|Classification and external resources|
Pancreatitis is inflammation of the pancreas. The pancreas is a large organ behind the stomach which produces digestive enzymes. There are two main types acute pancreatitis and chronic pancreatitis. Symptoms of pancreatitis include pain in the upper abdomen, nausea and vomiting. The pain often goes into the back and is usually severe. In acute pancreatitis a fever may occur and symptoms typically resolve in a few days. In chronic pancreatitis weight loss, fatty stool, and diarrhea may occur. Complications may include infection, bleeding, diabetes, or problems with other organs.
The most common causes of acute pancreatitis is gallstones and heavy alcohol use. Other causes include direct trauma, certain medications, infections such as mumps, and tumors among others. Chronic pancreatitis may develop as a result of acute pancreatitis. It is most commonly due to many years of heavy alcohol use. Other causes include high levels of blood fats, high blood calcium, some medications, and certain genetic disorders such as cystic fibrosis among others. Smoking increases the risk of both acute and chronic pancreatitis. Diagnosis of acute pancreatitis is based on a three fold increase in the blood of either amylase or lipase. In chronic pancreatitis these tests may be normal. Medical imaging such as ultrasound and CT scan may also be useful.
Acute pancreatitis is usually treated with intravenous fluids, pain medication, and sometimes antibiotics. Typically no eating or drinking is allowed and a tube may be placed into the stomach. A procedure known as a endoscopic retrograde cholangiopancreatography (ERCP) may be done to open the pancreatic duct if blocked. In those with gallstones the gallbladder is often also removed. In chronic pancreatitis, in addition to the above, temporary feeding through a nasogastric tube may be used to provide adequate nutrition. Long term dietary changes and pancreatic enzyme replacement may be required. And occasionally surgery is done to remove parts of the pancreas.
Acute pancreatitis occurs in about 30 per 100,000 people a year. New cases of chronic pancreatitis develop in about 8 per 100,000 people a year and currently affect about 50 per 100,000 people in the United States. Globally, in 2013 pancreatitis resulted in 123,000 deaths up from 83,000 deaths in 1990. It is more common in men than women. Often chronic pancreatitis starts between the ages of 30 and 40 while it is rare in children. Acute pancreatitis was first described on autopsy in 1882 while chronic pancreatitis was first described in 1946.
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.
Eighty percent of cases of pancreatitis are caused by alcohol or gallstones. Gallstones are the single most common cause of acute pancreatitis. Alcohol is the single most common cause of chronic pancreatitis.
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, and antihyperglycemic agents like metformin, vildagliptin, and sitagliptin. 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.
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.
Less common causes include pancreatic cancer, pancreatic duct stones, vasculitis (inflammation of the small blood vessels in the pancreas), coxsackievirus infection, and porphyria—particularly acute intermittent porphyria and erythropoietic protoporphyria.
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.
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
A number of infectious agents have been recognized as causes of pancreatitis including:
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.
- Characteristic CT scan
Amylase or lipase is frequently part of the diagnosis; lipase is generally considered a better indicator, but this is disputed. 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.
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.
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, which means that a narcotic pain killer may be required.
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, combined with appropriate analgesia.
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 alcohol consumption and 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. Oral intake, especially fats, is generally restricted initially but early enteral feeding within 48 hours has been shown to improve clinical outcomes. 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.
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:
- Age > 55 years
- Blood levels:
This can be remembered using the mnemonic PANCREAS:
- P02 Oxygen < 60mmHg or 7.9kPa
- Age > 55
- Neutrophilia White blood cells > 15
- Calcium < 2 mmol/L
- Renal Urea > 16 mmol/L
- Enzymes Lactate dehydrogenase (LDH) > 600iu/L Aspartate transaminase (AST) > 200iu/L
- Albumin < 32g/L
- Sugar Glucose > 10 mmol/L
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.
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 to relieve the pressure.
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.
In 2013 pancreatitis resulted in 123,000 deaths up from 83,000 deaths in 1990.
- "Pancreatitis". http://www.niddk.nih.gov. August 16, 2012. Retrieved 1 March 2015.
- Lankisch, PG; Apte, M; Banks, PA (20 January 2015). "Acute pancreatitis.". Lancet. PMID 25616312.
- Yadav, D; Lowenfels, AB (June 2013). "The epidemiology of pancreatitis and pancreatic cancer.". Gastroenterology 144 (6): 1252–61. PMID 23622135.
- Muniraj, T; Aslanian, HR; Farrell, J; Jamidar, PA (December 2014). "Chronic pancreatitis, a comprehensive review and update. Part I: epidemiology, etiology, risk factors, genetics, pathophysiology, and clinical features.". Disease-a-month : DM 60 (12): 530–50. PMID 25510320.
- GBD 2013 Mortality and Causes of Death, Collaborators (17 December 2014). "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013.". Lancet. doi:10.1016/S0140-6736(14)61682-2. PMID 25530442.
- NIDDK (July 2008). "Pancreatitis". National Digestive Diseases Information Clearinghouse. U.S. National Institute of Diabetes and Digestive and Kidney Diseases. 08–1596.
- "Pancreatitis". A.D.A.M., Inc. Retrieved 2013-01-05.
- Apte MV, Pirola RC, Wilson JS (June 2009). "Pancreas: alcoholic pancreatitis—it's the alcohol, stupid". Nature Reviews Gastroenterology & Hepatology 6 (6): 321–2. doi:10.1038/nrgastro.2009.84. PMID 19494819. [at Medscape Today Lay summary].
- 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. doi:10.1001/archinternmed.2009.125. PMID 19506173. [Study Redefines Roles Of Alcohol, Smoking In Risk For Pancreatitis Lay summary] – ScienceDaily (8 June 2009).
- "Pancreatitis Explained". Better Health Channel. State Government of Victoria. 2011.
- 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. doi:10.1136/gut.32.11.1401. PMC 1379177. PMID 1752477.
- 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. ISBN 0-19-856837-1.
- Ben MH, Thabet H, Zaghdoudi I, Amamou M (2002). "Metformin associated acute pancreatitis". Veterinary and human toxicology 44 (1): 47–48. PMID 11824780.
- Kunjathaya P, Ramaswami PK, Krishnamurthy AN, Bhat N (2013). "Acute necrotizing pancreatitis associated with vildagliptin". JOP : Journal of the pancreas 14 (1): 81–84. doi:10.6092/1590-8577/1203. PMID 23306341.
- 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. doi:10.2337/db09-0058. PMC 2699878. PMID 19403868.
- 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. doi:10.2337/dc08-1755. PMC 2671118. PMID 19208917.
- 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. doi:10.1016/s0022-5347(01)64524-5. PMID 9224338.
- D. Whitcomb (2006). "Genetic Testing for Pancreatitis".
- Parenti DM, Steinberg W, Kang P (November 1996). "Infectious causes of acute pancreatitis". Pancreas 13 (4): 356–71. doi:10.1097/00006676-199611000-00005. PMID 8899796.
- Lawrence W. Tierney, Stephen J. McPhee. Medicine. McGraw-Hill. ISBN 0-07-144441-6.
- Banks PA, Freeman ML (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.
- UK Working Party on Acute Pancreatitis (2005). "UK guidelines for the management of acute pancreatitis". Gut 54 (Suppl 3): iii1–9. doi:10.1136/gut.2004.057026. PMC 1867800. PMID 15831893.
- 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. doi:10.1111/j.1445-2197.2005.03391.x. PMID 15943725.
- 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. doi:10.1046/j.1445-2197.2001.02220.x. PMID 11552931.
- 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. doi:10.7326/0003-4819-102-5-576. PMID 2580467.
- 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. doi:10.1097/00004836-198902000-00011. PMID 2466075.
- 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. doi:10.1097/00006676-199801000-00008. PMID 9436862.
- 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. doi:10.1515/CCLM.2000.173. PMID 11156345.
- 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. doi:10.4065/71.12.1138. PMID 8945483.
- 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. doi:10.1136/gut.29.10.1402. PMC 1434014. PMID 3197985.
- E Medicine Health , Jerry R. Balentine, DO, FACEP , Melissa Conrad Stöppler, MD, Chief Medical Editor
- 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. doi:10.1371/journal.pone.0064926. PMID 23762266.
- Muddana V, Whitcomb DC, Papachristou GI (August 2009). "Current management and novel insights in acute pancreatitis". Expert Rev Gastroenterol Hepatol 3 (4): 435–44. doi:10.1586/egh.09.27. PMID 19673630.
- Munoz A, Katerndahl DA (July 2000). "Diagnosis and management of acute pancreatitis". Am Fam Physician 62 (1): 164–74. PMID 10905786.
- 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. doi:10.1016/S0140-6736(85)92733-3. PMID 2863441.
- 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. doi:10.1038/ajg.2009.622. PMID 19861954.
- 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. doi:10.1111/j.1742-481X.2012.00953.x. PMID 22487377.
- Pancreatic abscess at eMedicine
|Wikimedia Commons has media related to Pancreatitis.|
- NHS Direct Health encyclopaedia
- Tutorial and discussion from Surgeons Net Education
- GeneReviews/NCBI/NIH/UW entry on PRSS1-Related Hereditary Pancreatitis
- Disease of the Pancreas and Biliary Tree