Splenic hemangioma is the most common benign neoplasm of the spleen, consisting of a hamartomatous vascular proliferation composed of cavernous vascular spaces lined by single-layer endothelium. It is found with a prevalence of 0.3-14% in autopsy series and is usually discovered incidentally. While most are asymptomatic, large lesions (>5 cm) may present with Kasabach-Merritt syndrome (consumptive coagulopathy), thrombocytopenia, or hemoperitoneum due to spontaneous rupture. On imaging, it demonstrates peripheral nodular enhancement with centripetal fill-in similar to hepatic hemangioma; this pattern is characteristic for the spleen as well. It may be associated with congenital vascular syndromes such as Klippel-Trenaunay or Beckwith-Wiedemann syndrome. Treatment is usually not required; however, splenectomy may be considered for large, symptomatic, or complicated lesions.
Age Range
20-70
Peak Age
45
Gender
Female predominant
Prevalence
Common
Splenic hemangioma is a benign vascular hamartomatous proliferation originating from vascular endothelial cells within the splenic parenchyma. Two main histopathological types are recognized: cavernous type (large, irregular blood-filled vascular spaces — more common) and capillary type (small, regular vascular channels — rarer). The cavernous spaces are lined by single-layer, mature endothelium and contain extremely slow blood flow. This slow flow forms the pathological basis for the peripheral nodular enhancement with centripetal (periphery to center) fill-in pattern observed on contrast-enhanced imaging: contrast agent first enters the vascular spaces at the lesion periphery, then slowly progresses toward the center. The marked hyperintensity on T2-weighted MRI ('light bulb sign') results from the long T2 relaxation time of static or very slowly flowing blood and high free water content within the cavernous spaces. Over time, thrombosis may develop within cavernous spaces, and thrombosed areas may undergo dystrophic calcification (phleboliths); these calcifications appear as punctate hyperdense foci on CT. In large hemangiomas, blood pooling can lead to platelet consumption, resulting in Kasabach-Merritt syndrome (consumptive coagulopathy + thrombocytopenia).
Globular enhancement foci at blood pool density at the periphery of the lesion in arterial phase, with progressive centripetal fill-in in portal venous and delayed phases, combined with marked CSF-like hyperintensity on T2-weighted MRI ('light bulb sign'). This combined pattern represents the splenic equivalent of the classic hepatic hemangioma pattern and is pathognomonic for splenic hemangioma.
On unenhanced CT, a well-defined, homogeneously hypodense lesion is seen relative to the splenic parenchyma. Density is typically between 20-40 HU, reflecting the water-like density of slowly flowing blood in cavernous spaces. Punctate calcifications from phleboliths may be visible in large lesions, representing dystrophic calcification in thrombosed vascular spaces. The lesion margins are smooth and sharp without invasive features. Rarely, heterogeneous density increase may be observed due to internal hemorrhage.
Report Sentence
A well-defined, homogeneously hypodense lesion is seen in the spleen on unenhanced CT with punctate calcifications that may represent phleboliths.
Globular (nodular) enhancement foci are seen at the periphery of the lesion in the arterial phase. Enhancement foci can be recognized independently from the normal zebra pattern enhancement of the splenic parenchyma. Peripheral enhancement foci typically enhance simultaneously with the aorta, with density values approaching blood pool density (near aortic). The lesion center has not yet enhanced — this peripheral nodular pattern represents the splenic equivalent of the hepatic hemangioma pattern. Note: The normal heterogeneous zebra pattern enhancement of the spleen in arterial phase can make hemangioma diagnosis challenging; therefore, portal venous and delayed phase evaluation is critical.
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The splenic lesion demonstrates peripheral nodular (globular) enhancement in the arterial phase with enhancement foci approaching aortic density; this pattern is similar to the hepatic hemangioma enhancement pattern.
In the portal venous phase, enhancement has progressed from the lesion periphery toward the center and the enhanced area has expanded. Areas showing peripheral nodular enhancement in the previous arterial phase begin to coalesce. However, the central portion of the lesion has not yet completely filled — centripetal filling continues. In this phase, the spleen parenchyma becomes homogeneous (zebra pattern disappears), allowing better evaluation of lesion-parenchyma contrast. The density of peripheral enhanced areas approaches or slightly exceeds splenic parenchyma.
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Progressive enhancement with centripetal progression is seen in the lesion in the portal venous phase, with peripheral enhanced areas becoming confluent; however, the central portion has not yet completely filled.
In the delayed phase (5-15 minutes), the lesion has filled completely or largely and appears isodense or slightly hyperdense relative to splenic parenchyma. This complete fill-in pattern represents the splenic equivalent of delayed phase filling in hepatic hemangioma and is of great diagnostic importance. In very large hemangiomas (>5 cm) or areas with thrombosis, central unfilled areas may persist. Homogeneous delayed filling confirms the vascular nature of the lesion and is critical in differentiation from solid tumors (lymphoma, metastasis).
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In the delayed phase, the lesion has completely filled and appears isodense to the splenic parenchyma; this progressive centripetal fill-in pattern is consistent with splenic hemangioma.
Markedly homogeneous hyperintense signal on T2-weighted MRI — 'light bulb sign'. Signal intensity is near or equal to cerebrospinal fluid (CSF). This marked T2 hyperintensity results from static or very slowly flowing blood and free water content in cavernous spaces. The homogeneous signal pattern distinguishes it from heterogeneous signal of solid tumors. In large hemangiomas, thrombosed areas may appear as focal T2 hypointense foci. Signal persists on T2 fat-sat sequences (not mixed with fat). Hyperintense signal becomes even more prominent with increasing TE.
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The splenic lesion demonstrates markedly homogeneous hyperintensity on T2-weighted MRI equal to CSF signal ('light bulb sign'), consistent with cavernous hemangioma.
On T1-weighted MRI, the lesion shows hypointense or isointense signal relative to the splenic parenchyma. Homogeneous signal pattern is typical. T1 hyperintense foci (subacute blood products — methemoglobin) may be seen in the presence of internal hemorrhage. Post-gadolinium T1 imaging shows a peripheral nodular enhancement with centripetal fill-in pattern similar to CT. In the delayed post-contrast phase (10-15 minutes), the lesion may fill completely.
Report Sentence
The splenic lesion shows mildly hypointense signal relative to the splenic parenchyma on T1-weighted MRI with peripheral nodular enhancement and centripetal fill-in pattern on post-contrast series.
On B-mode ultrasound, small hemangiomas (<2 cm) appear as well-defined, homogeneously hyperechoic masses. The hyperechoic appearance results from multiple acoustic interfaces created by cavernous spaces. In large hemangiomas (>3-4 cm), mixed echogenicity, internal cystic (anechoic) areas, and heterogeneous structure may be seen — this heterogeneity reflects areas of thrombosis, hemorrhage, or cystic degeneration. Posterior acoustic enhancement may be present due to fluid-filled cavernous spaces. Lesion margins are smooth and well-defined.
Report Sentence
A well-defined, homogeneously hyperechoic mass is seen in the spleen on B-mode US with posterior acoustic enhancement; consistent with splenic hemangioma.
Criteria
Large, irregular blood-filled vascular spaces; most common type (90%). Wide sinusoids lined by single-layer endothelium.
Distinct Features
Classic peripheral nodular enhancement and centripetal fill-in pattern is most prominent in this type. T2 hyperintensity is more homogeneous and pronounced. Can reach large sizes (>10 cm).
Criteria
Composed of small, regular vascular channels; rare type. Usually small in size (<2 cm).
Distinct Features
May show more homogeneous and rapid enhancement. Peripheral nodular pattern may be less prominent. More homogeneous hyperechoic appearance on US.
Criteria
Size >5 cm; increased risk of complications (Kasabach-Merritt, rupture, hemorrhage).
Distinct Features
Heterogeneous structure; internal thrombosis, hemorrhage, fibrosis, and calcification areas. May not completely fill even in delayed phase (central thrombosis/fibrosis). Risk of Kasabach-Merritt syndrome.
Criteria
Associated with Klippel-Trenaunay, Beckwith-Wiedemann, or diffuse hemangiomatosis. Multiple splenic hemangiomas or multi-organ hemangiomatosis.
Distinct Features
Multiple lesions; concomitant hemangiomas in other organs (liver, skin, bone). Young age onset. Splenomegaly may accompany.
Distinguishing Feature
Lymphangioma shows no or minimal enhancement (lymphatic spaces rather than vascular); hemangioma shows progressive enhancement. Lymphangioma has a multilocular cystic structure with septa.
Distinguishing Feature
Hamartoma shows homogeneous early enhancement (red pulp structure) without centripetal fill-in pattern; hemangioma shows peripheral nodular enhancement with late fill-in.
Distinguishing Feature
Littoral cell angioma is isointense or mildly hyperintense to spleen on T2 (no marked 'light bulb sign') and shows Tc-99m sulfur colloid / iron oxide uptake; hemangioma is markedly hyperintense on T2 and does not show RES uptake.
Distinguishing Feature
Hemangioendothelioma shows irregular margins, heterogeneous enhancement without complete fill-in pattern; hemangioma has smooth margins and fills completely in delayed phase. Hemangioendothelioma has malignant potential.
Distinguishing Feature
Simple cyst shows no enhancement (water density, 0-20 HU, thin smooth wall); hemangioma shows progressive enhancement. Cyst is hyperintense on T2 but has lower density than hemangioma on unenhanced CT.
Urgency
routineManagement
surveillanceBiopsy
Not NeededFollow-up
annualSplenic hemangioma generally has a benign course and does not require treatment. Annual US follow-up is sufficient for small, asymptomatic lesions. For >5 cm lesions, closer follow-up or splenectomy should be considered due to complication risk (Kasabach-Merritt syndrome, spontaneous rupture, hemoperitoneum). Biopsy carries high bleeding risk due to the rich vascularity of the spleen and is generally contraindicated. Diagnosis can be confidently made by imaging — typical enhancement pattern is diagnostic. Multi-organ evaluation is required in syndrome-associated cases (Klippel-Trenaunay, Beckwith-Wiedemann).
Splenic hemangioma is usually asymptomatic and incidentally discovered. Biopsy is not needed when typical imaging features are present. Giant hemangiomas rarely carry risk of spontaneous rupture.