Chronic pancreatitis: Difference between revisions
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==Clinical Features<ref>Braganza, J. M., Lee, S. H., McCloy, R. F., & McMahon, M. J. (2011). Chronic pancreatitis. Lancet, 377(9772), 1184–1197. doi:10.1016/S0140-6736(10)61852-1</ref><ref>Steer, M. L., Waxman, I., & Freedman, S. (1995). Chronic pancreatitis. New England Journal of Medicine, 332(22), 1482–1490. doi:10.1056/NEJM199506013322206</ref>== | ==Clinical Features<ref>Braganza, J. M., Lee, S. H., McCloy, R. F., & McMahon, M. J. (2011). Chronic pancreatitis. Lancet, 377(9772), 1184–1197. doi:10.1016/S0140-6736(10)61852-1</ref><ref>Steer, M. L., Waxman, I., & Freedman, S. (1995). Chronic pancreatitis. New England Journal of Medicine, 332(22), 1482–1490. doi:10.1056/NEJM199506013322206</ref>== | ||
*Pain | *[[Abdominal pain|Pain]] | ||
**Episodic (1wk) or constant | **Episodic (1wk) or constant | ||
**Epigastric, radiating to back and left infrascapular region | **Epigastric, radiating to back and left infrascapular region | ||
**Associated with nausea/vomiting | **Associated with nausea/vomiting | ||
**Improved with sitting up or leaning forward | **Improved with sitting up or leaning forward | ||
*Steatorrhea/DM | *Steatorrhea/[[DM]] | ||
**Late finding | **Late finding | ||
**Requires >80-90% loss of exocrine and endocrine function | **Requires >80-90% loss of exocrine and endocrine function | ||
| Line 22: | Line 22: | ||
*Labs | *Labs | ||
**Lipase: Normal or slightly elevated | **Lipase: Normal or slightly elevated | ||
**Increased [[Hyperbilirubinemia|bilirubin]], alkaline phosphatase: Associated with compression of intrapancreatic bile duct (10-15%) | **[[LFTs]]: Increased [[Hyperbilirubinemia|bilirubin]], alkaline phosphatase: Associated with compression of intrapancreatic bile duct (10-15%) | ||
**Pancreatic function tests: Secretin stimulation | **Pancreatic function tests: Secretin stimulation | ||
**Gamma-globulin IgG elevation (IgG4) in autoimmune | **Gamma-globulin IgG elevation (IgG4) in autoimmune | ||
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*Lifestyle modifications (alcohol and tobacco cessation), dietary changes | *Lifestyle modifications (alcohol and tobacco cessation), dietary changes | ||
*Pancreatic enzyme supplements | *Pancreatic enzyme supplements | ||
*Acid suppression (H2 | *Acid suppression ([[H2 antagonist]], [[PPI]]) | ||
*Analgesics ([[NSAIDs]], [[opioids]], [[pregabalin]]) | *[[analgesia|Analgesics]] ([[NSAIDs]], [[opioids]], [[pregabalin]]) | ||
*Specialist referral for refractory pain | *Specialist referral for refractory pain | ||
Revision as of 19:51, 29 September 2019
Background
- Chronic imflammatory changes of the pancreas causing permanent structural damage
- Can be minimally symptomatic and presents with acute exacerbations.
- Can lead to both long term endocrine and exocrine dysfunction
Clinical Features[1][2]
- Pain
- Episodic (1wk) or constant
- Epigastric, radiating to back and left infrascapular region
- Associated with nausea/vomiting
- Improved with sitting up or leaning forward
- Steatorrhea/DM
- Late finding
- Requires >80-90% loss of exocrine and endocrine function
- Erythema ab igne
- Hyperpigmentation of upper abdomen
Differential Diagnosis
Epigastric Pain
- Gastroesophageal reflux disease (GERD)
- Peptic ulcer disease with or without perforation
- Gastritis
- Pancreatitis
- Gallbladder disease
- Myocardial Ischemia
- Splenic Infarctionenlargement/rupture/aneurysm
- Pericarditis/Myocarditis
- Aortic dissection
- Hepatitis
- Pyelonephritis
- Pneumonia
- Pyogenic liver abscess
- Fitz-Hugh-Curtis Syndrome
- Hepatomegaly due to CHF
- Bowel obstruction
- SMA syndrome
- Pulmonary embolism
- Bezoar
- Ingested foreign body
Evaluation
- Labs
- Imaging[3][4]
- Plain film: pancreatic calcifications (30%)
- CT: intraductal calcifications (insensitive for early disease)
- ERCP: gold standard
Management
- Lifestyle modifications (alcohol and tobacco cessation), dietary changes
- Pancreatic enzyme supplements
- Acid suppression (H2 antagonist, PPI)
- Analgesics (NSAIDs, opioids, pregabalin)
- Specialist referral for refractory pain
See Also
References
- ↑ Braganza, J. M., Lee, S. H., McCloy, R. F., & McMahon, M. J. (2011). Chronic pancreatitis. Lancet, 377(9772), 1184–1197. doi:10.1016/S0140-6736(10)61852-1
- ↑ Steer, M. L., Waxman, I., & Freedman, S. (1995). Chronic pancreatitis. New England Journal of Medicine, 332(22), 1482–1490. doi:10.1056/NEJM199506013322206
- ↑ Choueiri, N. E., Balci, N. C., Alkaade, S., & Burton, F. R. (2010). Advanced imaging of chronic pancreatitis. Current gastroenterology reports, 12(2), 114–120. doi:10.1007/s11894-010-0093-4
- ↑ Remer, E. M., & Baker, M. E. (2002). Imaging of chronic pancreatitis. Radiologic clinics of North America, 40(6), 1229–42– v.