Chronic Pancreatitis — Viva Defence

Long case viva — alcohol-related chronic pancreatitis

Candidate's opening statement (SASPOP)

"Doctor, my patient is a 49-year-old man with a 20-year history of heavy alcohol use and established chronic pancreatitis in the burnt-out phase. His problems are: chronic recurrent epigastric pain radiating to the back; severe exocrine insufficiency with steatorrhoea and a faecal elastase of 65 micrograms per gram; type 3c (pancreatogenic) brittle diabetes complicated by a recent severe hypoglycaemic episode; malnutrition with a 10-kilogram weight loss; and alcohol use disorder. The disease is irreversible but manageable, and the priority is structured replacement of exocrine and endocrine function, a stepped pain strategy that avoids opioid harm, and active 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 with a recent hypoglycaemic episode.
4. Chronic pain requiring a stepped analgesic strategy.
5. Alcohol use disorder.
6. Malnutrition with probable fat-soluble vitamin deficiency and osteoporosis risk.
7. Pancreatic cancer surveillance need and complication risk (pseudocyst, biliary obstruction, splenic vein thrombosis). [1]

Integrated management plan

Eliminate precipitants. Complete alcohol abstinence and smoking cessation (smoking accelerates fibrosis and magnifies pancreatic cancer risk). Addiction-medicine input, thiamine for Wernicke prevention, and supervised detoxification planning. [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 to enhance efficacy, titrated to symptoms. The de la Iglesia-García meta-analysis confirms PERT improves fat absorption, nutrition, and quality of life [7]. Fat-soluble vitamin supplementation (A, D, E, K), a DEXA scan, dietetic input, and medium-chain triglycerides.

Endocrine insufficiency. 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. Type 3c diabetes is brittle because of the loss of glucagon counter-regulation, and severe hypoglycaemia is a leading cause of death [4]. PERT improves glycaemic control by restoring nutrient absorption.

Pain. Stepped approach — abstinence and smoking cessation, paracetamol and NSAIDs, neuropathic adjuncts (pregabalin, a tricyclic), then weak and strong opioids with an addiction-medicine plan. For refractory pain with his dilated duct and dominant stricture, endoscopic ERCP (stent, stone removal, ESWL) and surgery (Puestow or Frey). The Cahen trial showed surgery provides superior durable pain relief to endoscopy in obstructive dilated-duct disease [8]; the decision is multidisciplinary.

Complications and surveillance. Assess for pseudocyst, biliary obstruction, and splenic vein thrombosis. Investigate any change in symptoms to exclude pancreatic cancer [5]. Smoking cessation is essential.

Examiner probing questions

Examiner: "Why is type 3c diabetes more dangerous than type 2 in this patient?" Because chronic pancreatitis destroys both beta cells and alpha cells. The loss of glucagon means there is no endogenous counter-regulatory recovery from insulin-induced hypoglycaemia, so the diabetes is brittle with wide excursions and severe hypoglycaemia is a leading cause of death. Insulin is still the mainstay, but the target is relaxed and hypoglycaemia avoidance is prioritised [4].

Examiner: "How do you titrate the pancreatic enzymes, and what do you do if they don't work?" First confirm adherence and timing — the enzymes must be taken during or immediately after food, and at an adequate dose (25,000 to 40,000 units of lipase with meals). If response is poor, increase the dose and add a proton pump inhibitor to reduce acid degradation. The meta-analysis supports titration and enteric-coated formulations with acid suppression [7]. Only after dose escalation and PPI addition should a poor response prompt re-evaluation of adherence or an alternative cause of diarrhoea.

Examiner: "When would you offer surgery over endoscopy for his pain?" For a fit patient with a dilated main duct and obstructive disease in whom endoscopic therapy is failing or unlikely to succeed. The Cahen trial showed surgery (pancreaticojejunostomy) provided superior durable pain relief to endoscopic drainage (75 versus 32 per cent partial or complete relief at two years; 80 versus 38 per cent at five years), with similar complication rates but fewer repeat procedures [8]. Endoscopy is a reasonable first step for a single dominant stricture or in those unfit for surgery; the decision is multidisciplinary.

Branching scenario — autoimmune pancreatitis

Examiner: "Now consider a 66-year-old man who presents with three weeks of painless progressive jaundice. CT shows a diffusely enlarged sausage-shaped pancreas with a capsule-like rim and irregular narrowing of the main pancreatic duct. His serum IgG4 is 4.2 g per litre, and he has a retroperitoneal soft-tissue mass. What is the diagnosis and management?" [1]

This is type 1 autoimmune pancreatitis, the pancreatic manifestation of IgG4-related disease. Diagnosis uses the International Consensus Diagnostic Criteria (ICDC), integrating imaging, serology, other organ involvement (the retroperitoneal fibrosis), histology, and an optional steroid response [6]. The treatment is prednisolone 0.6 to 1 mg per kg per day for two to four weeks with a taper; the dramatic response is itself diagnostic. Relapse is common (40 to 50 per cent) and requires maintenance immunosuppression (azathioprine, mycophenolate, or rituximab). The cardinal error is operating for presumed pancreatic cancer without considering the diagnosis.

Branching scenario — tropical calcific pancreatitis

Examiner: "And what if the patient were a 22-year-old thin man from Kerala who drinks no alcohol, with severe insulin-requiring diabetes, large dense intraductal calculi, and a markedly dilated main duct?" [1]

This is tropical calcific pancreatitis (fibrocalculous pancreatic diabetes). The cassava (cyanogenic glycoside) hypothesis, chronic protein-calorie malnutrition, and a high prevalence of SPINK1 mutations are implicated. It causes early, severe insulin-requiring type 3c diabetes and malnutrition, and the large dense intraductal calculi are characteristic. Management is insulin for the diabetes, pancreatic enzyme replacement for exocrine insufficiency, and pain management as for other forms [2].

Branching scenario — splenic vein thrombosis

Examiner: "If this patient presented with haematemesis and was found to have isolated gastric fundal varices with a normal liver, how would you explain and manage it?" [1]

Chronic peripancreatic inflammation can thrombose the splenic vein, producing left-sided (sinistral) portal hypertension. The splenic vein drains via the short gastric and left gastric veins, so thrombosis causes isolated gastric (especially fundal) varices while the liver, portal vein, and liver synthetic function remain normal. When variceal bleeding occurs, splenectomy is curative because it removes the distal venous bed driving the variceal hypertension [3].

Short-case discussion — abdominal examination

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

My routine: general inspection for cachexia, jaundice, and the stigmata of chronic alcohol use (spider naevi, palmar erythema, parotid enlargement); hands for clubbing and Dupuytren contracture; face for scleral icterus and conjunctival pallor; neck for lymphadenopathy; abdomen — inspect for scars and distension, palpate for epigastric tenderness, a palpable mass (a pseudocyst or inflammatory head), hepatosplenomegaly, and shifting dullness, and auscultate bowel sounds. [1]

Presentation: "On general inspection the patient is cachectic with stigmata of chronic alcohol use. The abdomen is soft with epigastric tenderness and a palpable mass in the epigastrium consistent with a pseudocyst or inflammatory head. There is no hepatosplenomegaly or ascites. These findings are consistent with chronic pancreatitis. I would review the imaging, assess exocrine and endocrine function, and exclude pancreatic cancer given the mass." [1]

Examiner: "What would you look for to suggest exocrine insufficiency?" Cachexia, easy bruising (vitamin K deficiency), and signs of fat-soluble vitamin deficiency, confirmed with faecal elastase. [1]

Examiner: "How would you exclude cancer in this patient with a mass?" Ca 19-9, contrast CT, and EUS-fine-needle aspiration; PET-CT where the picture remains indeterminate. Any change in symptoms mandates this workup [5].