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Liver abses

The liver receives blood from both systemic and portal circulations. Increased susceptibility
to infections would be expected given the increased exposure to bacteria. However, Kupffer
cells lining the hepatic sinusoids clear bacteria so efficiently that infection rarely occurs.
Multiple processes have been associated with the development of hepatic abscesses (see the
image below).

Table 4: Underlying etiology of


1086 cases of liver abscess compiled from the literature.
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Appendicitis was traditionally the major cause of liver abscess. As diagnosis and treatment of
this condition has advanced, its frequency as a cause for liver abscess has decreased to 10%.

Biliary tract disease is now the most common source of pyogenic liver abscess (PLA).
Obstruction of bile flow allows for bacterial proliferation. Biliary stone disease, obstructive
malignancy affecting the biliary tree, stricture, and congenital diseases are common inciting
conditions. With a biliary source, abscesses usually are multiple, unless they are associated
with surgical interventions or indwelling biliary stents. In these instances, solitary lesions can
be seen.

Infections in organs in the portal bed can result in a localized septic thrombophlebitis, which
can lead to liver abscess. Septic emboli are released into the portal circulation, trapped by the
hepatic sinusoids, and become the nidus for microabscess formation. These microabscesses
initially are multiple but usually coalesce into a solitary lesion.

Microabscess formation can also be due to hematogenous dissemination of organisms in


association with systemic bacteremia, such as endocarditis and pyelonephritis. Cases also are
reported in children with underlying defects in immunity, such as chronic granulomatous
disease and leukemia.

Approximately 4% of liver abscesses result from fistula formation between local intra-
abdominal infections.

Despite advances in diagnostic imaging, cryptogenic causes account for a significant


proportion of cases; surgical exploration has impacted this minimally. These lesions usually
are solitary in nature.
Penetrating hepatic trauma can inoculate organisms directly into the liver parenchyma,
resulting in pyogenic liver abscess. Nonpenetrating trauma can also be the precursor to
pyogenic liver abscess by causing localized hepatic necrosis, intrahepatic hemorrhage, and
bile leakage. The resulting tissue environment permits bacterial growth, which may lead to
pyogenic liver abscess. These lesions are typically solitary.

PLA has been reported as a secondary infection of amebic abscess, hydatid cystic cavities,
and metastatic and primary hepatic tumors. It is also a known complication of liver
transplantation, hepatic artery embolization in the treatment of hepatocellular carcinoma, and
the ingestion of foreign bodies, which penetrate the liver parenchyma. Trauma and
secondarily infected liver pathology account for a small percentage of liver abscess cases.

The right hepatic lobe is affected more often than the left hepatic lobe by a factor of 2:1.
Bilateral involvement is seen in 5% of cases. The predilection for the right hepatic lobe can
be attributed to anatomic considerations. The right hepatic lobe receives blood from both the
superior mesenteric and portal veins, whereas the left hepatic lobe receives inferior
mesenteric and splenic drainage. It also contains a denser network of biliary canaliculi and,
overall, accounts for more hepatic mass. Studies have suggested that a streaming effect in the
portal circulation is causative.