Chapter 121. Intraabdominal Infections and Abscesses (Part 5)

Intraperitoneal AbscessesAbscess formation is common in untreated peritonitis if overt gramnegative sepsis either does not develop or develops but is not fatal. In experimental models of abscess formation, mixed aerobic and anaerobic organisms have been implanted intraperitoneally. Without therapy directed at anaerobes, animals develop intraabdominal abscesses. As in humans, these experimental abscesses may stud the peritoneal cavity, lie within the omentum or mesentery, or even develop on the surface of or within viscera such as the liver.Pathogenesis and ImmunityThere is often disagreement about whether an abscess represents a disease state or a host response. ...
Nội dung trích xuất từ tài liệu:
Chapter 121. Intraabdominal Infections and Abscesses (Part 5) Chapter 121. Intraabdominal Infections and Abscesses (Part 5) Intraperitoneal Abscesses Abscess formation is common in untreated peritonitis if overt gram-negative sepsis either does not develop or develops but is not fatal. Inexperimental models of abscess formation, mixed aerobic and anaerobicorganisms have been implanted intraperitoneally. Without therapy directed atanaerobes, animals develop intraabdominal abscesses. As in humans, theseexperimental abscesses may stud the peritoneal cavity, lie within the omentum ormesentery, or even develop on the surface of or within viscera such as the liver. Pathogenesis and Immunity There is often disagreement about whether an abscess represents a diseasestate or a host response. In a sense, it represents both: while an abscess is aninfection in which viable infecting organisms and PMNs are contained in a fibrouscapsule, it is also a process by which the host confines microbes to a limited space,thereby preventing further spread of infection. In any event, abscesses do causesignificant symptoms, and patients with abscesses can be quite ill. Experimentalwork has helped to define both the host cells and the bacterial virulence factorsresponsible—most notably, in the case of B. fragilis. This organism, althoughaccounting for only 0.5% of the normal colonic flora, is the anaerobe mostfrequently isolated from intraabdominal infections, is especially prominent inabscesses, and is the most common anaerobic bloodstream isolate. On clinicalgrounds, therefore, B. fragilis appears to be uniquely virulent. Moreover, B.fragilis acts alone to cause abscesses in animal models of intraabdominalinfection, whereas most other Bacteroides species must act synergistically with afacultative organism to induce abscess formation. Of the several virulence factors identified in B. fragilis, one is critical: thecapsular polysaccharide complex (CPC) found on the bacterial surface. The CPCcomprises at least eight distinct surface polysaccharides. Structural analysis ofthese polysaccharides has shown an unusual motif of oppositely charged sugars.Polysaccharides having these zwitterionic characteristics, such as polysaccharideA (PSA), evoke a host response in the peritoneal cavity that localizes bacteria intoabscesses. B. fragilis and PSA have been found to adhere to primary mesothelialcells in vitro; this adherence, in turn, stimulates the production of tumor necrosisfactor α (TNF-α) and intercellular adhesion molecule 1 (ICAM-1) by peritonealmacrophages. Although abscesses characteristically contain PMNs, the process ofabscess induction depends on the stimulation of T lymphocytes by these uniquezwitterionic polysaccharides. The stimulated CD4+ T lymphocytes secreteleukoattractant cytokines and chemokines. The alternative pathway of complementand fibrinogen also participate in abscess formation. While antibodies to the CPC enhance bloodstream clearance of B. fragilis,CD4+ T cells are critical in immunity to abscesses. When administeredsubcutaneously, B. fragilis PSA has immunomodulatory characteristics andstimulates CD4+ T regulatory cells via an interleukin (IL) 2–dependentmechanism to produce IL-10. IL-10 downregulates the inflammatory response,thereby preventing abscess formation. Clinical Presentation Of all intraabdominal abscesses, 74% are intraperitoneal or retroperitonealand are not visceral. Most intraperitoneal abscesses result from fecal spillage froma colonic source, such as an inflamed appendix. Abscesses can also arise fromother processes. They usually form within weeks of the development of peritonitisand may be found in a variety of locations—from omentum to mesentery, pelvis topsoas muscles, and subphrenic space to a visceral organ such as the liver, wherethey may develop either on the surface of the organ or within it. Periappendicealand diverticular abscesses occur commonly. Diverticular abscesses are least likelyto rupture. Infections of the female genital tract and pancreatitis are also amongthe more common causative events. When abscesses occur in the female genitaltract—either as a primary infection (e.g., tuboovarian abscess) or as an infectionextending into the pelvic cavity or peritoneum—B. fragilis figures prominentlyamong the organisms isolated. B. fragilis is not found in large numbers in thenormal vaginal flora. For example, it is encountered less commonly in pelvicinflammatory disease and endometritis without an associated abscess. Inpancreatitis with leakage of damaging pancreatic enzymes, inflammation isprominent. Therefore, clinical findings such as fever, leukocytosis, and evenabdominal pain do not distinguish pancreatitis itself from complications such aspancreatic pseudocyst, pancreatic abscess (Chap. 307), or intraabdominalcollections of pus. Especially in cases of necrotizing pancreatitis, in which theincidence of local pancreatic infection may be as high as 30%, needle aspirationunder CT guidance is performed to sample fluid for culture. Many centersprescribe preemptive antibiotics for patients with necrotizing pancreatitis.Imipenem is frequently used for this purpose since it reaches high tissue levels inthe pancreas (although it is not unique in this regard). If needle aspiration yieldsinfected fluid, most experts agree that surgery is superior to percutaneousdrainage.