Pancreatic Necrosis and Pancreatic Abscess ?>

Pancreatic Necrosis and Pancreatic Abscess

Pancreatic Necrosis and Pancreatic Abscess


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.

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.

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%.

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 develop 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.
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.

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.
Diagnosed pancreatitis with an unexpectedly prolonged course, hemodynamic instability, fever, failure of medical therapy, or the presence of fluid collections on CT scan all point to the possibility of necrosis and, potentially, abscess formation later in the course.
Abscess formation takes weeks, and infected pancreatic necrosis may be diagnosed earlier in the course.
Abdominal pain with or without a mass on palpation of the epigastrium is suggestive of parietal peritoneal irritation.
Classic physical examination findings, such as Grey-Turner sign or Cullen sign, are supposedly characteristic of pancreatitis but rarely are noted in clinical practice.
Other physical findings are nonspecific and include abnormal vital signs consistent with sepsis, abdominal guarding, and rebound tenderness.
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.
Superinfection of pseudocysts is one way that pancreatic abscesses may form, though pseudocysts are not a prerequisite for abscess formation.
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.

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