Acute Pancreatitis

• Audio chapter
  Single-voice audio, listen on the commute.
• ABIM-format MCQs
  5-option vignettes with full wrong-answer teaching.
• Study guide
  Tables, decision trees, primary sources.
• AI tutor
  Chapter-grounded, answers the question you're stuck on.

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 hinges 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 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 affects 3 to 15 percent of cases overall and is the most common ERCP complication.

• 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 (cross-link 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: The First Hours

   Episode one of the Acute Pancreatitis chapter follows a single mechanism from trypsin escaping its compartment to the cytokine cascade, third-spacing, and lost pancreatic perfusion. The organizing idea: every first-hours decision reaches back to that mechanism. The two-of-three rule diagnoses around the failure modes of pain, enzymes, and imaging alone; the cause is worked up on admission because the trigger reshapes management; severity stays provisional while organ failure declares; and fluids are moderate lactated Ringer's titrated to hematocrit and BUN. The trial that asked whether more fluid was better answered no and stopped early.

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2. 02

   Feeding, ERCP, and the Gallbladder

   Episode two works through three first-days decisions where the intuitive older instinct turns out to be net harmful. Pancreatic rest with TPN increases infection because an empty lumen lets villi atrophy and gut bacteria translocate into necrotic tissue, so early enteral feeding wins. Universal urgent ERCP was wrong because most triggering stones have already passed, leaving an empty duct and only post-ERCP risk. And interval cholecystectomy costs roughly one in six patients a recurrent biliary event, so same-admission surgery is now standard. The unifying logic: each intervention earns its place against its own complication profile.

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3. 03

   Necrosis, Vascular Traps, and Recurrence

   Episode three picks up where the pancreas has declared itself necrotic and organizes the collection nomenclature on timing and content. Necrosis is managed by delay, drain, then debride, with endoscopic transmural drainage now favored because it never crosses the peritoneum. The vascular complications split by vessel: venous thrombosis usually self-resolves, while a pseudoaneurysm mandates CT angiography and embolization before any drainage. The post-ERCP triad attacks three independent nodes, and recurrent disease is worked up by escalation from baseline labs to MRCP to endoscopic ultrasound for microlithiasis, with the pancreas divisum trap waiting at the end.

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Key topics

• ·Mechanism: trypsin activation and the calcium convergence point
• ·Triggers: gallstones, alcohol, triglycerides, calcium
• ·Systemic inflammation, third-spacing, and necrosis
• ·Clinical presentation and lipase versus amylase
• ·Revised Atlanta two-of-three diagnosis
• ·Severity grading by organ failure
• ·Etiology workup during the index admission
• ·Severity scores and first-day hematocrit and BUN trends
• ·Moderate goal-directed lactated Ringer's resuscitation
• ·Pancreatic rest versus early enteral feeding
• ·The gut barrier and bacterial translocation
• ·Feeding rules in mild disease
• ·Feeding in predicted severe disease and tube level
• ·TPN as the failure path
• ·ERCP indications and the passed-stone anatomy
• ·The three-patient ERCP decision
• ·Same-admission versus interval cholecystectomy
• ·Exceptions: severe disease and the non-surgical patient
• ·Recognizing necrosis and infected necrosis
• ·Collection nomenclature by timing and content
• ·Step-up management: delay, drain, debride
• ·Endoscopic versus surgical step-up
• ·Splanchnic venous thrombosis and left-sided portal hypertension
• ·Arterial pseudoaneurysm and pre-drainage angiography
• ·Post-ERCP pancreatitis and its prevention triad
• ·Recurrent and idiopathic disease workup
• ·Pancreas divisum and prevention by stopping the cause