii oph Feeding
Acute Pancreatitis

87. ,NipByDBPBugtlgBrpgoEoDgoIOJ When Do I Start Antibiotics?P
rISgiBUtpIlitgogoOBoOBIFEBopsiIgoDpBHBA-G
P
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P
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a
*DpglD'ilOotA
P
7DBEipisogBopBaoA Br3*cBUtpIlitgogoO
P
PaoUipiaBDlBailDUipiaBopBpiIlDgoIophBUtpIlitgogoO
P
uiAiIgo'iBhSgB iIDpgtaoptgoDpBatVBEiBEipisoIotA
P
rE<B DBpDgBtUUitlBgDBUlDaDgiBsSphtABopsiIgoDp
P
6ipiltABliIDaaip tgoDpOBsDlBSOiC
a
&oAotlVBUtpIlitgogoOBTogNBOohpOBDsBINDAtphogoO
a
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•Acute pancreatitis is c/b infection ~ 10%
•30-50% of those with necrosis get infection
•Prophylactic antibiotics
–Controversial
•No benefit in mild ALC. pancreatitis
•Imipenem or meropenem in necrotizing pancreatitis
•Selective gut decontamination may be beneficial
•Abx do not appear to promote fungal infection
•General recommendations for use:
–Biliary pancreatitis with signs of cholangitis
–> 30% necrosis on CT scan
Acute Pancreatitis

88. rpgoEoDgoIOB(BG&M Antibiotics - EBMrpgoEoDgoIBgNiltUVBsDlBUlDUNVAt<oOBthtopOgB
opsiIgoDpBDsBUtpIlitgoIBpiIlDOoOBopBtISgiB
UtpIlitgogoOc
*DINltpiBytgtEtOiBDsBuVOgiatgoIB)i'oiTOcB8/B0--4
Antibiotic therapy for prophylaxis against
infection of pancreatic necrosis in acute
pancreatitis.
Cochrane Database of Systematic Reviews. 3, 2005
Acute PancreatitisyiOUogiB'tlotgoDpOBopB lShBthipg/BItOiBao</B SltgoDpBDsBglitgaipgBtp B
aigND DADhoItABdStAogVB=iOUiIotAAVBgNiBAtIBBDsB DSEAiBEAop i BOgS oiO>/B
gNiliBTtOBOglDphBi'o ipIiBgNtg Bopglt'ipDSOBtpgoEoDgoIBUlDUNVAtIgoIB
gNiltUVBsDlBA-BgDBA5B tVOB iIlitOi BgNiBloOBBDsBOSUil(opsiIgoDpBDsB
piIlDgoIBgoOOSiBtp BaDlgtAogVBopBUtgoipgOBTogNBOi'iliBtISgiBUtpIlitgogoOB
TogNBUlD'ipBUtpIlitgoIBpiIlDOoOBtgB*H
Despite variations in drug agent, case mix, duration of treatment and
methodological quality (especially the lack of double blinded studies),
there was strong evidence that intravenous antibiotic prophylactic
therapy for 10 to 14 days decreased the risk of super-infection of
necrotic tissue and mortality in patients with severe acute pancreatitis
with proven pancreatic necrosis at CT

89. rBsoptABTDl BDpBtpgoEoDgoIO A final word on antibioticsP
yDBpDgBSOiBiaUoloItAAVBitlAVBopBaoA B
UtpIlitgogoO
P
vi'ilBitlAV BopBgNiB oOitOiBUlDIiOOBoOB tAaDOgB
Spo'ilOtAAVBOiIDp tlVBgD BgNiB opsAtaatgDlVB
liOUDpOi Btp B7eHBtpBopsiIgoDSOBUlDIiOO
•Do not use empirically early in mild
pancreatitis
•Fever early in the disease process is almost
universally secondary to the inflammatory
response and NOT an infectious process
Acute Pancreatitis

90. When can he eat ?
Nutritional issues in AP
•TPN vs. enteral feeding
–Not TPN per meta-analysis but …*
–NJ not NG
•Early initiation of enteral nutrition in severe AP
•tube feed if anticipate NPO > 1 week
•may be unnecessary for mild AP
–Reduce microbial translocation
–Enhance gut mucosal blood flow
–Promote gut mucosal surface immunity
Acute Pancreatitis)i SIiBopIo ipIiBDsB
)i SIiBopIo ipIiBDsB
opsiIgi BpiIlDOoO
opsiIgi BpiIlDOoO
Reduce incidence of Reduce incidence of
infected necrosisinfected necrosis
* * 6 older studies, relationship b/w glycemic control and infectious risk may confound vs. TPN6 older studies, relationship b/w glycemic control and infectious risk may confound vs. TPN

91. 7SglogoDp NutritionP
MoA BUtpIlitgogoO
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tliBOSssoIoipg
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t ogoDptABpSglogoDptAB
OSUUDlg
a
eltABopgtBiBt 'tpIophBgDB
ADTBstgB oigBDpIiB
UtopFtpDli<otBliODA'iB
•Mild pancreatitis
–Calories from IVF (D5W)
are sufficient
–No benefit from
additional nutritional
support
–Oral intake advancing to
low fat diet once
pain/anorexia resolve P
MD iltgiFui'ili
a
&ihopBpSglogoDptABOSUUDlgB
tOBitlAVBtOBUDOOoEAi
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P
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KiKSptABtIIiOO
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nptEAiBgDBaiigBItADloIB
iatp OBipgiltAAV
•Moderate/Severe
–Begin nutritional support
as early as possible
•NJ tube preferred
–TPN only if :
•Can’t maintain adequate
jejunal access
•Unable to meet caloric
demands enterally
Acute Pancreatitis

92. Acute Pancreatitis

93. PathopyosoiyhlgABoDsoOtMlyhoI When Do I Consult GI Person ?P
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a
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P
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P
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•Evidence of biliary pancreatitis
–Elevated LFTs + pancreatitis
•No matter what the US shows
•Severe pancreatitis
•Recurrent unexplained pancreatitis
•Rule out infected necrosis
•EUS FNA sampling of fluid collections
•Endoscopic treatment of necrosis/abscess
Acute Pancreatitis

94. ) A VMToGVhSMtVB B l Biliary pancreatitisP
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NdiO o, BaoNHco LlolBVhUVMUoBatMVGTo ho& A VMToJO
•Q: When should I suspect it ?
–A: Always
•Q: How do I evaluate for it ?
–A: EUS and LFTs
•Q: When is ERCP indicated ?
–A: 3 studies looked at emergency (within 24-72h)
ERCP with EUS vs standard therapy in biliary AP
Acute Pancreatitis

95. Management of Pancreatic
Complications- objectivesP
JSgBtoEAg UoSyAAtSB yhl
a
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a
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•Acute fluid collections
–Occur early, seen not felt
–No defined wall \ usually resolve spontaneously
–NO routine percutaneous or operative drainage
•may infect otherwise sterile tissue
•Infected pancreatic necrosis
•Pancreatic abscess
•Pseudocysts
•Gallstones with CBD stones
•Pancreatic duct disruption with ascites
Acute Pancreatitis

96. Management of Pancreatic
Complications
•Infected Pancreatic
necrosis
–Organisms on gram stain
after aspirate
–Surgical drainage
–Trans-gastric drainage
–Try to delay necrosectomy 2-
3wk for demarcation of
necrosisP
OVhSMtVB SoV&lStll
a
ivoyMoNHco'g UtUo
UMV hV't
P
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P
c u AVMoByouVhV'tuthBo
yEoGltgUySTlB
•Pancreatic abscess
–CT or EUS guided
drainage
•Walled collection of pus
•Similar to management
of pseudocyst
Acute Pancreatitis

97. Acute Pancreatitis

98. OltgUySTlBl PseudocystsP
iyAAtSB yhoyEoGVhSMtVB SoEAg UothSAyltUo&Tohyh3
tG BatA VA :tUo,VAAoyEo'MVhgAVB yhoB llgt
P
iyuGA SVBtlo;3<=>oSVltloyEoJO
P
?o2o,tt/loVEBtMo hlgAB
P
1;3;=>oMtlyALtolGyhBVhtyglAT
•Collection of pancreatic fluid enclosed by non-
epithelialized wall of granulation tissue
•Complicates 5-10% cases of AP
•~ 4 weeks after insult
•25-50% resolve spontaneously
Acute Pancreatitis

99. Pseudocyst
Acute Pancreatitis

100. iyuGA SVB yhloyEoOltgUySTlB Complications of PseudocystP
shEtSB yho3o<2>
P
dgGBgMto3o@AB>
P
-tuyMMaV'to3o@A;>o
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iyuuyho& AtoUgSBoy&lBMgSB yho3o@A.>
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Dsoy&lBMgSB yho3o1A@>
•Infection - 14%
•Rupture - 6.8%
•Hemorrhage - 6.5%
•Common bile duct obstruction - 6.3%
•GI obstruction - 2.6%
Acute Pancreatitis

101. Pseudocyst ManagementP
8AUoBayg'aB
a
OltgUySTlBloCo;oSuoBaVBoaVLto&tthoGMtlthBoCo@o
,tt/louglBo&toUMV htU
P
igMMthBoGMVSB St
a
JlTuGByuVB SoGltgUySTlBl9oMt'VMUAtlloyEol :t9oUyo
hyBoMtDg MtoBMtVButhB
•Old thought
–Pseudocysts > 5 cm that have been present > 6
weeks must be drained
•Current practice
–Asymptomatic pseudocysts, regardless of size, do
not require treatment
Acute Pancreatitis

102. OltgUySTlBopMV hV'tovtSah Dgtl Pseudocyst Drainage TechniquesP
NhUylSyG S
P
cgM' SVA
P
dVU yAy' S
•Endoscopic
•Surgical
•Radiologic
Acute Pancreatitis
LiverLiver
PCPC
PCPC
StomStom

103. NhUylSyG SoOltgUySTlBo
6VhV'tuthB Endoscopic Pseudocyst
Management
Acute PancreatitisP
OltgUySTlBoSAVll E SVB yh
a
iyuugh SVB h'
a
nyh3Syuugh SVB h'
•Pseudocyst classification
–Communicating
–Non-communicating

104. Endoscopic Pseudocyst
Management
Acute Pancreatitis

105. OtMSgBVhtygl
OltgUySTlB
pMV hV't Percutaneous
Pseudocyst
Drainage
Acute Pancreatitis8GthoiTlB'VlBMylByuT
Open Cystgastrostomy

106. FVGVMylSyG SoiTlBoDVlBMylByuT Laparoscopic Cyst Gastrostomy
Acute Pancreatitis

107. OVhSMtVB SoJlS BtloVhUoOVhSMtVB SyGAtgMVAoe lBgAVl o Pancreatic Ascites and Pancreaticopleural Fistulas
Acute PancreatitisJ&Uyu hVAoUMV hV'tothUylSyG SoGAVStuthBoGVhSMtVB SolBthBo
VSMylloBatoU lMgGB yhAo
cgM' SVAoU lBVAoMtltSB yhoVhUoSAylgMtoyEoBatoGMy, uVAolBguGo
Abdominal drainage endoscopic placement pancreatic stent
across the disruption.
Surgical distal resection and closure of the proximal stump

108. ntSMtltSByuT Necresectomy
Acute PancreatitiscgM' SVAo hBtMLthB yho3ou h uVAATo hLVl LtoyMoSyhLthB yhVAoyGtho
BtSah Dgtl9o lo hU SVBtUo,athoVhoVhVByu SoSyuGA SVB yho
VuthV&AtoByoVoutSaVh SVAolyAgB yho loGMtlthBo0t'9oVSgBto
htSMyB : h'oGVhSMtVB B l5o
vatohtSMyB SoGaAt'uyho lot,S ltUoByoA u BoBatolygMStoyEoltGl loyMo
atuyMMaV' SoGVhSMtVB B loByooSyhBMyAoyEo&AttU h'o
ptGthU h'oyhoBatol BgVB yhoVhUoAySVAot,GtMB lt9oBa louVToMtDg Mto
BatoBVAthBloyEoVho hBtMLthB yhVAoMVU yAy' lB9oVho hBtMLthB yhVAo
thUylSyG lB9oyMolgM'tyho0 hU L UgVAAToyMo hoSyu& hVB yh5A
Surgical intervention - minimally invasive or conventional open
techniques, is indicated when an anatomic complication
amenable to a mechanical solution is present (eg, acute
necrotizing pancreatitis)
The necrotic phlegmon is excised to limit the source of sepsis or
hemorrhagic pancreatitis to control of bleeding
Depending on the situation and local expertise, this may require
the talents of an interventional radiologist, an interventional
endoscopist, or surgeon (individually or in combination).

109. ntSMyltSByuToAVG Necrosectomy lap
Acute Pancreatitis

110. ntSMyltSByuT Necrosectomy
Acute Pancreatitis

111. EVlSgAVMoiyuGA SVB yhlo Vascular Complications
Acute PancreatitiscGAth SoVMBtMT9olgGtM yMoutlthBtM S9oSTlB SoVhUo'VlBMyUgyUthVAoVMBtM tlo
OVhSMtVB SotAVlBVltoUVuV'tloBatoLtlltAlo, BaoGltgUyVhtgMTluo
EyMuVB yhAo
cGyhBVhtygloMgGBgMtouVll Lto&AttU h'olgUUthoyhltBoyEoV&Uyu hVAoGV h9o
BVSaTSVMU VoVhUoaTGyBthl yh9o
v(vo3
JMBtM VAotu&yA :VB yhAodtEMVSByMToSVltloMtDg MtoA 'VB yhoyEoBatoLtlltAo
VEEtSBtUouyMBVA BTo1B>oByo;@>A
EVlSgAVMoBaMyu&yl lolGAth SoLt hoGyMBVAoLthyglolTlBtuA
o dtSgMMthBotG lyUtloyEoHDsoAo&AttU h'o(LthygloaTGtMBthl yhoCoo
lGAthtSByuTo
Splenic artery, superior mesenteric, cystic and gastroduodenal arteries
Pancreatic elastase damages the vessels with pseudoaneurysm
formation.
Spontaneous rupture massive bleeding sudden onset of abdominal pain,
tachycardia and hypotension,
T/T -
Arterial embolization. Refractory cases require ligation of the vessel
affected mortality 28% to 56%.
Vascular thrombosis splenic vein portal venous system.
Recurrent episodes of UGI l bleeding /venous hypertension >
splenectomy

112. DVAAlByhtoGVhSMtVB B l Gallstone pancreatitis
Acute PancreatitisPattho pysilaygAsao Bo BhioDaoiBhiypo iAshlpyOByMio pihIllpAo BNsi
o DsAalLipAi BoDiahgsyOByMigDptayMBo Bhi BoDi pAhsyByMihBMyhi
ayOihLUlopUhipSipEho AIgo Bpy& isaAtLisyOphgplBgiAso ApMAaOsi
gDptayMBplaygAsao pMAalDLiVTGFevi Bo DihlDBygo sApopULiayOi
ho pysisro Aago BpyiBhiByOBgao sOc
Gallstone pancreatitis that is not responding to supportive
therapy or with ascending cholangitis with worsening signs
and symptoms of obstruction, early endoscopic retrograde
cholangiopancreatography (ERCP) with sphincterotomy and
stone extraction is indicated.dalaAphgplBgipAiplsyigDptsgLho sgo pULiopiEsiOpysiaSosAi,i
o piHi ssnh
Laparoscopic or open cholecystectomy to be done after 4
to 6 weeks

113. OVhSMtVB SoUgSBoU lMgGB yh Pancreatic duct disruption
Acute PancreatitisJaUaMsio pio DsilaygAsaoBgiOIgo atihL hosUiUaLiattp ilaygAsao Bgi
uIBgsio pitsaniSApUio DsiMtayOci' DsihIOOsyiOsNstplUsyo ipSi
DLlpgatgsUBaipAiaiAalBOiBygAsahsiByiAso AplsABo pysatiStIBOipyi
gpUlIo sOio pUpMAalDLiVF' v
Damage to the pancreatic ductal system may allow pancreatic
juice to leak from the gland. The sudden development of
hypocalcemia or a rapid increase in retroperitoneal fluid on
computed tomography (CT)esAgIoayspIhiltagsUsyoipSiaiOAaByaMsioIEsiByopioDsiStIBOigpttsgoBpy
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Percutaneous placement of a drainage tube into the fluid collection
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nasopancreatic tube attached to an external bulb suction device
Refractory cases may warrant surgery. If the persistent leak is present in
the tail of the gland, a distal pancreatectomy is preferred. If the leak is in
the head of the gland, a Whipple procedure is the operation of choice.

114. OVhSMtVB SoV&lStll Pancreatic abscess
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Pancreatic abscesses generally occur late in the course of pancreatitis. Many of
these respond to percutaneous catheter drainage and antibiotics. Those that
do not respond require surgical debridement and drainage.

115. Algorithm for A.P T/t
Acute Pancreatitis

116. Acute Pancreatitis

117. dtSoOVhSMtVB B loVA'yM BauoyEov(B Rec Pancreatitis algorithm of T/t
Acute Pancreatitis

118. eVuygloGtyGAto,ayoaVLtoaVUo
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•Alexander the Great
•Ludwig von Beethoven
•Dizzie Gillespie
•Maximilian Schell
•Matthew Perry
•John Ashcroft
Acute Pancreatitis

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•4 out of 5 patients have mild uneventful pancreatitis
•If the patient is not getting considerably better in 36-
48 hrs, start thinking about that “5th patient”
•A CT is that 5th patient’s friend
•If you are thinking about antibiotics, you should be
thinking about a CT and a few consultations.
•The pancreas is a mean organ….respect it
Acute Pancreatitis

120. Pathopyshoshiialh Take home messageoo ghAhBDOMoyIoaNLOho aUNBhaODODioaUSo aUNBhaODNoUhNByiDioNaUoyUEMo&hoBhEDa&EMo
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Severity of acute pancreatitis and pancreatic necrosis can only be reliably
assessed by imaging after 72 hours.
•Absence of pancreatic parenchymal necrosis does not preclude a serious
course of the illness.
•CT cannot reliably differentiate between collections that consist of fluid and
those that contain solid debris.
•In these cases MRI can be of additional value.
•Name collections always according to 2012 Atlanta definitions.
•Central gland necrosis is a subtype of necrotizing pancreatitis with important
implications.
•ERCP is the procedure of choice in mild to mod. Cases, with CBD stone
induced pancreatitis, Gallstone t/t after 4-6 weeks.

121. Acute Pancreatitis