Chronic pancreatitis is a relapsing inflammatory process that results in irreversible fibrotic changes to the pancreas, causing abdominal pain, exocrine and endocrine insufficiency. It is most commonly caused by prolonged alcohol abuse. Other causes include genetic mutations, autoimmune disorders, and obstructive factors. Diagnosis involves imaging tests like CT, MRI, and ERCP to identify morphological changes and complications. Treatment focuses on pain management, enzyme supplementation, endoscopic procedures to address duct abnormalities, and surgery for refractory cases or complications. Surgical options aim to relieve pain by draining the pancreatic duct or resecting inflamed areas, while preserving function.

1. Chronic pancreatitis
Dr Suhas U

2. • Chronic pancreatitis is a relapsing inflammatory
process that results in a variable degree of
parenchymal destruction and irreversible fibrotic
change in the pancreas with consequent clinical
manifestations typically including characteristic
abdominal pain, exocrine and endocrine insufficiency.

3. Types
Chronic obstructive pancreatitis
• is characterized by exocrine atrophy and is associated with duct
stenosis caused by tumors, pseudocyst, or scarring from prior acute
pancreatitis.
Chronic calcifying pancreatitis
• is characterized by intraductal calcifications and protein plugs, and
is often associated with atrophy, stenotic ducts, and areas of acute
inflammation or pseudocyst.
Chronic inflammatory pancreatitis
• consists of dense infiltration of mononuclear inflammatory cells.

4. Risk factors
• Alcohol 70%
• Idiopathic 20%
• Other 10%
Hereditary
Hyperparathyroidism
Hypertryglyceridemia
Autoimmune pancreatitis
Obstruction
Trauma
Pancreatic divisum

5. TIGAR O system by Whitmore

6. Toxic / metabolic
Alcohol
• Prolonged alcohol abuse
• 3-7%
1. Increased protein concentration
• Lithostathine secretion by acinar cells
• Increased glycoprotein 2 secretion
• Protein precipitation( protein plugs and stone)
• Obstruction – acinar cells not able to secrete enzymes –
autodigestion
2. Abnormal secretion of enzymes
• Metabolites of alcohol – fatty acid ethyl esters and reactive oxygen
species

7. 3. Direct acinar injury – acetaldehyde
4. Activation of pancreatic stellate cells- extensive fibrosis
Smoking
• Increases the risk of alcohol induced chronic pancreatitis
• Increased risk for pancreatic calcifications and diabetes
• Younger age

8. Idiopathic
• 20% of cases – no obvious risk factor
• Unidentified genetic or molecular
derangements

9. Genetic mutations
• Cationic tryosinogen gene(PRSS1)
Mutation
Cationic trypsinogen gene(PRSS1)
•Secreted by acinar cells
•Cleaved by duodenal enteropeptidase to trypsin
•Trypsin
Hydrolyse dietary proteins
Activate other pancreatic zymogens
Subsequent proteolytic inactivation
Trypsin
Resists autolytic inactivation
Premature and extended activation
CFTR gene
Chloride ion channel
Water , chloride and bicarbonate secretion from
epithelial cells
Viscous low volume low bicarbonate
secretions
Enzyme hyperconcentrations
Intraglandular enzyme activation
Duct sludge
SPINK 1
From acinar cells
Regulates premature activation of enzymes
1-2 % of normal individuals
Lowers the threshold for chronic
pancreatitis.

10. Autoimmune
Lymphoplasmocytic sclerosing pancreatitis
• Duct origin antigen
• Infiltration of CD4/CD8 lymophocytes and IgG4
postive plasma cells
o Diffuse glandular enlargement
o Diffuse ductal narrowing

11. Recurrent or severe acute pancreatitis
• Prior episodes of pancreatitis with
1. Prior episodes of necrosis
2. Postpancreatic ductal scarring
3. Persistent activation of pancreatic stellate cells

12. Obstructive
• Post traumatic duct strictures
• Cystic neoplasms / pancreatic
adenocarcinoma
• Anamolous anatomic variations of duct

13. Clinical presentation
Pain abdomen
• Left upper quadrant/epigastrium
• Radiating to back
• Variable pain pattern
• Recurrent attacks of moderate or severe pain
with periods of quisence
• Persistent pain with significant incapacitation
Weight loss and malnutrtion
• Decreased intake and exocrine insufficiency with
protein and fat malabsorption

14. Exocrine insufficiency – steatorrhoea
Endocrine deficiency
• Late presentation - Diabetes
• >90% parenchyma fibrosed
Fat soluble vitamin deficiency
• Bleeding, osteopenia, osteoporosis
Extrapancreatitic
• Pseudocyst – intestinal or biliary obstruction
• GI haemorrhage

15. Diagnosis
Appropriate history and imaging
Lab investigations – limited value
• Acute exacerbation – increased amylase or
lipase
• Nomal with acinar cell destruction
• Increased bilirubin with ALP – biliary
obstruction

16. CT abdomen
• Morphologic, duration and complications
CT findings
• Dilated pancreatic duct(68%)
• Parenchymal atrophy(54%)
• Pancreatic calcifications(50%)
• Peripancretic fluid
• Focal pancreatic enlargement
• Biliary duct obstruction
• Irregular parenchymal contour
Assessing complications
• Pancreatic duct disruption
• Pseudocyst
• Portal and splenic vein thrombosis
• Splenic or pancreaticoduodenal artery aneurysms

19. Toxic/ Idiopathic/ Genetic Autoimmune Obstructive
Focal or scattered calcifications
Focal enlarged lesions in the head –
inflammatory head mass
Segmental or diffuse pancreatic dilatation
Extrapancreatic complications
Calcifications are absent
Diffusely enlarged
pancreas
Dilated duct
upstream to stenosis

20. MRI
• Reliable alternative
• Changes in pancreatic parenchyma
Pancreatic atrophy
Irregularities in contour
• Secretin MRCP to evaluate
Enhanced duct visualisation
Assess pancreatic exocrine function

21. ERCP
• Historically the gold standard investigation
• Indications – when MRI/CT have inconclusive
findings
Main role as therapeutic procedure
• Pancreatic duct complications like
stones/strictures/pseudocysts / biliary stenosis

23. EUS
• Evaluation of pancreatic mass and cystic lesions
• More sensitive for early parenchymal changes
• EUS directed biopsy of pancreatic mass to rule
out malignancy

24. Functional assessment
1. Fecal elastase level
Using monoclonal / polyclonal elastase antibodies
>200mcg/g feces – normal
100-200mcg/g – mild to moderate exocrine deficiency
<100mcg/g – severe
2. Steatorrhea
Fecal fat weight
After intake of 100g fat for 3days
>7g/day – Steatorrhea

25. Treatment
PAIN management
• Main symptom
• Initial – NSAID’s and escalated accordingly
(Step up approach)
• Intractable severe pain – started with
narcotics ( top down approach)
• Infusion pumps for intrathecal delivery of
analgesics

27. Habit modification
• Cessation of alcohol/ smoking
• Avoidance of fatty food
Neurolysis
• Failed medical management
• Persistent pain
• Radiologic/ endoscopic approach
• 100% alcohol injection into the celiac ganglion
• Mixed results – transient improvement for not
>6months

28. Endoscopic procedures
• Pancreatic duct stenting
• Proximal pancreatic duct stenosis
• Decompression of pancreatic duct leak
• Drainage of pseudocysts
• Endoscopic stone removal
• ESWL for stones

29. Results are
• <50% effective improvement in pain /
frequency of attacks
• Multiple procedures
• Recurrent stones/ strictures

30. Surgery
• Indications
1) Pain intractable to pharmaco/ endoscopic
therapy – 90%
2) Complications of pancreatitis
– Relieve biliary/ gastrointestinal obstruction
– Drain symptomatic pseudocyst
– Vascular complications of chronic pancreatitis

31. Types
Drainage procedures
• Puestow/ Modified Puestow
Parenchymal resection
• Beger procedure
• Whipples procedure
• Berni procedure
Combination
• Frey’s
Also depends on the
anatomical
morphology and
diameter of the duct

32. I - Large duct disease
• Enlarged duct with diameter >7-8mm
• Puestow’s
Longitudinal unroofing of dilated pancreatic duct in the
body and neck
Resection of pancreatic tail
Longitudinal pancreaticojejunostomy
• Modified Puestow / Partington Rochelle procedure
Eliminated distal pancreatectomy

37. Outcomes
• 75-80% pain releif over 5-10years with diffusely
dilated duct and no mass
• Perioperative mortality low
• Endocrine and exocrine levels generally preserved
at preoperative levels

38. Chronic pancreatitis with dominat
head mass
• Pure resection / resection and drainage
procedures
• 4 procedures
1) Pancreaticoduodenectomy
2) Beger
3) Berne
4) Frey
Duodenum preserving

39. Whipple’s
Indication –
Chronic pancreaatitis with head mass with
• Biliary obstruction
• Imaging characteristics suspicious of malignancy
Can be classical / pylorus preserving
pancreaticoduodenectomy

40. More radical procedure for benign lesions

41. Beger Procedure
Dominant head mass without main duct dilatation /
biliary obstruction
This involves
• Resection of the head of pancreas
• A rim of head attached to the duodenum preserved
• Common bile duct left intact in the rim
• Pancreaticoenteric drainage through two sided Roux
en Y pancreaticojejunostomy

44. Frey’s
Disadvantage with Beger
• Does not address the disease that may coexist
in body and tail of pancreas
• Dominant head mass with dilated pancreatic
duct
• Local resection of head + lateral
pancreaticojejunostomy

46. Berni’ modification of Beger
• No transaction at neck of pancreas
• Anterior surface of mass palpated and cored
out using electrocautery
• Roux limb is sewn to the remainder rim of
pancreas

47. Small duct disease or diffuse sclerosis
• Total pancreatectomy with islet cell transplantation
• Izbicki procedure
• Long term analgesic support

48. Total pancreatectomy
• More commonly done as staged procedure with left
pancreatectomy followed by head resection
• Allowing initial processing of islet cells from body
and tail
• Isolation process relies on enzymatic and
mechanical steps to dissociate islet cells from acinar
cells

49. • Depending on proximity of islet isolation
facilities and efficiency of the process
• Infusion of islet cells into the portal circulation
be performed in same anesthesia or
postoperatively(radiological guidance)

50. Outcomes of islet cell transplantation
• Pain relief achieved in 50-60% but recurrence of pain
after 1year
• Insulin independence in 40-50%, but steady decline
of islet function at 10year followup.
• The indications for islet autotransplantation are
controversial and the overall safety and efficacy of
the procedure have not been fully validated outside a
handful of centers.

51. • Currently, the strongest arguments in favor of total
pancreatectomy and islet autotransplantation
• limited subset of patients with hereditary pancreatitis, who
otherwise carry a significant long-term risk of developing
pancreatic cancer

52. Izbicki procedure
• V shaped longitudinal pancreatic resection
• Entire pancreas is excavated along the trajectory of
the main pancreatic duct from the pancreatic head (as
with the Frey procedure) across the body and tail of
the organ.
• Pancreaticoenteric drainage is established by Roux-
en-Y lateral pancreaticojejunostomy

53. Pancreatic enzyme supplements
• Various formulations with varying composition
of lipase and protease
• Classical vs enteric coated enzymes
• Dosing schedule is before meals
• Uses
For pain relief
For steatorrhoea

54. Classical Enteric coated
Pain relief ( suppressing CCK induced
stimulation of pancreas)
Steatorrhoea
H2 blockers or PPI to suppress acid secretion Not necessary