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 antibiotics that penetrate necrosis).
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 a carbapenem or piperacillin-tazobactam for the infected necrosis, with a plan to de-escalate and stop once source control is achieved and inflammatory markers settle. ^[4]

Fluid and organ support. Lactated Ringer's, WATERFALL moderate (10 mL per kg bolus only if hypovolaemic, then 1.5 mL per kg per hour), with reassessment at 12, 24, 48, and 72 hours. Aggressive bolus resuscitation causes fluid overload without benefit; I will avoid the 20 then 3 mL per kg regimen. 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 for steatorrhoea from exocrine insufficiency. ^[4]

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. Parenteral then oral thiamine (Wernicke prevention). 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 WATERFALL moderate: 10 mL per kg bolus only if hypovolaemic, then 1.5 mL per kg per hour, reassessed at 12, 24, 48, and 72 hours. I avoid the aggressive 20 then 3 mL per kg regimen. Wu 2011 supports lactated Ringer's over saline (SIRS 84 per cent reduction versus 0 per cent). ^[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 antibiotics that penetrate necrosis are therapeutic, not prophylactic ^[2][10].

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. ACG 2013: delay drainage in stable infected necrosis, preferably 4 weeks, to allow a wall to form. ^[10][4]

Examiner: "What are the revised Atlanta morphological terms and why do they matter?" Atlanta names peripancreatic fluid collections, necrosis (sterile or infected), pseudocyst, and walled-off necrosis. Mapping "pancreatic abscess" or "phlegmon" onto infected necrosis, and pairing the four names with a 4-week unwalled/walled clock, is exam convention — not an Atlanta-abstract sentence. ACG 2013 supplies the sourced 4-week delay for drainage in stable infected necrosis. ^[1][10][2]

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]