MBBS SAQ · Gastroenterology
Chronic pancreatitis — diagnosis, investigation and management
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A 48-year-old man with a 20-year history of heavy alcohol use presents with 12 months of recurrent, severe epigastric pain that radiates through to his back and is worsened by food. He has lost 8 kg, has noticed his stools are bulky, pale and oily and difficult to flush, and was recently diagnosed with diabetes. Examination reveals a cachectic man with a BMI of 18.5, epigastric tenderness, and a brown reticular discolouration on his anterior abdominal wall. Outline your diagnostic approach, the investigations you would order and interpret, and your stepwise management.
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a) Clinical diagnosis and principle (2 marks)
The combination of recurrent epigastric pain radiating to the back, steatorrhoea, new-onset diabetes and weight loss in a heavy drinker is the classic triad of chronic pancreatitis (CP) — a progressive, fibrotic, inflammatory disease producing irreversible loss of exocrine and endocrine function.[1][2]
The reticular brown abdominal discolouration is erythema ab igni — chronic heat-pad use, a bedside sign of chronic pancreatic pain. The diagnostic principle is that no single test is gold-standard: diagnosis rests on a combination of structural imaging (calcification, ductal change, atrophy) and functional testing (exocrine insufficiency). Pancreatic cancer must always be actively excluded, because CP and cancer coexist and CP is itself a cancer risk factor.[1]
b) Investigations (3 marks)
Structural imaging:
- Abdominal X-ray — pancreatic calcification is pathognomonic when present (found in 30 to 50 percent).
- Contrast CT pancreas (the most useful single test) — parenchymal calcification, dilated main pancreatic duct, gland atrophy, pseudocysts, inflammatory head mass; excludes cancer; graded by the Cambridge classification (mild / moderate / marked).
- MRCP / secretin-MRCP or endoscopic ultrasound (EUS) with the Rosemont criteria if early / equivocal.
- The 'chain of lakes' / 'string of pearls' ductal appearance (alternating strictures and dilatation) is classic on ERCP (now used mainly therapeutically).
Functional tests:
- Faecal elastase-1 — under 200 microg/g = exocrine insufficiency (moderate); under 100 = severe; not affected by PERT.
- Fasting glucose / HbA1c — type 3c diabetes (low C-peptide).
Adjuncts:
- LFTs, coagulation, CA 19-9, and EUS-FNA of any mass — to exclude pancreatic cancer.
- Fat-soluble vitamins (A, D, E, K), B12, folate, calcium, magnesium, zinc — deficiency from malabsorption.
- IgG4 — if autoimmune pancreatitis suspected (painless jaundice, 'sausage' pancreas).
- DEXA scan — osteoporosis / osteomalacia; genetic testing (PRSS1, SPINK1, CFTR) if young / familial / idiopathic.
c) Management — definitive and stepwise (3 marks)
- Correctable causes and conservative measures — complete alcohol abstinence (slows progression, improves survival) and smoking cessation (independent benefit); small, frequent, low-fat, high-protein diet with medium-chain triglycerides (MCTs); nutritional supplements and fat-soluble vitamins; thiamine 100 mg daily (alcoholic).
- Pancreatic enzyme replacement therapy (PERT) — pancreatin (Creon) 25,000 to 40,000 units of lipase with each main meal, 10,000 to 25,000 with snacks, with a PPI (omeprazole 20 to 40 mg daily); taken WITH food, throughout the meal. Treats both steatorrhoea and (via CCK negative feedback) pain.
- Stepwise analgesia (WHO ladder) — paracetamol 1 g 6-hourly; then NSAID (ibuprofen 400 mg 8-hourly, with caution); then tramadol 50 to 100 mg 4 to 6-hourly; then a strong opioid (morphine or fentanyl patch) — pethidine is NOT preferred. Add a neuromodulator (pregabalin, amitriptyline) for the neuropathic component; refer to a chronic-pain service to limit opioid harm.
- Type 3c diabetes — insulin (often low doses); avoid sulfonylureas (hypoglycaemia).
- Endoscopic therapy if refractory pain from large calcified ductal stones (over 5 mm) — ESWL; stricture stenting and sphincterotomy.
- Surgery for dilated-duct (over 7 mm) disease failing endoscopy — lateral pancreaticojejunostomy (Puestow); resection (Beger, Frey, Whipple) for an inflammatory head mass; total pancreatectomy with islet autotransplantation (TPIAT) for intractable small-duct disease.
d) Complications and prognosis (2 marks)
- Complications: pancreatic pseudocyst (drain if symptomatic / infected / over 6 cm), bile-duct stricture (jaundice, cholangitis), duodenal obstruction, splenic vein thrombosis with isolated gastric fundal varices (left-sided portal hypertension; splenectomy is curative), visceral pseudoaneurysm (catastrophic bleed — angiography and embolisation), fat-soluble vitamin deficiency / osteoporosis, opioid dependence, and pancreatic cancer (cumulative risk about 4 percent at 20 years).[3]
- Prognosis — CP is progressive and shortens life expectancy by about 10 to 20 years; the main drivers of mortality are diabetes, malnutrition, addiction, pancreatic cancer and cardiovascular disease. Annual follow-up reviews pain, glucose, nutrition, micronutrients, bone density and adherence.[1]
References3ShowHide
- [1]Majumder S, Chari ST. Chronic pancreatitis. Lancet, 2016.PMID 26948434
- [2]Kleeff J, Whitcomb DC, Shimosegawa T, et al. Chronic pancreatitis. Nature Reviews Disease Primers, 2017.PMID 28880010
- [3]Yadav D, Lowenfels AB. The epidemiology of pancreatitis and pancreatic cancer. Gastroenterology, 2013.PMID 23622135