Acute Pancreatitis — DCE Clinical Case

Long case

Patient scenario

Mr RT is a 58-year-old man who was admitted 12 days ago with 24 hours of severe constant epigastric pain radiating to the back, with repeated vomiting. He had a low-grade fever. On admission his lipase was 2400 U per litre (ULN 60), ALT 220 IU per litre, bilirubin 45 micromol per litre, and abdominal ultrasound showed multiple gallstones with a normal-calibre common bile duct. He was diagnosed with acute gallstone pancreatitis. Over the first 48 hours he developed acute kidney injury (creatinine rising from 95 to 210 micromol per litre, oliguria) and respiratory compromise (oxygen saturation 90 per cent on room air requiring 4 litres of nasal specs), meeting criteria for severe pancreatitis per the Revised Atlanta Classification (persistent organ failure beyond 48 hours). A contrast-enhanced CT on day 5 showed extensive pancreatic and peripancreatic necrosis with gas bubbles within the collection, consistent with infected necrosis. He was commenced on meropenem 1 g IV every 8 hours and underwent EUS-guided endoscopic cystgastrostomy and drainage of the walled-off necrosis on day 8, with two sessions of endoscopic necrosectomy. His organ failure is now resolving: creatinine 145 micromol per litre, saturating at 95 per cent on 2 litres nasal specs. His blood glucose has been labile, with readings between 4 and 22 mmol per litre, and he has been commenced on a basal-bolus insulin regimen by the endocrinology team. He is on nasojejunal feeding at 60 mL per hour and has intermittent steatorrhoea. He drinks 60 to 80 grams of alcohol daily and smokes 15 cigarettes per day. He works as a truck driver. He has hypertension (on perindopril 5 mg daily) and has no known diabetes prior to this admission. He is keen to return home and is frustrated by the prolonged admission. [1]

Examination findings

The patient is in bed, comfortable but visibly deconditioned. He is afebrile, heart rate 88, blood pressure 132 over 78, respiratory rate 18, oxygen saturation 95 per cent on 2 litres nasal specs. He has mild scleral icterus. The abdomen is soft with mild epigastric tenderness, a palpable fullness in the epigastrium (consistent with the residual walled-off collection), and sparse bowel sounds. There is no guarding, rigidity, or Cullen or Grey Turner sign. He has a nasojejunal tube in situ and a triple-lumen central line in the right internal jugular vein. He has mild bilateral basal crackures. There is no peripheral oedema. [1]

Candidate's opening statement (SASPOP)

"Doctor, my patient is Mr RT, a 58-year-old man and truck driver, now on day 12 of an admission for severe acute gallstone pancreatitis complicated by persistent organ failure (acute kidney injury and respiratory compromise, both resolving), infected walled-off necrosis managed with endoscopic step-up drainage, new-onset diabetes of the pancreas, and malnutrition on nasojejunal feeding. He drinks 60 to 80 grams of alcohol daily. His problems are: severe necrotising gallstone pancreatitis with infected walled-off necrosis; resolving multi-organ failure; new-onset diabetes of the pancreas; malnutrition; alcohol use disorder; hypertension; and deconditioning requiring rehabilitation." [1]

Problem list

1. Severe necrotising gallstone pancreatitis with infected walled-off necrosis (managed with endoscopic drainage and meropenem).
2. Resolving multi-organ failure (acute kidney injury recovering, respiratory compromise improving).
3. New-onset diabetes of the pancreas (pancreoprivic, on basal-bolus insulin).
4. Malnutrition and ongoing catabolism (nasojejunal feeding at 60 mL per hour).
5. Alcohol use disorder (60 to 80 grams daily; withdrawal risk, need for cessation).
6. Smoking (15 cigarettes per day).
7. Hypertension (on perindopril).
8. Deconditioning and the need for rehabilitation. [1]

Integrated management plan

Source control for the infected necrosis. Continue endoscopic drainage of the walled-off necrosis via the established cystgastrostomy; repeat endoscopic necrosectomy if the collection re-accumulates or clinical parameters deteriorate. Continue meropenem 1 g IV every 8 hours, with a plan to de-escalate and stop once source control is achieved, inflammatory markers have settled, and the patient is clinically improving. The PANTER trial established the step-up approach as the standard — primary open necrosectomy is not indicated [4].

Organ support. Ringer lactate, moderately aggressive and goal-directed, with reassessment of blood urea and creatinine every 6 hours (the WATERFALL trial showed aggressive bolus resuscitation causes harm). Renal replacement therapy is on standby if the acute kidney injury worsens. Wean high-flow to low-flow oxygen as tolerated [3].

Nutrition. Continue nasojejunal enteral feeding and advance to target rate as tolerated; early enteral feeding reduces infectious complications and mortality compared with NPO and parenteral nutrition. Plan to transition to an oral low-fat diet as ileus resolves. Add pancreatic enzyme replacement (pancreatin 25,000 to 40,000 units with meals) for the steatorrhoea from exocrine insufficiency. [1]

Diabetes. Continue the endocrinology-guided basal-bolus insulin regimen. Pancreoprivic diabetes is often brittle (loss of glucagon counter-regulation makes hypoglycaemia dangerous). Educate the patient about hypoglycaemia recognition and management. Monitor HbA1c in 3 months. [1]

Alcohol and smoking. Thiamine 100 mg daily (Wernicke prevention). Addiction medicine consultation for cessation counselling and supervised detoxification planning. Counsel that continued drinking will cause recurrent pancreatitis and progression to chronic pancreatitis. Smoking cessation counselling (smoking increases the risk of pancreatic cancer in chronic pancreatitis). [1]

Definitive biliary management. Laparoscopic cholecystectomy once the patient has fully recovered from the acute episode (typically 3 to 6 months after severe necrotising pancreatitis, because the inflammation makes early dissection hazardous). Intraoperative cholangiogram to exclude retained common bile duct stones. For mild gallstone pancreatitis, cholecystectomy during the index admission would be appropriate, but for this severe case, delayed cholecystectomy is the standard [6].

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

Discussion questions

Examiner: "How would the fluid strategy differ if this patient had presented today, given the WATERFALL trial?" The 2024 ACG guideline recommends moderately aggressive, goal-directed fluid resuscitation with Ringer lactate — NOT the old approach of aggressive 250 to 500 mL per hour. The WATERFALL trial stopped early because aggressive resuscitation (20 mL per kg bolus, then 3 mL per kg per hour) caused significantly more fluid overload without improving disease-specific outcomes. The practical approach is 5 to 10 mL per kg per hour of Ringer lactate, with reassessment of blood urea, haematocrit, and urine output every 6 hours, reducing the rate once the urea is normalising. I would avoid boluses unless he was hypotensive [3].

Examiner: "Why was ERCP not performed at admission despite the gallstone aetiology?" ERCP within 24 hours is indicated in acute biliary pancreatitis only when there is concomitant cholangitis or persistent biliary obstruction. This patient had no cholangitis (no fever, no rigors, no ongoing jaundice at presentation beyond the initial bilirubin of 45) and no evidence of a persistent obstructing stone (normal-calibre common bile duct on ultrasound). The gallstone had likely already passed into the duodenum. ERCP would have exposed him to the risk of post-procedure pancreatitis without therapeutic benefit. The ACG guideline is clear on this point [2].

Examiner: "What is the BISAP score and why is it useful?" The Bedside Index of Severity in Acute Pancreatitis (BISAP) was derived from a population of nearly 18,000 patients to provide early risk stratification using data available within 24 hours. One point each for: Blood urea nitrogen above 8.9 mmol per litre, Impaired mental status, SIRS, Age above 60, and Pleural effusion. A score of 3 or above identifies severe disease with a mortality of 5 to 20 per cent. The advantage over Ranson (which requires 48 hours to complete) and APACHE II (which is complex and requires ICU) is that it is simple, early, and bedside-available [5].

Examiner: "Why does he have diabetes and what makes pancreoprivic diabetes different from type 2?" Necrotising pancreatitis destroys the endocrine pancreas. The resulting type 3c (pancreoprivic) 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 — wide glucose excursions, difficult to control, and prone to severe hypoglycaemia. Treatment requires insulin, but with education about hypoglycaemia. Pancreatic enzyme replacement improves glycaemic control by restoring nutrient absorption and reducing the mismatch between insulin and absorbed glucose. [1]

Examiner: "When would you perform the cholecystectomy?" Because this is severe necrotising pancreatitis with ongoing walled-off necrosis and organ failure recovery, I would defer cholecystectomy for 3 to 6 months until the inflammation has fully resolved. Operating during the acute phase would be hazardous because of the inflammation and the risk of enteric fistula. For mild gallstone pancreatitis, the standard is cholecystectomy during the index admission or within 2 weeks (meta-analyses show this reduces recurrent biliary events without increasing surgical complications), but for severe disease, delayed cholecystectomy is the standard [6].

Short case — focused abdominal examination

Instruction

"Examine this patient's abdomen. He is recovering from acute pancreatitis." [1]

Systematic examination routine

1. End of bed inspection. Assess for distress, pain posture (sitting forward), jaundice, and signs of chronic alcohol use (spider naevi, palmar erythema, parotid enlargement, gynaecomastia, muscle wasting). Look for the periumbilical and flank discolouration (Cullen and Grey Turner signs) in haemorrhagic disease. Note any lines, tubes, and drains.
2. Hands and arms. Look for clubbing, palmar erythema, asterixis (hepatic encephalopathy), and Dupuytren contracture (alcohol association).
3. Face. Conjunctival pallor, scleral icterus, parotid enlargement, and perioral signs of hyperlipidaemia (xanthelasma, corneal arcus).
4. Neck. Jugular venous pressure (hypovolaemia or fluid overload), cervical lymphadenopathy.
5. Chest. Look for pleural effusion (especially left-sided — a BISAP criterion and a sign of severity). Examine for basal crackures indicating fluid overload or ARDS.
6. Abdomen. Inspect for scars (previous surgery), distension (ileus, ascites), and visible peristalsis. Palpate for epigastric tenderness, guarding, and a palpable mass (pseudocyst, walled-off necrosis, or inflammatory mass). Check for shifting dullness (ascites). Auscultate bowel sounds (absent or tinkling in ileus).
7. Back. Look for Grey Turner sign (flank discolouration in haemorrhagic disease). [1]

Key signs this patient demonstrates

• Mild epigastric tenderness with a palpable fullness (consistent with residual walled-off necrosis).
• Sparse bowel sounds (resolving paralytic ileus).
• Mild scleral icterus (resolving biliary obstruction).
• Deconditioning and bilateral basal crackures (fluid overload and resolving ARDS). [1]

Presentation template

"Doctor, I examined Mr RT's abdominal system. He is comfortable in bed but visibly deconditioned, with mild scleral icterus. He has a nasojejunal tube and a right internal jugular central line in situ. The abdomen is soft with mild epigastric tenderness and a palpable fullness in the epigastrium, consistent with a residual walled-off collection. There is no guarding, rigidity, or hepatosplenomegaly. Bowel sounds are sparse, consistent with a resolving paralytic ileus. There is no Cullen or Grey Turner sign. Chest examination reveals bilateral basal crackures. These findings are consistent with severe necrotising pancreatitis in the recovery phase, with a residual walled-off collection. I would review the recent CT and inflammatory markers, confirm that the endoscopic drainage is functioning, and assess his nutritional status and glycaemic control." [1]

Discussion — severity assessment and the Revised Atlanta Classification

Examiner: "How do you classify the severity of this patient's pancreatitis and what are the determinants?" Per the Revised Atlanta Classification, this patient has severe pancreatitis. The three tiers are: mild (no organ failure, no local or systemic complications), moderately severe (transient organ failure resolving within 48 hours, or local complications without persistent organ failure), and severe (persistent organ failure beyond 48 hours). This patient developed acute kidney injury (creatinine 210 micromol per litre, oliguria) and respiratory compromise (oxygen requirement) that persisted beyond 48 hours, meeting the criteria for severe disease. The BISAP score, calculated early, would have stratified him as high-risk. The CRP above 150 mg per litre at 48 hours further supported the presence of significant necrosis. The determinants of severity are: the presence and persistence of organ failure, the extent of necrosis on CT, and the development of infected necrosis — the single most important determinant of mortality [1].

Examiner: "What are the Cullen and Grey Turner signs and when do they appear?" Cullen sign is periumbilical bluish discolouration from blood tracking via the falciform ligament from the retroperitoneum. Grey Turner sign is flank discolouration from blood tracking to the flanks. Both indicate haemorrhagic necrotising pancreatitis and, when present, are associated with a high mortality. They are rare (under 3 per cent of cases) and typically appear 24 to 72 hours after onset. They are not pathognomonic — Cullen sign also occurs in ruptured ectopic pregnancy and haemorrhagic ascites. [1]

Examiner: "What is the single most discriminating blood test for 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 traverses the biliary tree. This patient had an ALT of 220 IU per litre, strongly supporting the gallstone aetiology, which was confirmed on ultrasound [2].