Intravenous contrast should be used to image the spleen. Multiphase imaging is appropriate in most settings. Single-phase imaging should be performed in the portal venous phase because the parenchyma demonstrates an arcuate enhancement pattern on arterial-phase imaging, making it difficult to assess splenic lesions (Fig. 8.3). If the primary concern is for vascular disease, early arterial imaging can be used. Oral contrast is not necessary in the trauma setting; indeed, the delay involved and the possible obscuration of blood products explain why oral contrast may not be used. In the nonemergency setting, oral contrast may help delineate primary splenic disease from adjacent gastric, small bowel, or colonic disease.

MRI has the advantages of providing multiplanar, multi-sequence images and not requiring radiation. When dedicated imaging of the spleen is required, routine sequences are sufficient to evaluate the liver. The normal adult spleen is isointense to muscle on T1-weighted images and hyperintense to the liver on T2-weighted images. Studies have demonstrated a lower T2 signal in neonate spleens; this should not be misinterpreted as a pathological abnormality [2].

Various pathological entities can be illustrated in Table 8.1.

Also referred to as splenules, accessory spleens occur in 30–40 % of patients. Accessory spleens are usually multifocal and most often are located in the hilum, but they can occur anywhere around the spleen [3] and, rarely, in the pancreatic tail (also termed splenic choristoma, discussed in the pancreas chapter). Splenules follow normal splenic CT and MR imaging attenuation and signaling on all phases and sequences (Fig. 8.4). When there is doubt as to whether a mass lesion represents a splenule, sulfur colloid scans can provide additional diagnostic information, because the radiolabeled particles are taken up by the splenules (as well as the spleen).

If surgical removal of the spleen is necessary, it is important to be aware of any accessory spleens, because these may need to be removed as well. Conversely, in the setting of traumatic splenectomy, preserving the splenules may allow splenic function to be maintained. Accessory spleens should not be overlooked during imaging interpretation because they can be affected by conditions similar to those involving the spleen (Fig. 8.5).

As mesenchymal components fuse, incomplete fusion can appear as splenic clefts or lobulations (Fig. 8.6). Although a normal splenic variant, it can be confused with traumatic injury.

Like other viscera, the spleen is involved in situs abnormalities. When the viscera are in their expected locations, this is referred as situs solitus; a complete mirror-image rearrangement is called situs inversus. Situs ambiguous applies when some organs are in their expected locations and others are not. If the purpose of a radiological test is to evaluate and characterize situs anomalies, attention should be paid to the location of the heart chambers, which is beyond the scope of the chapter. There is a significant overlap of findings between heterotaxy and polysplenia or asplenia [4, 5].

The spleen is attached to surrounding structures by splenorenal, gastrosplenic, and phrenocolic ligaments. If these ligaments are absent, the spleen is no longer anchored in position and can “wander” through the abdominal cavity (Fig. 8.7). Such displacement can lead to twisting on the vascular pedicle, causing infarction [6].

A splenogonadal fusion is an anomaly characterized by the presence of splenic tissue in the testis, epididymis, and spermatic cord [7]. A few rare cases of ovarian fusion have been reported as well [8]. Splenorenal fusion is another rare anomaly that is characterized by the presence of splenic tissue in the renal parenchyma [9, 10].

As discussed in the pancreas chapter, intrapancreatic splenules are typically located in the pancreatic tail and can mimic hypervascular pancreatic masses.

Polysplenia is characterized by a complex set of congenital anomalies, including multiple rounded lesions with typical features of splenic tissue (Fig. 8.8), bilateral bilobed lungs, hyparterial bronchi, a midline or left-sided liver, and a variable stomach location [11]. An association between polysplenia, congenital lobar emphysema and azygos continuation of the inferior vena cava has been reported [12]. The splenic bodies lie along the greater curvature of the stomach and appear as multiple similar appearing lesions that measure 1–6 cm [13]. Without knowledge of congenital anomalies, this can be difficult to differentiate from splenosis in the setting of prior trauma (Fig. 8.8).

Splenosis is the presence of viable splenic tissues in other anatomical compartments of the body that occur secondarily to traumatic or iatrogenic rupture of the spleen. Splenosis can be differentiated from accessory splenules on the basis of the patient’s history and the location and number of lesions (Fig. 8.9). Hypertrophied splenic components in splenosis are usually large and are not found in the typical location for splenules (i.e., in the splenic hilum). Hypertrophied components can exist in either intraperitoneal or extraperitoneal locations compatible with the splenic hilum lying in the retroperitoneal space and the rest of the spleen lying in the intraperitoneal space (Fig. 8.9).

Asplenia refers to an absent spleen. With this condition, the liver is usually midline, the inferior vena cava is left-sided, and the stomach is often absent [4] (Fig. 8.10). Associated cardiac anomalies are complex and severe and carry 80 % mortality rate for the first year of life [4].

Congenital splenic cysts have an endothelial lining and are therefore true cysts [15]. On CT images, they appear homogeneous and well-circumscribed and have a thin or almost imperceptible wall. Internal septations may be present. On precontrast imaging, cysts have a density of less than 20 HU and no enhancement. Lesions are typically markedly hyperintense on T2-weighted MR images and homogeneously hypointense, without enhancing components, on T1-weighted MR image (Fig. 8.11). If symptomatic, these lesions can be treated by cystectomy [14, 16].

Pyogenic abscess is usually secondary to hematogenous spread. Risk factors include intravenous drug abuse, trauma, endocarditis, systemic infection, and immunodeficiency [17]. Direct inoculation in the setting of trauma has also been described. On CT images, these abscesses exhibit low attenuation, whereas on MR images, they demonstrate central T2 hyperintensity and low T1 signal intensity (Fig. 8.12). A rim-like enhancement may be noted. The presence of gas is consistent with a diagnosis of abscess formation. Pyogenic abscesses also demonstrate restricted diffusion, although this is not specific to the condition. Splenic abscesses should be suspected in febrile patients with leukocytosis, left upper quadrant pain, and left-sided pleural effusion [18]. Splenectomy and antibiotics have been used to treat these lesions [19, 20]. Abscesses <4 cm have been successfully treated with antibiotics only; a favorable outcome for larger lesions has been reached with percutaneous drainage and intravenous antibiotics [21].

Because lymphangiomas are composed of dilated lymphatic ducts, the contents are chylous. They appear as non-enhancing cystic structures with lobulated contours. Thin internal septations can also be seen. Calcification and internal debris are absent. Lymphangiomas are sharply demarcated, with no enhancement on post-contrast imaging (Fig. 8.13). Multiple lymphangiomas can be seen in the setting of lymphangiomatosis [22].

Multiple fungal microabscesses in the spleen usually occur in immunocompromised patients. In such cases, Candida is the most common fungus, followed by Aspergillus and Cryptococcus. Mycobacterial abscesses can be caused by Mycobacterium tuberculosis, Salmonella spp., Pneumocystis jiroveci, and Mycobacterium avium-intracellulare. Microabscesses appear on CT images as multiple small hypodense lesions less than 2 cm in the longest dimension, usually ranging from 2 to 5 mm (Fig. 8.14). On MR images, these lesions are isointense on T1-weighted images and mildly hyperintense on T2-weighted images. Peripheral enhancement can be difficult to appreciate on CT and MR images. Treatment and diagnosis of the abscesses depend on the etiological agent, environmental risk factors, and cause of immunodeficiency.

Secondary cysts in the spleen are often traumatic [23, 24]. In the acute and subacute stages, layering blood products can be seen. Acute cysts may contain fluid with higher attenuation than simple fluid does. Variable signal intensities of blood degradation products can be seen on MR images (Fig. 8.15). Peripheral calcification is not seen in the acute setting. On MR images, acute traumatic cysts have an increased signal on T1-weighted images.

A long-standing post-traumatic cyst has a homogeneously increased T2 signal and low T1 signal intensity. The rim has a low signal on all sequences, with evidence of blooming on gradient echo (GRE) sequences. On CT images, chronic post-traumatic cysts commonly demonstrate central low density and have a peripheral calcified rim (Fig. 8.16). Internal calcifications and septations are usually absent. Treatment is indicated if the cysts are symptomatic or at high risk of rupture (>5 cm) [25]. Both splenectomy and laparoscopic cystectomy can be performed [26]. Cystectomy preserves residual splenic tissue, allowing certain immune-based functions to be maintained [27]. Percutaneous drainage has not been found to be successful in treating these cases [28].

The liver is the most common organ involved in echinococcosis, which is most commonly caused by Echinococcus granulosus and less commonly by E. multilocularis. Early echinococcal cysts (also called hydatid cysts) may appear simple on CT images, with central low density, or they may have a high T2 signal on MR images. Unlike simple cysts, echinococcal cysts often have a perceptible wall that exhibits low signal intensity on T2-weighted images. The presence of floating membranes (intracystic linear or serpiginous low T2 signal structures) or daughter cysts (intracystic small cysts) is diagnostic. MR imaging allows for better demonstration of the cyst and layering membranes. Wall calcification may be also present and is thought to be correlated with disease activity; calcified cysts may indicate inactive disease [29] (Fig. 8.17). Current treatment strategies include splenectomy or, if possible, partial cyst excision [30]. Sclerotherapy has also been used successfully, especially for smaller cysts (<5 cm) [31].

Multilobulated cystic lesions include pyogenic abscesses and lymphangioma (Fig. 8.18), which were discussed above.