For a more detailed discussion, see Baron MJ, Kasper DL: Intraabdominal Infections and Abscesses, Chap. 127, p. 1077, in HPIM-18.
Intraperitoneal infections result when normal anatomic barriers are disrupted. Organisms contained within the bowel or an intraabdominal organ enter the sterile peritoneal cavity, causing peritonitis and—if the infection goes untreated and the pt survives—abscesses.
Peritonitis is a life-threatening event that is often accompanied by bacteremia and sepsis. Primary peritonitis has no apparent source, whereas secondary peritonitis is caused by spillage from an intraabdominal viscus; the etiologic organisms and the clinical presentation of these two processes are different.
• Epidemiology Primary bacterial peritonitis (PBP) is most common among pts with cirrhosis (usually due to alcoholism) and preexisting ascites, but ≤10% of these pts develop PBP. PBP is also described in other settings (e.g., malignancy, hepatitis).
• Pathogenesis PBP is due to hematogenous spread of organisms to ascitic fluid in pts in whom a diseased liver and altered portal circulation compromise the liver’s filtration function.
• Microbiology Enteric gram-negative bacilli such as Escherichia coli or gram-positive organisms such as streptococci, enterococci, and pneumococci are the most common etiologic agents.
– A single organism is typically isolated.
– If a polymicrobial infection including anaerobes is identified, the diagnosis of PBP should be reconsidered and a source of secondary peritonitis should be sought.
• Clinical manifestations Although some pts experience acute-onset abdominal pain or signs of peritoneal irritation, other pts have only nonspecific and nonlocalizing manifestations (e.g., malaise, fatigue, encephalopathy). Fever is common (~80% of pts).
• Diagnosis PBP is diagnosed if peritoneal fluid is sampled and contains >250 PMNs/μL.
– Culture yield is improved if a 10-mL volume of peritoneal fluid is placed directly into blood culture bottles.
– Blood cultures should be performed because bacteremia is common.
TREATMENT Primary (Spontaneous) Bacterial Peritonitis
• A third-generation cephalosporin (e.g., ceftriaxone, 2 g q24h IV; or cefotaxime, 2 g q8h IV) or piperacillin/tazobactam (3.375 g qid IV) constitutes appropriate empirical treatment.
• The regimen should be narrowed after the etiology is identified.
• Treatment should continue for at least 5 days, but longer courses (up to 2 weeks) may be needed for pts with coexisting bacteremia or for those whose improvement is slow.
• Prevention Up to 70% of pts have a recurrence of PBP within 1 year. Prophylaxis with fluoroquinolones (e.g., ciprofloxacin, 750 mg weekly) or trimethoprim-sulfamethoxazole (TMP-SMX; one double-strength tablet daily) reduces this rate to 20% but increases the risk of serious staphylococcal infections over time.
• Pathogenesis Secondary peritonitis develops when bacteria contaminate the peritoneum as a result of spillage from an intraabdominal viscus.
• Microbiology Infection almost always involves a mixed flora in which gram-negative bacilli and anaerobes predominate, especially when the contaminating source is colonic. The specific organisms depend on the flora present at the site of the initial process.
• Clinical manifestations Initial symptoms may be localized or vague and depend on the primary organ involved. Once infection has spread to the peritoneal cavity, pain increases; pts lie motionless, often with knees drawn up to avoid stretching the nerve fibers of the peritoneal cavity. Coughing or sneezing causes severe, sharp pain. There is marked voluntary and involuntary guarding of anterior abdominal musculature, tenderness (often with rebound), and fever.
• Diagnosis Although recovery of organisms from peritoneal fluid is easier in secondary than in primary peritonitis, radiographic studies to find the source of peritoneal contamination or immediate surgical intervention should usually be part of the initial diagnostic evaluation. Abdominal taps are done only to exclude hemoperitoneum in trauma cases.
• Treatment Antibiotics aimed at the inciting flora—e.g., penicillin/β-lactamase inhibitor combinations or a combination of a fluoroquino-lone or a third-generation cephalosporin plus metronidazole—should be administered early.
– For critically ill pts in the ICU, imipenem (500 mg q6h IV) or drug combinations such as ampicillin plus metronidazole plus ciprofloxacin should be used.
– Surgical intervention is often needed.
• Pathogenesis In a phenomenon similar to that seen in intravascular device–related infections, organisms migrate along the catheter, a foreign body that serves as an entry point.
• Microbiology CAPD-associated peritonitis usually involves skin organisms, with Staphylococcus spp. such as coagulase-negative staphylococci and Staphylococcus aureus accounting for ~45% of cases; gram-negative bacilli and fungi (e.g., Candida) are occasionally identified.
• Clinical manifestations CAPD-associated peritonitis presents similarly to secondary peritonitis, in that diffuse pain and peritoneal signs are common.
• Diagnosis Several hundred milliliters of removed dialysis fluid should be centrifuged and sent for culture.
– Use of blood culture bottles improves the diagnostic yield.
– The dialysate is usually cloudy and contains >100 WBCs/μL, with >50% neutrophils.
• Treatment Empirical therapy should be directed against staphylococcal species and gram-negative bacilli (e.g., cefazolin plus a fluoroquinolone or a third-generation cephalosporin such as ceftazidime). Vancomycin should be used instead of cefazolin if methicillin resistance is prevalent, if the pt has an overt exit-site infection, or if the pt appears toxic.
– Antibiotics are given by the intraperitoneal route either continuously (e.g., with each exchange) or intermittently (e.g., once daily, with the dose allowed to remain in the peritoneal cavity for 6 h). Severely ill pts should be given the same regimen by the IV route.
– Catheter removal should be considered if the pt’s condition does not improve within 48 h.
Intraabdominal abscesses are generally diagnosed through radiographic studies, of which abdominal CT is typically most useful.
• Epidemiology Of intraabdominal abscesses, 74% are intraperitoneal or retroperitoneal, not visceral.
• Pathogenesis Most abscesses arise from colonic sources. Abscesses develop in untreated peritonitis as an extension of the disease process and represent host defense activity aimed at containing the infection.
• Microbiology Bacteroides fragilis accounts for only 0.5% of the normal colonic flora, but is the anaerobe most frequently isolated from intraabdominal abscesses and from blood.
• Treatment Antimicrobial therapy is adjunctive to drainage and/or surgical correction of an underlying lesion or process.
– Diverticular abscesses usually wall off locally, and surgical intervention is not routinely needed.
– Antimicrobial agents with activity against gram-negative bacilli and anaerobic organisms are indicated (see “Secondary Peritonitis,” above).
• Epidemiology and Microbiology Liver abscesses account for up to half of visceral intraabdominal abscesses and are caused most commonly by biliary tract disease (due to aerobic gram-negative bacilli or enterococci) and less often by local spread from pelvic and other intraperitoneal sources (due to mixed flora including aerobic and anaerobic species, among which B. fragilis is most common) or hematogenous seeding (infection with a single species, usually S. aureus or streptococci such as S. milleri).
– Amebic liver abscesses are not uncommon.
– Amebic serology has yielded positive results in >95% of affected pts.
• Clinical manifestations Pts have fever, anorexia, weight loss, nausea, and vomiting, but only ~50% have signs localized to the RUQ, such as pain, tenderness, hepatomegaly, and jaundice. Serum levels of alkaline phosphatase are elevated in ~70% of pts, and leukocytosis is common. One-third to one-half of pts are bacteremic.
• Treatment Drainage is the mainstay of treatment, but medical management with long courses of antibiotics can be successful.
– Empirical therapy is the same as for intraabdominal sepsis and SBP.
– Percutaneous drainage tends to fail in cases with multiple, sizable abscesses; with viscous abscess contents that plug the pigtail catheter; with associated disease (e.g., of the biliary tract); or with lack of response in 4–7 days.
• Epidemiology Splenic abscesses are much less common than liver abscesses and usually develop via hematogenous spread of infection (e.g., due to endocarditis). The diagnosis is often made only after the pt’s death; the condition is frequently fatal if left untreated.
• Microbiology Splenic abscesses are most often caused by streptococci; S. aureus is the next most common cause. Gram-negative bacilli can cause splenic abscess in pts with urinary tract foci, with associated bacteremia, or with infection from another intraabdominal source; salmonellae are fairly commonly isolated, particularly from pts with sickle cell disease.
• Clinical manifestations Abdominal pain or splenomegaly occurs in ~50% of cases and pain localized to the LUQ in ~25%. Fever and leukocytosis are common.
• Treatment Pts with multiple or complex multilocular abscesses should undergo splenectomy, receive adjunctive antibiotics, and be vaccinated against encapsulated organisms (Streptococcus pneumoniae, Haemophilus influenzae, and Neisseria meningitidis). Percutaneous drainage has been successful for single, small (<3-cm) abscesses and may also be useful for pts at high surgical risk.
• Epidemiology Perinephric and renal abscesses are uncommon. More than 75% of these abscesses are due to ascending infection and are preceded by pyelonephritis. The most important risk factor is the presence of renal calculi that produce local obstruction to urinary flow.
• Microbiology E. coli, Proteus spp. (associated with struvite stones), and Klebsiella spp. are the most common etiologic agents; Candida species are sometimes identified.
• Clinical manifestations Clinical signs are nonspecific and include flank pain, abdominal pain, and fever. The diagnosis should be considered if pts with pyelonephritis have persistent fever after 4 or 5 days of treatment, if a urine culture yields a polymicrobial flora in pts with known renal stone disease, or if fever and pyuria occur in conjunction with a sterile urine culture.
• Treatment Drainage and the administration of antibiotics active against the organisms recovered are essential. Percutaneous drainage is usually successful for perinephric abscesses.
For a more detailed discussion, see Baron MJ, Kasper DL: Intraabdominal Infections and Abscesses, Chap. 127, p. 1077, in HPIM-18.