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Harrison’s Manual of Medicine



Intraperitoneal Abscesses
PATHOGENESIS   Intraperitoneal infections generally arise when a normal anatomic barrier is disrupted and the usually sterile peritoneal space becomes seeded with microorganisms. Peritonitis is either primary (without an apparent inciting event) or secondary. In adults, primary or spontaneous bacterial peritonitis (SBP) is most common among pts with cirrhosis of the liver due to alcoholism. Pts with preexisting ascites are predisposed to infection at this site. The pathogenic mechanism is presumed to be seeding of ascites when the diseased liver with altered portal circulation is unable to perform its usual filtration function. A single bacterial species usually causes SBP, and accompanying bacteremia is common. Secondary peritonitis develops when bacteria contaminate the peritoneum as a result of spillage from a ruptured viscus. Mixed aerobic and anaerobic bacteria are the rule in secondary peritonitis.
CLINICAL MANIFESTATIONS   SBP   Fever, the most common presenting symptom, is documented in 80% of cases of SBP. Abdominal pain, acute onset of symptoms, and peritoneal signs on physical examination are diagnostically helpful, but absence of these findings does not exclude this subtle diagnosis. Ascites virtually always predates infection.
Secondary Peritonitis   Localized symptoms, if present, depend on the inciting event. In cases of perforated gastric ulcer, epigastric pain is evident. In appendicitis, initial symptoms may be vague and may include nausea or periumbilical discomfort gradually localizing to the RLQ. Symptoms of secondary peritonitis include abdominal pain that increases with motion, coughing, or sneezing. Pts often lie with knees drawn up to avoid stretching peritoneal nerve fibers. Findings on abdominal exam include voluntary and involuntary guarding, tenderness, and, at a later stage, rebound tenderness.
DIAGNOSIS   To diagnose SBP, a primary intraabdominal source of infection must be excluded; abdominal CT with contrast may be helpful. A tap of the ascites is essential in every febrile cirrhotic pt to diagnose SBP. Peritoneal fluid should be placed in a blood culture bottle to increase yield. Blood should be cultured. For secondary peritonitis, diagnosis should focus on identifying the inciting event; a tap of peritoneal fluid is rarely needed.

Therapy for SBP should be directed at the organism recovered. Empirical therapy should include coverage for gram-negative aerobic bacilli and gram- positive cocci. Third-generation cephalosporins, carbapenems, or broad-spectrum penicillin/b-lactamase inhibitor combinations are reasonable initial options. After the infecting organism is identified, therapy should be narrowed to target that specific pathogen. If mixed flora (particularly anaerobes) are recovered in suspected SBP, the pt should be evaluated for secondary peritonitis. Treatment for secondary peritonitis includes antibiotics directed at aerobic gram-negative bacilli and at anaerobes as well as surgical intervention for the inciting process.

PATHOGENESIS   Intraperitoneal abscesses represent both a disease process and a host response. Anaerobic organisms, particularly Bacteroides fragilis, are critical in the development of these abscesses. The most important virulence factor of this organism is the capsular polysaccharide, which is responsible for the development of abscesses. Several host factors, including peritoneal macrophages, PMNs, and T cells, also appear to interact and stimulate abscess formation.
CLINICAL MANIFESTATIONS   Intraabdominal abscesses can be either intraperitoneal or retroperitoneal and are not visceral in 74% of cases. Infections of the female genital tract and pancreatitis are common causative events. Fever is the most common presenting symptom. As in secondary peritonitis, localizing symptoms depend on the inciting process. In psoas abscess, back or abdominal pain is common and associated osteomyelitis is found frequently.
VISCERAL ABSCESSES   Liver Abscesses   The liver is the intraabdominal organ in which abscesses develop most often. Fever is the most common presenting symptom. Only 50% of pts have signs or symptoms that direct attention to the RUQ, including hepatomegaly, tenderness, or jaundice.
Splenic Abscesses   These frequently are diagnosed only at autopsy. Generally, abscesses in the spleen arise from hematogenous spread. Bacterial endocarditis is the most common associated infection. Abdominal pain is reported in 50% of cases but is localized to the LUQ in only half of these instances. Fever is common; splenomegaly is documented in about 50% of cases.
Perinephric and Renal Abscesses   These are not common and generally arise from an initial UTI, often in association with nephrolithiasis. The clinical presentation is nonspecific. Pts may have flank and abdominal pain; 50% have fever. Pain may be referred to the groin or leg.
DIAGNOSIS   Scanning procedures generally are diagnostic; CT is most useful. Ultrasonography is particularly helpful for the RUQ, kidneys, and pelvis. Gallium- and indium-labeled WBCs localize in abscesses and may be useful in finding a collection. If one study is negative, a second study is sometimes revealing.

Treatment of intraabdominal infections involves establishment of an initial focus of infection, administration of antibiotics targeted at likely organisms, and performance of a drainage procedure if one or more definitive abscesses are found. Antibiotic treatment is adjunctive to drainage (percutaneous or surgical) and is usually directed at organisms involved in the inciting infection, which generally include aerobic gram-negative bacilli and anaerobes. Against gram-negative aerobic and facultative bacteria, aminoglycosides, third-generation cephalosporins, and the quinolones are the most widely tested agents, but they must be used in combination with another antibiotic active against anaerobes (e.g., metronidazole) when the latter organisms are likely to be involved in the process.


For a more detailed discussion, see Zaleznik DF, Kasper DL: Intraabdominal Infections and Abscesses, Chap. 130, p. 829, in HPIM-15; and Anaerobic Infections, Chap. 95, p. 441, in the Clinical Manual.


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