IS Case 127: Autosplenectomy

Daniel Ginat, MD

Imaging Sciences URMC 2008
Publication Date: 2009-05-21


Patient is an 43-year-old male with history of sickle cell disease.


Extensive atrophy and calcifications of the splenic parenchyma with sparing of focal rounded areas, as a sequela of sickle cell disease.




Splenic infarction is an uncommon entity. Etiologies include the following:

Emboli and thrombi are the most common etiologies. While many cases are asymptomatic, splenic infarcts typically present with sudden left upper quadrant pain that is referred to the shoulder.

On CT, acute splenic infarction typically appears and an area of low attenuation in a wedge-shaped configuration in the periphery of the organ. Ultrasound often demonstrates a hypoechoic or anechoic defect. Splenic infarction may also manifest as heterogeneous masses. On ultrasound, acute infarcts appear as poorly marginated hypoechoic lesions, but become hyperechoic with age. Chronic infarcts develop scarring and focal atrophy. Calcifications associated with splenic infarcts are usually coarse. In patients with sickle cell disease, thalassemia, and Hemoglobin C, calcifications are widespread and associated with loss of splenic function.

Differential diagnoses include lymphoma, metastasis, and abscess.

Potential complications of splenic infarction include rupture and infection. Therefore, follow-up imaging is recommended.


  1. Shirkhoda A, Wallace S, Sokhandan M. Computed tomography and ultrasonography in splenic infarction. J Can Assoc Radiol. 1985 Mar;36(1):29-33. [PMID: 3884618]
  2. Johnson CD, Schmit GD. Mayo Clinic Gastrointestinal Imaging Review. Mayo CLinic Scientific Press. 2005.

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