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), 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.

FIGURE 84-1

Algorithm for the management of pts with intraabdominal abscesses by percutaneous drainage. Antimicrobial therapy should be administered concomitantly. (Reprinted with permission from Lorber B [ed]: Atlas of Infectious Diseases, vol VII: Intraabdominal Infections, Hepatitis, and Gastroenteritis. Philadelphia, Current Medicine, 1996, p 1.30, as adapted from Rotstein OD, Simmons RL, in Gorbach SL et al [eds]: Infectious Diseases. Philadelphia, Saunders, 1992, p 668.)