MDCT findings of Splenic Pathology

Abstract

The delineation and characterization of splenic lesions and other abnormalities can be challenging on computed tomography (CT). Many splenic lesions are incidentally found, imaging features tend to overlap, and without the appropriate clinical context, differentials can range from benign to malignant. Radiologists should be familiar with the wide variety of pathologies seen on CT as it is often the first imaging modality a splenic lesion is seen. The purpose of this MDCT-focused review is to understand normal splenic anatomy and its variants, to illustrate and describe typical and atypical imaging patters of inflammatory, infectious, vascular, traumatic, benign and malignant tumors of the spleen and provide clues in reaching the appropriate differential diagnosis and management.

Introduction

The spleen is an intraabdominal organ, typically located in the left upper quadrant, and is the largest lymphatic organ. Anatomically, it is completely covered by visceral peritoneum, except at its hilum. The spleen has an upper and lower pole and contains two main types of tissue: red pulp, which is comprised of vascular sinuses, and white pulp, which is comprised of lymphoid tissue. The main functions of the spleen include immunologic surveillance, red blood cell breakdown, and acting as a reservoir for blood volume expansion.

Splenic lesions are frequently encountered in radiology practice and can be a diagnostic challenge which may ultimately influence management [1–5]. Knowing CT features of benign and malignant lesions each can help to differentiate the two, with a sensitivity of 72% and specificity as high as 89% [6]. CT is critical in trauma especially when deciding between active extravasation which greatly changes management and decisions often need to be made urgently. Another example includes discerning masses from microabscesses in a lymphoma patient, as treatment can be very different. Although MRI has a sensitivity of 100% and specificity of 97% for infections, a combination of CT and laboratory values can be useful to differentiate the two [7]. Percutaneous biopsy for splenic lesions is rarely used for diagnosis and, if performed, may be limited to fine needle aspiration in some practices [3]. Therefore, an adequate knowledge of the imaging patterns is essential to avoid unnecessary invasive diagnostic procedures. This MDCT focused pictorial review provides a concise overview of the different pathologies described above, as well as many additional lesions in a single source for easy access.

The purpose of this MDCT-focused review is to understand normal splenic anatomy and its variants, to illustrate and describe typical and atypical imaging patters of inflammatory, infectious, vascular, traumatic, benign and malignant tumors of the spleen and provide clues in reaching the appropriate differential diagnosis and management.

Imaging features of normal spleen

On CT, the spleen’s density is usually 10 Hounsfield units less than the liver on unenhanced CT phase and typically shows a heterogeneous serpentine enhancement in the first 25–45 seconds after injection of contrast due to differences in the circulatory route between the red and white pulp. For specific indications, such as bleeding, aneurysms, and vascular malformations, an optimal contrast-enhanced splenic evaluation requires dual phase arterial (approximately 30 seconds) and venous (approximately 60 seconds) acquisitions. The arterial phase is not indicated for parenchymal evaluation but is useful for vascular assessment [1–4].

Congenital variations and anomalies

Congenital variations and anomalies can be categorized by shape, location, and number. Shape variations include clefts, due to incomplete fusion, and lobulations that are commonly medial. Wandering spleen is a location anomaly related to absence or underdevelopment of one or all splenic ligaments (Fig. 1). It is represented by a mobile spleen that is attached only by an elongated vascular pedicle, migrating to any part of the abdomen with increased risk of axial torsion and infarction [3]. It occurs very rarely with only about 500 cases reported worldwide [8]. It has a variable clinical presentation with ranging from an incidental finding to a surgical emergency [9]. On precontrast imaging, it can appear as normal spleen, but post contrast, the present of a whirl sign of the vessels or poor enhancement can represent infarct. [9]. Treatment is splenopexy or splenectomy depending on severity of the symptoms [9].

Fig. 1.

Wandering spleen. Contrast enhanced coronal CT shows the spleen in the RUQ of the abdomen below the liver. The long vascular pedicle (arrows) increases the patient’s risk of torsion.

Number anomalies include asplenia, the congenital absence of the spleen. This can be isolated or part of a clinical sequela of a broader syndrome such as Ivermark syndrome, a heterotaxy syndrome occurring in 1 in 10,000 to 40,000 cases [10, 11]. CT will show lack of spleen and Tc-99 red blood cell scan will show lack of uptake [10].

Other number anomalies include right isomerism/polysplenia (Fig. 2). This is a rare anomaly with CT findings showing multiple systemic and visceral organ anomalies in addition to the multiple spleens. [11, 12]. Most patients with isomerism die secondary to cardiac complications by the age of 5 [12]. The key diagnosis is to associate the multiple spleens to an underlying syndrome and not a separate pathologic process [12].

Fig. 2.

55 y/o male with history of situs inversus totalis. Contrast enhanced axial CT shows the spleen in the right upper quadrant of the abdomen. Posterior to the spleen, there are smaller, isodense and ovoid lesions (arrows) consistent with accessory spleen.

Accessory spleen is a frequent congenital variation (20% of autopsy) due to failure in coalescence of mesodermal buds in the dorsal mesogastrium [1, 3]. The accessory spleen is supplied by the splenic artery and most are located near the splenic hilum. On pre- and post-contrast imaging, this enhances similarly to splenic parenchyma [13]. This entity is important to recognize because it could be responsible for the recurrence of hematologic disorders after splenectomy [3].

Splenosis in an acquired condition that occurs after splenectomy or splenic rupture is represented by seeding or implantation of splenic cells in any location, frequently simulating tumors (Fig. 3) [14]. On pre- and post-contrast, imaging, splenosis appears similar to the normal spleen [14]. When ectopic splenic tissue or splenosis is in the differential for a mass around the splenic hilum or splenectomy bed, a technetium tagged heat-damaged red blood cell scan is a nuclear medicine examination that can delineate ectopic splenic tissue [15]. Splenosis is usually managed conservatively and history is key to help differentiate it from other lesions [14]

Fig. 3.

47 y/o male with history of gunshot wound showing intrathoracic splenosis. A nodular opacity is projected in the posterior aspect of the chest suggestive of a pulmonary mass (short arrow) on the lateral chest radiograph; note the bullet (long arrow) from prior gunshot (a). Non-contrast (b) and venous (c) axial CT images demonstrate a homogenously enhancing left hemithoracic mass consistent with ectopic splenic tissue.

Cystic lesions

Intrasplenic cystic lesions are the most frequently encountered benign lesions of the spleen. They include true cysts, pseudocysts, and cystic neoplasms. It is usually not possible to distinguish a true cyst from other types by imaging alone, and there is little practical significance in doing so. However, differentiating cysts from abscesses or tumors may be a diagnostic challenge with significant clinical impact [3, 5, 16, 17]. A combination of imaging findings described below, clinical presentation, and laboratory values (increased WBC in abscesses, cytopenia in lymphoma, etc.) are necessary to establish appropriate diagnosis. True cysts can be classified into two groups: nonparasitic or parasitic (related to Echinococcus infection).

Nonparasitic cysts are congenital/epidermoid cysts accounting for less than 20% of all splenic cysts [18]. They are usually unilocular, solitary (80%), and typically large (>6 cm) [16]. They are typically sharply defined masses showing water density (<20 Hounsfield units {HU}) with no enhancement (change in density of <20 HU) [16]. They may contain cholesterol crystals, fat, and blood, but mural calcifications are uncommon (less than 25%), and they are managed conservatively (Fig. 4) [5, 16, 17]. Clinical context is important as epidermoid cyst can be mistaken for splenic abscess, hydatid cyst, or post traumatic pseudocyst, however definitive diagnosis is seen in pathology [19].

Fig. 4.

55 y/o male with early satiety found to have epidermoid cyst. Double (a) and single (b) contrast upper GI study showing an extrinsic compression of the gastric fundus with no abnormality in the gastric mucosal folds. Ultrasound (c) of the left upper quadrant shows a well-defined heterogenous mass with internal echoes (arrows). Echogenic foci are representing intralesional cholesterol crystals, fat and blood. Contrast-enhanced axial CT (d) images show a large intra-splenic homogeneous fluid density mass (arrow).

Pseudocysts are non-epithelial cystic lesions that constitute 75% of non-parasitic cysts [16]. Calcifications and septations are more common than in true cysts [16]. They appear following trauma, infarction, or inflammation. Posttraumatic cysts are final stage in the evolution of splenic hematoma and are becoming more common (Fig. 8) [20]. Postinfarction or inflammation cysts are usually solitary, sharply delineated, and slightly hyperdense. The wall is composed of dense fibrous tissue, often calcified, with no epithelial lining [5]. The content is a mixture of blood and necrotic debris. Intrasplenic pancreatic pseudocyst is a specific post-inflammatory pseudocyst that occurs in 1–5 % of patients with pancreatitis [3, 5, 16].

Fig. 8.

42 y/o male status post MVC showing post-traumatic splenic pseudocyst. Contrast enhanced axial CT image immediately after polytrauma shows multiple parenchymal lacerations and extensive hemoperitoneum (a). Subcapsular splenic hematoma is also seen (a, arrow). Contrast enhanced axial CT performed 30 days after traumatic event demonstrates a homogenous well-defined fluid containing collection compatible with pseudocyst (b, arrow).

Parasitic cysts are related to hydatid disease, which is a manifestation of infection with Echinococcus granulosus or multilocularis. Although the liver (75%) and lung (15%) are the most involved organs, secondary involvement due to hematogenous dissemination may be seen in almost any anatomic locations [21, 22]. Splenic involvement varies from 0.2–8%, and hydatid cyst should be considered higher in the differential when coming from an endemic area such as India or South America [23]. The description of cystic echinococcosis imaging features is commonly based on Gharbi’s ultrasound (US) classification, resulting in a standardized WHO classification. On contrast-enhanced CT, the lesions can be solitary or multiple, present with daughter cysts, and occasionally showing localized rupture (Fig. 5–7). Additional imaging features of hydatid cysts includes in folded membranes or calcifications. The cystic component may be either enhancing or avascular. Splenectomy is the treatment of choice due to the cysts’ high risk of rupture [5, 16, 17, 21, 22, 23].

Fig. 5.

Type I hydatid cyst. Axial non-contrast contrast enhanced CT images show a rounded well-defined homogeneous intrasplenic cyst. Courtesy of Dr. Moguillansky

Fig. 7.

Type IIB hydatid cyst. Axial post contrast CT showing a large intrasplenic hydatid cyst with multiple internal daughter cysts and mural as well as internal calcifications (arrow). Multiple cystic lesions are also seen in the liver. Courtesy of Dr. Moguillansky

Infectious pseudocysts include pyogenic abscess and microabscesses. Pyogenic abscesses are produced from hematogenous spread of infection and they are potentially fatal (Fig. 9). They are a rare disease with a rate of 0.05–0.7% on autopsy [24]. Typically, it is a low attenuated lesion showing irregular borders, without capsule, with peripheral enhancement. Gas may be present in a small number of cases [3, 5]. Microabscesses are seen in immunosuppressed patients and are produced by fungi (aspergillus, cryptococcus, PCP) and tuberculosis (Tb). Microabscesses may have similar imaging characteristics to solitary large pyogenic abscesses including rounded hypoattenuating lesions with peripheral rim enhancement or, alternatively, may show central enhancement [3, 25]. Appropriate history is important when deciding if a cyst could be infectious especially in the immunocompromised, with percutaneous drainage and antibiotics as possible treatment options [24].

Fig. 9.

98 y/o female with history of left upper quadrant pain. Abdominal radiograph showing clustered distribution of gas (arrow) in the left upper (a). Axial (b, c) CT images show large non-delineated foci of intrasplenic gas (arrows), with minimal amount of associated fluid. The patient died immediately after the examination. Autopsy confirmed splenic abscess.

Spleen traumatic injury

The spleen is the most injured solid organ ranging from 25–49% of the cases (Fig. 10–14) [26]. CT may demonstrate a variety of different splenic parenchymal injuries including lacerations, parenchymal and subcapsular hematomas. A laceration is a linear branching hypodensity from the splenic capsule; a parenchymal hematoma is the result of contusion and hemorrhage restricted in parenchyma with intact capsule; and a subcapsular hematoma is located between the intact capsule and parenchyma with lenticular shape [26, 27]. The standard CT grade of splenic injury of the American Association for the Surgery of Trauma (AAST) has recently been revised with grade 4 injuries accounted for by active bleeding confided to the splenic parenchyma and grade 5 injuries extending beyond the splenic parenchyma in the peritoneum [28]. Traditionally, the AAST scale has not predicted the success rate of a non-operative management; however, no studies have been carried out with the recently revised scoring system. The presence of active bleeding has substantial impact on the management because failure of non-operative management occurs in 80% of the cases and the need of intervention is almost 10 times higher compared to patients without extravasation [26, 27]. It is important not to dismiss an enlarging hyperdense focus only seen on delayed phase as non-arterial or venous as hypotension from blood loss, inaccurate phase acquisition timing, and varying flow characteristics of distal arteries (especially if there is associated vasoconstriction) are some of the reasons for the delayed appearance of active arterial bleed [26]. Subtle splenic injuries should be considered when patients with any left sided abdominal trauma and left lower chest trauma [26].

Fig. 10.

43 y/o female after abdominal trauma with grade I splenic injury. Axial contrast-enhanced CT images show a linear parenchymal laceration (< 1 cm in depth) after splenic trauma (arrows). Perisplenic blood is noted (arrowheads).

Fig. 14.

14 y/o male without any past medical history presenting after polytrauma. Contrast-enhanced venous phase axial CT image (a) shows a complete devascularization of the spleen consistent with grade V injury.

Benign Neoplasms

Primary benign or malignant splenic tumors are rare with certain imaging characteristics that help to differentiate two [Table 1]. Hemangioma is the most frequent benign tumor [1]. Hemangiomas may be solitary or multiple and associated with hemangiomas in other organs, particularly the liver. Multiple hemangiomas can be manifestations of systemic diseases such as Beckwith-Wiedemann and Klippel-Trenauney-Weber, and very large hemangiomas encasing the entire spleen can be an imaging manifestation of Kasabach-Merrit Syndrome [16, 29]. Hemangiomas are often asymptomatic, diagnosed incidentally, and managed conservatively; however spontaneous rupture occurs in 25% of cases [30]. They are typically hypodense or isodense lesions to adjacent splenic parenchyma on noncontrast images. On post-contrast acquisition, there is a smooth margin with a variable internal appearance (Fig. 15). Capillary type hemangiomas enhance homogeneously, whereas cavernous type hemangiomas show heterogeneous enhancement [1, 3, 16, 30].

Table 1.

CT characteristics of benign and malignant splenic lesions.

Benign	Non contrast	Arterial	Portal Venous	Delayed	Other features
Hemangioma	Isodense to surrounding parenchyma	Hyperdense	Variable	Variable
Sclerosing angiomatoid nodular transformation	Hypodense	Peripheral enhancement	Variable	Variable	Central scar may be present
Littoral cell angioma	Hypodense	Hypodense	Hypodense	May become isodense to surrounding parenchyma
Lymphangioma	Hypodense. Calcifications and septations	Variable	Variable	Variable	Cystic is most common
Hamartoma	Isodense to surrounding parenchyma	hypodense	Slow progressive enhancement	Slow progressive enhancement	May simulate hemangioma
Malignant	Non contrast	Arterial	Portal Venous	Delayed	Other features
Lymphoma	Variable	Hypodense	hypodense	hypodense	Diffuse infiltration with or without splenomegaly
Metastases	Solid or cystic	Peripheral rim enhancement	Variable	Variable	Usually multiple
Angiosarcoma	Heterogenous solid mass	Hypervascular	Variable	Variable	Splenomegaly and involves entire spleen; Rare

Fig. 15.

Splenic flash filling hemangioma. Axial post-contrast image of the spleen demonstrates a well-defined, rounded, hyper-vascular intraparenchymal lesion (a, arrow). Three-minute delayed image shows intralesional isoattenuation with the normal splenic parenchyma (b, arrows).

Sclerosing angiomatoid nodular transformation is a benign splenic mass, often discovered incidentally and has been very rarely reported [31]. Its pathogenesis is not well understood and no correlation with other diseases have been identified. Suggestive characteristics include a well-circumscribed hypodense solitary mass with peripheral enhancement that becomes homogeneous on delayed imaging, and a central scar becoming apparent on delayed images [31]. It is a well-circumscribed mass composed of numerous nodules derived from red pulp, alternating with bands of fibrous tissue but the small number of cases precludes definitive assessment [1, 31].

Littoral cell angioma is another rare primary benign neoplasm arising from littoral cells, which normally line the splenic sinuses of the red pulp. Patients can present with splenomegaly, abdominal pain or hypersplenism. This diagnosis must be suspected in case of multiple hypodense splenic masses in a patient with clinic symptoms of hypersplenism, however, multiple hemangiomas, lymphoma, metastatic disease, disseminated infections can have similar imaging appearances [32]. Isoattenuation to surrounding parenchyma on delayed phases may aid in the differential diagnosis: definitive diagnosis can only be made at pathology after splenectomy (Fig. 16) [1, 5]. Although it is a benign tumor, it has been associated with visceral malignancies, and close follow up is recommended [32].

Fig. 16.

Littoral cell angioma in a patient with hypersplenism. Pre-contrast (a), post-contrast early venous (b), and delayed (C) axial images of the spleen demonstrate a poorly marginated hypovascular lesion with no peripheral nodular arterial enhancement (b). PET/CT fusion image (d) shows a FDG-avid mass. Pathology confirmed: Littoral cell angioma (e, arrow).

Lymphangioma is relatively uncommon benign malformation composed of dilated lymphatic channels lined by endothelium and filed with proteinaceous fluid [33]. It can be capillary, cavernous, or cystic and composed of single or multiples cysts of various sizes that do not enhance with contrast material. They are often subcapsular lesions where lymphatics are concentrated. Imaging features are determined by the subtype and proteinaceous content, with cystic type being most common and indistinguishable from other cystic lesions of the spleen [1, 3, 5, 33].

Hamartomas are incidentally found, asymptomatic, nonneoplastic lesions composed of a mixture of normal splenic elements and often associated with hamartomatous syndromes such as tuberous sclerosis [1, 16]. They are hypo or isodense in noncontrast images with slow progressive enhancement, which may help differentiate it from malignant tumors of the spleen [1, 5, 16].

Malignant Neoplasms

Lymphoma is the most common malignant tumor of the spleen and primary involvement is rare [1, 7, 16]. The typical presentation is diffuse infiltration with or without splenomegaly. CT is not reliable to confirm splenic involvement, and a normal appearing spleen may contain tumor cells in 30% of cases [7, 33]. Loss of normal heterogeneity in the early phase may suggest infiltration [7]. FDG PET/CT is more accurate than other cross-sectional technique with the sensitivity and specificity reaching as high as 100% and 95 % respectively [7]. Solitary or multifocal masses presentation are represented by hypodense lesions (Fig. 17), with calcifications in treated patients [1, 3, 5, 6, 7, 33,].

Fig. 17.

Multifocal splenic involvement in lymphoma. Axial contrast-enhanced CT images (a–b) shows an enlarged spleen with multiple well-defined hypovascular parenchymal lesions. Retrocrural, retroperitoneal and intraperitoneal adenopathy are seen (a–b, arrows).

Patients suffering lymphoma are immunocompromised and vulnerable to disseminated fungal infections, so the differentiation of multinodular splenic lymphoma from fungal microabscesses is critical and challenging. Fungal microabscesses typically are smaller than lymphoma nodules and characteristically occur in the absence of lymphadenopathy. On the other hand, in comparison with the homogeneous enhancement typical of lymphoma nodules, the contrast enhancement of fungal microabscesses tend to be more heterogeneous: common patterns include enhancement in the center of a nodule and peripheral rim-like enhancement [3, 25]. In addition, patients with fungal microabscesses are usually febrile and neutropenic.

Metastases are rare, often asymptomatic, and most often occurs in disseminated cancer [1, 16]. The primary cancers typically involved include melanoma, gynecologic tumors, breast, lung and stomach. Typically, they present as multiple lesions, but sometimes are solitary; they may also present as diffuse solid or cystic hypodense lesions with central or peripheral enhancement (Fig. 18). Calcifications are rare except for mucinous tumors [5, 6]. Spontaneous rupture, secondary to metastatic tumors, is rare [34]. MRI is more accurate than CT for the detection of splenic metastases when hemorrhagic or necrotic [33].

Fig. 18.

Breast cancer splenic metastases. Axial (a) and coronal (c) contrast enhanced CT images of the spleen demonstrate a complex cystic appearing lesion (arrows), not visualized on prior exam consistent with metastatic deposit.

Angiosarcoma is an extremely rare tumor but is the most common primary non-hematolymphoid malignancy. It is an extremely aggressive neoplasm with widespread metastasis and splenic rupture common presenting manifestations [1, 33, 34]. The most common CT finding is a patient with splenomegaly (60%) containing a large heterogenous solid mass or masses that nearly replace the spleen [1, 5]. MRI dynamic imaging may be a useful problem-solving tool in uncertain cases, showing heterogenous enhancement, corresponding with the pathological diagnosis of solid parenchyma with necrosis [33].

Splenomegaly

Splenomegaly is a common radiologic finding in many diseases, and there is a wide range of variation by age, patient size, or nutritional status. The splenic size must be measured anterior to the mid axillary line. There is controversy in the CT definition of splenomegaly. Some have reported a craniocaudal length more than 10 cm should be considered abnormal whereas others allow up to 13 cm for maximum length [35]. An alternative definition is extension below lower pole of left kidney. The splenic index is its volume calculated by three dimensions and ranges up to 315–440 cm3 in healthy individuals. There are many causes of splenomegaly, which may be accounted for by hyperplasia or hypertrophy of splenic parenchyma, passive congestion, or infiltrative disease [1]. Treating the underlying condition helps avoid the complications of splenomegaly, the most significant being rupture [35].

Hematologic disorders like myelofibrosis, hemolytic anemia, and polycythemia vera produce splenomegaly due to extramedullary hematopoiesis. Certain infections such as histoplasmosis, TB, mononucleosis, brucellosis, can also cause enlargement of the spleen [1, 3].

Passive splenic congestion is due to portal hypertension in patients with cirrhosis, ascites, varices. Gamma Gandy bodies-foci are siderotic nodules encountered in portal hypertension. Many storage diseases are involved too, such as Gaucher, hemochromatosis and amyloidosis. The imaging pattern varies from hypo to hyperdense foci, depending on the presence of calcium deposition (Fig. 19) [1, 3]. Thalassemia, hemochromatosis/hemosiderosis, treated lymphoma and cases using thorotrast, a radioactive radiographic contrast agent, all produce similar imaging findings. Gamma-Gandy bodies deposition can be detected in 9–12% of patients with portal hypertension using MRI, due to its sensitivity to iron containing structures [36].

Fig. 19.

Gamna-Gandy bodies in portal hypertension. Contrast-enhanced axial CT image (a) shows multiple scattered sub-centimeter hypodense splenic lesions. Axial MRI T1 (b) and T2 (c) weighted images demonstrate multiple well-defined hypointense in T1 and T2 splenic lesions compatible with deposits of hemosiderin secondary to microfollicular hemorrhage. Gross specimen (d) confirmed Gamna-Gandy bodies (arrows).

Vascular and Miscellaneous

Infarcts are an important cause of focal splenic defects which may be secondary to embolic, hematologic, or splenic vascular diseases [37]. CT findings are a well-defined, wedge-shape, peripheral low-density lesions and may either completely heal, usually within a month, or result in pseudocysts and/or posterior contour defects [3, 20].

Splenic artery aneurysms are the most frequent of visceral artery aneurysms (Fig. 20) [38]. Splenic artery aneurysms may be intra or extra-splenic and most of the cases are calcified [38]. If it measures more than 2.0 cm, there is high risk of rupture (76% fatal), and are often treated [26, 28, 38]. Women with more than two pregnancies have high predisposition to aneurysm rupture and are often treated more aggressively [38].

Fig. 20.

Splenic artery Aneurysms. Contrast-enhanced axial (a, b), coronal MIP (c), and volume rendered reconstruction (d) CT images showing two saccular aneurysmal dilatations in the splenic artery (arrows), the largest measuring 3 cm (b, c, d, arrows).

Miscellaneous conditions affecting the spleen may include infectious or non-infectious granulomatous diseases or hematological disorders. The most common infectious cause is histoplasmosis, transmitted through inhalation of soil infected with bird or bat excrement. Histoplasmosis shows multiples punctate calcifications, usually representing healed disease, and it is associated with calcifications in other organs. Sarcoidosis is a common non-infectious granulomatous disease that may present with splenomegaly or hypodense lesions (Fig. 21). When patients have sarcoidosis or if other features of sarcoidosis are seen, focal splenic lesions can confidently be attributed to sarcoidosis [1]. Increased splenic density is a CT finding seen in pathologies like sickle cell disease (Fig. 22), due to increased turnover, vascular occlusions, and infarctions. Sickle cell disease often progresses to atrophy and auto-infarction [1, 3].

Fig. 21.

Sarcoidosis. Contrast-enhanced axial (a–b) CT images of the spleen demonstrate solid hypovascular partially defined splenic lesions. Axial CT scan of the lungs (c) revealed a typical perilymphatic distribution of micronodules and alveolar sarcoid pattern of nodular consolidations (black arrows). Hepatic involvement is incidentally noted (a).

Fig. 22.

Multiple appearances of splenic abnormalities in patients with sickle cell disease. The spleen contains a slow, tortuous microcirculation that subjects it to congestion and polymerization. First patient shows an enlarged spleen with linear calcifications likely sequela from prior infarcts (a, arrows). The second patient demonstrates small spleen with confluent calcifications (b). The third patient shows minute fully calcified spleen consistent with autosplenectomy (c, arrow).

Conclusion

Normal splenic anatomy, congenital variations, focal lesions, causes of splenomegaly, traumatic injury, and various conditions were reviewed in this article. A brief schematic on how to approach CT lesions is shown below (Fig. 23). Isolated splenic pathology on CT can be challenging to generate an accurate differential diagnosis on imaging findings alone. Integration with clinical history can help radiologists to accurately diagnose splenic pathology.

Fig 23.

Simple schematic to help differentiate splenic lesions based on certain characteristics seen on CT and history findings.

Fig. 6.

Type IIC hydatid cyst. Axial contrast enhanced CT scan demonstrate a complex cystic mass in the spleen. Internal calcifications are present (arrows). This patient also shows liver involvement. Courtesy of Dr. Moguillansky

Fig. 11.

21 y/o male status post MVC with grade 2 splenic injury. Contrast-enhanced venous phase axial (a) CT images demonstrate large ill-defined parenchymal splenic contusion (arrow). A subcapsular hematoma is well identified on the coronal images (b) (arrow).

Fig. 12.

68 y/o male with presenting after trauma with grade III splenic injury. Contrast-enhanced venous phase coronal images show large subcapsular hematomas (arrows) > 50% of the surface area consistent with a grade III splenic injury. No active extravasation is seen.

Fig. 13.

33 y/o male with after trauma presenting with grade IV splenic injury. Contrast-enhanced arterial phase axial CT image show a peripheral splenic laceration with intraparenchymal and peri splenic active bleeding (yellow arrows). The active bleeding stays within the confines of the splenic capsule. The patient was taken to angiography suite, which showed persistent active bleeding (b, arrow) which was successfully embolized (c).