The differential diagnosis of cystic lesions of the liver includes bilomas, abscesses, parasitic disease, simple cysts, polycystic liver disease (PCLD), biliary cystadenoma, and cystadenocarcinoma.1 The disease spectrum includes infectious, traumatic, congenital, and neoplastic hepatic lesions that are relatively uncommon. While significant improvements have been made in the diagnosis, treatment, and outcome of many of these cystic hepatic lesions, controversy continues regarding the best treatment option. Many classification systems exist for these lesions; however, the one used in this chapter is presented in Table 43-1.
Table 43-1: Classification of Cystic Hepatic Lesions |Favorite Table|Download (.pdf)
Table 43-1: Classification of Cystic Hepatic Lesions
|I. Infectious hepatic cysts|
|A. Pyogenic liver abscess|
|B. Amebic liver abscess|
|C. Hydatid liver cysts|
|II. Congenital hepatic cysts|
|A. Simple cysts|
|B. Polycystic liver disease|
|III. Neoplastic hepatic cysts|
|IV. Traumatic hepatic cysts|
The first description of a hepatic abscess is credited to Hippocrates in the year 4000 BC. Ochsner's classic 1938 paper2 described this disease as one that occurred in young males with pylephlebitis, usually due to appendicitis, and resulting in liver abscess. At that time, pyogenic liver abscesses carried a case-fatality rate of 77%2 and open surgical drainage remained the treatment of choice for many years. In 1953, McFadzean and associates3 in Hong Kong advocated closed aspiration and antibiotics for treatment of solitary pyogenic liver abscess; however, this treatment did not gain widespread acceptance until imaging advancements in the 1980s allowed for precise localization and a percutaneous approach to treatment. In recent decades, the predominant etiology of pyogenic liver abscess has changed from pylephlebitis to a biliary origin, and more recent reports from Asia and the United States have noted an increase in incidence of cryptogenic liver abscesses. Fortunately, advanced imaging techniques and improved therapeutic modalities have decreased the case-fatality rate for this disease to 6–26%.4,5
Kupffer cells act as a filter for the clearance of microorganisms in the liver. These organisms reach the liver through the bloodstream, biliary tree, or direct extension. Abscesses occur when normal hepatic clearance mechanisms fail or the system is overwhelmed. Parenchymal necrosis and hematoma secondary to trauma, obstructive biliary processes, ischemia, and malignancy also promote invasion of microorganisms.
In order to appropriately treat the abscess, source control is required. Six distinct categories have been identified as potential sources: (1) bile ducts, causing ascending cholangitis; (2) portal vein, causing pylephlebitis from appendicitis or diverticulitis; (3) direct extension from a contiguous disease; (4) trauma due to blunt or penetrating injuries; (5) hepatic artery due to septicemia; and (6) cryptogenic6,7 (Fig. 43-1).
Biliary disease accounts for 35–40% of all pyogenic liver abscesses, and 40% of pyogenic liver abscesses of biliary origin are related to an underlying malignancy.6 Obstruction of the biliary tree is ...