Splenic Abscess after Infarction

Emboli (septic or sterile) are the most common cause of splenic infarctions, followed by local thrombosis (e.g., myelofibrosis, sickle cell disease, leukemia, and lymphoma), vasculitiides, pancreatic disease, splenic artery aneurysm, and splenic torsion.

In the acute phase, splenic infarctions are characterized peripheral low-attenuation lesions that may be wedge-shaped (classic), round or irregular (more common). In some cases, they may present as heterogeneous and poorly marginated lesions that are similar to abscesses and tumors. Later on, there is progressive volume loss and possibly calcification with hypertrophy of the surrounding normal spleen. Liquefaction and necrosis may also occur, with the risk of outward expansion, subcapsular hemorrhage, peritoneal hemorrhage.

Splenic infarctions may be complicated by abscess. The presence of gas in an intrasplenic collection suggests an abscess, but the majority of splenic abscesses do not contain gas. When gas is seen in an infarcted spleen, however, the issue is a bit more complicated. This is because gas in an organ following infarction does not always point to an infectious etiology. Gas formation has been reported in the kidney, liver, and spleen after transcatheter embolization, and is thought to be due to liberation of oxygen from oxyhemoglobin.

Therefore, it is important to differentiate gas in an abscess from gas following infarction. Multiple small gas bubbles throughout the organ, with most of the gas in the more central portions suggests a nonsuppurative origin.

References

• Levy JM, Wasserman PI, Weiland DE. Nonsuppurative gas formation in the spleen after transcatheter splenic infarction. Radiology. 1981 May;139(2):375-6.
• Rabushka LS, Kawashima A, Fishman EK. Imaging of the spleen: CT with supplemental MR examination. Radiographics. 1994 Mar;14(2):307-32.