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Acute pancreatitis 1

Acute pancreatitis
Acute pancreatitis
(acute pancreatic necrosis)
Classification and external resources

Pancreas

ICD-10 [1]
K 85.

ICD-9 [2]
577.0

DiseasesDB [3]
9539

MedlinePlus [4]
000287

eMedicine [5] [6]
med/1720 radio/521

Acute pancreatitis or acute pancreatic necrosis[7] is a sudden inflammation of the pancreas. Depending on its
severity, it can have severe complications and high mortality despite treatment. While mild cases are often
successfully treated with conservative measures, such as NPO (nil by mouth or NBM) and IV fluid rehydration,
severe cases may require admission to the ICU or even surgery (often requiring more than one intervention) to deal
with complications of the disease process.

Symptoms and signs
The most common symptoms and signs include:
• Severe epigastric pain radiating to the back
• Nausea, vomiting, diarrhea and loss of appetite
• Fever/chills
• Hemodynamic instability, including shock
Signs which are less common, and indicate severe disease, include:
• Grey-Turner's sign (hemorrhagic discoloration of the flanks)
• Cullen's sign (hemorrhagic discoloration of the umbilicus)
• Grünwald sign (appearance of ecchymosis around the umbilicus due to local toxic lesion of the vessels.)

Thought to be hypertensive sphincter or microlithiasis.mumps (paramyxovirus) and other viruses (Epstein-Barr virus. and also snake bites • H . or steroids.g.)[8] Other conditions to consider are: • Pancreatic pseudocyst • Pancreatic dysfunction (diabetes mellitus. & didanosine) and duodenal ulcers. Two patients died. the U.ethanol (alcohol) • T .steroids & sulfonamides.gallstone. Cytomegalovirus) • A . NSAIDS. As an example.Acute pancreatitis 2 • Körte's sign (pain or resistance in the zone where the head of pancreas is located (in epigastrium. • G . a diabetes medicine approved in 2005. malabsorption due to exocrine failure) • Pancreatic cancer Although these are common symptoms. . azathioprine.idiopathic.[9] This mnemonic is also roughly arranged according to the frequency of its causes.a procedure that combines endoscopy and fluoroscopy) • D . Causes Most common causes A common mnemonic for the causes of pancreatitis spells "I get smashed". diuretics such as furosemide and thiazides. an allusion to heavy drinking (one of the many causes): • I . trauma.scorpion sting (e. The backflow of these digestive juices causes lysis (dissolving) of pancreatic cells and subsequent pancreatitis. Thus: Gallstone pancreatitis is more common than pancreatitis caused by alcohol. • Kamenchik's sign (pain with pressure under the xiphoid process.autoimmune disease (Polyarteritis nodosa.steroids • M . • E . they are not always present. The FDA previously reported 30 other cases of pancreatitis.S. Systemic lupus erythematosus) • S .drugs (SAND .trauma • S . 6-7 cm above the umbilicus).) • Mayo-Robson's sign (pain while pressing at the top of the angle lateral to the Erector spinae muscles and below the left 12th rib (left costovertebral angle (CVA)). Food and Drug Administration (FDA) reported in August 2008 six cases of hemorrhagic or necrotizing pancreatitis in patients taking Byetta. Gallstones that travel down the common bile duct and which subsequently get stuck in the Ampulla of Vater can cause obstruction in the outflow of pancreatic juices from the pancreas into the duodenum. hyperlipidemia/hypertriglyceridemia and hypothermia • E . Tityus trinitatis).ERCP (Endoscopic Retrograde Cholangio-Pancreatography . Patients taking Byetta should promptly seek medical care if they experience unexplained severe abdominal pain with or without nausea and vomiting. Simple abdominal pain may be the sole symptom.hypercalcemia.

chronic alcoholism and gallstones accounting for more than 85% of all cases • Eastern countries . • cystic fibrosis • valproic acid • Anorexia or bulimia • Codeine reaction[10] [11] Causes by demographic The most common causes of pancreatitis. Inflammatory infiltrate is rich in neutrophils. In acute pancreatitis. focal enzymic necrosis of pancreatic fat and vessel necrosis . Necrotic fat cells appear as shadows. lipases. are as follows : • Western countries . Lipase activation produces the necrosis of fat tissue in pancreatic interstitium and peripancreatic spaces. and saccharidases. lacking the nucleus. pink. It is possible to find calcium precipitates (hematoxylinophilic). These are produced by intrapancreatic activation of pancreatic enzymes. Digestion of vascular walls results in thrombosis and hemorrhage.Acute pancreatitis 3 Less common causes • pancreas divisum • long common duct • carcinoma of the head of pancreas. the worst offender among these enzymes may well be the protease trypsinogen which converts to the active trypsin. finely granular cytoplasm. Trypsin is most responsible for auto-digestion of the pancreas which in turn causes the pain and complications of pancreatitis.trauma • Adolescents and young adults . Histopathology The acute pancreatitis (acute hemorrhagic pancreatic necrosis) is characterized by acute inflammation and necrosis of pancreas parenchyma. .gallstones • Children .hemorrhage. including varicella zoster • repeated marathon running. These enzymes contribute to food digestion by breaking down food tissues. such as proteases. contours of cells.mumps Pathogenesis The exocrine pancreas produces a variety of enzymes. and other cancer • ascaris blocking pancreatic outflow • chinese liver fluke • ischemia from bypass surgery • fatty necrosis • pregnancy • infections other than mumps.

PMID 9436862). parotitis. two practice guidelines state: "It is usually not necessary to measure both serum amylase and lipase. gas bubbles. Computed tomography Regarding the need for computed tomography. Liver Function. edema. In one large study." [13] 2005: "Patients with persisting organ failure.Full blood count. but not all (PMID 11156345. fluid in the lessar sac. Serum lipase may be preferable because it remains normal in some nonpancreatic conditions that increase serum amylase including macroamylasemia. PMID 2466075. serum amylase and lipase. Renal function tests. For example. a CT scan is usually not essential in patients with recurrent mild pancreatitis caused by alcohol."[14] CT abdomen should not be performed before the 1st 48 hours of onset of symptoms as early CT (<48 h) may result in equivocal or normal findings. often trigger the initial diagnosis of acute pancreatitis. there were no patients with pancreatitis who had an elevated amylase with a normal lipase [15] . serum lipase is thought to be more sensitive and specific than serum amylase in the diagnosis of acute pancreatitis" [13] "Although amylase is widely available and provides acceptable accuracy of diagnosis. and gallstones which are radioopaque in 10%) and CT abdomen Amylase and lipase • Elevated serum amylase and lipase levels.Acute pancreatitis 4 Investigations and diagnosis • Blood Investigations . pancreatic pseudocysts and phlegmons/abscesses (which present 4 to 6 wks after initial onset) • Peripancreatic / extrapancreatic . Another study found that the amylase could add diagnostic value to the lipase. it is an indication of pancreatitis due to alcohol. PMID 8945483) individual studies support the superiority of the lipase. fluid in the left anterior pararenal space . signs of sepsis. obliterated peripancreatic fat. serum calcium. • Reasons for false positive elevated serum amylase include salivary gland disease (elevated salivary amylase) and macroamylasemia. such as a perforated ulcer. A reasonable indication for a CT scan at admission (but not necessarily a CT with IV contrast) is to distinguish acute pancreatitis from another serious intra-abdominal condition. in combination with severe abdominal pain. In general. or deterioration in clinical status 6–10 days after admission will require CT (recommendation grade B). retroperitoneal edema.irregular pancreatic outline. where lipase is available it is preferred for the diagnosis of acute pancreatitis (recommendation grade A)"[14] Most (PMID 15943725.diffuse or segmental enlargement. Arterial blood gas • Imaging .[12] Regarding selection on these tests. and some carcinomas.5 to 3 times that of amylase.Chest Xray (for exclusion of perforated viscus). Abdominal Xrays (for detection of "sentinel loop" dilated duodenum sign. PMID 2580467. • If the lipase level is about 2. practice guidelines state: 2006: "Many patients with acute pancreatitis do not require a CT scan at admission or at any time during the hospitalization. but only if the results of the two tests were combined with a discriminant function equation [16] . • Serum lipase rises 4 to 8 hours from the onset of symptoms and normalizes within 7 to 14 days after treatment. CT Findings can be classified into the following categories for easy recall : • Intrapancreatic . PMID 11552931. • Serum amylase may be normal (in 10% of cases) for cases of acute or chronic pancreatitis (depleted acinar cell mass) and hypertriglyceridemia.

the Apache II 24 hr score was used rather than the 48 hour score. Most[22] [23] . pseudoaneurysms. however. body mass index. vascular complications.Gerota's fascia sign (thickening of inflamed Gerota's fascia. The further clinical course is then determined by bacterial infection. As the Apache II is more cumbersome to calculate. all patients in the study received an ultrasound twice which may have influenced allocation of co-interventions. Regardless. respiratory. chest x ray. Practice guidelines state: 2006: "The two tests that are most helpful at admission in distinguishing mild from severe acute pancreatitis are APACHE-II score and serum hematocrit."[13] 2005: "Immediate assessment should include clinical evaluation. particularly of any cardiovascular. About 20% of the acute pancreatitis are severe with a mortality of about 20%. but with the benefits of being less invasive and causing fewer complications. presumably patients whose only laboratory abnormality is an elevated lipase or amylase do not need prognostication with the Apache II. pleural effusion (seen on basal cuts of the pleural cavity). the presence of tiny biliary stones (choledocholithiasis or cholelithiasis) and duct anomalies.org [25] . and an overall greater sensitivity to hemorrhage.[17] magnetic resonance imaging (MRI) has become increasingly valuable as a tool for the visualization of the pancreas. Prognostic indices In predicting the prognosis. Mostly the Atlanta classification (1992) is used. Magnetic resonance imaging While computed tomography is considered the gold standard in diagnostic imaging for acute pancreatitis. which becomes visible). etc. but not all [24] studies report that the Apache score may be more accurate..[19] Another advantage of MRI is its utilization of magnetic resonance cholangiopancreatography (MRCP) sequences. MRCP provides useful information regarding the etiology of acute pancreatitis.[18] Clinical trials indicate that MRCP can be as effective a diagnostic tool for acute pancreatitis with biliary etiology as endoscopic retrograde cholangiopancreatography. particularly of pancreatic fluid collections and necrotized debris. pancreatic ascites. and renal compromise. 12 h after admission. Age and Chronic Health Evaluation) indices. It is recommended that APACHE-II scores be generated during the first 3 days of hospitalization and thereafter as needed to help in this distinction. Two such scoring systems are the Ranson criteria and APACHE II (Acute Physiology. One is the above mentioned Ranson Score. i.e. and APACHE II score" [14] . Necrosis will be followed by a systemic inflammatory response syndrome (SIRS) and will determine the immediate clinical course. The Apache II score can be calculated at www. and 24 h after admission to help gauge adequacy of fluid resuscitation. SIRS is the cause of bacterial (Gram negative) translocation from the patients colon. there are several scoring indices that have been used as predictors of survival. In severe pancreatitis serious amount of necrosis determine the further clinical outcome. This is an important classification as severe pancreatitis will need intensive care therapy whereas mild pancreatitis can be treated on the common ward.sfar. It is also recommended that serum hematocrit be obtained at admission. this approach is not studied.[20] [21] Classification by severity Progression of pathophysiology Acute pancreatitis can be further divided into mild and severe pancreatitis.[18] Additional utility of MRI includes its indication for imaging of patients with an allergy to CT's contrast material. adynamic ileus. There are several ways to help distinguish between these two forms. In the negative study of the Apache II [24] . and venous thrombosis.Acute pancreatitis 5 • Locoregional . In addition. only the Apache II can be fully calculated upon admission.

so that in some situations it can be calculated shortly after admission. AST. Alternatively.0 mg/dL) • Hematocrit fall > 10% • Oxygen (hypoxemia PO2 < 60 mmHg) • BUN increased by 1. hematocrit. O2. WBC count) At 48 hours: "C Hobbs" (i. LDH. sequestration (of fluid) greater than 6 L (see: fluid balance) APACHE "Acute Physiology And Chronic Health Evaluation" (APACHE II) score > 8 points predicts 11% to 18% mortality [13] Online calculator [25] • Hemorrhagic peritoneal fluid • Obesity • Indicators of organ failure • Hypotension (SBP <90 mmHG) or tachycardia > 130 beat/min • PO2 <60 mmHg • Oliguria (<50 mL/h) or increasing BUN and creatinine • Serum calcium < 1.0 mmol/L (< 8.2.g/dL)> .90 mmol/L (<8. It was introduced in 1974. Calvin and Hobbes): (calcium.[1] At admission • age in years > 55 years • white blood cell count > 16000 cells/mm3 • blood glucose > 11 mmol/L (> 200 mg/dL) • serum AST > 250 IU/L • serum LDH > 350 IU/L At 48 hours • Calcium (serum calcium < 2. Base deficit. age.0 mg/dL) or serum albumin <33 g/L (<3. pancreatitis can be diagnosed by meeting any of the following:[2] APACHE II score Apache score of ≥ 8 Organ failure Substantial pancreatic necrosis (at least 30% glandular necrosis according to contrast-enhanced CT) Interpretation If the score ≥ 3. severe pancreatitis likely.e. BUN. If the score < 3.Acute pancreatitis 6 Ranson Score Ranson criteria is a clinical prediction rule for predicting the severity of acute pancreatitis. severe pancreatitis is unlikely Or Score 0 to 2 : 2% mortality Score 3 to 4 : 15% mortality Score 5 to 6 : 40% mortality Score 7 to 8 : 100% mortality Mnemonic for memorizing Ranson's criteria At admission: "GA LAW" (glucose. It is applicable to both gallstone and alcoholic pancreatitis.8 or more mmol/L (5 or more mg/dL) after IV fluid hydration • Base deficit (negative base excess) > 4 mEq/L • Sequestration of fluids > 6 L The criteria for point assignment is that a certain breakpoint be met at anytime during that 48 hour period.

so the drug of choice was meperidine. and C-reactive protein (CRP) level. nor is it an accurate predictor of AP severity. The numerical CTSI has a maximum of ten points.Acute pancreatitis 7 Balthazar scoring Developed in the early 1990s by Emil J.[33] IMRIE scoring is also useful. more recent studies have found morphine the analgesic of choice.[31] [32] Treatment Pain control Originally it was thought that analgesia should not be provided by morphine because it may cause spasm of the sphincter of Oddi and worsen the pain. due to lack of efficacy and risk of toxicity of meperidine. Meperidine may still be used by some practitioners in more minor cases. Approximately 20% of patients have a relapse of pain during acute pancreatitis. Ranson. the treatment is to stop feeding the patient. . and sufficient pain control. Bowel rest In the management of acute pancreatitis. As the pancreas is stimulated to secrete enzymes by the presence of food in the stomach. giving him or her nothing by mouth. However.. a few studies indicate that CTSI is not significantly associated with the prognosis of hospitalization in patients with pancreatic necrosis. The incidence of relapse after oral refeeding may be reduced by post-pyloric enteral rather than parenteral feeding prior to oral refeeding. or where morphine is contraindicated. Balthazar et al. giving intravenous fluids to prevent dehydration.[33] Approximately 75% of relapses occur within 48 hours of oral refeeding. and is the sum of the Balthazar grade points and pancreatic necrosis grade points: Balthazar Grade Balthazar Grade Appearance on CT CT Grade Points Grade A Normal CT 0 points Grade B Focal or diffuse enlargement of the pancreas 1 point Grade C Pancreatic gland abnormalities and peripancreatic inflammation 2 points Grade D Fluid collection in a single location 3 points Grade E Two or more fluid collections and / or gas bubbles in or adjacent to pancreas 4 points Necrosis Score Necrosis Points Percentage No necrosis 0 points 0 to 30% necrosis 2 points 30 to 50% necrosis 4 points Over 50% necrosis 6 points CTSI's staging of acute pancreatitis severity has been shown by a number of studies to provide more accurate assessment than APACHE II.[26] the Computed Tomography Severity Index (CTSI) is a grading system used to determine the severity of acute pancreatitis.[27] [28] [29] [30] However. having no food pass through the system allows the pancreas to rest.

Antibiotics A meta-analysis by the Cochrane Collaboration concluded that antibiotics help with a number needed to treat of 11 patients to reduce mortality [34] . The advantage of enteral feeding is that it is more physiological. In addition. bleeding It is worth noting that ERCP itself can be a cause of pancreatitis. The additional advantages of post-pyloric feeding are the inverse relationship of pancreatic exocrine secretions and distance of nutrient delivery from the pylorus.[39] ERCP Early ERCP (endoscopic retrograde cholangiopancreatography).Acute pancreatitis 8 Nutritional support Recently. the role of antibiotics is controversial. as well as reduced risk of aspiration. performed within 24 to 72 hours of presentation. Carbapenems An early randomized controlled trial of imipenem 0. however. 28% of patients in the group subsequently required open antibiotic treatment vs.[40] The indications for early ERCP are as follows : • Clinical deterioration or lack of improvement after 24 hours • Detection of common bile duct stones or dilated intrahepatic or extrahepatic ducts on CT abdomen The disadvantages of ERCP are as follows : • ERCP precipitates pancreatitis. . prevents gut mucosal atrophy.e. and is free from the side effects of TPN (such as fungemia). the one study in the meta-analysis that used a quinolone. However. Disadvantages of a naso-enteric feeding tube include increased risk of sinusitis (especially if the tube remains in place greater than two weeks) and a still-present risk of accidentally intubating the bronchus even in intubated patients (contrary to popular belief.[36] Another randomized controlled trial with patients who had at least 50% pancreatic necrosis found a benefit from imipenem compared to pefloxacin with a reduction in infected necrosis from 34% to 20%[37] A subsequent randomized controlled trial that used meropenem 1 gram intravenously every 8 hours for 7 to 21 days stated no benefit. One recent expert opinion (prior to the last negative trial of meropenem[38] ) suggested the use of imipenem if CT scan showed more than 30% necrosis of the pancreas. the endotracheal tube cuff alone is not always sufficient to prevent NG tube entry into the trachea). is known to reduce morbidity and mortality.[38] Summary In summary. 46% in the placebo group. there has been a shift in the management paradigm from TPN (total parenteral nutrition) to early.5 gram intravenously every eight hours for two weeks showed a reduction in from pancreatic sepsis from 30% to 12%. and can introduce infection to sterile pancreatitis • The inherent risks of ERCP i. the control group had only 18% incidence of peripancreatic infections and less biliary pancreatitis that the treatment group (44% versus 24%). post-pyloric enteral feeding (in which a feeding tube is endoscopically or radiographically introduced to the third portion of the duodenum). and a subsequent randomized controlled trial that studied ciprofloxacin were both negative [35] .

necrosectomy with closed continuous postoperative lavage • Open management . DIC.9 per 100. mortality remained stable as a result of better outcomes. hemorrhage from erosions into splenic artery and vein.000 annually from 1985 to 1995. duodenal obstruction.000 population. splenic artery pseudoaneurysms.necrosectomy with simple drainage • Closed management . multiple organ dysfunction syndrome. however. In a European cross-sectional study. Infection is diagnosed based on 2 criteria • Gas bubbles on CT scan (present in 20 to 50% of infected necrosis) • Positive bacterial culture on FNA (fine needle aspiration. is 18 per 100. • Systemic complications include ARDS. common bile duct obstruction. The most common cause of death in acute pancreatitis is secondary infection.S.necrosectomy through small incision in skin (left flank) or stomach • Conventional management .4 to 15.8 per 100.[41] • The use of octreotide has not been shown to improve outcome.[43] Another study showed a lower incidence of 9. progression to chronic pancreatitis Epidemiology • Annual incidence in the U.[42] Complications Complications can be systemic or locoregional.9 in 1963-74) over time. thrombosis of the splenic vein. hyperglycemia and insulin dependent diabetes mellitus (from pancreatic insulin producing beta cell damage) • Locoregional complications include pancreatic pseudocyst and phlegmon / abscess formation. hypocalcemia (from fat saponification).Acute pancreatitis 9 Surgery Surgery is indicated for (i) infected pancreatic necrosis and (ii) diagnostic uncertainty and (iii) complications.necrosectomy with planned staged reoperations at definite intervals (up to 20+ reoperations in some cases) Other measures • Pancreatic enzyme inhibitors are not proven to work.[44] See also • Chronic pancreatitis . Surgical options for infected necrosis include: • Minimally invasive management . superior mesenteric vein and portal veins (in descending order of frequency). usually CT or US guided) of the pancreas.000 but a similar worsening trend (increasing from 4. incidence of acute pancreatits increased from 12.

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DrSasha. Andrew73. Todfox. Jaganath. Galletto. Stevenfruitsmaak. Medicalan. Rjwilmsi.php?title=File:Illu_pancrease. Ostmoe. 0/ . Mike2vil.tawfik.wikipedia. Fearless Son. Ixfd64. Dr Davids. Arcadian. Hughesdavidw. D6. Serrin. Peterl. Yang Ling Nee. Greystork. Radon210. Mackermer. Sirprojects. Jalan z. Agentmoose. Choosebrad. Ground Zero. Gorx. JevriS. Luna Santin. Kubigula. Nunquam Dormio. Maxxicum. JohnnyCalifornia. Renato Caniatti. Jmarchn. Meggyok. Wouterstomp.wikipedia. Irbisgreif. Licenses and Contributors File:Illu pancrease. Jeremykemp. SunCreator. Lipothymia. Cereis.Article Sources and Contributors 12 Article Sources and Contributors Acute pancreatitis  Source: http://en. Jr. Stusemple. Belovedfreak. DoctorC. Puldis. org/ licenses/ by-sa/ 3. Acctorp. LibLord. Rich Farmbrough. Boston. Badgettrg. Dreadstar. Stemonitis. Cradel. Bobblewik. DaveBurstein. Dr. Triggtay. Aoxiang. Mikolasz.org/w/index.svg  License: Public Domain  Contributors: User:Cradel License Creative Commons Attribution-Share Alike 3. Gholam. Goodnightmush. Mdanciu. Taksim Shinawat. LordFoppington. Woohookitty. DocJohnny. Debbybriggs.org/w/index.svg  Source: http://en.0 Unported http:/ / creativecommons. Fluppy. Planetary. ‫דוד‬55. Choledocho. SMcCandlish. Jfdwolff. Riotrocket8676.php?oldid=367170753  Contributors: 2004-12-29T22:45Z. 141 anonymous edits Image Sources. George Burgess. James Baraldi. Afr77. Spellinator.. Thomasimov.