Pancreatitis

Anatomy of the Pancreas

• Head - sits within the duodenal C-loop; the main pancreatic duct (duct of Wirsung) joins the common bile duct here to form the ampulla of Vater, draining via the sphincter of Oddi
• Body - traverses posterior to the stomach
• Tail - abuts the splenic hilum

Pathophysiology

1. Inappropriate activation of trypsinogen → trypsin within the gland
2. Trypsin activates other digestive enzymes, causing autodigestion of pancreatic tissue
3. Macrophage and neutrophil recruitment amplify destruction
4. Cytokine release increases vascular permeability → edema, hemorrhage, and necrosis
5. A heightened systemic inflammatory response can cause SIRS → sepsis → shock
6. Bacteremia may occur via translocation of intestinal flora through a compromised gut barrier
7. Extrapancreatic complications include pleural effusions, ARDS, and renal failure

• Rosen's Emergency Medicine, p. 1265

Causes

• Rosen's Emergency Medicine, Box 77.1, p. 1266

Types

1. Acute Pancreatitis (AP)

2. Chronic Pancreatitis (CP)

• Textbook of Family Medicine, p. 1139

Clinical Features of Acute Pancreatitis

• Persistent epigastric or LUQ pain radiating to the back, chest, or flanks
• Pain is moderate to severe; classically relieved by sitting forward or leaning ahead
• Nausea, vomiting, and anorexia (oral intake worsens pain)

• Vital signs may be normal in mild disease; tachycardia and fever are common
• Jaundice suggests biliary obstruction (gallstone pancreatitis or tumor)
• Shallow respirations, basilar crackles (pulmonary complications)
• Epigastric tenderness with guarding; absent bowel sounds (ileus)
• Cullen sign - bluish periumbilical discoloration (hemoperitoneum) - rare but poor prognosis
• Grey Turner sign - reddish-brown flank discoloration (retroperitoneal bleeding) - rare but poor prognosis

• Pulmonary: pleural effusions (in up to 50%, more often left-sided), atelectasis, ARDS
• Cardiovascular: hypotension, shock from fluid shifts
• Renal: failure from hypoperfusion and inflammatory mediators
• Metabolic: hyperglycemia (decreased insulin), hypocalcemia (from low albumin/magnesium), coagulopathy/DIC
• Rosen's Emergency Medicine, pp. 1265-1266

Diagnosis

1. Abdominal pain characteristic of acute pancreatitis
2. Serum lipase or amylase ≥ 3× the upper limit of normal
3. Characteristic findings on abdominal imaging

• Lipase - preferred; more sensitive and specific than amylase; rises within hours, remains elevated for 1-2 weeks
• Amylase - less specific (also elevated in renal failure, salivary gland disease, cholecystitis, bowel obstruction); stays elevated for 3-5 days
• CBC (leukocytosis), metabolic panel (renal function, LFTs, calcium, glucose), lipid panel
• Note: normal enzyme levels do not exclude pancreatitis in alcohol-related cases

• CT abdomen with contrast - gold standard for severity assessment; shows peripancreatic fat stranding, fluid collections, and necrosis
• Ultrasound - first-line to detect gallstones as etiology; limited for pancreas visualization
• MRCP/MRI - useful to evaluate pancreatic/biliary ducts without radiation
• Plain films and chest X-ray are supportive (may show ileus, pleural effusions, "colon cut-off sign")

Severity Classification (Revised 2012 Atlanta Classification)

• Rosen's Emergency Medicine, Box 77.4, p. 1268

Local Complications

Management

Acute Pancreatitis

1. Fluid resuscitation - aggressive IV hydration (Lactated Ringer's preferred); corrects hypovolemia, maintains pancreatic perfusion, and limits SIRS progression
2. Analgesia - IV opioids for pain control (no evidence that any opioid worsens pancreatitis)
3. NPO vs. early enteral nutrition (EN):
   • Historical practice of NPO (to "rest the pancreas") is no longer standard
   • Mild-moderate AP: oral diet should be offered as tolerated; EN considered only if diet cannot be advanced after 4 days
   • Severe AP with SIRS/ICU admission: nasogastric (NG) or nasojejunal (NJ) tube feeding should be initiated within 24-36 hours
   • Two meta-analyses show EN vs. parenteral nutrition (PN) provides a ~2-fold reduction in infectious complications and a ~2.5-fold reduction in mortality risk
   • The AGA technical review of 12 RCTs confirms EN reduces infected peripancreatic necrosis (OR 0.28), single organ failure (OR 0.25), and multiorgan failure (OR 0.41)
4. Antibiotics - NOT routinely indicated; reserved for confirmed infected necrosis or other bacterial complications
5. ERCP with sphincterotomy - indicated within 24-48 hours for gallstone pancreatitis with concurrent cholangitis or biliary obstruction

Chronic Pancreatitis

• Pain management: analgesics, antioxidants (selenium, ascorbic acid, β-carotene, vitamin E - evidence mixed), nerve blocks, ERCP, or surgery for selected patients
• Exocrine insufficiency: pancreatic enzyme replacement with each meal
• Endocrine insufficiency: insulin therapy for diabetes
• Alcohol abstinence - essential; continued use drives recurrent attacks
• Jejunal feeding can improve weight and reduce pain in malnourished patients
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease, pp. 2935-2941

Differential Diagnosis

• Abdominal: peptic ulcer disease, acute cholecystitis/cholangitis, bowel obstruction, mesenteric ischemia, perforated viscus, ruptured AAA, ectopic pregnancy
• Cardiopulmonary: myocardial infarction, pneumonia, pericarditis
• Systemic: DKA, sickle cell crisis

Key Points

• Gallstones and alcohol together cause ~65-80% of cases
• Lipase is preferred over amylase (more sensitive and specific)
• Atlanta 2012 classifies severity as mild/moderately severe/severe based on organ failure duration
• Early enteral nutrition in severe AP is strongly preferred over parenteral nutrition
• Antibiotics are NOT routinely given - only for infected necrosis
• Chronic pancreatitis causes irreversible damage, malabsorption, and diabetes

• Rosen's Emergency Medicine: Concepts and Clinical Practice, Chapter 77
• Sleisenger and Fordtran's Gastrointestinal and Liver Disease
• Textbook of Family Medicine, 9e