This slide covers etiology, pathogenesis and management of gall stone induced acute and chronic pancreatitis. It includes details about latest trials and has information taken from standard textbooks.

2. PANCREATITIS
Dr M Surya Pratap
Moderator : Dr Ranveer Singh
Date : 22/06/23

3. INTRODUCTION
• Acute Inflammatory condition –acinar cell destruction
• Most common GI disease for acute hospitalisations
• 80 %- mild-resolve within one week
• 20% -severe acute pancreatitis – organ failure / necrotizing
pancreatitis
• Sterile pancreatic necrosis- conservative management
• 30 % - secondary infection , 3-4 weeks after onset
• Mortality:
– Mild – 0-1%
– Severe -15-30%
– Within 7 days-Half of total mortality

4. ETIOLOGY
• Gall Stone Induced: 4 to 8 % of Gall Stones lead to
pancreatitis
• 60 to 80% of pancreatitis- Gall stones
• Mechanism:
– Transient obstruction - stone or edema due to stone
passage
– Extravasation of pancreatic juice into interstitium
(calcineurin dependent)
– Common channel formation – bile salt reflux
• Risk factors:
– Stone size < 5mm
– Wide cystic duct >5mm
– High stone load >20
– Mulberry shaped stones

5. • Alcoholic Pancreatitis:
– More common in men-due to higher tendency to drink
– Peak incidence-40-60 years
– Avg consumption 100-150g/ day
– Genetic and environmental factors play a role
ETIOLOGY

6. • Mechanism:
– MULITIFACETED
– Alcohol increases GP2 and lithostathine
– Secrete in pancreatic juice and calcify-intraductal calculi
– Increases trypsinogen, chymotripsin exocytosis
– Upregulation of pro inflammatory cytokines
– Increased autophagy due to cathepsin B and L
– Oxidative and Non oxidative alcohol metabolites-acinar
cell injury
– Activation of Matrix metalloproteinases - Pancreatic
stellate cell activation

7. ETIOLOGY
• Hypertriglyceridemia:
– 1 to 10 % of cases
– Serum TG > 10mmol/L fasting
– Type 1, 4, 5 hyperlipidemia
– Mechanism:
• Excessive TG – hydrolysed by pancreatic lipase-high FFA
• High FFA- pancreatic capillary injury-ischemia and acid
mileu
• Increased chylomicrons –Increased blood viscosity
• Hypercalcemia:
– 1-4 % of cases
– Activation of enzymes by trypsin based mechanism
– Pancreatic calculi formation –ductal obstruction
– Direct toxic effects of elevated parathormone

8. ETIOLOGY
• Inborn Errors of Metabolism:
• Neonatal and Pediatric cases
• Hyperlipidemias
• Disorders of branched-chain amino acid degradation
• Homocystinuria
• Hemolytic disorders
• Acute intermittent porphyria
• Von Gierke.
– Mechanism:
• Not clear
• Hyperlipidemia, lactic acidosis, hypoglycemia, and
hyperuricemia, any of which could initiate pancreatitis.

9. ETIOLOGY
• Inborn Errors of Metabolism:
• Neonatal and Pediatric cases
• Hyperlipidemias
• Disorders of branched-chain amino acid degradation
• Homocystinuria
• Hemolytic disorders
• Acute intermittent porphyria
• Von Gierke.
– Mechanism:
• Not clear
• Hyperlipidemia, lactic acidosis, hypoglycemia, and
hyperuricemia, any of which could initiate pancreatitis.

10. ASSESSMENT OF PANCREATITIS
• The diagnosis of AP requires at least 2 of the following
features:
(1) characteristic abdominal pain;
– acute and constant pain localized in the epigastrium or
right upper quadrant that usually radiates to the back.
With nausea and vomiting
(2) biochemical evidence of pancreatitis (i.e., amylase or lipase
elevated >3 times the upper limit of normal);
(3) evidence of pancreatitis on cross-sectional imaging

11. Phases of Acute Pancreatitis
• Traditionally 2 phases
– Early
– Late
• Early phase:
• SIRS(Systemic Inflammatory Response Syndrome)
• Lasts 1 to 2 weeks
• Activated cytokine cascades in response to local pancreatic
disease
• Persistent SIRS leads to Organ failure
• Unreliable morphological abnormalities (peri pancreatic
necrosis)
• Other infections lead to early organ failure

12. Phases of Acute Pancreatitis
• Late phase:
• CARS –Compensatory Anti inflammatory Response Syndrome
• Weeks to months
• Organ Failure related to extent of local complications
• CECT to characterise local complications

13. CLASSIFICATION SYSTEM FOR SEVERITY OF
PANCREATITIS - ATLANTA CLASSIFICATION(2012)
• MILD
– No organ failure
– No local or systemic complications
– Mortality is very rare.
• MODERATE
– Presence of transient organ failure (usually resolves within 48 hr)
– Local or systemic complications without persistent organ failure
– Mortality is much lower than that of severe acute pancreatitis
• SEVERE
– Persistent organ failure: may be single or multiple
– Usually have at least 1 local complications.
– Infected necrosis with persistent organ failure
– Extremely high mortality, reported as high as 36%–50%

14. CLASSIFICATION SYSTEM FOR SEVERITY OF
PANCREATITIS – DETERMINANT BASED CLASSIFICATION
• MILD
– No peripancreatic necrosis
– No organ failure
– Mortality 0%
• MODERATE
– Presence of sterile peripancreatic necrosis
– Transient organ failure
– Mortality 3.6%
• SEVERE
– Presence of either infected peripancreatic necrosis
– Persistent organ failure
– Mortality 33.8
• CRITICAL
– Presence of infected peripancreatic necrosis and persistent
organ failure Mortality 87.5%

15. ORGAN FAILURE
• ATLANTA CLASSIFICATION: MODIFIED MARSHAL SCORE(>1 IN ONE OF 3
ORGAN SYSTEMS)
• DBC
– Persistent organ failure: >48 hr
– Transient organ failure: <48 hr
– Cardiovascular: need for inotropic agent
– Renal: creatinine: >= 171 mmol/L
– Respiratory: Pao2/Fio2 =<300 mm Hg

16. CT IN PANCREATITIS
• Indications of cross-sectional imaging in AP:
• Confirmation of the diagnosis in cases of diagnostic
uncertainty
• Prognostication and detection of complications in the latter
course of disease
• CECT scan is the imaging modality of choice
• Done after 72 hours-to detect necrosis

17. • Unenhanced CT scoring systems
• evaluate the extent of pancreatic and peripancreatic
inflammatory changes
• Balthazar grade
• pancreatic size index (PSI)
• Both peripancreatic inflammatory changes and
extrapancreatic complications
• mesenteric edema and peritoneal fluid” (MOP) score
• extrapancreatic score (EP)
• extrapancreatic inflammation on CT (EPIC) score.
• CECT scores determine the presence and extent of necrosis,
• CTSI
• MCTSI

19. LOCAL COMPLICATIONS (< 4 WEEKS)
• Acute peripancreatic fluid
collection:
• Fluid seen usually develops
in early phase
• Associated with interstitial
edematous pancreatitis
• CECT: no well-defined wall,
homogeneous, confined by
normal fascial planes in
retroperitoneum; may be
multiple
• Acute necrotic collection
(ANC):
• Containing variable
amounts of fluid and
necrotic tissue
• Infected necrosis: diagnosis
of infection of ANC or WON
suspected by patient’s
clinical course or by
presence of gas within
collection on CECT

20. Acute peripancreatic fluid
Acute necrotic collection

21. LOCAL COMPLICATIONS (> 4 WEEKS)
• Pancreatic pseudocyst:
• fluid collection in
peripancreatic tissues
• well-defined wall with
minimal or no necrosis
• Walled-off necrosis (WON):
• mature, encapsulated
collection of pancreatic
• peripancreatic necrosis with
well-defined inflammatory
wall; after onset of
necrotizing pancreatitis
• Infected necrosis: infection
of ANC or WON, suspected
by patient’s clinical course
or by presence of gas within
collection on CECT

22. pseudocyst
WON

23. Classification of pseuodocysts
TYPE PANCREATITIS DUCTAL
DISRUPTION
1 ACUTE
PANCREATITIS
RARELY
2 ACUTE
EXACERBATION OF
CHRONIC
PANCREATITIS
SOMETIMES
3 RETENTION
PSEUDOCYST
`OBSTRUCTION
AND DILATION
OF PANCREATIC
DUCT

24. NEALON CLASSIFICATION

25. Prognostic Scores-RANSON

26. PROGNOSTIC SCORES
SOFA Sepsis-related Organ Failure Assessment MAP, Pao2/Fio2, creatinine, GCS, platelet count,
bilirubin Score: 1–5, based on severity of each
parameter
SIRS Systemic inflammatory response syndrome Temperature (<36°C or >38°C), heart rate (>90/min),
respiratory rate (>20/min) or Paco2 (<32 mm Hg),
WBC (<4000/mm3, > 12,000/mm3, or >10% bands)
POP Pancreatitis Outcome Prediction score Age, MAP, Pao2/Fio2, arterial pH, BUN, calcium (these
scores use normal ranges)
PANC 3 Hematocrit (>44 mg/dL), body mass index (>30
kg/m2), pleural effusion
Haps
Harmless Acute Pancreatitis Score
Abdominal tenderness, hematocrit (>43 mg/dL for
men or >39.6 mg/dL for women), creatinine (>2
mg/dL)
JSS
Japanese Severity Score
Base excess (=< 3 mEq/L), Pao2 (=< 60 mm Hg or
respiratory failure), BUN (>=40 mg/dL) or creatinine
(>=2 mg/dL), LDH (>= 2 X upper limit of normal),
platelet (<100,000/mm3), calcium (=< 7.5 mg/dL), C-
reactive protein (>= 15 mg/dL), SIRS (>=3), age (>=70
yr)
Pancreatitis Activity Scoring System (PASS) Organ failure x100 (for each system),SIRS x 35 for each
criteria, Abdominal pain (0–10) x5, Morphine
equivalent dose (mg) x5, Tolerating solid diet (yes = 0,
no = 1) X 40

27. Lab markers
• CRP:
– > 150mg/dl within first 48 hours – severe AP
– 70 to 80 percent accuracy
– Peaks at 72-96 hours
• Hematocrit:
– Hct >44 or no fall in first 24 hours-increased risk for
necrosis
– Hct> 50
• Procalcitonin:
– >1.8ng/ml in pancreatitis –marker for infected necrosis
– Sensitivity and specifity > 90%
• IL6, IL 8, Trypsinogen, Trypsinogen activated peptide

28. MANAGEMENT

29. • ANALGESIA:
• Intense abdominal pain present
• WHO analgesic ladder is recommended
• Opiod analgesia – treatment of choice
• Associated with decreased supplementary analgesia
• No evidence of complications due to opioids(Cochrane
review 2013)
• Patient controlled analgesia may be required

30. • FLUID THERAPY:
• Appropriate fluid therapy in first 24 hours decreases SIRS
• Decreased SIRS when RL used instead of NS
• Rate of fluid administration – 5 to 10 ml/Kg/hr-decreased
complications
• Controlled hemodilution with target HCT > 35 % within 48
hours-decreased sepsis
• Resuscitation to be guided by Urine output, lactate, Base
deficit

31. • Oxygen Supplementation:
• Avoid anemia: rare in hemoconcentrated patient in
pancreatitis
• Administer supplemental oxygen via face mask, intubation of
mech ventilation
• Cardiac Output monitoring-preload and after load
mangement

32. • ANTIBIOTICS
• Secondary infection of necrotic collection –second peak of
mortality
• No benefit from prophylactic antibiotics
• Indicated if co existing cholangitis present
• No role of probiotics(PROPATRIA trial)
• ERCP
• No benefit of early ERCP on mortality or local complications
• Indicated in cholangitis, jaundice with SIRS
• Jaundice without SIRS-MRCP

33. • ORGAN FAILURE:
• Identified by Modified Marseille Score
• Respiratory failure: Oxygen supplementation and mechanical
ventilation with lung protective strategies
• Cardiovascular: Volume resuscitation and vasoactive agents
• Renal:
• Due to impaired renal perfusion
• Restoration of circulating volume and may require
dialysis

34. • Gastrointestinal:
• Reduced perfusion and splanchanic vasoconstriction
• Clinically nausea, vomiting, abdominal distention
• Leads to
• Failure to tolerate enteral nutrition
• Bacterial translocation infected pancreatic necrosis

35. • INTRA ABDOMINAL HYPERTENSION:
• ACS: IAP>20 mm Hg (with or without abdominal arterial
pressure <60 mm Hg) with new onset organ failure
• Surrogate marker of impending negative outcome
1. IAP measured in mechanical ventilated patient with
Severe AP
2. Medical intervention targeting hollow viscus volume,
abdominal wall compliance, Volume status
3. Invasive treatment: NO strong indication/ evidence
• Methods: Percutaneous catheter drainage of
ascites, laparostomy, Sub cutaneous line alba
fasciotomy

36. • ROLE OF CHOLECYSTECTOMY
• PONCHO trail
• Early cholecystectomy –reduces gall stone related
complications
• Just before discharge after resolutions of
symptoms
• Cholecystectomy: All resolutions of signs of
pancreatitis(mild)/ persistent for > 6 weeks

37. • NUTRITION:
• Enteral nutritional superior to parentral nutrition
• Reduces organ failure, infected necrosis, mortality
• Maintains bowel motility and restore bowel mucosa
• PYTHON trail:
• early nasoenteral nutrition did not reduce end point of
mortality and infection
• Only recommended when oral nutrition not tolerated in 3-5
days of onset

38. Management of Necrosis
• Acute fluid collections without necrosis resolve within 4 weeks
• Acute pancreatic pseudocyst: collection without or minimal
necrosis
– Rare
• Collections may be sterile or infected
• Persistent SIRS and organ failure- Increased risk of infected necrosis-
Increased mortality
• Acute Fluid collections-
– Puddles in the vicinity of pancreas
– Do Not require intervention
– Failure to resolve-Duct disruption or necrosis

39. Infected Pancreatic Necrosis
• Intervention Avoided in first 2 weeks-High morbidity and
mortality
• Indicated only if bleeding or bowel ischemia present
• Intervention required in infected collection
– Evidenced by Secondary clinical and biochemical
parameters
– Small pockets of gas on CT
– Air fluid level –associated spontaneous enteric discharge
of collection

40. PANTER Trial
• PAncreatitis, Necrosectomy versus sTEp up appRoach
• Step up approach:
– Early organ support and nutritional Optimisation
– Endoscopic or percutaneous drainage
– f/b retroperitoneal drainage with lavage , if not improved.
• Significant benefit in composite end point or death with Step
up Approach
• Previously, Solid predominant or infected necrotic collection-
MIRP or VARD technique
• Late Well Organised –endoscopic or laproscopic transgastric
drainage

41. • Recent Approach
– Lateral collections extending behind the colon-Percutaneous
drainage from the left / right flank
– Drain as lateral and inferior as possible-for possibility of step up
approach
– Avoid coastal margins
– Alternative drain if initial placement sub optimal
– Minimum 12 Fr drain used, irrigated thrice daily with 250ml NS
– Medial collections by endoscopic route-if collection behind liver,
spleen, bowel

42. Retroperitoneal Step up Techniques
• MIRP-Minimally Invasive Retropancreatic necrosectomy
• VARD-Video assisted Retroperitoneal Debridement
• Modifications of open necrosectomy
• Open procedure : Major morbidities
– Enteric fistula-45%
– Hemorrhage-40%
– Colonic necrosis-15%

43. • Videos

44. Management of Late Walled Off Pancreatic
Necrosis
• Intervention indication in WPON:
– Infection, radiologically or clinical picture
– Nutritional failure
– Persistent abdominal pain
• Cystogastrostomy
– EUS guided
– Laparoscopic

45. • Endoscopic complications:
– Fatal air embolism
– Bleeding and perforation
– Time consuming and ineffective
– Blockage of stents via solid material

46. Open Techniques
• 3 types-based on method to prevent recurrence
1. Open or Closed Packing
2. Continuous closed peritoneal lavage
3. Programmed Open Necrosectomy
• Approach
– Midline laparotomy or B/l Sub coastal incision
– Gastro colic omentum divided

47. • Open Packing
– Leaving the abdomen open and packing the peritoneal cavity
– Sequential pack changes and healing by secondary intention
– Drains may be placed
– Higher incidence of fistulas, bleeding, incisional hernia, mortality
rate
• Closed Packing
– Primary closure over guaze stuffed Penrose drains
– Silicone drains (Jackson Pratt) additionally in lesser sac
– Sequential removal for gradual involution of cavity

48. • Closed Post operative lavage
– Closed cavity reconstituted by suturing gastro colic and duodenocolic
ligaments
– Large bore drains allowing side to side lavage
– 1 to 10 litres perday
– End Point: Clinical and Lab parameters improvement and clear effluent
• Programmed Necrosectomy
– Conservative debridement every 48 hours
– Pancreatic bed packed and abdomen closed with suturing mesh/zipper

49. Early Complications
• SIRS
– Requires critical care and vasopressor therapy
– Minimally invasive – resolves in 24-36 hours
– More sever in Open Procedure
• Acute/Delayed Hemorrhage
– Intra op venous bleeding common during early/over
necrosectomy
– Controlled by compression by Sengstaken blakemore tube,
gastric balloon, guage packing

50. Early Complications
• Secondary Hemorrhage
– Arterial Origin
– Massive and sudden preceeded by Herald bleed
– Herald bleed-hemorrhage into a retro peritoneal drain/ gi
bleed
– Due to uncontrolled sepsis
– Requires CT Angiography and embolisation
– No role of UGIE

51. Late Complications
• Pancreatic fistulation
• Disruption of the pancreatic duct following significant
parenchymal loss
• Early endoscopic interventionintroduce infection in the
collection
• ERCP following resolution of sepsis and collection-Pancreatic duct
stenting
• May require large volume paracentesis
• Respond in 4 to 6 weeks
• Persistent drainage-Extensive parenchymal loss and disconnected
tail

52. • Can be
– internal-biliary system, pleural, small bowel
– External
• Internal fistula
– anteriorly-ascitis;
– Posterioly- pleural effusiom

53. Early Complications
• Enteric fistulation:
• Spontaneous discharge into GI tractresolving symptoms
• Colonic fistula-Poorly controlled collection and persistent
sepsis
• May require resection/ileostomy

54. • Pancreatic Duct disruption
• Complication of AP and CP
• 80% disruption in head of pancreas
• Presents as non resolving or recurrent pancreatic fluid
collection
• MRCP / ERCP- diagnostic
• Significant functional Pancreatic Tissue present-
Pancreaticojejunostomy
• Small isolated segment: Distal pancreatectomy

55. Extra Pancreatic Complications
• Splenic Vein Thrombosis:
• Occurs due to peripancreatic fibrosis due to splenic location
• Incidental finding on imaging
• No anti coagulation or splenectomy required
• Variceal bleeding- Splenectomy indicated
• Medically unfit for surgery-Splenic artery embolisation
• Asymptomatic gastric varices + pancreatic surgery
Splenectomy indicated

56. • Pseudoaneurysm and Hemorrhage
• Less common than venous thrombosis,but life threatening
• Direct erosion of pancreatic necrotic collection into splenic
artery
• Presents 2 to 8 months after episode
• Angioembolisation: First line of management
• If structure cannot be sacrificied( Hepatic artery), stenting can
be done
• Obstruction
• Commonly due to gastric ileus
• Compression due to pseudocyst can occur anywhere along
the intestine

57. CHRONIC PANCREATITIS

58. INTRODUCTION
• Chronic progressive pancreatic inflammation and scarring
• Loss of exocrine and endocrine function
• Multiple Hypothesis
– Necrosis-fibrosis
– Toxic metabolic causes
– Oxidative stress
– Duct obstruction
– Sentinel Acute Pancreatic Event

59. Pathogenesis
• Necrosis Fibrosis Hypothesis
• Distinct episodic APnecrosis and fibrosis
• Contradiction: Collagen after pancreatitis: Type 3 and pro
collagen 4
Ongoing
Inflammati
on
Fibriosis
Scarring and
sacculation of
glands
Obstruction
of bile flow
Protein
precipitation
and
calcification

60. • Protein Plug /Ductal Obstruction Theory
– Lithogenicity of pancreatic fluid in the pancreatic ductule
– Esonophilc proteinaceous aggregates
– Lithostathine/Pancreatic Stone Protein deficiency(PSP)
– CalcificationStone formationUlceration of ductal
epithelium
– Inflammation and Fibrosis of parenchyma
• Contradiction: Stones and plugs are seen in late stages.
• Alcohol
– Decreased Pancreatic juice formationIncreasing viscosity
– Increases CCK

61. • Oxidative Stress Theory
• Hepatic metabolites of xenobiotics
• Steady exposure of acinar cells to
– Free radicals
– Lipid Peroxidation products
– Toxic epoxides
• Reach parenchyma via bile duct/systemic circulation
• Cyt P450 induced  Glutathione reduced
• Inflammatory damage of ductules and acinar cells
• Alcohol –depletes scavengers of free radicals
– Vit E and C, Riboflavin, Selenium

62. • Toxic Metabolic Theory
• Alcohol Increased intracellular lipid component
• Alteration in lipid metabolismapoptosis and scarring and
damage to microcirculation
• Direct damage to pancreatic pericytes Scarring
• Analogy similar to liver cirrhosis

63. • Primary Duct Hypothesis
• Immunologic attack to specific genetic/structural/acquired
antigen in ductal epithelial cells
• 2 mechanisms:
– MHC molecules aberrant expression in ductal epithelium
– Infiltration of activated lympocytescytotoxic response
• Analogous to PSC

64. • Sentinel Acute Pancreatitis Event Hypothesis
– SAPE is esstential to initiate inflammatory and
immunologic process
– Multiple risk factors necessary to propagate CP through
membrane or mitochondrial injury
– Susceptibility is essential through genetic/ ongoing injury
• Sustained Intracinar Nuclear Factor –kB
– Trypsinogen independent mechanism for chronic
pancreatitis

65. DIAGNOSIS

66. Imaging Modalities
• X Ray Abdomen:
– Focal / Diffuse pancreatic calcifications noted (30 – 40%)
• USG
– First imaging in patients with abdominal complains
– High Specificity low sensitivity for CP
– Criteria :
• Irregular contour (lobulations)
• Pancreatic duct dilation and irregularity
• Loss or reduction of pancreatic parenchyma
• Cysts/ cavities
• Pancreatic calcifications

68. PSEUDOCYSTS

69. • CT Findings:
– Main pancreatic duct dilation
– Intra ductal calcifications
– Gland atrophy
– Cystic lesions
– Heterogenous gland with enlargment or atrophy
• Cannot detect early parenchymal changes or small pancreatic
duct chnages
• 5mm slice thickness for CECT

70. • NCCT for detections of pancreatic calculi
• Exclusion of extra pancreatic CP complications can be done
– Pseudoaneurysms
– Pseudocysts
– Pancreatopleural fistula
– Pleural effusuion
– SVT

71. • ERCP
• Chain of lake appearance in advanced cases

73. • EUS
– Detects subtle changes in duct and parenchyma
– Rosemont criteria

75. • MRCP
– More sensitive than CT and US
– Secretin stimulated MRCP-pancreatic duct and
parenchyma evaluation
– IV secretin-increases duct diameter upto 1mm, recover
after 10min( Pancreatic duct compliance)
– Evaluates peri pancreatic fibrosis,
– duct ectasia, side branch abnormalities

76. Etiologies
• TIGARO classification
• T-Toxic Metabolic
• I-Idiopathic
• G-Genetic
• A-Autoimmune
• R-Recurrent pancreatitis
• O-Obstructive mechanical
Causes
• M-ANNHEIM
• M- multiple risk factors
• A-Alcohol
• N-Nicotine
• N-Nutritional factors
• H-Hereditary factors
• E-Efferent duct factors
• I –Immunological factors
• M-Miscellaneous

77. Management of pain
• Pain reduces quality of life
• Medical management - first line therapy. Relief in 40 to 70 %
• Mechanism of pain generation in the absence of local
complications:
• (1) inflammatory changes of pancreatic parenchyma with
intrapancreatic and peripancreatic neural alterations
• (2) ductal and intraparenchymal hypertension
• (3) altered nociception of pain

79. • MEDICAL
• 1 Alcohol abstinence and diet.
• 2. anti oxidants reduce pain in mild CP
• 3. Analgesics are used in a step up pattern. Opioids can be
used
• INTERVENTIONS FOR PAIN
• Celiac plexus block - destruction of celiac plexus/ blocking of
visceral fibres
• Alcohol or phenol for lysis
• Bupivacaine and triamcinolone for block
• USG / CT guided

80. ENDOSCOPIC TREATMENT
• AIM: Decompress and drain the pancreatic ductal system
• Surgery –better pain relief than endoscopical methods

81. Indications:
1. Proximal stenosis and no calcifications or inflammatory mass
endoscopically.
two to three repetitive endoscopic treatments fail, the
option of surgery must be evaluated.
2. Distal duct obstruction, calcifications, or local complications,
surgery is superior to endoscopic treatment.
Patients should undergo surgery early in the course of
the disease to prevent further deterioration of exocrine or
endocrine function.
3. Pancreatic pseudocysts may be treated endoscopically.
If endoscopic treatment fails, a surgical drainage
procedure is recommended.

83. Decompression of Pancreatic Pseudocysts
• Late complication of pseoducyst
• 40% regress after 6 weeks
• Indications
– Symptomatic patients like pain, obstruction, bile stasis,
hemorrhage
– Asymptomatic > 5cm for >6weeks
• Transgastric/ transduodenal apprach-requires bulge into the
cavity
• EUS can be used to guide

84. • Transduodenal better than transgastric
• Selective endoscopic pancreating stenting and retrograde
pancreatography
– Double pigtail used over a guide wire
• Cannot be used if stone or strictures present between cysts
and opening
• Percutaneous drainage have a risk of fistula formation

85. • Selective endoscopic pancreating stenting and retrograde
pancreatography
– Double pigtail used over a guide wire
• Cannot be used if stone or strictures present between cysts
and opening
• Percutaneous drainage have a risk of fistula formation

86. • CBD Stenting
• Used in CBD stenosis patients
• Cholestasis can be treated
• Complications:
– Plastic stent clogging
– Migration
– Cholangitis
• SEMS (Self Expanding Metallic Stents ) can be used

89. Pancreatic Insufficiency
• impairment of fat digestion compared with protein and
carbohydrate digestion in patients with pancreatic
insufficiency
(1) impairment of pancreatic lipase synthesis and secretion
occurs earlier
(2) more rapid and complete inactivation of lipase occurs in the
acidic duodenum as a result of impaired bicarbonate output
(3) proteolytic degradation of lipase occurs earlier during aboral
transit than that of amylase and proteases

90. (4) impairment of pancreatic bicarbonate secretion decreases
duodenal pH, resulting in precipitation of glycine-conjugated bile
acids and further deterioration of fat digestion
(5) extrapancreatic sources of lipase are unable to compensate
for loss of pancreatic lipase activity.

91. Pancreatic Insufficiency
• Tests of Exocrine Pancreatic Function
• Minor role in CP
(1) noninvasive tests of exocrine pancreatic function show high
sensitivity only in advanced stages of CP
(2) there is low clinical availability of most direct tests
(3) utility of function tests is limited to the diagnosis of more
advanced disease
(4) these tests have low specificity (70%)
Pancreatic Insufficiency appears late (90% parenchyma
destroyed)

92. • Invasive Tests
• Secretin stimulation test: detects functional impairment in all
stages
• Gold standard
• 60 min of duodenal aspirate done after IV secretin
• Bicarbonate levels
– <50-consistent with CP
– 50-75-Normal
• False Positive tests : DM, Bilroth II gastrectomy, Celiac sprue,
Cirrhosis
• Alternately, endoscopically collected at 15 min interval
• Invasive, cumbersome and need specialists.

93. • Indirect tests
• Assess fat absorption
• Low sensitivity in early CP
• Quantitative stool tests: Chymotrypsin, fecal elastase
• FE assay: Best accuaracy, limited specificity in watery stools,
– Measures only human elastase. Supplements does not
alter
• Chymotrypsin: Not acceptable accuaracy.

94. • Supplementation
• Weight loss or Steatorrhea >15g/day
• Can also be used for the treatment of pain
• To reach adequate lipase in duodenum
• Protein malabsorption eliminated, steatorrhea reduced with
current supplementation

95. • Uncoated preparations:
– Required high dosage
– Inactivation by gastric acid
– Used in achlorhydria/ hypochlorhydria
• Enteric coated tablets: Erratic enzyme release
• Enteric coated microsphere preparation:
– Protected by low PH polymer
– Release only at pH 4.5
– Concomitant antacids decrease availability
Dosage:
20-40000U before meal
10-20000U before snack

96. SURGICAL MANAGEMENT
• Preservation of tissue via drainage
– Protects against further loss of pancreatic function
• Pancreatic resection
– Nondilated pancreatic ducts
– Pancreatic head enlargement
– Pancreatic carcinoma is suspected

97. • Drainage Procedures:
• Puestow procedure:
• Resection of tail of pancreasLongitudinal incision of the
pancreatic ductRous en y anstamosis of jejunal loops
• Parington Rochelle modification: Omits the resection of tail of
pancreas
– Preserves more pancreatic tissue and decreases mortality
and morbidity
• Only useful if duct dilation >7mm
• In isolated pseudocysts with recurrent severe pancreatitis:
Cystojejunostomy with Rous en Y reconstruction treatment of
choice

100. • RESECTIVE PROCEDURES
• Inflammatory mass in pancreatic head : Pancreatic head
resection is treatment of choice
• Indications
– Intractable pain
– Symptomatic local complications
– Unsuccessful endoscopic management
– Suspicion of malignancy

101. • Partial Pancreatoduodenectomy:(Kaush –Whipple procedure)
– Indications:
• Head of pancreas enlarged with cysts and
calcificatnions
• Ineefective endoscopic treatment
• Malignancy suspicion
• Extent of resection: Pancreatic head with duodenum with
lower 1/3rd of stomach
• Pylorus preserving: Lower 1/3rd of stomac not resected
• Operative mortality 2 to 5%
• Complications:
– Dumping
– Diarrhoea
– Peptic Ulcer
– Dyspeptic symptoms(bile reflux gastritis)

103. • Duodenum preserving Pancreatic Head
resection(DPPHR):BEGER procedure
• The pancreas is dissected on the level of the portal vein.
• The pancreatic head is excavated, and the duodenum is
preserved with a thin layer of pancreatic tissue.
• If the bile duct is obstructed, it can be opened, and an
internal anastomosis with the excavated pancreatic head can
be performed
• The reconstruction is performed with a Roux-en-Y jejunal loop
including two anastomoses, one to the pancreatic tail
remnant and one to the excavated pancreatic head.

105. • Advantages
– Greater weight gain
– Better Glucose tolerance
– Higher insulin secretion capacity
– Relief of pain 91% cases

106. • FREY PROCEDURE
• Laterolateral Pancreaticojejunostomy
• Combination of BEGER with Parington Rochelle Method
• Indicated: Smaller head mass with obstruction in head and tail
• BERN
• No division of pancreas at the head
• Single anastamosis
• Indicated: No tail duct obstruction

107. FREY
BERN

108. • Pancreatic Left Resection
• Pseudocysts and fistulae in the tail of pancreas
• May or may not be splenectomy
• Splenectomy done in:
– Fibrotic encasement of splenic vessels
– Peri splenic cysts
• Total Pancreatectomy with islet cell transplantation
– No inciting organ for pain and complications
– Prevention of diabetes by islet transplantaion in liver
– Relief from pain

109. THANK YOU