Abscesses are well-defined collections of infected purulent material that are walled off from the rest of the peritoneal cavity by inflammatory adhesions, loops of intestine and their mesentery, the greater omentum, or other abdominal viscera. Abscesses may occur in the peritoneal cavity, either within or outside of abdominal viscera (extravisceral), as well as in the retroperitoneum.1 Most relevant to the surgeon are extravisceral abscesses that usually arise in one of two situations: (1) after resolution of diffuse peritonitis in which a loculated area of infection persists and evolves into an abscess and (2) after perforation of a viscus or an anastomotic breakdown that is successfully walled off by peritoneal defense mechanisms. More than 80% of intra-abdominal abscesses occur in the postoperative period, the majority of which occur after pancreaticobiliary or colorectal surgery and are usually related to anastomotic dehiscence.2,3 Occasionally, postsurgical abscesses result from infection of an intraperitoneal hematoma that develops following surgery. Less frequently, intra-abdominal abscesses are unassociated with previous surgery and are usually attributable to spontaneous inflammatory processes associated with a small, localized perforation, such as in appendicitis, diverticulitis, and Crohn's disease.3,4 Visceral abscesses are most commonly caused by hematogenous or lymphatic spread of bacteria to the organ. Retroperitoneal abscesses may be caused by several mechanisms, including perforation of the gastrointestinal (GI) tract into the retroperitoneum and hematogenous or lymphatic spread of bacteria to retroperitoneal organs, particularly the inflamed pancreas.
Pathophysiology of Abscess Formation
After bacterial contamination of the peritoneal cavity, a complex series of events is initiated that, under ideal circumstances, effects complete eradication of invading bacteria. The three major defense mechanisms in the peritoneal cavity are (1) mechanical clearance of bacteria via the diaphragmatic lymphatics, (2) phagocytosis and destruction of suspended or adherent bacteria by phagocytic cells, and (3) sequestration and walling off of bacteria coupled with delayed clearance by phagocytic cells.5 The first two mechanisms act rapidly, usually within hours. Egress of bacteria from the peritoneal cavity via the lymphatics is responsible for the early septic response due to bacteremia and initiation of the innate immune response to infection.
The initial peritoneal response to bacterial contamination is characterized by hyperemia, exudation of protein-rich fluid into the peritoneal cavity, and a marked influx of phagocytic cells. Resident peritoneal macrophages predominate early in the infection, but the rapid influx of neutrophils after a 2- to 4-hour delay makes them the predominant phagocytic cell in the peritoneal cavity for the first 48–72 hours.6 The combination of resident peritoneal cells plus the influxing into the peritoneum serves to propagate the initiation of the innate immune response, including the elaboration of inflammatory cytokines and the procoagulant response. In humans with severe intra-abdominal infection, peritoneal levels of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1, and IL-6 are higher than levels measured simultaneously in plasma.7,8 Haecker and colleagues reported that TNF-α and ...