Non-parasitic splenic cysts are rare benign lesions, typically classified as true epithelial (epidermoid) cysts or post-traumatic pseudocysts. Imaging differentiation can be challenging, especially when calcifications are present. On CT, both appear as well-defined hypodense lesions; pseudocysts more often show thicker, irregular rim calcification and a history of prior injury, whereas epidermoid cysts have thin, smooth walls and occur in younger patients (Figure 1). When features overlap, the term ‘benign non-parasitic splenic cyst’ is appropriate.

Key teaching point: The absence of internal septations or daughter membranes helps distinguish benign non-parasitic splenic cysts (including pseudocysts and epidermoid cysts) from parasitic cysts such as hydatid disease on imaging.¹

Splenic haemangiomas are the most common benign primary splenic neoplasm often showing peripheral nodular discontinuous enhancement with progressive centripetal fill-in, paralleling hepatic haemangiomas. Imaging overlap with hamartoma can occur; both entities can present as solitary, well-defined splenic masses with variable enhancement patterns (Figure 2a–c), occasionally making the distinction on imaging alone challenging. Histopathologic correlation is often required for definitive diagnosis.²

Torsion is a rare but critical complication of a wandering spleen, resulting from twisting of the elongated vascular pedicle on its axis. The torsion may be partial or complete, with consequent venous congestion, splenic enlargement (Figure 3), and, if prolonged, parenchymal infarction (Figure 4a and b). On imaging, the ‘whorled’ or ‘whirlpool’ sign, characterised by concentric twisting of the splenic vessels and pedicle (Figure 4c and d), is the key diagnostic feature on both Doppler ultrasound and contrast-enhanced CT or MRI. Additional findings may include a displaced spleen, variable splenic enhancement depending on the degree of vascular compromise, and associated ascites. Timely recognition of these imaging features enables splenopexy in salvageable cases; delayed diagnosis often necessitates splenectomy.³

Key teaching point: Early recognition of the ‘whirlpool sign’ is crucial to prevent irreversible infarction.³

Splenic hydatid disease is a rare manifestation of Echinococcus granulosus, accounting for < 2% of abdominal echinococcosis.⁴ Isolated splenic involvement typically reflects haematogenous seeding. Imaging features include a well-defined cystic lesion with daughter cysts, floating or detached membranes (‘water-lily sign’)⁴ (Figure 5a–c) and curvilinear or rim calcification, the latter two findings being highly specific.

In contrast, multiorgan hydatid disease reflects more extensive dissemination with concurrent hepatic, peritoneal and splenic involvement (Figure 6a–c). Liver cysts are the most common manifestations and may act as the source of peritoneal seeding through spontaneous rupture or iatrogenic spread.⁵ Peritoneal implants often present as multiple thin-walled cysts scattered along serosal surfaces.

Across both isolated and disseminated forms, complications such as secondary infection, rupture, anaphylaxis, or mass effect dictate the urgency of management. CT and MRI play crucial roles not only in diagnosis but also in classification and surgical planning.⁵

Key teaching point: It is essential to identify the ‘water-lily sign’ and assess for vascular complications as well as peritoneal seeding.⁴

Venous and arterial vascular abnormalities of the spleen represent a rare and often under-recognised subset of splenic pathology. In this review, two illustrative cases highlight this spectrum, with the first demonstrating a venous abnormality and the second an arterial lesion. The initial case illustrates a splenic venous pseudoaneurysm (also referred to as a splenic vein varix), an exceptionally uncommon entity most often described in association with trauma, pancreatitis, infection or adjacent inflammatory processes. On cross-sectional imaging, the lesion appears as a focal, contrast-opacified venous outpouching contiguous with the splenic vein, with well-defined margins and enhancement characteristics concordant with the venous system on arterial and portal venous phases. Recognition is critical, as splenic venous pseudoaneurysms carry a significant risk of rupture, haemorrhage or thrombosis and may necessitate urgent endovascular or surgical management depending on clinical stability (Figure 7a and b).

Key teaching point: Pseudoaneurysms may rupture even when small; early detection and vascular intervention are critical.⁶

Splenic artery aneurysms (Figure 8a–d) are the most common visceral arterial aneurysms and are more prevalent in conditions associated with increased splenic arterial flow, such as portal hypertension and pregnancy. Although often asymptomatic, they pose a significant risk of rupture, particularly when larger than 3 cm, and early identification is essential.⁶ The accompanying variceal network and enlarged spleen not only contextualise the underlying pathophysiology but also underscore the importance of detailed vascular assessment in patients with portal hypertensive states.

Key teaching point: There are diverse vascular manifestations that may involve the spleen, and there is a need for careful evaluation of both arterial and venous structures during abdominal imaging.

Polysplenia is part of the heterotaxy (left isomerism) spectrum, characterised by multiple splenunculi and abnormal thoracoabdominal arrangement (e.g. interrupted inferior vena cava with azygos continuation and midline liver). Identification of multiple splenunculi and associated anomalies on CT/MRI is diagnostic; evaluation of cardiovascular anomalies is essential for patient management and surgical planning⁷ (Figure 9a–c).

Key teaching point: Evaluate for associated cardiovascular and visceral anomalies.⁷

In sickle cell disease, repeated vaso-occlusive infarctions lead to progressive splenic fibrosis, atrophy, and eventual ‘autosplenectomy’. Early childhood may show splenomegaly from sequestration and extramedullary haematopoiesis, but chronic infarction results in a small, calcified, non-functioning spleen.⁸ CT demonstrates marked atrophy and dense calcification (Figure 10a–d), while MRI shows diffusely low signal from fibrosis and hemosiderin. Recognising these features is key, as functional asplenia increases the risk of overwhelming post-splenectomy infection.

Key teaching point: Splenic calcification in a young patient strongly suggests haemoglobinopathy.⁹

Granulomatous diseases such as tuberculosis and sarcoidosis commonly involve the spleen as part of multi-system disease processes, producing overlapping imaging features that may mimic neoplastic or infectious aetiologies. In splenic tuberculosis, lesions may be solitary or multiple, often hypodense on CT, with caseating necrosis leading to central low attenuation and peripheral rim enhancement (Figure 11a and b); chronic lesions may calcify.¹⁰ Sarcoidosis, by contrast, typically manifests as diffuse splenomegaly or numerous tiny hypodense nodules that are non-enhancing and frequently accompanied by hepatic or nodal involvement (Figure 11c). On MRI, both entities demonstrate low T1 and variably low T2 signal intensities depending on the fibrotic content, with minimal enhancement. Other granulomatous or inflammatory conditions such as histoplasmosis or brucellosis can appear similar,¹⁰ necessitating clinical correlation and supportive laboratory or histopathological confirmation. Awareness of these overlapping appearances helps avoid misdiagnosis of metastatic or lymphomatous disease, guiding appropriate medical rather than surgical management.

Key teaching point: Differentiating microabscesses in disseminated infection (tuberculosis, fungal) is based on clinical and systemic findings.¹⁰

In Hodgkin lymphoma, splenic involvement is a common manifestation of advanced disease and typically occurs through haematogenous or contiguous spread. On CT, the spleen may appear enlarged with or without discrete hypodense nodules. The nodules are often well-circumscribed, non-enhancing, and homogeneous, reflecting lymphomatous infiltration (Figure 12a–b).¹⁰ The imaging appearance of multiple rounded hypoattenuating lesions with splenomegaly in a patient with known Hodgkin lymphoma is characteristic (Figure 13a–b) and should not be mistaken for metastatic disease or infection.

Splenic metastases are uncommon and typically seen with disseminated disease (melanoma, breast, lung, ovarian and colorectal).¹¹ Lesions are usually hypodense on CT and variable on MRI; FDG-PET is typically avid. Their presence signifies advanced disease with prognostic implications (Figure 14).

Key teaching point: Consider splenic involvement in patients with disseminated malignancy.¹¹

Several extra-splenic processes may project onto or above the spleen, creating the false impression of a primary splenic lesion.¹² Peritoneal deposits, particularly in mucinous gastrointestinal malignancies, may adhere to the splenic capsule and mimic parenchymal disease, often showing calcifications or FDG avidity (Figure 15). Careful evaluation of the capsular versus intraparenchymal location on multiplanar imaging helps avoid misclassification of splenic involvement (Figure 15a–c).

Key teaching point: The importance of careful evaluation of lesion location and morphology to avoid misclassification of peritoneal deposits as primary splenic pathology.¹²