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Intra-abdominal abscess continues to be an important and serious problem in surgical practice. Appropriate treatment is often delayed because of the obscure nature of many conditions resulting in abscess formation, which can make diagnosis and localization difficult. Associated pathophysiologic effects may become life threatening or lead to extended periods of morbidity with prolonged hospitalization. Delayed diagnosis and treatment can also lead to increased mortality rates; therefore, the economic impact of delaying treatment is significant.
A better understanding of intra-abdominal abscess pathophysiology and a high clinical index of suspicion should allow for earlier recognition, definitive treatment, and reduced morbidity and mortality.
Etiology
Although multiple causes of intra-abdominal abscesses exist, the following are the most common: (1) perforation of a diseased viscus, which includes peptic ulcer perforation, (2) perforated appendicitis and diverticulitis, (3) gangrenous cholecystitis, (4) mesenteric ischemia with bowel infarction, and (5) pancreatitis or pancreatic necrosis progressing to pancreatic abscess.
Other causes include untreated penetrating trauma to the abdominal viscera and postoperative complications, such as anastomotic leak or missed gallstones during laparoscopic cholecystectomy.
Microbiology includes a mixture of aerobic and anaerobic organisms. The most commonly isolated aerobic organism is Escherichia coli, and the most commonly observed anaerobic organism is Bacteroides fragilis. A synergistic relationship exists between these organisms. In patients who receive prolonged antibiotic therapy, yeast colonies (eg, candidal species) or a variety of nosocomial pathogens may be recovered from abscess fluids.
Skin flora may be responsible for abscesses following a penetrating abdominal injury. Neisseria gonorrhoeae and chlamydial species are the most common organisms involved in pelvic abscesses in females as part of pelvic inflammatory disease. The type and density of aerobic and anaerobic bacteria isolated from intra-abdominal abscesses depend upon the nature of the microflora associated with the diseased or injured organ.
Microbial flora of the GI tract shifts from small numbers of aerobic streptococci, including enterococci and facultative gram-negative bacilli in the stomach and proximal small bowel, to larger numbers of these species with an excess of anaerobic gram-negative bacilli (particularly Bacteroides species) and anaerobic gram-positive flora (streptococci and clostridia) in the terminal ileum and colon. Differences in microorganisms observed from the upper to the lower portion of the GI tract partially account for differences in septic complications associated with injuries or diseases to the upper and lower gut. Sepsis occurring after upper GI perforations or leaks causes less morbidity and mortality than sepsis after leaks from colonic insults.
Pathophysiology
Intra-abdominal abscesses are localized collections of pus that are confined in the peritoneal cavity by an inflammatory barrier. This barrier may include the omentum, inflammatory adhesions, or contiguous viscera. The abscesses usually contain a mixture of aerobic and anaerobic bacteria from the GI tract.