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Acute Pancreatitis Workup

  • Author: Timothy B Gardner, MD; Chief Editor: BS Anand, MD  more...
 
Updated: Apr 01, 2015
 

Approach Considerations

Once a working diagnosis of acute pancreatitis is reached, laboratory tests are obtained to support the clinical impression. In addition to confirming the diagnosis, laboratory tests are helpful in defining an etiology and looking for complications.

Although diagnostic imaging is unnecessary in most cases of pancreatitis, visualization of inflammatory changes within the pancreas provides morphologic confirmation of the diagnosis. Obtain imaging tests when the diagnosis is in doubt, when severe pancreatitis is present, or when a given imaging study might provide specific information needed to answer a clinical question.

Image-guided aspiration may be useful for differentiating infected from sterile necrosis and for draining fluid collections. Genetic testing for mutations associated with acute pancreatitis may be considered, even if effective treatments for these genetic conditions are lacking.

In 2013, the American College of Gastroenterology issued guidelines for the management of acute pancreatitis, including the following[15] :

  • Because acute pancreatitis can usually be diagnosed based on clinical symptoms and laboratory testing, contrast-enhanced computed tomography (CT) scanning and/or magnetic resonance imaging (MRI) of the pancreas should be performed only in the absence of clinical improvement or if the diagnosis is unclear
  • Assessment of the patient’s hemodynamic status should occur immediately upon presentation, with resuscitative measures initiated as necessary
  • Patients with systemic inflammatory response syndrome (SIRS) and/or organ failure should, if possible, be admitted to an intensive care unit (ICU) or an intermediary care setting
  • All patients should receive aggressive hydration, unless this is precluded by cardiovascular and/or renal comorbidities; aggressive intravenous (IV) hydration is most effective within the first 12-24 hours, with possibly little benefit derived from its administration after this point
  • Within 24 hours of admission, patients with concurrent acute cholangitis should undergo endoscopic retrograde cholangiopancreatography (ERCP); in high-risk patients, the risk of severe post-ERCP pancreatitis should be reduced through the use of postprocedure rectal nonsteroidal anti-inflammatory drug (NSAID) suppositories and/or pancreatic duct stents
  • The guidelines recommend against routinely using prophylactic antibiotics in cases of severe acute pancreatitis and/or sterile necrosis; however, intervention in patients with infected necrosis may be delayed through the use of antibiotics that do not penetrate the necrotic tissue
  • In mild cases of acute pancreatitis with no nausea and vomiting, oral feeding can be initiated immediately; enteral nutrition should be used in severe cases to prevent infectious complications, and parenteral nutrition should be avoided
  • Regardless of lesion size, location, and/or extension, intervention is not necessary for asymptomatic pancreatic and/or extrapancreatic necrosis and/or pseudocysts
  • Surgical, radiologic, and/or endoscopic drainage in stable patients with infected necrosis should be postponed (for 4 weeks if possible) to permit a wall to develop around the necrosis
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Laboratory Studies

Amylase and lipase

Serum amylase and lipase levels are typically elevated in persons with acute pancreatitis. However, these elevations may only indicate pancreastasis. In research studies, amylase or lipase levels at least 3 times above the reference range are generally considered diagnostic of acute pancreatitis.

Serum amylase determinations are routinely available, but they are not specific for pancreatitis. Preferably, the amylase P level should be measured, which is somewhat more specific to pancreatic pathology. Elevations can occur in patients with small intestinal obstruction, mesenteric ischemia, tubo-ovarian disease, renal insufficiency, or macroamylasemia. Rarely, elevations may reflect parotitis. The serum half-life of amylase is short, and elevations generally return to the reference ranges within a few days.

Lipase has a slightly longer half-life and its abnormalities may support the diagnosis if a delay occurs between the pain episode and the time the patient seeks medical attention. Elevated lipase levels are more specific to the pancreas than elevated amylase levels. Lipase levels remain high for 12 days. In patients with chronic pancreatitis (usually caused by alcohol abuse), lipase levels may be elevated in the presence of a normal serum amylase level.

The level of serum amylase or lipase does not indicate whether the disease is mild, moderate, or severe, and monitoring levels serially during the course of hospitalization does not offer insight into the prognosis.

Liver-associated enzymes

Determine alkaline phosphatase, total bilirubin, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels to search for evidence of gallstone pancreatitis. An ALT level higher than 150 U/L suggests gallstone pancreatitis and a more fulminant disease course.

Serum electrolytes, BUN, creatinine, glucose, cholesterol, and triglycerides

Obtain measurements for blood urea nitrogen (BUN), creatinine, and electrolytes; a great disturbance in the electrolyte balance is usually found, secondary to third spacing of fluids. Measure blood glucose level because it may be elevated from B-cell injury in the pancreas.

Measure calcium, cholesterol, and triglyceride levels to search for an etiology of pancreatitis (eg, hypercalcemia or hyperlipidemia) or complications of pancreatitis (eg, hypocalcemia resulting from saponification of fats in the retroperitoneum). However, be aware that baseline serum triglyceride levels can be falsely lowered during an episode of acute pancreatitis.

Complete blood count and hematocrit

A complete blood count (CBC) demonstrates leukocytosis (white blood cell [WBC] count higher than 12,000/µL) with the differential being shifted toward the segmented polymorphonuclear (PMN) cells. Leukocytosis may represent inflammation or infection.

Hemoconcentration at admission (an admission hematocrit value greater than 47%) has been proposed as a sensitive measure of more severe disease. However, this has subsequently been shown to have value only as a negative predictor—that is, a lack of hemoconcentration effectively rules out severe disease.

If blood transfusion is necessary, as in cases of hemorrhagic pancreatitis, obtain type and cross-match.

C-reactive protein

A C-reactive protein (CRP) value can be obtained 24-48 hours after presentation to provide some indication of prognosis. Higher levels have been shown to correlate with a propensity toward organ failure. A CRP value in double figures (ie, ≥ 10 mg/dL) strongly indicates severe pancreatitis. CRP is an acute-phase reactant that is not specific for pancreatitis.

Other tests

Evaluate arterial blood gases if a patient is dyspneic. Whether tachypnea is due to acute respiratory distress syndrome (ARDS) or diaphragmatic irritation must be determined.

Lactic dehydrogenase (LDH), BUN, and bicarbonate levels should be measured both at admission and at 48 hours in order to help determine the Ranson criteria for survival.

Immunoglobulin G4 (IgG4) levels can be checked to evaluate for autoimmune pancreatitis. However, this test is not specific, because IgG4 levels can be elevated in as many as 10% of patients with acute pancreatitis who do not have autoimmune pancreatitis.

Trypsin and its precursor trypsinogen-2 in both the urine and the peritoneal fluid have been evaluated as possible markers for acute pancreatitis (especially post-ERCP pancreatitis) but are not widely used. Trypsinogen activation peptide (TAP) is formed when trypsinogen is cleaved to form trypsin and can be measured commercially in the urine to diagnose acute pancreatitis and to help determine severity.

Although not currently in use clinically, polymorphisms in the chemokine monocyte chemotactic protein 1 (MCP-1) gene may also predict severity. This is the first gene identified that plays a role strictly in predicting the severity of disease.

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Abdominal Radiography

Abdominal radiographs have a limited role in acute pancreatitis. Kidneys-ureters-bladder (KUB) radiography with the patient in the upright position is primarily performed to detect free air in the abdomen, indicating a perforated viscus, as would be the case in a penetrating, perforated duodenal ulcer. In some cases, the inflammatory process may damage peripancreatic structures, resulting in a colon cut-off sign, a sentinel loop, or an ileus. The presence of calcifications within or around the pancreas may indicate chronic pancreatitis.

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Ultrasonography

Abdominal ultrasonography

Ultrasonography of the abdomen is the most useful initial test in determining the etiology of pancreatitis and is the technique of choice for detecting gallstones. In the setting of acute pancreatitis, sensitivity is reduced to 70-80%. In addition, the ability to identify choledocholithiasis is limited. Although ultrasonography can be used as a screening test, it may not be specific if overlying gas shadows secondary to bowel distention are present. Ultrasonography cannot measure the severity of disease.

Endoscopic ultrasonography

Endoscopic ultrasonography (EUS) is an endoscopic procedure that allows a high-frequency ultrasound transducer to be inserted into the gastrointestinal (GI) tract to visualize the pancreas and the biliary tract. This study allows a more detailed image to be obtained than with transcutaneous ultrasonography because the high-frequency transducer can be introduced directly adjacent to the pancreas.

Its principal role in the evaluation of acute pancreatitis is the detection of microlithiasis and periampullary lesions not easily revealed by other methods. This modality should not be used to help identify chronic pancreatitis until several months after the episode of acute pancreatitis.

In specialized centers with highly trained medical staff, a secretin-stimulated EUS study may reveal resistance to ductal outflow at the level of the papilla, as evidenced by dilatation of the pancreatic duct to a greater extent and longer duration than in a healthy population. This can be helpful in evaluating patients with recurrent idiopathic pancreatitis.

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Computed Tomography

Abdominal computed tomography (CT) scanning is generally not indicated for patients with mild pancreatitis unless a pancreatic tumor is suspected (usually in elderly patients). It is always indicated in patients with severe acute pancreatitis and is the imaging study of choice for assessing complications. Scans are seldom needed within the first 72 hours after symptom onset unless the diagnosis is uncertain, because inflammatory changes are often not radiographically present until this time.[16]

Abdominal CT scans also provide prognostic information based on the following grading scale developed by Balthazar and colleagues[17, 18, 19] :

  • Grade A - Normal pancreas
  • Grade B - Focal or diffuse gland enlargement
  • Grade C - Intrinsic gland abnormality recognized by haziness on the scan
  • Grade D - Single ill-defined collection or phlegmon
  • Grade E - Two or more ill-defined collections or the presence of gas in or nearby the pancreas

The chances of infection and death are virtually nil in grades A and B but steadily increase in grades C through E. Patients with grade E pancreatitis have a 50% chance of developing an infection and a 15% chance of dying.

Dynamic spiral CT scanning is used to determine the presence and extent of pancreatic necrosis. After the administration of an oral agent to define bowel structures, a study of the upper abdomen is performed twice, before and after administration of an intravenous (IV) bolus of iodine contrast agent.

For a healthy pancreas, density numbers are in the range of 30-40 Hounsfield units on an unenhanced study, increasing to 100-150 Hounsfield units on an enhanced study. When pancreatic necrosis is present, focal or diffuse areas of unenhanced parenchyma on the second study suggest pancreatic necrosis. Pancreatic necrosis for research purposes is defined as loss of enhancement in at least 30% of the pancreatic parenchyma.

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Magnetic Resonance Cholangiopancreatography

Magnetic resonance cholangiopancreatography (MRCP) has an emerging role in the diagnosis of suspected biliary and pancreatic duct obstruction in the setting of pancreatitis. Heavily T2–weighted images provide a noninvasive image of the biliary and pancreatic ducts.[2]

Although MRCP is not as sensitive as endoscopic retrograde cholangiopancreatography (ERCP), it is safer, noninvasive, and fast, and it provides images useful in guiding clinical care decisions. MRCP should be used if choledocholithiasis is suspected but there is concern that pancreatitis might worsen if ERCP is performed.

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Endoscopic Retrograde Cholangiopancreatography

ERCP is an endoscopic procedure used to evaluate the biliary and pancreatic ductal system and is indicated in a subset of patients with acute pancreatitis (see the image below). However, ERCP should be used with extreme caution in patients with acute pancreatitis and should never be used as a first-line diagnostic tool in this disease.[2] It should be performed only in the following situations:

  • The patient has severe acute pancreatitis that is believed, and is seen on other radiographic studies, to be secondary to choledocholithiasis
  • The patient has biliary pancreatitis and is experiencing worsening jaundice and clinical deterioration despite maximal supportive therapy
    This patient with acute gallstone pancreatitis und This patient with acute gallstone pancreatitis underwent endoscopic retrograde cholangiopancreatography. Cholangiogram shows no stones in common bile duct and multiple small stones in gallbladder. Pancreatogram shows narrowing of pancreatic duct in area of genu, resulting from extrinsic compression of ductal system by inflammatory changes in pancreas.

When combined with sphincterotomy and stone extraction, ERCP may reduce the length of hospital stay, the complication rate, and, possibly, mortality.

In the case of biliary pancreatitis where a dilated obstructed common bile duct is diagnosed on the basis of CT or any other imaging modality and an elevated plasma bilirubin level (> 5 mg/dL), ERCP with sphincterotomy is warranted within the first 72 hours. Biliary pancreatitis should always be treated eventually with a cholecystectomy after the process has subsided.

Occasionally, ERCP with sphincter of Oddi manometry reveals sphincter of Oddi dysfunction as the cause of recurrent idiopathic pancreatitis. However, in the setting of suspected sphincter of Oddi dysfunction (SOD), the risk of procedure-induced pancreatitis is at least 30%.

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Image-Guided Aspiration and Drainage

CT-guided needle aspiration is used to differentiate infected necrosis from sterile necrosis in patients with severe necrotizing pancreatitis. The needle is placed into an area of low attenuation in or around the pancreas of a patient with fever and tachycardia or other signs of a systemic inflammatory response syndrome, generally following the first week of severe pancreatitis. The procedure may be repeated weekly if clinically indicated.

The specimen should be delivered to the laboratory within an hour and interpreted promptly. The specimen should always be evaluated for Gram stain, culture, and sensitivity. If the Gram stain shows bacteria or fungi, surgical debridement of the infected necrosis is generally indicated. An exception would be if the patient cannot tolerate surgery; in that case, CT-guided catheter drainage may be more effective.

EUS-guided needle aspiration can often be used to differentiate infected necrosis from sterile necrosis in the same manner as CT-guided needle aspiration. EUS can also be used to guide drainage of pancreatic and peripancreatic fluid collections that have complicated an episode of acute pancreatitis. These procedures should only be carried out once the pseudocyst has had the opportunity to mature.

A complete description of these procedures is beyond the scope of this article.

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Genetic Testing

With the advent of molecular medicine, various genetic abnormalities have been associated with pancreatitis. Although effective treatments for these conditions have yet to be discovered, it is sometimes reasonable to begin testing for these mutations in patients with otherwise idiopathic pancreatitis, rather than subjecting the entire group to the risks of endoscopic sphincterotomy or stent placement for presumptive sphincter of Oddi dysfunction.

As more is learned about molecular mechanisms and therapy, logical novel treatments can eventually be offered to these patients as part of clinical trials. Of course, as with any type of genetic testing, expert genetic counseling that addresses social, familial, insurance, and financial issues is essential for all persons before testing. In fact, it is the author’s policy not to perform any genetic testing unless patients are first counseled by a qualified genetic counselor.

Hereditary pancreatitis has been associated with a mutation of cationic trypsinogen (PRSS1). At least 4 mutations have thus far been identified. These mutations appear to render the protein resistant to second-line proteolytic defense mechanisms. Patients with PRSS1 mutations typically develop their first episode of pancreatitis by the time they are in their mid teens. Most often, there is a strong family history of pancreatic disease (eg, acute or chronic pancreatitis, pancreatic malignancy). It should be noted that PRSS1 -induced pancreatitis is very rare.

Some patients with idiopathic pancreatitis have atypical mutations in the CFTR gene, which follows an autosomal recessive pattern of inheritance. This is a fascinating advance in understanding the spectrum of cystic fibrosis, in which phenotypic expression depends on the degree to which the mutation affects the activity of the CFTR enzyme’s function. Relatively minor mutations that do not affect pulmonary function may influence chloride transport in the pancreas enough to predispose individuals to recurrent idiopathic pancreatitis.

Mutations in the SPINK1 gene can predispose patients to acute pancreatitis. The SPINK1 protein blocks the active binding site of trypsin, rendering it inactive. However, approximately 1 in 100 persons in the United States are at least heterozygotes for SPINK1. It is an autosomal recessive gene pattern of inheritance. Therefore, although mutations of the SPINK1 gene are not usually enough to cause pancreatitis, they are likely to be a cofactor responsible for pancreatitis in some individuals.

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Histologic Findings

For practical purposes, the infinite spectrum of pancreatitis severity is usually subdivided into mild and severe categories as follows:

  • Mild pancreatitis - The gland exhibits interstitial edema and an inflammatory infiltrate without hemorrhage or necrosis, usually with minimal or no organ dysfunction
  • Severe pancreatitis - Extensive inflammation and necrosis of the pancreatic parenchyma are present, often associated with severe gland dysfunction and multiorgan system failure

At surgery, peripancreatic fatty tissue is predominantly involved by necrosis, whereas the gland is usually less affected; hence, the extent of pancreatic necrosis is commonly overestimated. In very severe cases, arterial thrombosis may lead to panlobular infarction, in which the gland becomes a hemorrhagic, necrotic, gangrenous mass. The natural history of fat necrosis depends on its location and extent; small areas (< 1 cm) may resolve entirely, whereas large areas (>5 cm) may liquefy within a fibrotic capsule.

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Staging

Various strategies have been used to predict the severity and outcome of acute pancreatitis, including the Ranson, Acute Physiology and Chronic Health Evaluation (APACHE) II, Glasgow, and Imrie scoring systems. Each has advantages and disadvantages, and none is currently recognized as a criterion standard.

For research purposes, the Atlanta classification of acute pancreatitis has been used to differentiate between severe and mild cases of acute pancreatitis.[3] According to this classification, patients are diagnosed with severe acute pancreatitis if they show the following:

  • Evidence of organ failure (eg, systolic blood pressure below 90 mm Hg, arterial partial pressure of oxygen [P a O 2] 60 mm Hg or lower, serum creatinine level 2 mg/dL or higher, GI bleeding amounting to 500 mL or more in 24 hours)
  • Local complications (eg, necrosis, abscess, pseudocyst)
  • Ranson score of 3 or higher or APACHE score of 8 or higher

Ranson criteria

Ranson used a series of different criteria for the severity of acute pancreatitis to formulate a scoring system that is still widely used.[20]

Criteria present on admission include the following:

  • Patient older than 55 years
  • WBC count higher than 16,000/µL
  • Blood glucose level higher than 200 mg/dL
  • Serum LDH level higher than 350 IU/L
  • AST level higher than 250 IU/L

Criteria developing during the first 48 hours include the following:

  • Hematocrit fall more than 10%
  • BUN level increased by more than 8 mg/dL
  • Serum calcium level lower than 8 mg/dL
  • P a O 2 less than 60 mm Hg
  • Base deficit higher than 4 mEq/L
  • Estimated fluid sequestration higher than 600 mL

Each of the above criteria counts for 1 point toward the score. A Ranson score of 0-2 has a minimal mortality, and the patient is admitted to the regular ward for medical therapy and support. A Ranson score of 3-5 has a 10-20% mortality rate, and the patient should be admitted to the intensive care unit (ICU). A Ranson score higher than 5 after 48 hours has a mortality of more than 50% and is associated with more systemic complications.

Although the Ranson criteria are perhaps the best known scoring system, they have several drawbacks. First, 11 criteria are used, some of which are evaluated on day 1 and others on day 2. The Ranson score is valid only at 48 hours after onset and not at any other time during the disease. Second, the threshold for an abnormal value depends on whether the pancreatitis is caused by alcohol or gallstones. Finally, the sensitivity is only 73% and the specificity is 77% for predicting mortality.

BUN

An elevated BUN level at admission has been associated with an increase in severe acute pancreatitis and/or death. This corresponds well with the APACHE II score. The rise in BUN is thought to be due to hemoconcentration, which is a surrogate marker for intravascular depletion. Intravascular depletion is thought to be a key mediator of the inflammatory response in acute pancreatitis.

APACHE II

The APACHE score has the advantage of being able to assess the patient at any point during the illness; however, it is very cumbersome for routine clinical use. Attempts have been made to make this evaluation user friendly (eg, with APACHE II, the Simplified Acute Physiology Score [SAPS], and the Imrie score), but it remains cumbersome. The sensitivity is 77%, and the specificity is 84%. See the APACHE II Scoring System calculator.

Biological markers

The most widely available biological marker for staging acute pancreatitis is the hematocrit value. Admission hemoconcentration to a hematocrit value greater than 47% had been reported as a sensitive predictor of pancreatic necrosis at admission. However, a subsequent study has revealed admission hematocrit to be useful only as a negative predictor for necrosis in patients without hemoconcentration.

CRP, a nonspecific acute-phase reactant produced by the liver in response to interleukin (IL)–6, is a useful marker at 36-48 hours. A CRP level greater than 6 at 24 hours or greater than 7 at 48 hours is consistent with severe acute pancreatitis. The sensitivity of this test is 73%, and the specificity is 71%.

IL-6 levels begin to rise in the first several hours of pancreatitis, stimulating the release of CRP. Early studies of IL-6 as a biological marker appear promising, indicating that this may be a reliable indicator of pancreatitis severity. However, this possibility is not yet validated, and IL-6 is not yet commercially available for clinical use in this setting.

Several other blood tests show promise in predicting the severity of acute pancreatitis. These include TAP, polymorphonuclear elastase, and phospholipase A2. Like IL-6, they are generally not used in clinical practice and are more expensive than typically used tests. Some are only slightly better than using CRP.

Genetic markers

Polymorphisms in the chemokine monocyte chemotactic protein 1 (MCP-1) gene may play a role in predisposing patients to severe acute pancreatitis, although this marker is still under investigation and is not used clinically.

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Contributor Information and Disclosures
Author

Timothy B Gardner, MD Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of Pancreatic Disorders, Section of Gastroenterology, Dartmouth-Hitchcock Medical Center

Timothy B Gardner, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, American Pancreatic Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Brian S Berk, MD Assistant Professor, Department of Medicine, Dartmouth Medical School; Director of End Stage Liver Disease, Section of Gastroenterology, Dartmouth Hitchcock Medical Center

Brian S Berk, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

Tushar Patel, MB, ChB Professor of Medicine, Ohio State University Medical Center

Tushar Patel, MB, ChB is a member of the following medical societies: American Association for the Study of Liver Diseases and American Gastroenterological Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Noel Williams, MD Professor Emeritus, Department of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; Professor, Department of Internal Medicine, Division of Gastroenterology, University of Alberta, Edmonton, Alberta, Canada

Noel Williams, MD is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Paul Yakshe, MD Assistant Professor of Medicine, University of Minnesota, Medical Director of Pancreas and Biliary Clinic, Department of Medicine, Division of Gastroenterology, Hepatology, and Nutrition, Fairview University Medical Center

Paul Yakshe, MD is a member of the following medical societies: American College of Gastroenterology, American Pancreatic Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

References
  1. Vege SS, Ziring B, Jain R, Moayyedi P, for the Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on the diagnosis and management of asymptomatic neoplastic pancreatic cysts. Gastroenterology. 2015 Apr. 148(4):819-22. [Medline].

  2. Telem DA, Bowman K, Hwang J, Chin EH, Nguyen SQ, Divino CM. Selective management of patients with acute biliary pancreatitis. J Gastrointest Surg. 2009 Dec. 13(12):2183-8. [Medline].

  3. Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013 Jan. 62(1):102-11. [Medline].

  4. Haydock MD, Mittal A, van den Heever M, Rossaak JI, Connor S, Rodgers M, et al. National Survey of Fluid Therapy in Acute Pancreatitis: Current Practice Lacks a Sound Evidence Base. World J Surg. 2013 May 30. [Medline].

  5. Ai X, Qian X, Pan W, Xu J, Hu W, Terai T, et al. Ultrasound-guided percutaneous drainage may decrease the mortality of severe acute pancreatitis. J Gastroenterol. 2010. 45(1):77-85. [Medline].

  6. Li H, Qian Z, Liu Z, Liu X, Han X, Kang H. Risk factors and outcome of acute renal failure in patients with severe acute pancreatitis. J Crit Care. 2010 Jun. 25(2):225-9. [Medline].

  7. Whitcomb DC, Yadav D, Adam S, et al. Multicenter approach to recurrent acute and chronic pancreatitis in the United States: the North American Pancreatitis Study 2 (NAPS2). Pancreatology. 2008. 8(4-5):520-31. [Medline]. [Full Text].

  8. Granger J, Remick D. Acute pancreatitis: models, markers, and mediators. Shock. 2005 Dec. 24 Suppl 1:45-51. [Medline].

  9. Singla A, Csikesz NG, Simons JP, Li YF, Ng SC, Tseng JF, et al. National hospital volume in acute pancreatitis: analysis of the Nationwide Inpatient Sample 1998-2006. HPB (Oxford). 2009 Aug. 11(5):391-7. [Medline]. [Full Text].

  10. Banks PA. Epidemiology, natural history, and predictors of disease outcome in acute and chronic pancreatitis. Gastrointest Endosc. 2002 Dec. 56(6 Suppl):S226-30. [Medline].

  11. Morinville VD, Barmada MM, Lowe ME. Increasing incidence of acute pancreatitis at an American pediatric tertiary care center: is greater awareness among physicians responsible?. Pancreas. 2010 Jan. 39(1):5-8. [Medline].

  12. Akhtar AJ, Shaheen M. Extrapancreatic manifestations of acute pancreatitis in African-American and Hispanic patients. Pancreas. 2004 Nov. 29(4):291-7. [Medline].

  13. Whitcomb DC. Clinical practice. Acute pancreatitis. N Engl J Med. 2006 May 18. 354(20):2142-50. [Medline].

  14. Suppiah A, Malde D, Arab T, Hamed M, Allgar V, Smith AM, et al. The Prognostic Value of the Neutrophil-Lymphocyte Ratio (NLR) in Acute Pancreatitis: Identification of an Optimal NLR. J Gastrointest Surg. 2013 Feb 1. [Medline].

  15. Tenner S, Baillie J, Dewitt J, et al. American College of Gastroenterology Guidelines: Management of Acute Pancreatitis. Am J Gastroenterol. 2013 Jul 30. [Medline].

  16. Imamura Y, Hirota M, Ida S, Hayashi N, Watanabe M, Takamori H, et al. Significance of renal rim grade on computed tomography in severity evaluation of acute pancreatitis. Pancreas. 2010 Jan. 39(1):41-6. [Medline].

  17. Balthazar EJ, Ranson JH, Naidich DP, Megibow AJ, Caccavale R, Cooper MM. Acute pancreatitis: prognostic value of CT. Radiology. 1985 Sep. 156(3):767-72. [Medline].

  18. Balthazar EJ, Robinson DL, Megibow AJ, Ranson JH. Acute pancreatitis: value of CT in establishing prognosis. Radiology. 1990 Feb. 174(2):331-6. [Medline].

  19. Balthazar EJ. Staging of acute pancreatitis. Radiol Clin North Am. 2002 Dec. 40(6):1199-209. [Medline].

  20. Imrie CW. Prognostic indicators in acute pancreatitis. Can J Gastroenterol. 2003 May. 17(5):325-8. [Medline].

  21. Jacobson BC, Vander Vliet MB, Hughes MD, Maurer R, McManus K, Banks PA. A prospective, randomized trial of clear liquids versus low-fat solid diet as the initial meal in mild acute pancreatitis. Clin Gastroenterol Hepatol. 2007 Aug. 5(8):946-51; quiz 886. [Medline]. [Full Text].

  22. Bakker OJ, van Brunschot S, van Santvoort HC, Besselink MG, Bollen TL, Boermeester MA, et al. Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med. 2014 Nov 20. 371(21):1983-93. [Medline].

  23. Maravi-Poma E, Gener J, Alvarez-Lerma F, Olaechea P, Blanco A, Dominguez-Munoz JE. Early antibiotic treatment (prophylaxis) of septic complications in severe acute necrotizing pancreatitis: a prospective, randomized, multicenter study comparing two regimens with imipenem-cilastatin. Intensive Care Med. 2003 Nov. 29(11):1974-80. [Medline].

  24. Isenmann R, Rünzi M, Kron M, et al. Prophylactic antibiotic treatment in patients with predicted severe acute pancreatitis: a placebo-controlled, double-blind trial. Gastroenterology. 2004 Apr. 126(4):997-1004. [Medline].

  25. Johnson CD, Kingsnorth AN, Imrie CW, et al. Double blind, randomised, placebo controlled study of a platelet activating factor antagonist, lexipafant, in the treatment and prevention of organ failure in predicted severe acute pancreatitis. Gut. 2001 Jan. 48(1):62-9. [Medline]. [Full Text].

  26. Aboulian A, Chan T, Yaghoubian A, Kaji AH, Putnam B, Neville A, et al. Early cholecystectomy safely decreases hospital stay in patients with mild gallstone pancreatitis: a randomized prospective study. Ann Surg. 2010 Apr. 251(4):615-9. [Medline].

  27. van Santvoort HC, Besselink MG, Bakker OJ, Hofker HS, Boermeester MA, Dejong CH, et al. A step-up approach or open necrosectomy for necrotizing pancreatitis. N Engl J Med. 2010 Apr 22. 362(16):1491-502. [Medline].

 
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Suspected acute pancreatitis. Etiologic factors and forms of acute pancreatitis. Ranson criteria.
Mild pancreatitis. Favorable prognostic signs for acute pancreatitis. Medical management and studies used for acute pancreatitis.
Prognostic indicators for severe pancreatitis and ICU management.
Diagnosis and treatment of necrotizing pancreatitis.
Treatment of and studies used for pancreatic pseudocysts.
Idiopathic recurrent pancreatitis. Etiologies for acute pancreatitis.
Pancreatic abscess. Definition of an abscess.
This patient with acute gallstone pancreatitis underwent endoscopic retrograde cholangiopancreatography. Cholangiogram shows no stones in common bile duct and multiple small stones in gallbladder. Pancreatogram shows narrowing of pancreatic duct in area of genu, resulting from extrinsic compression of ductal system by inflammatory changes in pancreas.
Pancreas divisum associated with minor papilla stenosis causing recurrent pancreatitis. Because pancreas divisum is relatively common in general population, it is best regarded as variant of normal anatomy and not necessarily as cause of pancreatitis. In this case, note bulbous contour of duct adjacent to cannula. This appearance has been termed Santorinicele. Dorsal duct outflow obstruction is a probable cause of pancreatitis when Santorinicele is present and associated with a minor papilla that accommodates only guide wire.
Normal-appearing ventral pancreas in a patient with recurrent acute pancreatitis. Dorsal pancreas (not pictured) showed evidence of chronic pancreatitis.
Endoscopic retrograde cholangiopancreatography excluded suppurative cholangitis and established presence of anular pancreas divisum. Dorsal pancreatogram showed extravasation into retroperitoneum, and sphincterotomy was performed on minor papilla. Pigtail nasopancreatic tube was then inserted into dorsal duct and out into retroperitoneal fluid collection. The other end of the tube was attached to bulb suction and monitored every shift.
While percutaneous drains remove loculated fluid collections elsewhere in the abdomen, nasopancreatic tube is containing retroperitoneal fluid collection. By 1 week later, retroperitoneal fluid collection is much smaller (image is reversed in horizontal direction). By this time, patient is off pressors and is ready to be extubated.
Recurrent pancreatitis associated with pancreas divisum in an elderly man. Pancreatogram of the dorsal duct shows distal stenosis with upstream chronic pancreatitis. After the stenosis was dilated and stented, pain resolved and the patient improved clinically during 1 year of quarterly stent exchanges. Follow-up CT scans showed resolution of the inflammatory mass. Although ductal biopsies and cytology were repeatedly negative, pain and pancreatitis returned when stents were removed. Patient developed duodenal outflow obstruction and was sent to surgery; Whipple procedure revealed periampullary adenocarcinoma (of minor papilla).
 
 
 
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