Peliosis splenis is a rare vascular condition characterized by formation of blood-filled sinusoidal and parenchymal spaces (lacunae) within the splenic parenchyma. It is not a true neoplasm but rather a vascular anomaly. Histopathologically, two forms are recognized: phlebitic type (endothelium-lined regular spaces) and parenchymal type (irregular spaces without endothelial lining — surrounded by fibrotic stroma). Hepatic involvement (peliosis hepatis) frequently coexists, and splenic involvement is usually seen together with hepatic involvement. Associated conditions include immunosuppression (HIV/AIDS), anabolic steroid use, oral contraceptives, azathioprine, tamoxifen, Bartonella henselae infection (bacillary peliosis), tuberculosis, and hematologic malignancies. Clinical presentation is mostly asymptomatic, but serious complications include spontaneous rupture and life-threatening hemoperitoneum. On imaging, the progressive enhancement pattern (fill-in phenomenon) of blood-filled spaces is characteristic and may resemble hemangioma. Treatment by correcting the underlying cause (drug discontinuation, infection treatment) may lead to lesion regression.
Age Range
20-70
Peak Age
45
Gender
Equal
Prevalence
Rare
Peliosis splenis is characterized by formation of blood-filled lacunae within splenic parenchyma and pathogenesis involves multiple mechanisms. The fundamental mechanism is sinusoidal endothelial damage: disruption of endothelial cell integrity leads to sinusoidal blood leakage into the parenchymal space, forming blood-filled spaces (lacunae). In the phlebitic type, endothelium is preserved with regular, round spaces, while in the parenchymal type, endothelial loss leads to irregular spaces with surrounding fibrotic stroma development. In Bartonella henselae infection (bacillary peliosis), bacteria directly infect endothelial cells and trigger VEGF (vascular endothelial growth factor) release — this angiogenic stimulus results in sinusoidal proliferation and dilation. Anabolic steroids and azathioprine create peliosis through endothelial cell apoptosis and sinusoidal integrity loss. The progressive enhancement (fill-in) pattern on imaging results from slow diffusion of contrast agent into blood-filled lacunae — a similar mechanism is seen in hemangioma, but in peliosis the lacunae are more irregular and directly continuous with splenic parenchyma. On T1-weighted MRI, the blood content of lacunae gives variable signal depending on methemoglobin (subacute blood) or deoxyhemoglobin (acute blood) state. On T2-weighted imaging, blood-filled lacunae appear hyperintense — the long T2 relaxation time of static blood produces high signal.
Slow contrast filling of blood-filled lacunae from periphery to center in peliosis — peripheral in arterial, partial in portal venous, complete in delayed phase. This pattern resembles hemangioma but peliosis lesions have more irregular borders and clinical context (immunosuppression, drug history) supports diagnosis.
In the arterial phase, peripheral or nodular enhancement foci are seen in the lesions — vascularized areas at the periphery of blood-filled lacunae show early contrast uptake. Progressive centripetal fill-in is observed on portal venous and delayed phases — contrast agent slowly progresses from periphery to center and lesions become increasingly homogeneous. On delayed phase (5-15 minutes), lesions may become isodense or mildly hyperdense to splenic parenchyma. This fill-in pattern may closely resemble hemangioma; however, in peliosis, lesions have more irregular contours and less defined borders with splenic parenchyma. Splenomegaly accompanies most cases. Concurrent liver lesions should be sought (hepatic peliosis).
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The splenic lesions demonstrate peripheral enhancement in the arterial phase with progressive centripetal fill-in pattern on delayed phases.
On unenhanced CT, multiple, variable-sized (from few mm to several cm), well or poorly defined hypodense lesions are seen in splenic parenchyma. Density typically ranges 20-40 HU — near blood density (fresh blood approximately 50-70 HU, but decreases due to stasis in lacunae). Hyperdense foci (60-80 HU) may be seen in lacunae with acute hemorrhage. Lesion margins are generally ill-defined with splenic parenchyma — different from hemangioma's well-circumscribed nature. Splenomegaly is common.
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Multiple, variable-sized, poorly defined hypodense lesions are seen in the splenic parenchyma on unenhanced CT.
On T2-weighted MRI, lesions appear hyperintense relative to splenic parenchyma — the high free water content of static or slowly flowing blood in blood-filled lacunae creates high signal through long T2 relaxation time. Lesions generally show heterogeneously hyperintense pattern — blood products of different ages give different T2 signal intensity. Deoxyhemoglobin in acutely hemorrhagic areas may create low T2 signal. T2 hypointense foci (superparamagnetic effect) may be seen in areas with chronic hemosiderin accumulation. Lesions are scattered and ill-defined within the splenomegalic splenic parenchyma.
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The splenic lesions appear heterogeneously hyperintense on T2W MRI, consistent with blood-filled lacunae.
On T1-weighted MRI, lesions show variable signal — depending on the age of blood products and hemoglobin state. Subacute blood-containing lacunae (methemoglobin) show T1 hyperintensity — T1 shortening from paramagnetic effect. Acute blood (deoxyhemoglobin) appears isointense or mildly hypointense. Fluid-fluid levels may be seen in chronic lacunae — methemoglobin (T1 hyperintense) on top, deoxyhemoglobin or hemosiderin (T1 hypointense) below. Post-gadolinium contrast sequences show progressive fill-in pattern similar to CT.
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The splenic lesions show variable signal on T1W MRI with T1 hyperintensity (subacute blood products) in some lesions.
On B-mode ultrasonography, multiple, variably echogenic lesions are seen in splenic parenchyma. Blood-filled lacunae generally appear hypoechoic or anechoic; internal echoes (blood products, debris) may be seen. Fluid-debris levels may be detected in large lacunae. Lesions may have ill-defined borders with splenic parenchyma. Splenomegaly usually accompanies. Color Doppler may show low-flow vascularity or avascularity within lacunae — helpful in assessing acute rupture risk. In some cases, diffuse heterogeneous echopattern may be seen — widespread parenchymal change rather than discrete focal lesions.
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Multiple, variably echogenic, poorly defined lesions are seen in the splenic parenchyma in the setting of splenomegaly, consistent with blood-filled lacunae.
On delayed phase (5-15 minutes), most lesions become isodense or mildly hyperdense to splenic parenchyma — progressive fill-in is completed. This delayed homogeneous enhancement reflects complete contrast filling of blood-filled lacunae. Persistent hypodense areas may indicate thrombosed or fibrosed lacunae. Complete isodensity helps differentiation from simple cysts (no enhancement) and solid tumors (different kinetics). This delayed fill-in pattern may closely resemble hemangioma — clinical context and lesion morphology (irregular borders) are critical for differential diagnosis.
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On delayed phase, the splenic lesions become isodense to splenic parenchyma with progressive fill-in.
Criteria
Regular, round spaces lined by endothelium. Generally no surrounding fibrotic stroma. More regular imaging pattern.
Distinct Features
More regular, round lesions on imaging. More closely resembles hemangioma. Well-defined enhancement pattern.
Criteria
Irregular spaces without endothelial lining. Surrounding fibrotic stroma present. More chaotic parenchymal damage pattern.
Distinct Features
More irregular, poorly defined lesions on imaging. More heterogeneous enhancement. Fibrotic stroma shows delayed enhancement.
Criteria
Associated with Bartonella henselae or B. quintana infection. Common in HIV/AIDS patients. Reversible with antibiotic treatment.
Distinct Features
Concurrent hepatic peliosis very common. Diffusely distributed small lesions. Lymphadenopathy may accompany. Dramatic regression with treatment.
Distinguishing Feature
Hemangioma is well-circumscribed, round with regular peripheral nodular enhancement and centripetal fill-in. Peliosis has poorly defined, irregular lesions with more heterogeneous filling. Clinical context (drugs, immunosuppression) important in peliosis.
Distinguishing Feature
Angiosarcoma shows more aggressive appearance, irregular margins, hemorrhagic components, and rapid progression. Peliosis may regress when underlying cause is corrected. Metastatic disease (liver, lung) may accompany angiosarcoma.
Distinguishing Feature
Lymphoma typically shows homogeneous hypodense lesions, homogeneously low T2 signal, and homogeneous enhancement — no fill-in pattern. Progressive fill-in pattern and variable T1/T2 signal (blood products) in peliosis are diagnostic clues.
Distinguishing Feature
Metastasis shows rim enhancement with central necrosis and known malignancy — no fill-in pattern. Progressive homogeneous filling and underlying etiological factor (drug, infection) support peliosis diagnosis.
Urgency
urgentManagement
medicalBiopsy
Not NeededFollow-up
3-monthPeliosis splenis is a potentially life-threatening condition — spontaneous rupture and massive hemoperitoneum risk exists. Mortality is high in rupture cases requiring emergent surgery. Identifying and correcting the underlying cause (discontinuation of responsible drug, doxycycline or erythromycin for Bartonella infection, HIV treatment optimization) may lead to lesion regression. In drug-related peliosis, regression is expected within weeks-months after drug discontinuation — should be confirmed with follow-up imaging. Splenectomy may be considered for large lesions with rupture risk. Concurrent hepatic peliosis should be investigated. Percutaneous biopsy is contraindicated — very high bleeding risk.
Splenic peliosis is usually asymptomatic but carries risk of spontaneous rupture. Regression may occur if the underlying cause (drug, immunosuppression) is treated. Splenectomy may be needed in severe cases.