Visceral Abscesses

Liver Abscess

Epidemiology, pathogenesis, 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 IP 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 Streptococcus milleri).
- Amebic liver abscesses are not uncommon, with positive serology 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 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
Liver Abscess Drainage is the mainstay of treatment (Fig. 84-1. Algorithm for the Management of Pts with Intraabdominal Abscesses by Percutaneous Drainage), but medical management with long courses of antibiotics can be successful. Empirical therapy is the same as for intraabdominal sepsis and secondary bacterial peritonitis. 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) requiring surgery; with the presence of yeast; or with lack of response in 4-7 days.

Splenic Abscess

Epidemiology and pathogenesis: 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
Splenic Abscess 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.

Perinephric and Renal Abscesses

Epidemiology and pathogenesis: 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 spp. are sometimes identified.
Clinical manifestations: Clinical signs are nonspecific and include flank pain, abdominal pain, and fever. This 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, if the pt has known renal stone disease, or if fever and pyuria occur in conjunction with a sterile urine culture.

TREATMENT
Perinephric and Renal Abscesses Drainage and the administration of antibiotics active against the organisms recovered are essential. Percutaneous drainage is usually successful for perinephric abscesses.