Pancreatic Necrosis and Pancreatic Abscess 

  • Author: Alan BR Thomson, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jul 15, 2010
 

Background

Although there can be overlap in the characterization of infections in the pancreas, recognizing the different terms used in describing this complication of acute pancreatitis is important. A pancreatic abscess (PA) is a collection of pus resulting from tissue necrosis, liquefaction, and infection. Infected necrosis refers to bacterial contamination of necrotic pancreatic tissue in the absence of abscess formation. A pseudocyst is a peripancreatic fluid collection containing high concentrations of pancreatic enzymes within a defined fibrous wall and lacking an epithelial lining.

Pancreatic abscess is a late complication of acute necrotizing pancreatitis (ANP), occurring more than 4 weeks after the initial attack. The mortality rate associated with pancreatic abscess is generally less than that of infected necrosis. The mortality rate of pancreatitis may exceed 20% or more with infected pancreatic necrosis and is largely related to sepsis and multiorgan failure.

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Pathophysiology

ANP is the most severe end of a spectrum of inflammation associated with pancreatitis. Inflammation causes cell death with resultant devitalized tissue, which is likely to become infected. The amount of necrotic tissue is the strongest predictor of mortality in ANP. After pancreatic necrosis occurs, 3 potential outcomes exist, resolution, pseudocyst, or abscess. The role of proinflammatory cytokines in this process is being vigorously examined.

Pancreatic abscesses form through various mechanisms, including fibrous wall formation around fluid collections, penetrating peptic ulcers, and secondary infection of pseudocysts. Pseudocysts arise as a complication of ANP. Over a period of 3-4 weeks, sequestration of necrotic tissue occurs, forming a fibrous capsule without an epithelial lining. At any point after the initial injury in ANP, infection of necrotic tissue may occur, leading to abscess formation. When this occurs prior to the formation of the fibrous wall, it is termed infected necrosis. Pseudocysts and abscesses can be single or multiple and vary greatly in size.

Of note, pseudocyst formation is directly related to the degree of necrosis present. Approximately 3% of patients with acute pancreatitis develop pancreatic abscess.

Severe acute pancreatitis (SAP) occurs in approximately 25% of persons with acute pancreatitis. About two thirds of SAP cases occur in the first week and are associated with early single- or multi-organ dysfunction, infection of associated necrosis, and extension of necrosis to more than 50% of the pancreas.[1] In the first 48-72 hours after the onset of acute pancreatitis, prediction of possible future development of infected necrosis, multi-organ failure syndrome (MOFS) and death can be done by using the Sepsis-Related Organ Failure Assessment (SOFA) score, elevated levels of procalcitonin and IL-8, and contrast-enhanced CT scan (which has the highest diagnostic accuracy).

Balthazar and Ranson's radiographic staging criteria predict the formation of pseudocysts and, therefore, abscesses.

  • Grade A – Normal pancreas
  • Grade B - Focal or diffuse enlargement
  • Grade C - Mild peripancreatic inflammatory changes
  • Grade D - Single fluid collection
  • Grade E - Two or more fluid collections or gas within the pancreas or within peripancreatic inflammation

In grade A, B, C, or D, the probability of abscess formation is less than 2%. With grade E disease (2 or more collections of peripancreatic fluid), the probability rises to 57%.

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Epidemiology

Frequency

United States

The incidence of pancreatitis is approximately 185,000 cases per year. At least 80% of cases are due to alcohol and cholelithiasis. ANP is reported by some to occur in approximately 20% of all episodes of pancreatitis. Although sterile necrosis may occur, a variable percentage develops infection of the necrotic tissue. Depending on the time course and the host's ability to encase the necrotic tissue, the lesion is either infected necrosis or an abscess.

Mortality/Morbidity

  • Some studies have indicated a worse prognosis in idiopathic acute pancreatitis compared to pancreatitis induced by alcohol or biliary stones.
  • Patients are at risk for sepsis and, ultimately, even death. The mortality rate approaches 100% if surgical intervention and drainage are not undertaken for infected necrosis or abscess.
  • Pseudocysts may result in prolonged abdominal pain, rupture leading to acute peritonitis, fistula formation, and erosion into vessels with acute hemorrhage. Pancreatic ascites or pleural effusion may result.
  • Pseudocysts or abscesses may also cause hollow viscus obstruction by compression of surrounding structures, including the colon, stomach, duodenum, and the common bile duct.
  • Even with aggressive intravenous fluid replacement, nutritional support, and early intervention of pancreatic necrosis or abscess, the hospital mortality rate of SAP is about 20%.
  • Overall, the mortality rate from acute pancreatitis is low (< 1% for acute edematous pancreatitis), but it depends upon the proportion of patients in the group with severe pancreatitis complicated by MODS, with or without associated sepsis.
  • The mortality rate from sterile pancreatic necrosis is 10% and rises to 30% with infection in the necrotic area.[2]

Sex

Differences in sexual predilection are based on the difference in frequency of causative factors of the pancreatitis.

  • Women are more likely to have gallstone pancreatitis than men.
  • Men have alcohol-induced pancreatitis more commonly than women.
  • A difference in the rate of abscess formation between men and women has not been clearly demonstrated.
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Contributor Information and Disclosures
Author

Alan BR Thomson, MD  Professor of Medicine, Division of Gastroenterology, University of Alberta, Canada

Alan BR Thomson, MD is a member of the following medical societies: Alberta Medical Association, American College of Gastroenterology, American Gastroenterological Association, Canadian Association of Gastroenterology, Canadian Medical Association, College of Physicians and Surgeons of Alberta, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Coauthor(s)

Eric R Frizzell, MD  Instructor of Medicine, Uniformed Services University of the Health Sciences; Consulting Staff, Department of Medicine, Division of Gastroenterology, Walter Reed Army Medical Center

Eric R Frizzell, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Specialty Editor Board

Jose A Perez Jr, MD, MSEd, MBA  Residency Director, Vice Chair of Education, Department of Medicine, Methodist Hospital, Houston; Associate Professor of Clinical Medicine, Weill Cornell Medical College

Jose A Perez Jr, MD, MSEd, MBA, is a member of the following medical societies: American College of Physician Executives, American College of Physicians, Society of General Internal Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Douglas M Heuman, MD, FACP, FACG, AGAF  Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

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Contrast-enhanced CT scan of infected pancreatic pseudocyst.
 
 
 
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