Chronic pancreatitis

Epidemiology

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Etiology

• Chronic heavy alcohol use (most common, esp. men)
• Pancreatic ductal obstruction
• Tobacco use
• Idiopathic pancreatitis
• Hereditary pancreatitis
  • PRSS1 gene mutation
  • Age of onset < 20 years
  • Characterized by a positive family history and the absence of other risk factors
• Systemic disease
  • Cystic fibrosis
  • Severe hypertriglyceridemia (levels > 1,000 mg/dL)

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Pathophysiology

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Clinical features

• Epigastric abdominal pain (main symptom)
  • Pain radiates to the back, is relieved on bending forward, and is exacerbated after eating. c
  • Often associated with nausea and vomiting
• Features of pancreatic insufficiency: late manifestation (after 90% of the pancreatic parenchyma is destroyed)
  • Steatorrhea (exocrine enzyme deficiency)
    • Cramping abdominal pain, bloating, diarrhea
    • Can lead to a deficiency of fat-soluble vitamins (A, D, E, and K)
  • Malabsorption and weight loss
  • Pancreatic diabetes (endocrine hormone deficiency)

Complications

Pancreatic pseudocysts

• Pathology
  • Fluid collection rich in enzymes (Amylase, Lipase) and necrotic debris.
  • Lined by granulation tissue/fibrosis (NOT epithelium) $\to$ “Pseudo” cyst. t
  • Most common cystic lesion of pancreas.
• Etiology
  • Acute Pancreatitis (complication appearing 4–6 weeks post-onset).
  • Chronic Pancreatitis (most common).
  • Trauma.
• Clinical Features
  • Persistent epigastric pain/mass.
  • Early satiety or N/V (mass effect on stomach/duodenum).
• Diagnostics
  • CT Scan: Best initial test.
  • Labs: Persistently $\uparrow$ Serum Amylase weeks after acute episode.
• Treatment
  • Asymptomatic / < 6 cm: Conservative (Observation); spontaneous resolution common.
  • Symptomatic / > 6 cm / > 6 weeks: Drainage required (Percutaneous, Endoscopic Cystogastrostomy, or Surgical).

Pancreatic ascites

Pathophysiology

• Ductal disruption (due to an acute attack of pancreatitis, pancreatic surgery and/or trauma) or a pseudocyst leak/rupture → pancreatic ascites
• Pancreatic ascites develops when the pancreatic leak is not walled off by fibrous/granulation tissue. It is a rare complication (∼ 1%) that is mostly seen in patients with chronic pancreatitis secondary to heavy alcohol use.

Diagnostics

Ascitic fluid analysis: exudate (high protein: inline-measurement; low SAAG: inline-measurement) with high amylase levels (> 1,000 IU/L)

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Diagnostics

• Key Labs:
  • Amylase & Lipase: Often normal or only mildly elevated in late-stage CP (burnt-out parenchyma). c
  • Fecal elastase-1: Most sensitive and specific non-invasive functional test (<200 mcg/g indicates pancreatic insufficiency).
  • 72-hour fecal fat collection: Diagnostic gold standard for steatorrhea but rarely used due to patient non-compliance.
• Imaging:
  • Abdominal X-ray: High-yield if it shows pancreatic calcifications (highly specific for CP, but low sensitivity).
  • Abdominal CT (Initial imaging of choice): Shows pancreatic calcifications, parenchymal atrophy, and pancreatic duct dilation. c
  • MRCP (Confirmatory non-invasive test of choice): Exquisite visualization of ductal anatomy; reveals “chain of lakes” (alternating stenosis and dilation) or ductal stones.
  • Endoscopic Ultrasound (EUS): Most sensitive test for early-stage CP when calcifications are not yet visible on CT/MRCP.

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Treatment

• First-Line:
  • EtOH and smoking cessation (most effective intervention to slow disease).
  • Low-fat, small meals.
  • Pancreatic Enzyme Replacement Therapy (PERT): Enteric-coated lipase, protease, and amylase taken with meals (to digest them).
    • Acid suppression (PPI or H2RA) to prevent gastric acid degradation of non-enteric-coated enzymes if symptoms persist.
    • Normal serum lipase does not contraindicate oral pancreatic enzymes. It reflects leakage of pancreatic enzymes into the bloodstream, not the intestinal lumen. c
  • Non-opioid analgesics (Acetaminophen, NSAIDs) ± TCAs/gabapentinoids.
  • Fat-soluble vitamin supplementation.
• Second-Line:
  • Judicious opioids for refractory pain.
  • ERCP with stenting or lithotripsy for ductal stones/strictures.
  • Celiac plexus neurolysis/block for refractory visceral pain.
• Refractory / Surgical:
  • Puestow procedure (ductal decompression) if main duct is dilated (≥5–7 mm).
  • Resection (Whipple procedure) for disease localized to the pancreatic head.
  • Low-dose insulin for Type 3c DM (caution: high risk of hypoglycemia).

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