Chronic Pancreatitis

Sobia Siddiqui

Definition

A syndrome characterized by irreversible chronic progressive pancreatic inflammation, fibrosis, and scarring, resulting in damage to and loss of exocrine (acinar), endocrine (islet cells), and ductal cells.

Etiology (TIGAR-O)

  • Toxic Metabolic: EtOH, tobacco use (independent risk factor), hyperCa (Ca >12), hypertriglyceridemia (fasting TG >300, nonfasting >500), CKD, medications, toxins.
  • Idiopathic: Early onset (age <35), late onset (age >35).
  • Genetic: Autosomal dominant (PRSS1 gene), recessive (CFTR, SPINK1, etc.).
  • Autoimmune: IgG4-related (AIP type 1), AIP type 2.
  • Recurrent, severe acute pancreatitis.
  • Obstructive: Pancreas divisum, ampullary stenosis, main duct pancreatic stones or strictures, widespread calcifications, mass causing duct obstruction.

Presentation

  • Abdominal pain (most common).
  • Exocrine insufficiency: Diarrhea, steatorrhea, weight loss (typically occurs later in disease process).
  • Endocrine insufficiency: Diabetes.
  • Occasionally asymptomatic.

Evaluation

  • Labs: 
    • BMP, LFTs, lipid panel, PEth.
    • Lipase and amylase levels can be elevated, but can be normal due to pancreatic scarring and fibrosis.
    • Gold standard for EPI: 72-hour fecal fat (>7g fat/ 100g stool/ day) - rarely done.
    • More practical: fecal elastase (<100 μg/g = severe EPI, 100-200 = indeterminate, >200 = normal. 
      • Note: Must be performed on formed stool, false positives occur with watery specimens, do not need to stop pancreatic enzymes to measure.
    • Consider genetic testing, especially in patients <35 years, those without clear etiology, or with family history of pancreatic disease.
    • Pancreatic function testing diagnoses exocrine insufficiency but is not necessary for diagnosis of CP.
  • Imaging: 
    • CT or MRI should be first-line imaging modalities (may be negative early in disease course) If CT or MRI negative but suspicion remains high, consider EUS ± biopsy or secretinenhanced MRCP.

Management

  • Lifestyle Modifications are 1st line: Tobacco and EtOH cessation.
  • Pancreatic enzyme replacement therapy: for any patient with symptoms of malabsorption or diagnosed exocrine insufficiency.
    • Usual dose: 50,000 units/meal + 25,000 units with snacks. 
      • Should take during the meal (distributed throughout) to maximize mixing with foo.
      • If lack of response: Increase dose, confirm compliance, add PPI, split dose throughout meal, evaluate for concurrent GI disorders (SIBO, celiac).
  • Pain: Follow analgesic ladder approach.
    •  Acetaminophen + NSAIDs -> pregabalin, gabapentin, TCAs, SNRIs ->tramadol ->strong opioids.
    • For refractory pain, celiac plexus block (temporary effect, bridge to surgery) or total pancreatectomy with islet autotransplantation (TPIAT).
  • Antioxidants (selenium, ascorbic acid, β-carotene, methionine, vitamin E): Mixed evidence, may be considered given potential benefit and absence of adverse effects.
  • Nutritional Support: MV, Vit D, Ca. 
    • Routine testing for osteoporosis and fat-soluble vitamin deficiencies.
    • Avoid dietary fat restriction (can worsen weight loss and vitamin deficiencies).
  • Screen for diabetes annually in chronic pancreatitis.
  • Pancreatic cancer routine surveillance is NOT recommended for non-hereditary chronic pancreatitis.
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