Pancreatic Necrosis and Pancreatic Abscess

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Fluid and necrotic collections can occur as complications of acute pancreatitis. According to the latest classification, these can be divided into acute or delayed, depending on whether such a collection is of less than or more than 4 weeks’ duration. [1]

In the acute period, the fluid collection is not well defined and is simply described as acute peripancreatic fluid collection. It is often associated with tissue edema. After 4 weeks, the fluid collection is much more organized with a definite wall and is described as a pseudocyt. A pseudocyst is a peripancreatic fluid collection containing high concentrations of pancreatic enzymes within a defined fibrous wall and lacking an epithelial lining. When a pseudocyst gets infected, it is called a pancreatic abscess.

Similarly, pancreatic necrosis is an acute necrotic collection in which there is a variable amount of fluid and necrosis. By around 4 weeks, a walled-off pancreatic necrosis (WOPN) may form, in which the collection is defined by a fibrotic and inflammatory wall. The term “infected necrosis” refers to bacterial invasion of necrotic pancreatic tissue.

Pancreatic abscess is often 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 in the presence of infected pancreatic necrosis and is largely related to sepsis and multiorgan failure.

A number of molecules mediating the inflammatory (NF-κB, cytokines/chemokines, adhesion molecules, and novel kinase C isoforms) and cell death responses (eg, caspases) play a role in the pathogenesis of acute pancreatitis.

Pancreatitis begins in acinar cells and leads to the premature, intra-acinar activation of digestive zymogens into their active forms (eg, trypsinogen to trypsin); accumulation of large vacuoles in acinar cells; inflammation; and parenchymal cell death through apoptosis and necrosis. [2] The activated pancreatic enzymes cause autodigestion. These inflammatory processes lead to collection of fluid in and around the pancreas. In addition injury to the pancreatic duct or its branches leads to leakage of pancreatic enzymes into the lesser sac and the retroperitoneum. The enzyme rich fluid and necrotic collections if persistent will eventually develop fibrosis around its periphery leading to pseudocysts and WOPN. These processes often follow severe acute pancreatitis (SAP) as opposed to mild acute pancreatitis.

Acute necrotic pancreatitis is the most severe end of a spectrum of inflammation associated with pancreatitis. Inflammation in this situation may cause cell death. The resultant devitalized tissue becomes a potential bed for infection. The amount of necrotic tissue is the strongest predictor of mortality in necrotic pancreatitis. After necrotic pancreatitis three potential outcomes exist: resolution, persistent fluid collection (pseudocyst)/necrosis (WOPN), or formation of abscess or infected necrosis.

Pseudocysts and abscesses can be single or multiple and vary greatly in size and location. Approximately 3% of patients with acute pancreatitis develop pancreatic abscess.

The inciting events for pancreatitis are legion; however, cholelithiasis and alcohol account for more than 80% of cases in the developed world.

Peripancreatic fluid encased in a fibrinous capsule defines pseudocysts. It is often the result of a ductal leak or disruption.

Superinfection of pseudocysts leads to the development of pancreatic abscesses. Evidence suggests that colonic translocation of bacterial flora accounts for many cases of pancreatic infection.

The most typical organisms isolated from infected necrosis and abscesses are enteric bacteria and Candida species.

The incidence of pancreatitis is approximately 185,000 cases per year. At least 80% of cases are due to alcohol and cholelithiasis. Acute necrotic pancreatitis (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.

Differences in sexual predilection are based on the difference in the frequency of causative factors of the pancreatitis and include the following:

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.

Risk assessment of acute pancreatitis (AP) depends upon clinical indices (eg, Ranson, Imrie, or Apache I/II Scores), the presence of extrapancreatic complications, an elevated C-reactive or hematocrit, an elevated procalcitonin, and the finding of pancreatic necrosis on CT scanning.

The prognosis may be worse in obese patients, after trauma, after organ transplantation, after coronary artery bypass surgery, or in idiopathic AP. [3]

In the first 48-72 hours after the onset of acute pancreatitis using the Sepsis-Related Organ Failure Assessment (SOFA) score and contrast-enhanced CT scan (which has the highest diagnostic accuracy) one can predict the future development of infected necrosis, multiorgan failure syndrome (MOFS) and death. Balthazar and Ranson’s radiographic staging criteria predict the formation of pseudocysts and, therefore, abscesses.

Note the following:

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 the 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%.

Patients are at risk for sepsis and, ultimately, even death. The mortality rate approaches 100% if intervention and drainage are not undertaken for infected necrosis or abscess.

Pseudocysts and abscesses may result in prolonged , 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 the 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 presence of pancreatic necrosis is associated with an overall increase in mortality. The mortality rate from sterile pancreatic necrosis is 10% and rises to 30% with infection in the necrotic area. [4] One meta-analysis concluded that when organ failure and infected pancreatic necrosis are present together, it portends an even worse prognosis, with mortality reaching 43%. [5]

Complications include the following:

Fistula formation (eg, enterocutaneous following surgery, entero-entero, enterovascular)

Recurrent pancreatitis

Bowel obstruction


Inform patients about the common causes of pancreatitis.

Offer cholecystectomy to patients with gallstone pancreatitis if they are surgical candidates.

Provide counseling for patients to abstain from alcohol use.

Monitor patients for steatorrhea, and inform them about the potential for pancreatic insufficiency and the potential need for pancreatic enzymes and fat-soluble vitamin supplementation.

For patient education resources, see Digestive Disorders Center, as well as Pancreatitis.

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Abraham Mathew, MD, MS Professor of Medicine, Department of Internal Medicine, Division of Gastroenterology and Hepatology, Hershey Medical Center, Pennsylvania State University College of Medicine

Abraham Mathew, MD, MS is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Received ownership interest from Hershey Endoscopy Center for partner of ambulatory surgery center, practice site; Received consulting fee from Boston Scientific for consulting.

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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, American Gastroenterological Association

Disclosure: Received grant/ funds from Novartis for other; Received grant/ funds from Bayer for other; Received grant/research funds from Otsuka for none; Received grant/research funds from Bristol Myers Squibb for other; Received none from Scynexis for none; Received grant/research funds from Salix for other; Received grant/research funds from MannKind for other.

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.

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

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

Disclosure: Nothing to disclose.

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.

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.

Pancreatic Necrosis and Pancreatic Abscess

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