Splenic granuloma is a granulomatous inflammatory lesion developing in the splenic parenchyma due to infectious or non-infectious causes. Most common causes are tuberculosis (TB), histoplasmosis, brucellosis, fungal infections (coccidioidomycosis, cryptococcosis), and sarcoidosis. Active granulomas appear as small hypodense nodules, while calcified granulomas are discovered incidentally as sequelae of prior infection and are generally benign findings. Calcified granulomas are the most common calcified lesion of the spleen. In immunosuppressed patients, active granulomatous infection may indicate disseminated disease requiring urgent treatment. Diagnosis is established by the combination of clinical context (endemic region, TB exposure, immunosuppression) and imaging findings.
Age Range
20-80
Peak Age
50
Gender
Equal
Prevalence
Common
Granuloma formation is the fundamental pathological mechanism of cell-mediated immune response (Type IV hypersensitivity). Intracellular pathogens like Mycobacterium tuberculosis or Histoplasma capsulatum are phagocytosed by macrophages but cannot be killed intracellularly. T lymphocytes activate and cytokine release (IFN-γ, TNF-α) activates macrophages — macrophages transform into epithelioid cells and giant cells (Langhans type). This organized immune response forms the granuloma structure: central necrosis (caseous necrosis — typical in TB), epithelioid cells, giant cells, and lymphocyte halo. Over time, the granuloma enters the healing process: fibrosis develops and central necrotic material calcifies — dystrophic calcification. Calcium crystals (hydroxyapatite) nucleate on necrotic tissue proteins. This calcification creates high density (>100 HU) on CT. On MRI, calcium exhibits diamagnetic properties and causes T2 signal loss. In active granulomas, increased vascular permeability leads to contrast uptake, while calcified granulomas are avascular and do not enhance. In sarcoidosis-related granulomas, caseous necrosis is absent — non-caseating granulomas are smaller and calcify more slowly.
Multiple small (1-10 mm) hyperdense calcified foci in splenic parenchyma on non-contrast CT — the most classic and common finding of granulomatous disease sequelae. Usually discovered incidentally, asymptomatic, and requires no treatment. Liver and lymph node calcifications may accompany.
On non-contrast CT, multiple small (1-10 mm) hyperdense foci are seen in the splenic parenchyma (>100-300 HU). Calcifications are punctate or small round in shape. Distribution is generally random and homogeneous. Number can range from a few to hundreds. Spleen size is usually normal (calcified granulomas represent inactive disease). Concurrent liver and lymph node calcifications may be seen.
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Multiple small punctate calcified foci in the splenic parenchyma on non-contrast CT, consistent with sequelae of prior granulomatous disease (TB/histoplasmosis).
In active granulomatous disease, multiple small (2-10 mm) hypodense nodules are seen in the splenic parenchyma on arterial phase. The nodules become conspicuous as low-density areas against the background of the spleen's zebra/arcuate enhancement. Some nodules may show thin rim enhancement — active granulomatous inflammation and surrounding vascular reaction. Splenomegaly may accompany.
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Multiple small hypodense nodules in the splenic parenchyma on arterial phase, consistent with active granulomatous disease; clinical correlation is recommended.
On T2-weighted sequences, granulomas appear as small hypointense nodules. Calcified granulomas show prominent T2 signal loss due to diamagnetic calcium content. Active granulomas show intermediate-to-low T2 signal due to dense cellular content (epithelioid cells, lymphocytes). Caseous necrosis areas may have variable T2 signal (dry necrosis: hypointense, liquefied necrosis: hyperintense). On GRE/SWI sequences, calcified granulomas show blooming artifact.
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Multiple small hypointense nodules in the splenic parenchyma on T2-weighted sequences, consistent with granulomatous disease.
In active granulomas, mild-to-moderate diffusion restriction may be observed on DWI (ADC: 0.8-1.2 × 10⁻³ mm²/s). Dense cellular inflammatory infiltration and the viscous nature of caseous necrosis restrict water diffusion. Calcified inactive granulomas do not show diffusion restriction. This finding helps differentiate active from inactive granulomas.
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Mild-to-moderate diffusion restriction in the splenic nodules on DWI, consistent with active granulomatous disease.
On B-mode US, calcified granulomas may appear as small hyperechoic foci — calcium creates strong reflection due to high acoustic impedance difference. Large calcified foci may produce posterior acoustic shadow. Active granulomas may appear as small hypoechoic nodules but most are too small to detect on US. Spleen size may be normal or mildly enlarged.
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Small hyperechoic foci are observed in the splenic parenchyma on B-mode US, consistent with calcified granulomas.
In the delayed phase, active granulomas may show thin rim enhancement or mild homogeneous enhancement — disrupted capillary permeability in the peripheral active inflammatory tissue causes late contrast accumulation. Calcified granulomas do not enhance in any phase. This phase helps differentiate active from inactive granulomas.
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Thin rim enhancement of the splenic nodules in the delayed phase, consistent with active granulomatous inflammation.
Criteria
Hyperdense calcified foci on CT, no enhancement, normal spleen size. Sequela of prior infection.
Distinct Features
Most common form, discovered incidentally. Asymptomatic, no treatment needed. High-density foci on CT are diagnostic.
Criteria
Hypodense nodules on CT, mild enhancement, splenomegaly may accompany. Infectious etiology such as TB, histoplasmosis, brucellosis.
Distinct Features
Clinical symptoms (fever, night sweats, weight loss) accompany. May indicate disseminated disease. PPD/IGRA, cultures, serology aid in diagnosis.
Criteria
Develops in the setting of sarcoidosis. No caseous necrosis. Nodules are generally smaller (<5 mm) and numerous.
Distinct Features
Hilar/mediastinal lymphadenopathy and pulmonary involvement accompany. Elevated ACE, hypercalcemia. Granulomas calcify more slowly or may not calcify.
Distinguishing Feature
Gamna-Gandy bodies are typically invisible on CT; prominent blooming on MR GRE/SWI. Calcified granulomas are easily visible as hyperdense foci on CT. Portal hypertension is present in Gamna-Gandy, generally absent in granulomas.
Distinguishing Feature
Sarcoidosis and infectious granuloma may appear very similar on imaging. Hilar lymphadenopathy and pulmonary involvement differentiate sarcoidosis. In infectious granuloma, endemic region history, PPD positivity, and culture results are diagnostic.
Distinguishing Feature
Lymphoma nodules are generally larger (>1 cm), more homogeneous, and do not show calcification. Granulomas are smaller (<10 mm) and may be calcified. B symptoms are more prominent in lymphoma.
Distinguishing Feature
Metastases are generally larger, fewer, and associated with known primary malignancy. Granulomas are small, numerous, and associated with infectious/inflammatory history. Metastases enhance while calcified granulomas do not.
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
no-follow-upCalcified granulomas are benign sequelae requiring no treatment or follow-up. In active granulomatous disease, treatment is etiology-directed: anti-tuberculous therapy for TB, antifungal for histoplasmosis, steroids for sarcoidosis. In immunosuppressed patients, active splenic granulomas may indicate disseminated infection requiring urgent treatment. Biopsy is generally not needed — clinical context and serological/microbiological tests are sufficient for diagnosis.
Splenic granulomas are benign remnants and require no treatment. Granuloma should be the first consideration when calcified splenic lesions are seen. Clinical evaluation is needed when active infection is suspected.