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CME Objective: To revuew current evidence for the prevention, diagnosis, and treatment of acute pancreatitis.
The information contained herein should never be used as a substitute for clinicaljudgment.
Who is at increased risk for acutepancreatitis?Of the many causes of acute pancre-atitis, gallstone disease (approximately35% to 40% of cases) and excessivealcohol consumption (approximately30% of cases) dominate (5) (Table 1).Gallstone disease is among the mostcommon disorders in the UnitedStates, affecting an estimated 6.3 mil-lion men and 14.2 million women 20to 74 years of age (6). It is difficult topredict which patients with eithersymptomatic or asymptomatic gall-stones will develop pancreatitis. Onerisk factor is the presence of stones inthe common bile duct (choledo-cholithiasis), especially small stones(<5 mm) or microlithiasis comprisingstones that measure <2 mm becausethey can obstruct the orifice of thepancreatic duct at the level of the am-pulla. Pancreatitis occurs when gall-stones pass into the bile duct and become trapped at the sphincter ofOddi, stopping the flow of pancreaticfluid containing digestive enzymesinto the duodenum. If the blockagecontinues, activated enzymes build upin the pancreas and cause severe in-flammation. To reduce the risk forsuch complications as pancreatitis, pa-tients with symptomatic gallstonesusually have cholecystectomy and
those with common bile duct stoneshave them removed by endoscopicretrograde cholangiopancreatography(ERCP), an imaging and therapeutictechnique that combines endoscopyand fluoroscopy.
Alcohol-related pancreatitis usuallyoccurs after long-term (>5 years),heavy alcohol consumption. Riskincreases with the amount of alco-hol consumed, indicative of a directtoxic effect on the pancreas whenthe alcohol is metabolized. Becauseonly about 5% of alcoholics developpancreatitis, additional unknowngenetic or other factors must in-crease susceptibility. Smoking to-bacco may play a role; it has beenreported to accelerate progressionof established alcoholic pancreatitis(7). One study found an associationbetween high intake of beer (>14drinks per week) and pancreatitis,but not for wine or spirits (8).
Hypertriglyceridemia is anotherimportant risk factor for pancreati-tis, especially during pregnancy (9).No clear risk profile can indicatewhich patients with elevatedtriglycerides will develop pancreati-tis, but the complication occursrarely in the absence of significant
1. Bradley EL. A clinicallybased classificationsystem for acute pan-creatitis: Summary ofthe InternationalSymposium on AcutePancreatitis, Atlanta,Ga; September 11-13,1992. ArchSurg;1993;128:586-90.[PMID: 8489394]
2. Fagenholz PJ, CastilloCF, Harris NS, PelletierAJ, Camargo CA Jr. In-creasing UnitedStates hospital ad-missions for acutepancreatitis, 1988-2003. Ann Epidemiol.2007;17:491-7.[PMID: 17448682]
3. Lowenfels AB,Maisonneuve P, Sulli-van T. The changingcharacter of acutepancreatitis: epidemi-ology, etiology, andprognosis. Curr Gas-troenterol Rep.2009;11:97-103.[PMID: 19281696]
4. Lankisch PG, BreuerN, Bruns A, et al. Nat-ural history of acutepancreatitis: a long-term population-based study. Am JGastroenterol.2009;104:2797-805.[PMID: 19603011]
5. Forsmark CE, Baillie J.AGA Institute ClinicalPractice and Eco-nomics Committee.AGA Institute techni-cal review on acutepancreatitis. Gas-troenterology.2007;132:2022-44.[PMID: 17484894]
Acute pancreatitis is an acute inflammatory process of the pancreasthat can occur as an isolated event or relapsing episodes. Acute pan-creatitis is a heterogeneous disease ranging from minimal pancreatic
inflammation seen in mild interstitial pancreatitis to extensive pancreaticnecrosis and liquefaction of severe attacks. Diagnosis is based on the pres-ence at least 2 of 3 features: abdominal pain; increased pancreatic enzyme,amylase, and/or lipase levels to !3 times the upper limit of normal; and im-aging tests showing characteristic findings of acute pancreatitis (1). Alcoholand gallstones are the two most common causes, but there are many lesscommon causes. Acute pancreatitis accounts for more than 200 000 hospi-tal admissions annually in the United States, and incidence has been in-creasing (2). The rates of acute pancreatitis per 1000 Americans 40 to 59years of age are the highest they have been in the past 20 years, and ratesare higher for blacks than for whites. Mortality from acute pancreatitis is<5% overall, but severe attacks cause longer hospitalization and significant-ly higher mortality (3). The annual relapse rate of acute pancreatitis rangesfrom 0.6% to 5.6%, depending on the cause, and is highest when pancre-atitis results from alcohol consumption (4).
Several drugs have been linked todevelopment of acute pancreatitis(Table 1), but the risk is generallylow. In one review, the authors as-sessed the evidence for specificdrugs causing acute pancreatitis aswell as their clinical presentationsand proposed a classification ofdrug-induced pancreatitis (11).Patients who develop apparentdrug-induced acute pancreatitisshould still be evaluated for othercauses before attributing anepisode to particular medications.While searching for another, morecommon cause of acute pancreati-
tis, the temporal association ofmedication use and developmentof the episode should be evaluat-ed. The clinician needs to recog-nize that drug-induced pancreati-tis can occur at any point in thecourse of a medication regimen,ranging from at or shortly afterinitiation to an idiosyncratic reaction after prolonged use. Itmay be necessary to rechallengewith the drug if it is critical forthe patient’s health. In general,drug-induced acute pancreatitis isless common than was previouslybelieved, and without strong evi-dence for drug-related pancreati-tis, medications can usually becontinued (12).
6. Everhart JE, Khare M,Hill M, Maurer KR.Prevalence and eth-nic differences ingallbladder disease inthe United States.Gastroenterology.1999;117:632-9.[PMID: 10464139]
7. Yadav D, WhitcombDC. The role of alco-hol and smoking inpancreatitis. Nat RevGastroenterol Hepa-tol. 2010;7:131-45.[PMID: 20125091]
8. Kristiansen L, Grøn-baek M, Becker U, Tol-strup JS. Risk of pan-creatitis according toalcohol drinkinghabits: a population-based cohort study.Am J Epidemiol.2008;168:932-7.[PMID: 18779386]
9. Ewald N, Hardt PD,Kloer HU. Severe hy-pertriglyceridemiaand pancreatitis:presentation andmanagement. CurrOpin Lipidol.2009;20:497-504.[PMID: 19770656]
11. Badalov N, Baradari-an R, Iswara K, Li J,Steinberg W, TennerS. Drug-inducedacute pancreatitis:an evidence-basedreview. Clin Gas-troenterol Hepatol.2007;5:648-61.[PMID: 17395548]
12. Nitsche CJ, JamiesonN, Lerch MM, Mayer-le JV. Drug inducedpancreatitis. BestPract Res Clin Gas-troenterol.2010;24:143-55.[PMID: 20227028].
Table 1. Causes of Acute PancreatitisMore Common Causes Comments
Gallstones and microlithiasis Most common cause Alcohol abuse Alcohol-related disease usually occurs only occurs after
>5–10 y of heavy drinking Drugs More common in older patients, HIV-positive persons, or in
those receiving immunomodulating agentsERCP Can be a trigger, particularly if performed by an inexperienced
clinician or if the patient has sphincter of Oddi dysfunctionHyperlipidemia Usually with extremely elevated triglyceride levels (>1000 mg/dL)Hypercalcemia Commonly caused by hyperparathyroidism or cancer, can be a
trigger by increasing activation of trypsinogenGenetic Hereditary, and research has linked gene mutations in cationic
trypsinogen (PRSS1), SPINK1, or CFTR genes with acute andchronic pancreatitis
Autoimmune pancreatitis Diffuse “sausage shaped” finding on imaging with rim enhance-ment or ductal abnormalities.
Infections Includes viruses: mumps, coxsackievirus, cytomegalovirus, varicella,HSV, HIV; bacteria: Mycoplasma, Legionella, Leptospira, Salmonella;Parasites: Toxoplasma, Cryptosporidium, Ascaris; and fungi: Aspergillus
Idiopathic Accounts for approximately 15%–20% of cases; causes includesphincter of Oddi dysfunction, microlithiasis, and biliary sludge;anatomical abnormalities
Less common causes
Cystic lesions of the pancreas More likely if cysts involve the main duct, such as pancreatic intraductal papillary mucinous tumor
Cystic fibrosis Rare, occurs when some viable pancreatic tissue remainsPancreas divisum Controversial as a cause so exclude all other causes first Pancreatic cancer Focal pancreatitis can indicate an underlying massPenetrating peptic ulcer Rare, clue is thickening of the duodenal wallPostsurgical Such as ischemia related to bypass surgeryTrauma History is usually compelling Tropical pancreatitis Endemic in some parts of Asia and AfricaVasculitis Rare even in patients with vasculitis
13. Cheng CL, ShermanS, Watkins JL, et al.Risk factors for post-ERCP pancreatitis: aprospective multi-center study. Am JGastroenterol.2006;101:139-47.[PMID: 16405547]
14. Saad AM, Fogel EL,McHenry L, et al.Pancreatic ductstent placementprevents post-ERCPpancreatitis in pa-tients with suspect-ed sphincter of Oddidysfunction but nor-mal manometry re-sults. GastrointestEndosc. 2008;67:255-61.[PMID: 18028920].
15. Nordback I, Pelli H,Lappalainen-Lehto R,et al. The recurrenceof acute alcohol-as-sociated pancreatitiscan be reduced: arandomized con-trolled trial. Gas-troenterology.2009;136:848-55.[PMID: 19162029]
An important iatrogenic risk factorfor development of acute pancreati-tis is ERCP. The risk for acute pan-creatitis related to ERCP rangesfrom 5% to 20%, depending onphysician-related factors, such asthe level of experience performingthe procedure, and patient charac-teristics, especially sphincter ofOddi dysfunction and a history ofprevious ERCP-related pancreatitis(13). From a technical standpoint,the incidence of ERCP-relatedpancreatitis seems to be decreasedby placement of a pancreatic ductstent at the time of ERCP (14).Careful patient selection and avoid-ance of ERCP, unless clearly indi-cated, will decrease the risk foracute pancreatitis resulting fromthis procedure.
Other less common causes ofacute pancreatitis are listed inTable 1. Rare causes of unex-plained acute pancreatitis includecancer; mucinous neoplasm; re-mote history of trauma; infectionscaused by parasites, such as toxo-plasmosis and cryptosporidiosis;and viruses (cytomegalovirus, Epstein Barr virus). Autoimmuneprocesses leading to pancreatitis,such as vasculitis and autoimmunepancreatitis, are well described butunderrecognized.
What behavioral advice shouldclinicians give to a patient tominimize the chance of a repeatedepisode of acute pancreatitis?After a clear cause of acute pan-creatitis has been identified, ef-forts should be made not only toeliminate the cause but also toprovide counseling and educationfor the patient about the need toavoid known risk factors for thedisease. When alcohol consump-tion has been identified as thecause, patients should be evaluatedfor alcohol abuse or dependence.The patient should receive inten-sive counseling about the exigencyof abstaining from alcohol toavoid repeated episodes of acute
pancreatitis or chronic pancreati-tis, as well as the other well-known complications of alcoholabuse and dependence. In this sit-uation, one brief alcohol counsel-ing session will not suffice.
In a randomized, controlled trial of 120patients hospitalized for a first episode ofalcohol-associated acute pancreatitis, 59patients received repeated 30-minute al-cohol reduction and social stressor coun-seling intervention both before dischargeand after 6-months while the 61 controlparticipants received only the initialcounseling session (15). Over the next 2 years, significantly fewer recurrentepisodes occurred in the patients with re-peated alcohol counseling.
In addition, referral to alcohol spe-cialty treatment will improve absti-nence, ideally with support to ensure that the patient receives this care.
As noted, there are few drugs witha definite link to acute pancreatitis(12). Physicians should be alertfor drug-induced pancreatitis incertain groups, such as the elderlyor patients with HIV infection orcancer, who often take multiplemedications (16). However, evenwhen the association seems to beclear, questions may linger withregard to whether it was the drugor the underlying condition forwhich the drug was prescribedthat caused the pancreatitis.
Patients who develop acute pan-creatitis because of hypertriglyc-eridemia should be counseledabout lifestyle modifications, suchas reducing sugars and unhealthyfats, and should have aggressivemedical interventions (fibrates ornicotinic acid) to reduce triglyc-eride levels to normal. When thetriglyceride level is !500 mg/dL,the first priority is to preventacute pancreatitis by reducing thelevel to <500; reducing the risk forcoronary heart disease is a second-ary goal, according to an expertpanel report (17).
17. Third Report of theExpert Panel on De-tection, Evaluation,and Treatment ofHigh Blood Choles-terol in Adults (ATPIII Final Report). Cir-culation.2002;106:3143-421.[PMID: 12485966].
sequestration seen in more severecases. Jaundice indicates biliary treeobstruction. The clinician shouldperform a careful abdominal exami-nation focusing especially on aus-cultation for bowel sounds, locationof pain, guarding (usually severe),rebound, and distention. Distentionwith absent bowel sounds indicatesileus. Ecchymosis in the flanks(Grey-Turner sign) or around theumbilicus (Cullen sign) are indica-tive of blood in the abdomen frompancreatic necrosis. Mental statusimpairment is also an indicator ofmore severe pancreatitis and mayoccur as a result of septicemia, hy-poxemia, electrolyte imbalance, oralcohol use. Multiorgan dysfunc-tion signifies a more severe episodewith complications, such as pancre-atic necrosis.
A patient with gallstones and a his-tory of fever, chills, and/or rigorssuggests ascending cholangitis, butthese symptoms may be due only tothe inflammatory process associat-ed with acute pancreatitis.
What laboratory tests are usefulin the evaluation of acutepancreatitis?Elevation of the serum amylaseand/or lipase levels at least threetimes the upper limit of normal is akey component of diagnosing acutepancreatitis. Measurement of serumamylase levels has good sensitivitybut low specificity, signifying a highfalse-positive rate (18). Other causes
What elements of the history and examination are helpful insuggesting a diagnosis of acutepancreatitis?The most common presentingsymptom of acute pancreatitis isabdominal pain, classically de-scribed as occurring in the upperabdomen and radiating to the back.The pain is typically severe andpersistent without alleviating or relieving factors and is usually asso-ciated with nausea and vomiting.When ileus is present, vomiting reduces the pain associated withacute pancreatitis only slightly.
In patients with suspected acutepancreatitis, a detailed historyshould address the potential causeslisted in Table 1. Previous cholecys-tectomy for gallstones in a personwith no or minimal use of alcoholincreases the likelihood of pancre-atitis due to retained gallstones.Careful history should assess forhyperlipidemia, abdominal trauma,similar previous episodes, or priorERCP. A detailed list of medica-tions must be reviewed, focusing onthe likelihood of a drug being thecause as well as timing of use (11).
On physical examination, vitalsigns including pulse, orthostaticblood pressure, and respiratory ratemust be performed to evaluate hy-dration status and indicate theseverity of pancreatitis. Tachycardiaand hypotension represent intravas-cular depletion secondary to fluid
Prevention... Gallstones and excessive alcohol consumption are the two mostcommon causes of acute pancreatitis. It is not possible to predict which patientswith these conditions will develop this complication. Removal of gallstones andalcohol cessation can help prevent recurrences. Other less common causes includehypertriglyceridemia and side effects of medications, but alcohol and gallstonesshould first be ruled out as sole or concurrent causes. Recurrent pancreatitis re-lated to hypercalcemia is best prevented through treatment of the underlyingcause. Iatrogenic acute pancreatitis due to ERCP can be reduced by careful pa-tient selection and possibly through placement of a pancreatic duct stent.
CLINICAL BOTTOM LINE
Diagnosis
19. Liu KJ, Atten MJ,Lichtor T, et al.Serum amylase andlipase elevation is as-sociated with in-tracranial events. AmSurg. 2001;67:215-9;discussion 219-20.[PMID: 11270877]
20. Seno T, Harada H,Ochi K, et al. Serumlevels of six pancre-atic enzymes as re-lated to the degreeof renal dysfunction.Am J Gastroenterol.1995;90:2002-5.
21. Manjuck J, Zein J,Carpati C, Astiz M.Clinical significanceof increased lipaselevels on admissionto the ICU. Chest.2005;127:246-50.[PMID: 15653991]
of elevated serum amylase levels in-clude disorders of salivary glands andfallopian tubes, intestinal ischemia,perforated peptic ulcer, and chronicrenal insufficiency. To improve speci-ficity, the level of the serum amylaseor lipase needs to be three times nor-mal. Measurement of lipase levels ismore sensitive than that of amylaselevels in acute alcoholic pancreatitisor when patients present to theemergency department days afterdisease onset because it remains ele-vated for a longer period. However,lipase can also be falsely elevated incases of renal insufficiency and headtrauma or an intracranial mass aswell as in patients receiving heparintherapy (through activation oflipoprotein lipase) (19, 20). Elevatedserum lipase levels are also commonamong critically ill patients in the in-tensive care unit (ICU) (21). Simul-taneous measurement of amylase andlipase levels does not seem to im-prove diagnostic accuracy (18).
No enzyme assay can assess theseverity or cause of an episode ofacute pancreatitis. Serum C-reactiveprotein at 48 hours is the best avail-able laboratory marker of severity.Liver enzymes should also be rou-tinely checked. Elevated liver en-zymes (alanine transaminase) >150IU/L has a 95% positive predictivevalue and a specificity of 96% butsensitivity of less than 50%; the ac-curacy of the aspartate transaminaseis similar (22). Elevations can sug-gest gallstone pancreatitis. Triglyc-eride levels should be checked because levels above >1000 mg /dLcan precipitate acute pancreatitis thatis often severe. A low serum calciumlevel can cause acute pancreatitis butmay also be a consequence of acutepancreatitis due to other causes (23).
The presence of leukocytosis oncomplete blood count may resultfrom the acute pancreatic inflam-mation alone or point to an underlying infectious process. In-creased hematocrit and blood ureanitrogen (BUN) levels may reveal
hemoconcentration, indicative offluid sequestration. Early changesin the serial BUN levels provide themost useful assessment of responseto initial resuscitation (24).
An acute drop in hemoglobin in anunstable patient may represent he-morrhagic pancreatitis. Patientswith pancreatitis may also developdisseminated intravascular coagu-lopathy, perhaps due to circulatingpancreatic enzymes or to vascularinjury precipitating consumption ofcoagulation factors (25).
What other diagnoses shouldclinicians consider in a patientwith possible acute pancreatitis?The clinical presentation of upperabdominal pain with nausea, vomit-ing, and fever has a broad differential(Table 2). Although peptic ulcer per-foration often mimics this presenta-tion, it is distinguished by free airseen on imaging studies. Acutecholecystitis, symptomatic choledo-cholithiasis, and cholangitis are typi-cally described as causing right upperquadrant pain but can also presentwith epigastric pain similar to that ofacute pancreatitis. Normal serumamylase and lipase levels as well ascharacteristic imaging findings, suchas gallbladder wall thickening(cholecystitis) or common bile ductstones (choledocholithiasis), helpdifferentiate biliary disease fromacute pancreatitis but, as noted, acutepancreatitis may also present withgallstone-related biliary obstruction.Patients with intestinal obstructionwill have abdominal distention, col-icky abdominal pain, and an obstruc-tive bowel pattern on imaging. Theymay also have elevated serum amy-lase levels but these levels are usuallylower than those associated withacute pancreatitis. Mesenteric vascu-lar obstruction should be suspectedin patients with underlying vascularor cardiac disease. Pain associatedwith nonobstructive mesenteric is-chemia is usually postprandial, andon rare occasions an abdominal bruitmay be heard. Table 2 lists additional
23. Schütte K, Malfer-theiner P. Markers forpredicting severityand progression ofacute pancreatitis.Best Pract Res ClinGastroenterol.2008;22:75-90.[PMID: 18206814]
24. Wu BU, Johannes RS,Sun X, Conwell DL,Banks PA. Earlychanges in bloodurea nitrogen pre-dict mortality inacute pancreatitis.Gastroenterology.2009;137:129-35.[PMID: 19344722]
25. Saif MW. DIC sec-ondary to acutepancreatitis. Clin LabHaematol.2005;27:278-82.[PMID: 16048498]
causes of upper abdominal pain thatshould be considered in the differen-tial of acute pancreatitis.
What is the role of imagingstudies in the evaluation of acute pancreatitis?Imaging plays an important role inidentify the cause of the attack ofacute pancreatitis and in assessingseverity (26). A plain abdominal ra-diograph may show nonspecificsigns of acute pancreatitis, such as asentinel loop (localized ileus involv-ing the jejunum), colon cutoff sign(isolated distention of the trans-verse colon), duodenal distentionwith air and fluid, and pleural effu-sion localized to the left thorax. Incases of abdominal distention withacute pain, the X-ray may reveal
free air showing a perforated viscusas the cause of pain.
However, the initial imaging studyof choice is ultrasonography of theright upper quadrant because it isreadily available, noninvasive, inex-pensive, and relatively sensitive(95%) for diagnosing gallstone dis-ease. The presence of gallstonesand/or dilatation of the common bileduct supports stones as the cause ofacute pancreatitis. However, the dis-tal common bile duct and pancreasare frequently obscured by overlyingbowel gas and limit the sensitivity ofultrasonography for diagnosing gall-stone-associated pancreatitis.
In this case, a contrast-enhanced,thin-sliced, triple-phase computedtomography (CT) scan provides an
Table 2. Differential Diagnosis of Acute PancreatitisDisease Characteristics Findings
Perforated viscus, especially peptic ulcer Sudden onset of pain that increases over 30-60 min Intraperitoneal air presentAcute cholecystitis and biliary colic Epigastric or right upper quadrant pain that radiates Liver enzymes often elevated; ultrasonography
to right shoulder or shoulder blade may show thickened gallbladder, pericholecystic fluid
Intestinal obstruction Constant colicky pain Obstructive pattern can be seen on CT scan orabdominal series
Mesenteric vascular occlusion Classic triad is postprandial abdominal pain, Discrepancy between symptoms (severe pain) andweight loss, and abdominal bruit examination (benign abdominal examination)
Dissecting aortic aneurysm Sudden onset; pain may radiate to the lower extremities
Renal colic Flank pain radiates to the genitals; dysuria may Urinalysis with active sediment be present
Myocardial infarction Upper abdominal or chest pain Electrocardiography usually abnormalConnective tissue disorders with vasculitis Acute pancreatitis can be due to vasculitis Other signs of vasculitis usually present (skin,
joint, eye, and kidney involvement)Appendicitis Pain may start in epigastrium or periumbilical then Ultrasonography and and CT aid in diagnosis
migrate to right lower quadrantEctopic pregnancy Sudden onset of pain; menstrual abnormalities Rapid drop in hematocrit and intraperitoneal
often precede pain pelvic fluid on imaging should raise suspicionPneumonia Fever, malaise, and other respiratory symptoms Changes on physical examination of the chest
(dyspnea, cough, sputum production, chest pain) and abnormalities on chest X-ray possibly due to usually present ARDS or pleural effusion
27. Lankisch PG, Struck-mann K, Assmus C,Lehnick D, Maison-neuve P, LowenfelsAB. Do we need acomputed tomogra-phy examination inall patients withacute pancreatitiswithin 72 h after ad-mission to hospitalfor the detection ofpancreatic necrosis?Scand J Gastroen-terol. 2001;36:432-6.[PMID: 11336171]
28. Arvanitakis M, Del-haye M, De Maerte-laere V, et al. Com-puted tomographyand magnetic reso-nance imaging inthe assessment ofacute pancreatitis.Gastroenterology.2004;126:715-23.[PMID: 14988825]
29. Makary MA, DuncanMD, Harmon JW, etal. The role of mag-netic resonancecholangiography inthe management ofpatients with gall-stone pancreatitis.Ann Surg.2005;241:119-24.[PMID: 15621999]
30. Liu CL, Lo CM, ChanJK, et al. Detection ofcholedocholithiasisby EUS in acute pan-creatitis: a prospec-tive evaluation in100 consecutive pa-tients. GastrointestEndosc. 2001;54:325-30. [PMID: 11522972]
excellent image of the pancreas andcan identify choledocholithiasis orother causes of abdominal pain. CTscanning can also be useful to assessthe severity of the pancreatitis and inidentifying complications, such asnecrosis (infected or not), pseudocystformation, and diffuse pancreatic flu-id collection (27). However, early inthe course of disease a CT scan maynot show signs of pancreatitis or itsassociated complications. In addi-tion, intravenous contrast may accel-erate renal injury. When these fac-tors are a concern, magneticresonance imaging (MRI) offers analternative at greater cost to diagnoseand evaluate the severity of acutepancreatitis (28).
Among newer but even more costlyimaging modalities, the noninvasivemagnetic resonance cholangiopan-creatography (MRCP) has highsensitivity (>90%) for choledo-cholithiasis and can identify otheranatomical abnormalities, such aspancreas divisum, pancreatic ductabnormalities, and mucinous neo-plasm in the pancreas (29). It canbe useful to exclude the presence ofa retained stone or debris if there isa high index of clinical suspicion.
Secretin-enhanced MRI is usefulfor evaluating pancreatic functionand anatomy when the patient issuspected of having underlyingchronic pancreatitis. However, sincesecretin stimulates pancreatic secre-tion, it should not be obtained dur-ing an acute episode because itcould worsen the disease.
Endoscopic ultrasonography is bothsensitive and specific in identifyingsmall (e.g., "5 mm) gallstones inthe bile ducts (30) and can identifyanatomical abnormalities of thepancreas. Although it is more inva-sive than MRI, it can detect smallerstones and can be used when MRIis not possible (e.g., in critically illpatients or when it is contraindicat-ed, such as in patients with a car-diac pacer) (31, 32).
Which factors help to predict theprognosis of a patient with acutepancreatitis?Patients should be stratified by riskfor severe morbidity and death relat-ed to acute pancreatitis because ofthe disease’s protean manifestations,unpredictable course, and the needto identify persons who require in-tensive care. The Atlanta Classifica-tion of Acute Pancreatitis was developed in 1992 to standardizewhat was a heterogeneous set of cri-teria to diagnose the disease and toassess severity (1). However, becauseof a changing understanding of thepathophysiology and epidemiologyof acute pancreatitis, in 2008 a revi-sion was proposed to the AtlantaClassification (still being reviewedwith final approval expected by2011) that recognizes 2 phases of thedisease that were not appreciated bythe original classification (see theBox) (33). First, there is a peak inmortality usually within the firstweek of onset and another 2 to 6weeks after onset. In the first week,the severity of the disease is usuallyreflected by the extent of organ fail-ure. After that, mortality can be pre-dicted more by the presence of pancreatic necrosis and infection.
Therefore, when a patient firstpresents, clinicians need to be alertto the possibility of organ failure(34). As expected, progression fromsingle to multiorgan failure is a pre-dictor of increased mortality (35).Coagulopathy bodes poorly for pa-tients as indicated by platelet count<100 000/mm3, fibrinogen <100mg/dL, and fibrin split products>80 µg/mL. Similarly, low serumcalcium levels (" 7.5 mg/dL) carrya poor prognosis.
The Atlanta symposium alsoidentified the development of lo-cal complications (necrosis andabscess and pseudocyst formation)as indicative of severe acute pan-creatitis. Pancreatic necrosis isdemonstrated by poor perfusionand nonenhancement on CT scan
Atlanta Classification of AcutePancreatitis*
Severe acute pancreatitis• Organ failure (systolic blood pressure
inflammation. When both organfailure and infected pancreaticnecrosis are present, relative riskfor mortality doubles (45).
A variety of other classificationshave been developed to assess theseverity of acute pancreatitis earlyin the course of disease (Table 3),including Ranson criteria; theAcute Physiology and ChronicHealth Evaluation (APACHE-II
of more than 3 cm or >30% of thepancreas (but these dimensionsare being debated) (39). Apseudocyst is a fluid collectionwithin the pancreas, separated bya nonepithelized wall, that devel-ops over a period of weeks (bydefinition >4 wk). Infection of either pancreatic necrosis or apseudocyst can lead to abscess for-mation. Pancreatic fluid can alsoextravasate as a result of the
Table 3. Clinical Criteria for Determining Severity of Acute PancreatitisClassification Predictors Outcomes Based on Score Comments
Ranson criteria Admission measurements Mortality: 0%–3% for <3 criteria, Scoring on admission and at 48 h after (1 point each): Age >55 years; 11%–15% for 3–5 criteria, presentation; limited predictive power reported inleukocyte count >16 000/mm3; and 40% for !6 criteria (36) meta-analysis (37)glucose >200 mg/dL; LDH >350 U/L; AST >250 U/L; fluid sequestration >6 LMeasurement at 48 h (1 point each): HCT decrease of 10 volume %; BUN increase of 5 mg/dL; calcium <8 mg/dL; PaO
2<60 mm Hg; base deficit
>4 mEq/LAcute Physiology and Chronic Daily: Based on diverse variables, Mortality: <4% for a score <8, Requires data usually only available when
Health Evaluation including age, physiology, and 11%–18% for a score !8 (39) patient is in ICU; an increasing APACHE-II (APACHE) II scoring system long-term health; equation score in the first few days of hospitalization
available at www.sfar.org/ indicates worsening severity whereas the oppo- scores2/apache22.html#calcul; site indicates improvement (38); APACHE-IIAdding BMI to APACHE-II and APACHE-III have a similar performance(the APACHE-O score)increases discrimination (1 point added for BMI 26-30; 2 points for BMI >30) (38)
Modified Glasgow prognostic At 48 h after admission (1 point Severe episode: score !3 within Takes 48 h to complete; similar performance to criteria (Imrie scoring system) each): PaO
Bedside Index for Severity in Within 24 h after presentation Mortality: <1% in the lowest Assessed at 24 h; prognostic accuracy similar to Acute Pancreatitis (BISAP) (1 point each): BUN >25 mg/dL; risk group and >20% in the other scoring systems (42)score impaired mental status; systemic highest risk group.
inflammatory response syndrome (see text for definition); age >60 y; presence of pleural effusion (41)
Modified CT severity index CT scan assessment of Correlated with length of stay Studied in small patient populationspancreatic inflammation and and clinical complications (44)necrosis, plus assessment ofextrapancreatic complications (43)
AST = aspartate transaminase; BMI = body mass index; BUN = blood urea nitrogen; CT = computed tomography; HCT = hematocrit; ICU = intensive care unit;LDH = lactate dehydrogenase; WBC = white blood cells.
32. Sedlack R, Affi A,Vazquez-Sequeiros E,Norton ID, Clain JE,Wiersema MJ. Utilityof EUS in the evalua-tion of cystic pancre-atic lesions. Gas-trointest Endosc.2002;56:543-7.[PMID: 12297771]
33. Acute PancreatitisClassification Work-ing Group. Revisionof the Atlanta classi-fication of acutepancreatitis (3rd re-vision). www.pan-creasclub.com/re-sources/AtlantaClassification.pdf. Ac-cessed 16 Septem-ber 2010.
34. Johnson CD, Abu-Hilal M. Persistent or-gan failure duringthe first week as amarker of fatal out-come in acute pan-creatitis. Gut.2004;53:1340-4.[PMID: 15306596]
35. Brown A, Orav J,Banks PA. Hemocon-centration is an earlymarker for organ fail-ure and necrotizingpancreatitis. Pan-creas. 2000;20:367-72. [PMID: 10824690]
36. Blum T, Maison-neuve P, LowenfelsAB, Lankisch PG. Fa-tal outcome in acutepancreatitis: its oc-currence and earlyprediction. Pancre-atology. 2001;1:237-41. [PMID: 12120201]
37. De Bernardinis M, Vi-oli V, Roncoroni L,Boselli AS, Giunta A,Peracchia A. Discrim-inant power and in-formation content ofRanson’s prognosticsigns in acute pan-creatitis: a meta-ana-lytic study. Crit CareMed. 1999;27:2272-83. [PMID: 10548220]
38. Banks PA, FreemanML. Practice Parame-ters Committee ofthe American Col-lege of Gastroen-terology. Practiceguidelines in acutepancreatitis. Am JGastroenterol.2006;101:2379-400.[PMID: 17032204]
39. Johnson CD, Toh SK,Campbell MJ. Com-bination of APACHE-II score and an obe-sity score(APACHE-O) for theprediction of severeacute pancreatitis.Pancreatology.2004;4:1-6.[PMID: 14988652]
and III) scale; the Modified Glas-gow prognostic criteria (also knownas the Imrie scoring system); Bed-side Index for Severity in AcutePancreatitis (BISAP) score; and theModified CT Severity Index.
It is important to note that neitherserum amylase nor lipase levels arepredictive of the severity of acutepancreatitis. On the other hand, C-reactive protein has been widelyused to predict the severity of acutepancreatitis (18), and in critically illpatients, it has been shown to beassociated with increased risk fororgan failure and death (46). Pro-calcitonin has been associated withpancreatic infection and can beused as an indicator of the need forfine-needle aspiration of pancreaticnecrosis (23).
What are the indications forhospitalization and for intensive care for a patient with acutepancreatitis?Patients with acute pancreatitisshould be hospitalized until they havebeen observed for a sufficient periodto evaluate disease severity and pro-gression. Essential management
includes aggressive intravenous fluidresuscitation with no fluids or solidsby mouth. Patients often require painmanagement with intravenous med-ications, typically opiates are used andmust be monitored for side effects,such as respiratory depression. Stablepatients having a mild episode whohave a history of multiple episodescan sometimes be managed on anoutpatient basis.
Such tests as ERCP are usually donein an inpatient setting when indicat-ed. Severe acute pancreatitis requiresclose inpatient monitoring, and thepatient should be transferred to ICUif organ failure develops (47). In eld-erly patients with underlying cardio-vascular disease, aggressive fluid resuscitation should be administeredin an ICU and may require a centralvenous catheter for more accuratefluid monitoring. Transfer to a spe-cialized monitored unit, althoughnot necessarily an ICU, should beconsidered for patients with highbody mass index (>30), decreasedurine output < 50 mL/h, tachycardia(pulse rate > 120 beats/min), signs ofencephalopathy, and/or need for ad-ditional narcotics (39).
Diagnosis... In acute pancreatitis, diagnosis is based on the presence at least 2 of 3features: abdominal pain; increased pancreatic enzyme, amylase, and/or lipase levelsto !3 times the upper limit of normal; and imaging tests showing characteristicfindings of acute pancreatitis. Ultrasonography of the right upper quadrant may re-veal stones or biliary duct dilatation and CT scan can be useful to assess for pancre-atic edema, necrosis, or pseudocyst formation. MRI offers an alternative but is morecostly. Assessing the severity of the attack of acute pancreatitis using clinical labora-tory parameters; imaging; and standard measurements, such as APACHE-II, BISAP, CTseverity index, or Ranson criteria, can guide management. Acute pancreatitis shouldbe managed in the inpatient setting with rare exceptions and patients with organfailure or severe comorbid conditions should be treated in the ICU.
CLINICAL BOTTOM LINE
Treatmentcan experience a significant loss ofintravascular volume due to thirdspacing and increased permeabilityfrom release of inflammatory media-tors. Compromised intravascular vol-ume can lead to decreased perfusion
How should clinicians managefluids in a patient with acutepancreatitis?Fluid resuscitation is a critical com-ponent of management of patientswith acute pancreatitis because they
40. Chatzicostas C,RoussomoustakakiM, Vlachonikolis IG,et al. Comparison ofRanson, APACHE IIand APACHE III scor-ing systems in acutepancreatitis. Pan-creas. 2002;25:331-5.[PMID: 12409825].
42. Wu BU, Johannes RS,Sun X, et al. The ear-ly prediction of mor-tality in acute pan-creatitis: a largepopulation-basedstudy. Gut.2008;57:1698-703.[PMID: 18519429] 43.Papachristou GI,Muddana V, Yadav D,et al. Comparison ofBISAP, Ranson’s,APACHE-II, and CTSIscores in predictingorgan failure, com-plications, and mor-tality in acute pan-creatitis. Am JGastroenterol.2010;105:435-41;quiz 442.[PMID: 19861954]
44. Mortele KJ, WiesnerW, Intriere L, et al. Amodified CT severityindex for evaluatingacute pancreatitis:improved correla-tion with patientoutcome. AJR Am JRoentgenol.2004;183:1261-5.[PMID: 15505289]
45. Petrov MS,Shanbhag S,Chakraborty M, et al.Organ failure and in-fection of pancreaticnecrosis as determi-nants of mortality inpatients with acutepancreatitis. Gas-troenterology. 2010Jun 9. [Epub aheadof print][PMID: 20540942]
46. Lobo SM, Lobo FR,Bota DP, et al. C-re-active protein levelscorrelate with mor-tality and organ fail-ure in critically ill pa-tients. Chest.2003;123:2043-9.[PMID: 12796187]
47. Zhang XP, Wang L,Zhou YF. The patho-genic mechanism ofsevere acute pancre-atitis complicatedwith renal injury: areview of currentknowledge. Dig DisSci. 2008;53:297-306.[PMID: 17597411]
48. Frossard J-L, SteerML, Pastor CM.Acute pancreatitis.Lancet.2008;371:143-52.[PMID: 18191686]
However, studies comparing naso-gastric with nasojejunal feedinghave not shown significant differ-ences in outcomes, but larger com-parative studies are required beforepractice recommendations arechanged.
A meta-analysis of 6 studies showed alower incidence of infections, reducedsurgical intervention and shorter hospitalstay in patients with acute pancreatitisreceiving nasojejunal feeding (50). In onestudy, nasojejunal feeding was associat-ed with a shorter hospital stay and fewercomplications than parental nutrition(sepsis, 4% vs. 33%; metabolic complica-tions, 15% vs. 52%, respectively), and asavings of $2362 (51).
An ongoing National Institutes ofHealth multi-center trial, called theStudy of Nutrition in Acute Pan-creatitis (SNAP), is evaluating na-sogastric vs. nasojejunal feeding.Difficulty placing or maintaining anasojejunal tube also requires par-enteral nutrition. Notably, parenter-al nutrition may be required insome critically ill patients as well asthose with severe ileus.
What other supportive care may bebeneficial for acute pancreatitis?Oxygen may reduce the acute res-piratory distress syndrome thatcan occur in the early stages ofacute pancreatitis. Pain manage-ment is another key aspect oftreatment. Due to the severity ofpain with acute pancreatitis andthe inability to take pills, par-enteral narcotic analgesics are es-sential. Opiates are usually admin-istered every 2 to 4 hours. Apatient-controlled analgesia pumpoffers an alternative when bolusesof pain medications provide inad-equate pain control. Morphine hasbeen theoretically implicated inincreasing pressure in the sphinc-ter of Oddi and potentially de-creasing pancreatic and biliaryflow into the small bowel lumen,but this has not been confirmed inclinical studies. Meperidine, mor-phine and hydromorphone are
of the pancreas and such complica-tions as pancreatic necrosis and renalfailure. Fluid administration shouldbe guided by vital signs, urine out-put, and change in hematocrit at ad-mission, 12 hours, and 24 hours(39). Increasing hematocrit or BUNis a poor prognostic sign and indi-cates worsening severity.
How should clinicians manage thenutritional needs of a patientwith acute pancreatitis?In mild acute pancreatitis, nutri-tional support is not necessary.Once pain has diminished alongwith nausea and vomiting, oral nu-trition can be started. It begins withclear liquids and clinical monitoringfor change in pain and symptoms ofnausea and vomiting. Resolution ofimaging findings and normalizationof amylase and lipase may not occurfor up to a week, so the diet shouldbe advanced based on how the pa-tient feels. There is no clear consen-sus about fat restriction.
Patients with moderate or severepancreatitis must usually abstainfrom solids and liquids for severaldays to weeks. Although mortalityrates do not differ substantially be-tween parenteral and enteral nutri-tion, the latter has been shown toreduce the rate of infection, surgicalinterventions, and noninfectiouscomplications (48). United King-dom guidelines for management ofacute pancreatitis recommend en-teral nutrition for all patients withsevere acute pancreatitis, but statethat the nasogastric route is pre-ferred for feeding because it is ef-fective in ! 80% of cases (49).However, the nasojejunal route isincreasingly being used in theUnited States. Although tubeplacement is more difficult, enteralfeeding beyond the ligament ofTreitz may decrease the risk for in-fectious complications that can oc-cur with feeding methods in whichthe small bowel can be affected byedema and permeability from in-flammatory mediators is increased.
49. UK Working Party onAcute Pancreatitis.UK guidelines for themanagement ofacute pancreatitis.Gut 2005;54(SupplIII):iii1-iii9.
50. Louie BE, NoseworthyT, Hailey D, GramlichLM, Jacobs P,Warnock GL. 2004MacLean-Muellerprize enteral or par-enteral nutrition forsevere pancreatitis: arandomized con-trolled trial andhealth technology as-sessment. Can J Surg.2005;48:298-306.[PMID: 16149365]
51.Abou-Assi S, Craig K,O’Keefe SJ.Hypocaloric jejunalfeeding is betterthan total parenteralnutrition in acutepancreatitis: resultsof a randomizedcomparative study.Am J Gastroenterol.2002;97:2255-62.[PMID: 12358242]
52. Villatoro E, Mulla M,Larvin M. Antibiotictherapy for prophy-laxis against infec-tion of pancreaticnecrosis in acutepancreatitis.Cochrane DatabaseSyst Rev. 2010 May12;5:CD002941.[PMID: 20464721]
53. Carter CR, McKay CJ,Imrie CW. Percuta-neous necrosectomyand sinus tract en-doscopy in the man-agement of infectedpancreatic necrosis:an initial experience.Ann Surg.2000;232:175-80.[PMID: 10903593]
54. Connor S, Ghaneh P,Raraty M, Sutton R,Rosso E, Garvey CJ,et al. Minimally inva-sive retroperitonealpancreatic necrosec-tomy. Dig Surg.2003;20:270-7.[PMID: 12748429].
55. van Santvoort HC,Besselink MG, BakkerOJ, et al. A step-upapproach or opennecrosectomy fornecrotizing pancre-atitis. N Engl J Med.2010;362:1491-502.[PMID: 20410514]
more commonly used narcotics forpain control in acute pancreatitis.
What is the role of antibiotics inthe management of patients withacute pancreatitis?Antibiotics are not currently rec-ommended for mild interstitialpancreatitis or even for moderate tosevere pancreatitis with sterilenecrosis. Studies of prophylacticadministration of antibiotics to de-crease infectious complicationshave been largely nonsupportive.
A recent Cochrane review found no benefitof antibiotics to prevent infection of pan-creatic necrosis or mortality, with the pos-sible exception of the #-lactam imipenem,that was associated with a significant de-crease in pancreatic infection (52). The re-viewers concluded that better-designedstudies would be required before antibioticprophylaxis could be recommended.
However, antibiotics are definitely re-quired to treat ascending cholangitis,infected pancreatic necrosis, or an in-fected pseudocyst. When the patientseems to be septic or infection is sus-pected, a fever workup should be con-ducted with cultures and a chest X-ray. If needed, CT-guided needleaspiration of a necrotic area of thepancreas should be cultured for bacte-ria and fungi. If the workup is nega-tive, continue antibiotics if the patienthas septicemia, organ failure, or !30%necrosis of the pancreas (5).
For an infected necrotic pancreas,the choice of antibiotic is guided bythe culture. For gram-negative or-ganisms, options include imipenem,meropenem, ofloxacin, orciprofloxacin with metronidazole, ora third-generation cephalosporinwith metronidazole. Patients withinfected pancreatic necrosis shouldbe closely observed to assess for re-sponse and surgical debridementshould be considered when the pa-tient does not improve—mortality ishigh if this disorder is not treatedaggressively (49).
There are multiple approaches fordebridement but no consensus on
which one is best. Open surgicaldebridement has been a standard,but debridement with a percuta-neous nephroscope offers an alter-native (53, 54).
A recent multicenter study randomly as-signed 88 patients with necrotizing pan-creatitis and suspected or confirmed in-fected necrotic tissue to primary opennecrosectomy or a step-up treatment ap-proach (percutaneous drainage followedby minimally invasive retroperitonealnecrosectomy if needed) (55). Major com-plications or death occurred in 69% of pa-tients in the open necrosectomy group vs.40% in the step-up treatment group.
Case reports have also describedendoscopic transgastric endoscopicdebridement of an infected area ofnecrosis in selected patients whoare poor surgical candidates (56).This approach should be consid-ered in advanced centers with ex-pertise in these techniques.
When should clinicians considerconsultation with a gastro-enterologist, a surgeon, or aninterventional radiologist?For patients who have mild acutepancreatitis with a known cause,consultation is usually unneces-sary. However, if the cause is un-clear or pancreatitis tends to recur,a gastroenterology consult may beuseful. In patients with more se-vere attacks, gastroenterology consultation can assist with man-agement and monitoring for complications. Further, when gall-stone pancreatitis is suspected,consultation for ERCP may benecessary, as noted below.
When a patient develops necrotizingpancreatitis or abscesses or pseudo-cysts, or pancreatic fluid collection isnecessary, both a surgeon and a gas-troenterologist should be consulted.These patients usually require a teamapproach because surgical, endoscop-ic, and percutaneous drainage meth-ods should be considered. Endoscopicdrainage of pseudocysts has been as-sociated with better outcomes (57).Because of limited data on endoscopic
57. Seewald S, Ang TL,Teng KC, SoehendraN. EUS-guideddrainage of pancre-atic pseudocysts, ab-scesses and infectednecrosis. Dig Endosc.2009;21 Suppl 1:S61-5. [PMID: 19691738]
58. Maniatis P, Delis S,Fagrezos D, et al. Theinterventional radio-logical procedures ofthe infections ofpancreas. Infect Dis-ord Drug Targets.2010;10:5-8.[PMID: 20180752]
59. Petrov MS, vanSantvoort HC,Besselink MG, et al.Early endoscopic ret-rograde cholan-giopancreatographyversus conservativemanagement inacute biliary pancre-atitis withoutcholangitis: a meta-analysis of random-ized trials. Ann Surg.2008;247:250-7.[PMID: 18216529]
60. Loveday BPT, Srini-vasa S, Vather R, etal. High quantity andvariable quality ofguidelines for acutepancreatitis: a sys-tematic review. Am JGastroenterol.2010;105:1466-76.
61. Nathens AB, CurtisJR, Beale RJ et al.Management of thecritically ill patientwith severe acutepancreatitis. CritCare Med.2004;32:2524-36.
drainage of pancreatic necrosis but especially when infected, surgical in-tervention may be required. An inter-ventional radiology consultation maybe useful for percutaneous CT-guidedcatheter drainage of infected pancre-atic pseudocysts (58). A trial of per-cutaneous drainage followed by minimally invasive retroperitonealnecrosectomy, if necessary, versus sur-gery with open necrosectomy foundthat the minimally invasive approachhad fewer major complications ordeath (55). When gallstones are pres-ent, patients need to be evaluated by asurgeon for cholecystectomy.
What are the indications for ERCP?Presence of a retained bile ductstone seen on imaging is an indi-cation for ERCP to perform bil-iary sphincterotomy and stone
removal. Urgent ERCP is indi-cated if cholangitis is suspected.In the absence of these criteria,studies have found that earlyERCP was associated with in-creased complications.
A meta-analysis of 7 randomized trialsfound no significant reduction in overallcomplications or mortality from earlyERCP in patients with predicted mild or se-vere acute biliary pancreatitis withoutacute cholangitis (59).
Several studies have shown an ad-vantage of ERCP in pancreatitisfrom obstructive biliary disease. Pa-tients presenting with complicatedacute pancreatitis due to a disruptedpancreatic duct with a leak may alsobenefit from ERCP and placementof a pancreatic duct stent.
What is the role of patienteducation in the management ofacute pancreatitis?Patient education plays an impor-tant role in preventing recurrentacute pancreatitis. Lifestyle meas-ures, such as cessation of alcoholconsumption, are critical. Educa-tion about the risks of certainmedications if implicated in theinitial episode should also be pro-vided with careful monitoring.Dietary modification and adher-ence to lipid-lowering medica-tions are both necessary in patients with pancreatitis due tohypertriglyceridemia.
What do professionalorganizations recommend withregard to the care of patientswith acute pancreatitis?A recent summary has assessed thequality of 30 clinical guidelines re-garding management of acute pan-creatitis that were published between1988 and 2008 (60). Among themore recent U.S. clinical guidelines,those from the American ThoracicSociety (2004), American College ofGastroenterology (2006), and theAmerican Gastroenterological Asso-ciation (2007) earned high qualityscores (5, 39, 61). The Box summa-rizes the most recent 2 guidelines.
Treatment... Aggressive fluid resuscitation is the most important approach to manageacute pancreatitis. Appropriate pain control and supportive care with oxygen supple-mentation are additional basic measures. In patients with a prolonged course, enteralnutrition is preferred to parenteral nutrition whenever possible. Antibiotics are onlyrecommended for a documented infectious process or if there is !30% necrosis. If thecause of acute pancreatitis is unclear or ERCP reveals retained gallstones, consultationby a gastroenterologist is indicated. A team approach with both a gastroenterologistand surgeon is indicated for patients with organized necrosis (sterile or infected),pseudocyst, or abscess. In some cases, an interventional radiologist should be consult-ed for specialized diagnostic and therapeutic imaging techniques.
CLINICAL BOTTOM LINE
PracticeImprovement
Inthe
C linicTool Kit
In the Clinic
AcutePancreatitis
PIER Modulewww.pier.acponline.orgAccess the PIER module on acute pancreatitis. PIER modules provide evidence-
based, updated information on current diagnosis and treatment in an electronicformat designed for rapid access at the point of care.
The PIER module on acute pancreatitis includes two tables to help guide diagnosis.
Patient Informationwww.annals.org/intheclinic/toolkit-acutepancreatitis.htmlAccess the Patient Information material that appears on the following page
for duplication and distribution to patients.http://digestive.niddk.nih.gov/ddiseases/pubs/pancreatitis/Access information on pancreatitis from the NIDDK’s National Digestive
Diseases Information Clearinghouse.www.nlm.nih.gov/medlineplus/ency/article/000287.htmwww.nlm.nih.gov/medlineplus/spanish/ency/article/000287.htmAccess information on acute pancreatitis in English and Spanish from the
National Library of Medicine’s Medline Plus.www.gastro.org/patient-center/digestive-conditions/pancreatitisAccess “Understanding Pancreatitis” from the American Gastroenterological
Association.
Clinical Guidelineswww.acg.gi.org/physicians/guidelines/AcutePancreatitis.pdfThe American College of Gastroenterology published practice guidelines in
acute pancreatitis in 2006.www.gastrojournal.org/article/S0016-5085%2807%2900592-6/fulltextThe American Gastroenterological Association Institute published a Medical Position
Statement on the management of acute pancreatitis in 2007.
The PIER module on acute pancreatitis includes two tablesto help guide diagnosis.
Quality MeasuresThere are currently no Centers for Medicare & Medicaid Services quality
American College of Gastroenterology Guidelines 2006• Diagnosis of acute pancreatitis requires 2 of the following 3 criteria: abdominal pain, amylase and/or lipase levels !3 times upper limit of
normal, and/or CT scan findings of acute pancreatitis.• Obesity, older age, and organ failure on admission; APACHE II score !8 and/or increasing in first 48 hours; and/or hematocrit !44 suggest
severe acute pancreatitis.• CT scan with intravenous contrast and C-reactive protein > 150 mg/L help to identify necrotizing pancreatitis.• Initial management includes aggressive intravenous hydration and supplemental oxygen. Patients with organ failure require ICU monitoring.• Prolonged illness requires nutritional support. Enteral is preferred to total parenteral nutrition when possible.• Antibiotics are not necessary for necrotizing pancreatitis, even with organ failure. If infection is suspected, CT-guided needle aspiration and
culture are recommended.• MRCP and endoscopic ultrasonography can identify choledocholithiasis. If bile duct stone is confirmed, urgent ERCP is recommended.• For complex necrotizing pancreatitis, pseudocyst, or infected necrosis, interventional options include open or laparoscopic surgery or
percutaneous or endoscopic drainage. Individualize management to the patient and available expertise.
American Gastroenterological Association Guidelines 2007• Clinical presentation, increased serum amylase and lipase levels, and imaging—especially contrast-enhanced CT scan—assist in diagnosis of
acute pancreatitis. • Organ failure and local pancreatic complications help to assess severity. Progressive organ failure predicts increased mortality.• ICU monitoring is recommended if severe comorbidity or severe disease is diagnosed on the basis of imaging or APACHE II score !8.• Identify the cause through imaging and laboratory studies, including liver enzyme and triglyceride levels.• Specialized imaging, such as endoscopic ultrasonography, is needed when choledocholithiasis is a concern before proceeding with ERCP.• Reserve ERCP for when less invasive methods are unavailable.• Supportive care should include fluid resuscitation, supplemental oxygen, correction of electrolyte abnormalities, and pain control.• Consider nutritional support with preference for enteral nutrition over total parenteral nutrition.• Reserve antibiotic prophylaxis for patients with > 30% of necrosis. Use CT-guided aspiration to guide antibiotic selection.• Base management of pseudocysts, fluid collections, and necrosis on symptoms and available expertise.
In the ClinicAnnals of Internal Medicine
Patie
nt In
form
atio
n
THINGS YOU SHOULDKNOW ABOUT ACUTEPANCREATITIS
What is acute pancreatitis?• The pancreas is a gland that lies behind the stomach
and produces fluid that goes into the small intestine tobreak down food.
• Acute pancreatitis occurs when something blocks theflow of this fluid or attacks the tissues of the pancreas.
• Severe acute cases can be fatal.
What are symptoms of acutepancreatitis?• Severe, constant pain in the upper abdomen may
spread to the back. • Nausea and vomiting can occur. • Sweating, fast heart rate, and fever can occur.
Who gets acute pancreatitis?• People with gallstone disease or who use alcohol
heavily are at risk.• Other, less common causes include some medications,
injury to the pancreas, high triglyceride levels (oftenchecked with cholesterol), and pancreas deformitiesfrom birth.
• Men are at higher risk than women.
How is it diagnosed?• Your doctor will ask you about risk factors for acute
pancreatitis, review your medications, and examineyour stomach area as well as check your vital signs.
• Your doctor will order blood tests of enzymes fromthe pancreas among other tests and do X-ray orultrasonography studies.
• Common tests used to diagnose acute pancreatitisinclude ultrasonography, computed tomography (CT)scan, and endoscopic retrograde cholangiopancrea-tography (ERCP), which examines the pancreasthrough a tube inserted down the throat into thestomach and pancreas.
How is it treated?• Hospitalization is necessary for nearly all patients
with acute pancreatitis. Sometimes intensive care isneeded.
• While in the hospital and under physician care, youmay need to stop eating for a few days to rest thepancreas.
• Pain medications and intravenous fluids are oftenneeded.
• Treatment may be needed for the underlying cause,such as for alcohol use or surgery to clear a bile ductblocked by a gallstone.
• It is important to avoid anything that can causepancreatitis after an episode, such as alcohol, certainmedications, or foods that increase triglyceride levelsin order to prevent the disease from coming back.
For More Informationhttp://digestive.niddk.nih.gov/ddiseases/pubs/pancreatitis/http://digestive.niddk.nih.gov/ddiseases/pubs/ercp/National Institute of Diabetes and Digestive and Kidney Diseases
information on acute pancreatitis and ERCP.
www.nlm.nih.gov/medlineplus/ency/article/000287.htmwww.nlm.nih.gov/medlineplus/spanish/ency/article/000287.htmInformation on acute pancreatitis in English and in Spanish from
A 42-year-old woman is evaluated in theemergency department for acute onsetof epigastric pain that radiates to theback and is associated with nausea andvomiting. The patient had previouslybeen healthy and has no history ofalcohol or tobacco use. Her onlymedication is an oral contraceptive pill.
On physical examination, thetemperature is 37.2° C (99° F), the bloodpressure is 158/90 mm Hg, the pulse rateis 101/min, and the respiration rate is20/min. There is no scleral icterus orjaundice. The abdomen is distended withmid-epigastric tenderness withoutrebound or guarding and with hypoactivebowel sounds. The results of laboratorystudies are follows: leukocyte count, 13 500/µL (13.5 $ 109/L); aspartateaminotransferase, 131 U/L; alanineaminotransferase, 567 U/L; bilirubin(total), 1.1 mg/dL (18.8 µmol/L); amylase,824 U/L; lipase, 1432 U/L.
Radiography of the abdomen shows mildileus.
Which of the following is the mostappropriate next step in the evaluationof this patient?
A. CT scan of the abdomen and pelvisB. Endoscopic retrograde
cholangiopancreatographyC. EsophagogastroduodenoscopyD. Ultrasonography of the abdomen
A 34-year-old woman is evaluated forcontinued severe mid-epigastric painthat radiates to the back, nausea, andvomiting 5 days after being hospitalizedfor acute alcohol-related pancreatitis.She has not been able eat or drink andhas not had a bowel movement sincebeing admitted.
On physical examination, thetemperature is 38.2° C (100.8° F), theblood pressure is 132/84 mm Hg, thepulse rate is 101/min, and the respirationrate is 20/min. There is no scleral icterusor jaundice. The abdomen is distended
and diffusely tender with hypoactivebowel sounds. The results of laboratorystudies are follows: leukocyte count, 15400/µL (15.4 $ 109/L); aspartateaminotransferase, 189 U/L; alanineaminotransferase, 151 U/L; bilirubin(total), 1.1 mg/dL (18.8 µmol/L); amylase,388 U/L; lipase, 924 U/L.
CT scan of the abdomen shows adiffusely edematous pancreas withmultiple peripancreatic fluid collections,and no evidence of pancreatic necrosis.
Which of the following is the mostappropriate next step in themanagement of this patient?
A. Enteral nutrition by nasojejunalfeeding tube
B. Intravenous imipenemC. Pancreatic débridementD. Parenteral nutrition
A 68-year-old man with a history ofalcoholism is evaluated in the emergencydepartment for a 7-month history ofdiarrhea during which he has noted anincreased volume of stool and decreasedconsistency. He has had intermittentabdominal pain but not severe enough toprevent him from eating or drinking. Heis not taking any medications.
On physical examination, he is afebrile;the blood pressure is 108/72 mm Hg, thepulse rate is 80/min, and the respirationrate is 16/min. The abdomen is soft withmild periumbilical tenderness but nodistention. The results of laboratorystudies are follows: aspartateaminotransferase, 155 U/L; alanineaminotransferase, 88 U/L; alkalinephosphatase, 96 U/L; bilirubin (total), 1.1 mg/dL (18.8 µmol/L); amylase, 65U/L; lipase, 70 U/L.
CT scan of the abdomen showscalcifications but no mass. There is fat inthe stool.
Which of the following is the mostappropriate management for thispatient?
A. FiberB. CholestyramineC. LoperamideD. Pancreatic enzymes
A 51-year-old man is evaluated for an 8-month history of mid-epigastric painthat is worse after eating, six to eightbowel movements a day usuallyoccurring after a meal, and loss of 6.8 kg(15 lb) over the past 6 months. Thepatient drinks six to eight cans of beer aday. He takes no medications.
On physical examination, the patient isthin (BMI 21) and has normal bowelsounds, mid-epigastric tenderness, butno evidence of hepatosplenomegaly ormasses. Rectal examination revealsbrown stool that is occult bloodnegative. The remainder of theexamination is normal. Plain radiographof the abdomen shows a normal bowelgas pattern and is otherwise normal. Theresults of laboratory studies are follows:leukocyte count, 6800/µL (6.8 ! 109/L);platelet count, 69 000/µL (69 ! 109/L);fasting plasma glucose, 104 mg/dL (5.77 mmol/L); aspartate amino -transferase, 191 U/L; alanine amino -transferase, 82 U/L; amylase, 122 U/L;lipase, 289 U/L.
Which of the following tests is mostlikely to establish the diagnosis in thispatient?
A. ColonoscopyB. CT scan of the abdomenC. Measurement of serum
antiendomysial antibodiesD. Stool for leukocytes, culture, ova,
and parasites
1.
2.
Questions are largely from the ACP’s Medical Knowledge Self-Assessment Program (MKSAP, accessed at http://www.acponline.org/products_services/mksap/15/?pr31). Go to www.annals.org/intheclinic/
to complete the quiz and earn up to 1.5 CME credits, or to purchase the complete MKSAP program.
