Acute Pancreatitis

Introduction

• Acute inflammatory process of the pancreas.
• Caused by an inciting event damaging the pancreatic parenchyma.
• Enzymes leak into the pancreas, causing autodigestion, further injury, and edema.
• Significant pancreatic edema and fat necrosis result.

Classification

• Mild Acute Pancreatitis: No organ failure or local/systemic complications.
• Moderately Severe Acute Pancreatitis: Transient organ failure (resolves within 48 hours) or local/systemic complications without persistent organ failure (>48 hours).
• Severe Acute Pancreatitis: Persistent organ failure, possibly affecting multiple organs.

Etiology

Mnemonic: GET SMASHED

• G: Gallstones – Obstruction of the duct causing backup into the pancreas (40-70% of cases).
• E: Ethanol – Damage to acinar cells from alcohol consumption (25-35% of cases).
• T: Trauma – Blunt abdominal trauma causing mechanical damage.
• S: Steroids
• M: Mumps
• A: Autoimmune Pancreatitis
• S: Scorpion Sting
• H: Hypercalcemia/Hypertriglyceridemia – High serum triglyceride concentrations leading to pancreatitis (1-14% of cases).
• E: ERCP – Post-ERCP pancreatitis in 3-25% of patients based on the procedure.
• D: Drugs – Especially sulfa drugs causing chemical injury.

Pathophysiology

• Different mechanisms for acinar cell injury:
  • Duct Obstruction: e.g., secondary to cholelithiasis, chronic alcoholism
  • Acinar Cell Injury: e.g., alcohol, certain drugs (Dido, valproic acid, tetracyclines)
  • Trauma, ischemia, viral infections (especially mumps)
• All causing enzyme activation, inflammation, edema, fat necrosis, and potential hemorrhage.

Signs and Symptoms

• Severe epigastric abdominal pain radiating to the back (90% of patients).
• Nausea and vomiting.
• Pain worsens when supine, improves in fetal position.
• Possible right upper quadrant pain or pain on the left side.
• Fever and tachycardia.
• Severe cases: dyspnea, pleural effusions, ARDS.
• Cullen Sign: Bluish discoloration around the umbilicus.
• Grey Turner Sign: Bluish-red discoloration along the flanks.
• Potential hypocalcemia, ARDS, hemodynamic instability.

Microscopic Findings

• Mild Form: Interstitial edema, focal areas of fat necrosis in pancreas and peri-pancreatic fat.

Gross Findings

• Red-black hemorrhagic areas with foci of yellow-white chalky fat necrosis.

Diagnosis

• Serum Levels: Elevated serum lipase (most specific), increased serum amylase, decreased calcium.

Imaging Modalities

• Abdominal and Chest Radiographs: Can range from unremarkable to localized ileus (sentinel loop/colon cutoff sign).
• Abdominal Ultrasound: Enlarge hypoechoic pancreas, possible gallstones.
• CT Scan: Focal/diffuse pancreatic enlargement, heterogeneous enhancement, peri-pancreatic fat stranding.

Diagnostic Criteria

• Acute persistent severe epigastric pain radiating to the back.
• Elevated serum lipase or amylase (>3 times normal).
• Characteristic imaging findings (CT/MRI/abdominal ultrasound).

Treatment

• Initial Management: Supportive care, fluid resuscitation, pain control, nutritional support.
• Fluid Replacement: Within first 12-24 hours to reduce morbidity/mortality.
• Mild Pancreatitis: Oral intake as tolerated once pain resolves.
• Severe Pancreatitis: Enteral nutrition in 24-48 hours, NPO, IV fluids, pancreatic rest.
• Gallstone Cause: Cholecystectomy.
• Pain Control: Intravenous opiates (morphine, fentanyl, PCA pump).

Possible Complications

• Multi-system organ failure (DIC, ARDS, serious cyst formation, necrotizing pancreatitis).

Key Takeaway

• Acute pancreatitis can be severe, requiring ICU care, and potential intubation.