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Pancreatitis

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Pancreatitis
SpecialtyGastroenterology Edit this on Wikidata

Pancreatitis is inflammation of the pancreas. It occurs when pancreatic enzymes (especially trypsin) that digest food are activated in the pancreas instead of the small intestine. It may be acute – beginning suddenly and lasting a few days, or chronic – occurring over many years. It has multiple causes and symptoms.

Symptoms

The most common symptoms of pancreatitis are severe upper abdominal pain radiating to the back, nausea, and vomiting that is worsened with eating. The physical exam will vary depending on severity and presence of internal bleeding. Blood pressure may be elevated by pain or decreased by dehydration or bleeding. Heart and respiratory rates are often elevated. The abdomen is usually tender but to a lesser degree than the pain itself. As is common in abdominal disease, bowel sounds may be reduced from reflex bowel paralysis. Fever or jaundice may be present. Chronic pancreatitis can lead to diabetes or pancreatic cancer. Unexplained weight loss may occur from a lack of pancreatic enzymes hindering digestion.

Causes

The most common cause of acute pancreatitis is gallstones, which can form to cause inflammation in the pancreas as they pass through the common bile duct.[1][2] Long-term alcohol abuse is the most common cause of the chronic form,[3][4][5][6] which can result from a single acute instance if the cause is not addressed.

Some medications are associated, commonly including the AIDS drugs didanosine and pentamidine, diuretics, the anticonvulsant valproic acid, the chemotherapeutic agents L-asparaginase andazathioprine, estrogen by way of increased blood triglycerides,[7] and cholesterol-lowering statins.[citation needed]

There is an inherited form that results in the activation of trypsinogen within the pancreas, leading to autodigestion. Involved genes may include Trypsin 1, which codes for trypsinogen, SPINK1, which codes for a trypsin inhibitor, or cystic fibrosis transmembrane conductance regulator.[8]

Other common causes include trauma, steroid use, mumps, autoimmune disease, scorpion stings, high blood calcium, high blood triglycerides, hypothermia, and endoscopic retrograde cholangiopancreatography (ERCP). Pancreas divisum is a common congenital malformation of the pancreas that may underlie some recurrent cases. Pregnancy can be a cause, possibly by increasing blood triglycerides. Diabetes mellitus type 2 is associated with a 2.8-fold higher risk.[9]

Less common causes include pancreatic cancer, pancreatic duct stones,[10] vasculitis (inflammation of the small blood vessels in the pancreas), coxsackievirus infection, and porphyria—particularly acute intermittent porphyria and erythropoietic protoporphyria.

Diagnosis

Diagnosing pancreatitis requires two of the following:

Amylase or lipase is frequently part of the diagnosis; lipase is generally considered a better indicator,[11][12][13][14][15][16][17] but this is disputed.[18][19] Cholecystitis, perforated peptic ulcer, bowel infarction, and diabetic ketoacidosis can mimic pancreatitis by causing similar abdominal pain and elevated enzymes.[citation needed] The diagnosis can be confirmed by ultrasound or CT, but this is usually unnecessary,[20] and CT contrast may exacerbate the condition.[21]

Treatment

The treatment of pancreatitis is supportive and depends on severity. Morphine is preferred for pain relief. Oral intake, especially fats, are restricted. Fluids and electrolytes are replaced intravenously. When possible, the underlying cause is treated, such as by ERCP for gallstones or antibiotics for a bacterial infection. The patient is monitored for complications.

Prognosis

Several scoring systems are used to predict the severity of an attack of pancreatitis. They each combine demographic and laboratory data to estimate severity or probability of death. Examples include APACHE II, Ranson, and Glasgow. Apache II is available on admission; Glasgow and Ranson are simpler but cannot be determined for 48 hours. One form of the Glasgow criteria suggests that a case be considered severe if at least three of the following are true:[22]

Complications

Early complications include shock, infection, systemic inflammatory response syndrome, low blood calcium, high blood glucose, and dehydration. Blood loss, dehydration, and fluid leaking into the abdominal cavity can lead to kidney failure. Respiratory complications are often severe. Pleural effusion is usually present. Shallow breathing from pain can lead to lung collapse. Pancreatic enzymes may attack the lungs, causing inflammation.

Late complications include recurrent pancreatitis and the development of pancreatic pseudocysts—collections of pancreatic secretions that have been walled off by scar tissue. These may cause pain, become infected, rupture and bleed, block the bile duct and cause jaundice, or migrate around the abdomen. Acute necrotizing pancreatitis can lead to a pancreatic abscess, a collection of pus caused by necrosis, liquefaction, and infection. This happens in approximately 3% of cases,[23] or almost 60% of cases involving more than two pseudocysts and gas in the pancreas.

References

  1. ^ Pancreatitis at hih.gov
  2. ^ http://www.umm.edu/altmed/articles/pancreatitis-000122.htm
  3. ^ http://www.medscape.com/viewarticle/706319
  4. ^ http://www.sciencedaily.com/releases/2009/06/090608162430.htm
  5. ^ http://www.betterhealth.vic.gov.au/bhcv2/bhcarticles.nsf/pages/pancreatitis_explained?opendocument
  6. ^ . PMC 1379177 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1379177. {{cite journal}}: Cite journal requires |journal= (help); Missing or empty |title= (help)
  7. ^ Page 584, Oxford Handbook of Clinical Medicine, 7th Edition, ISBN 9780198568377
  8. ^ D. Whitcomb (2006). "Genetic Testing for Pancreatitis".
  9. ^ http://care.diabetesjournals.org/content/32/5/834.abstract
  10. ^ Macaluso JN: Editorial Comment: re ESWL for obstructing pancreatic calculi. Journal of Urology, Vol 158, #2, 522–525, August 1997
  11. ^ a b Banks P, Freeman M (2006). "Practice guidelines in acute pancreatitis". Am J Gastroenterol. 101 (2379–400): 2379–400. doi:10.1111/j.1572-0241.2006.00856.x. PMID 17032204.
  12. ^ UK Working Party on Acute Pancreatitis (2005). "UK guidelines for the management of acute pancreatitis". Gut. 54 Suppl 3: iii1. doi:10.1136/gut.2004.057026. PMC 1867800. PMID 15831893.
  13. ^ Smith RC, Southwell-Keely J, Chesher D (2005). "Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis?". ANZ J Surg. 75 (6): 399–404. doi:10.1111/j.1445-2197.2005.03391.x. PMID 15943725. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  14. ^ Treacy J, Williams A, Bais R; et al. (2001). "Evaluation of amylase and lipase in the diagnosis of acute pancreatitis". ANZ J Surg. 71 (10): 577–82. doi:10.1046/j.1445-2197.2001.02220.x. PMID 11552931. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  15. ^ Steinberg WM, Goldstein SS, Davis ND, Shamma'a J, Anderson K (1985). "Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity". Ann. Intern. Med. 102 (5): 576–80. PMID 2580467. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  16. ^ Lin XZ, Wang SS, Tsai YT; et al. (1989). "Serum amylase, isoamylase, and lipase in the acute abdomen. Their diagnostic value for acute pancreatitis". J. Clin. Gastroenterol. 11 (1): 47–52. doi:10.1097/00004836-198902000-00011. PMID 2466075. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  17. ^ Keim V, Teich N, Fiedler F, Hartig W, Thiele G, Mössner J (1998). "A comparison of lipase and amylase in the diagnosis of acute pancreatitis in patients with abdominal pain". Pancreas. 16 (1): 45–9. doi:10.1097/00006676-199801000-00008. PMID 9436862. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  18. ^ Ignjatović S, Majkić-Singh N, Mitrović M, Gvozdenović M (2000). "Biochemical evaluation of patients with acute pancreatitis". Clin. Chem. Lab. Med. 38 (11): 1141–4. doi:10.1515/CCLM.2000.173. PMID 11156345. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  19. ^ Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP (1996). "What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study". Mayo Clin. Proc. 71 (12): 1138–44. doi:10.4065/71.12.1138. PMID 8945483. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  20. ^ Fleszler F, Friedenberg F, Krevsky B, Friedel D, Braitman L (2003). "Abdominal computed tomography prolongs length of stay and is frequently unnecessary in the evaluation of acute pancreatitis". Am J Med Sci. 325 (5): 251–5. doi:10.1097/00000441-200305000-00001. PMID 12792243.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ McMenamin D, Gates L (1996). "A retrospective analysis of the effect of contrast-enhanced CT on the outcome of acute pancreatitis". Am J Gastroenterol. 91 (7): 1384–7. PMID 8678000.
  22. ^ Corfield AP, Cooper MJ, Williamson RC; et al. (1985). "Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices". Lancet. 2 (8452): 403–7. doi:10.1016/S0140-6736(85)92733-3. PMID 2863441. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  23. ^ "Pancreatic abscess". Retrieved 2010-04-19.
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