The Spleen

• Imaging techniques
• Normal anatomy
• Splenomegaly
• Malignant mass lesions
• Splenic infection
• Splenic trauma
• Other splenic disorders
IMAGING TECHNIQUES

Plain radiography is not routinely used in the evaluation of the spleen. The splenic outline may be seen on a plain radiograph especially if it is enlarged ( Fig. 73.1 ).

Figure 73.1 Splenomegaly. Plain radiograph showing the splenic outline in a patient with splenomegaly due to chronic myeloid leukaemia.

On ultrasound (US) the spleen is readily visualized. The normal splenic parenchyma shows a homogenous low-level echo pattern, which is generally of slightly lower reflectivity than hepatic parenchyma. Ultrasound is useful for detecting and characterizing focal lesions within the spleen as cystic or solid. Colour Doppler US is useful for differentiating vascular structures such as normal vessels from nonvascular structures such as pancreatic pseudocysts.

The use of microbubble US contrast media may aid in identifying and characterizing splenic abnormalities[1].

On non-enhanced computed tomography (CT) the normal spleen is homogeneous and has an attenuation of 35–55 HU, that is 5–10 HU less than that of liver. The spleen is optimally evaluated following intravenous injection of contrast medium. The spleen normally enhances heterogeneously immediately after injection of a bolus of contrast material. Only after a minute or more does the splenic parenchyma achieve uniform homogeneous enhancement ( Fig. 73.2 ). This is thought to reflect the variable blood flow within different compartments of the spleen and should not be misinterpreted for disease.

Figure 73.2 Normal splenic enhancement on CT. (A) Dynamic contrast-enhanced CT obtained 30 s after bolus injection of contrast media showing the heterogeneous enhancement pattern. (B) A delayed image shows uniform opacification of the spleen.

On magnetic resonance imaging (MRI) the splenic parenchyma is of lower signal intensity than the liver and slightly greater signal than muscle on T1-weighted images. On T2-weighted sequences, the spleen shows higher signal intensity than the liver ( Fig. 73.3 ). The signal intensity of normal splenic parenchyma and many pathological processes are similar. Consequently, the use of contrast enhanced MRI is important for evaluating the spleen. Intravenous gadolinium-based contrast agents are most commonly used. Images are acquired using a dynamic breath-hold T1-weighted spoiled gradient echo sequence after injection of a bolus of gadolinium intravenously. As on CT, the spleen shows heterogeneous enhancement on the dynamic contrast enhanced MRI ( Fig. 73.4 ). Supraparamagnetic iron oxide particles injected intravenously have been used to evaluate the spleen. These particles are taken up by the reticuloendothelial system and lower the signal intensity of the normal spleen, thereby increasing the conspicuousness of focal abnormalities in the spleen.

Figure 73.3 Normal spleen on MRI. Axial (A) T1-weighted spin-echo and (B) T2-weighted fast-spin-echo images showing the normal signal intensity of the spleen.

Figure 73.4 Normal splenic enhancement on MRI. (A) A dynamic breath-hold axial T1-weighted spoiled gradient-echo image obtained 30 s after bolus injection of gadolinium shows inhomogeneous enhancement. (B) The delayed image shows uniform enhancement of the spleen.

Radionuclide imaging with technetium-99m (99mTc) labelled sulphur or tin colloid imaging of the spleen for the detection of focal abnormalities has been replaced by cross-sectional imaging. For specific imaging of the spleen, 99mTc-labelled denatured autologous red blood cells are used.

Angiography with selective catheterization of the coeliac axis or splenic artery provides excellent visualization of the splenic and portal veins. In many patients it is possible to show the main splenic artery and normal splenic and portal veins using intravenous subtraction angiography.

Percutaneous biopsy of splenic lesions may be performed for cytological or histological diagnosis. This results in a high diagnostic rate (55–90%) and the complication rate is low[2]. Splenic abscess may be treated successfully with aspiration or percutaneous drainage.

NORMAL ANATOMY

The spleen forms from multiple foci of mesenchymal cells in the dorsal mesogastrium. During embryological development, the dorsal mesentery moves to the left with the development of the stomach. As it grows to the left the spleen becomes covered with peritoneum of the greater sac. The anterior portion of the dorsal mesogastrium that extends from the greater curvature of the stomach to the spleen becomes the gastrosplenic ligament. The posterior portion of the dorsal mesogastrium extending from the spleen to the left kidney becomes the splenorenal ligament, which transmits the tip of the pancreatic tail and splenic vessels towards the splenic hilum. Both ligaments carry veins, which are potential anastomotic channels between the portal and systemic venous system.

The adult spleen lies in the left hypochondrium at the level of the 10th rib in the mid axillary line. The spleen has diaphragmatic and visceral surfaces. The visceral surface is related to the stomach and left kidney. The spleen has a superior and inferior border and is notched on its inferior border. The vessels and nerve enter the spleen at the hilum on the visceral surface.

The spleen is composed of a supporting connective tissue framework comprising its capsule and trabeculae, and a unique functional parenchyma made up of red and white pulp. The spleen has important haematological and immunological functions.

Spleen size

The normal adult spleen measures approximately 12–15 cm length, 4–8 cm in antero-posterior diameter and 3–4 cm in thickness[3]. However, the irregular shape and oblique orientation of spleen mean that these linear measurements are of limited use. Furthermore, splenic volume varies greatly from one individual to another, and the normal spleen decreases in size with age. Normal in vivo adult splenic volume ranges from 107 to 314 cm [3] [4]. Splenic size can be assessed on imaging. On plain radiography vertical length measurement is the single best indicator of splenic size. A length greater than 11 cm is associated with a 70% probability of splenomegaly[5]. Ultrasound can be used to determine changes in spleen size with serial measurement and the long axis of the spleen is less than 12 cm in 95% of the population[6]. Ultrasound assessment of splenic size correlates well with CT splenic volume[7]. Determination of splenic volume on CT using summation of cross-sectional areas is very accurate with errors in the range of 3–5%[7]. However, this technique is cumbersome and, in practice, on CT or MRI most observers judge splenic volume by subjective evaluation. Rounding of the normally crescentic shape, extension of the spleen anterior to the aorta or below the right hepatic lobe or rib cage are further clues to splenomegaly. On cross-sectional imaging a more accurate method for the assessment of the splenic volume is the splenic index, i.e., the product of the length, width and thickness. The normal splenic index is between 120 and 480 cm [3] [8].

Normal variants and congenital anomalies

The shape and position of the normal spleen can vary considerably. Commonly, a bulge from the posterior margin of the spleen may extend medially and simulate a mass on urography. In 15–20% of individuals the posterolateral border of the spleen lies posterior to the left kidney. This is known as a retrorenal spleen. Residual clefts between adjacent lobulations may mimic lacerations. The upside down spleen is a variant in which the splenic hilum is directed superiorly towards the hemidiaphragm.

Accessory spleen (splenunculus) refers to ectopic splenic tissue of congenital origin, unlike splenosis, which refers to ectopic splenic tissue that results from trauma (see below). Accessory spleens are present in 10–30% of the population, and can be single or multiple. They usually occur near the splenic hilum (75%), but may be found in its suspensory ligaments or in the tail of the pancreas and, rarely, elsewhere in the abdomen. The blood supply to an accessory spleen is usually derived from the splenic artery with drainage into the splenic vein. Accessory spleens vary in size from a few millimetres to several centimetres in diameter. After splenectomy, an accessory spleen can hypertrophy dramatically causing recurrence of problems in patients who have undergone splenectomy for hypersplenism. The typical accessory spleen has a smooth, round or ovoid shape (Figs 73.5, 73.6 [5] [6]). Its imaging appearance (i.e., echo-texture, or attenuation, or signal intensity) is similar to that of the parent spleen.

Figure 73.5 Accessory spleen. Contrast-enhanced CT shows a small accessory spleen (arrow) anterior to the spleen. Note the draining vein (curved arrow) from the accessory spleen can be seen to join the other veins draining the main spleen.

Figure 73.6 Accessory spleen on MRI. Axial (A) T1-weighted spin-echo and (B) T2-weighted fast-spin-echo images shows a small accessory spleen (arrow) anterior to the spleen. The signal intensity of the accessory spleen corresponds to that of the spleen on all sequences.

The wandering spleen is a congenital variant in which laxity of the suspensory ligament permits the spleen to move about in the abdomen. It affects children and women of child-bearing age and is usually asymptomatic unless torsion occurs. The imaging findings are of an abdominal mass with a size appropriate for the spleen with the absence of the spleen in the normal location. It may be possible to recognise the characteristic shape of the spleen and to trace the splenic vasculature back to its origin. The density and pattern of enhancement may also suggest the diagnosis. However, if there is uncertainty as to whether the mass is truly an ectopically located spleen, radionuclide scintigraphy with 99mTc-labelled denatured autologous red blood cells usually resolves the issue.

Polysplenia is a rare complex congenital syndrome characterized by partial visceral heterotaxia (situs ambiguous) and concomitant levo-isomerism (bilateral left-sidedness). It is associated with multiple, highly variable cardiovascular and visceral anomalies. The abdominal anomalies include a right-sided stomach, midline or left-sided liver, malrotation of the intestine, a short pancreas and inferior vena cava anomalies. The spleen is divided into 2–16 masses, which are located in either the right or left upper quadrant along the greater curve of the stomach. Less commonly, there are one or two large spleens along with several smaller splenunculi.

The congenital asplenia syndrome (right isomerism) is characterized by an absent spleen and multiple anomalies in both the abdomen and thorax. Many of its features are those of right isomerism, e.g., situs ambiguous with bilateral right sidedness.

Splenogonadal fusion is a rare congenital anomaly characterized by fusion of splenic tissue and gonad[9]. It is thought that this anomaly is due to an adhesion between the gonadal primordia and developing spleen prior to gonadal descent. The functioning splenic tissue is located in close proximity to gonadal tissue. Splenogonadal fusion occurs predominantly in male patients and the left gonad is nearly always affected. It is usually asymptomatic but may cause confusion with testicular malignancy.

SPLENOMEGALY

There are many causes of splenomegaly ( Table 73.1 ). The imaging appearances are usually non-specific and only occasionally can imaging provide a clue to the underlying cause, e.g., abdominal lymph node enlargement may suggest lymphoma or sarcoidosis.

Table 73.1 — CAUSES OF SPLENOMEGALY
Congestive
Portal hypertension
Cirrhosis
Cystic fibrosis
Splenic vein obstruction
Neoplasms
Leukaemia/lymphoma
Storage disease
Gaucher’s disease
Niemann–Pick disease
Amyloidosis
Histiocytosis
Collagen vascular
Systemic lupus erythematosus
Rheumatoid/Felty syndrome
Haemolytic anaemias
Haemoglobinopathies
Hereditary spherocytosis
Infections
Hepatitis
Malaria
Infectious mononucleosis
Tuberculosis
Typhoid
Extramedullary haematopoiesis
Myelofibrosis
Miscellaneous
Sarcoidosis
Porphyria

Benign mass lesions

Splenic cyst

Non-neoplastic splenic cysts can be divided into true (primary) cysts, which possess a cellular lining, and false (secondary) cysts, which have no cellular lining. True cysts are either parasitic (echinococcal) or nonparasitic (epithelial). True, nonparasitic, i.e., epithelial (also called epidermoid, mesothelial, or primary) cysts are congenital in origin. They are more common in women than in men and usually occur in childhood or adolescence[10]. In 80% of cases congenital splenic cysts are unilocular and solitary. A false cyst, i.e., pseudocyst, is post-traumatic in origin and is thought to represent the final stage in the evolution of a splenic haematoma.

On CT/MRI, splenic cysts are well defined, of water density or signal intensity, and show no enhancement after intravenous injection of contrast medium (Figs 73.7, 73.8 [7] [8]). It is usually difficult to distinguish between true and false cysts on imaging, but certain characteristics may be useful in differentiating between them. On US, false cysts may contain internal echoes from debris and show echogenic foci with distal shadowing due to calcification in the wall. On CT, cyst wall calcification can be seen in 14% of true cysts and 50% of false cysts[11]. Cyst wall trabeculation or peripheral septation occurs in 86% of true cysts and 17% of false cysts. High attenuation cysts may occur in up to one third of false cysts. On MRI, false cysts may have variable signal intensity on T1-weighted images, depending on the degree of proteinaceous material or haemorrhage present.

Figure 73.7 Splenic cyst. (A) Ultrasound and (B) contrast-enhanced CT showing the typical appearances of a splenic cyst (arrow).

Figure 73.8 Splenic cyst on MRI. (A) Coronal T2-weighted fast-spin-echo and (B) a dynamic breath-hold coronal T1-weighted spoiled gradient-echo image obtained 2 minutes after gadolinium injection shows the typical appearance of splenic cyst (arrow) on MRI.

Splenic hydatid cysts occur in less than 5% of cases of echinococcosis, and in approximately 75% of patients with echinoccoccal involvement of the spleen other structures are involved, the liver being the most common. The appearance on imaging of splenic hydatidosis depends on the age of the cyst and any associated complication. On US, a hydatid cyst may be anechoic or have mixed echogenicity due to intracystic components, e.g., scolices. Separation of the membrane produces the ‘water-lily’ sign—an undulating, linear collection of echoes within the cyst. Daughter cysts give the characteristic appearance of a cyst enclosed within a cyst. On CT, hydatid cysts are well-defined low-density lesions that do not enhance after intravenous injection of contrast medium, except for possible ring-like enhancement of the external cyst wall. The cyst wall may calcify, and the presence of a complete ring of calcification suggests an inactive lesion. On MRI, hydatid cysts are well-defined, rounded spaces occupying lesions with signal intensity similar to water. However, depending on the protein content or haemorrhage in the cyst, the signal intensity on T1-weighted sequences may vary. Daughter cysts have slightly lower signal than the main cyst on T1-weighted images. A thick, low-intensity rim surrounding the cyst is usually present. This rim corresponds to a dense fibrous capsule encasing the parasitic membrane. As the appearance of a hydatid cyst is non-specific, differentiating hydatid cysts from other cystic lesions can be difficult. The presence of daughter cyst, hepatic involvement and positive serology may be helpful in the differential diagnosis.

The differential diagnosis of a splenic cyst includes abscess, acute haematoma, intrasplenic pancreatic pseudocyst, cystic neoplasm (lymphangioma or haemangioma) and cystic metastasis.

Haemangioma

Haemangioma is the most common primary benign neoplasm of the spleen, occurring in 0.03–14% of cases at autopsy[12]. Splenic haemangiomas can be multiple ( Fig. 73.9 ) and part of a generalised angiomatosis as in Klippel–Trénaunay–Weber syndrome. Most lesions are detected incidentally but large haemangiomas can lead to splenic rupture and anaemia, thrombocytopenia and coagulopathy (Kasabach–Merritt syndrome).

Figure 73.9 Multiple splenic haemangiomata. (A) Contrast-enhanced CT shows multiple poorly enhancing lesions in the spleen. On the (B) axial T1-weighted spin-echo no lesions can be seen but the (C) T2-weighted fast-spin-echo shows multiple haemangiomata with the typical high signal intensity. Dynamic breath-hold T1-weighted spoiled gradient-echo images acquired (D) before, (E) immediately after, (F) 60 s after and (G) 3 minutes after bolus injection of intravenous gadolinium shows the typical enhancement pattern for haemangioma. On the early phase images, there is peripheral enhancement of the lesions and the delayed image shows the haemangioma to be isointense to the rest of the spleen.

The imaging characteristics of splenic haemangiomas range from solid to mixed to purely cystic lesions[13]. The US appearance is non-specific, and may show cystic areas. On CT, haemangiomas may appear either solid or cystic and may enhance in a similar pattern to hepatic haemangioma[14]. Some lesions are relatively avascular or show slow filling of contrast material. The MRI appearance is also similar to hepatic haemangioma. The lesion is of lower signal intensity than, or isointense to, the spleen on T1-weighted images, and of high signal intensity on T2-weighted images. T2-weighted images may show heterogeneous signal intensity representing mixed solid and cystic component of the haemangioma. T1-weighted images may shows areas of high signal due to subacute haemorrhage or proteinaceous fluid.

Lymphangioma

Lymphangioma may occur as single or multiple lesions, are usually asymptomatic, and are categorized as capillary, cavernous, or cystic depending on the size of the abnormal lymphatic channels. In the spleen the cystic type is most common. On US they appear as hypoechoic masses occasionally containing septation and debris[15]. CT shows multiple thin-walled, well-marginated cysts, often subcapsular in location. No enhancement is seen and the attenuation measurements vary from 15–35 HU[16].

Hamartoma

Splenic hamartomas (also called splenomas, or nodular hyperplasia of the spleen) are rare benign lesions composed of an anomalous mixture of normal splenic elements with red pulp predominating[17]. The hamartoma occurs singly or less commonly as multiple nodules. On US, hamartomas are hyperechoic relative to the spleen and sometimes have a cystic component[18]. On CT, they appear iso- or hypodense on unenhanced images with occasional lesions showing cystic components. On MRI, they are isointense on T1-weighted and hyperintense on T2-weighted sequences[15]. On CT and MRI, following intravenous contrast material, they usually show slow enhancement with late ‘filling in’[19].

MALIGNANT MASS LESIONS

Lymphoma (see Chapter 72 )

Splenic lymphoma is usually a manifestation of generalized lymphoma and is the most common splenic malignancy. Primary splenic lymphoma, which is usually of the non-Hodgkin type, is rare and comprises 1–2% of all lymphomas[20]. It is estimated that, at the time of diagnosis, splenic involvement is present in 25–35% of patients with Hodgkin’s or non-Hodgkin lymphoma (NHL)[21]. In patients with NHL splenic involvement is associated with infiltrated para-aortic nodes in approximately 70% of patients. On imaging, splenic involvement in lymphoma can take several forms: (A) homogeneous enlargement, (B) miliary nodules, (C) multifocal, 1–10 cm lesions (Figs 73.10, 73.11 [10] [11]), or (D) single solitary mass. Necrosis of a large lesion can give rise to an irregular cystic lesion[22]. Radiologically visible calcification has been reported in aggressive lesions and after chemotherapy[23].

Figure 73.10 Lymphoma. (A) Ultrasound and (B) contrast-enhanced CT in a patient with non-Hodgkin’s lymphoma involving the spleen. The ultrasound shows a large spleen (arrows) with multiple, poorly defined hypoechoic lesions. On the CT, enlarged intra-abdominal lymph nodes (arrows) can also be seen.

Figure 73.11 Lymphoma. Contrast-enhanced CT in a patient with non-Hodgkin’s lymphoma involving the liver and spleen. Multiple small poorly defined nodules can be seen in both liver and spleen. A trace of ascites can also be seen anterior to the liver.

Other primary malignant tumours

Splenic angiosarcoma is very rare but is the most common non-lymphoid primary malignant tumour of the spleen. The prognosis is very poor as only 20% of patients survive lon ger than 6 months. Approximately 70% of all angiosarcoma metastasize to the liver and approximately 30% undergo spontaneous rupture[24]. Imaging reveals an enlarged spleen with a poorly defined mass, and there may be areas of haemorrhage.

Other primary tumours of the spleen are very rare and include fibrosarcoma, leiomyosarcoma, malignant teratoma and malignant fibrous histocytoma.

Metastatic disease

Metastatic deposits in the spleen are unusual, occurring in only 0.3–10.3% of patients with malignancy where metastases have occurred in multiple organs[25]. Splenic metastases are usually asymptomatic and are usually found at autopsy or at imaging. The most common primary site for splenic metastases are the breast, lung, colorectal, ovary and skin (melanoma). Splenic involvement may either be due to surface disease from peritoneal spread of cancer or parenchymal disease from haematogenous spread.

Parenchymal splenic metastases most frequently appear as multiple nodules. On CT, nodular metastases appear as rounded hypodense lesions ( Fig. 73.12 ). Cystic lesions may occur with metastases from ovary ( Fig. 73.13 ), breast, endometrium and skin (melanoma). Calcification is uncommon but occurs typically in patients with a mucinous adenocarcinoma primary. Peritoneal implants in patients with ovarian, gastrointestinal, or pancreatic cancer can cause scalloping of the splenic capsular surface.

Figure 73.12 Splenic metastases. Contrast-enhanced CT showing multiple deposits (arrows) from malignant melanoma.

Figure 73.13 Cystic splenic metastasis. Contrast-enhanced CT shows a cystic splenic metastasis (arrow) in a patient with advanced ovarian cancer. There are also peritoneal deposits (open arrow) and malignant ascites present.

SPLENIC INFECTION

Splenic infection is uncommon and in 70% of cases is the result of haematogenous spread from primary infection elsewhere. Endocarditis is the most common cause; others include urinary tract infection, wound infection, appendicitis and pneumonia. Abscesses are present in other organs in 15–20% of patients with splenic abscess[26]. Direct spread of infection from adjacent organs may also occur. Noninfectious predisposing factors include diabetes, immunosuppression, sickle-cell disease, splenic injury and infarction.

Bacterial splenic abscess is most commonly due to staphylococci, streptococci, or salmonella. On US, splenic abscesses have a variable appearance: they may be hypoechoic or cystic with an irregular wall containing debris, septation and air bubbles. On CT, splenic abscesses appear as spherical or slightly lobulated non-enhancing areas of low attenuation. The rim is often of equal attenuation to the surrounding spleen but an enhancing capsule may be seen. Gas is present in only a small number of splenic abscesses. The use of CT or US-guided drainage is becoming an acceptable alternative to splenectomy[27].

Infection of the spleen with Mycobacterium tuberculosis usually occurs in a miliary form by haematogenous dissemination. Miliary tuberculosis may appear as irregular areas of low attenuation. Often there is mild splenomegaly, and infarcts from septic emboli may be present. Other evidence of intra-abdominal tuberculosis may be present, such as lymphadenopathy, high attenuation ascites on CT, peritoneal thickening, or hepatomegaly. Evolution of the splenic lesions ultimately gives rise to healed calcified granuloma often incidentally noted on CT.

With increasing prevalence of immunosuppression, fungal infection is becoming more common. The most common pathogens are candida, aspergillus and cryptococcus[28]. Fungal infection in the spleen is most likely to appear as a miliary or multifocal process. On CT, hepatosplenic candidiasis ( Fig. 73.14 ) may appear as multiple rounded areas of decreased attenuation producing a “bull’s-eye” lesion with hypoattenuating foci and a central core of higher attenuation; or as tiny 2–5 mm lesions of increased attenuation due to calcification. Calcification is seen in treated candida microabscesses and lesions caused by other fungi, especially histoplasma, mycobacteria and Pneumocystis carinii. Fungal abscesses in neutropenic patients are often small and not always detectable with any imaging technique.

Figure 73.14 Splenic candidiasis. Contrast-enhanced CT shows multiple tiny hypodense lesions in the spleen from candidal microabscess. A small accessory spleen (curved arrow) at the splenic hilum is also involved.

Patients with acquired immune deficiency syndrome (AIDS) infrequently have fungal microabscesses seen in other immunocompromised patients. More often, several small hypoattenuating foci seen in the spleen are due to granulomas or abscesses caused by mycobacteria or P. carinii. On CT, this appears as splenomegaly with focal lesion and several scattered punctuate calcification. Calcification may occur before or after treatment.

SPLENIC TRAUMA

Splenic trauma may follow blunt or penetrating injuries and may be spontaneous or iatrogenic. The spleen is the most commonly injured organ in cases of blunt abdominal trauma. Ultrasound may be used to evaluate the abdomen and may show splenic injury ( Fig. 73.15 ). However, CT is the investigation of choice for the evaluation and delineation of the extent of splenic injury. Intravenous administration of contrast material is needed for adequate evaluation of splenic trauma as areas of haematoma and laceration may be isodense to splenic parenchyma on non-contrast-enhanced CT. Injury to the spleen can take the form of laceration, intrasplenic haematoma, subcapsular haematoma, or infarction. Splenic laceration appears as an irregular linear area of hypodensity on contrast-enhanced CT ( Fig. 73.16 ); intrasplenic haematoma as a hypodense area of nonperfused spleen on the contrast-enhanced CT; a subcapsular haematoma as a crescentic collection of fluid that distorts the underlying spleen. A congenital splenic cleft may mimic laceration, but typically these are smooth and there is no perisplenic blood. A decrease in the overall splenic enhancement to less than that of the liver has been noted in traumatized hypotensive patients and should not be misinterpreted as representing splenic vascular injury. Haemoperitoneum almost always accompanies significant splenic injury. If there is significant intra-abdominal fluid, the presence of local perisplenic clot (i.e., a ‘sentinel clot’) suggests splenic injury as the site of bleeding. This sentinel clot has a homogeneous appearance with an attenuation coefficient greater than 60 HU[29]. Perisplenic haematoma may have a multilayered or ‘onion skin’ appearance if there are repeated episodes of bleeding. Pseudoaneurysm formation can occur following trauma, which appears as a focal well-circumscribed area of vascular enhancement within the splenic parenchyma.

Figure 73.15 Splenic injury. A longitudinal ultrasound showing splenic lacerations (open arrows) and perisplenic fluid/haematoma (asterisks) around the spleen (arrows). (Courtesy of Dr J.A.W. Webb.)

Figure 73.16 Splenic injury. Contrast-enhanced CT in a man who fell from a ladder. (A)There is fracture of the left 10th rib (arrow) with perisplenic fluid and ascites. (B) Splenic laceration (open arrow) was also identified on CT.

Several CT grading systems have been devised in an attempt to identify patients with splenic trauma who may undergo successful nonsurgical treatment [30] [31]. Recent studies have shown that although CT is an accurate means of evaluating splenic injury it cannot be used to reliably determine the need for surgical intervention or to predict clinical outcome [31] [32].

Delayed splenic rupture—i.e., haemorrhage from splenic rupture occurring more than 48 hours after trauma—may occur in a few patients in whom the initial CT was normal[32]. This may be genuinely delayed and secondary to a splenic fracture in which there is little initial haemorrhage. Alternatively, poor contrast opacification of the spleen, rendering the haematoma isodense with splenic parenchyma on images acquired soon after trauma, may result in splenic trauma being unidentified if unenhanced images were not obtained[32].

CT may be used to monitor healing of splenic injury, as documented by progressive diminution of perisplenic and intrasplenic haematoma or laceration. Progressive enlargement on serial CT is not an indicator of clinical deterioration. It is likely that, in acutely injured patients, the spleen contracts secondary to intravascular volume depletion and sympathetic drive. With time and volume replacement the spleen returns to normal size.

Splenosis

Splenosis represents the heterotopic autotransplantation of splenic tissue that usually follows traumatic rupture of the splenic capsule. The splenic remnant implants on the serosal surfaces of the abdomen and chest, derives its blood supply from surrounding tissues, and is indistinguishable from normal spleen histologically. The radiological diagnosis of splenosis requires awareness of the condition and a history of splenic trauma. Imaging may show one or several homogeneous, solid, well-circumscribed, noncalcified soft tissue nodules. The splenules have a variable shape, are poorly marginated and are closely related to the tissue from which they receive their blood supply. 99mTc-sulphur colloid or 99mTc-labelled heat denatured erythrocytes show uptake in splenic tissue and may be used to diagnose splenosis[33]. MRI with supramagnetic iron-oxide particles has also been used to diagnose splenosis[34]

OTHER SPLENIC DISORDERS

Splenic infarcts may occur from embolic disease, atherosclerosis, arteritis, splenic artery aneurysm, sickle-cell disease, or mass lesion compressing splenic vasculature, e.g., pancreatic masses. Splenic infarction may be diffuse or focal. On CT, infarcts typically appear as sharply marginated, low-density wedge-shaped areas ( Fig. 73.17 ). Occasionally infarcts may be multiple, resulting in poorly defined hypodense lesions. When the entire spleen is infarcted, only rim enhancement of the capsule occurs from capsular vessels[3]. Splenic infarction can also been seen on MRI, and haemorrhagic infarcts have a high signal on T1- and T2-weighted images.

Figure 73.17 Splenic infarct. Contrast-enhanced CT shows a tumour mass (arrows) in the tail of the pancreas is causing occlusion to the splenic vein and a splenic infarct (black arrow)

Splenic sarcoidosis is usually asymptomatic, and the spleen may be involved in up to 60% of patients. The presentation and appearance of the spleen may mimic lymphoma. Imaging findings include splenomegaly, hypodense nodules in the spleen on CT, and coexistent lymphadenopathy. The chest radiograph may be normal in 25% of patients with splenomegaly or discrete nodules in the spleen[35].

Iron deposition in the reticuloendothelial system, haemosiderosis, may occur in patients receiving multiple blood transfusions and can sometimes be identified on CT by its increased attenuation. MRI is more sensitive than CT for demonstrating iron deposition. The paramagnetic properties of deposited iron results in diffuse diminished signal intensity of the spleen relative to the musculature on T1- and T2-weighted images ( Fig. 73.18 ).

Figure 73.18 Haemosiderosis. Axial (A) T1-weighted spin-echo and (B) T2-weighted fast-spin-echo images show the very low signal intensity of the liver and spleen with respect to the skeletal muscle due to iron deposition in a patient with leukaemia who has had multiple blood transfusions.

Splenic involvement in amyloidosis may be nodular or diffuse[36]. The nodular form involves the lymphoid follicle, and appears on CT as discrete low-attenuation masses within an enlarged spleen. In the diffuse form, with infiltration of the red pulp, the spleen is of low attenuation with poor contrast enhancement. Spontaneous splenic rupture may occur due to vascular fragility and acquired coagulopathy associated with amyloidosis. On MRI, low signal intensity in the spleen has been noted on T2-weighted images[37].

In sickle-cell anaemia the appearance of the spleen depends on the duration of the disease and whether the patient has the homozygous (sickle-cell disease) or the heterozygous (sickle-cell trait) form of the condition. Disease complications will also alter the appearance of the spleen. Splenic infarction is common in both forms of sickle-cell anaemia. Repeated infarction in sickle-cell anaemia eventually results in a shrunken spleen containing diffuse microscopic deposits of calcium and iron. Acute splenic sequestration is a common complication of sickle-cell disease during childhood and may occur in the heterozygous form of the condition at any age. It results from sudden trapping of a large amount of blood in the spleen, resulting in splenic enlargement and a rapid decrease in haematocrit. On CT, the spleen is enlarged with peripheral low-attenuation regions from infarcts interspersed with higher attenuation areas from haemorrhage and pooling of blood. MRI shows the corresponding changes due to infarction and haemorrhage. Functional asplenia occurs in sickle-cell anaemia and may be indicated by the absence of tracer uptake on a 99mTc-sulphur colloid scintigraphy. Deposition of iron (haemosiderois) and calcium in sickle-cell anaemia results in an echogenic spleen on US, high attenuation on CT and low signal intensity on T1- and T2-weighted MRI.

ACKNOWLEDGEMENTS

We would like to thanks Mrs Julie Jessop for help with the manuscript preparations.

REFERENCES

1. Peddu P, Shah M, Sidhu PS: Splenic abnormalities: a comparative review of ultrasound, microbubble-enhanced ultrasound and computed tomography. Clin Radiol 2004; 59:777-792.

2. Lucey BC, Boland GW, Maher MM, Hahn PF, Gervais DA, Mueller PR: Percutaneous nonvascular splenic intervention: a 10-year review. Am J Roentgenol 2002; 179:1591-1596.

3. Warshauer DM, Koehler RE: Spleen. In: Lee JK, Sagel SS, Stanley RJ, Heiken JP, ed. CT with MRI Correlation, Philadelphia: Lippencott-Raven; 1998:845-872.

4. Prassopoulos P, Daskalogiannaki M, Raissaki M, Hatjidakis A, Gourtsoyiannis N: Determination of normal splenic volume on computed tomography in relation to age, gender and body habitus. Eur Radiol 1997; 7:246-248.

5. Whitley JE, Maynard CD, Rhyne AL: A computer approach to the prediction of spleen weight from routine films. Radiology 1966; 86:73-76.

6. Dardenne AN: The Spleen. In: Cosgrove DO, Meire HB, Dewbury KCD, ed. Clinical Ultrasound, Edinburgh: Churchill Livingstone; 1993:353-365.

7. Lamb PM, Lund A, Kanagasabay RR, Martin A, Webb JA, Reznek RH: Spleen size: how well do linear ultrasound measurements correlate with three-dimensional CT volume assessments?. Br J Radiol 2002; 75:573-577.

8. Strijk SP, Wagener DJ, Bogman MJ, de Pauw BE, Wobbes T: The spleen in Hodgkin disease: diagnostic value of CT. Radiology 1985; 154:753-757.

9. Carragher AM: One hundred years of splenogonadal fusion. Urology 1990; 35:47175.

10. Younger KA, Hall CM: Epidermoid cyst of the spleen: a case report and review of the literature. Br J Radiol 1990; 63:652-653.

11. Dawes LG, Malangoni MA: Cystic masses of the spleen. Am Surg 1986; 52:333-336.

12. Rabushka LS, Kawashima A, Fishman EK: Imaging of the spleen: CT with supplemental MR examination. Radiographics 1994; 14:307-332.

13. Duddy MJ, Calder CJ: Cystic haemangioma of the spleen: findings on ultrasound and computed tomography. Br J Radiol 1989; 62:180-182.

14. Ros PR, Moser RPJ, Dachman AH, Murari PJ, Olmsted WW: Hemangioma of the spleen: radiologic-pathologic correlation in ten cases. Radiology 1987; 162:73-77.

15. Mortelé KJ, Merjo PJ, Kunnen M: Tumoral pathology of the spleen. In: DeSchepper AM, Vanhoenacker F, ed. Medical Imaging of the Spleen, Berlin: Spinger-Verlag; 2000:101-123.

16. Pistoia F, Markowitz SK: Splenic lymphangiomatosis: CT diagnosis. Am J Roentgenol 1988; 150:121-122.

17. Dachman AH, Friedman AC: Radiology of the Spleen, St Louis, Mosby-Year Book Inc, 1993.

18. Norowitz DG, Morehouse HT: Isodense splenic mass: hamartoma, a case report. Comput Med Imaging Graph 1989; 13:347-350.

19. Ohtomo K, Fukuda H, Mori K, Minami M, Itai Y, Inoue Y: CT and MR appearances of splenic hamartoma. J Comput Assist Tomogr 1992; 16:425-428.

20. Long JC, Aisenberg AC: Malignant lymphoma diagnosed at splenectomy and idiopathic splenomegaly. A clinicopathologic comparison. Cancer 1974; 33:1054-1061.

21. Castellino RA: Hodgkin disease: practical concepts for the diagnostic radiologist. Radiology 1986; 159:305-310.

22. Harris NL, Aisenberg AC, Meyer JE, Ellman L, Elman A: Diffuse large cell (histiocytic) lymphoma of the spleen. Clinical and pathologic characteristics of ten cases. Cancer 1984; 54:2460-2467.

23. Marti-Bonmati L, Ballesta A, Chirivella M: Unusual presentation of non-Hodgkin lymphoma of the spleen. Can Assoc Radiol J 1989; 40:49-50.

24. Mahony B, Jeffrey RB, Federle MP: Spontaneous rupture of hepatic and splenic angiosarcoma demonstrated by CT. Am J Roentgenol 1982; 138:965-966.

25. Lam KY, Tang V: Metastatic tumors to the spleen: a 25-year clinicopathologic study. Arch Pathol Lab Med 2000; 124:526-530.

26. Tikkakoski T, Siniluoto T, Paivansalo M, et al: Splenic abscess. Imaging and intervention. Acta Radiol 1992; 33:561-565.

27. Thanos L, Dailiana T, Papaioannou G, Nikita A, Koutrouvelis H, Kelekis DA: Percutaneous CT-guided drainage of splenic abscess. Am J Roentgenol 2002; 179:629-632.

28. Chew FS, Smith PL, Barboriak D: Candidal splenic abscesses. AJR Am J Roentgenol 1991; 156:474.

29. Orwig D, Federle MP: Localized clotted blood as evidence of visceral trauma on CT: the sentinel clot sign. Am J Roentgenol 1989; 153:747-749.

30. Buntain WL, Gould HR, Maull KI: Predictability of splenic salvage by computed tomography. J Trauma 1988; 28:24-34.

31. Mirvis SE, Whitley NO, Gens DR: Blunt splenic trauma in adults: CT-based classification and correlation with prognosis and treatment. Radiology 1989; 171:33-39.

32. Umlas SL, Cronan JJ: Splenic trauma: can CT grading systems enable prediction of successful nonsurgical treatment?. Radiology 1991; 178:481-487.

33. Gunes I, Yilmazlar T, Sarikaya I, Akbunar T, Irgil C: Scintigraphic detection of splenosis: superiority of tomographic selective spleen scintigraphy. Clin Radiol 1994; 49:115-117.

34. Storm BL, Abbitt PL, Allen DA, Ros PR: Splenosis: superparamagnetic iron oxide-enhanced MR imaging. Am J Roentgenol 1992; 159:333-335.

35. Warshauer DM, Dumbleton SA, Molina PL, Yankaskas BC, Parker LA, Woosley JT: Abdominal CT findings in sarcoidosis: radiologic and clinical correlation. Radiology 1994; 192:93-98.

36. Kozicky OJ, Brandt LJ, Lederman M, Milcu M: Splenic amyloidosis: a case report of spontaneous splenic rupture with a review of the pertinent literature. Am J Gastroenterol 1987; 82:582-587.

37. Rafal RB, Jennis R, Kosovsky PA, Markisz JA: MRI of primary amyloidosis. Gastrointest Radiol 1990; 15:199-201.

FURTHER READING

Dachman AH, Friedman AC: Radiology of the Spleen, St Louis, Mosby-Year Book Inc, 1993.

DeSchepper AM, Vanhoenacker F: Medical Imaging of the Spleen, Berlin, Spinger-Verlag, 2000.

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