Findings and procedure details
Non-traumatic focal splenic lesions are a true challenge to the radiologist because the majority of them are incidental findings in asymptomatic patients and their findings usually overlap. Lesions can be classified according to their number, size, composition (reflected in echogenicity, density and signal intensity), growth-rate and behavior with contrast agents. Ancillary sings like the spleen size, lymph nodes and vascular abnormalities are used to narrowing our differential diagnosis spectrum. We review the main findings of twenty different spleen focal lesions through cross-sectional imaging after systematizing the approach to them in order to survive the spleen challenge. Fig. 1 and Fig. 2 .
CYSTIC LESIONS
Splenic cysts are usually common findings in imaging studies. It is unusual that splenic cysts become symptomatic by growing enough to cause a mass effect on adjacent organs or present complications such as bleeding, rupture or secondary infection. Fig. 3 and Fig. 4 .
They can be divided into primary or secondary.
Primary cysts are called epidermoid cysts where it is rare to observe the presence of calcifications (less than 5%).
Secondary or false cysts are pseudocysts with epithelial lining. They represent 80% of the total splenic cysts and their origin is considered to be posttraumatic.
INFECTIONS
Single or multiple lesions
Hydatic or echinococcal cyst:
Systemic dissemination and intraperitoneal dissemination of a broken liver cyst constitute the two pathways of splenic involvement. The imaging characteristics vary according to the age of the cyst and complications, such as superinfection or rupture.
In computed tomography (CT) it is presented as a single rounded or ovoid mass of liquid attenuation with a peripheral wall which can present calcifications.
The presence of a lesion with greater denisity occurs as a result of the presence of detached membranes as daughter vesicles or entire calcification cyst can also be observed. Fig. 5 , Fig. 6 and Fig. 7 .
Pyogenic abscesses:
Despite being a rare entity, its incidence has increased recently. It usually occurs as a result of hematogenous dissemination of primary focus, usually endocariditis. It can occur as multiple lesions or a single lesion.
Ultrasound (US) usually shows as hypoechogenic or anechogenic image depending on the content. On CT they appear as low density collections with thick walls that show slight enhancement after contrast media administration. Fig. 8 .
Sarcoidosis:
It is a systemic granulomatous disease of unknown etiology. Spleen involvement is rare. It is commonly presented as splenomegaly. After administration of the contrast agent, nodular lesions of 2-3 cm are observed although it can also present as a single lesion. It is observed as a well defined hypoechogenic mass without vascularization with Doppler.
On CT it is observed as a hypodense mass that does not show enhancement. In MR it has low signal intensity in all sequences. Fig. 9 , Fig. 10 and Fig. 11 .
Tuberculosis:
Is an infectious disease that is caused by the bacillus of Koch and rarely affects the spleen. Splenic involvement is caused by hematogenous spread. Its presentation can be either micronodular or macronodular.
In the micronodular form small hypodense nodules are seen on CT. Fig. 12 .
SOLID FOCAL LESIONS
HYPOVASCULAR
Benign
Littoral cell angyoma:
A rare vascular tumor. It originates in the splenic sinusoid littoral cells of the red pulp. Its size is usually variable. By CT it can be seen as hypodense masses with or without contrast enhancement. In MR it is usually observed as heterogeneous masses in T1 and T2 sequences.
Malignant
Lymphoma:
Is the most common malignant tumor. It can present in different ways; splenomegaly, multiple solid masses of different sizes or a large mass.
In patients with NHL with systemic involvement, the spleen is involved in up to 70%. In the HL it is important to detect splenic involvement since it affects both prognosis and treatment.
HYPERVASCULAR
Benign
Hemangioma:
Although rare, it is the most common primary benign neoplasm. Most lesions are small and incidental findings.
On ultrasound they are observed as well-defined hyperechogenic lesions. On CT they usually present peripherical and nodular enhancement with centripetal progression. This finding may vary as there are also atypical hemangioma that have different patterns of enhancement. On MR splenic hemangiomas are hypointense to isointense in T1-weighted images and hyperintense in T2-weighted images. Dynamic MRI after contrast administration has shown that splenic hemangiomas have three patterns of enhancement.
Malignant
Metastasis:
Splenic metastases are atypical (less than 10%). Melanoma is the most frequent primary tumor that metastasizes. Metastases of breast, lung, prostate and ovarian neoplasms are also frequent due to their prevalence. On MR they are observed as hypointense in T1 and hyperintense in T2. Fig. 13 and Fig. 14 .
VASCULAR AFFECTION
Infarction:
Splenic infarctions usually occur secondary to an occlusion of the splenic artery or a thrombosis of the splenic vein.
The causes of arterial occlusion can be various from emboligenic foci, inflammation as seen in vasculitis, aneurysms, neoplasms or trauma among others. Fig. 15 .
Splenic vein thrombosis is usually seen in trauma, inflammation or neoplastic processes.
The US infarcts usually appear as hypoechogenic wedge-shaped areas with peripheral base and center with hilar orientation.
The CT finding is of a wedged-shaped area that does not enhance in the venous phase although a slight peripheral enhance can be observed.
SANT (sclerosing nodular angiomatous transformation):
Is a benign vascular condition which occurs due to a proliferation of angiomatoid / vascular nodules. It is usually an incidental finding in asymptomatic patients, mostly women.
The differential diagnosis should be established with metastases, hemangioma and angioma of littoral cells, lymphoma and other benign and malignant lesions.
Heterogeneous appearance during the arterial and portal venous phases are seen in both CT and MR with progression in the late phases. Fig. 16.