Chronic pancreatitis (CP) is caused by progressive inflammation and irreversible damage to the structure and function (exocrine and endocrine) of the pancreas. Chronic heavy alcohol use is the most common cause, followed by pancreatic ductal obstruction. Idiopathic pancreatitis accounts for up to 30% of cases. Patients may be asymptomatic or present with abdominal pain and features of pancreatic enzyme insufficiency (e.g., steatorrhea, weight loss, impaired glucose tolerance). Diagnosis is confirmed on imaging, which demonstrates pancreatic calcifications, ductal strictures, and ductal dilations. Pancreatic function tests (e.g., fecal elastase-1 measurement, 72-hour ) assess the degree of enzyme deficiency. Symptomatic patients are managed with oral pancreatic enzyme replacements and analgesics. Patients with chronic pain require additional interventions (e.g., celiac ganglion block, partial/complete pancreatic resection).
- Chronic heavy alcohol use (60–70% of cases, esp. men) 
- Pancreatic ductal obstruction (< 10%): strictures (e.g., due to trauma, stones)
- Tobacco use
- Idiopathic pancreatitis (20–30%)
- Hereditary pancreatitis (∼ 1%) 
- Systemic disease
- Most common cause in the tropics (esp. southern India)
- Young age at onset
- Autodigestion and inflammation: damage to pancreatic acinar cells; (e.g., alcohol), outflow obstruction of pancreatic enzymes or premature activation of trypsinogen to trypsin; → intrapancreatic activation of digestive enzymes (e.g., amylase and lipase) → autodigestion of pancreatic tissue → inflammatory reaction
- Fibrosis: exposure to toxins and/or inflammatory mediators (e.g., alcohol, cytokines) → activation of pancreatic stellate cells
- Epigastric abdominal pain (main symptom)
- Features of pancreatic insufficiency: late manifestation (after 90% of the pancreatic parenchyma is destroyed)
Subtypes and variants
|Autoimmune pancreatitis |
|Autoimmune pancreatitis type I||Autoimmune pancreatitis type II|
|Etiology|| || |
|Diagnostics||Serology|| || |
|Prognosis || || |
- Initial survey: medical history, risk factors, clinical features suggestive of chronic pancreatitis
- Laboratory testing: helps identify the underlying cause and possible complications (CBC, calcium levels, triglycerides, fasting glucose, liver function tests, pancreatic enzyme levels)
- Confirm diagnosis: via imaging and pancreatic function tests
- Assess disease severity: (e.g., fecal elastase-1 activity) are used to determine the extent of pancreatic insufficiency.
- Genetic testing: indicated in young patients with idiopathic pancreatitis or a family history of chronic pancreatitis
The STEP-wise approach involves Survey, Tomography/imaging, Endoscopy, and Pancreatic function testing.
In chronic pancreatitis, pancreatic enzyme levels are often normal and cannot be used to confirm or rule out the diagnosis. In contrast, acute pancreatitis typically causes significant enzyme elevation.
- Fecal elastase-1 (FE-1) activity: confirms that steatorrhea is due to pancreatic lipase insufficiency 
72-hour quantitative fecal fat estimation
- Patients are asked to consume 100 g of fat per day for 3 days, after which the fecal fat content of their stool is measured.
- Fecal fat > 7 g per day is diagnostic of steatorrhea.
Direct tests 
- Cholecystokinin test: Cholecystokinin analog (cerulein) is administered intravenously, which stimulates pancreatic enzyme and bicarbonate secretion. This secretion is collected in a tube placed in the duodenum during endoscopy and analyzed.
- Secretin test: Secretin stimulates pancreatic bicarbonate secretion. The test is performed in the same way as the cholecystokinin test.
- Cholecystokinin-secretin pancreatic function test: Both of the secretagogues are administered simultaneously and the collected secretion is quantitatively analyzed.
- Abdominal CT (plain and contrast-enhanced CT): best initial imaging modality to screen for CP
ERCP: detection of early pathologies and simultaneous treatment possible (e.g., duct dilation, stent insertion)
- Ductal stones, which are visible as filling defects
- “Chain of lakes” or “string of pearls” appearance (characteristic feature)
- Irregularity and/or dilation of the main pancreatic duct
- Indicated when CT findings are equivocal but clinical suspicion of CP is high
- Ductal strictures and dilations
- Pancreatic calcifications
- Indistinct margins and enlargement
- Pancreatic calcifications
- Ductal strictures, dilation, or stones
- Endoscopic ultrasound (EUS)
- Abdominal x-ray: visible pancreatic calcifications (highly specific, but only seen in ∼ 30% of cases)
Genetic testing 
- Abstinence from alcohol and nicotine
- Pancreatic enzyme replacement (with meals)
- Small, regular meals (rich in carbohydrates, low in fat)
- Supplementation with medium-chain triglycerides (MCT)
- Parenteral administration of (A, D, E, K) if necessary
- Endocrine insufficiency: insulin administration
- For more information on the management of acute attacks, see “”.
- Analgesics: NSAIDs, opioids for severe pain (e.g., long-acting fentanyl/morphine), low-dose (e.g., amitriptyline)
- Intractable pain
- → deficiency of lipase, amylase, and protease → maldigestion, steatorrhea, malabsorption
- Destruction of beta cells → endocrine insufficiency with pancreatic diabetes 
Pancreatic pseudocysts 
- Definition: encapsulated collection of pancreatic fluid that develops 4 weeks after an acute attack of pancreatitis (can occur in both acute and chronic pancreatitis )
- Pathophysiology: pancreatic secretions leak from damaged ducts → inflammatory reaction of surrounding tissue → encapsulation of secretions by granulation tissue
- Clinical features 
Diagnostics: abdominal ultrasound/CT/MRI
- Extrapancreatic fluid collection within well-defined wall/capsule
- No solid cyst components detectable
Splenic vein thrombosis 
- Epidemiology: Occurs in 10% of patients with chronic pancreatitis
- Pathophysiology: inflammation of the splenic vein → thrombus formation → left-sided portal hypertension → gastric varices
- Clinical features: can present with upper GI bleeding, ascites, and splenomegaly
- Diagnostics: ultrasound with doppler, CT/MR angiography
- Acute: anticoagulation and/or thrombectomy
- Chronic and symptomatic: splenectomy
- Pathophysiology: ductal disruption (due to an acute attack of pancreatitis, pancreatic surgery and/or trauma) or a pseudocyst leak/rupture → pancreatic ascites
- Clinical features
- Conservative management: indicated in all patients; ∼ 30% require no further treatment
- Stenting of the pancreatic duct: if ERCP shows ductal disruption 
- Surgery: indicated in patients showing no improvement after 4 weeks of conservative management (see “ ”)
We list the most important complications. The selection is not exhaustive.