Pancreatitis

1. Acute Pancreatitis

2. Outline
• Introduction
• Epidemiology
• Pathophysiology
• Etiology
• Clinical Presentation
• Workup
• Severity ScoringSystem
• Treatment
• Prognosis
• Complications

3. PANCREATITIS
Inflammation in pancreas associated with injuryto
exocrine parenchyma
P
ANCREAS
Stroma
Parenchyma
Exocrine
Primary injury causing
P
ANCREA
TITIS
Endocrine
Involved secondarilyor
asa complication
P
ANCREASGreek word with literal meaning ‘pan’ (all/whole) , ‘creas’ (flesh):sweatbread

4. CLINICALCLASSIFICATION
*Considered aphaseof chronic pancreatitis
** resulting from fibrosis within pancreas

5. ACUTEPANCREATITIS
• CLINICALDEFINITION
– An acute condition presenting with abdominal pain-usually associatedwith
raised blood/urine pancreatic enzymes asaresult of pancreatic inflammation
• P
A
THOLOGICALDEFINITION
– Reversible* pancreatic parenchymal injury associated with inflammation
*ifunderlying causeof pancreatitis is removed, heal without any impairment of
function or morphologic lossof gland
*Recurrent attacks with irreversible parenchymal injury leading toimpairment of
function and morphologic lossis chronic pancreatitis

6. CLASSIFICATIONOFACUTEPANCREATITIS
Atlanta* criteria(1992)
• Mild acute pancreatitis (80%cases)
(Acute Interstitial/edematous pancreatitis)
– AcuteAbsenceof organfailure
– Absenceof localcomplications
• Severeacute pancreatitis(20 %cases)
(Acute Hemorrhagic Necrotizing(fulminant)
pancreatitis)
– Localcomplications +/-
– Organfailure definedas
• SBP<90 mm Hg
• PaO2≤ 60 mm Hg
• GIbleed ≥ 500 ml/24 hrs
• Cret ≥ 2 mg/dL afterrehydration
– Ransonscore ≥ 3 or AP
ACHE≥8
RevisedAtlanta criteria(2012)
• Mild acutepancreatitis
– Absenceof organfailure
– Absenceof localcomplications
• Moderately severeacute
pancreatitis
– Localcomplications +/-
– Transient organ failure(<48h)
• Severeacute pancreatitis
– Persistent organ failure**(>48 h)
and/or death
*defined asascore of 2 or more for one of these(CVS, Renal, Resp)organ systems usingthe
modified Marshall scoring system

7. Modified Marshall ScoringSystem for organ failure

8. TwoDistinct phases of AcutePancreatitis
Early Phase(within 1week)
• Characterized by SIRS+/-
organ failure
• Severity assessedby
functional/clinical Severity
Scoring System
(Ranson/Galsgow etc)
LatePhase (>1week)
• Characterized by local
complication
• Severity assessedby
morphological scoring
system(BalthazarScoring)
*Early clinical and the later morphologic classifications do not necessarily
overlap and do not necessarily correlate with oneanother

9. Epidemiology
World wide incidence
ranges between 5 and 80 per 100,000 population
GEOGRAPHICAL
Highest incidence(worldwide) recorded in the
United States and Finland(73.4 casesper 100,000)

10. Epidemiology
Median agesof onset for variousetiologies
Etiology Median Ages ofonset
Alcohol-related 39years
Biliary tract–related 69years
Trauma-related 66 years
Drug-induced etiology 42 years
ERCP-related 58 years
AIDS-related 31 years
Vasculitis-related 36 years

11. Epidemiology
Gender Predilection
Generally M>F
In males more often related toalcohol
In females more often related tobiliary tract disease
Idiopathic pancreatitis no clear gender predilection
AGE
Youngmales and Old Females

12. Epidemiology
RACE
Hospitalization rates3 times higher for blacks than whites
(racial differences more pronounced for males thanfemales)
Riskfor African Americans aged35-64 years10 times higher
than for any other group

13. PATHOPHYSIOLOGY
Autodigestionof pancreatic substance by
inappropriately activated pancreatic enzymes
(especially trypsinogen)

14. PATHOPHYSIOLOGY
TRYPSINOGEN
TRYPSIN
(hydrolysis of N-
terminus
hexapeptide by
brush border
enterokinase)
Activation of prekallikrein Activation of kininsystem
Activation of Hagemanfactor-XII Activation of clotting and
complement systemsthrombosis
and inflammation
Activation of Phospholipase Activation of Prostaglandinsand
Bradykinins
Lipase activation Triglycerides
Glycerol +Fatty acids
Fatty acids+ calcium saponified
fat Hypocalcemia
Elastase activation Digestion of
elastic fibers Capillary
leak/rupture/ Pseudoaneurysm
3rd spaceSequestration of
blood/fluid Hemorrhage+
Hypovolemicshock
Activation of Lysolecithinase
(derived from bile)
Membrane damageNecrosis
Releaseof inflammatory mediators
into circulation
systemic complications

15. MICROBIOLOGY-ininfected necrosis
• Commonly polymicrobial infection-60%
• Source:
– gall bladder, colon, small bowel(Transmural) or hematogenousspread
• INCIDENCE:
– 24%(1week) and 70 %(3 weeks)
• ORGANISMS:
– E.Coli(35%),klebsiella( 25%),Enterococcus (25%)
– Others…..Staphlyococci, pseudomonas, proteus, enterobacter,
anaerobes, candida(10%)

16. ACUTEP
ANCREA
TITIS
Drinks like FISH (Dehydration)
Burrows like
RODENT
(produces fistula)
Stings like
SC
ORPION
(severe pain)
Kills like LEOP
ARD (Life threatening)
Eatslike WOLF
(Pancreatic
Necrosis)

17. Etiology
• Mechanical causes
• Metabolic causes
• Infective causes
• Genetic causes
• Vascular causes
• Idiopathic AP

18. MECHANICAL CAUSES OFACUTEPANCREATITIS
Gall stones  Choledocholithiasis(40-70%)
• Most common biliary tract disease leading toAP
• MOA: Ductal obstruction causing ductal hypertension and acinar cell injury
• “Common channel hypothesis”-Opie in 1901(bile/activated enzymesreflux)-
CONTROVERSIAL
• Riskfactors: inverse relation to size,wide cysticduct
• 5 %of gall stones causespancreatitis
• M:F=1:3
Ampullary tumor
sphincter of Oddidysfunction
Pancreatic CA(1-2%)
• 5 %present asAP
Choledochoceles, biliary sludge
Abdominal trauma(1.5 %cases)
• 17 %caseshave high enzymes and 5 %have clinical AP
• Penetrating>Blunt
Iatrogenic Injury
• Operative injury - Endoscopic procedures with dye injection

19. METABOLIC CAUSES OF ACUTE PANCREATITIS
Alcoholism (25-35%)
• M:F=6:1
Hyperlipoproteinemia (1-4 %)
• TypeI and Vhyperlipidemia
• >1000 mg/dL(diagnostic criteria)
• More severe than alcohol/gallstone
Malnutrition
Diabetes,Azotemia
Porphyria
Hypercalcemia/hyperparathyroidism
• Hyper secretion and formation of calcified stones intraductallyAcinar injury
Drugs (2 %cases)(usually mild)
Definite association ( azathioprine, sulfonamaides, sulindac, tetracycline,valproic acid,Didanosine,
Methyldopa,estrogens, furosemide, 6-Mercaptopurine, pentamidine, 5-ASA,steriods,octreotide)
Probable association (thiazides, Flagyl, Methandienone, Nitrofurantoin, phenformin,piroxicam,procainamide,
Colaspase,chlorthalidone, asparagine,cimetidine,cisplatin, cytosine arabinoside, diphenoxylate, ethacrynic acid)

20. INFECTIVE CAUSES OFACUTEPANCREATITIS
Viruses
• MMR, Denguevirus(complication of dengue hemorrhagic fever MOA:
Capillary leak3rd spaceloss),Coxsackie B, Hepatitis virus, CMV,EBV
,Echovirus,
VZV
,HSV
Bacteria
• M. tuberculosis,M. avium complex, Mycoplasma, Legionella, Leptospira, Salmonella,
Campylobacter, Yersinia,Brucella, Nocarbia
Fungi
• Aspergillus
Parasites
• Clonorchis sinensis, Toxoplasma,Cryptosporidium, Ascaris, Echinococcus granulosus,
• FasciolaHepatica, Opistorhcis spand Dicrocoelium dendriticym
Scorpion and snake bite
• Trinidalian scorpion* (Tityus trinitatis)
• MOA: Neurotransmitter discharge from cholinergic nerve terminals, leading to
massiveproduction of pancreatic juice(same MOAin antiacetylcholinesterase/OPC
insecticide)
*Most commoncauseofAPin RepublicofTrinidadandTobago,atwin island country off the northern edge of
SouthAmerica

21. GENETIC CAUSES OFAUTEPANCREATITIS
Pancreasdivisum (unfused ducts of Wirsung and Santorini)
• Seenin 20-45 %cases
• MOA(controversial): stenotic minor papillae and atretic duct ofsantorini
Anomalous union of pancreaticobiliary duct(annular pancreas)
Autoimmune pancreatitis-associated with IBD
Hereditary pancreatitis-
• Autosomal dominant, gain of function, mutations in cationic
trypsinogen(PRSS1)with 80 %penetrance premature activation of trypsinogen
• Mutation in trypsin inhibitor (SPINK1)genesblockade of active bindingof
trypsin rendering it inactive
• Acute pancreatitis in teens
• Chronic in next 2decades
• 40 %risk of pancreatic cancer by 70year
Celiac disease
Cystic fibrosis-CFTRmutation  abnormality of ductalsecretion

22. VASCULAR CAUSES OFACUTEPANCREATITIS
Shock
Hypothermia
Atheroembolism
Vasculitis(Polyarteritis nodosa, SLE)

23. How Alcohol  AcutePancreatitis??
 Effects of diet
 Malnutrition
 Direct toxicity ofalcohol
 Concomitant tobaccosmoking
 Hypersecretion of gastric and
pancreatic juices(rich inprotein,
low in bicarbonate/ trypsin
inhibitor)protein plugsduct
obstruction/reflux
 Hyperlipidemia
 Increased ductal
permeability enzymes
extrusion damage
 Releaseof freeradicals-
superoxide, hydroxyl
 Spasmof sphincter of Oddi

24. Alcohol-induced Pancreatitis
• Manifests asaspectrum, ranging from discrete episodes of
APto chronic irreversible silent changes.
• Diagnosis should not be entertained unless a person has a
history of over 5-(15) years of heavy(>50 g per day,types
less significant) alcoholconsumption.
• Clinically evident APoccurs in <5%of heavy drinkers; thus,
there are likely other factors that sensitize individuals to
the effects of alcohol, such asgenetic factors and tobacco
use.
• 1st attack is considered alcohol inducedAP
– Although it may be 1st manifestation of (acute on)chronic
pancreatitis

25. Idiopathic AcutePancreatitis
• Defined aspancreatitis with noetiology established after initial
laboratory (includinglipid and calciumlevel,autoimmunemarkers,
viral titers) and imaging tests(USGand CTin the appropriate
patient)
– In somepatients an etiology mayeventually be found(70 %of IAPdue
to microlithiasis), yet in others no definitecauseis ever established.
• Patients with IAPshould be evaluated at centers of excellence
focusing on pancreatic disease,providing advancedendoscopy
servicesand acombined multidisciplinary approach.
Careful search for the etiology must be made in all cases,and nomore
than 20 %of casesshould fall into the idiopathiccategory

26. Hyperlipidemia induced AP
• In the absence of gallstones and/or history of significant history of
alcohol use, aserum triglyceride should be obtained andconsidered
the etiology if >1,000mg /dl
• Lactescent (milky) serum hasbeen observed in asmany as20 % of
patients with AP
• Therefore afasting triglyceride level should be re-evaluated 1 monthafter
discharge when hypertriglyceridemia issuspected
• MOA:Lipaseliberate large amounts of toxic fatty acids into
pancreatic microcirculation
• Leadingto endothelial injury, sludging of blood cells, and consequent ischemic
states

27. Iatrogenic-Operative Pancreatitis
• Surgeriesperformed on/close to pancreas
– Pancreatic biopsy
– Biliary duct exploration
– Distal or Billroth IIgastrectomy
– Jejunostomy
– Splenectomy
• Surgeries that uselow systemicperfusion
– Cardiopulmonary bypass(also due to hypothermia, atheromatous
emboli)
– Cardiactransplantation

28. Post-ERCPPancreatitis
• 3rd Most common causeof AP(after gallstone and alcohol) i.e. 4%
• Most common complication of ERCP
• INCIDENCE
– 2-4 %(Historically, 5-10%)patients undergoing ERCPdevelop acute pancreatitis
– Riskof severeAP<1/500.
• CAUSE
– Duct disruption , enzymeextravasation
• PREDISPOSINGF
ACTORS
– Sphincter of Oddi dysfunction(risk increasesto30 %)
– H/O recurrent pancreatitis
– Sphincterotomy
– Balloon dilation ofsphincter
– Inexperienced endoscopist

29. CLINICAL MANIFESTATION

30. ABDOMENPAIN-CardinalSymptom
• SITE:usually experienced first in theepigastrium
– but may be localized to either upper quadrant or felt diffusely throughout the abdomen or lowerchest
• ONSET: characteristically develops quickly, generally following substantial meal and precedesNV
• SEVERITY: frequently severe, reaching max. intensity withinminutes rather than hours
• NATURE: “boring through”, “knifing”(illimitable agony)
• DURATION:hours-days
• COURSE:constant (refractory to usualdoses of analgesics, not relieved by vomiting)
• RADIATION: directly to back(50%),chest orflanks
• RELEIVING FACTOR:sitting or leaning/stooping forward (MUHAMMEDANPRA
YERSIGN)
– due to shifting forward of abdominal contents and taking pressure off from inflamedpancreas
• AGGRAVATING FACTOR:food/alcohol intake, walking, lyingsupine
_
Paindescribed asdull, colicky, or located in the lower abdominal region isnot
consistent with APand suggestsan alternativeetiology

31. OTHERMANIFESTATIONS
• Nausea,frequent and effortless vomiting, anorexia,diarrhea
– Due to reflex pylorospasm
– More intense in necrotizing than in edematouspancreatitis
• Persistent retching
– despite empty stomach
• Hiccups
– Dueto gastric distension/diaphragmatic irritation
• Fever
– Low grade, seenin infective pancreatitis
• Weakness,Anxiety, Sweating
– Indicates severe attack
• Polyarthritis

32. General PhysicalExamination
• Appearance: well  gravely ill with profoundshock, toxicity
and confusion
• Vitals: Tachypnea(and dyspnea-10%),Tachycardia(65%),
Hypotension, temp  high(76%)/normal/low (acute
swinging pyrexia in cholangitis)
• Icterus(28%)
– gallstone pancreatitis or due to edema of pancreatichead
• Cyanosis
– Improper lung perfusion
• Pallor, cold clammy skin,diaphoretic

33. ABDOMENEXAMINATION
• Tenderness+Rebound tenderness:
– epigastrium/upper abdomen
• Distension:
– Ileus(BSdecreased or absent)
– ascites with shiftingdullness
• Massin epigastrium(usually absent)
– due to inflammation
• Guarding(also called “defense musculaire” )-upper abdomen
– tensing of the abdominal wall muscles toguard inflamed organs within the
abdomen from the pain of pressure upon them(i.e.during palpation)
• Rigidity(involuntary stiffness)-unusual
– Tensingof the abdominal wall musclesto guard inflamed organseven if patient not
touched

34. Cutaneous Ecchymosis(1%cases)*
Acute Hemorrhagic Necrotizing/fulminant
PancreatitisPeriperitoneal/retroperitoneal
Hemorrhage
Methemalbumin formed from digested bloodtracks around
Fascialplanes
 hemorrhagic
spots and
ecchymosisin
flanks
(GREYTURNER’S
SIGN)**
FALCIFORM
LIGAMENT Bluish
Discolorationaround
umbilicus
(CULLEN’SSIGN)
(umbllical blackeye)
Below inguinal ligament
(FOX SIGN)
*Neither sign is pathognomonic of acutepancreatitis
*takes 24-48 hours to develop with 10-40 %mortality
**More commonly, ruddy
erythema in flanks due to
extravasated pancreatic exudate

35. Differential Diagnosis
GREYTURNER/CULLEN/FOXSIGNs
• Acute Pancreatitis
• Pancreatic Hemorrhage
• RupturedAAA
• Blunt abdominaltrauma
• Ruptured ectopicpregnancy
• Retroperitonealhemorrhage
• Coagulopathy
Above: GeorgeGreyTurner Above: ThomasStephen Cullen

36. GREY TURNER1 SIGN CULLEN2 SIGN FOX3 SIGN
1.Named after British surgeon GeorgeGreyTurner(1877-1951)
2.Named for ThomasStephen Cullen (1869-1953), Canadiangynecologist who first
described the sign in ruptured ectopic pregnancy in1916
3.Named after George Henry Fox(1846-1937),American dermatologist

37. RESPIRATORYEXAMINATION
Leftsided* Pleural effusion(10-20%) +pulmonary edema+ pneumonitis
Reducedchest movements+
decreased vocal fremitus/resonance +
stony dull percussionnote+
decreased air entry basally bilaterally +
basalfine mid/end-inspiratory crepitation's- don’t change
with cough
*Due to close approximation of body and tail of pancreas to the left sided diaphragm

38. Neurological Examination
Mild
Psychosis
Coma
Toxemia
FatEmbolism
Hypoxia
R
espiratory
distress
Uremic
encephlopathy
Hypovolemic
shock
DIC

39. Other Manifestations
• Subcutaneous fat necrosis
– Small(<1 cm), red, tender nodules on extensor
skin of legs
• Purtscher retinopathy(on fundoscopy)
– Activation of complement and agglutination of
blood cells within retinal vesselscausingIschemic
injury of retina
– May causetemporary or permanentblindness

40. MANIFESTAIONSOFCOMPLICATIONS
• Hypocalcaemia
– circumoral numbness or paresthesia (1st symtpom to develop) /tingling of
distal extremities
– carpopedal spasm(=main d'accoucheur-French "hand of the obstetrician”)
• Flexion of wrist and MCPjoints with extension ofIPjoints
– laryngospasm
– generalized seizures
– Chvostek*(-Weiss) sign
• Dependingon calciumlevel, gradedresponse occur: twitching first at angle of mouth,
then by nose, the eye and the facialmuscles
• Positive in 10 %population in absenceofhypocalcaemia
– Trousseau** sign of latent tetany
• BPcuff around arm and inflating to 20 mmHg above SBPfor 3-5minutes
• Carpal spasmobserved
• More specific and sensitive than chvostek sign(postive even beforetetany/hyperreflxia)
*František Chvostek (German: Franz Chvostek)Czech-Austrian military physician (1835 – 1884), described this signin1876.
**Armand Trousseau, Frenchphysican (1801-1867) described this phenomenon in1861

41. MANIFESTAIONSOFCOMPLICATIONS
Hematemesis/
melena
(5%)
DIC
Peripancreatic
(duodenal)
necrosis
Gastric
erosions

42. DIFFERENTIALDIAGNOSIS
ABDOMINAL CONDITONS
• Perforated peptic ulcer/gastroentritis
• Biliary colic/acute cholecystitis/Cholangitis
• Mesentric Ischemia
• RupturedAorticAnuerysm
• Intestinal Obstruction
• Gastric/colon/pancreatic CA
• Viral Hepatitis
• IBS
SYSTEMIC CONDITIONS
• DKA
THORAXCONDITIONS
• Pneumonia/ARDS
• Pleuritic pain
• MI
GYNECOLOGICALCONDITONS
• Ectopic pregnancy
• Salpingtis

43. Diagnostic criteria
• Most often established by the presence of two of the three
following criteria:
– (i) abdominal pain consistent with thedisease,
– (ii) serum amylaseand/or lipase greater than three times theupper
limit of normal,and/or
– (iii) characteristic findings from abdominalimaging.
CTand/or MRI of the pancreas should be reserved forpatients
– in whom the diagnosis is unclear(typical pain with normal enzymes)
– who fail to improve clinically within the first 48–72 h after hospital
admission (e.g., persistent pain, fever, nausea, unable to begin oral
feeding)
– to evaluatecomplications

44. WORKUP
• HEMATOLOGICALinvestigations
• RADIOLOGICALinvestigations
• Miscellaneous investigations

45. HEMATOLOGICAL
• BASELINES
– CBC:
• LowHb: prolonged hemetemesis/melena, internal hemorrhage
• Leucocytosis (10,000-30,000/mcL)-infection, non infectious inflammation
• Low platelets-DIC
• Hct –raised in hemoconcentration
– LFT’s:
• raised bilirubin, AST/ALT/LDH,ALP
,GGTP-gall stonepancreatitis
– RFT’s:
• raised BUN/cretainine-ATNARF
– Coagulation profile:
• increased INR-DIC
– BSR:
• >180 mg/dl-diabetes as asequelae or cause
– Serum electrolytes:
• Low sodium/potassium: persistent vomiting
• Hypocalcemia- saponification/fat necrosis
– Serum Protein:
• low protein/ albumin
Diabetes Mellitus AP

46. HEMATOLOGICAL
• ABG’
s
• Etiology specific investigations
– Serumfasting lipid profile
– Viral titers
– SerumCalcium (HypercalcemiaAPHypocalcemia)
– Autoimmune markers
• increased serum levels of IgG4
• serum autoantibodies such asanti-nuclear antibody (ANA),anti-lactoferrin
antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF),
Acid-Base Disturbance Etiology
Metabolic (Lactic)acidosis with high aniongap Hypovolemic shock
Cholride-responsive Hypokalemic Hypochloremic metabolic alkalosis
(Urine chloride <20 mEq/L)
persistent vomiting
Respiratory acidosis ARDS/resp failure

47. HEMATOLOGICAL
• Pancreatic Enzymes’Assays
– SerumAmylase:
• ONSET
:almostimmediately
• PEAK:within severalhours
– Serum Lipase:
• more sensitive/specific than amylase
• Remainselevated longer than amylase(12days)
• Useful if latepresentation
RaisedAmylase  may notAP
Normal Amylase  may beAP
– 3-4 times upper limit of normal within 24 hrs(90%)
• RETURNto normal depends on severity(3-5days)
• normal at time of admission in20%cases
• Compared with lipase, returns more quickly to values below
the upper limit ofnormal.
SERUM INDICATOR OFHIGHEST
PROBABILITYOFDISEASE

48. • Pancreatic Enzymes’Assays
– UrineAmylase
• More sensitive than serumlevels
• Remain elevated for several daysafter serum levels returnedto
normal
– Pancreatic-specific amylase(p-amylase)
• Measuring p-amylase instead to total amylase(alsoincludes
salivary amylase) makesdiagnosis more specific(88-93%)

49. CONDITIONS ASSOCIATEDWITH RAISED SERUM AMYLASE
ABDOMEN
• Small bowelobstruction
– strangulation ileus
– mesenteric ischemia
• Acuteappendicitis
• Cholecystitis
• Perforated Duodenal Ulcer
• Gastroenteritis
• Biliary peritonitis
• Spasmof sphincter of Oddi
GYNE
• Ruptured Ectopicpregnancy
• Torsion of an ovarian cyst
OTHERS
• Parotitis (Mumps)
• Macroamylasaemia
• Opioids administration
• LowGFR
• Brain injury(CVA)- hyperstimulation
of pancreas

50. Plain CXR-PAview
• Leftsided Pleural effusion: blunting of costophrenicand
cardiophrenic angles +hazinessin lower zones
• Elevated diaphragm on left side
• Linear focal atelactasis of lower lobe oflungs
• ARDS:diffuse alveolar interstitialshadowing
• Pulmonary edema: prominent vascularmarkings
Not diagnosticof Acute Pancreatitis;useful in differential diagnosis

51. Plain X-rayabdomen erect APview
• Sentinel* loopsign
– Localizedisolated Distended gut loop (Ileus) seennear the site of injuredviscus
or inflamed organ
– RATIONALE: body's effort to localize the traumatic or inflamed lesions
– ETIOLOGY:Localizedparalysis followed by accumulation ofgas
– SITE:
• Acute Pancreatitis Left hypochondrium (PROXIMALJEJUNUM)
• AcuteAppendicitis Right iliac fossa
• Acute Cholecystitis Right Hypochondrium
• Diverticulitis Left iliac fossa
*SENTINEL:Asoldier stationed as a guard to challenge all comers and prevent a surprise
attack
Not diagnostic of Acute Pancreatitis; useful in differentialdiagnosis

52. SENTINELLOOPSIGN

53. Plain X-rayabdomen erect APview
• Colon cut-off sign
– Gasfilled (Distended) segment of proximal(mainly transverse) colon
associated with narrowing of the splenicflexure
– abruptly ending at the area of pancreaticinflammation
– with collapse of descendingcolon
– RANTIONALE: Extension of inflammatory process from the pancreas intothe
phrenicocolic ligament via the transversemesocolon
• resulting in functional spasmand/or mechanical narrowing ofthe splenic flexure at
the level where the colon returns to theretroperitoneum.
– Differential DIAGNOSIS:
• IBD
• Carcinoma of colon
• Mesenteric Ischemia
Not diagnostic of Acute Pancreatitis; useful in differentialdiagnosis

54. COLONCUT-OFFSIGN

55. Plain X-rayabdomen erect APview
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis
• increased gastrocolic separation
• Gastric curvature distortion
• T
orule out perforated DU(gas
under diaphragm)
• Renal halo sign
– RATIONALE: peripancreatic inflammatory reaction extension into pararenal
space
– ETIOLOGY:water-density (radiolucent-halo)of inflammation in anterior
pararenal spacecontrasts with perirenal fat; more common on left side
• OTHERS
• Obliteration of psoas shadow • Air in the duodenalC-loop
• Localized ground glassappearance
( localized increased high soft tissue
density)
• Calcified gall stones
• Pancreatic calcification(chronic
pancreatitis)

56. RenalHalo Sign
NORMAL RENALHALOSIGN

57. Transcutaneous Abdominal Ultrasonography
• Not diagnostic
• Should be performed within 24 hours in all patientsto
– detect gall stones* asapotential cause
– Ruleout acute cholecystits asdifferentialdiagnosis
– Detect dilated CBD
– sensitivity-(70-80%)
– DEMERIT
:overlying gasshadows 2ndary to bowel distension
• THERAPEUTIC:
– USG-guided aspiration for gram staining andculture
– USG-guided pig tail catheterinsertion
* Identification of gallstones asthe etiology should prompt referral for cholecystectomy to
prevent recurrent attacks and potential biliary sepsis.
Gallstone pancreatitis is usually an acute event and resolves when the stone is removedor
passes spontaneously.

58. IV Contrast enhanced Computed TomographyScan
• Provides over 90 % sensitivity and specificityfor
the diagnosis of AP…..BUT
• Routine usein patients with APis unwarranted,
asthe diagnosis is apparent in many patientsand
most haveamild, uncomplicatedcourse.

59. IV Contrast enhanced Computed TomographyScan*
• INDICATIONS-DIAGNOSTIC
– Diagnostic uncertainty (differentiating pancreatitis from other possible intra-
abdominal catastrophes)
– Severeacute pancreatitis- distinguish interstitial from necrotizingpancreatitis
• Necrosis( non enhancement area >30 %or 3 cm) done at 72 hrs*
– Systemic complications:
• Progressive deterioration, MOF
,sepsis
– Localized complications:
• Altered fat and fascial planes, Fluid collection, pseudocyst,
psduoaneurysm,
• Bowel distension, mesenteric edema, hemorrhage
*INVESTIGATIONOFCHOICE
**Seldom needed within first 72 hrs after symptom onset unless the
diagnosis is uncertain, because inflammatory changesare often not
radiological present until thistime

60. IV Contrast* enhanced Computed TomographyScan
• INDICATIONS-DIAGNOSTIC
– Initial assessmentof prognosis(CTseverityindex)
– Perfusion CTat 3rd day  area of ischemia predict pancreaticnecrosis
• INDICATIONS-THERAPEUTIC:
– CT-guidedaspiration of fluid collection/necrotic tissue for gram staining and
culture(sterile vsinfected necrosis)
– specimenshould be delivered to the laboratory within an hour and interpreted
promptly
– CT-guided pig tail catheterinsertion
*Use of IVcontrast mayincreaserisk of complications of pancreatitisandAKI
*Avoided if serumcreatinine >1.5mg/dL
*MRI suitable alternative

61. BALTHAZARCTseverity index(CTSI)-1994
Mild (0-3) moderate (4-6) severe(7-10)
CTSeverity Index Inflammation score +Necrosisscore

62. Magnetic ResonantImaging
Suitable alternative to CTin patients with a
contrast allergy and renal insufficiency where
T2-weighted imageswithout gadolinium
contrast candiagnose pancreatic necrosis

63. Magnetic ResonantCholangiopancreatography
• INDICATION:
– diagnosis of suspected biliary and pancreatic duct obstructionin
the setting of pancreatitis.
– Repeated attacks of idiopathic acutepancreatitis
• Merit
– used if choledocholithiasis is suspected but there is concernthat
pancreatitis might worsen is ERCPisperformed
– Provide non-invasive/fast/safe high-quality (Heavily T2–
weighted) imaging for diagnostic and/or severitypurposes

64. Endoscopic UltraSonography
• INDICATIONS
– Repeatedidiopathic acute pancreatitis*
• occult biliary disease- smallstones/sludge
• secretin-stimulatedEUS study may reveal resistance to ductal outflow at the
level of thepapilla,
– asevidenced by dilatation of the pancreatic duct to agreater extent and longerduration
than in ahealthypopulation
– Age>40to excludemalignancy
• especiallythose with prolong or recurrent course
• RATIONALE:5 %CApancreaspresent asAP
*Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, asthe
risks and benefits of investigation in these patients areunclear and should be referred to centers
of expertise.

65. Endoscopic Retrograde Cholangiopancreatography
INDICATION
• SeveregallstoneAPor APwith concurrent acute cholangitis/biliary
obstruction/ biliary sepsis/jaundice (due topersistent stone)
• ERCPwithin 24(-72) h ofadmission
• Sphincterotomy/stent and bile duct clearance reducesinfective
complications/mortality
NOTINDICATED
• Not needed early in most patients withgallstone pancreatitis who lack
laboratory or clinical evidence of ongoing biliaryobstruction
– Asmost of gallstones causingAPreadily passto duodenum and are lost in stool
– MRCPor EUSrecommended if CBDstone still suspected
• asrisk of post-ERCPpancreatitis is greater with normal calibre bile duct and normal
bilirubin
• MRCP/EUSasaccurate asdiagnostic ERCP

66. MISCELLANEOUS
• Peritoneal(sensitivity 54%,specificity 93%)/Pleural fluidtap
– High amylase/lipase/protein
• Urine CompleteExamination
– Proteinuria, granular cast,glycosuria
• Electrocardiography
– ST-Twavechanges
• BileAspiration
– Crystal analysis, if suspicion of microlithiasis
• Manometry
– Sphincterof Oddi dysfunction asa cause
• Genetictesting
– may be considered in young(<30 yrs) patients if no causeis evident and a
family history (especially if >1family member)of pancreatic disease ispresent

67. SEVERITYSCORINGSYSTEMS
ACUTEP
ANCREA
TITISSPECIFIC SCORINGSYSTEMS
– Ranson score
– Glagsow score
– Bedside Index for Severity in Acute Pancreatitis(BISAP) score
– Harmless Acute Pancreatitis Score(HAPS)
– HongKong Criteria
ACUTEP
ANCREA
TITISNON-SPECIFIC SCORINGSYSTEMS
(ICUSCORINGSYSTEMS)
– Acute Physiology And Chronic Health Evaluation(APACHE) II score
– Sequential Organ Failure Assessment(SOFA)score

68. Eachsystem hasmerits and demerits, and none
is currently recognized asacriterion standard

69. Although amylase/lipase are used in diagnosing
pancreatitis, they are NOT usefor predictingseverity
of disease
– i.e. patient with normal amylase(raised in 90%cases)
levels may still have severe acute pancreatitis

70. RANSONSCORE-1974
(for alcohol pancreatitis)
• TLC>16,000/mm3
• BSR>200mg/dL
• AST>250IU/L
• LDH>350IU/L
ONADMISSION WITHIN 48HOURS
• Age> 55 yrs • BUNrise >5mg/dL
• Pa02<60 mmHg( 8 KPa)
• SerumCalcium <8 mg/dL
• Basedeficit >4 meq/L
• Fluid Sequestration >6000 mL
• Hct fall >10%
NOTE:Diseaseclassified asSEVEREwhen 3 or more factors arepresent

71. RevisedRANSONSCORE-1979
(for Gallstone pancreatitis)
ONADMISSION
• Age>70 years
• TLC>18000/mm3
• BSR>220 mg/dL
• AST>250IU/L
• LDH>400IU/L
WITHIN 48HOURS
• BUNrise >5 mg/dL
• Pa02<60 mmHg ( 8 KPa)
• Serum Calcium <8 mg/dL
• Basedeficit >5 meq/L
• Fluid Sequestration >4 litres
• Hct fall >10%
NOTE:Diseaseclassified asSEVEREwhen 3 or more factors arepresent

72. RANSONSCORE
Ranson
score
Mortality rate SEVERITY Interpretation
0-2 ≈ 0-2 %i.e. minimal mortality Mild AP Admit in regularward
3-5 10-20 %
SevereAP
Admit in ICU/HDU
6-7 40 % Associated with moresystemic
complications
>7 >50 % Sameas above
SCORING SYSTEM SENSITIVITY SPECIFICITY
Ranson Criteria 73% 77%
APACHEII 77% 84%
CRP 73% 71%

73. RANSONSCORE…….
DRAWBACKS
• Onehasto measure all 11 signsto achieve the best predictabilityof
prognosis
• 2 full daysare needed to complete theprofile.
– Adelay of 48 hours after admission merely for assessmentmay
squander avaluable opportunity to prevent acomplication duringthis
time.
• Best used within the initial 48 hours ofhospitalization and have not
been validated for later timeintervals.
• Threshold for abnormal valve depends on whether causeis
gallstone or alcohol
• Only 73 %sensitive and 77 %specific in predicting mortality

74. Glasgow-Imrie score
ONADMISSION
• Age>55 yrs
• TLC>15 x109 l-1
• BSR>180mg/dL (10 mmol l-1)
(no H/Odiabetes)
• BUN>16 mmol l-1
(no response to IVfluids)
• Pa02<60 mmHg( 8 KPa)
WITHIN 48HOURS
• SerumCalcium <2.0 mmol l-1
• Serumalbumin <32gl-1
• LDH>600 unitsl-1
• AST/ALT>200 unitsl-1
NOTE:Diseaseclassified asSEVEREwhen 3 or more factors arepresent

75. Modified Glasgow/PANCREASscore
• PaO2 <8kPa(60mmhg)
• Age>55 years
• Neutrophils: WBC >15x109/l
• Calcium <2mmol/l
• Renal function: (Urea >16mmol/l)
• Enzymes:(AST/ALT>200 iu/L or LDH >600 iu/L)
• Albumin <32g/l
• Sugar: (Glucose>10mmol/L)
*Applicable for both gallstone and alcohol induced pancreatitis within 48 hours ofadmission
*Omission of age/serum transaminase increases the predictive valve of scoring system as
serum transaminase did not differ significantly between mild and severepancreatitis
*Bold 4 factors are independently significant in predicting theseverity

76. Acute Physiology And Chronic Health Evaluation IIscore-1985
NOTE:Diseaseclassified asSEVEREif clinical impression of very ill patient with
AP
ACHEII score above8

77. APACHEScoringSystem
MERIT
• Immediate assessmentof the severity ofpancreatitis
possible
• Canbe used even after 48hours
• Unlike ALLpancreatic specific scoring systems,APACHE(and SOFA)also
includes clinical features of patient besides laboratoryvalues
(Clinical findings are more important than lab findings inpredicting
SIRS,sepsisand othercomplications)
• Best validated(medscape)

78. DEMERITS OFAP-specific scoring systems(ACG2013)
• Uniformly cumbersome, typically requiring 48h to become accurate
– when the score demonstrates severe disease, the patient’s conditionis
obvious regardless of thescore.
• Havealimited value, asthey provide little additional information tothe
clinician in the evaluation of patients and maydelay appropriate
management.
• Nolaboratory test is practically available or consistently accurate to
predict severity in patients withAP
.
– Eventhe acute-phase reactant CRP, the most widely studied inflammatory
marker in AP
, is not practical asit takes 72 h to becomeaccurate.
– CTand/or MRIimaging also cannot reliably determine severity early in the
course of AP
,asnecrosis usually is not present on admission and may develop
after 24 – 48 h.
Thus,in the absenceof any available test to determine severity, close
examination to assessearly fluid losses,hypovolemic shock,andsymptoms
suggestive of organ dysfunction iscrucial.

79. Predicting Severe AP(ACG2013)
Sorather than depending on ascoring system to
predict severity ofAP
,
one need to be awareof intrinsic patient-
related risk factors, includinglaboratory
and imaging risk factors, for the
development of severedisease.

80. Clinicalfindings associated witha severe coursefor initial risk assessment
Patient characteristics Age>55 years
Obesity (BMI >30 kg/m2)
Altered mental status
Comorbid disease
SIRS(>2 of the following criteria) pulse >90 bpm
Resprate >20/min or PaCO2>4.3 KPa(32mmHg)
Temperature >38 °C(100.4oF)or <36 °C(96.8oF)
TLC>12,000 or <4,000 cells/mm3 or >10%
immature neutrophils (bands)
Laboratory findings BUN>20 mg/dl
Rising BUN
Hct >44%
Rising Hct
Elevated creatinine
Radiology findings Pleural effusions
Pulmonary infiltrates
Multiple or extensive extrapancreaticcollections

81. MANAGEMENT
• Mild acutepancreatitis
– ConservativeApproach
– Admit in generalward
– Non invasive monitoring
• (Moderate)Severe acutepancreatitis
– AggressiveApproach
– Admit in HDU/ICU
– Invasive monitoring
Recognizing patients with severe acute pancreatitis ASAPis
critical for achieving optimaloutcomes

82. Mild AcutePancreatitis
• mild and self-limiting, needing only briefhospitalization.
• Rehydration by IV fluids
• Frequent non-invasive observation/monitoring(atleast 8hrly)
• Brief period of fasting tillpain/vomiting settles
– Little physiological justification forprolonged NPO
• No medication required other than analgesics(important) andanti-emetics
– Antibiotics not indicated in absenceof signsor documented sources of infection
– Painresults in ongoing cholinergic discharge,stimulatinggastric and pancreatic secretions
– Analgesics: WHOanalgesic ladder-1986
– Avoid Morphine-cause sphincter of Oddispasm
• Metabolicsupport
– Correction of electrolyte imbalance

83. Modified WHOanalgesic Ladder

84. No or little roleof………………..
• Nasogastric suction and H2-blockers
• Secretion-inhibiting drugs
– Atropine, calcitonin, somatostatin and its analogue(Octreotide)
– glucagon andfluorouracil
• Protease inhibiting drugs
– Aprotinin, gabexatemesylate,camostate, phospholipase A2inhibitors,
FFP
• Indomethacin or PGinhibitors
• P
AFantagonists
– P
AFacetylhydrolase, Lexipafant

85. SevereAcute Pancreatitis
• P:
– Painrelief
– Proton pump inhibitors-omeprazole
– Peritoneal lavage
• A
– Admit in HDU/ICU
– Antibiotics
• N
– Nasogastric intubation(if vomiting)
– Nasaloxygen
– Nutrition support
• C
– Calciumgluconate
– CVPline
– Catherisation-Foley
• R
• E
– Rehydration by IV fluids,plasma,blood
– Ranitidine(for stress ulcer)
– Radiology: CTscan,USG
– Resuscitation when required
– Endotracheal intubation
– Electrolytes management
– ERCP
• A
– Antacids
• S
– Swan-Ganzcatheter for CVPandTPN
– Suction-in caseof aspiration
– Steroids in caseof ARDS
– Supportive therapy for organfailure
• Inotropes
• Hemofiltration
• Ventilator(PEEP)

86. Monitoring
CLINICAL
• Vitals
• UOP
• CVpressure
INVESTIGATIONS
• Baselines
• SerialABGs
• Serial BSR
• Serumcalcium/magnesium

87. ACG2013Recommendations
• Despite dozensof randomized trials, no
medication hasbeen shown to beeffective
in treatingAP
.
• However, an effective intervention hasbeen
well described: EARLYAGRESSIVE IV
hydration.

88. Rationale for EARLYAGRESSIVE IVhydration
• Frequent hypovolemia due to
– vomiting,
– reduced oral intake,
– third spacingof fluids(increased vascularpermeability)
– increased respiratory losses,and
– diaphoresis.
• Combination of microangiopathic effects and edema of the
inflamed pancreas decreasesblood flow, leading to increased
cellular death, necrosis, and ongoing release of pancreaticenzymes
activating numerous cascades.
*provides micro- and macrocirculatory support to preventserious
complications suchaspancreatic necrosis

89. EARLYAGRESSIVE IV hydration
Kon sa? Lactated Ringer ’ssolution may be the preferred isotoniccrystalloid
replacement fluid
• Ringer lactate is better electrolyte balance and more pH-balanced
• Normal saline given in large volumes may lead to the
development of anon-anion gap, hyperchloremicmetabolic
acidosis and increased chancesof SIRS
• Low pHactivates the trypsinogen, makesthe acinar cells more
susceptible toinjury and increases the severity of established AP
Kab? Early aggressiveIVhydration is most beneficial during the first 12– 24h, and
may have little benefit beyond this timeperiod
Kitna? Aggressivehydration, defined as250– 500ml per hour of isotonic crystalloid
solution should be provided to all patients, unless cardiovascular, renal, or
other related comorbid factorsexist.
• In apatient with severe volume depletion, manifest ashypotension
and tachycardia, more rapid repletion (bolus) may be needed
• Fluid requirements should be reassessed at frequent intervals within 6
h of admission and for the next24 – 48 h.

90. EARLYAGRESSIVE IV hydration
– Hematocrit and BUNhasbeen widely recommended as
surrogate markers for successfulhydration
• No absolute numbers recommended
• Goal to decrease Hct and BUNand maintain normalcret
– In elderly and cardiac/renal comorbidities hydrationis
monitored by
• Central venous pressure via CVlineor
• Intrathoracic blood volumeindex
– Better/more accurate correlate with cardiac index thanCVP

91. Antibiotics
• Routine use* NOTrecommended(ACG2013) as
– Prophylaxis in severeAP
– Preventive measure in sterile necrosis toprevent
development of infectednecrosis
• Indicated in
– Established infected pancreatic necrosisor
– Extraperitoneal infections
• Cholangitis, catheter-acquired infections, bacteremia, UTIs,
pneumonia
*Routine useof antifungal agents along with prophylactic or therapeutic antibioticsNOT
recommended(ACG2013)

92. Antibiotics
• AsSIRSmay be indistinguishable from sepsis
syndrome, soif infection is suspected,antibiotics
should be given while source of infection isbeing
investigated
– Onceblood and other cultures are foundnegative,
antibiotics should bediscontinued
• Fewantibiotics penetrate due to consistencyof
pancreatic necrosis
– cefuroxime, or imipenem, or ciprofloxacinplus
metronidazole

93. Antibiotics
• Useof probiotics is associated with increasedmortality
in severeAP
• Selective decontamination of bowel, targetingboth
bacteria and fungi, in order to prevent infected
necrosis
– Controversial
• Relatively stable patients with infected necrosis canbe
managed conservatively on antibiotics withoutneeding
surgery(necrosectomy) or intervention (percutaneous
or endoscopicdrainage)
– Surgical debridement recommended if no responseto
conservative treatment or deterioratesclinically

94. …………………………………………………….
Rather than preventing infection, the role of antibiotics in patients with
necrotizing APis NOWto treat established infectednecrosis

95. Nutrition
• In mildAP
– oral feedings canbe started immediately if there is no
nausea/vomiting, and the abdominal pain/tenderness/Ileus has
resolved(amylase return tonormal, patient feel hunger)
– Initiation of feeding withasmall and slowly increasing low-fat
(low-protein) soft diet appears assafeasaclear liquid diet,
providing more calories
• Stepwisemanner increase from clear liquids to soft dietNOTnecessary
• In severeAP
– Enteral route is recommended to prevent infectiouscomplications
– Parenteral nutrition should be avoided, unless enteral route isnot
available, not tolerated, or not meeting caloric requirements

96. RATIONALEOFEARLYENTERALNUTRITION
• Theneed to place pancreas at rest untilcomplete
resolution of APno longer seemimperative
– Bowel rest associated withintestinal mucosal atrophy and
bacterial translocation from gut and increased infectious
complications
• Early enteral feeding maintains the gut mucosalbarrier,
prevents disruption, and prevents translocation of
bacteria that seedpancreaticnecrosis
– Decreasein infectious complications, organ failureand
mortality

97. ………………………………………………..
Rather than using antibiotics to prevent infected necrosis………….start early
enteral feeding to prevent translocation of bacteria
RATIONALE MANAGEMENT
PREVENTIONOFSTERILENECROSIS Early aggressiveIV hydration
PREVENTIONOFINFECTEDNECCROSIS Early enteral feeding( NOTantibiotics)
TREATMENTOFINFECTEDNECROSIS Antibiotics, drainage, necrosectomy

98. Route of enteralNutrition
• Traditionally nasojejunal route hasbeenpreferred
to avoid the gastric phase of stimulationBUT
– Nasogastric route appears comparable in efficacyand
safety
MERITS OFNASOGASTRIC ROUTE DEMERITS OF NASOGASTRICROUTE
NGtube placement is far easier than
nasojejunal tube placement( requiring
interventional radiology or endoscopy,thus
expensive) especially in HDU/ICUsetting
Slight increased risk of aspiration
(Canbe overcome by placing patient in upright
position and be placed on aspiration
precautions)

99. Roleof Surgery in AP
• In caseof mild gallstoneAP
,cholecystectomy should be performed before
discharge to prevent arecurrence ofAP
– Within 48-72 hour od admission or briefly delay intervention(after 72 hrsbut
during sameadmission
– Along with intraoperative cholangiography and any remaining CBDstones can
be dealt with intra/post operative ERCPor
– Along with preoperative EUSorMRCP
• In caseof necrotizing biliary AP
,in order to prevent infection,
cholecystectomy is to be deferred until active inflammationsubsidesand
fluid collections resolve orstabilize
• Cholecysectomydone for recurrent AP(IAP)with no stones/sludge onUSG
and no significant elevation of LFT
sis associated with >50%recurrence of
AP
If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone
maybe effective to reduce further attacks ofAP

100. Sterilenecrosis infectednecrosis
Asymptomatic doesnot mandate
intervention regardless of
size,location andextension
surgical, radiologic, and/or
endoscopic drainage should be
delayed preferably for more
than 4weeks
• to allow liquefaction of
the contents and the
development of a
fibrous wall aroundthe
necrosis
• Initially treated with
antibiotics
Stable
Symptomatic
(associated with
GOOor bile
obstruction)
minimally invasivemethods
of necrosectomy are
preferred to open
necrosectomy
Urgentdebridement unstable
Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach),
percutaneous radiologic catheter drainage or debridement, video-assisted or small incision-
basedleft retroperitoneal debridement, andendoscopy

101. When toDischarge
• Painis well controlled with oralanalgesia
• Able to tolerate an oral diet that maintains their caloric needs, and
• all complications havebeen addressedadequately
Followup
• Routine clinical follow-up care (typically including physical examinationand
amylase and lipase assays)is needed to monitor for potential complications ofthe
pancreatitis, especially pseudocysts.
• Within 7-10days

102. Recurrent AP
CTscan
• If neoplasiaor chronicpancreatitis is found
• addressed and treatedaccordingly.
MRCP
• shows developmentalabnormalities, strictures, or evidenceof chronicpancreatitis
• endoscopicor surgical treatmentmaybe of benefitin a subset of patients
EUS
• Microlithiasis/biliary sludgeCholecystectomy
• Periammpullarymass missed onCTor MRCP
Genetic • cationic trypsinogen mutations, SPINK1mutations, or CFTRmutations
ERCP
• sphincter of Oddimanometry
• Placedlast becauseveryhigh rateof post-ERCPpancreatitis(benefits< risk)

103. Prognosis
TYPEOF AP MORTALITY
Overall 10-15 %
(Biliary>alcholic)
Mild Acute Pancreatitis(80 %cases) 1 %
SevereAcute Pancreatitis(20 %cases) Severe 20-50 %
<1week 1/3 cases MOF
>1week 2/3 cases Sepsis
(+MO
F)

104. SYSTEMICCOMPLICATIONS
• CARDIOVASCULAR
– Shock-hypovolemic and septic
– Arrhythmias/pericardial effusion/sudden death
– ST-Tnonspecificchanges
• Pulmonary
– Respiratory failure/pneumonia/atelectasis/pleural effusion
– Acute Respiratory Distress Syndrome (ARDS)
• Renal Failure
– Oliguria
– Azotemia
– Renalartery/vein thrombosis
• Hematological
– Hemoconcentation
– Disseminated Intravascular Coagulopathy (DIC)

105. SYSTEMICCOMPLICATIONS
• Metabolic
– Hypocalcemia
– Hyperglycemia
– Hyperlipidemia
• Gastrointestinal
– Peptic Ulcer/Erosive gastritis
– Ileus
– Portal vein or splenic vein thrombosis withvarices
• Neurological
– Visual disturbances-Sudden blindness(Purtscher’sretinopathy)
– Confusion,irritability,psychosis
– Fatemboli
– Alcohol withdrawal syndrome
– Encephalopathy
• Miscellaneous
– Subcutaneousfat necrosis
– Intra-abdominal saponification
– Arthralgia

106. LOCALCOMPLICATIONS
• Peripancreatic fluid collections
• (Peri)Pancreatic necrosis( sterile +infected)
• Pancreatic abscess(Phlegmon)
• Pseudocyst
• Pancreatic ascites
• Pseudoaneurysm
• Involvement of adjacent organs,with hemorrhage, thrombosis,bowel
infraction, obstructive jaundice, fistula formation, or mechanical
obstruction

107. THANK YOU……….