Chronic Pancreatitis

What is Chronic pancreatitis?

(MCQ) CP is characterised by all except ?

• A-Progressive and permanent endocrine and exocrine insufficiency • B-Activation of stellate cells • C-Abdominal pain is present in all patients • D-recurrent episodes of acute pancreatitis can cause CP

Explanation

• Stages of Chronic Pancreatitis:
  • Stage A- recurrent pain (absent in 15%-20% of cases)
  • Stage B- complications
  • Stage C-endocrine and exocrine insufficiency ( 90% of gland has to be damaged to cause these)
    • Last thing to go is Endocrine function
• Irreversible destruction of exocrine and endocrine tissue of pancreas
  • Endocrine and exocrine insufficiency
• Pancreatic Stellate Cells (PSC)- fibrosis of gland which is progressive

• Advanced stage:

  • ductal dilatation and stricture with calcification
  • parenchymal calcification

  

Risk Factors of Chronic Pancreatitis

(MCQ) Not a risk factor for CP ?

• A-Hypercalcemia • B-Hyperlipidemia • C-Gall stones • D-Chronic renal failure

Explanation:

• But if there is recurrent acute episodes of pancreatitis due to gall stones then it can also lead to chronic pancreatitis

• Most Common cause of CP = Alcohol

MCQ: Clinical Features of Chronic Pancreatitis (CP) – All are true except:

• A: 4-30% have exocrine insufficiency
• B: Fat soluble vitamin deficiency
• C: Diabetes more common in hereditary pancreatitis (Correct answer)
• D: Endocrine insufficiency occurs in last when 90% of parenchyma is destroyed

Explanation:

• Hereditary pancreatitis: Has a lower incidence of diabetes compared to other types, particularly alcoholic pancreatitis, where diabetes is more common.
• Exocrine insufficiency: Occurs in 4-30% of chronic pancreatitis patients due to the loss of pancreatic enzyme production.
• Diabetes: Tends to appear last in the course of chronic pancreatitis, when 90% of the pancreatic parenchyma is destroyed. It is more commonly seen in alcoholic pancreatitis.
• Fat-soluble vitamin deficiency: Results from lipase loss, leading to malabsorption of vitamins such as A, D, E, K.

Hereditary Pancreatitis

MCQ: Which of the following is not true about hereditary pancreatitis?

• A: Most patients are asymptomatic
• B: 35% lifetime risk of pancreatic cancer
• C: Associated with cationic PRSS1 mutation
• D: Recurrent episodes of pain with calcification is hallmark (Correct answer: D)

Explanation:

• Hereditary pancreatitis is an autosomal dominant (AD) disorder.
• Caused by a mutation in the PRSS1 gene (cationic trypsinogen mutation).
• Bimodal pattern of onset, often presenting in childhood and later in life.
• 80% penetrance with recurrent episodes of acute pancreatitis (AP). Most patients may be asymptomatic, but when symptomatic, pain is the most common feature.
• Patients have a 50-fold increased risk of developing pancreatic ductal adenocarcinoma (PDAC), with a 35% lifetime risk.
• R122H mutation in PRSS1 results in a proteolytic-resistant form of trypsinogen, leading to autodigestion of the gland.
• Calcification is not a hallmark of hereditary pancreatitis. It is also not characteristic of:
  • Obstructive pancreatitis
  • Autoimmune pancreatitis
  • Cystic fibrosis-related chronic pancreatitis

Chronic Pancreatitis: Most Common Mutation

MCQ: What is the most common mutation associated with chronic pancreatitis?

• A: Cationic PRSS1
• B: Anionic PRSS1
• C: SPINK1 (Correct answer)
• D: CFTR

Explanation:

• SPINK1 is the most common mutation seen in various forms of pancreatitis, including:
  • Hereditary pancreatitis
  • Alcoholic pancreatitis
  • Tropical pancreatitis
• SPINK1 mutation alone cannot cause chronic pancreatitis; other contributing factors are necessary for the development of the disease.
• Key Research:
  • Witt et al. studied 96 unrelated children and adolescents with idiopathic chronic pancreatitis and found frequent mutations in the serine protease inhibitor Kazal Type 1 (SPINK1), a pancreatic trypsin inhibitor.
  • SPINK1 is co-localized with trypsinogen in zymogen granules and is believed to prevent inappropriate intrapancreatic protease activation.
• N34S Mutation:
  • The most frequent mutation associated with chronic pancreatitis is the N34S amino acid substitution in exon 3 of the SPINK1 gene.
• Mechanism:
  • Mutations in SPINK1 or PRSS1 create an imbalance favoring intrapancreatic trypsin activation, leading to autodigestion of the pancreas and subsequent inflammation.
  • It is hypothesized that SPINK1 mutations are not directly responsible for causing pancreatitis but lower the threshold for the disease in the presence of other risk factors.

MCQ: Tropical Pancreatitis – Most Likely Genetic Mutation

A 20-year-old male from India presents with recurrent abdominal pain and diabetes mellitus. CT scan shows a dilated duct with multiple calcifications. The most likely genetic mutation in him is:

• A: PRSS1
• B: SPINK1 (Correct answer)
• C: CFTR
• D: None of the above

Explanation:

• Tropical Calcific Pancreatitis is the most common form of chronic pancreatitis in India, affecting children and adolescents.
• It presents with recurrent abdominal pain, pancreatic calculi, and early-onset diabetes.
• Unlike other forms of pancreatitis, tropical pancreatitis is not related to cassava beans or malnutrition.
• SPINK1 gene mutation is found in 25% of patients, making it the most common mutation associated with tropical pancreatitis.
• Other genes such as Cathepsin B, CFTR, and Carboxypeptidase A1 may also contribute by causing intrapancreatic activation of trypsin, leading to autodigestion of the pancreas.

Extrapancreatic complication

• Most Common is Biliary obstruction
• 2% will have Duodenal obstruction
• Splenic vein thrombosis: Asymptomatic = generally dont bleed but have varices
• Pancreatic cancer
  • 2% per decade (non hereditary)
  • equal for alcoholic and other risk factor

DIAGNOSIS OF CHRONIC PANCREATITIS:

Functional Assessment of Pancreatic Function

1. Assessment of Endocrine Function:

• C-peptide levels
• HbA1C
• Oral Glucose Tolerance Test (OGTT)

2. Assessment of Exocrine Function:

(MCQ)

Most sensitive test to detect exocrine insufficiency in pancreas?

• A: Fecal elastase-1
• B: Pancreaolauryl test
• C: Secretin-CCK test (Correct answer)
• D: C13 mixed triglyceride breath test

Explanation:

• The Secretin-CCK test is the most sensitive test for detecting exocrine insufficiency, as it directly measures pancreatic enzyme secretion after stimulation. However, it is not commonly used due to its invasive nature.

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(MCQ)

Indirect tests for exocrine pancreatic function?

• A: Fecal elastase-1
• B: Lundh test
• C: C13 mixed triglyceride breath test (Correct answer)
• D: Secretin-enhanced MRCP

Explanation:

• Indirect tests for pancreatic exocrine function do not measure enzyme levels directly. The C13 mixed triglyceride breath test is an indirect test that assesses pancreatic lipase activity and response to enzyme supplementation.

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(MCQ)

Not true about fecal elastase-1 used for the assessment of exocrine insufficiency?

• A: Investigation of choice to assess response after PERT (Correct answer)
• B: Level less than 200 ug/g is diagnostic
• C: Not sensitive for assessment after pancreatic surgery
• D: Level less than 100 ug/g indicates severe insufficiency

Explanation:

• Fecal elastase-1 cannot assess the response to PERT (Pancreatic Enzyme Replacement Therapy), making option A incorrect. It is commonly used to diagnose exocrine insufficiency, with levels less than 200 ug/g indicating insufficiency and less than 100 ug/g indicating severe insufficiency.

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Non-Invasive vs Invasive Tests for Pancreatic Function

Non-Invasive Tests:

• Enzyme levels may be altered in conditions like:
  • Diarrhea
  • Malabsorption
  • Chronic renal failure
  • Diabetes
• These tests are not sensitive in the early phase of pancreatic insufficiency because exocrine and endocrine insufficiency generally appear in the late stages of chronic pancreatitis.

Invasive Tests:

• Invasive tests involve intubation of the duodenum and stimulation of the pancreas using agents such as secretin or CCK.
• After stimulation, levels of bicarbonate and enzymes (e.g., trypsin, lipase) are measured directly.
• More accurate than non-invasive tests, especially for detecting early pancreatic insufficiency.

Sensitivity:

• Invasive tests are generally more sensitive than non-invasive tests.
• Non-invasive tests (e.g., fecal elastase-1, C13 breath test) are not sensitive for detecting early stages of chronic pancreatitis.
  • Imaging with EUS is considered the best investigation for diagnosing early-stage chronic pancreatitis.

Direct vs Indirect Tests:

• Direct tests are more sensitive than indirect tests because they directly measure enzyme levels.
  • Direct Tests (Invasive):
    • Measure enzyme secretion after stimulating the pancreas (e.g., Secretin or CCK test).
    • Secretin test is the most sensitive but invasive and impractical.
    • Diagnostic thresholds:
      • Bicarbonate <80 mEq/L = insufficiency.
      • Bicarbonate <50 mEq/L = moderate to severe insufficiency.
  • Non-Invasive/Indirect Tests:
    • Less sensitive, especially in the early phases of pancreatic insufficiency.
    • Imaging with EUS is the best investigation for diagnosing early chronic pancreatitis.
• Fecal Elastase-1:
  • Most commonly performed test (though not the most sensitive).
  • <200 ug/g indicates chronic pancreatitis.
  • <100 ug/g indicates severe insufficiency.
  • Cannot assess the response to PERT.

Note: Most sensitive is Secretin CCK test but not practical ; therefore Most Commonly done test is Fecal Elastase -1 test

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Indirect Tests:

• These tests are used for assessing response to PERT.
• Fecal Fat Test:
  • The patient is put on a 100g fat diet for 5 days.
  • If >7g/day of fecal fat is found on days 3-5, it indicates steatorrhea.
• C13 Mixed Triglyceride Breath Test:
  • Measures pancreatic lipase activity.
  • Useful for assessing the response to PERT.
  • Investigation of choice (IOC) to assess the response after PERT.

Imaging in Chronic Pancreatitis

(MCQ) EUS use in CP as a diagnostic test, which is not true?

• A: Increased ductal wall echogenicity
• B: Calcification
• C: Accentuation of lobular pattern
• D: High sensitivity and specificity (Correct answer)

Explanation:

• Although EUS is highly sensitive for detecting early changes in chronic pancreatitis, its specificity is lower because many features seen in CP (e.g., increased ductal wall echogenicity, calcifications) can also be present in normal pancreas.

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(MCQ) Major ductal feature on EUS according to Rosemont criteria for CP?

• A: Dilated side branches
• B: MPD > 3.5 mm in body
• C: Hyperechoic MPD
• D: Main pancreatic duct calculi (Correct answer)

Explanation:

• According to Rosemont criteria, the presence of main pancreatic duct (MPD) calculi is a major feature in diagnosing chronic pancreatitis.

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(MCQ) Not used in the diagnosis of CP?

• A: EUS-guided true cut biopsy of gland (Correct answer)
• B: Secretin-MRCP
• C: CECT abdomen
• D: Glucose tolerance test

Explanation:

• Biopsy is not typically used to diagnose chronic pancreatitis, though it may be performed to rule out malignancy. Imaging techniques like Secretin-MRCP, CECT abdomen, and EUS are more commonly used for diagnosis.

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Imaging Modalities and Their Role

• X-ray:
  • Can detect calcifications in 30-40% of chronic pancreatitis cases.
• CECT Abdomen:
  • Most sensitive for detecting calcifications (especially in the non-contrast phase).
  • Also detects duct dilation, head mass, underlying malignancy, and surrounding structures.
  • Commonly used for diagnosis because it provides a broad view of pancreatic and surrounding structures.

• EUS:

  • Most sensitive for identifying early changes in chronic pancreatitis.
  • Can help take biopsies to rule out malignancy.

  • Features seen on EUS include:

    • Increased ductal wall echogenicity
    • Calcification
    • Accentuation of lobular pattern
    • Main pancreatic duct (MPD) calculi (per Rosemont criteria).

    

• Secretin-MRCP:

  • Allows visualization of the pancreatic duct and its function, especially helpful in early disease stages.

• ERCP:

  • chain of lake appearance
  • Cambridge Criteria:

  

Sensitivity and Specificity of various tests:

MANAGEMENT OF CHRONIC PANCREATITIS:

• 3 types:
  • Medical:
    • Pain Killers , Opiates ,SSRI’s ( venlaflaxine) = by WHO PAIN LADDER
    • Role of Enzymes in Pain Management = Use of uncoated enzyme preparation = because whenever patient eats ⇒ CCK released ⇒ which causes pain ⇒ therefore uncoated enzymes release in proximal duodenum and ameliorate CCK response
    • Anti Oxidants = Methionine and Selenium ⇒ decrease oxidative stress response on pancreas
  • Endoscopic therapy:
    • ERCP / EUS
    • used mainly for complications like pseudocyst( EUS guided stent placement) , pancreatic ascites (ERCP with stent will resolve) will resolve
  • Surgical = mainly used for pain

MEDICAL MANAGEMENT OF CHRONIC PANCREATITIS:

• Pain management:
  • WHO step ladder:
    • Step 1- Non opiods
    • Step 2- mild opiods (Tramadol)
    • Step 3- Potent opiods - Morphine
    • Step 4- intervention
  • Gabapentin, Venlaflaxine
  • Antioxidant
    • Selenium, Vit C, Beta carotene, alpha topocherol, Methionine (Betamore G)
  • Fat restriction no longer recommended.
    • Can give MCT
    • Small frequent meals
  • PERT
    • • Enteric coated = to decrease the exocrine insufficiency = used classically • Uncoated ( given with PPI) = to decrease pain
    • CCK - release factor- pain
    • 10% of pancreatic enzyme activity
    • Porcine origin
    • For exocrine insufficiency - Dose is 90000 USP of lipase with meals

• Indications for surgical therapy in CP:
  • A-Pain not managed with medical management
  • B-Suspicion of malignancy (Head mass)
  • C- Symptomatic local Complications-
    • Pseudocyst
    • Bile duct/duodenal stenosis
  • D- Failed endoscopic management
• Endocrine & Exocrine insufficiency in absence of pain is not an indication for surgery

ENDOSCOPIC MANAGEMENT OF CHRONIC PANCREATITIS

• Role of Endotherapy = is for complications

• Endoscopic Therapy Options , Indications and limitations of Endoscopic Management:

  

SURGICAL MANAGEMENT OF CHRONIC PANCREATITIS

There are 3 types of surgeries usually performed:

1. Decompressive = when duct is dilated >7mm without head mass
   1. Child Duval
   2. Peustow
   3. Partington Rochelle ( modified peustow) = LPJ
   4. izbicki procedure = V shaped excision of duct = for small duct <3mm
2. Resectional
   1. Whipples
   2. Pylorus preserving PD = Traverso Longmire
   3. Near Total or total pancreatectomy
   4. DPPHR
      1. Beger =Division of pancreas at neck
3. Hybrid
   1. DPPHR:
      1. Frey’s = head coring + LPJ
      2. Berne modification = modification of beger
         • done in cases of Chronic Pancreatitis with Portal Hypertension
         • because it is difficult to divide the pancreas at the neck here so, we do head coring only [ donot open the duct and donot divide pancreas ] and anastomose jejunum.
      3. Hamburg Modification = done in non dilated duct
         • modification of frey’s
         • izbicki + Frey’s

Techniques of Pancreatic Head Resection for Chronic Pancreatitis

A. Partial Pancreatoduodenectomy (Pylorus-Preserving Procedure)

• Resection:
  • Removal of the pancreatic head and duodenum.
  • Pylorus-preserving option shown.
• Reconstruction:
  • Pancreaticojejunostomy.
  • Hepaticojejunostomy.
  • Duodenojejunostomy (if pylorus-preserving).

B,C,D : Duodenum-Preserving Pancreatic Head Resection Procedures

B. Beger Procedure (Duodenum-Preserving Pancreatic Head Resection)

• Resection:
  • Dissection at the level of the portal vein.
  • The pancreatic head is excavated, with the duodenum preserved.
  • If the bile duct is obstructed, an internal anastomosis can be performed (not shown).
• Reconstruction:
  • Roux-en-Y jejunal loop with two anastomoses:
    • One to the pancreatic tail remnant.
    • One to the excavated pancreatic head.

C. Frey Procedure (Duodenum-Preserving Pancreatic Head Resection)

• Resection:
  • Combines circumscribed excision of the pancreatic head with a longitudinal dissection of the pancreatic duct toward the tail.
• Reconstruction:
  • Roux-en-Y jejunal loop with a single anastomosis.
  • Less extensive head resection than the Beger procedure.
  • Easier reconstruction because it only requires one anastomosis.

D. Bern Modification (Duodenum-Preserving Pancreatic Head Resection)

• Resection:
  • Similar to the Beger procedure in terms of the extent of pancreatic head resection.
  • Portal vein dissection is not performed.
• Reconstruction:
  • One anastomosis to a Roux-en-Y jejunal loop.
  • The bile duct may be opened for an internal anastomosis if necessary.
  • The pancreatic duct toward the tail must be probed to rule out distal stenosis.

High-Yield Points: Surgical Procedures for Chronic Pancreatitis (CP)

(MCQ) True about Modified Puestow procedure?

• A: Used for duct >7mm with head mass
• B: 30% of patients have recurrence of pain after 5 years
• C: Preserves endocrine and exocrine function
• D: Both B and C (Correct answer)

Explanation:

• Puestow procedure involves distal pancreatectomy + LPJ (longitudinal pancreaticojejunostomy).
• Modified Puestow (Partington-Rochelle modification):
  • Only LPJ is done.
  • No drainage of the head or uncinate process.
  • Used when the duct >7mm.
  • 80% of patients experience pain relief.
  • 30% have recurrence of pain after 3-5 years.
  • The procedure aims to preserve endocrine and exocrine function.

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(MCQ) CP with head mass and non-dilated duct. Most appropriate surgical procedure?

• A: Frey’s
• B: Beger’s
• C: ppPD (pylorus-preserving pancreaticoduodenectomy)
• D: Both B and C (Correct answer)

Explanation:

• Frey’s procedure requires a dilated duct to be performed, so it cannot be used in cases of non-dilated ducts.
• Beger’s and ppPD are better options for patients with head mass and non-dilated duct.

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(MCQ) Frey’s procedure for CP includes all except:

• A: Division of gastroduodenal artery
• B: Preservation of duodenum
• C: Head coring
• D: Division of pancreas at neck (Correct answer)

Explanation:

• Frey’s procedure involves a combination of head coring and ductal drainage, preserving the duodenum.
• There is no division of the pancreas at the neck, as this is part of other procedures like the Whipple.

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(MCQ) 50-year-old male presents with chronic abdominal pain. CT scan shows pancreatic calcification with inflammatory head mass and left-sided ductal stenosis. Duct diameter is 7mm. Procedure of choice?

• A: Beger’s
• B: Whipple’s
• C: Hamburg modification
• D: Frey’s (Correct answer)

Explanation:

• Frey’s procedure is a hybrid approach combining head resection with ductal drainage, especially useful when there is a head mass and multiple levels of ductal obstruction (body and tail).
• 90% of patients have pain relief with this procedure.
• However, 35% may develop endocrine and exocrine insufficiency postoperatively.

High-Yield Points: Surgical Procedures and Outcomes in Chronic Pancreatitis (CP)

(MCQ) Beger’s procedure for CP?

• A: Also called as duodenum-preserving head resection
• B: Two anastomoses with head and body along with division at neck
• C: Mesoduodenal vessels are preserved
• D: Pain control is better than ppPD (Correct answer)

Explanation:

• Beger’s procedure is a duodenum-preserving head resection (DPPHR).
• Pain control with Beger’s, Frey’s, and Whipple's is comparable, and better than LPJ alone.
• The choice between Frey’s and Beger’s is based on ductal characteristics:
  • Dilated left-sided duct = Frey’s.
  • Non-dilated left-sided duct = Beger’s.

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(MCQ) Outcomes after surgery for CP: Which is not true?

• A: Pain control is similar in ppPD and DPPHR
• B: DPPHR stops progression of exocrine and endocrine insufficiency on long term (Correct answer)
• C: Endocrine and exocrine insufficiency is equal in long term in ppPD and DPPHR
• D: Berne technique is used in portal hypertension

Explanation:

• Pain control is similar across procedures like ppPD, Frey’s, and Beger’s, while LPJ offers inferior pain control.
• Surgery does not alter the progression of exocrine and endocrine insufficiency over the long term.
• Berne technique is used in cases with portal hypertension.

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(MCQ) 35-year-old male with obstructive jaundice and long segment symmetrical biliary stricture. Most appropriate treatment?

• A: ERCP and stenting
• B: Frey’s procedure
• C: Frey’s procedure with hepaticojejunostomy
• D: Choledochojejunostomy alone (Correct answer)

Explanation:

• Diagnosis: Chronic pancreatitis with a benign biliary stricture (long segment symmetrical).
• Endotherapy (ERCP and stenting) is indicated in cases of cholangitis, but here, it's not feasible due to calcification.
• Since the patient has jaundice without pain, Frey’s is not appropriate.
• The best treatment is a biliary drainage procedure, specifically choledochojejunostomy to relieve the jaundice.

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Key Takeaways:

• Beger’s procedure is a duodenum-preserving head resection for chronic pancreatitis, offering comparable pain relief to other surgical options like Frey’s and ppPD.
• Surgery does not stop the progression of exocrine and endocrine insufficiency in chronic pancreatitis.
• For benign biliary strictures causing jaundice in chronic pancreatitis without pain, choledochojejunostomy / HJ alone is the most appropriate procedure.

High-Yield Points: Biliary Stricture and Pseudocyst in Chronic Pancreatitis (CP)

(MCQ) Biliary stricture in CP: Which statement is not true?

• A: 1/3rd of CP patients have bile duct dilatation
• B: Long segment symmetrical narrowing of intrapancreatic portion
• C: ERCP with metallic stenting offers long-term relief (Correct answer)
• D: 6% have evidence of cholestasis

Explanation:

• 1/3 of CP patients may have CBD dilatation, but most are asymptomatic.
  • In asymptomatic cases, addressing the pancreatic disease (e.g., Frey’s procedure if there is a head mass) often resolves the biliary dilatation, and hepaticojejunostomy (HJ) is usually not needed.
  • In symptomatic cases (e.g., jaundice or cholangitis), biliary drainage through ERCP stenting, HJ, or choledochojejunostomy is performed.
• 6% of CP patients present with significant biliary obstruction and cholestasis.
• Biliary strictures typically show long, symmetrical narrowing of the intrapancreatic portion of the bile duct on MRCP or ERCP.
• ERCP with metallic stenting does not offer long-term relief in most cases.

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(MCQ) Not true about pseudocyst arising in CP?

• A: 30-40% have spontaneous remission (Correct answer)
• B: External drainage can be done in sepsis
• C: EUS-guided internal drainage is comparable to open drainage
• D: Have ductal communication in majority of cases

Explanation:

• Pseudocysts are more commonly seen in chronic pancreatitis (CP) than in acute pancreatitis (AP) because CP is associated with ductal obstruction, leading to persistent pseudocyst formation.
  • In acute pancreatitis (AP), pseudocysts often resolve spontaneously because there is no obstruction in the duct, unlike CP.
• 10% of pseudocysts in CP resolve spontaneously, not 30-40%.
• The majority of pseudocysts in CP have a ductal communication due to ductal obstruction.
• EUS-guided internal drainage is as effective as open surgical drainage.
• In the presence of sepsis, external drainage can be performed.

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Key Takeaways:

• Biliary strictures in chronic pancreatitis typically involve long, symmetrical narrowing of the intrapancreatic portion of the bile duct. In symptomatic cases, biliary drainage is necessary.
• Pseudocysts in chronic pancreatitis usually do not resolve spontaneously due to ductal obstruction and often require intervention. Ductal communication is common in these cases.

Recent Advances in Chronic Pancreatitis

ESCAPE Trial: Early Surgery vs Endoscopy-First Approach for Pain in Chronic Pancreatitis

• ESCAPE Randomized Clinical Trial:
  • Compared early surgery to an endoscopy-first approach for pain management in patients with chronic pancreatitis.
  • Outcome: Early surgery resulted in better clinical outcomes in terms of pain relief and long-term management of the disease.

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ChroPac Trial: Partial Pancreatoduodenectomy vs Duodenum-Preserving Pancreatic Head Resection (DPPHR)

• ChroPac Trial:
  • A multicenter, randomized, controlled, double-blind trial comparing partial pancreatoduodenectomy (PD) with duodenum-preserving pancreatic head resection (DPPHR) in patients with chronic pancreatitis.
• Key Findings:
  • Quality of life was similar between both groups after 24 months.
  • Pain control and pancreatic function (endocrine and exocrine) were also similar between the two approaches.
  • Fewer readmissions were observed in patients undergoing partial pancreatoduodenectomy (PD).

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Chronic Pancreatitis ( live class)

Classification Systems for Chronic Pancreatitis

Major Consensus Conferences and Studies:

• Marseille (1963) and Marseille-Rome (1986).
• Cambridge (1984).
• Zurich symposium.
• Manchester classification.

Key Classification Systems:

1. Cambridge and Rosemont Classification:
   • Based on morphologic changes seen on CT and EUS.
   • Useful for categorizing the disease based on imaging findings.
   • Limitation: Imperfect correlation between morphologic changes and clinical symptoms.
   • Does not include etiology.
2. TIGAR-O Classification:
   • Focuses on major etiologic sources of chronic pancreatitis.
   • Limitation: Does not provide clinical severity staging.
3. Manchester and Heidelberg Classification:
   • Classify patients based on discrete clinical features.
   • Includes three severity stages for easier clinical use.
   • Heidelberg classification offers guidance on which clinical stages are most likely to require surgery.

Shortcomings:

• Each system offers some clinical utility but has shortcomings.
• None of these systems fully account for the heterogeneity of chronic pancreatitis.
• A combination of clinical and etiologic systems may be needed for comprehensive patient care.

M-ANNHEIM Classification:

• Most comprehensive classification at present.
• Includes:
  • Severity scoring.
  • Diagnostic criteria.
  • Multifactorial risk factor classification.
• M-ANNHEIM Acronym:
  • M: Multiple risk factors.
  • A: Alcohol.
  • N: Nicotine.
  • N: Nutrition.
  • H: Hereditary.
  • E: Efferent duct factors.
  • I: Immunological.
  • M: Miscellaneous.
• Strength: Provides a complete classification and grading tool.
• Limitation: May be too detailed for easy clinical use in some situations.
• Conclusion: Remains the most complete tool for exploring the etiology and grading the severity of chronic pancreatitis.

Clinical Features:

• Pain:
  • Abdominal pain is a hallmark symptom.
  • Neuropathic pain may develop later, which often does not respond to surgery.
  • Early surgery is recommended to address the pain before it becomes neuropathic.
  • Pain may be absent in 15-20% of cases.
• Endocrine and Exocrine Insufficiency:
  • Exocrine insufficiency appears earlier due to the destruction of acinar cells.
  • Endocrine insufficiency (involving islet cells) appears later, after >90% of the gland is destroyed, resulting in burnt-out disease.
  • By the time endocrine insufficiency appears, pain is often gone, or it persists as neuropathic pain.
• Progressive Disease:
  • The pancreas undergoes fibrosis, leading to both endocrine and exocrine insufficiency.
• Surgery:
  • While surgery may help with early pain management, it does not alter the natural course of the disease.

Etiology:

• Most Common Cause: Alcohol.
• Gallstones:
  • Do not cause chronic pancreatitis because gallstone-related issues do not result in morphological changes in the gland, unlike chronic pancreatitis.

TIGAR-O Classification:

• A system used to classify the causes of chronic pancreatitis based on:

  • T: Toxic-metabolic (e.g., alcohol)
  • I: Idiopathic
  • G: Genetic
  • A: Autoimmune
  • R: Recurrent and severe acute pancreatitis
  • O: Obstructive (e.g., ductal issues)

  

Idiopathic (Tropical) Pancreatitis and Genetic Mutations

Idiopathic (Tropical) Pancreatitis

• Commonly seen in India.
• No genetic causes should be associated with true idiopathic (tropical) pancreatitis.

Genetic Mutations in Pancreatitis

• PRSS1 Mutation:
  • Involved in activation of trypsin in the pancreas.
  • Associated with hereditary pancreatitis.
• SPINK1 Mutation:
  • Most common mutation found in pancreatitis.
  • Regulates activation of trypsin.
  • Present in 1-2% of normal individuals.
  • Seen in alcoholic, hereditary, and tropical pancreatitis.
• CFTR Mutation:
  • Involved in bicarbonate production.
  • Homozygous mutation leads to cystic fibrosis.
  • Heterozygous mutation is associated with chronic pancreatitis.

Tropical Pancreatitis

• Prevalence:
  • Most common form of pancreatitis in India.
• Common Mutation:
  • SPINK1-N34S mutation (seen in alcoholic and idiopathic cases).
• Clinical Features:
  • Pancreatic calcification.
  • Endocrine and exocrine insufficiency.
  • Not related to cassava toxicity.

Diagnosis

• X-ray:
  • Detects pancreatic calcifications.
• Ultrasound (USG) Abdomen:
  • Shows calcifications.
• Contrast-Enhanced CT (CECT):
  • Used in advanced stages of the disease.
  • Detects calcifications, ductal dilatation, pseudocyst, pseudoaneurysm, and local complications (e.g., duodenal and biliary strictures).
• Secretin MRCP (SMRCP):
  • Shows ductal anatomy, but cannot detect calcifications.

Chain of Lake Appearance on ERCP also can be seen on MRCP as well :

CT images showing calcification and atrophy:

Pancreatic Function Tests and Risk of Malignancy in Chronic Pancreatitis

Pancreatic Function Tests

• Fecal Elastase:
  • Levels not related to PERT (Pancreatic Enzyme Replacement Therapy).
  • < 200 is considered abnormal.
  • < 100 indicates severe exocrine insufficiency.
• Most Sensitive Test:
  • The secretin stimulation test is the most sensitive test for assessing pancreatic function.

Risk of Malignancy in Chronic Pancreatitis

• General Population:
  • There is a 4-5 fold increased risk of developing pancreatic malignancy in chronic pancreatitis patients (previously thought to be 16 times).
• Hereditary Chronic Pancreatitis (CP):
  • Patients have a 40-50 times increased risk of developing pancreatic cancer.
  • Lifetime probability of developing pancreatic cancer is around 40% for hereditary CP.

Medical and Endoscopic Management of Chronic Pancreatitis

Medical Management

• Pain Management:
  • NSAIDs and opioids.
  • SSRIs for neuropathic pain.
  • Celiac plexus block.
  • Antioxidants: Selenium-based formulations.
  • Uncoated PERT (Pancreatic Enzyme Replacement Therapy) for pain relief.
• Exocrine Insufficiency:
  • PERT given with PPI (Proton Pump Inhibitors).
  • Dosage: 25,000 to 75,000 units of lipase.
  • Fat restriction is no longer recommended. A normal diet high in protein and low in carbohydrates and fats is suggested.

Endoscopic Therapy

• Proximal Duct Stenosis (No calcifications or inflammatory mass):
  • Endoscopic treatment can be attempted.
  • If 2-3 endoscopic treatments fail, consider surgery.
• Distal Duct Obstruction, Calcifications, or Local Complications:
  • Surgery is superior to endoscopic treatment.
  • Early surgery is recommended to preserve exocrine and endocrine function.
• Pancreatic Pseudocysts:
  • May be treated endoscopically.
  • If endoscopic treatment fails, a surgical drainage procedure is recommended.

Surgical Management:

Surgical Procedures for Chronic Pancreatitis

Child-Duval Procedure:

• Distal pancreatectomy combined with a drainage procedure.

Peustow Procedure:

• Involves opening the pancreatic duct in the body and tail.
• Distal pancreatectomy is performed.
• The remaining pancreas is invaginated into the jejunum.

Partington-Rochelle Modification of Peustow:

• No distal pancreatectomy performed.
• Instead, a longitudinal pancreaticojejunostomy (LPJ) is done, preserving the pancreas.