Splenic Pathology: Splenic Infarction

On CT, infarcts are regions of wedged shape hypodensity extending to the capsule of the spleen reflecting the lack of vascular supply. Infarcts may also be poorly defined and heterogeneous in attenuation. The appearance can be similar to abscesses, tumors, or hematomas. Therefore, clinical information can be crucial to correct diagnosis. When infarcts are large, involving the majority of the spleen, there is often a rim of peripheral enhancement from maintained capsular vessel perfusion. This is known as the "rim" sign and is specific for infarction. The appearance is similar to the rim sign in the kidney.

With time, infarcts become more well defined and hypodense. These areas may develop into regions of scaring and fibrosis with only residual irregularity of the border of the spleen. Infarcts leave the spleen prone to rupture and superimposed infection. Individuals with multiple, ongoing infarctions, as in sickle cell disease, develop progressive atrophy and calcification of the spleen. This processes is called autosplenectomy. Infarcts may also develop into pseudocysts leaving hypodense, water attenuation regions years later as the only finding.

Pancreatitis and pancreatic cancer are the most common causes of vascular occlusion in the spleen. Other etiologies include ischemia and infarction due to blood dyscrasias including sickle cell disease, myelofibrosis, and lymphoma/leukemia. Vasculitis may lead to splenic infarctions. Embolic occlusion of the splenic artery results from endocarditis, mitral valve disease, and potentially during transcatheter procedures of the hepatic artery. Prolonged hypoperfusion due to decreased cardiac output is a cause of infarction. Marked splenomegaly may also cause relative hypoperfusion leading to regions of infarct.