• Clinical science

Chronic pancreatitis

Summary

Chronic pancreatitis (CP) is caused by progressive inflammation and irreversible damage to the structure and function (exocrine and endocrine) of the pancreas. Chronic heavy alcohol use is the most common cause, followed by pancreatic ductal obstruction. Idiopathic pancreatitis accounts for up to 30% of cases. Patients may be asymptomatic or present with abdominal pain and features of pancreatic enzyme insufficiency (e.g., steatorrhea, weight loss, impaired glucose tolerance). Diagnosis is confirmed on imaging, which demonstrates pancreatic calcifications, ductal strictures, and ductal dilations. Pancreatic function tests (e.g., fecal elastase-1 measurement, 72-hour fecal fat estimation) assess the degree of enzyme deficiency. Symptomatic patients are managed with oral pancreatic enzyme replacements and analgesics. Patients with chronic pain require additional interventions (e.g., celiac ganglion block, partial/complete pancreatic resection).

Etiology

Pathophysiology

  • Autodigestion and inflammation: damage to pancreatic acinar cells; (e.g., alcohol), outflow obstruction of pancreatic enzymes or premature activation of trypsinogen to trypsin intrapancreatic activation of digestive enzymes (e.g., amylase and lipase) → autodigestion of pancreatic tissue inflammatory reaction
  • Fibrosis: exposure to toxins and/or inflammatory mediators (e.g., alcohol, cytokines) → activation of pancreatic stellate cells

References:[4]

Clinical features

In the later stages of chronic pancreatitis, patients may not experience any pain.References:[1][5]

Subtypes and variants

Autoimmune pancreatitis [6]
Autoimmune pancreatitis type I Autoimmune pancreatitis type II
Definition
Epidemiology
  • >
  • =
Etiology
Clinical features
  • Asymptomatic jaundice (∼ 60%)
  • Epigastric pain and features of pancreatic insufficiency (see “Clinical features” above)
  • Multiorgan involvement (IgG4-associated autoimmune diseases)
  • Obstructive jaundice
  • Epigastric pain and features of pancreatic insufficiency (see “Clinical features” above)
Diagnostics Serology
  • Characterized by ↑ IgG4
  • Often normal findings
Histology
Management
Prognosis [7]
  • Relapse rate: ∼ 50%
  • Rarely relapses

Diagnostics

Approach [8]

The STEP-wise approach involves Survey, Tomography/imaging, Endoscopy, and Pancreatic function testing.

Laboratory tests

  • Serum pancreatic enzyme levels: Lipase (specific) and amylase (nonspecific) are often normal .

In chronic pancreatitis, pancreatic enzyme levels are often normal and cannot be used to confirm or rule out the diagnosis. In contrast, acute pancreatitis typically causes significant enzyme elevation.

Pancreatic function tests

Imaging [8][11]

  • Abdominal CT (plain and contrast-enhanced CT): best initial imaging modality to screen for CP
  • ERCP: detection of early pathologies and simultaneous treatment possible (e.g., duct dilation, stent insertion)
    • Ductal stones, which are visible as filling defects
    • Chain of lakes” or “string of pearls” appearance (characteristic feature)
    • Irregularity and/or dilation of the main pancreatic duct
  • MRCP [12]
    • Indicated when CT findings are equivocal but clinical suspicion of CP is high
    • Findings
      • Ductal strictures and dilations
      • Pancreatic calcifications
  • Abdominal ultrasound
    • Indistinct margins and enlargement
    • Pancreatic calcifications
    • Ductal strictures, dilation, or stones
  • Endoscopic ultrasound (EUS)
    • An invasive test that is reserved for cases in which a CT scan and/or MRCP are nondiagnostic (can detect early changes of CP )
    • Findings
      • Parenchymal lobularity and hyperechoic foci
      • Ductal dilation and calcification [13]
  • Abdominal x-ray: visible pancreatic calcifications (highly specific, but only seen in ∼ 30% of cases)

Genetic testing [14]

Indications: family history of chronic pancreatitis, young patients with idiopathic pancreatitis

Treatment

General measures

  • Abstinence from alcohol and nicotine
  • Pancreatic enzyme replacement (with meals)
  • Small, regular meals (rich in carbohydrates, low in fat)
  • Supplementation with medium-chain triglycerides (MCT)
  • Parenteral administration of fat-soluble vitamins (A, D, E, K) if necessary
  • Endocrine insufficiency: insulin administration
  • For more information on the management of acute attacks, see “Acute pancreatitis”.

Pain management

Surgery

Complications

Pancreatic insufficiency

Tissue atrophy and fibrosis cause:

Pancreatic pseudocysts [17]

  • Definition: encapsulated collection of pancreatic fluid that develops 4 weeks after an acute attack of pancreatitis; (can occur in both acute and chronic pancreatitis )
  • Pathophysiology: pancreatic secretions leak from damaged ducts → inflammatory reaction of surrounding tissue → encapsulation of secretions by granulation tissue
  • Clinical features [18]
  • Diagnostics: abdominal ultrasound/CT/MRI
    • Extrapancreatic fluid collection within well-defined wall/capsule
    • No solid cyst components detectable
  • Treatment
    • Cystogastrostomy/cystoduodenostomy/cystojejunostomy
    • Ultrasound/CT-guided percutaneous drainage
  • Complications
    • Infection → fever, abdominal pain, sepsis
    • Pseudocyst rupture → pancreatic ascites/pancreaticopleural fistula
    • Erosion into an abdominal vessel → hemorrhage into the cyst → sudden abdominal pain, signs of hemorrhagic shock

Splenic vein thrombosis [19]

Pancreatic ascites

Further complications

We list the most important complications. The selection is not exhaustive.

  • 1. Apte MV, Pirola RC, Wilson JS. Mechanisms of alcoholic pancreatitis. J Gastroenterol Hepatol. 2010; 25(12): pp. 1816–1826. doi: 10.1111/j.1440-1746.2010.06445.x.
  • 2. Howes N, Greenhalf W, Stocken DD, Neoptolemos JP. Cationic Trypsinogen Mutations and Pancreatitis. Clin Lab Med. 2005; 25(1): pp. 39–59. doi: 10.1016/j.cll.2004.12.004.
  • 3. De Boeck K, Weren M, Proesmans M, Kerem E. Pancreatitis among patients with cystic fibrosis: correlation with pancreatic status and genotype. Pediatrics. 2005; 115(4): pp. e463–469. doi: 10.1542/peds.2004-1764.
  • 4. Masamune A, Watanabe T, Kikuta K, Shimosegawa T. Roles of pancreatic stellate cells in pancreatic inflammation and fibrosis. Clin Gastroenterol Hepatol. 2009; 7(11 Suppl): pp. S48–54. doi: 10.1016/j.cgh.2009.07.038.
  • 5. Kalloo AN, Norwitz L, Yeo CJ. Chronic Pancreatitis. url: http://www.hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/pancreas_biliary_tract/chronic_pancreatitis.pdf Accessed March 20, 2017.
  • 6. De Pretis N, Frulloni L. Autoimmune pancreatitis type 2. Curr Opin Gastroenterol. 2020; 36(5): pp. 417–420. doi: 10.1097/mog.0000000000000655.
  • 7. Sah RP, Chari ST, Pannala R, et al. Differences in Clinical Profile and Relapse Rate of Type 1 Versus Type 2 Autoimmune Pancreatitis. Gastroenterology. 2010; 139(1): pp. 140–148. doi: 10.1053/j.gastro.2010.03.054.
  • 8. Barry K. Chronic Pancreatitis: Diagnosis and Treatment. Am Fam Physician. 2018; 97(6): pp. 385–393. pmid: 29671537.
  • 9. Nandhakumar N, Green MR. Interpretations: How to use faecal elastase testing. Archives of Disease in Childhood - Education and Practice. 2010; 95(4): pp. 119–123. doi: 10.1136/adc.2009.174359.
  • 10. DiMagno MJ. Pancreatic Function Tests. Elsevier; 2004: pp. 76–77.
  • 11. Conwell DL et al. American Pancreatic Association Practice Guidelines in Chronic Pancreatitis: evidence-based report on diagnostic guidelines. Pancreas. 2014; 43(8): pp. 1143–62. doi: 10.1097/MPA.0000000000000237.
  • 12. Conwell DL, Wu BU. Chronic Pancreatitis: Making the Diagnosis. Clinical Gastroenterology and Hepatology. 2012; 10(10): pp. 1088–1095. doi: 10.1016/j.cgh.2012.05.015.
  • 13. Duggan SN, Chonchubhair HMN, Lawal O, O'Connor DB, Conlon KC. Chronic pancreatitis: A diagnostic dilemma. World J Gastroenterol. 2016; 22(7): pp. 2304–2313. doi: 10.3748/wjg.v22.i7.2304.
  • 14. Witt H. The SPINK in chronic pancreatitis: similar finds, different minds. Gut. 2002; 50(5): pp. 590–591. doi: 10.1136/gut.50.5.590.
  • 15. Maher JW, Johlin FC, Pearson D. Thoracoscopic splanchnicectomy for chronic pancreatitis pain. Surgery. 1996; 120(4): pp. 603–609. pmid: 8862367.
  • 16. Hart PA, et al. Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer. The Lancet Gastroenterology & Hepatology. 2016; 1(3): pp. 226–237. doi: 10.1016/s2468-1253(16)30106-6.
  • 17. U.S. National Library of Medicine. Pancreatic pseudocyst. https://medlineplus.gov/ency/article/000272.htm. Updated October 16, 2019. Accessed November 13, 2020.
  • 18. Go VLW, Maule WF, Reber HA. The Pancreas: biology, pathobiology, and disease. Raven Press; 1993.
  • 19. Akhondi H, Ganjali S, Nagalli S. Splanchnic Venous Thrombosis. StatPearls. 2020. pmid: 31985963.
  • 20. Kozarek RA. Management of pancreatic ascites. Gastroenterol Hepatol. 2007; 3(5): pp. 362–264. url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3099317/.
  • 21. Kanneganti K, Srikakarlapudi S, Acharya B, Sindhaghatta V, Chilimuri S. Successful Management of Pancreatic Ascites with both Conservative Management and Pancreatic Duct Stenting. Gastroenterology Res. 2009; 2(4): pp. 245–247. doi: 10.4021/gr2009.08.1306.
  • Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
  • Jackson CS, Piscoya A. Chronic pancreatitis. http://www.dynamed.com/topics/dmp~AN~T116518/Chronic-pancreatitis. Updated November 16, 2018. Accessed July 8, 2019.
last updated 11/26/2020
{{uncollapseSections(['MC0MsR', 'KC0UGR', 'WPcPdc0', 'JC0sGR', 'PPcWUc0', 'rC0ftR', 'sC0ttR', 'GC0BtR'])}}