Splenic pseudocyst is a cystic lesion without true epithelial lining, surrounded by a fibrous wall, comprising approximately 70-80% of all splenic cysts. It most commonly develops after trauma (blunt abdominal trauma — organized hematoma) or infarction; less commonly, it may result from extension of pancreatic pseudocyst into the spleen as a complication of pancreatitis. Histopathologically, the wall consists of fibrous tissue, granulation tissue, and hemosiderin-laden macrophages — the absence of epithelial lining is the key feature distinguishing it from true cysts (simple cyst, epidermoid cyst). Cyst contents may include old blood products (hemosiderin, cholesterol crystals, fibrin), serous or hemorrhagic fluid. Wall calcification is common, and the 'eggshell' pattern is characteristic. Size can range from a few cm to 15-20 cm. Most patients are asymptomatic; large pseudocysts may develop left upper quadrant pain, splenomegaly, or rarely rupture and infection. Treatment is generally symptomatic or surgical for large/complicated lesions.
Age Range
20-60
Peak Age
35
Gender
Male predominant
Prevalence
Uncommon
Splenic pseudocyst develops from organization and subsequent central liquefaction of hematoma or necrotic area formed in splenic parenchyma after trauma or infarction. In the post-traumatic process, an intraparenchymal hematoma initially forms — a clot composed of fibrin mesh and erythrocytes organizes. Over weeks-months, granulation tissue at the periphery forms a fibrous capsule; necrotic material in the center liquefies through enzymatic degradation and a cystic cavity develops. Macrophages phagocytize hemoglobin degradation products (hemosiderin, hematoidin) — hemosiderin accumulates in the wall and surrounding tissue, forming the basis for wall calcification on CT and T2 hypointense wall signal on MRI. Cholesterol crystals originate from erythrocyte membrane lipid degradation and increase the density of cyst contents — values above water density (15-35 HU) are seen on CT. Wall calcification occurs through dystrophic mechanism: local calcium-phosphate precipitation in necrotic and fibrous tissue. Calcification is typically peripheral and layered — termed 'eggshell' pattern and most prominently seen on CT. Extension of pancreatic pseudocysts into the spleen occurs through pancreatic enzymes (lipase, amylase) eroding the splenic parenchyma — in this type, high amylase level in cyst fluid is diagnostic.
Peripheral, layered, curvilinear calcification on CT in the cyst wall — 'eggshell' pattern is near-pathognomonic for pseudocyst. This calcification reflects dystrophic calcium deposition in the fibrous wall of organized post-traumatic/post-infarction hematoma and is not seen in simple cysts (epithelial wall, no calcification).
On unenhanced CT, a well-defined, round-oval, thick-walled cystic lesion is seen in the spleen. Wall thickness is generally 2-5 mm and frequently shows peripheral 'eggshell' calcification — this calcification is layered, curvilinear, and smooth-bordered. Cyst content density typically ranges between 15-35 HU — higher than pure water (0 HU), reflecting hemoglobin degradation products, protein, and cholesterol crystal content. In acutely hemorrhagic cysts, density may increase to 50-70 HU. The cyst is usually unilocular, though thin septa may rarely be seen. Internal debris or fluid-debris levels may be present.
Report Sentence
A thick fibrous-walled cystic lesion is seen in the spleen with peripheral 'eggshell' calcification of the wall.
On portal venous phase, cyst contents show no enhancement — confirming simple cystic nature. The fibrous cyst wall may show thin, smooth enhancement — capillary vascularity within the wall enhances. Wall enhancement is generally mild and homogeneous; thick, irregular, or nodular enhancement should raise suspicion for abscess or malignancy. Enhancement assessment is difficult in calcified wall segments — high density of calcification masks the contrast effect.
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The cystic lesion contents show no enhancement while the fibrous wall demonstrates mild smooth enhancement.
On T2-weighted MRI, cyst contents appear markedly hyperintense — long T2 relaxation time of fluid content produces high signal. However, with proteinaceous or hemorrhagic content, T2 signal may be slightly lower than pure water. The fibrous cyst wall appears markedly hypointense — short T2 relaxation time of collagen. If the wall contains hemosiderin, T2 hypointensity becomes more pronounced through superparamagnetic effect. Calcified wall segments also appear markedly hypointense — signal-void nature of calcium (no protons). Fluid-debris levels may be visible — hyperintense fluid above, low-signal debris below.
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The splenic cystic lesion shows hyperintense cyst contents and hypointense thick fibrous wall on T2W MRI.
On T1-weighted MRI, cyst content signal varies depending on content composition. Cysts with serous fluid content show low T1 signal. Cysts with proteinaceous content show intermediate T1 signal — protein T1-shortening effect. Hemorrhagic cysts show marked T1 hyperintensity with methemoglobin presence — paramagnetic effect. The fibrous wall appears hypointense or isointense. Calcified segments show signal void. Post-gadolinium, the fibrous wall mildly enhances but cyst contents do not.
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The splenic cystic lesion shows mildly hyperintense signal on T1W MRI consistent with proteinaceous/hemorrhagic cyst contents.
On B-mode ultrasonography, a well-defined, usually unilocular, thick hyperechoic-walled cystic lesion is seen in the spleen. Contents may be anechoic or contain low-level internal echoes (debris, old blood products). Wall calcification appears as a hyperechoic curvilinear line with prominent posterior acoustic shadowing — this calcification finding is diagnostic for pseudocyst. Posterior acoustic enhancement is prominent in the fluid-containing area but shadowing predominates behind calcified wall segments. Fluid-debris levels may be seen in large cysts. Doppler shows no flow in wall or contents (avascular lesion).
Report Sentence
A thick hyperechoic-walled cystic lesion is seen in the spleen on US with wall calcification demonstrating acoustic shadowing.
The pseudocyst shows no diffusion restriction on DWI — signal loss at high b-values with high signal on ADC maps (>2.0 × 10⁻³ mm²/s). This finding is critical for differentiation from abscess (viscous purulent content with diffusion restriction). T2 shine-through must be carefully evaluated — hyperintense appearance at high b-values may be misleading, confirmation with ADC maps is mandatory.
Report Sentence
The splenic cystic lesion shows no diffusion restriction on DWI with high signal on ADC maps supporting simple cystic nature.
Criteria
History of blunt or penetrating abdominal trauma. Develops from liquefaction of organized hematoma. Most common type.
Distinct Features
Contents may be hemorrhagic (high density, T1 hyperintensity). Hemosiderin-laden wall. Trauma usually months-years prior.
Criteria
Develops from liquefaction of necrotic area after splenic infarction (embolic, sickle cell). Cystic transformation in wedge-shaped infarction area.
Distinct Features
May be wedge-shaped or peripherally located — reflects morphology of infarction area. May be bilateral/multiple in sickle cell patients.
Criteria
Extension of pancreatic pseudocyst into spleen as pancreatitis complication. Pancreatic enzymes erode splenic parenchyma.
Distinct Features
Cystic tract may be visible between pancreatic tail and splenic hilum. High amylase in cyst fluid diagnostic. Pancreatic calcifications may accompany.
Distinguishing Feature
Simple cyst has thin (<1 mm) smooth wall, water density (0-10 HU), no calcification, no trauma history. Pseudocyst has thick wall (2-5 mm), elevated density (15-35 HU), eggshell calcification, trauma history.
Distinguishing Feature
Abscess shows diffusion restriction on DWI, thick irregular wall with rim enhancement, clinical fever/leukocytosis. Pseudocyst shows no diffusion restriction, smooth wall, low inflammatory markers.
Distinguishing Feature
Lymphangioma is multiloculated, thin septa, no wall calcification, young patient, no trauma history. Pseudocyst is unilocular, thick wall, eggshell calcification, trauma history.
Distinguishing Feature
Hemangioma shows peripheral nodular enhancement with centripetal fill-in — vascular pattern. Pseudocyst has non-enhancing cystic contents and non-enhancing thick wall — cystic pattern. Hemangioma calcification is punctate (phleboliths), pseudocyst is peripheral layered.
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
12-monthSplenic pseudocyst is benign and most cases require no treatment — annual US follow-up is sufficient for asymptomatic cysts. Surgery (splenectomy, partial splenectomy, or percutaneous drainage) is considered for large (>5 cm), symptomatic, or growing cysts. Rupture or infected pseudocyst may require emergent surgery. In pancreatic extension pseudocysts, pancreatitis treatment is the primary approach. In patients without trauma history, other cystic lesions (simple cyst, hydatid cyst, cystic neoplasm) must be excluded. Percutaneous aspiration may be diagnostic — high amylase in cyst fluid supports pancreatic origin, hemosiderin supports traumatic origin.
Splenic pseudocyst is usually asymptomatic and follows a benign course. Follow-up is sufficient for small lesions with typical features. Drainage or splenectomy may be considered for large or symptomatic cysts.