Acute pancreatitis is an inflammation of the pancreas that presents with severe abdominal pain and elevated pancreatic enzymes. It can be caused by gallstones, alcohol use, metabolic disorders, infections, genetic factors, or trauma. The clinical presentation includes epigastric pain radiating to the back that is relieved by sitting forward, nausea, vomiting, and fever in severe cases.

1. Acute Pancreatitis
[Acute inflammation of abdominal tiger]
(According to American College of Gastroenterology 2013 guidelines)
Jibran Mohsin
Resident, Surgical Unit I
SIMS/Services Hospital Lahore

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

3. PANCREATITIS
Inflammation in pancreas associated with injury to
exocrine parenchyma
PANCREAS
Stroma
Parenchyma
Exocrine
Primary injury causing
PANCREATITIS
Endocrine
Involved secondarily or
as a complication
PANCREAS Greek word with literal meaning ‘pan’ (all/whole) , ‘creas’ (flesh): sweatbread

4. CLINICAL CLASSIFICATION
*Considered a phase of chronic pancreatitis
** resulting from fibrosis within pancreas

5. ACUTE PANCREATITIS
• CLINICAL DEFINITION
– An acute condition presenting with abdominal pain-usually associated with
raised blood/urine pancreatic enzymes as a result of pancreatic inflammation
• PATHOLOGICAL DEFINITION
– Reversible* pancreatic parenchymal injury associated with inflammation
___________________________________________________________
*if underlying cause of pancreatitis is removed, heal without any impairment of
function or morphologic loss of gland
*Recurrent attacks with irreversible parenchymal injury leading to impairment of
function and morphologic loss is chronic pancreatitis

6. CLASSIFICATION OF ACUTE PANCREATITIS
Atlanta* criteria (1992)
• Mild acute pancreatitis (80% cases)
(Acute Interstitial/edematous pancreatitis)
– Acute Absence of organ failure
– Absence of local complications
• Severe acute pancreatitis(20 % cases)
(Acute Hemorrhagic Necrotizing (fulminant)
pancreatitis)
– Local complications +/-
– Organ failure defined as
• SBP < 90 mm Hg
• PaO2 ≤ 60 mm Hg
• GI bleed ≥ 500 ml/24 hrs
• Cret ≥ 2 mg/dL after rehydration
– Ranson score ≥ 3 or APACHE ≥ 8
Revised Atlanta criteria (2012)
• Mild acute pancreatitis
– Absence of organ failure
– Absence of local complications
• Moderately severe acute
pancreatitis
– Local complications +/-
– Transient organ failure(<48 h)
• Severe acute pancreatitis
– Persistent organ failure**(>48 h)
and/or death
*defined as a score of 2 or more for one of these(CVS, Renal, Resp) organ systems using the
modified Marshall scoring system

7. Modified Marshall Scoring System for organ failure

8. Two Distinct phases of Acute Pancreatitis
Early Phase(within 1 week)
• Characterized by SIRS +/-
organ failure
• Severity assessed by
functional/clinical Severity
Scoring System
(Ranson/Galsgow etc)
Late Phase (>1 week)
• Characterized by local
complication
• Severity assessed by
morphological scoring
system(Balthazar Scoring)
__________________________________________________________________________
*Early clinical and the later morphologic classifications do not necessarily
overlap and do not necessarily correlate with one another

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 cases per 100,000)

10. Epidemiology
Median ages of onset for various etiologies
Etiology Median Ages of onset
Alcohol-related 39 years
Biliary tract–related 69 years
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 to alcohol
In females more often related to biliary tract disease
Idiopathic pancreatitis no clear gender predilection
AGE
Young males and Old Females

12. Epidemiology
RACE
Hospitalization rates3 times higher for blacks than whites
(racial differences more pronounced for males than females)
Risk for African Americans aged 35-64 years10 times higher
than for any other group

13. PATHOPHYSIOLOGY
Autodigestion of 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 kinin system
Activation of Hageman factor-XII Activation of clotting and
complement systems thrombosis
and inflammation
Activation of Phospholipase Activation of Prostaglandins and
Bradykinins
Lipase activation Triglycerides
Glycerol + Fatty acids
Fatty acids+ calcium saponified
fat Hypocalcemia
Elastase activation Digestion of
elastic fibers Capillary
leak/rupture/ Pseudoaneurysm
3rd space Sequestration of
blood/fluid Hemorrhage+
Hypovolemic shock
Activation of Lysolecithinase
(derived from bile)
Membrane damage Necrosis
Release of inflammatory mediators
into circulation
systemic complications

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

16. ACUTE
PANCREATITIS
Drinks like FISH (Dehydration)
Burrows like
RODENT
(produces fistula)
Stings like
SCORPION
(severe pain)
Kills like LEOPARD (Life threatening)
Eats like WOLF
(Pancreatic
Necrosis)

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

18. MECHANICAL CAUSES OF ACUTE PANCREATITIS
Gall stones  Choledocholithiasis(40-70 %)
• Most common biliary tract disease leading to AP
• MOA: Ductal obstruction causing ductal hypertension and acinar cell injury
• “Common channel hypothesis”-Opie in 1901(bile/activated enzymes reflux)-
CONTROVERSIAL
• Risk factors: inverse relation to size, wide cystic duct
• 5 % of gall stones causes pancreatitis
• M:F=1:3
Ampullary tumor
sphincter of Oddi dysfunction
Pancreatic CA(1-2 % )
• 5 % present as AP
Choledochoceles, biliary sludge
Abdominal trauma(1.5 %cases)
• 17 % cases have 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 %)
• Type I and V hyperlipidemia
• >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 OF ACUTE PANCREATITIS
Viruses
• MMR, Dengue virus(complication of dengue hemorrhagic fever MOA:
Capillary leak3rd space loss), 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,
• Fasciola Hepatica, Opistorhcis sp and Dicrocoelium dendriticym
Scorpion and snake bite
• Trinidalian scorpion* (Tityus trinitatis)
• MOA: Neurotransmitter discharge from cholinergic nerve terminals, leading to
massive production of pancreatic juice(same MOA in antiacetylcholinesterase/OPC
insecticide)
*Most common cause of AP in Republic of Trinidad and Tobago, a twin island country off the northern edge of
South America

21. GENETIC CAUSES OF AUTE PANCREATITIS
Pancreas divisum (unfused ducts of Wirsung and Santorini)
• Seen in 20-45 % cases
• MOA(controversial): stenotic minor papillae and atretic duct of santorini
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 binding of
trypsin rendering it inactive
• Acute pancreatitis in teens
• Chronic in next 2 decades
• 40 % risk of pancreatic cancer by 70 year
Celiac disease
Cystic fibrosis-CFTR mutation  abnormality of ductal secretion

22. VASCULAR CAUSES OF ACUTE PANCREATITIS
Shock
Hypothermia
Atheroembolism
Vasculitis(Polyarteritis nodosa, SLE)

23. How Alcohol  Acute Pancreatitis??
 Effects of diet
 Malnutrition
 Direct toxicity of alcohol
 Concomitant tobacco smoking
 Hypersecretion of gastric and
pancreatic juices(rich in protein,
low in bicarbonate/ trypsin
inhibitor)protein plugsduct
obstruction/reflux
 Hyperlipidemia
 Increased ductal
permeability enzymes
extrusion damage
 Release of free radicals-
superoxide, hydroxyl
 Spasm of sphincter of Oddi

24. Alcohol-induced Pancreatitis
• Manifests as a spectrum, ranging from discrete episodes of
AP to 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) alcohol consumption.
• Clinically evident AP occurs in <5 % of heavy drinkers; thus,
there are likely other factors that sensitize individuals to
the effects of alcohol, such as genetic factors and tobacco
use.
• 1st attack is considered alcohol induced AP
– Although it may be 1st manifestation of (acute on) chronic
pancreatitis

25. Idiopathic Acute Pancreatitis
• Defined as pancreatitis with no etiology established after initial
laboratory (including lipid and calcium level,autoimmune markers,
viral titers) and imaging tests (USG and CT in the appropriate
patient)
– In some patients an etiology may eventually be found(70 % of IAP due
to microlithiasis), yet in others no definite cause is ever established.
• Patients with IAP should be evaluated at centers of excellence
focusing on pancreatic disease, providing advanced endoscopy
services and a combined multidisciplinary approach.
________________________________________________________
Careful search for the etiology must be made in all cases, and no more
than 20 % of cases should fall into the idiopathic category

26. Hyperlipidemia induced AP
• In the absence of gallstones and/or history of significant history of
alcohol use, a serum triglyceride should be obtained and considered
the etiology if > 1,000 mg /d l
• Lactescent (milky) serum has been observed in as many as 20 % of
patients with AP
• Therefore a fasting triglyceride level should be re-evaluated 1 month after
discharge when hypertriglyceridemia is suspected
• MOA: Lipase liberate large amounts of toxic fatty acids into
pancreatic microcirculation
• Leading to endothelial injury, sludging of blood cells, and consequent ischemic
states

27. Iatrogenic-Operative Pancreatitis
• Surgeries performed on/close to pancreas
– Pancreatic biopsy
– Biliary duct exploration
– Distal or Billroth II gastrectomy
– Jejunostomy
– Splenectomy
• Surgeries that use low systemic perfusion
– Cardiopulmonary bypass (also due to hypothermia, atheromatous
emboli)
– Cardiac transplantation

28. Post-ERCP Pancreatitis
• 3rd Most common cause of AP(after gallstone and alcohol) i.e. 4%
• Most common complication of ERCP
• INCIDENCE
– 2-4 % (Historically, 5-10%) patients undergoing ERCP develop acute pancreatitis
– Risk of severe AP < 1/500.
• CAUSE
– Duct disruption , enzyme extravasation
• PREDISPOSING FACTORS
– Sphincter of Oddi dysfunction(risk increases to 30 %)
– H/O recurrent pancreatitis
– Sphincterotomy
– Balloon dilation of sphincter
– Inexperienced endoscopist

29. CLINICAL MANIFESTATION

30. ABDOMEN PAIN-Cardinal Symptom
• SITE: usually experienced first in the epigastrium
– but may be localized to either upper quadrant or felt diffusely throughout the abdomen or lower chest
• ONSET: characteristically develops quickly, generally following substantial meal and precedes NV
• SEVERITY: frequently severe, reaching max. intensity within minutes rather than hours
• NATURE: “boring through”, “knifing” (illimitable agony)
• DURATION: hours-days
• COURSE: constant (refractory to usual doses of analgesics, not relieved by vomiting)
• RADIATION: directly to back(50%), chest or flanks
• RELEIVING FACTOR: sitting or leaning/stooping forward (MUHAMMEDAN PRAYER SIGN)
– due to shifting forward of abdominal contents and taking pressure off from inflamed pancreas
• AGGRAVATING FACTOR: food/alcohol intake, walking, lying supine
_______________________________________________________________________________
Pain described as dull, colicky, or located in the lower abdominal region is not
consistent with AP and suggests an alternative etiology

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

32. General Physical Examination
• Appearance: well  gravely ill with profound shock, 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 pancreatic head
• Cyanosis
– Improper lung perfusion
• Pallor, cold clammy skin,diaphoretic

33. ABDOMEN EXAMINATION
• Tenderness + Rebound tenderness:
– epigastrium/upper abdomen
• Distension:
– Ileus(BS decreased or absent)
– ascites with shifting dullness
• Mass in epigastrium(usually absent)
– due to inflammation
• Guarding(also called “defense musculaire” )-upper abdomen
– tensing of the abdominal wall muscles to guard inflamed organs within the
abdomen from the pain of pressure upon them(i.e. during palpation)
• Rigidity(involuntary stiffness)-unusual
– Tensing of the abdominal wall muscles to guard inflamed organs even if patient not
touched

34. Cutaneous Ecchymosis(1 % cases)*
Acute Hemorrhagic Necrotizing/fulminant
Pancreatitis Periperitoneal/retroperitoneal
Hemorrhage
Methemalbumin formed from digested blood tracks around
Fascial planes 
hemorrhagic spots
and ecchymosis in
flanks
(GREY TURNER’S
SIGN)**
FALCIFORM
LIGAMENT  Bluish
Discoloration around
umbilicus
(CULLEN’S SIGN)
(umbllical black eye)
Below inguinal ligament
(FOX SIGN)
*Neither sign is pathognomonic of acute pancreatitis
*takes 24-48 hours to develop with 10-40 % mortality
**More commonly, ruddy
erythema in flanks due to
extravasated pancreatic exudate

35. Differential Diagnosis
GREY TURNER/CULLEN/FOX SIGNs
• Acute Pancreatitis
• Pancreatic Hemorrhage
• Ruptured AAA
• Blunt abdominal trauma
• Ruptured ectopic pregnancy
• Retroperitoneal hemorrhage
• Coagulopathy
Above: George Grey Turner Above: Thomas Stephen Cullen

36. GREY TURNER1 SIGN CULLEN2 SIGN FOX3 SIGN
1. Named after British surgeon George Grey Turner(1877-1951)
2. Named for Thomas Stephen Cullen (1869-1953), Canadian gynecologist who first
described the sign in ruptured ectopic pregnancy in 1916
3.Named after George Henry Fox(1846-1937), American dermatologist

37. RESPIRATORY EXAMINATION
Left sided* Pleural effusion(10-20%) + pulmonary edema+ pneumonitis
Reduced chest movements+
decreased vocal fremitus/resonance +
stony dull percussion note+
decreased air entry basally bilaterally +
basal fine 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
Fat Embolism
Hypoxia
Respiratory
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 vessels causing Ischemic
injury of retina
– May cause temporary or permanent blindness

40. MANIFESTAIONS OF COMPLICATIONS
• 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 MCP joints with extension of IP joints
– laryngospasm
– generalized seizures
– Chvostek*(-Weiss) sign
• Depending on calcium level, graded response occur: twitching first at angle of mouth,
then by nose, the eye and the facial muscles
• Positive in 10 % population in absence of hypocalcaemia
– Trousseau** sign of latent tetany
• BP cuff around arm and inflating to 20 mmHg above SBP for 3-5 minutes
• Carpal spasm observed
• More specific and sensitive than chvostek sign(postive even before tetany/hyperreflxia)
*František Chvostek (German: Franz Chvostek) Czech-Austrian military physician (1835 – 1884), described this sign in 1876.
**Armand Trousseau, French physican (1801-1867) described this phenomenon in 1861

41. MANIFESTAIONS OF COMPLICATIONS
Hematemesis/
melena
(5%)
DIC
Peripancreatic
(duodenal)
necrosis
Gastric
erosions

42. DIFFERENTIAL DIAGNOSIS
ABDOMINAL CONDITONS
• Perforated peptic ulcer/gastroentritis
• Biliary colic/acute cholecystitis/ Cholangitis
• Mesentric Ischemia
• Ruptured Aortic Anuerysm
• Intestinal Obstruction
• Gastric/colon/pancreatic CA
• Viral Hepatitis
• IBS
SYSTEMIC CONDITIONS
• DKA
THORAX CONDITIONS
• Pneumonia/ARDS
• Pleuritic pain
• MI
GYNECOLOGICAL CONDITONS
• Ectopic pregnancy
• Salpingtis

43. Diagnostic criteria
• Most often established by the presence of two of the three
following criteria:
– (i) abdominal pain consistent with the disease,
– (ii) serum amylase and/or lipase greater than three times the upper
limit of normal, and/or
– (iii) characteristic findings from abdominal imaging.
_________________________________________________________
CT and/or MRI of the pancreas should be reserved for patients
– 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 evaluate complications

44. WORKUP
• HEMATOLOGICAL investigations
• RADIOLOGICAL investigations
• Miscellaneous investigations

45. HEMATOLOGICAL
• BASELINES
– CBC:
• Low Hb: 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 stone pancreatitis
– RFT’s:
• raised BUN/cretainine- ATN ARF
– Coagulation profile:
• increased INR-DIC
– BSR:
• > 180 mg/dl-diabetes as a sequelae 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
– Serum fasting lipid profile
– Viral titers
– Serum Calcium (HypercalcemiaAPHypocalcemia)
– Autoimmune markers
• increased serum levels of IgG4
• serum autoantibodies such as anti-nuclear antibody (ANA), anti-lactoferrin
antibody, anti-carbonic anhydrase II antibody, and rheumatoid factor (RF),
Acid-Base Disturbance Etiology
Metabolic (Lactic)acidosis with high anion gap 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
– Serum Amylase:
• ONSET: almost immediately
• PEAK: within several hours
– 3-4 times upper limit of normal within 24 hrs (90%)
• RETURN to normal depends on severity(3-5 days)
• normal at time of admission in 20% cases
• Compared with lipase, returns more quickly to values below
the upper limit of normal.
– Serum Lipase:
• more sensitive/specific than amylase
• Remains elevated longer than amylase(12 days)
• Useful if late presentation
Raised Amylase  may not AP
Normal Amylase  may be AP
SERUM INDICATOR OF HIGHEST
PROBABILITY OF DISEASE

48. • Pancreatic Enzymes’ Assays
– Urine Amylase
• More sensitive than serum levels
• Remain elevated for several days after serum levels returned to
normal
– Pancreatic-specific amylase(p-amylase)
• Measuring p-amylase instead to total amylase(also includes
salivary amylase) makes diagnosis more specific(88-93%)

49. CONDITIONS ASSOCIATED WITH RAISED SERUM AMYLASE
ABDOMEN
• Small bowel obstruction
– strangulation ileus
– mesenteric ischemia
• Acute appendicitis
• Cholecystitis
• Perforated Duodenal Ulcer
• Gastroenteritis
• Biliary peritonitis
• Spasm of sphincter of Oddi
GYNE
• Ruptured Ectopic pregnancy
• Torsion of an ovarian cyst
OTHERS
• Parotitis (Mumps)
• Macroamylasaemia
• Opioids administration
• Low GFR
• Brain injury(CVA)- hyperstimulation
of pancreas

50. Plain CXR-PA view
• Left sided Pleural effusion: blunting of costophrenic and
cardiophrenic angles + haziness in lower zones
• Elevated diaphragm on left side
• Linear focal atelactasis of lower lobe of lungs
• ARDS: diffuse alveolar interstitial shadowing
• Pulmonary edema: prominent vascular markings
_________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

51. Plain X-ray abdomen erect AP view
• Sentinel* loop sign
– Localized isolated Distended gut loop (Ileus) seen near the site of injured viscus
or inflamed organ
– RATIONALE: body's effort to localize the traumatic or inflamed lesions
– ETIOLOGY: Localized paralysis followed by accumulation of gas
– SITE:
• Acute Pancreatitis Left hypochondrium (PROXIMAL JEJUNUM)
• Acute Appendicitis Right iliac fossa
• Acute Cholecystitis Right Hypochondrium
• Diverticulitis Left iliac fossa
*SENTINEL:A soldier stationed as a guard to challenge all comers and prevent a surprise
attack
_______________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

52. SENTINEL LOOP SIGN

53. Plain X-ray abdomen erect AP view
• Colon cut-off sign
– Gas filled (Distended) segment of proximal(mainly transverse) colon
associated with narrowing of the splenic flexure
– abruptly ending at the area of pancreatic inflammation
– with collapse of descending colon
– RANTIONALE: Extension of inflammatory process from the pancreas into the
phrenicocolic ligament via the transverse mesocolon
• resulting in functional spasm and/or mechanical narrowing of the splenic flexure at
the level where the colon returns to the retroperitoneum.
– Differential DIAGNOSIS:
• IBD
• Carcinoma of colon
• Mesenteric Ischemia
____________________________________________________________________________________
Not diagnostic of Acute Pancreatitis; useful in differential diagnosis

54. COLON CUT-OFF SIGN

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

56. Renal Halo Sign
NORMAL RENAL HALO SIGN

57. Transcutaneous Abdominal Ultrasonography
• Not diagnostic
• Should be performed within 24 hours in all patients to
– detect gall stones* as a potential cause
– Rule out acute cholecystits as differential diagnosis
– Detect dilated CBD
– sensitivity-(70-80%)
– DEMERIT: overlying gas shadows 2ndary to bowel distension
• THERAPEUTIC:
– USG-guided aspiration for gram staining and culture
– USG-guided pig tail catheter insertion
______________________________________________________________________________
* Identification of gallstones as the 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 removed or
passes spontaneously.

58. IV Contrast enhanced Computed Tomography Scan
• Provides over 90 % sensitivity and specificity for
the diagnosis of AP….. BUT
• Routine use in patients with AP is unwarranted,
as the diagnosis is apparent in many patients and
most have a mild, uncomplicated course.

59. IV Contrast enhanced Computed Tomography Scan*
• INDICATIONS-DIAGNOSTIC
– Diagnostic uncertainty (differentiating pancreatitis from other possible intra-
abdominal catastrophes)
– Severe acute pancreatitis- distinguish interstitial from necrotizing pancreatitis
• 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
_____________________________________________________________
*INVESTIGATION OF CHOICE
**Seldom needed within first 72 hrs after symptom onset unless the
diagnosis is uncertain, because inflammatory changes are often not
radiological present until this time

60. IV Contrast* enhanced Computed Tomography Scan
• INDICATIONS-DIAGNOSTIC
– Initial assessment of prognosis(CT severity index)
– Perfusion CT at 3rd day  area of ischemia predict pancreatic necrosis
• INDICATIONS-THERAPEUTIC:
– CT-guided aspiration of fluid collection/necrotic tissue for gram staining and
culture(sterile vs infected necrosis)
– specimen should be delivered to the laboratory within an hour and interpreted
promptly
– CT-guided pig tail catheter insertion
______________________________________________________________
*Use of IV contrast may increase risk of complications of pancreatitis and AKI
*Avoided if serum creatinine >1.5 mg/dL
*MRI suitable alternative

61. BALTHAZAR CT severity index(CTSI)-1994
___________________________________________________________________
Mild (0-3) moderate (4-6) severe (7-10)
CT Severity Index Inflammation score + Necrosis score

62. Magnetic Resonant Imaging
Suitable alternative to CT in patients with a
contrast allergy and renal insufficiency where
T2-weighted images without gadolinium
contrast can diagnose pancreatic necrosis

63. Magnetic Resonant Cholangiopancreatography
• INDICATION:
– diagnosis of suspected biliary and pancreatic duct obstruction in
the setting of pancreatitis.
– Repeated attacks of idiopathic acute pancreatitis
• Merit
– used if choledocholithiasis is suspected but there is concern that
pancreatitis might worsen is ERCP is performed
– Provide non-invasive/fast/safe high-quality (Heavily T2–
weighted) imaging for diagnostic and/or severity purposes

64. Endoscopic UltraSonography
• INDICATIONS
– Repeated idiopathic acute pancreatitis*
• occult biliary disease- small stones/sludge
• secretin-stimulated EUS study may reveal resistance to ductal outflow at the
level of the papilla,
– as evidenced by dilatation of the pancreatic duct to a greater extent and longer duration
than in a healthy population
– Age >40 to exclude malignancy
• especially those with prolong or recurrent course
• RATIONALE: 5 % CA pancreas present as AP
_________________________________________
*Endoscopic investigation in patients with acute idiopathic pancreatitis should be limited, as the
risks and benefits of investigation in these patients are unclear and should be referred to centers
of expertise.

65. Endoscopic Retrograde Cholangiopancreatography
INDICATION
• Severe gallstone AP or AP with concurrent acute cholangitis/biliary
obstruction/ biliary sepsis/jaundice (due to persistent stone)
• ERCP within 24(-72) h of admission
• Sphincterotomy/stent and bile duct clearance reduces infective
complications/mortality
NOT INDICATED
• Not needed early in most patients with gallstone pancreatitis who lack
laboratory or clinical evidence of ongoing biliary obstruction
– As most of gallstones causing AP readily pass to duodenum and are lost in stool
– MRCP or EUS recommended if CBD stone still suspected
• as risk of post-ERCP pancreatitis is greater with normal calibre bile duct and normal
bilirubin
• MRCP /EUS as accurate as diagnostic ERCP

66. MISCELLANEOUS
• Peritoneal(sensitivity 54%,specificity 93%)/Pleural fluid tap
– High amylase/lipase/protein
• Urine Complete Examination
– Proteinuria, granular cast, glycosuria
• Electrocardiography
– ST-T wave changes
• Bile Aspiration
– Crystal analysis, if suspicion of microlithiasis
• Manometry
– Sphincterof Oddi dysfunction as a cause
• Genetic testing
– may be considered in young(<30 yrs) patients if no cause is evident and a
family history (especially if >1 family member)of pancreatic disease is present

67. SEVERITY SCORING SYSTEMS
ACUTE PANCREATITIS SPECIFIC SCORING SYSTEMS
– Ranson score
– Glagsow score
– Bedside Index for Severity in Acute Pancreatitis(BISAP) score
– Harmless Acute Pancreatitis Score(HAPS)
– Hong Kong Criteria
ACUTE PANCREATITIS NON-SPECIFIC SCORING SYSTEMS
(ICU SCORING SYSTEMS)
– Acute Physiology And Chronic Health Evaluation(APACHE) II score
– Sequential Organ Failure Assessment(SOFA) score

68. Each system has merits and demerits, and none
is currently recognized as a criterion standard
______________________________________

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

70. RANSON SCORE-1974
(for alcohol pancreatitis)
ON ADMISSION
• Age > 55 yrs
• TLC > 16,000/mm3
• BSR> 200 mg/dL
• AST > 250 IU/L
• LDH > 350 IU/L
WITHIN 48 HOURS
• BUN rise >5 mg/dL
• Pa02 < 60 mmHg ( 8 KPa)
• Serum Calcium < 8 mg/dL
• Base deficit > 4 meq/L
• Fluid Sequestration > 6000 mL
• Hct fall > 10 %
NOTE: Disease classified as SEVERE when 3 or more factors are present

71. Revised RANSON SCORE-1979
(for Gallstone pancreatitis)
ON ADMISSION
• Age > 70 years
• TLC > 18000/mm3
• BSR > 220 mg/dL
• AST> 250 IU/L
• LDH >400 IU/L
WITHIN 48 HOURS
• BUN rise >5 mg/dL
• Pa02 < 60 mmHg ( 8 KPa)
• Serum Calcium < 8 mg/dL
• Base deficit > 5 meq/L
• Fluid Sequestration > 4 litres
• Hct fall > 10 %
NOTE: Disease classified as SEVERE when 3 or more factors are present

72. RANSON SCORE
Ranson
score
Mortality rate SEVERITY Interpretation
0-2 ≈ 0-2 % i.e. minimal mortality Mild AP Admit in regular ward
3-5 10-20 %
Severe AP
Admit in ICU/HDU
6-7 40 % Associated with more systemic
complications
>7 >50 % Same as above
SCORING SYSTEM SENSITIVITY SPECIFICITY
Ranson Criteria 73% 77%
APACHE II 77% 84%
CRP 73% 71%

73. RANSON SCORE…….
DRAWBACKS
• One has to measure all 11 signs to achieve the best predictability of
prognosis
• 2 full days are needed to complete the profile.
– A delay of 48 hours after admission merely for assessment may
squander a valuable opportunity to prevent a complication during this
time.
• Best used within the initial 48 hours of hospitalization and have not
been validated for later time intervals.
• Threshold for abnormal valve depends on whether cause is
gallstone or alcohol
• Only 73 % sensitive and 77 % specific in predicting mortality

74. Glasgow-Imrie score
ON ADMISSION
• Age > 55 yrs
• TLC > 15 x 109 l-1
• BSR>180 mg/dL (10 mmol l-1)
(no H/O diabetes)
• BUN > 16 mmol l-1
(no response to IV fluids)
• Pa02 < 60 mmHg ( 8 KPa)
WITHIN 48 HOURS
• Serum Calcium < 2.0 mmol l-1
• Serum albumin <32 g l-1
• LDH > 600 units l-1
• AST/ALT > 200 units l-1
NOTE: Disease classified as SEVERE when 3 or more factors are present

75. Modified Glasgow/PANCREAS score
• PaO2 < 8kPa (60mmhg)
• Age > 55 years
• Neutrophils: WBC >15 x109/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 of admission
*Omission of age/serum transaminase increases the predictive valve of scoring system as
serum transaminase did not differ significantly between mild and severe pancreatitis
*Bold 4 factors are independently significant in predicting the severity

76. Acute Physiology And Chronic Health Evaluation II score-1985
NOTE: Disease classified as SEVERE if clinical impression of very ill patient with
APACHE II score above 8

77. APACHE Scoring System
MERIT
• Immediate assessment of the severity of pancreatitis
possible
• Can be used even after 48 hours
• Unlike ALL pancreatic specific scoring systems, APACHE (and SOFA) also
includes clinical features of patient besides laboratory values
(Clinical findings are more important than lab findings in predicting
SIRS,sepsis and other complications)
• Best validated(medscape)

78. DEMERITS OF AP-specific scoring systems(ACG 2013)
• Uniformly cumbersome, typically requiring 48 h to become accurate
– when the score demonstrates severe disease, the patient’s condition is
obvious regardless of the score.
• Have a limited value, as they provide little additional information to the
clinician in the evaluation of patients and may delay appropriate
management.
• No laboratory test is practically available or consistently accurate to
predict severity in patients with AP.
– Even the acute-phase reactant CRP, the most widely studied inflammatory
marker in AP, is not practical as it takes 72 h to become accurate.
– CT and/or MRI imaging also cannot reliably determine severity early in the
course of AP, as necrosis usually is not present on admission and may develop
after 24 – 48 h.
_________________________________________________________________
Thus, in the absence of any available test to determine severity, close
examination to assess early fluid losses, hypovolemic shock, and symptoms
suggestive of organ dysfunction is crucial.

79. Predicting Severe AP(ACG 2013)
So rather than depending on a scoring system to
predict severity of AP,
one need to be aware of intrinsic patient-
related risk factors, including laboratory
and imaging risk factors, for the
development of severe disease.

80. Clinical findings associated with a severe course for 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
Resp rate > 20/min or PaCO2 >4.3 KPa(32 mmHg)
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 extrapancreatic collections

81. MANAGEMENT
• Mild acute pancreatitis
– Conservative Approach
– Admit in general ward
– Non invasive monitoring
• (Moderate)Severe acute pancreatitis
– Aggressive Approach
– Admit in HDU/ICU
– Invasive monitoring
__________________________________________
Recognizing patients with severe acute pancreatitis ASAP is
critical for achieving optimal outcomes

82. Mild Acute Pancreatitis
• mild and self-limiting, needing only brief hospitalization.
• Rehydration by IV fluids
• Frequent non-invasive observation/monitoring(atleast 8 hrly)
• Brief period of fasting till pain/vomiting settles
– Little physiological justification for prolonged NPO
• No medication required other than analgesics(important) and anti-emetics
– Antibiotics not indicated in absence of signs or documented sources of infection
– Pain results in ongoing cholinergic discharge, stimulating gastric and pancreatic secretions
– Analgesics: WHO analgesic ladder-1986
– Avoid Morphine-cause sphincter of Oddi spasm
• Metabolic support
– Correction of electrolyte imbalance

83. Modified WHO analgesic Ladder

84. No or little role of………………..
• Nasogastric suction and H2-blockers
• Secretion-inhibiting drugs
– Atropine, calcitonin, somatostatin and its analogue(Octreotide)
– glucagon and fluorouracil
• Protease inhibiting drugs
– Aprotinin, gabexate mesylate,camostate, phospholipase A2 inhibitors,
FFP
• Indomethacin or PG inhibitors
• PAF antagonists
– PAF acetylhydrolase, Lexipafant

85. Severe Acute Pancreatitis
• P:
– Pain relief
– Proton pump inhibitors-omeprazole
– Peritoneal lavage
• A
– Admit in HDU/ICU
– Antibiotics
• N
– Nasogastric intubation(if vomiting)
– Nasal oxygen
– Nutrition support
• C
– Calcium gluconate
– CVP line
– Catherisation- Foley
• R
– Rehydration by IV fluids,plasma,blood
– Ranitidine(for stress ulcer)
– Radiology: CT scan, USG
– Resuscitation when required
• E
– Endotracheal intubation
– Electrolytes management
– ERCP
• A
– Antacids
• S
– Swan-Ganz catheter for CVP and TPN
– Suction-in case of aspiration
– Steroids in case of ARDS
– Supportive therapy for organ failure
• Inotropes
• Hemofiltration
• Ventilator(PEEP)

86. Monitoring
CLINICAL
• Vitals
• UOP
• CV pressure
INVESTIGATIONS
• Baselines
• Serial ABGs
• Serial BSR
• Serum calcium/magnesium

87. ACG 2013 Recommendations
• Despite dozens of randomized trials, no
medication has been shown to be effective
in treating AP.
• However, an effective intervention has been
well described: EARLY AGRESSIVE IV
hydration.

88. Rationale for EARLY AGRESSIVE IV hydration
• Frequent hypovolemia due to
– vomiting,
– reduced oral intake,
– third spacing of fluids(increased vascular permeability)
– increased respiratory losses, and
– diaphoresis.
• Combination of microangiopathic effects and edema of the
inflamed pancreas decreases blood flow, leading to increased
cellular death, necrosis, and ongoing release of pancreatic enzymes
activating numerous cascades.
_________________________________________________________
*provides micro- and macrocirculatory support to prevent serious
complications such as pancreatic necrosis

89. EARLY AGRESSIVE IV hydration
Kon sa? Lactated Ringer ’s solution may be the preferred isotonic crystalloid
replacement fluid
• Ringer lactate is better electrolyte balance and more pH-balanced
• Normal saline given in large volumes may lead to the
development of a non-anion gap, hyperchloremic metabolic
acidosis and increased chances of SIRS
• Low pH activates the trypsinogen, makes the acinar cells more
susceptible to injury and increases the severity of established AP
Kab? Early aggressive IV hydration is most beneficial during the first 12 – 24 h, and
may have little benefit beyond this time period
Kitna? Aggressive hydration, defined as 250 – 500 ml per hour of isotonic crystalloid
solution should be provided to all patients, unless cardiovascular, renal, or
other related comorbid factors exist.
• In a patient with severe volume depletion, manifest as hypotension
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 next 24 – 48 h.

90. EARLY AGRESSIVE IV hydration
– Hematocrit and BUN has been widely recommended as
surrogate markers for successful hydration
• No absolute numbers recommended
• Goal to decrease Hct and BUN and maintain normal cret
– In elderly and cardiac/renal comorbidities hydration is
monitored by
• Central venous pressure via CV line or
• Intrathoracic blood volume index
– Better/more accurate correlate with cardiac index than CVP

91. Antibiotics
• Routine use* NOT recommended(ACG 2013) as
– Prophylaxis in severe AP
– Preventive measure in sterile necrosis to prevent
development of infected necrosis
• Indicated in
– Established infected pancreatic necrosis or
– Extraperitoneal infections
• Cholangitis, catheter-acquired infections, bacteremia, UTIs,
pneumonia
______________________________________________
*Routine use of antifungal agents along with prophylactic or therapeutic antibiotics NOT
recommended(ACG 2013)

92. Antibiotics
• As SIRS may be indistinguishable from sepsis
syndrome, so if infection is suspected, antibiotics
should be given while source of infection is being
investigated
– Once blood and other cultures are found negative,
antibiotics should be discontinued
• Few antibiotics penetrate due to consistency of
pancreatic necrosis
– cefuroxime, or imipenem, or ciprofloxacin plus
metronidazole

93. Antibiotics
• Use of probiotics is associated with increased mortality
in severe AP
• Selective decontamination of bowel, targeting both
bacteria and fungi, in order to prevent infected
necrosis
– Controversial
• Relatively stable patients with infected necrosis can be
managed conservatively on antibiotics without needing
surgery(necrosectomy) or intervention (percutaneous
or endoscopic drainage)
– Surgical debridement recommended if no response to
conservative treatment or deteriorates clinically

94. …………………………………………………….
Rather than preventing infection, the role of antibiotics in patients with
necrotizing AP is NOW to treat established infected necrosis

95. Nutrition
• In mild AP
– oral feedings can be started immediately if there is no
nausea/vomiting, and the abdominal pain/tenderness/Ileus has
resolved(amylase return to normal, patient feel hunger)
– Initiation of feeding with a small and slowly increasing low-fat
(low-protein) soft diet appears as safe as a clear liquid diet,
providing more calories
• Stepwise manner increase from clear liquids to soft diet NOT necessary
• In severe AP
– Enteral route is recommended to prevent infectious complications
– Parenteral nutrition should be avoided, unless enteral route is not
available, not tolerated, or not meeting caloric requirements

96. RATIONALE OF EARLY ENTERAL NUTRITION
• The need to place pancreas at rest until complete
resolution of AP no longer seem imperative
– Bowel rest associated with intestinal mucosal atrophy and
bacterial translocation from gut and increased infectious
complications
• Early enteral feeding maintains the gut mucosal barrier,
prevents disruption, and prevents translocation of
bacteria that seed pancreatic necrosis
– Decrease in infectious complications, organ failure and
mortality

97. ………………………………………………..
Rather than using antibiotics to prevent infected necrosis………….start early
enteral feeding to prevent translocation of bacteria
RATIONALE MANAGEMENT
PREVENTION OF STERILE NECROSIS Early aggressive IV hydration
PREVENTION OF INFECTED NECCROSIS Early enteral feeding( NOT antibiotics)
TREATMENT OF INFECTED NECROSIS Antibiotics, drainage, necrosectomy

98. Route of enteral Nutrition
• Traditionally nasojejunal route has been preferred
to avoid the gastric phase of stimulation BUT
– Nasogastric route appears comparable in efficacy and
safety
MERITS OF NASOGASTRIC ROUTE DEMERITS OF NASOGASTRIC ROUTE
NG tube placement is far easier than
nasojejunal tube placement( requiring
interventional radiology or endoscopy, thus
expensive) especially in HDU/ICU setting
Slight increased risk of aspiration
(Can be overcome by placing patient in upright
position and be placed on aspiration
precautions)

99. Role of Surgery in AP
• In case of mild gallstone AP, cholecystectomy should be performed before
discharge to prevent a recurrence of AP
– Within 48-72 hour od admission or briefly delay intervention(after 72 hrs but
during same admission
– Along with intraoperative cholangiography and any remaining CBD stones can
be dealt with intra/post operative ERCP or
– Along with preoperative EUS or MRCP
• In case of necrotizing biliary AP, in order to prevent infection,
cholecystectomy is to be deferred until active inflammation subsides and
fluid collections resolve or stabilize
• Cholecysectomy done for recurrent AP (IAP) with no stones/sludge on USG
and no significant elevation of LFTs is associated with >50 % recurrence of
AP
_________________________________________________________
If patient unfit for surgery(comorbid/elderly), biliary sphincherotomy alone
may be effective to reduce further attacks of AP

100. Sterile necrosis infected necrosis
Asymptomatic doesnot mandate
intervention regardless of
size, location and extension
surgical, radiologic, and/or
endoscopic drainage should be
delayed preferably for more
than 4 weeks
• to allow liquefaction of
the contents and the
development of a
fibrous wall around the
necrosis
• Initially treated with
antibiotics
Stable
Symptomatic
(associated with
GOO or bile
obstruction)
minimally invasive methods
of necrosectomy are
preferred to open
necrosectomy
Urgent debridement unstable
Minimally invasive approach: laparoscopic surgery(ant or retroperitoneal approach),
percutaneous radiologic catheter drainage or debridement, video-assisted or small incision-
based left retroperitoneal debridement, and endoscopy

101. When to Discharge
• Pain is well controlled with oral analgesia
• Able to tolerate an oral diet that maintains their caloric needs, and
• all complications have been addressed adequately
Follow up
• Routine clinical follow-up care (typically including physical examination and
amylase and lipase assays) is needed to monitor for potential complications of the
pancreatitis, especially pseudocysts.
• Within 7-10 days

102. Recurrent AP
CT scan
•If neoplasia or chronic pancreatitis is found
•addressed and treated accordingly.
MRCP
•shows developmental abnormalities, strictures, or evidence of chronic pancreatitis
•endoscopic or surgical treatment may be of benefit in a subset of patients
EUS
•Microlithiasis/biliary sludge Cholecystectomy
•Periammpullary mass missed on CT or MRCP
Genetic •cationic trypsinogen mutations, SPINK1 mutations, or CFTR mutations
ERCP
•sphincter of Oddi manometry
•Placed last because very high rate of post-ERCP pancreatitis(benefits< risk)

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

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

105. SYSTEMIC COMPLICATIONS
• Metabolic
– Hypocalcemia
– Hyperglycemia
– Hyperlipidemia
• Gastrointestinal
– Peptic Ulcer/Erosive gastritis
– Ileus
– Portal vein or splenic vein thrombosis with varices
• Neurological
– Visual disturbances-Sudden blindness(Purtscher’s retinopathy)
– Confusion,irritability,psychosis
– Fat emboli
– Alcohol withdrawal syndrome
– Encephalopathy
• Miscellaneous
– Subcutaneous fat necrosis
– Intra-abdominal saponification
– Arthralgia

106. LOCAL COMPLICATIONS
• 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……….