Splenic Infarction

Global or segmental parenchymal splenic ischemia and necrosis caused by vascular occlusion

Acute findings on CECT

• Diagnosis best made on portal venous-phase images due to heterogeneous arterial-phase enhancement

• Global infarction: Complete nonenhancement of spleen

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    ± cortical rim sign: Preserved enhancement of peripheral rim of spleen in massive infarction

• Segmental infarction: Wedge-shaped or rounded low-attenuation area usually at periphery of spleen

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    Can be multiple, especially when caused by emboli

Chronic findings on CECT

• Most often results in scarring and volume loss

• Multiple repetitive infarcts in sickle cell disease can lead to small, calcified spleen (autoinfarcted spleen)

• Infarct can develop into splenic cyst

MR findings: Low signal on T1WI, heterogeneous high signal on T2WI, and hypoenhancing on T1WI C+ images

Complications (< 20% of patients)

• Perisplenic fluid/hematoma suggests splenic rupture

• Development of rim-enhancing fluid collection: Splenic abscess

Splenic laceration

Splenic cyst or abscess

Heterogeneous arterial-phase enhancement of spleen

Splenic tumors

Many different causes but 2 most common are

• Hematologic disease or hematologic malignancies (sickle cell, myelofibrosis, leukemia, etc.)

• Embolic conditions (septic emboli, cardiac emboli from atrial fibrillation, etc.)

Most cases require no treatment but rarely surgery or intervention for pain or complications

Global or segmental parenchymal splenic ischemia and necrosis caused by vascular occlusion

Best diagnostic clue

• Peripheral, wedge-shaped, nonenhancing areas within splenic parenchyma on CECT in patients with LUQ pain

Location

• Entire spleen may be infarcted or more commonly segmental areas

Size

• Variable: Global or segmental

• Spleen may or may not demonstrate splenomegaly

Morphology

• Most commonly wedge-shaped areas of nonenhancement when infarct is segmental

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    Straight margins indicate vascular etiology (rather than mass or fluid collection)

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    May very rarely be rounded (atypical appearance)

Radiography

• May be associated with lower left lobe atelectasis and pleural effusion on chest x-ray

NECT

• Infarcts may be difficult (or impossible) to visualize without intravenous contrast

• Areas of hemorrhagic transformation within infarcts appear hyperdense

CECT

• Acute findings

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    Diagnosis best made on portal venous-phase images: Heterogeneous enhancement during arterial phase (due to differential enhancement of red and white pulp) makes identification of subtle infarcts difficult

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    Global: Complete nonenhancement of spleen

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      ± cortical rim sign: Preserved enhancement of peripheral rim of spleen in massive infarction due to preserved flow from capsular vessels

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      Mottled higher density areas within infarcted spleen may represent either tiny islands of residual enhancing splenic tissue or hemorrhage

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    Segmental: Wedge-shaped or rounded low-attenuation area usually at periphery of spleen

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      Can be multiple, especially when caused by emboli

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      In some instances, accessory spleens (splenules) may be infarcted

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      Spleen may or may not be enlarged in acute phase

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    Complications (< 20% of patients)

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      Presence of fluid or hematoma surrounding spleen in setting of infarct suggests splenic rupture (most often in setting of large or global infarct)

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      Development of discrete rim-enhancing fluid collection ± internal gas should raise concern for splenic abscess

• Chronic findings

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    Infarcts should evolve over time, leaving areas of scarring and volume loss in spleen

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      Sites of old infarcts may show calcification

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      Remaining spleen may undergo compensatory hypertrophy

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    Multiple repetitive infarcts in sickle cell disease can lead to small, calcified spleen (autoinfarcted spleen)

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    Infarct can develop into splenic cyst (secondary or acquired cyst)