Acute Pancreatitis
Revised Atlanta classification, lactated Ringer's resuscitation per WATERFALL, the etiologic workflow, same-admission cholecystectomy per PONCHO, the step-up necrosis pathway with LAMS, and post-ERCP pancreatitis prevention with rectal indomethacin and the prophylactic PD stent.
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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 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).