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Pancreatitis

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Pancreatitis

Pancreatitis
Classification and external resources
ICD-10 K85, K86.0–K86.1
ICD-9 577.0-577.1
OMIM 167800
DiseasesDB 24092
MedlinePlus 001144
eMedicine emerg/354
MeSH D010195

Pancreatitis is defined as inflammation of the pancreas. It has several causes and symptoms and requires immediate medical attention. 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.

Signs and symptoms

The most common symptoms of pancreatitis are severe upper abdominal or left upper quadrant burning pain radiating to the back, nausea, and vomiting that is worsened with eating. The physical examination 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

Eighty percent of cases of pancreatitis are caused by alcohol or gallstones. Gallstones are the single most common etiology of acute pancreatitis.[1] Alcohol is the single most common etiology of chronic pancreatitis.[2][3][4][5][6]

Some medications are commonly associated with pancreatitis, most commonly corticosteroids such as prednisolone, but also including the HIV drugs didanosine and pentamidine, diuretics, the anticonvulsant valproic acid, the chemotherapeutic agents L-asparaginase and azathioprine, estrogen by way of increased blood triglycerides,[7] and antihyperglycemic agents like metformin,[8] vildagliptin,[9] sitagliptin.[10] It may be noted here that the drugs which are used to treat conditions which are themselves associated with increased events of pancreatitis may also be incidentally linked to pancreatitis. Examples include statins in dyslipidemia and gliptins in diabetes. According to the Food and Drug Administration's MedWatch Surveillance System and Published Reports Atypical, atypical antipsychotics such as clozapine, risperidone, and olanzapine can also be responsible for causing pancreatitis.[11]

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.[12]

Other common causes include trauma, mumps, autoimmune disease, high blood calcium, hypothermia, and endoscopic retrograde cholangiopancreatography (ERCP). Pancreas divisum is a common congenital malformation of the pancreas that may underlie some recurrent cases. Diabetes mellitus type 2 is associated with a 2.8-fold higher risk.[13]

Less common causes include pancreatic cancer, pancreatic duct stones,[14] vasculitis (inflammation of the small blood vessels in the pancreas), coxsackievirus infection, and porphyria—particularly acute intermittent porphyria and erythropoietic protoporphyria.

The mnemonic GETSMASHED is often used to remember the common causes of Pancreatitis: G - Gall stones E - Ethanol T - Trauma S - Steroids M - Mumps A - Autoimmune Pancreatitis S - Scorpion sting H - Hyperlipidaemia, Hypothermia, Hyperparathyroidism E - Endoscopic retrograde cholangiopancreatography D - Drugs commonly azathioprine, valproic acid

Infectious causes

A number of infectious agents have been recognized as causes of pancreatitis including:[15]

Diagnosis

Acute exudative pancreatitis on CT scan

Diagnosing pancreatitis requires two of the following:

  • Characteristic abdominal pain
  • Blood amylase or lipase will be 4-6 times higher than the normal variations, but this will be dependent on the laboratory that is testing the blood.
  • Abdominal ultrasound is generally performed first, which is advantageous for the diagnosis of the causes of the pancreas, for example, detecting gallstones, diagnosing alcoholic fatty liver (combined with history of alcohol consumption). They are both the main causes of pancreatitis. Abdominal ultrasound also shows an inflamed pancreas clearly. It is convenient, simple, non-invasive, and inexpensive.[16]
  • Characteristic CT scan[17]

Amylase or lipase is frequently part of the diagnosis; lipase is generally considered a better indicator,[17][18][19][20][21][22][23] but this is disputed.[24][25] Cholecystitis, perforated peptic ulcer, bowel infarction, and diabetic ketoacidosis can mimic pancreatitis by causing similar abdominal pain and elevated enzymes. The diagnosis can be confirmed by ultrasound and/or CT.

Treatment

The treatment of pancreatitis is supportive and depends on severity. Morphine generally is suitable for pain control. There is a claim that morphine may constrict the sphincter of Oddi, but this is controversial. There are no clinical studies to suggest that morphine can aggravate or cause pancreatitis or cholecystitis.[26]

The treatment that is received for acute pancreatitis will depend on whether the diagnosis is for the mild form of the condition, which causes no complications, or the severe form, which can cause serious complications.

Mild acute pancreatitis

The treatment of mild acute pancreatitis is successfully carried out by admission to a general hospital ward. Eating should not be allowed until pancreatic inflammation has resolved, which usually takes around five days, as the digestion process places strain on the pancreas. Because pancreatitis can cause lung damage and affect normal lung function, oxygen is usually delivered through breathing tubes that are connected via the nose. The tubes can then be removed after a few days once it is clear that the condition is improving. Dehydration may result during an episode of acute pancreatitis, so fluids will be provided intravenously. The pain associated with even mild or moderate cases of acute pancreatitis can be severe, so it likely will require a strong, opiate-based painkiller.

Severe acute pancreatitis

Severe pancreatitis is associated with organ failure, necrosis, infected necrosis, pseudocyst and abscess. If diagnosed with severe acute pancreatitis, patients will need to be admitted to a high dependency unit or intensive care unit. It is likely that the levels of fluids inside the body will have dropped significantly as it diverts bodily fluids and nutrients in an attempt to repair the pancreas. The drop in fluid levels can lead to a reduction in the volume of blood within the body, which is known as hypovolemic shock. Hypovolemic shock can be life-threatening as it can very quickly starve the body of the oxygen-rich blood that it needs to survive. To avoid going into hypovolemic shock, fluids will be pumped intravenously. Oxygen will be supplied through tubes attached to the nose and ventilation equipment may be used to assist with breathing. Feeding tubes may be used to provide nutrients, while painkillers can help to relieve the pain.

As with mild acute pancreatitis, it will be necessary to treat the underlying cause - gallstones, discontinuing medications, cessation of alcohol, etc. If the cause is gallstones, it is likely that an ERCP procedure or removal of the gallbladder will be recommended. If the cause of pancreatitis is alcohol, cessation of drinking and receiving treatment for alcohol dependency may improve the pancreatitis. Even if the underlying cause is not related to alcohol consumption, doctors recommend avoiding it for at least six months as this can cause further damage to the pancreas during the recovery process.[27] Oral intake, especially fats, is generally restricted initially but early enteral feeding within 48 hours has been shown to improve clinical outcomes.[28] Fluids and electrolytes are replaced intravenously. Nutritional support is initiated via tube feeding to surpass the portion of the digestive tract most affected by secreted pancreatic enzymes if there is no improvement in the first 72–96 hours of treatment.[29]

Prognosis

Severe acute pancreatitis has mortality rates around 2-9%, higher where necrosis of the pancreas has occurred.[30]

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, BISAP, and Glasgow. The Modified Glasgow criteria suggests that a case be considered severe if at least three of the following are true:[31]

This can be remembered using the mnemonic PANCREAS:

The BISAP score (Blood urea nitrogen level >25 mg/dL, Impaired mental status, Systemic inflammatory response syndrome, age over 60 years, pleural effusion) has been validated as similar to other prognostic scoring systems.[32]

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 (ascites) 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. Severe inflammation can lead to intra-abdominal hypertension and abdominal compartment syndrome, further impairing renal and respiratory function and potentially requiring management with an open abdomen (laparostomy) to relieve the pressure.[33]

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, or almost 60% of cases involving more than two pseudocysts and gas in the pancreas.[34]

See also

References

  1. ^ NIDDK (July 2008). "Pancreatitis". National Digestive Diseases Information Clearinghouse. U.S. National Institute of Diabetes and Digestive and Kidney Diseases. 08–1596. 
  2. ^ "Pancreatitis". A.D.A.M., Inc. Retrieved 2013-01-05. 
  3. ^ Apte MV, Pirola RC, Wilson JS (June 2009). "Pancreas: alcoholic pancreatitis—it's the alcohol, stupid". Nature Reviews Gastroenterology & Hepatology 6 (6): 321–2.  
  4. ^ Yadav D, Hawes RH, Brand RE, Anderson MA, Money ME, Banks PA, Bishop MD, Baillie J, Sherman S, DiSario J, Burton FR, Gardner TB, Amann ST, Gelrud A, Lawrence C, Elinoff B, Greer JB, O'Connell M, Barmada MM, Slivka A, Whitcomb DC (June 2009). "Alcohol consumption, cigarette smoking, and the risk of recurrent acute and chronic pancreatitis". Arch. Intern. Med. 169 (11): 1035–45.  
  5. ^ "Pancreatitis Explained". Better Health Channel. State Government of Victoria. 2011. 
  6. ^ Johnson CD, Hosking S (1991). "National statistics for diet, alcohol consumption, and chronic pancreatitis in England and Wales, 1960–88". Gut 32 (11): 1401–5.  
  7. ^ Smith, Emma; Murray Longmore; Wilkinson, Ian; Tom Turmezei; Chee Kay Cheung (2007). Oxford handbook of clinical medicine (7th ed.). Oxford [Oxfordshire]: Oxford University Press. p. 584.  
  8. ^ Ben MH, Thabet H, Zaghdoudi I, Amamou M (2002). "Metformin associated acute pancreatitis". Veterinary and human toxicology 44 (1): 47–48.  
  9. ^ Kunjathaya P, Ramaswami PK, Krishnamurthy AN, Bhat N (2013). "Acute necrotizing pancreatitis associated with vildagliptin". JOP : Journal of the pancreas 14 (1): 81–84.  
  10. ^ Matveyenko AV, Dry S, Cox HI, Moshtaghian A, Gurlo T, Galasso R, Butler AE, Butler PC (July 2009). "Beneficial endocrine but adverse exocrine effects of sitagliptin in the human islet amyloid polypeptide transgenic rat model of type 2 diabetes: interactions with metformin". Diabetes 58 (7): 1604–15.  
  11. ^ http://www.medscape.com/viewarticle/461398_3
  12. ^ D. Whitcomb (2006). "Genetic Testing for Pancreatitis". 
  13. ^ Noel RA, Braun DK, Patterson RE, Bloomgren GL (May 2009). "Increased risk of acute pancreatitis and biliary disease observed in patients with type 2 diabetes: a retrospective cohort study". Diabetes Care 32 (5): 834–8.  
  14. ^ Macaluso JN (August 1997). "Editorial Comment". J. Urol. 158 (2): 522.  on Matthews K, Correa RJ, Gibbons RP, Weissman RM, Kozarek RA (August 1997). "Extracorporeal shock wave lithotripsy for obstructing pancreatic duct calculi". J. Urol. 158 (2): 522–5.  
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  16. ^ Lawrence W. Tierney, Stephen J. McPhee. Medicine. McGraw-Hill.  
  17. ^ a b Banks PA, Freeman ML (2006). "Practice guidelines in acute pancreatitis". Am J Gastroenterol 101 (2379–400): 2379–400.  
  18. ^ UK Working Party on Acute Pancreatitis (2005). "UK guidelines for the management of acute pancreatitis". Gut 54 (Suppl 3): iii1–9.  
  19. ^ Smith RC, Southwell-Keely J, Chesher D (June 2005). "Should serum pancreatic lipase replace serum amylase as a biomarker of acute pancreatitis?". ANZ J Surg 75 (6): 399–404.  
  20. ^ Treacy J, Williams A, Bais R, Willson K, Worthley C, Reece J, Bessell J, Thomas D (October 2001). "Evaluation of amylase and lipase in the diagnosis of acute pancreatitis". ANZ J Surg 71 (10): 577–82.  
  21. ^ Steinberg WM, Goldstein SS, Davis ND, Shamma'a J, Anderson K (May 1985). "Diagnostic assays in acute pancreatitis. A study of sensitivity and specificity". Ann. Intern. Med. 102 (5): 576–80.  
  22. ^ Lin XZ, Wang SS, Tsai YT, Lee SD, Shiesh SC, Pan HB, Su CH, Lin CY (February 1989). "Serum amylase, isoamylase, and lipase in the acute abdomen. Their diagnostic value for acute pancreatitis". J. Clin. Gastroenterol. 11 (1): 47–52.  
  23. ^ Keim V, Teich N, Fiedler F, Hartig W, Thiele G, Mössner J (January 1998). "A comparison of lipase and amylase in the diagnosis of acute pancreatitis in patients with abdominal pain". Pancreas 16 (1): 45–9.  
  24. ^ Ignjatović S, Majkić-Singh N, Mitrović M, Gvozdenović M (November 2000). "Biochemical evaluation of patients with acute pancreatitis". Clin. Chem. Lab. Med. 38 (11): 1141–4.  
  25. ^ Sternby B, O'Brien JF, Zinsmeister AR, DiMagno EP (December 1996). "What is the best biochemical test to diagnose acute pancreatitis? A prospective clinical study". Mayo Clin. Proc. 71 (12): 1138–44.  
  26. ^ Helm JF, Venu RP, Geenen JE, Hogan WJ, Dodds WJ, Toouli J, Arndorfer RC (October 1988). "Effects of morphine on the human sphincter of Oddi". Gut 29 (10): 1402–7.  
  27. ^ E Medicine Health , Jerry R. Balentine, DO, FACEP , Melissa Conrad Stöppler, MD, Chief Medical Editor
  28. ^ Li JY, Yu T, Chen GC, Yuan YH, Zhong W, Zhao LN, Chen QK. (Jun 6, 2013). "Enteral Nutrition within 48 Hours of Admission Improves Clinical Outcomes of Acute Pancreatitis by Reducing Complications: A Meta-Analysis.". PLoS One. 8 (6): e64926.  
  29. ^ Muddana V, Whitcomb DC, Papachristou GI (August 2009). "Current management and novel insights in acute pancreatitis". Expert Rev Gastroenterol Hepatol 3 (4): 435–44.  
  30. ^ Munoz A, Katerndahl DA (July 2000). "Diagnosis and management of acute pancreatitis". Am Fam Physician 62 (1): 164–74.  
  31. ^ Corfield AP, Cooper MJ, Williamson RC, Mayer AD, McMahon MJ, Dickson AP, Shearer MG, Imrie CW (1985). "Prediction of severity in acute pancreatitis: prospective comparison of three prognostic indices". Lancet 2 (8452): 403–7.  
  32. ^ Papachristou GI, Muddana V, Yadav D, O'Connell M, Sanders MK, Slivka A, Whitcomb DC (Feb 2010). "Comparison of BISAP, Ranson's, APACHE-II, and CTSI scores in predicting organ failure, complications, and mortality in acute pancreatitis.". Am J Gastroenterol. 105 (2): 435–41.  
  33. ^ Fitzgerald JE, Gupta S, Masterson S, Sigurdsson HH (April 2012). "Laparostomy management using the ABThera™ open abdomen negative pressure therapy system in a grade IV open abdomen secondary to acute pancreatitis". Int Wound J 10 (2): 138–144.  
  34. ^ Pancreatic abscess at eMedicine

External links

  • Disease overview from USC
  • Pancreatitis Support Network (UK)
  • National Pancreas Foundation [1] (US)
  • NHS Direct Health encyclopaedia
  • Tutorial and discussion from Surgeons Net Education
  • GeneReviews/NCBI/NIH/UW entry on PRSS1-Related Hereditary Pancreatitis
  • Pancreatitis causes and treatment
  • Disease of the Pancreas and Biliary Tree
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