Chronic Pancreatitis Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: This is an important, though not ubiquitous, cause of chronic abdominal pain and malabsorption presenting to our gastroenterology clinics and general medical wards. While often linked to alcohol, a significant portion in our population is idiopathic. It causes immense morbidity and requires long-term multidisciplinary management.
High-Yield Definition: Chronic pancreatitis is a progressive pathological fibro-inflammatory syndrome of the pancreas in individuals with genetic, environmental, and/or other risk factors who develop persistent pathological responses to parenchymal injury or stress. Key features are pancreatic atrophy, fibrosis, pain syndromes, ductal strictures, calcifications, and exocrine and endocrine insufficiency. (Source: United European Gastroenterology Journal, 2018; UpToDate, 2024).
Clinical One-Liner: Essentially, the pancreas is slowly destroying and scarring itself, causing severe, persistent pain and eventually stopping it from producing digestive enzymes and insulin.
II. Etiology & Risk Factors
The most widely used classification system is TIGAR-O.
Etiology (TIGAR-O Classification):
Toxic-metabolic: Alcohol (most common), Smoking (independent risk factor and disease accelerator), hypercalcaemia, chronic kidney disease.
Idiopathic: The second most common cause after alcohol.
Genetic: Mutations in genes like PRSS1, SPINK1, CFTR.
Autoimmune: IgG4-related disease.
Recurrent and Severe Acute Pancreatitis: Post-necrotic changes leading to chronic fibrosis.
Obstructive: Pancreas divisum, obstructive tumours, sphincter of Oddi dysfunction, post-traumatic ductal strictures.
Key Risk Factors in the Malaysian Context:
Modifiable: Chronic heavy alcohol consumption, cigarette smoking.
Non-modifiable: History of recurrent acute pancreatitis, genetic predisposition, anatomical variants like pancreas divisum.
III. Quick Pathophysiology
It's a vicious cycle of injury and scarring. An initial insult (e.g., alcohol toxicity) causes acinar cell injury and inflammation. Instead of resolving completely, this process activates pancreatic stellate cells, which are the key drivers of fibrosis. They deposit collagen and extracellular matrix, leading to scarring. This fibrosis distorts and obstructs the small pancreatic ducts, causing increased intraductal pressure, further inflammation, and ischemia. This progressive process destroys both the exocrine (acinar cells -> maldigestion) and endocrine (islet cells -> diabetes) parenchyma.
IV. Clinical Assessment
Red Flags & Immediate Actions:
Fever, persistent tachycardia, hypotension: Suspect infected pseudocyst or cholangitis → Alert senior, secure IV access, start broad-spectrum IV antibiotics (e.g., Tazocin), and arrange for urgent imaging (CT abdomen).
New-onset or worsening jaundice: Suspect common bile duct (CBD) obstruction from a stricture or pancreatic head mass → Alert senior, send off LFTs/GGT, arrange urgent ultrasound or MRCP.
Intractable pain unresponsive to oral analgesia: Requires admission for parenteral analgesia and investigation of the underlying cause (e.g., pseudocyst).
Signs of GI bleeding (melena, hematemesis): Suspect pseudoaneurysm or bleeding from gastric varices (due to splenic vein thrombosis) → ABCDE approach, alert senior and gastroenterology team immediately.
History:
Common (>50%):
Abdominal Pain: Typically epigastric, often severe, persistent, and boring through to the back. Worsened by eating, especially fatty foods.
Steatorrhea: Pale, bulky, foul-smelling, greasy stools that are difficult to flush. This is a hallmark of exocrine insufficiency.
Weight Loss: Due to malabsorption and fear of eating (sitophobia).
Less Common (10-50%):
Nausea and vomiting.
Symptoms of diabetes mellitus (Type 3c): polyuria, polydipsia.
Physical Examination:
Often unremarkable in between acute flares.
Epigastric tenderness may be present.
Signs of malnutrition: muscle wasting, reduced subcutaneous fat.
Signs of fat-soluble vitamin (A, D, E, K) deficiency in advanced disease.
A palpable epigastric mass may indicate a pseudocyst.
Clinical Pearl: Don't just ask about diarrhoea. Ask specifically about the character of the stool. Many patients won't volunteer that they have greasy, floating stools unless prompted. This is your single biggest clue for exocrine insufficiency.
V. Diagnostic Workflow
Differential Diagnosis:
Pancreatic Cancer:
Points For: Epigastric pain, weight loss, jaundice.
Points Against: Chronic pancreatitis usually has a longer history of recurrent pain attacks over years. "Painless jaundice" is a classic red flag for cancer.
How to Differentiate: High-quality contrast-enhanced CT (pancreatic protocol) or EUS with biopsy is essential. CA 19-9 can be elevated in both but is more suggestive of malignancy.
Peptic Ulcer Disease (PUD):
Points For: Epigastric pain related to meals.
Points Against: PUD pain is classically relieved by food, whereas pancreatitis pain is exacerbated.
How to Differentiate: Oesophagogastroduodenoscopy (OGDS).
Biliary Colic/Choledocholithiasis:
Points For: Post-prandial RUQ/epigastric pain.
Points Against: Pain is typically more colicky and resolves within hours, unlike the persistent pain of pancreatitis.
How to Differentiate: Liver function tests (obstructive pattern) and ultrasound of the hepatobiliary system.
Investigations Plan:
Bedside / Initial:
Blood glucose (to check for diabetes).
In an acute flare: Serum amylase/lipase (note: may be normal in "burnt-out" chronic pancreatitis).
First-Line Labs & Imaging:
Labs: FBC, LFT, Renal profile, HbA1c.
Faecal Elastase-1: The best non-invasive test for pancreatic exocrine insufficiency. A level <200 µg/g indicates insufficiency.
Ultrasound Abdomen: Useful to rule out gallstones but has poor sensitivity for chronic pancreatitis.
Confirmatory / Gold Standard Imaging:
CT Abdomen (Pancreatic Protocol): The workhorse imaging modality. Look for the classic triad: pancreatic calcifications, ductal dilatation, and parenchymal atrophy.
Magnetic Resonance Cholangiopancreatography (MRCP): Excellent for visualizing the pancreatic and biliary ducts without radiation.
Endoscopic Ultrasound (EUS): The most sensitive imaging test for detecting early changes of chronic pancreatitis (e.g., parenchymal and ductal irregularities).
VI. Staging & Severity Assessment
Severity is determined clinically based on the presence of pain, malabsorption, diabetes, and morphological changes. The M-ANNHEIM classification is a comprehensive system based on risk factors and clinical stage, but for practical purposes, we stage based on functional impairment.
Mild: Intermittent pain, no exocrine or endocrine insufficiency.
Moderate: More frequent pain, evidence of exocrine insufficiency (requiring PERT).
Severe: Intractable pain, established exocrine and endocrine insufficiency, significant morphological changes (e.g., large pseudocysts, severe ductal dilatation).
Impact on Management: The stage dictates the intensity of management. Severe disease requires a multidisciplinary approach with pain specialists, endocrinologists, and potentially surgeons.
VII. Management Plan
This is based on three pillars: pain control, and management of exocrine and endocrine insufficiency.
Immediate Stabilisation (During an Acute Flare):
A/B/C: Standard resuscitation. Keep NBM, provide IV fluids.
Analgesia: Start with IV Paracetamol 1g QDS. Escalate to IV Tramadol 50-100mg TDS or IV Morphine 2.5-5mg titrated to effect.
Nutrition: Enteral nutrition via nasojejunal tube should be considered if the patient cannot tolerate oral intake for >72 hours. Avoid TPN unless absolutely necessary.
Definitive Treatment (The Ward Round Plan):
1. Pain Control & Lifestyle:
Absolute cessation of alcohol and smoking. This is non-negotiable and is the most important intervention to slow disease progression.
Analgesia Ladder:
Step 1: Paracetamol ± NSAIDs (use with caution due to GI risk).
Step 2: Weak opioids (e.g., Tramadol SR 100-200mg BD).
Step 3: Strong opioids (involve the pain service). Consider agents for neuropathic pain like Pregabalin or Amitriptyline.
2. Exocrine Insufficiency (Malabsorption):
Pancreatic Enzyme Replacement Therapy (PERT): This is crucial to prevent malnutrition.
Drug: Pancrelipase (Brand: Creon).
Dose: Start with 25,000 - 50,000 units of lipase taken with each main meal and 10,000 - 25,000 units with snacks. Titrate dose based on resolution of steatorrhea.
Supplementation: Monitor and replace fat-soluble vitamins (A, D, E, K) and check DEXA scan for osteoporosis.
3. Endocrine Insufficiency (Type 3c Diabetes):
This form of diabetes is brittle, with a high risk of hypoglycemia due to loss of glucagon-producing alpha cells.
First-line: Metformin can be used if insulin resistance is a factor.
Insulin: Most patients will eventually require insulin. Start with a simple regimen and titrate carefully. Involve the endocrinology team early.
Endoscopic / Surgical Management:
ERCP: For dominant pancreatic duct strictures (stenting) or stone removal.
EUS: For drainage of pseudocysts or celiac plexus neurolysis for pain.
Surgery: Considered for intractable pain with a dilated main pancreatic duct (e.g., lateral pancreaticojejunostomy - Puestow procedure).
VIII. Complications
Short-Term:
Pancreatic pseudocyst: Management: Watchful waiting if asymptomatic; endoscopic or surgical drainage if symptomatic or infected.
Biliary obstruction: Management: ERCP with stenting.
Long-Term:
Pancreatic cancer: Significantly increased risk. Surveillance may be considered in some high-risk groups.
Splenic vein thrombosis: Can lead to gastric varices.
Osteoporosis/Osteopenia: Due to Vitamin D malabsorption.
IX. Prognosis
Morbidity is high due to chronic pain, malnutrition, and diabetes, significantly impacting quality of life.
Mortality is increased compared to the general population.
Key Negative Prognostic Factors: Continued alcohol consumption and smoking, development of diabetes, and the need for long-term opioid analgesia.
X. How to Present to Your Senior
"Dr., for review please. This is Mr. Chen in Clinic Room 2, a 50-year-old man with a history of heavy alcohol intake, presenting with a 2-year history of chronic epigastric pain boring to the back and a 10kg weight loss. He confirms his stools are pale and oily. My primary differential is chronic pancreatitis with exocrine insufficiency. I plan to send a faecal elastase test and request a CT abdomen to look for pancreatic calcifications and ductal changes. I would like to ask if we should start him on empirical PERT like Creon while awaiting investigation results."
XI. Summary & Further Reading
Top 3 Takeaways:
Suspect chronic pancreatitis in any patient with chronic epigastric pain, especially with risk factors like alcohol use. The clinical triad is abdominal pain, steatorrhea, and diabetes.
Diagnosis relies on imaging (CT/MRCP) to show calcifications/ductal changes and functional testing (faecal elastase) for exocrine failure.
Management is a triad: (1) Absolute alcohol/smoking cessation, (2) Stepwise pain management, and (3) Replacing lost function with PERT (Creon) for malabsorption and insulin for diabetes.
Key Resources:
UpToDate: "Clinical manifestations and diagnosis of chronic pancreatitis in adults"
Amboss: "Chronic pancreatitis"
Review Article: [Link to a high-quality review from NEJM or Lancet, e.g., https://www.google.com/search?q=https://www.nejm.org/doi/full/10.1056/NEJMra1204620 - This is an older landmark review but principles remain valid]
