Chronic Pancreatitis
Summary
Chronic pancreatitis is a progressive inflammatory disease of the pancreas characterised by irreversible structural damage, fibrosis, and loss of exocrine and endocrine function. Alcohol is the most common cause in Western countries (~70%), followed by idiopathic, genetic, autoimmune, and obstructive causes. Patients typically present with recurrent episodes of abdominal pain, and over time develop exocrine insufficiency (malabsorption, steatorrhoea) and endocrine insufficiency (diabetes mellitus). Imaging may show pancreatic calcifications, ductal dilatation, and parenchymal atrophy. Management focuses on pain control, abstinence from alcohol, pancreatic enzyme replacement therapy (PERT) for exocrine insufficiency, and management of diabetes. Surgery (drainage, resection) is reserved for medically refractory pain or complications.
Key Facts
- Aetiology: Alcohol (~70%), Idiopathic (20%), Genetic (PRSS1, SPINK1, CFTR), Autoimmune, Obstructive
- TIGAR-O classification: Toxic, Idiopathic, Genetic, Autoimmune, Recurrent acute, Obstructive
- Cardinal feature: Recurrent/persistent abdominal pain
- Exocrine insufficiency: Steatorrhoea, weight loss, fat-soluble vitamin deficiency
- Endocrine insufficiency: "Type 3c" diabetes mellitus
- Imaging: CT (calcifications, atrophy), MRCP/EUS (ductal changes)
- Cambridge classification: Grades ductal changes on imaging
- Treatment: Pain management, PERT (Creon), diabetes control, alcohol cessation
- Surgery: Frey, Beger, or Puestow procedures for refractory pain
Clinical Pearls
"Pain Is the Presenting Feature": Chronic epigastric pain, often radiating to the back and relieved by leaning forward, is the hallmark. Pain may "burn out" later in the disease as the pancreas becomes atrophic.
"Steatorrhoea = 90% Loss of Function": Exocrine insufficiency only manifests clinically when >90% of pancreatic function is lost. Steatorrhoea (pale, floating, foul-smelling stools) indicates severe disease.
"Calcifications = Chronic Pancreatitis": Pancreatic calcifications on CT are virtually diagnostic of chronic pancreatitis. However, early disease may have no calcifications.
"Type 3c Diabetes Is Different": Diabetes from chronic pancreatitis (pancreatogenic diabetes) lacks the typical insulin resistance of type 2 and also involves glucagon deficiency, creating a "brittle" diabetes with hypoglycaemia risk.
"Alcohol Cessation Slows Progression": Abstinence from alcohol is essential — it reduces pain, slows progression, and improves response to treatment.
Why This Matters Clinically
Chronic pancreatitis is often underdiagnosed and undertreated. Recognising the clinical features, understanding the role of pancreatic enzyme replacement, and managing pain effectively can significantly improve quality of life. The increased risk of pancreatic cancer in chronic pancreatitis requires vigilance.[1,2]
Incidence & Prevalence
| Parameter | Data |
|---|---|
| Incidence | 5-12 per 100,000/year (Western countries) |
| Prevalence | 50 per 100,000 |
| Peak onset | 40-50 years |
| Sex ratio | Male predominance (alcohol-related) |
Risk Factors and Causes (TIGAR-O)
| Category | Causes |
|---|---|
| Toxic-metabolic | Alcohol (~70%), Smoking, Hyperlipidaemia, Hypercalcaemia, CKD, Medications |
| Idiopathic | Early-onset (20-30 years), Late-onset (>50 years) |
| Genetic | PRSS1, SPINK1, CFTR, CTRC mutations; Hereditary pancreatitis |
| Autoimmune | Type 1 (IgG4-related), Type 2 (associated with IBD) |
| Recurrent acute | Repeated episodes of acute pancreatitis |
| Obstructive | Pancreatic duct stricture, pancreas divisum, tumour |
Mechanism
Step 1: Initial Injury
- Alcohol, genetic mutations, obstruction, autoimmune attack
- Repeated episodes of pancreatic inflammation
Step 2: Necrosis-Fibrosis Cycle
- Repeated acute pancreatitis leads to necrosis
- Activated stellate cells produce collagen
- Progressive fibrosis replaces functional parenchyma
Step 3: Ductal Changes
- Main pancreatic duct dilatation and strictures
- Calcification of protein plugs (calcifications)
- "Chain of lakes" appearance
Step 4: Exocrine Insufficiency
- Loss of acinar cells
- Reduced enzyme secretion
- Maldigestion and malabsorption (steatorrhoea)
- Fat-soluble vitamin deficiency (A, D, E, K)
Step 5: Endocrine Insufficiency
- Loss of islet cells (beta and alpha cells)
- Diabetes mellitus ("Type 3c")
- Glucagon deficiency → risk of hypoglycaemia
Pathological Features
| Feature | Description |
|---|---|
| Fibrosis | Replacement of parenchyma with fibrous tissue |
| Calcifications | Calcium deposits in ducts and parenchyma |
| Atrophy | Small, shrunken pancreas (late stage) |
| Ductal dilatation | Irregular, "chain of lakes" |
| Pseudocysts | Fluid collections without epithelial lining |
Symptoms
| Symptom | Frequency | Notes |
|---|---|---|
| Epigastric pain | 80-90% | Radiates to back; relieved by leaning forward |
| Steatorrhoea | 30-40% (late) | Pale, bulky, foul-smelling, floating stools |
| Weight loss | Common | Malabsorption + reduced oral intake |
| Nausea/vomiting | Variable | During pain exacerbations |
| Diabetes symptoms | 30-50% | Polydipsia, polyuria, late complication |
Signs
| Sign | Notes |
|---|---|
| Epigastric tenderness | Mild; not peritonism |
| Cachexia | Advanced disease |
| Jaundice | Bile duct obstruction (head of pancreas mass or stricture) |
| Splenomegaly | Splenic vein thrombosis |
Pain Pattern
| Feature | Description |
|---|---|
| Location | Epigastric, radiates to back |
| Character | Dull, constant, gnawing |
| Relief | Leaning forward; fasting; analgesics |
| Triggers | Eating (post-prandial); alcohol |
| "Burn-out" | Pain may improve as pancreas becomes atrophic (late stage) |
Red Flags
[!CAUTION] Red Flags — Urgent Assessment:
- New jaundice (bile duct obstruction, ?cancer)
- Unexplained new weight loss (malignancy risk)
- Large/symptomatic pseudocyst (infection, bleeding, compression)
- GI bleeding (splenic vein thrombosis → gastric varices)
- Uncontrolled or new diabetes
Approach
General:
- Cachexia (malnutrition)
- Jaundice
- Signs of chronic liver disease (if alcoholic)
Abdominal:
- Epigastric tenderness
- Mass (pseudocyst)
- Hepatomegaly (if concurrent alcoholic liver disease)
- Splenomegaly (splenic vein thrombosis)
- Ascites (rare in chronic pancreatitis alone)
Features of Complications
| Complication | Examination Finding |
|---|---|
| Pseudocyst | Epigastric mass; may be tender |
| Splenic vein thrombosis | Splenomegaly; gastric varices (haematemesis) |
| Bile duct obstruction | Jaundice; palpable gallbladder (if malignant) |
First-Line Investigations
| Investigation | Expected Findings |
|---|---|
| FBC | May be normal; macrocytosis if alcohol |
| LFTs | Elevated ALP/Bilirubin if bile duct obstruction |
| Amylase/Lipase | Often normal (burned-out gland); elevated in acute exacerbations |
| Glucose / HbA1c | Diabetes |
| Faecal elastase-1 | <200 μg/g indicates exocrine insufficiency; <100 = severe |
| Fat-soluble vitamins | Low A, D, E, K (malabsorption) |
| Lipids, Calcium | Hypertriglyceridaemia, hypercalcaemia as causes |
Imaging
| Modality | Findings |
|---|---|
| CT Abdomen | Calcifications (diagnostic), ductal dilatation, atrophy, pseudocyst |
| MRCP | Ductal changes; "chain of lakes"; strictures |
| EUS | Parenchymal and ductal changes; most sensitive for early disease |
| ERCP | Now mainly therapeutic; Cambridge classification |
Cambridge Classification (Ductal Changes)
| Grade | Findings |
|---|---|
| Normal | No abnormalities |
| Equivocal | <3 abnormal side branches |
| Mild | ≥3 abnormal side branches |
| Moderate | Abnormal main duct + side branches |
| Marked | Severe; large cavity, stricture, calculi, obstruction |
Management Algorithm
CHRONIC PANCREATITIS MANAGEMENT
↓
┌──────────────────────────────────────────────────────────────┐
│ LIFESTYLE │
├──────────────────────────────────────────────────────────────┤
│ ➤ Alcohol cessation (ESSENTIAL) │
│ ➤ Smoking cessation │
│ ➤ Small, frequent, low-fat meals │
│ ➤ Nutritional support (dietitian) │
└──────────────────────────────────────────────────────────────┘
↓
┌──────────────────────────────────────────────────────────────┐
│ PAIN MANAGEMENT │
├──────────────────────────────────────────────────────────────┤
│ ➤ WHO analgesic ladder: │
│ • Paracetamol │
│ • Weak opioid (tramadol) │
│ • Strong opioid (morphine, oxycodone) │
│ ➤ Adjuvants: Amitriptyline, pregabalin │
│ ➤ Avoid large doses of opioids if possible (dependence) │
│ ➤ Antioxidants (limited evidence) │
│ │
│ ⚠️ Pain clinic referral for chronic pain management │
└──────────────────────────────────────────────────────────────┘
↓
┌──────────────────────────────────────────────────────────────┐
│ EXOCRINE INSUFFICIENCY │
├──────────────────────────────────────────────────────────────┤
│ ➤ Pancreatic Enzyme Replacement Therapy (PERT): │
│ • Creon (pancreatin) │
│ • Minimum 40,000-50,000 units lipase per meal │
│ • 25,000 units with snacks │
│ • Take at the start of meals │
│ │
│ ➤ Add PPI if suboptimal response (protects enzymes) │
│ ➤ Fat-soluble vitamin supplementation (A, D, E, K) │
│ ➤ Monitor nutritional status; dietitian input │
└──────────────────────────────────────────────────────────────┘
↓
┌──────────────────────────────────────────────────────────────┐
│ ENDOCRINE INSUFFICIENCY │
├──────────────────────────────────────────────────────────────┤
│ ➤ Type 3c diabetes management: │
│ • Metformin (first-line) │
│ • Insulin (often required; "brittle" diabetes) │
│ ⚠️ Glucagon deficiency → high hypoglycaemia risk │
│ ➤ Avoid sulfonylureas if possible (hypoglycaemia) │
│ ➤ Careful glucose monitoring │
└──────────────────────────────────────────────────────────────┘
↓
┌──────────────────────────────────────────────────────────────┐
│ ENDOSCOPIC TREATMENT │
├──────────────────────────────────────────────────────────────┤
│ ➤ ERCP + sphincterotomy for dominant stricture │
│ ➤ Stenting of pancreatic duct strictures │
│ ➤ Stone extraction (with ESWL if needed) │
│ ➤ Pseudocyst drainage (transgastric) │
└──────────────────────────────────────────────────────────────┘
↓
┌──────────────────────────────────────────────────────────────┐
│ SURGERY │
├──────────────────────────────────────────────────────────────┤
│ INDICATIONS: │
│ ➤ Refractory pain despite maximal medical/endoscopic Rx │
│ ➤ Suspected malignancy │
│ ➤ Complications (pseudocyst, bile duct obstruction) │
│ │
│ PROCEDURES: │
│ ➤ Drainage: Puestow (lateral pancreaticojejunostomy) │
│ ➤ Resection + Drainage: Frey (partial head resection) │
│ ➤ Resection: Whipple (head); Distal pancreatectomy (tail) │
│ ➤ Total pancreatectomy + Islet autotransplant (TPIAT) │
└──────────────────────────────────────────────────────────────┘
Local Complications
| Complication | Incidence | Management |
|---|---|---|
| Pseudocyst | 20-40% | Observation if small; drainage if symptomatic |
| Bile duct stricture | 5-10% | Stent; surgery if refractory |
| Duodenal obstruction | Rare | Surgical bypass |
| Splenic vein thrombosis | 10% | Gastric varices; splenectomy if bleeding |
| Pancreatic fistula | Variable | Conservative; stent; surgery |
Systemic Complications
| Complication | Notes |
|---|---|
| Malnutrition | PERT, nutritional support |
| Osteoporosis | Vitamin D deficiency |
| Diabetes (Type 3c) | Insulin often required |
| Pancreatic cancer | 4-8% lifetime risk; surveillance controversial |
Survival
| Factor | Impact |
|---|---|
| Continued alcohol use | Accelerates progression; worse outcomes |
| Smoking | Independent risk factor for progression |
| Surgery | 60-80% pain relief in selected patients |
| Cancer risk | ~5% develop pancreatic cancer; increased surveillance not routine |
Quality of Life
- Chronic pain significantly impairs QOL
- Opioid dependence is a major concern
- Diabetes and malabsorption require lifelong management
Key Guidelines
| Guideline | Organisation | Year | Key Points |
|---|---|---|---|
| UEG Chronic Pancreatitis Guideline | United European Gastroenterology | 2017 | Comprehensive management guidance |
| ACG Chronic Pancreatitis Guideline | American College of Gastroenterology | 2020 | Diagnosis and management |
Key Studies
EUROPAC Trial (2014)
- Antioxidant supplementation in chronic pancreatitis
- No significant benefit on pain
- PMID: 24813469
Puestow vs Frey Procedures
- Frey procedure (partial head resection + drainage) shows better pain outcomes in some studies
- Lower morbidity than Whipple
What is Chronic Pancreatitis?
Chronic pancreatitis is long-term inflammation and scarring of the pancreas — an organ that helps digest food and control blood sugar. Over time, the pancreas becomes damaged and doesn't work properly.
What causes it?
The most common cause is drinking too much alcohol over many years. Other causes include genetic conditions, autoimmune disease, and sometimes no cause is found (idiopathic).
What are the symptoms?
- Pain: The main symptom is pain in the upper tummy that goes through to the back
- Digestive problems: Pale, oily, bad-smelling stools (because fat isn't absorbed properly)
- Weight loss: From poor absorption of food
- Diabetes: Because the pancreas also controls blood sugar
What is the treatment?
- Stop alcohol and smoking — essential to slow down the disease
- Pain relief — tablets, pain clinic
- Enzyme capsules (Creon) — to help digest food
- Diabetes treatment — if blood sugar becomes too high
- Surgery — in severe cases to relieve pain
Guidelines
-
Löhr JM, et al. United European Gastroenterology evidence-based guidelines for the diagnosis and therapy of chronic pancreatitis. United European Gastroenterol J. 2017;5(2):153-199. PMID: 28344786
-
Gardner TB, et al. ACG Clinical Guideline: Chronic Pancreatitis. Am J Gastroenterol. 2020;115(3):322-339. PMID: 32022720
High-Yield Exam Topics
| Topic | Key Points |
|---|---|
| TIGAR-O | Toxic, Idiopathic, Genetic, Autoimmune, Recurrent, Obstructive |
| CT findings | Calcifications, atrophy, ductal dilatation |
| Exocrine insufficiency | Faecal elastase <200; steatorrhoea; PERT (Creon) |
| Type 3c diabetes | Pancreatogenic; glucagon deficiency; hypoglycaemia risk |
| Surgery options | Frey, Puestow, Whipple; for refractory pain |
Sample Viva Questions
Q1: A patient with chronic alcoholic pancreatitis complains of greasy, foul-smelling stools. What is the diagnosis and management?
Model Answer: This is steatorrhoea due to exocrine pancreatic insufficiency. It occurs when >90% of pancreatic function is lost. I would confirm with faecal elastase-1 (<200 μg/g indicates insufficiency). Management: Pancreatic enzyme replacement therapy (PERT) — Creon 40,000-50,000 units lipase with each main meal. Add a PPI if response is suboptimal to protect enzymes from acid. Supplement fat-soluble vitamins (A, D, E, K). Reinforce alcohol cessation. Dietitian referral for nutritional optimisation.
Q2: What are the surgical options for chronic pancreatitis and their indications?
Model Answer: Surgery is indicated for refractory pain despite maximal medical and endoscopic treatment, complications (pseudocyst, bile duct obstruction), or suspicion of malignancy.
Options:
- Puestow (lateral pancreaticojejunostomy): For dilated pancreatic duct (>7mm); decompresses duct
- Frey procedure: Partial head resection + drainage; for inflammatory head mass and dilated duct
- Beger procedure: Duodenum-preserving head resection
- Whipple (pancreaticoduodenectomy): For inflammatory head mass or suspected malignancy
- Distal pancreatectomy: For distal (tail) disease
- Total pancreatectomy + islet autotransplant (TPIAT): For refractory pain when preserving islets is possible
Common Exam Errors
| Error | Correct Approach |
|---|---|
| Relying on amylase for diagnosis | Amylase is often normal in chronic pancreatitis (burned-out gland) |
| Missing faecal elastase | Key test for exocrine insufficiency |
| Treating Type 3c diabetes like Type 2 | Type 3c has glucagon deficiency; high hypo risk; avoid sulfonylureas |
| Forgetting alcohol/smoking cessation | Essential; slows progression |
Last Reviewed: 2025-12-24 | MedVellum Editorial Team
Medical Disclaimer: MedVellum content is for educational purposes and clinical reference. Clinical decisions should account for individual patient circumstances. Always consult appropriate specialists.