Chronic Pancreatitis

Snapshot

  • A 32-year-old female is brought to the emergency room by her husband for severe abdominal pain. The patient reports that the pain began 4 hours again and is 10/10, sharp, and radiates to her back. She has had multiple similar episodes in the past that have resolved with opioid analgesics. She reports a 6-lbs. weight loss over the past 4 months and stools that are difficult to flush.  A CT scan demonstrastes dystrophic calcifications of the pancreas.

Introduction

  • Clinical definition
    • condition characterized by a long-standing, progressive inflammation of the pancreas leading to permanent alterations in the organ’s normal structure and functions
    • damage of the organ leads to impairment of exocrine and endocrine function 
      • malabsorption leading to fat soluble vitamin (D, E, A, and K) deficiencies 
      • diabetes due to pancreas’ inability to produce insulin
  • Epidemiology
    • demographics
      • alcoholism is the most common cause in the United States
  • Pathogenesis
    • there are various etiologies that can lead to chronic pancreatitis 
      • alcohol abuse  
      • smoking
      • genetic causes (e.g., cystic fibrosis or hereditary pancreatitis)
      • ductal obstruction (e.g., trauma, pseudocysts, stones, tumors, or pancreas divisum)
      • tropical pancreatitis
      • systemic diseases (e.g., systemic lupus erythematous, hypertriglyceridemia, or hyperparathyroidism)
      • autoimmune pancreatitis
      • idiopathic pancreatitis
    • the pathophysiology of chronic pancreatitis is not fully understood but some theories to its development are as follows
      • proteinaceous ductal plug secondary to increased secretion of pancreatitic proteins
        • plugs acts a nidus for calcification leading to stone formation, ductal lesions, and subsequent inflammatory changes
      • ischemia likely important in exacerbating and facilitating the disease
      • lack of antioxidants (e.g., selenium, vitamin C and E, and methionine) leading to increases in free radicals
      • autoimmune mechanisms, as a number of autoimmune disorders (e.g., autoimmune pancreatitis) have been linked to chronic pancreatitis
  • Associations 
  • increased risk of pancreatic cancer 

Presentation

  • Symptoms
    • abdominal pain
      • often epigastric with radiation to the back relieved by leaning forward
      • worse 15-30 minutes after eating
      • repeated pain attacks
    • nausea
    • vomiting
    • steatorrhea
    • constipation
    • flatulence
  • Physical exam
  • weight loss

Imaging

  • Abdominal computed tomography (CT) with contrast
    • best initial imaging
    • positive findings include calcifications within the pancreas, ductal dilation, enlargement of the pancreas, and fluid collections (e.g., pseudocysts) adjacent to the gland  
  • Magnetic resonance cholangiopancreatography (MRCP)
    • becoming the diagnostic test of choice
    • no radiation risk
    • allows for better detection of calcifications and pancreatic duct obstruction consistent with chronic pancreatitis
  • Endoscopic retrograde cholangiopancreatography
  • indicated in patients with no calcifications on imaging and have the potential need of therapeutic intervention

Studies 

  • Laboratory studies
    • normal to minimally elevated of amylase and/or lipase
      • should not be used for the diagnosis of chronic pancreatitis
    • CBC, electrolytes, and liver functions tests
      • typically normal
      • may see elevations in serum bilirubin and alkaline phosphatase
    • HbA1c levels for evaluation of diabetes
  • Pancreatic function tests
    • secretin pancreatitic function test
      • low levels of bicarbonate concentration following secretin administration indicates exocrine pancreatic insufficiency
    • stool elastase (< 200 mcg/g)
  • low serum trypsinogen (< 20ng/mL)

Differential 

  • Pancreatic cancer
    • differentiating factors
      • lesion will be visible on imaging with further support from ERCP findings if needed
  • Acute pancreatitis
    • differentiating factors
  • clinical presentation (e.g., pain characteristic) and history as well as serum lipase and/or amylase levels

Treatment

  • Lifestyle and dietary modifications 
    • cessation of alcohol and tobacco
    • dietary modifications (eat small meals that are low in fat)
    • acid suppression (e.g.. proton pump inhibitor) along with pancreatic enzyme supplements (e.g., lipase) for pain management and malabsorption
    • oral hypoglycemic agents or insulin therapy if needed
    • vitamin supplementations (e.g., vitamins A, D, E, K, and B12)
  • Pain management 
    • analgesics with opiates and/or nonsteroidal anti-inflammatory agents
      • indicated if pancreatic enzyme therapy fails to control pain
      • can be used with adjuvant pregabalin
    • other approaches for pain management include
      • endoscopic therapy
      • extracorporeal shock wave lithotripsy
      • celiac nerve block
  • Surgery 
    • generally indicated in patients who fail medical therapy
  • approaches include decompression/drainage, pancreatic resections, and denervation procedures

Complications 

  • Chronic pain with addiction to analgesics
  • May have exocrine and endocrine insufficiency
  • Pancreatic pseudocyst
  • Ductal obstruction
  • Increased risk of pancreatic cancer