Acute Pancreatitis

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• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
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What this chapter covers

• Section 25.1: Pathophysiology of acute pancreatitis

  Acute pancreatitis begins inside the acinar cell with premature intracellular activation of trypsinogen to trypsin, which then cleaves and activates the rest of the digestive zymogen pool (chymotrypsinogen, proelastase, prophospholipase A2, procarboxypeptidase) before they reach the duodenum.

• Section 25.2: Diagnosis and Atlanta classification

  The Revised Atlanta Classification establishes the diagnosis of acute pancreatitis when two of three criteria are present: characteristic upper abdominal pain (typically epigastric, often radiating to the back, peaking within minutes to hours, exacerbated by oral intake), serum lipase or amylase greater than three times the upper limit of normal, and characteristic findings on cross-sectional imaging (CT or MRI showing focal or diffuse pancreatic enlargement, peripancreatic stranding, or fluid collections).

• Section 25.3: Etiologic workflow

  Gallstones (40 to 50 percent) and alcohol (25 to 35 percent) account for the majority of acute pancreatitis.

• Section 25.4: Severity stratification

  Severity depends on organ failure quantified by the modified Marshall score in renal, pulmonary, and cardiovascular systems, with a score of 2 or more in any system defining failure.

• Section 25.5: Initial fluid resuscitation and the WATERFALL trial

  The mechanism of fluid therapy in acute pancreatitis is reversal of intravascular hypovolemia from third-spacing in order to restore pancreatic perfusion within the time-sensitive 6 to 12 hour window before ischemia drives further necrosis.

• Section 25.6: Nutrition route and timing

  Older teaching of pancreatic rest with NPO and TPN has been overturned because enteral nutrition maintains gut mucosal integrity and prevents bacterial translocation that drives infected necrosis, while TPN allows bacterial translocation across an atrophic gut barrier and doubles the infectious complication rate.

• Section 25.7: ERCP timing in gallstone pancreatitis

  Most bile duct stones have already passed at the onset of gallstone pancreatitis, so empty ERCP exposes the patient to post-ERCP pancreatitis risk for no benefit.

• Section 25.8: Same-admission cholecystectomy and PONCHO

  The PONCHO trial (da Costa, Lancet 2015) randomized 264 patients with mild gallstone pancreatitis to same-admission laparoscopic cholecystectomy (within 3 days of pain resolution) versus interval cholecystectomy at 25 to 30 days.

• Section 25.9: Necrosis classification and step-up approach

  About 20 to 25 percent of patients develop necrotizing pancreatitis, distinguished from interstitial edematous pancreatitis on contrast-enhanced CT by absence of pancreatic enhancement (no perfusion of the gland).

• Section 25.10: Vascular complications of acute pancreatitis

  Splanchnic venous thrombosis (splenic, portal, or superior mesenteric vein) develops from peripancreatic inflammatory damage to the venous wall.

• Section 25.11: Post-ERCP pancreatitis prevention

  Post-ERCP pancreatitis (3 to 15 percent of ERCPs) is the most common ERCP complication and an etiology of acute pancreatitis that the inpatient gastroenterologist manages.

• Section 25.12: Recurrent and idiopathic acute pancreatitis

  Roughly 17 to 23 percent of patients have a second attack within 5 years, and recurrent acute pancreatitis is a major risk factor for chronic pancreatitis (see Ch 26 for the recurrent-acute-to-chronic pancreatitis transition, the TIGAR-O classification, and the management of established chronic pancreatitis).

Podcast episodes

1. 01

   Acute Pancreatitis: From Acinar Cell to Severity

   Acute pancreatitis starts with premature trypsin activation inside the acinar cell, driven by sustained intracellular calcium whatever the trigger, and it becomes dangerous through capillary leak, third spacing, and necrosis that takes days to show. The episode begins with diagnosis by two of three criteria, so a CT on day one is unnecessary, and with why lipase is the better enzyme and why very high triglycerides can hide it. It then works through the cause: gallstones, alcohol, triglycerides, drugs, calcium, tumor after forty, structural, autoimmune, and genetic causes. It ends with severity, defined by organ failure, the early scores and bedside markers, and the timing of CT.

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2. 02

   Acute Pancreatitis: First Days of Treatment

   The organizing idea is that early treatment in acute pancreatitis works by restoring perfusion, feeding the gut, and acting on the bile duct only when there is a reason. The episode starts with fluid: which fluid, how much, how to judge response at six to twelve hours, and when a non-responder moves to the ICU. It then covers feeding, from early oral diet in mild disease to tube choice and the limited role of parenteral nutrition. Last come the biliary decisions: who needs ERCP and when, timing of cholecystectomy in mild versus necrotizing disease, and sphincterotomy for patients who cannot have surgery.

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3. 03

   Acute Pancreatitis: Necrosis and Recurrence

   Necrosis changes the tempo of acute pancreatitis, and the organizing idea is that timing and cause decide every step. The episode begins with a man in week three whose gas-containing collection proves infected necrosis, treated with antibiotics that penetrate tissue, while sterile necrosis gets none. It then names collections by content and time, applies the delay, drain, debride sequence, and requires excluding a pseudoaneurysm before drainage and deciding whether venous thrombosis needs anticoagulation. The second half turns to a young woman with recurrent attacks: second-pass MRCP and EUS, genetic testing, divisum, post-ERCP pancreatitis prevention, cholecystectomy, removing the cause, and screening for diabetes and exocrine insufficiency.

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Key topics

• ·Trypsin activation and the calcium pathway
• ·Systemic inflammation and necrosis timing
• ·Revised Atlanta diagnostic criteria
• ·When to skip the CT
• ·Lipase versus amylase
• ·Lipemic serum and falsely normal enzymes
• ·Gallstone, alcohol, and triglyceride causes
• ·Drugs, calcium, tumors, and genetics
• ·Organ failure and the Marshall score
• ·Early scores, bedside markers, and CT severity index
• ·Why fluid resuscitation is urgent
• ·Lactated Ringer's versus normal saline
• ·Moderate goal-directed fluid dosing
• ·Reassessing response and escalating to the ICU
• ·Fluid caution in heart and kidney disease
• ·Early oral and enteral feeding
• ·Tube choice and parenteral nutrition
• ·ERCP indications and timing
• ·Cholecystectomy timing
• ·Sphincterotomy when surgery is not possible
• ·Infected pancreatic necrosis
• ·Antibiotics for infected versus sterile necrosis
• ·Atlanta collection terms
• ·Delay, drain, debride step-up
• ·Pseudoaneurysm and splanchnic vein thrombosis
• ·Recurrent and idiopathic pancreatitis workup
• ·Genetic testing
• ·Pancreas divisum
• ·Post-ERCP pancreatitis prevention
• ·Cholecystectomy and follow-up after discharge