Pancreatitis

1. Anatomy Recap

2. Pathophysiology

1. Inappropriate activation of trypsinogen → trypsin - activating other digestive enzymes
2. Autodigestion of pancreatic parenchyma and surrounding fat
3. Inflammatory cascade - macrophage and neutrophil recruitment, cytokine release
4. Increased vascular permeability - edema, hemorrhage, necrosis
5. SIRS → sepsis, shock if uncontrolled, with bacteremia from intestinal flora translocation
6. Extrapancreatic organ dysfunction - ARDS, pleural effusions, renal failure - Rosen's Emergency Medicine, p. 1265

3. Etiology

4. Pathology

Acute Pancreatitis

• Edematous: interstitial edema, fat necrosis, minimal parenchymal necrosis
• Necrotizing: widespread hemorrhagic necrosis; in 40-60% of necrotizing cases, debris becomes infected - greatly worsening prognosis

Chronic Pancreatitis

• Gross: Hard gland, dilated ducts, visible calcific concretions
• Microscopy: Parenchymal fibrosis, loss of acini, variable ductal dilation, chronic inflammatory infiltrate around lobules and ducts; relative sparing of islets of Langerhans initially, but eventual islet destruction leads to diabetes
• Autoimmune pancreatitis (IgG4-related): Dense lymphoplasmacytic infiltrate with IgG4+ plasma cells, "swirling" fibrosis, venulitis (lymphocytic sclerosing pancreatitis) - Robbins & Kumar, p. 644-645

5. Clinical Features

Acute Pancreatitis

• Pain: Persistent epigastric or LUQ pain, radiating to the back/chest/flanks; moderate to severe; intensity does not correlate with severity; may be alleviated by sitting forward
• Associated: Nausea, vomiting, anorexia (oral intake worsens pain)
• Signs:
  • Fever, tachycardia, tachypnea (SIRS)
  • Hypotension/shock in severe disease
  • Epigastric tenderness ± guarding
  • Cullen sign (periumbilical bluish discoloration - hemoperitoneum) - rare, poor prognosis
  • Grey Turner sign (reddish-brown flank discoloration - retroperitoneal bleed) - rare, poor prognosis
  • Jaundice suggests obstruction (gallstone, tumor)
  • Diminished/absent bowel sounds with ileus
  • Pleural effusions in up to 50% (more often left-sided)
• Systemic complications: ARDS, cardiovascular collapse, renal failure, DIC, coagulopathy, hyperglycemia, hypocalcemia - Rosen's Emergency Medicine, p. 1265-1266

Chronic Pancreatitis

• Recurrent or persistent abdominal and back pain (most common symptom)
• Jaundice from ductal compression
• Weight loss, hypermetabolism, malabsorption
• Exocrine insufficiency (steatorrhea)
• Diabetes mellitus (from eventual islet destruction)
• May be silent until complications develop - Robbins & Kumar, p. 645

6. Diagnosis

Diagnostic Criteria (Atlanta Classification)

1. Characteristic abdominal pain
2. Serum lipase or amylase >3x upper limit of normal
3. Characteristic findings on imaging

Laboratory Tests

Imaging

• Abdominal US: First-line for biliary etiology (gallstones); limited for direct pancreatic visualization (obscured by bowel gas)
• CT with IV contrast: NOT routine; indicated for: (1) diagnostic uncertainty, (2) ruling out other pathology, (3) assessing complications at 48-72h of non-response - best done at 3-7 days; >90% sensitivity and specificity; pancreatic necrosis = non-enhancing areas; normal in 15-30% of mild cases
• MRI/MRCP: Superior biliary/ductal imaging; useful when contrast is contraindicated
• EUS: Biliary tract assessment, surgical planning

Local Complications (Revised Atlanta 2012)

7. Severity Scoring

• Severe AP: persistent multi-organ failure >48 hours, ICU admission, mechanical ventilation
• Scoring systems (Ranson, APACHE-II, BISAP, CT Severity Index/CTSI) are used to predict mortality and guide disposition

8. Management

Acute Pancreatitis - General Principles

• Aggressive early IV fluid resuscitation is the cornerstone of management
• Recent evidence (2025 meta-analysis, PMID 40085761) favors Lactated Ringer's solution over normal saline for reducing progression to moderate-to-severe AP

• Adequate pain control; IV opioids as needed

• Previous practice of NPO ("pancreatic rest") has been replaced by early enteral nutrition (EN)
• Severe AP (ICU, SIRS, mechanical ventilation): NG/NJ tube + EN initiated within 24-36 hours of admission
• Mild-moderate AP (ward patient): Oral diet as tolerated; EN only if diet fails to advance after 4 days
• EN vs. PN: Meta-analyses show EN provides 2-fold reduction in infectious complications and 2.5-fold reduction in mortality vs. parenteral nutrition (PN)
• Gastric vs. jejunal feeding: No significant clinical difference in severe AP - Sleisenger & Fordtran, p. 2935-2939

• Gallstone pancreatitis + cholangitis/obstruction: urgent ERCP
• Hypertriglyceridemia: insulin infusion, plasmapheresis if triglycerides >1000 mg/dL
• Drugs: discontinue offending agent

• Antibiotics + drainage (endoscopic, percutaneous, or surgical - "step-up approach")
• Surgery reserved for failed minimally invasive drainage or abdominal compartment syndrome

• Watch for ARDS, renal failure, DIC, hyperglycemia, hypocalcemia, splenic/portal vein thrombosis

Chronic Pancreatitis Management

• Alcohol/smoking cessation
• Pancreatic enzyme replacement for exocrine insufficiency
• Pain management: NSAIDs, opioids, antioxidants (selenium, ascorbic acid, beta-carotene, alpha-tocopherol, methionine - evidence mixed)
• Jejunal feeding to improve weight and reduce pain in severe cases
• Endoscopic or surgical decompression for ductal hypertension
• Autoimmune pancreatitis: Steroids ± anti-B cell therapy (responds well)
• Monitor and treat diabetes mellitus

9. Differential Diagnosis

• Peptic ulcer disease / perforated peptic ulcer
• Acute cholecystitis / cholangitis / choledocholithiasis
• Mesenteric ischemia / bowel infarction
• Aortic dissection / abdominal aortic aneurysm
• Myocardial infarction (inferior/posterior)
• Pneumonia, pericarditis
• Sickle cell crisis, DKA

Recent Evidence (2024-2026)