Chronic Pancreatitis — DCE Clinical Case

Long case

Patient scenario

Mr DK is a 49-year-old man referred to the gastroenterology outpatient clinic for management of established chronic pancreatitis. He has a 20-year history of heavy alcohol use (80 to 100 grams per day) and smokes 20 cigarettes per day. He first presented five years ago with recurrent acute pancreatitis, and over the last two years has developed chronic persistent epigastric pain radiating to the back, progressive weight loss of 10 kilograms (BMI now 18), and foul bulky greasy stools that are difficult to flush. He describes recent thirst, polyuria, and one episode of symptomatic hypoglycaemia with sweating and confusion that resolved with food. He takes oral morphine 20 mg twice daily for pain (started by his general practitioner), with poor control and escalating use. He has no other past medical history. He works as a labourer and is increasingly unable to work because of pain and fatigue. [1]

Recent investigations: faecal elastase 65 micrograms per gram, HbA1c 58 mmol per mol, normal full blood count and liver function apart from a slightly low albumin of 32 g per litre, Ca 19-9 within normal range. CT abdomen shows a dilated irregular main pancreatic duct (8 mm) with multiple intraductal calcifications, parenchymal atrophy, and a 4 cm low-density inflammatory mass in the pancreatic head without definite malignant features. There is no biliary dilatation. A DEXA scan shows osteopenia. Vitamin D is low at 38 nmol per litre. [1]

Examination findings

The patient is thin and cachectic, alert and oriented, in no acute distress. He is afebrile, heart rate 78, blood pressure 118 over 72, respiratory rate 16, oxygen saturation 98 per cent on room air. He has several spider naevi on the chest and mild palmar erythema. The abdomen is soft with mild epigastric tenderness and a palpable, poorly defined fullness in the epigastrium. There is no guarding, rigidity, hepatosplenomegaly, shifting dullness, or detectable ascites. Bowel sounds are normal. There is no peripheral oedema. Neurological examination is normal. There are no stigmata of chronic liver decompensation (no jaundice, ascites, or encephalopathy). [1]

Candidate's opening statement (SASPOP)

"Doctor, my patient is Mr DK, a 49-year-old labourer with established alcohol-related chronic pancreatitis now in the burnt-out phase. His problems are: chronic recurrent epigastric pain poorly controlled on escalating oral morphine; severe exocrine insufficiency with steatorrhoea (faecal elastase 65) and malnutrition; type 3c brittle diabetes (HbA1c 58) with a recent hypoglycaemic episode; an inflammatory pancreatic head mass requiring active exclusion of pancreatic cancer; alcohol use disorder and tobacco smoking; and osteopenia with vitamin D deficiency. The disease is irreversible but manageable, and my priorities are structured replacement of exocrine and endocrine function, a stepped pain strategy that reduces opioid harm, and definitive exclusion of pancreatic cancer." [1]

Problem list

1. Alcohol-related chronic pancreatitis, burnt-out phase (TIGAR-O toxic-metabolic).
2. Severe exocrine insufficiency (faecal elastase 65) with steatorrhoea and malnutrition.
3. Type 3c brittle diabetes (HbA1c 58) with a recent hypoglycaemic episode.
4. Chronic pain, poorly controlled on escalating oral morphine.
5. Inflammatory pancreatic head mass — pancreatic cancer not yet excluded.
6. Alcohol use disorder and tobacco smoking.
7. Malnutrition, osteopenia, and vitamin D deficiency. [1]

Integrated management plan

Eliminate precipitants. Complete alcohol abstinence and smoking cessation. Addiction-medicine consultation, supervised detoxification planning, thiamine for Wernicke prevention, and counselling that continued drinking accelerates progression and magnifies pancreatic cancer risk. [1]

Exocrine insufficiency. Enteric-coated pancreatin 25,000 to 40,000 units of lipase with meals and half with snacks, taken during or immediately after food, with a proton pump inhibitor (omeprazole 20 mg) to enhance efficacy, titrated to symptoms [7]. Fat-soluble vitamin supplementation (including vitamin D replacement), dietetic input, and medium-chain triglycerides. The de la Iglesia-García meta-analysis confirms that PERT improves fat absorption, nutrition, and quality of life [7].

Type 3c diabetes. Insulin as the mainstay (basal-bolus, cautiously titrated), avoiding metformin in this malnourished patient and sulphonylureas (hypoglycaemia risk), with a relaxed glycaemic target that prioritises avoidance of hypoglycaemia over tight control. Structured education on hypoglycaemia recognition and management. The diabetes is brittle because of the loss of glucagon counter-regulation, and severe hypoglycaemia is a leading cause of death [4].

Pain. A multidisciplinary stepped approach — abstinence, paracetamol and NSAIDs with gastroprotection, neuropathic adjuncts (pregabalin, a tricyclic), then cautious opioid use with an addiction-medicine plan to address the escalating morphine. For his dilated duct with a dominant stricture and stones, endoscopic ERCP (stricture stenting, stone removal, ESWL for large calculi), and surgery (Puestow longitudinal pancreaticojejunostomy, or Frey if the head is diseased). The Cahen trial showed surgery provides superior durable pain relief to endoscopy in obstructive dilated-duct disease [8]; the decision is multidisciplinary.

Exclude pancreatic cancer. The inflammatory head mass requires active exclusion of pancreatic adenocarcinoma: EUS-fine-needle aspiration of the mass, with PET-CT if the picture remains indeterminate [5]. The normal Ca 19-9 is reassuring but does not exclude cancer. Any change in symptoms mandates repeat imaging.

Surveillance and complications. Assess for pseudocyst, biliary obstruction, and splenic vein thrombosis. Osteoporosis management (vitamin D, calcium, a bisphosphonate if osteoporotic). [1]

Discussion questions

Examiner: "How does type 3c diabetes differ from type 2, and why did he have a hypoglycaemic episode?" Type 3c diabetes results from destruction of both beta cells and alpha cells. The loss of glucagon means there is no endogenous recovery from insulin-induced or fasting hypoglycaemia, so the diabetes is brittle and hypoglycaemia is dangerous and potentially fatal. His hypoglycaemic episode likely reflected the combination of malabsorption (reduced and unpredictable glucose delivery), exocrine insufficiency, and the absence of glucagon counter-regulation. Insulin is the mainstay, with a relaxed target and hypoglycaemia-focused education [4].

Examiner: "Why is he on escalating morphine, and what is your plan?" His pain is poorly controlled because the underlying mechanical obstruction (a dominant stricture with upstream dilatation and stones) has not been addressed, and the escalating opioid use reflects tolerance and emerging dependence rather than analgesic efficacy. My plan is to address the mechanical problem definitively (ERCP with stent and stone removal, ESWL, or surgery), introduce neuropathic adjuncts, and engage addiction medicine to manage the opioid component. The Cahen trial supports earlier definitive surgical drainage in fit patients with obstructive dilated-duct disease [8].

Examiner: "How will you exclude pancreatic cancer in the head mass?" With EUS-fine-needle aspiration for tissue, a Ca 19-9 trend, and PET-CT if the picture remains indeterminate. A mass in chronic pancreatitis that changes, a rising Ca 19-9, or new weight loss or jaundice all heighten suspicion. The Kirkegård meta-analysis confirms that pancreatic cancer risk is real and highest in the first two years after diagnosis, partly reflecting surveillance bias and undiagnosed cancer [5].

Examiner: "Could this be autoimmune pancreatitis rather than alcoholic?" Autoimmune pancreatitis (type 1, IgG4-related) is the one reversible form and must not be missed. The clues would be painless obstructive jaundice, a diffuse sausage-shaped gland with a capsule-like rim, elevated serum IgG4, and other organ involvement, with a dramatic steroid response on the ICDC criteria [6]. This patient's intraductal calcifications and long alcohol history point to alcoholic disease, but I would check serum IgG4 to exclude coexistent or alternative autoimmune pancreatitis.

Short case — focused abdominal examination

Instruction

"Examine this patient's abdomen. He has chronic pancreatitis." [1]

Systematic examination routine

1. End of bed inspection. Assess for cachexia, jaundice, and the stigmata of chronic alcohol use (spider naevi, palmar erythema, parotid enlargement, gynaecomastia, muscle wasting). Note any lines, drains, or surgical scars.
2. Hands and face. Clubbing, Dupuytren contracture, conjunctival pallor, scleral icterus.
3. Neck. Virchow's node, jugular venous pressure.
4. Abdomen. Inspect for distension and scars; superficial then deep palpation for epigastric tenderness, a palpable mass (a pseudocyst or inflammatory head), hepatosplenomegaly, and shifting dullness for ascites; palpate for a palpable gallbladder (Courvoisier). Auscultate bowel sounds and bruits.
5. Back and legs. Examine for pitting oedema and spinal tenderness (osteomalacia). [1]

Key signs this patient demonstrates

• Cachexia and stigmata of chronic alcohol use.
• Mild epigastric tenderness with a palpable, poorly defined epigastric fullness (the inflammatory head mass or pseudocyst).
• No hepatosplenomegaly or ascites (excluding decompensated cirrhosis as the cause of his findings). [1]

Presentation template

"Doctor, I examined Mr DK's abdominal system. He is cachectic with stigmata of chronic alcohol use. The abdomen is soft with mild epigastric tenderness and a palpable, poorly defined fullness in the epigastrium consistent with an inflammatory mass or pseudocyst. There is no guarding, rigidity, hepatosplenomegaly, or ascites. These findings are consistent with chronic pancreatitis with a probable inflammatory head mass. I would review the imaging, assess exocrine and endocrine function, and actively exclude pancreatic cancer given the mass." [1]

Discussion — aetiology, pain strategy, and cancer surveillance

Examiner: "How would you classify the aetiology?" Using the TIGAR-O mechanistic classification — toxic-metabolic (alcohol, smoking), idiopathic, genetic (PRSS1, SPINK1, CFTR, CTRC), autoimmune, recurrent and severe acute pancreatitis, and obstructive. This patient is toxic-metabolic (alcohol with smoking as the cofactor) [2].

Examiner: "Outline the analgesic ladder." Abstinence and smoking cessation; non-opioids (paracetamol, NSAIDs with gastroprotection); neuropathic adjuncts (pregabalin, a tricyclic); then weak and strong opioids with an addiction-medicine plan; coeliac plexus block and thoracoscopic splanchnicectomy for refractory pain; and definitive endoscopic or surgical drainage for obstructive disease [3] [8].

Examiner: "Who warrants pancreatic cancer surveillance?" Surveillance is selective, not universal. It is recommended for high-risk groups — hereditary pancreatitis (PRSS1), genetic syndromes, and selected familial clusters — because the absolute risk in ordinary alcoholic chronic pancreatitis is too low to justify universal imaging. Any change in symptoms (new weight loss, a change in pain pattern, jaundice) mandates investigation to exclude cancer [5]. Smoking cessation is essential.