Chronic pancreatitis (CP) is characterized by progressive inflammation that results in irreversible damage to the structure and function of the pancreas. Chronic heavy alcohol use is the most common cause of CP, followed by pancreatic ductal obstruction. Approximately 30% of CP cases are idiopathic. Affected individuals may be asymptomatic or present with abdominal pain and features of exocrine pancreatic insufficiency (e.g., steatorrhea, weight loss) or endocrine pancreatic insufficiency (e.g., prediabetes, diabetes). Diagnosis is confirmed with imaging, which typically shows pancreatic calcifications, ductal strictures, and ductal dilations. Pancreatic function tests (e.g., fecal elastase-1 measurement, 72-hour ) assess the degree of enzyme deficiency. Medical therapy should include patient counseling and education, pain management, and monitoring and management of complications (e.g., via oral pancreatic enzyme replacement therapy). Interventional therapy may be required for patients with intractable pain or other complications (e.g., celiac ganglion block, partial or complete pancreatic resection).
- Chronic heavy alcohol use (most common, esp. men) 
- Pancreatic ductal obstruction: strictures (e.g., due to trauma, stones)
- Tobacco use
- Idiopathic pancreatitis
- Hereditary pancreatitis 
- 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|
|Diagnostics||Serology|| || |
|Prognosis || || |
Rule out underlying pancreatic malignancies before starting steroids for autoimmune pancreatitis; reassess for pancreatic malignancy in the case of autoimmune pancreatitis that does not respond to treatment. 
There is no single test for the diagnosis of chronic pancreatitis; risk factors, clinical features, imaging studies, and pancreatic function tests may all be considered in the determination of a diagnosis.
- Initial survey: Identify findings raising suspicion for chronic pancreatitis.
- Imaging studies (most important) to confirm structural changes
- Laboratory testing to assess for complications and identify the underlying cause
- Additional studies: if initial studies were nondiagnostic
A STEP-wise approach to diagnosing chronic pancreatitis may include: Survey, Tomography/imaging, Endoscopic imaging, and Pancreatic function testing.
Abdominal CT (with and without contrast) or MRI/MRCP
- Best initial imaging modalities to establish a diagnosis
- Can exclude gastrointestinal malignancies (e.g., pancreatic carcinoma)
- Supportive findings
Additional imaging 
- Abdominal ultrasound 
- Abdominal x-ray: visible pancreatic calcifications (highly specific, but only seen in ∼ 30% of cases) 
- Endoscopic ultrasound (EUS)
- Secretin-enhanced MRCP
- ERCP: Not routinely recommended because of availability of noninvasive imaging, high risk, and cost 
Laboratory studies 
- Serum pancreatic enzyme levels: Lipase (specific) and amylase (nonspecific) are often normal.
- CBC: WBCs may be elevated in infection or abscess.
- Calcium: Hypercalcemia may suggest hyperparathyroidism, a rare cause of chronic pancreatitis.
- Triglycerides: Severe hypertriglyceridemia can cause pancreatitis.
- Liver enzymes and liver function tests: elevated in biliary or ductal obstruction
- HbA1c: elevated levels could suggest type 3c diabetes (pancreatogenic diabetes mellitus) and/or
- Fat-soluble vitamins and zinc: to identify deficiency and establish baseline
Pancreatic enzyme levels are often normal in chronic pancreatitis and cannot be used to confirm or rule out the diagnosis. In contrast, acute pancreatitis typically causes significant enzyme elevation.
Pancreatic function tests 
- Fecal elastase-1 (FE-1): most common test
72-hour quantitative fecal fat estimation: confirmatory test for steatorrhea
- Patients consume 100 g of fat per day for 72 hours.
- Interpretation: Fecal fat > 7 g per day is diagnostic of steatorrhea.
- Serum trypsinogen: not routinely recommended 
- Direct tests of pancreatic function
- Indications: reserved for high-risk patients if the diagnosis has not been established after thorough evaluation
- Characteristic findings 
Genetic testing 
- Indications include:
- Tests include:
- Provide patient education: Chronic pancreatitis is a relapsing and remitting disease.
- Recommend abstinence from nicotine and alcohol for all patients. 
- Monitor for and manage (e.g., pancreatic enzyme replacement therapy for ).
- Initiate directed treatment of the underlying
Patients with CP may benefit from a multidisciplinary team providing individualized pain management and addressing psychosocial factors. 
Pharmacological pain management 
- Start with nonopioid (e.g., NSAIDs and acetaminophen if not contraindicated).
- Consider . 
- Consider antioxidant therapy (e.g., combinations of selenium, ascorbic acid, beta carotene, and methionine).
- Limit .
- Indication: pain not adequately managed with pharmacotherapy
- Thoracoscopic bilateral splanchnicectomy 
- Surgical decompression
- Surgical resection
Recurrent acute pancreatitis 
See “Acute pancreatitis.”
- Long-standing chronic pancreatitis
- Weight loss, malnutrition
- Diarrhea, steatorrhea
- Osteoporosis or osteopenia
- Clinical diagnosis
- Consider testing for diagnostic confirmation (see also “Diagnostics”)
- Advise small, frequent meals without fat restriction.
- Check indications for pancreatic enzyme replacement therapy (e.g., with pancrelipase) , which include: 
- Screen for vitamins A, D, E, and K) and zinc. (
Endocrine pancreatic insufficiency
- Pathophysiology: Destruction of beta cells leads to endocrine insufficiency with (type 3c diabetes mellitus). 
- Clinical features: Brittle, insulin-dependent diabetes
Pancreatic pseudocysts 
Clinical features 
- Often asymptomatic
- Painless abdominal mass
- Pressure effects
- First line: CT abdomen with contrast
- Findings: Extrapancreatic fluid collection within well-defined wall or capsule with contrast enhancement
- Other imaging modalities
- Symptomatic cysts
- Large asymptomatic cysts
- Urgent intervention may be needed if patients develop complications.
- Infection: fever, abdominal pain, sepsis
- Pseudocyst rupture: pancreatic ascites/pancreaticopleural fistula
- Erosion into an abdominal vessel: hemorrhage into the cyst
- Abdominal distention; variable abdominal pain
- Peripheral edema
- Free fluid in the peritoneal cavity
- Ascitic fluid analysis: exudate (high protein: > 3 g/dL; low SAAG: < 1.1 g/dL) with high amylase levels (> 1,000 IU/L)
- Imaging: ERCP, CECT, MRCP
- Conservative management
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
- Acute: anticoagulation and/or thrombectomy
- Chronic and symptomatic: splenectomy
General screening for pancreatic cancer is not currently recommended. Screen patients (with a triphasic pancreas protocol CT) who develop weight loss, protracted abdominal pain, or functional decline. 
We list the most important complications. The selection is not exhaustive.