| 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 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.
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Contents
- 1 Signs and symptoms
- 2 Causes
- 3 Diagnosis
- 4 Treatment
- 4.1 Mild acute pancreatitis
- 4.2 Severe acute pancreatitis
- 5 Prognosis
- 6 Complications
- 7 See also
- 8 References
- 9 External links
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Signs and symptoms [edit]
The most common symptoms of pancreatitis are severe upper abdominal 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 [edit]
Eighty percent of cases of pancreatitis are caused by alcohol and 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] cholesterol-lowering statins[citation needed] and the 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 sich 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, 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.[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 [edit]
A number of infectious agents have been recognized as causes of pancreatitis including:[15]
- Viruses
- Coxsackie virus
- Cytomegalovirus
- Hepatitis B
- Herpes simplex virus
- Mumps
- Varicella-zoster virus
- Bacteria
- Legionella
- Leptospira
- Mycoplasma
- Salmonella
- Fungi
- Parasites
- Ascaris
- Cryptosporidium
- Toxoplasma
Diagnosis [edit]
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.[citation needed] The diagnosis can be confirmed by ultrasound and/or CT.
Treatment [edit]
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 [edit]
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 cases of acute pancreatitis can be severe, so it may require quite a strong, opiate-based painkiller.
Severe acute pancreatitis [edit]
If diagnosed with severe acute pancreatitis, they 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. If the cause is gallstones, it is likely that an ERCP procedure or removal of your gallbladder will be recommended. For more information about ERCP, see Acute pancreatitis - ERCP. If the cause is alcohol use, stopping drinking and receiving treatment for alcohol dependency will be recommended (as discussed above). Though, as mentioned above, even if the underlying cause is not alcohol-related, consumption should still be avoided 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 at first. Fluids and electrolytes are replaced intravenously. Nutritional support should be initiated via tube feeding to surpass the portion of the digestive tract most affected by secreted pancreatic enzymes.[28] The underlying cause should also be treated (targeting gallstones, discontinuing medications, cessation of alcohol etc.) The patient is monitored for complications.
Prognosis [edit]
Severe acute pancreatitis has mortality rates around 2-9%, higher where necrosis of the pancreas has occurred.[29]
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:[30]
- Age > 55 years
- Blood levels:
- P02 Oxygen < 60mmHg or 7.9kPa
- White blood cells > 15
- Calcium < 2 mmol/L
- Urea > 16 mmol/L
- Lactate dehydrogenase (LDH) > 600iu/L
- Aspartate transaminase (AST) > 200iu/L
- Albumin < 32g/L
- Glucose > 10 mmol/L
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
Complications [edit]
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.[31]
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.[32]
See also [edit]
- Acute pancreatitis
- Autoimmune pancreatitis
- Chronic pancreatitis
- Exocrine pancreatic insufficiency
References [edit]
- ^ 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". Nat Rev Gastroenterol Hepatol 6 (6): 321–2. doi:10.1038/nrgastro.2009.84. PMID 19494819. [at Medscape Today Lay summary].
- ^ Yadav D., Hawes R. H., Brand R. E., et al. (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. 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.
- ^ http://www.ncbi.nlm.nih.gov/pubmed/11824780
- ^ http://www.ncbi.nlm.nih.gov/pubmed/23306341
- ^ Matveyenko AV, Dry S, Cox HI, et al. (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.
- ^ http://www.medscape.com/viewarticle/461398_3
- ^ D. Whitcomb (2006). "Genetic Testing for Pancreatitis".
- ^ 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. PMID 9224338.
- ^ Parenti D. M., Steinberg W., Kang P. (November 1996). "Infectious causes of acute pancreatitis". Pancreas 13 (4): 356–71. PMID 8899796.
- ^ Lawrence W. Tierney, Stephen J. McPhee. Medicine. McGraw-Hill. ISBN 0-07-144441-6.
- ^ 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.
- ^ 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., et al. (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. PMID 2580467.
- ^ Lin XZ, Wang SS, Tsai YT, et al. (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, et al. (October 1988). "Effects of morphine on the human sphincter of Oddi". Gut 29 (10): 1402–7. PMC 1434014. PMID 3197985.
- ^ E Medicine Health , Jerry R. Balentine, DO, FACEP , Melissa Conrad Stöppler, MD, Chief Medical Editor
- ^ 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 A. P., Cooper M. J., Williamson R. C., 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.
- ^ 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. doi:10.1111/j.1742-481X.2012.00953.x. PMID 22487377.
- ^ Pancreatic abscess at eMedicine
External links [edit]
- 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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Inflammation
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| Acute |
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Plasma derived mediators
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Bradykinin · complement (C3, C5a, MAC) · coagulation (Factor XII, Plasmin, Thrombin)
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Cell derived mediators
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preformed: Lysosome granules · vasoactive amines (Histamine, Serotonin)
synthesized on demand: cytokines (IFN-γ, IL-8, TNF-α, IL-1) · eicosanoids (Leukotriene B4, Prostaglandins) · Nitric oxide · Kinins
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| Chronic |
Macrophage · Epithelioid cell · Giant cell · Granuloma
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| Processes |
Traditional: Rubor · Calor · Tumor · Dolor (pain) · Functio laesa
Modern: Acute-phase reaction/Fever · Vasodilation · Increased vascular permeability · Exudate · Leukocyte extravasation · Chemotaxis
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| Specific locations |
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Nervous
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CNS (Encephalitis, Myelitis) · Meningitis (Arachnoiditis) · PNS (Neuritis) · eye (Dacryoadenitis, Scleritis, Episcleritis, Keratitis, Choroiditis, Retinitis, Chorioretinitis, Blepharitis, Conjunctivitis, Uveitis) · ear (Otitis, Labyrinthitis, Mastoiditis)
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Cardiovascular
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Carditis (Endocarditis, Myocarditis, Pericarditis) · Vasculitis (Arteritis, Phlebitis, Capillaritis)
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Respiratory
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upper (Sinusitis, Rhinitis, Pharyngitis, Laryngitis) · lower (Tracheitis, Bronchitis, Bronchiolitis, Pneumonitis, Pleuritis) · Mediastinitis
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Digestive
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mouth (Stomatitis, Gingivitis, Gingivostomatitis, Glossitis, Tonsillitis, Sialadenitis/Parotitis, Cheilitis, Pulpitis, Gnathitis) · tract (Esophagitis, Gastritis, Gastroenteritis, Enteritis, Colitis, Enterocolitis, Duodenitis, Ileitis, Caecitis, Appendicitis, Proctitis) · accessory (Hepatitis, Cholangitis, Cholecystitis, Pancreatitis) · Peritonitis
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Integumentary
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Dermatitis (Folliculitis) · Cellulitis · Hidradenitis
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Musculoskeletal
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Arthritis · Dermatomyositis · soft tissue (Myositis, Synovitis/Tenosynovitis, Bursitis, Enthesitis, Fasciitis, Capsulitis, Epicondylitis, Tendinitis, Panniculitis)
Osteochondritis: Osteitis (Spondylitis, Periostitis) · Chondritis
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Urinary
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Nephritis (Glomerulonephritis, Pyelonephritis) · Ureteritis · Cystitis · Urethritis
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Reproductive
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female: Oophoritis · Salpingitis · Endometritis · Parametritis · Cervicitis · Vaginitis · Vulvitis · Mastitis
male: Orchitis · Epididymitis · Prostatitis · Balanitis · Balanoposthitis
pregnancy/newborn: Chorioamnionitis · Omphalitis
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Endocrine
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Insulitis · Hypophysitis · Thyroiditis · Parathyroiditis · Adrenalitis
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Lymphatic
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Lymphangitis · Lymphadenitis
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Alcohol and health
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Ethanol
classifications |
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Dependency
and harm
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- Physical dependence
- ISCD harm and damaging rating: 72/100
- IARC Group 1 carcinogen
- Neurotoxin
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Pathophysiology
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- Anxiolytic
- Depressant
- Euphoriant
- Hypnotic/sedative
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Pharmacology
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- Glutamatergic: NMDA antagonist
Serotonergic: 5-HT3 agonist responsible for GABAergic (GABAA receptor PAM), glycinergic, and cholinergic (mAChR agonist) effects
Research: Adenosinergic: ENT inhibitor. Dopaminergic: Reversible MAO-B inhibitor. Norepinephrine reuptake inhibitor. Opioid
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Specific
interactions |
Note: see Template:Psychoactive substance use for diagnoses. Cancer (breast cancer) · Aging · Brain · Sleep · Tolerance · Weight · Alcohol induced mood disorders
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Substance
abuse
prevention |
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Sobriety
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- Alcohol detoxification
- Alcohol rehabilitation
- Alcoholics Anonymous
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Alcohol
limitation
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- 0-0-1-3
- Alcohol education
- Alcohol server training
- Recommended maximum intake of alcoholic beverages
- Group Against Liquor Advertising (GALA)
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Addiction medicine
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Anti-addictive entheogens: Ibogaine, Salvia divinorum
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Religion and alcohol
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- Christian views on alcohol
- Islam and alcohol
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| Social issues |
- Alcohol advertising/alcohol advertising on college campuses
- Alcohol-free beverage definition controversy
- Sex
- High-functioning alcoholic (HFA)
- Family systems
- College student alcoholism
- Drunkorexia
- rum-running (black market)
- Blackout (alcohol-related amnesia)
- American Indian alcoholism
- Binge drinking
- Drinking games/pregaming
- Domestic violence
- Driving under the influence
- French paradox
- Impure alcohol (methanol outbreaks, moonshine contamination)
- Alcohol self-medication
- Sin tax/Pigovian tax
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| General |
- Alternative alcohol use
- Short-term effects of alcohol
- Long-term effects of alcohol
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