Abscesses of the liver are generally due to infection by bacteria or, less commonly in the United States, by amebae. The diagnosis is often missed, since many patients have only subtle clinical indications of liver disease or none at all.
Pyogenic liver abscess is a disease seen predominantly among individuals with other underlying disorders. Structural and neoplastic diseases involving the biliary tract predominate. Obstruction to biliary drainage allows infected bile to produce ascending infection of the liver. Inﬂammatory diseases of the bowel such as appendicitis and diverticulitis also predispose to hepatic abscess via spread through portal veins. On occasion, penetrating or blunt trauma predisposes to hepatic abscess; tissue injury may allow bacterial infection by seeding during transient episodes of portal bacteremia.
Hepatic abscess complicates fewer than 2 per cent of cases of colitis due to Entamoeba histolytica, presumably occurring via portal spread.
Clinical and Laboratory Features
Clinical findings in patients with hepatic abscess are often nonspecific. Most are febrile, but only about half have abdominal pain and tenderness; two thirds have palpable hepatomegaly; less than one in four is jaundiced, although half have elevated serum bilirubin liver abscess have positive blood cultures. In patients with liver abscess the alkaline phosphatase is generally elevated and disproportionate to the modest elevation in bilirubin. In contrast, patients with the nonspecific jaundice that occasionally accompanies bacterial infection at other sites generally have elevated bilirubin levels (as much as 5 to 10 mg/dl or more) and only slightly elevated alkaline phosphatase levels.
In liver abscess, chest roentgenogram may reveal an elevated right hemi diaphragm and atelectasis or effusion at the right lung base. The diagnosis is best achieved by contrast-enhanced computerized tomography of the abdomen. Pyogenic abscesses may be single or multiple; multiple abscesses often arise from a biliary source of infection. Amebic abscesses are generally single and are usually located in the right lobe of the liver. Only a minority of patients with amebic liver abscess have concurrent intestinal amebiasis; a positive stool examination for amebae, however, may suggest the diagnosis. Antibody titers against E. histolytica are almost always positive in patients with amebic liver abscess.
Anaerobes, microaerophilic streptococci, and gram-negative bacilli are the predominant agents of pyogenic liver abscess. Occasionally Staphylococcus aureus causes multiple hepatic abscesses during the course of bacteremic seeding of multiple organs. Of the protozoa, only Entamoeba histolytica is known to cause hepatic abscess.
In patients with bacteremia and abnormal liver function studies, the jaundice of sepsis may be distinguished from the mild jaundice of liver abscess by a relatively high bilirubin/alkaline phosphatase ratio and clinical indications of a primary extra-hepatic source of bacteremia. Patients with cholecystitis and cholangitis are at risk, albeit low, for the development of hepatic abscess. In both cholecystitis and cholangitis the onset of illness is more abrupt than in patients with hepatic abscess. Tenderness among patients with cholecystitis is generally quite localized over the gallbladder. Patients with cholangitis are often very ill and jaundiced.
The Fitz-Hugh-Curtis syndrome or gonococcal perihepatitis may share some clinical manifestations of hepatic abscess and should be suspected in the young sexually active woman with fever and right upper quadrant tenderness. Tumors involving the liver may produce fever and a clinical and radiologic picture mimicking hepatic abscess. This is complicated by the occasional concurrence of malignancy with hepatic abscess. Patients with echinococcal cysts may present with a slowly expanding mass in the liver. Fever in the absence of cyst rupture is rare.
Diagnosis and Treatment
If pyogenic abscess is suspected, needle aspiration is indicated. Using ultrasound or CT guidance, a percutaneous catheter can be inserted into the abscess cavity for both diagnostic, and therapeutic purposes. The pus should be Gram s stained and cultured aerobically and anaerobically. Unless the Gram s stain indicates otherwise, initial therapy for pyogenic liver abscess should include a drug active against anaerobes (clindamycin or chloramphenicol) plus an aminoglycoside. Antibiotics should be continued for at least four to six weeks. Duration of therapy may be guided by serial CT scans. Surgery is required to relieve biliary tract obstruction and to drain loculated abscesses or abscesses that do not respond to percutaneous drainage and antibiotics. Patients with pyogenic liver abscess should be evaluated for an intra-abdominal source of infection.
Dr. Afsaneh Jeddi