Acute Pancreatitis — Viva Defence

Long case viva — severe necrotising alcohol-related pancreatitis

Candidate's opening statement (SASPOP)

"Doctor, my patient is a 58-year-old man who presented with severe acute pancreatitis, now on day 14 of his admission, complicated by persistent organ failure (acute kidney injury and respiratory compromise requiring high-flow nasal cannula), infected walled-off necrosis managed with endoscopic step-up drainage, and new-onset diabetes. He drinks approximately 80 grams of alcohol daily. His problems are: severe acute pancreatitis (Revised Atlanta severe) with infected walled-off necrosis; resolving multi-organ failure; malnutrition requiring nasojejunal feeding; alcohol use disorder; new-onset diabetes of the pancreas; and the need for rehabilitation and future alcohol and pancreatic surveillance." [1]

Problem list

1. Severe necrotising pancreatitis with infected walled-off necrosis (managed with endoscopic drainage and meropenem).
2. Resolving multi-organ failure (acute kidney injury recovering, respiratory compromise improving on high-flow nasal cannula).
3. Malnutrition and ongoing catabolism (nasojejunal feeding at target rate).
4. Alcohol use disorder (withdrawal risk, need for cessation counselling and thiamine).
5. New-onset diabetes of the pancreas (pancreoprivic, likely brittle).
6. Deconditioning and the need for rehabilitation. [1]

Integrated management plan

Source control. Continue endoscopic drainage of the walled-off necrosis via the established cystgastrostomy; repeat endoscopic necrosectomy if the collection re-accumulates or if clinical parameters deteriorate. Continue meropenem 1 g IV every 8 hours for the infected necrosis, with a plan to de-escalate and stop once source control is achieved and inflammatory markers settle. [1]

Fluid and organ support. Ringer lactate, moderately aggressive and goal-directed, with reassessment of the blood urea, creatinine, and urine output every 6 hours. The WATERFALL trial established that aggressive bolus resuscitation causes fluid overload without benefit; I will avoid boluses unless he is hypotensive. Renal replacement therapy is on standby if the acute kidney injury worsens. High-flow nasal cannula for respiratory support, weaning as tolerated. [1]

Nutrition. Nasojejunal enteral feeding at target rate to achieve positive nitrogen balance. Multiple trials show early enteral feeding reduces infectious complications and mortality compared with NPO and parenteral nutrition. Plan to transition to an oral diet as ileus resolves. Pancreatic enzyme replacement (pancreatin 25,000 to 40,000 units with meals) for steatorrhoea from exocrine insufficiency. [1]

Diabetes. Endocrinology consultation. Pancreoprivic diabetes after necrotising pancreatitis is often brittle because of the loss of both insulin and glucagon counter-regulation, making hypoglycaemia dangerous. Likely requires insulin (basal-bolus regimen) with careful blood glucose monitoring and patient education about hypoglycaemia recognition. [1]

Alcohol use disorder. Thiamine 100 mg IV daily for 5 days (Wernicke prevention), followed by oral thiamine. Benzodiazepines for withdrawal symptoms if they develop (CIWA-guided). Addiction medicine consultation for cessation counselling and planning for supervised detoxification after discharge. Counsel that continued drinking will cause recurrent attacks and progression to chronic pancreatitis with chronic pain, exocrine and endocrine insufficiency, and elevated pancreatic cancer risk. [1]

Rehabilitation. Early mobilisation, physiotherapy, and functional recovery. Deconditioning after a prolonged ICU stay is a major contributor to length of stay and morbidity. [1]

Examiner probing questions

Examiner: "Why did you choose Ringer lactate over normal saline, and what rate?" Ringer lactate is preferred over normal saline for three reasons: the WATERFALL trial established that moderately aggressive resuscitation is superior to aggressive bolus resuscitation; Ringer lactate reduces the systemic inflammatory response compared with normal saline; and normal saline causes hyperchloraemic metabolic acidosis, which may worsen splanchnic vasoconstriction and pancreatic perfusion. The rate I use is 5 to 10 mL per kg per hour for the first 24 to 48 hours, with reassessment of the blood urea, haematocrit, and urine output every 6 hours, reducing the rate once the urea is normalising. I avoid boluses unless the patient is hypotensive [3].

Examiner: "Why no prophylactic antibiotics?" Prophylactic antibiotics are NOT recommended in acute pancreatitis, including in severe necrotising disease. Multiple randomised trials and meta-analyses confirm they do not reduce infected necrosis or mortality, and they increase fungal superinfection and antibiotic resistance. I use antibiotics only when infection is proven or strongly suspected — for this patient, the gas in the necrotic collection on CT was definitive evidence of infected necrosis, so meropenem is therapeutic, not prophylactic [2].

Examiner: "What is the step-up approach and what did PANTER show?" The step-up approach means treating infected necrosis with the least invasive effective intervention first, escalating only if that fails. The sequence is: antibiotics and supportive care; percutaneous or endoscopic catheter drainage; minimally invasive necrosectomy (endoscopic or VARD); and open necrosectomy as the last resort. The PANTER trial (van Santvoort, NEJM 2010) randomised 88 patients with infected necrosis to primary open necrosectomy versus the step-up approach. The step-up approach reduced the primary composite endpoint (major complications or death) from 69 to 40 per cent, and 35 per cent of patients needed drainage alone. The key timing principle is to intervene late, allowing the collection to wall off (usually after 4 weeks) [4].

Examiner: "What are the revised Atlanta morphological terms and why do they matter?" The Revised Atlanta Classification standardises the terminology for local complications based on two questions: is there necrosis, and has the collection been present for more or less than 4 weeks. For interstitial oedematous pancreatitis (about 90 per cent), the terms are acute peripancreatic fluid collection (less than 4 weeks) and pseudocyst (more than 4 weeks, encapsulated fluid without necrosis). For necrotising pancreatitis (about 10 per cent), the terms are acute necrotic collection (less than 4 weeks) and walled-off necrosis (more than 4 weeks, necrosis within a capsule). These terms matter because they determine management: sterile fluid collections usually resolve spontaneously, sterile necrosis is managed conservatively unless symptomatic, and infected necrosis requires antibiotics and the step-up approach. The old terms pancreatic abscess and phlegmon are discouraged [1].

Examiner: "Why does he have diabetes and what makes it different from type 2?" Necrotising pancreatitis destroys the endocrine pancreas. The resulting pancreoprivic (type 3c) diabetes is different from type 2 because it involves the loss of both insulin-secreting beta cells and glucagon-secreting alpha cells. Without glucagon counter-regulation, hypoglycaemia is more dangerous and the diabetes is brittle — difficult to control, with wide glucose excursions. Treatment requires insulin, but with caution and education about hypoglycaemia. Pancreatic enzyme replacement improves glycaemic control by restoring nutrient absorption and reducing the mismatch between insulin and absorbed glucose. [1]

Branching scenario — autoimmune pancreatitis

Examiner: "Now consider a 65-year-old man who presents with painless progressive jaundice over three weeks. CT shows diffuse sausage-shaped enlargement of the pancreas with a capsule-like rim and irregular narrowing of the main pancreatic duct. His serum IgG4 is 4.2 g per litre. Biopsy shows a dense lymphoplasmacytic infiltrate with storiform fibrosis and abundant IgG4-positive plasma cells. What is the diagnosis and management?" [1]

This is type 1 autoimmune pancreatitis (AIP), the pancreatic manifestation of IgG4-related disease. The diagnosis is established by the HISORt criteria: characteristic histology (lymphoplasmacytic infiltrate, storiform fibrosis, IgG4-positive plasma cells), characteristic imaging (diffuse pancreatic enlargement with a capsule-like rim and irregular duct narrowing), elevated serum IgG4, and other organ involvement. The management is prednisolone 0.6 to 1 mg per kg per day (typically 30 to 40 mg daily) for 2 to 4 weeks, then taper. The response is dramatic and is so characteristic that it is used diagnostically. About 40 to 50 per cent relapse and require maintenance immunosuppression (azathioprine or mycophenolate). The critical trap is to avoid operating for presumed pancreatic cancer without considering AIP — a dramatic steroid response is the clinical hallmark. Type 2 AIP is separate (idiopathic duct-centric, IgG4-negative, younger patients, associated with IBD). [1]

Branching scenario — hypertriglyceridaemic pancreatitis

Examiner: "And what if the patient were a 30-year-old woman with poorly controlled type 1 diabetes, a lactescent (milky) serum, triglycerides of 18 mmol per litre, and pancreatitis? How does the management differ?" [1]

This is hypertriglyceridaemic pancreatitis. The mechanism is that pancreatic lipase hydrolyses the excess triglycerides to free fatty acids, which are directly toxic to the pancreatic vascular endothelium and acinar cells. The diagnostic clue is the lactescent serum and triglycerides above 11 mmol per litre. The management has the same resuscitation principles (goal-directed Ringer lactate, early enteral feeding, no prophylactic antibiotics) plus specific measures: insulin infusion (insulin activates lipoprotein lipase, accelerating triglyceride clearance), plasmapheresis or apheresis in severe cases (removes triglycerides rapidly and is used in selected centres for severe disease or pregnancy), and treatment of the underlying lipid disorder (fibrate such as fenofibrate, omega-3 fatty acids, diabetic control, avoidance of alcohol and oestrogen, and genetic evaluation for familial chylomicronaemia). Target triglycerides below 5 mmol per litre to prevent recurrence. Note that the serum lipase may be falsely low because the lactescent serum interferes with the assay — dilute and re-test if the clinical picture is consistent but the lipase is not elevated. [1]

Short-case discussion — abdominal examination

Examiner: "Examine this patient's abdomen. He is recovering from pancreatitis."

My routine: general inspection for distress, pain posture (sitting forward), and signs of chronic alcohol use (spider naevi, palmar erythema, parotid enlargement, muscle wasting); hands for clubbing and Dupuytren contracture; face for conjunctival pallor, scleral icterus, and perioral signs of hyperlipidaemia; neck for jugular venous pressure and lymphadenopathy; chest for pleural effusion (especially left-sided); abdomen — inspect for scars and distension, palpate for epigastric tenderness, guarding, and a palpable mass (pseudocyst or inflammatory mass), check for shifting dullness, and auscultate bowel sounds (sparse or tinkling in ileus); examine the back for Grey Turner sign (flank discolouration in haemorrhagic disease). [1]

Presentation: "On general inspection the patient is comfortable but sitting forward. There are no stigmata of chronic liver disease. The abdomen is soft with mild epigastric tenderness and no guarding or rigidity. There is no palpable mass, hepatosplenomegaly, or ascites. Bowel sounds are sparse, consistent with a resolving paralytic ileus. There is no Cullen or Grey Turner sign. These findings are consistent with resolving acute pancreatitis without evidence of haemorrhagic or necrotising complications. I would review the observations, confirm the diagnosis with a serum lipase, and organise an abdominal ultrasound to identify the cause." [1]

Examiner: "What would Cullen and Grey Turner signs indicate?" Haemorrhagic necrotising pancreatitis. Cullen sign is periumbilical discolouration from blood tracking via the falciform ligament; Grey Turner sign is flank discolouration from blood tracking to the flanks. Both are rare (under 3 per cent of cases) but, when present, indicate severe haemorrhagic disease with a high mortality. They are not pathognomonic — Cullen sign also occurs in ruptured ectopic pregnancy. [1]

Examiner: "What single blood test most strongly suggests gallstone aetiology?" An ALT above 150 IU per litre has a positive predictive value of 95 per cent for gallstone pancreatitis. The mechanism is that the obstructing gallstone causes hepatocellular injury as it passes through the biliary tree. A mildly elevated ALT is less specific, but a markedly elevated ALT in the context of acute pancreatitis points strongly to gallstones. [1]