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Q1: Diagnosis and severity (2 min)
- Define acute pancreatitis — acute inflammatory disorder of the pancreas with premature intracellular trypsin activation and autodigestion.
- Diagnose with 2 of 3 — epigastric pain radiating to the back, lipase or amylase over 3 × ULN, characteristic imaging. Lipase is preferred (higher sensitivity and specificity than amylase, longer half-life for late presentation); amylase may be normal in hypertriglyceridaemia and late presentation.[18]
- Reproduce the Revised Atlanta severity grades — mild (no organ failure, no complications), moderately severe (transient organ failure under 48 h or local/systemic complications), severe (persistent organ failure over 48 h; Marshall-style assessment of respiratory, renal and cardiovascular function).
- Name the bedside scores — BISAP within 24 hours (BUN over 25 mg/dL, impaired mental status, SIRS, age over 60, pleural effusion; in-hospital mortality ranged from over 20 percent in the highest-risk group to under 1 percent in the lowest; AUC 0.82 versus APACHE-II 0.83). Ranson and Glasgow/Imrie mature at 48 hours. Severity itself is Revised Atlanta organ failure persisting beyond 48 hours, not a score cut-off.[4][1]
Q2: Causes (1 min)
- Two big causes: gallstones and alcohol together about 80% of episodes (one prospective series: gallstones 56%, alcohol 16%).
- Reproduce I GET SMASHED (Idiopathic, Gallstones, Ethanol, Trauma, Steroids/Smoking, Mumps/Malignancy, Autoimmune, Scorpion sting, HyperCa/HyperTG, ERCP, Drugs).
- Admission transaminase predicted gallstones with 75% sensitivity, 74% specificity and PPV 78.8% in Davidson's one-factor system — not a 95% PPV for ALT over 150.[11][10]
Q3: Initial management (3 min)
- ABCDE, oxygen, two IV cannulae, urinary catheter, ICU referral for severe disease.
- Goal-directed moderate lactated Ringer's — 10 mL/kg bolus only if hypovolaemic, then 1.5 mL/kg per hour. Avoid aggressive boluses (20 mL/kg then 3 mL/kg per hour) — WATERFALL: fluid overload 20.5 versus 6.3 percent, no improvement in moderately severe or severe disease.[2]
- Adequate IV opioid analgesia.
- Early enteral feeding within 24 to 48 h — no prolonged nil by mouth; NG/NJ if oral-intolerant.
Q4: Definitive management (3 min)
- No routine prophylactic antibiotics (Poropat 2022: no significant effect on infected necrosis or mortality) — only for infected necrosis or cholangitis.[7]
- ERCP within 24 h ONLY for cholangitis or persistent biliary obstruction — NOT routine (Cochrane: no evidence early routine ERCP changes mortality or complications).[8]
- Same-admission laparoscopic cholecystectomy in mild gallstone pancreatitis (ACG: surgery to prevent recurrent biliary disease; Ranson: 33% further pancreatitis if discharged without a biliary operation); delay in severe disease with collections.[3][20]
- Hypertriglyceridaemic pancreatitis: risk rises above 11.3 mmol/L (~5%) and 15 to 20 percent of severe HTG >1000 mg/dL develop AP; insulin infusion ± plasmapheresis, then fibrate.[18]
- Infected necrosis: step-up drainage at ~4 weeks — percutaneous or endoscopic drainage first, minimally invasive necrosectomy if it fails (PANTER 2010). Avoid open necrosectomy.[5]
Q5: Complications (2 min)
- Local (by content and timing — Revised Atlanta): APFC, pseudocyst, ANC, walled-off necrosis; infected necrosis; haemorrhage; splenic/portal vein thrombosis.[1]
- Systemic: SIRS/sepsis, ARDS (phospholipase A2 destroys surfactant), AKI, shock, DIC, hypocalcaemia (saponification), diabetes.
- Long-term: exocrine and endocrine insufficiency (type 3c diabetes), chronic pancreatitis, recurrence.
Q6: Prognosis and pitfalls (1 min)
- Mortality — Ranson's prognostic split: mild 1.8%, severe 17%; infected necrosis higher.[20]
- Predictors of severity — organ failure, obesity, age, comorbidity; CRP over 150 mg/L at 48 h, persistent SIRS, rising scores.
- Three classic errors: aggressive fluids (WATERFALL); prolonged NPO; routine prophylactic antibiotics; early surgery for necrosis; missing a leaking AAA or mesenteric ischaemia that raises amylase.
- Cullen's (periumbilical) and Grey-Turner's (flank) signs — rare but specific for severe necrotising or haemorrhagic disease.
References11ShowHide
- [1]Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus Gut, 2013.PMID 23100216
- [2]de-Madaria E, Buxbaum JL, Maisonneuve P, et al. Aggressive or Moderate Fluid Resuscitation in Acute Pancreatitis N Engl J Med, 2022.PMID 36103415
- [3]Tenner S, Vege SS, Sheth SG, et al. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis Am J Gastroenterol, 2024.PMID 38857482
- [4]Wu BU, Johannes RS, Sun X, et al. The early prediction of mortality in acute pancreatitis: a large population-based study Gut, 2008.PMID 18519429
- [5]van Santvoort HC, Besselink MG, Bakker OJ, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis N Engl J Med, 2010.PMID 20410514
- [7]Poropat G, Goričanec K, Lacković A, et al. Systematic Review with Trial Sequential Analysis of Prophylactic Antibiotics for Acute Pancreatitis Antibiotics (Basel), 2022.PMID 36139970
- [8]Tse F, Yuan Y. Early routine endoscopic retrograde cholangiopancreatography strategy versus early conservative management strategy in acute gallstone pancreatitis Cochrane Database Syst Rev, 2012.PMID 22592743
- [10]Davidson BR, Neoptolemos JP, Leese T Biochemical prediction of gallstones in acute pancreatitis: a prospective study of three systems Br J Surg, 1988.PMID 2450614
- [11]Hasibeder WR, Torgersen C, Rieger M Critical care of the patient with acute pancreatitis Anaesth Intensive Care, 2009.PMID 19400483
- [18]Hu Q, Hu Y, Tan C Acute pancreatitis: mechanisms and therapeutic approaches Signal Transduct Target Ther, 2026.PMID 41530118
- [20]Ranson JH The timing of biliary surgery in acute pancreatitis Ann Surg, 1979.PMID 443917