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CHRONIC PANCREATITIS
 DR.JAYA SAKTHI.S
 PG 1ST YEAR
 PROF.DR.LALITH KUMAR UNIT
 GENERAL SURGERY
DEFINITION
 Ongoing inflammatory and fibrosing Disorder.
 Irreversible morphologic changes.
 Progressive and permanent loss of exocrine and
endocrine function.
 Clinical pattern of either recurrent exacerbation or
persistent pain.
 Histopathologic changes:
i)Fibrosis
ii)Reduced number of acinar cells
iii)Reduced number of islet cells of langerhans
iv)Development of strictures
v)Dilatation of pancreatic duct
vi)Pancreatic ductal Calculi
 Classified into:
 Chronic pancreatitis with focal or segmental or diffuse
fibrosis
 Chronic pancreatitis with or without stones
 Obstructive chronic pancreatitis
 Chronic Calcifying Pancreatitis
 Chronic inflammatory Pancreatitis
Cambridge conference classification of Chronic Pancreatitis: ERCP
Terminology Main duct Abnormal Side
Ducts
Additional
features
Normal Normal None
Equivocal Normal <3
Mild changes Normal >=3
Moderate
changes
Abnormal >3
Marked changes Abnormal >3 1 or more of
Large cavity
obstruction
Filling defects
Severe dilatation
RISK FACTORS
 !!!ALCOHOL
Byproducts of
Alcohol
metabolism
Acinar cell
injury
Pancreatic
enzyme
activation and
local tissue
damage
Alcohol
Increase protein
concentration in pancreatic
juice
Intraductal calcium stone formation,
ductal epithelial ulceration,
inflammation and fibrosis
 Toxic/Metabolic
• Tobacco use potentiate the progression of Chronic
pancreatitis
• Hyperparathyroidism and Hypercalcemia
• MEN 2A
• CRF
• Medications  Statins, Steroids, OCP, IF
 Idiopathic
• 20%
• Bimodal distribution
 Genetic
• Hereditary Chronic Pancreatitis – Autosomal Dominant-
chromosome 7 q.
• Transition mutation in the cationic trypsinogen gene
PRSS1.
• Mutation in Serine Protease inhibitor- SPINK1
• Mutation in the Cystic Fibrosis Transmembrane
Conductance Regulator gene CFTR.
• Mutation in Anionic Trypsinogen PRSS2.
• Mutation in Chymotrypsin C.
 Autoimmune
• Lymphoplasmacytic sclerosing Pancreatitis
• Gland enlargement, diffuse duct narrowing, stenosis of
intra pancreatic portion of bile duct.
• HPE  Pancreas Parenchyma infiltrated by both CD4+
and CD8+ lymphocytes and IgG4 plasma cells with
Interstitial Fibrosis and Acinar cell atrophy.
• ABx against Peptide homologous to PBP in H.Pylori and
Ubiquitin-protein ligase E3 component n-recognin 2.
• Primary treatment is Steroids.
 Recurrent acute
• Of any etiology
• Accumulated effects of post inflammatory scarring and
necrosis.
• Priming of pancreatic stellate cells to induce fibrosis.
• Radiation and scarring.
 Obstruction
• Congenital / Functional / Acquired
• Pancreatic / Ampullary tumors
• Post injury pancreatic duct fibrosis
• Anatomical variation in the pancreatic ductal system
CLINICAL MANIFESTATIONS
 Abdominal pain.
 Nausea /vomiting
 Weight loss
 Bloating /Flatulence/ Steatorrhoea
 Endocrine Insufficiency (90% Fibrosis)
ETIOLOGIC RISK FACTORS ASSOCIATED WITH
CHRONIC PANCREATITIS : TIGAR O
Toxic-metabolic Alcohol, Tobacco smoking,
Hypercalcemia, Hyperlipidemia, CRF,
Medications, Toxins
Idiopathic Tropical
Genetic Cationic/Anionic Trypsinogen, CFTR,
SPINK1
Autoimmune Isolated or associated with
Autoimmune disorders
Recurrent acute Post necrotic
Vascular disease/Ischemia
Postirradiation
Obstuctive Pancreatic divisum
Sphincter of oddi disorders
Duct obstruction
Posttraumatic duct scars
Preampullary duodenal wall cysts
!!!PAIN
Obstruction of
main pancreatic
duct
Increased ductal
pressure
Stretch activated
neural pathways
Mistargeted secretion
of pancreatic
enzymes
Protease activates
nociceptive
pathways
Chronic
inflammation
Fibrosis of
peripancreatic
capsule & perilobular
parenchyma
Impair regional
and local
blood flow
Pain through
ischemia
Consequent
tissue acidosis
DIAGNOSIS
 History / Physical examination
 Serum Amylase/ Lipase / Glucose
 IgG4 protein levels , ANA, RF, ESR AIP
 Plain radiograph  Calcifications
 USG Abdomen
 CECT
 ERCP/ MRCP
TREATMENT OPTIONS
 Lifestyle modifications
 Pain control
NSAIDs
Narcotics
Celiac plexus nerve block
PAIN MANAGEMENT STRATEGY REFLECTS PRESUMED MECHANISM
Local inflammation Pharmacotherapy (pancreatic enzymes,
Analgesics, Narcotics)
Ductal Hypertension Decompression (Puestow, Endoscopic
Stenting)
Organ Hypertension Resection (Whipple, Frey procedure)
Retroperitoneal Damage Neuroablation (Celiac Block,
Splanchnicectomy)
Altered Nociception Psychosocial intervention (counseling,
Detoxification)
 ENDOSCOPIC MANAGEMENT
• Pancreatic sphincterotomy
• Endoscopic Polyethylene stents
 SURGICAL MANAGEMENT
Indications:
• Intractable abdominal pain
• Secondary complications of Chronic pancreatitis 
biliary stricture, Duodenal stenosis, pseudocyst
• Suspected neoplasm
OPTIONS:
i)Resection
ii)Decompression
iii)Hybrid Procedures
SURGICAL TREATMENTS FOR CHRONIC PANCREATITIS
RESECTION DECOMPRESSION HYBRID
Pancreatico
duodenectomy
(Kaush-Whipple
procedure)
Duval procedure Frey Procedure
Pylorus preserving
Pancreatico
duodenectomy
(Transverse Longmire)
Puestow-Gillesby
procedure
Hamburg Modification
Beger Procedure Partington- Rochelle
Procedure (Puestow)
Berne Modification
Near total or total
Pancreatectomy
Izbicki Procedure
SURGICAL TREATMENT OPTION BASED ON PANCREAS MORPHOLOGY
DILATED PANCREATIC
DUCT
SMALL OR NON DILATED
PANCFREATIC DUCT
No Focal Mass
Decompressive :
Partington-Rochelle
Procedure (Puestow)
Observation
Resection: Pancreatico
Duodenectomy, Total
Pancreatectomy
Hybrid Procedure: Frey Decompressive: Izbicki
Procedure
Focal Mass
Resection: Pancreatico
Duodenectomy, Beger
Procedure
Resection: Pancreatico
Duodenectomy , Beger
Procedure
Hybrid Procedure: Frey
WHIPPLE PROCEDURE
 Resection of Head of Pancreas with CBD, Distal Stomach,
Duodenum and Proximal Jejunum.
 Two layered end to side Pancreatico jejunostomy and a
gastrojejunostomy
 Pain releif  85%
 Diabetes  50% subsequent 10 years.
 Exocrine insufficiency 50%
 Mortality <5%
TRANSVERSE LONGMIRE PPPD
DPPHR
 Division of pancreatic neck
 Removal of head of pancreas
 Leaving small rim of pancreatic tissue
 End to end and side to side Roux en Y pancreatico
jejunostomy
DUVAL PROCEDURE
 Lateral Pancreatico Jejunostomy
 Retrocolic side to side Roux en Y Pancreatico
Jejunostomy
 Without Splenectomy and distal Pancreatic
ojejunostomy.
 Duodenum sparing resectio of pancreatic head
 Without division of pancreatic neck
 Longitudinal pancreaticojejunostomy
 75% releif of pain
IZBICKI PROCEDURE
 Excavation of pancreatic head
 V shaped longitudinal wedge resection
 Larearal decompressive pancreatico jejunostomy.
 92% Pain releif
 Small duct disease with diffuse parenchymal
inflammation.
 Heriditary syndromes
 Prior pancreatic operations.
 Pain releif 75%.
Chronic pancreatitis

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Chronic pancreatitis

  • 1. CHRONIC PANCREATITIS  DR.JAYA SAKTHI.S  PG 1ST YEAR  PROF.DR.LALITH KUMAR UNIT  GENERAL SURGERY
  • 2. DEFINITION  Ongoing inflammatory and fibrosing Disorder.  Irreversible morphologic changes.  Progressive and permanent loss of exocrine and endocrine function.  Clinical pattern of either recurrent exacerbation or persistent pain.
  • 3.  Histopathologic changes: i)Fibrosis ii)Reduced number of acinar cells iii)Reduced number of islet cells of langerhans iv)Development of strictures v)Dilatation of pancreatic duct vi)Pancreatic ductal Calculi
  • 4.
  • 5.  Classified into:  Chronic pancreatitis with focal or segmental or diffuse fibrosis  Chronic pancreatitis with or without stones  Obstructive chronic pancreatitis  Chronic Calcifying Pancreatitis  Chronic inflammatory Pancreatitis
  • 6. Cambridge conference classification of Chronic Pancreatitis: ERCP Terminology Main duct Abnormal Side Ducts Additional features Normal Normal None Equivocal Normal <3 Mild changes Normal >=3 Moderate changes Abnormal >3 Marked changes Abnormal >3 1 or more of Large cavity obstruction Filling defects Severe dilatation
  • 7. RISK FACTORS  !!!ALCOHOL Byproducts of Alcohol metabolism Acinar cell injury Pancreatic enzyme activation and local tissue damage
  • 8. Alcohol Increase protein concentration in pancreatic juice Intraductal calcium stone formation, ductal epithelial ulceration, inflammation and fibrosis
  • 9.  Toxic/Metabolic • Tobacco use potentiate the progression of Chronic pancreatitis • Hyperparathyroidism and Hypercalcemia • MEN 2A • CRF • Medications  Statins, Steroids, OCP, IF
  • 10.  Idiopathic • 20% • Bimodal distribution
  • 11.  Genetic • Hereditary Chronic Pancreatitis – Autosomal Dominant- chromosome 7 q. • Transition mutation in the cationic trypsinogen gene PRSS1. • Mutation in Serine Protease inhibitor- SPINK1 • Mutation in the Cystic Fibrosis Transmembrane Conductance Regulator gene CFTR. • Mutation in Anionic Trypsinogen PRSS2. • Mutation in Chymotrypsin C.
  • 12.  Autoimmune • Lymphoplasmacytic sclerosing Pancreatitis • Gland enlargement, diffuse duct narrowing, stenosis of intra pancreatic portion of bile duct. • HPE  Pancreas Parenchyma infiltrated by both CD4+ and CD8+ lymphocytes and IgG4 plasma cells with Interstitial Fibrosis and Acinar cell atrophy. • ABx against Peptide homologous to PBP in H.Pylori and Ubiquitin-protein ligase E3 component n-recognin 2. • Primary treatment is Steroids.
  • 13.  Recurrent acute • Of any etiology • Accumulated effects of post inflammatory scarring and necrosis. • Priming of pancreatic stellate cells to induce fibrosis. • Radiation and scarring.
  • 14.  Obstruction • Congenital / Functional / Acquired • Pancreatic / Ampullary tumors • Post injury pancreatic duct fibrosis • Anatomical variation in the pancreatic ductal system
  • 15. CLINICAL MANIFESTATIONS  Abdominal pain.  Nausea /vomiting  Weight loss  Bloating /Flatulence/ Steatorrhoea  Endocrine Insufficiency (90% Fibrosis)
  • 16. ETIOLOGIC RISK FACTORS ASSOCIATED WITH CHRONIC PANCREATITIS : TIGAR O Toxic-metabolic Alcohol, Tobacco smoking, Hypercalcemia, Hyperlipidemia, CRF, Medications, Toxins Idiopathic Tropical Genetic Cationic/Anionic Trypsinogen, CFTR, SPINK1 Autoimmune Isolated or associated with Autoimmune disorders Recurrent acute Post necrotic Vascular disease/Ischemia Postirradiation Obstuctive Pancreatic divisum Sphincter of oddi disorders Duct obstruction Posttraumatic duct scars Preampullary duodenal wall cysts
  • 17. !!!PAIN Obstruction of main pancreatic duct Increased ductal pressure Stretch activated neural pathways Mistargeted secretion of pancreatic enzymes Protease activates nociceptive pathways
  • 18. Chronic inflammation Fibrosis of peripancreatic capsule & perilobular parenchyma Impair regional and local blood flow Pain through ischemia Consequent tissue acidosis
  • 19. DIAGNOSIS  History / Physical examination  Serum Amylase/ Lipase / Glucose  IgG4 protein levels , ANA, RF, ESR AIP  Plain radiograph  Calcifications  USG Abdomen  CECT  ERCP/ MRCP
  • 20.
  • 21.
  • 22.
  • 23. TREATMENT OPTIONS  Lifestyle modifications  Pain control NSAIDs Narcotics Celiac plexus nerve block
  • 24. PAIN MANAGEMENT STRATEGY REFLECTS PRESUMED MECHANISM Local inflammation Pharmacotherapy (pancreatic enzymes, Analgesics, Narcotics) Ductal Hypertension Decompression (Puestow, Endoscopic Stenting) Organ Hypertension Resection (Whipple, Frey procedure) Retroperitoneal Damage Neuroablation (Celiac Block, Splanchnicectomy) Altered Nociception Psychosocial intervention (counseling, Detoxification)
  • 25.  ENDOSCOPIC MANAGEMENT • Pancreatic sphincterotomy • Endoscopic Polyethylene stents
  • 26.  SURGICAL MANAGEMENT Indications: • Intractable abdominal pain • Secondary complications of Chronic pancreatitis  biliary stricture, Duodenal stenosis, pseudocyst • Suspected neoplasm OPTIONS: i)Resection ii)Decompression iii)Hybrid Procedures
  • 27. SURGICAL TREATMENTS FOR CHRONIC PANCREATITIS RESECTION DECOMPRESSION HYBRID Pancreatico duodenectomy (Kaush-Whipple procedure) Duval procedure Frey Procedure Pylorus preserving Pancreatico duodenectomy (Transverse Longmire) Puestow-Gillesby procedure Hamburg Modification Beger Procedure Partington- Rochelle Procedure (Puestow) Berne Modification Near total or total Pancreatectomy Izbicki Procedure
  • 28. SURGICAL TREATMENT OPTION BASED ON PANCREAS MORPHOLOGY DILATED PANCREATIC DUCT SMALL OR NON DILATED PANCFREATIC DUCT No Focal Mass Decompressive : Partington-Rochelle Procedure (Puestow) Observation Resection: Pancreatico Duodenectomy, Total Pancreatectomy Hybrid Procedure: Frey Decompressive: Izbicki Procedure Focal Mass Resection: Pancreatico Duodenectomy, Beger Procedure Resection: Pancreatico Duodenectomy , Beger Procedure Hybrid Procedure: Frey
  • 30.  Resection of Head of Pancreas with CBD, Distal Stomach, Duodenum and Proximal Jejunum.  Two layered end to side Pancreatico jejunostomy and a gastrojejunostomy  Pain releif  85%  Diabetes  50% subsequent 10 years.  Exocrine insufficiency 50%  Mortality <5%
  • 32. DPPHR
  • 33.  Division of pancreatic neck  Removal of head of pancreas  Leaving small rim of pancreatic tissue  End to end and side to side Roux en Y pancreatico jejunostomy
  • 34.
  • 36.
  • 37.
  • 38.  Lateral Pancreatico Jejunostomy  Retrocolic side to side Roux en Y Pancreatico Jejunostomy  Without Splenectomy and distal Pancreatic ojejunostomy.
  • 39.
  • 40.
  • 41.
  • 42.  Duodenum sparing resectio of pancreatic head  Without division of pancreatic neck  Longitudinal pancreaticojejunostomy  75% releif of pain
  • 43. IZBICKI PROCEDURE  Excavation of pancreatic head  V shaped longitudinal wedge resection  Larearal decompressive pancreatico jejunostomy.  92% Pain releif
  • 44.
  • 45.  Small duct disease with diffuse parenchymal inflammation.  Heriditary syndromes  Prior pancreatic operations.  Pain releif 75%.