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الانزيمات
Intraperitoneal Abscesses
المؤلف:
Longo, D., Fauci, A. S., Kasper, D. L., Hauser, S., Jameson, J. L., Loscalzo, J., Holland, S. M., & Langford, C. A.
المصدر:
Harrisons Principles of Internal Medicine (2025)
الجزء والصفحة:
22e , p1072-1074
2025-09-16
35
Abscess formation is common in untreated peritonitis if overt gram negative 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 Immunity
There is often disagreement about whether an abscess represents a disease state or a host response. In a sense, it represents both: while an abscess is an infection in which viable infecting organisms and PMNs are contained in a fibrous capsule, 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 cause significant symptoms, and patients with abscesses can be quite ill. Experimental work has helped to define both the host cells and the bacterial virulence factors responsible—most notably in the case of B. fragilis. This organism, although accounting for only 0.5% of the normal colonic flora, is the anaerobe most frequently isolated from intraabdominal infections, is especially prominent in abscesses, and is the most common anaerobic bloodstream isolate. On clinical grounds, therefore, B. fragilis appears to be uniquely virulent. Moreover, B. fragilis acts alone to cause abscesses in animal models of intraabdominal infection, whereas most other Bacteroides species must act synergistically with a facultative organism to induce abscess formation.
Of the several virulence factors identified in B. fragilis, one is critical: the capsular polysaccharide complex found on the bacterial surface. This complex comprises at least eight distinct surface polysaccharides. Structural analysis of these polysaccharides has shown an unusual motif of oppositely charged sugars. Polysaccharides having these zwitterionic characteristics, such as polysaccharide A, evoke a host response in the peritoneal cavity that localizes bacteria into abscesses. B. fragilis and polysaccharide A have been found to adhere to primary mesothelial cells in vitro; this adherence, in turn, stimulates the pro duction of tumor necrosis factor α and intercellular adhesion molecule 1 by peritoneal macrophages. Although abscesses characteristically contain PMNs, the process of abscess induction depends on the stimulation of T lymphocytes by these unique zwitterionic polysaccharides. The stimulated CD4+ T lymphocytes secrete leukoattractant cytokines and chemokines. The alternative pathways of complement and fibrinogen also participate in abscess formation.
While antibodies to the capsular polysaccharide complex enhance bloodstream clearance of B. fragilis, CD4+ T cells are critical in immunity to abscesses. When administered experimentally, B. fragilis poly saccharide A has immunomodulatory characteristics and stimulates CD4+ T regulatory cells via an interleukin 2–dependent mechanism to produce interleukin 10. Interleukin 10 downregulates the inflammatory response, thereby preventing abscess formation.
Clinical Presentation
Of all intraabdominal abscesses, 74% are intraperitoneal or retroperitoneal and are not visceral. Most intraperitoneal abscesses result from fecal spillage from a colonic source, such as an inflamed appendix. Abscesses can also arise from other processes. They usually form within weeks of the development of peritonitis and may be found in a variety of locations from omentum to mesentery, pelvis to psoas muscles, and subphrenic space to a visceral organ such as the liver, where they may develop either on the surface of the organ or within it. Periappendiceal and diverticular abscesses occur commonly. Diverticular abscesses are least likely to rupture. Infections of the female genital tract and pancreatitis also are among the more common causative events. When abscesses occur in the female genital tract—either as a primary infection (e.g., tuboovarian abscess) or as an infection extending into the pelvic cavity or peritoneum—B. fragilis figures prominently among the organisms isolated. B. fragilis is not found in large numbers in the normal vaginal flora. For example, it is encountered less commonly in pelvic inflammatory disease and endo metritis without an associated abscess. In pancreatitis with leakage of damaging pancreatic enzymes, inflammation is prominent. Therefore, clinical findings such as fever, leukocytosis, and even abdominal pain do not distinguish pancreatitis itself from complications such as pancreatic pseudocyst, pancreatic abscess, or intraabdominal collections of pus. Especially in cases of necrotizing pancreatitis, in which the incidence of local pancreatic infection may be as high as 30%, needle aspiration under CT guidance is performed to sample fluid for culture. Traditionally, many centers have prescribed preemptive antibiotics for patients with necrotizing pancreatitis. Imipenem is frequently used for this purpose because it reaches high tissue levels in the pancreas (although it is not unique in this regard). Randomized controlled studies have not demonstrated a benefit from this practice, and guidelines no longer recommend preemptive antibiotics for patients with acute pancreatitis. If needle aspiration yields infected fluid in the setting of acute necrotizing pancreatitis, antibiotic treatment is appropriate in conjunction with surgical and/or percutaneous drainage of infected material. Infected pseudocysts that occur remotely from acute pancreatitis are unlikely to be associated with significant amounts of necrotic tissue and may be treated with either surgical or percutaneous catheter drainage in conjunction with appropriate anti biotic therapy.
Diagnosis
Scanning procedures have considerably facilitated the diagnosis of intraabdominal abscesses. Abdominal CT probably has the highest yield, although ultrasonography is particularly useful for the right upper quadrant, kidneys, and pelvis. Both indium-labeled WBCs and gallium tend to localize in abscesses and may be useful in finding a collection. Because gallium is taken up in the bowel, indium labeled WBCs may have a slightly greater yield for abscesses near the bowel. Neither indium-labeled WBC scans nor gallium scans serve as a basis for a definitive diagnosis, however; both need to be followed by other, more specific studies, such as CT, if an area of possible abnormality is identified. PET scanning should also be considered due to its ready availability and because it provides more resolution. Abscesses contiguous with or contained within diverticula are particularly difficult to diagnose with scanning procedures. Although barium should not be injected if a perforation is suspected, a barium enema occasionally may detect a diverticular abscess not diagnosed by other procedures. If one study is negative, a second study sometimes reveals a collection. Although exploratory laparotomy has been less commonly used since the advent of CT, this procedure still must be undertaken on occasion if an abscess is strongly suspected on clinical grounds.
TREATMENT
Intraperitoneal Abscesses
An algorithm for the management of patients with intraabdominal (including intraperitoneal) abscesses by percutaneous drainage is presented in Fig. 1. Treatment of intraabdominal infections involves determination of the initial focus of infection, administration of broad-spectrum antibiotics targeting the organisms involved, and performance of a drainage procedure if one or more definitive abscesses have formed. Antimicrobial therapy, in general, is adjunctive to drainage and/or surgical correction of an underlying lesion or process in intraabdominal abscesses. Results of cultures from drain sites are not reliable for defining the etiology of infections. Unlike the intraabdominal abscesses resulting from most causes, for which drainage of some kind is generally required, abscesses associated with diverticulitis usually wall off locally after rupture of a diverticulum, so that surgical intervention is not routinely required.
Fig1. Algorithm for the management of patients with intraabdominal abscesses by percutaneous drainage. Antimicrobial therapy should be administered concomitantly. (Reproduced with permission from B Lorber [ed]: Atlas of Infectious Diseases, vol VII: Intra-abdominal infections, hepatitis, and gastroenteritis. Philadelphia, Current Medicine, 1996, p 1.30, as adapted from OD Rotstein, RL Simmons, in SL Gorbach et al [eds]: Infectious Diseases. Philadelphia, Saunders; 1992.)
A number of agents exhibit excellent activity against aerobic gram-negative bacilli. Because death in intraabdominal sepsis is linked to gram-negative bacteremia, empirical therapy for intra- abdominal infection always needs to include adequate coverage of gram-negative aerobic, facultative, and anaerobic organisms. Even if anaerobes are not cultured from clinical specimens, they still must be covered by the therapeutic regimen. Empirical antibiotic therapy should be the same as that discussed above for secondary peritonitis. Most clinical treatment failures are due to failure to drain the abscess and thereby achieve source control. The appropriate duration of antibiotic treatment for abdominal abscesses depends on whether the presumptive source of the intraabdominal infection has been controlled. With adequate source control, antibiotic treatment may be limited to 4 or 5 days.
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