Technique
Magnetic Resonance
Magnetic resonance (MR) relaxation character- istics of focal tumors tend to be similar to normal splenic tissue and thus difficult to detect. With the spleen located in the left upper abdomen close to the left hemidiaphragm, mag- netic resonance imaging (MRI) of the spleen requires control of motion artifacts. A number of breath-hold techniques have been developed that allow dynamic contrast-enhanced images.
Faster MRI techniques allow postcontrast images to be obtained during perfusion, equi- librium, and more delayed phases. Some focal lesions equilibrate with normal splenic parenchyma within several minutes after con- trast injection and thus early postcontrast images accentuate tumors compared to normal tissue.
Superparamagnetic iron oxide contrast agents are taken up by the reticuloendothelial cells and shorten T2, making high signal inten- sity tumors more conspicuous. While these agents are theoretically advantageous in the spleen, research activity in this field peaked about a decade ago, and little current clinical application exists in the spleen.
Scintigraphy
Some of the more common radiopharmaceu- ticals useful in splenic imaging are technetium-
99m (Tc-99m)–sulfur colloid, indium-111–
white blood cells, and Tc-99m–red blood cells.
Biopsy/Drainage
Splenic biopsies are performed in both adults and children with few complications. A variety of needles are used, with 20- and 22-gauge needles being the most common (1). Biopsies establish a specific diagnosis in most patients with a focal splenic abnormality.
Congenital Anomalies
Malposition
The spleen is normally located in the left upper quadrant of the abdomen. Malposition is due to either a congenital maldevelopment or an acquired condition, such as a prior surgical procedure. Excessive mobility to the spleen is secondary to laxity of the splenic suspensory ligaments, including the lienorenal ligament. At times the splenic hilum is located along the superior aspect of the spleen, a condition that is probably a normal variant. The spleen can her- niate into a prior lumbar incision.
Many patients with a hypermobile spleen are asymptomatic, and these “wandering spleens”
are discovered incidentally when an imaging study is performed for other purposes. An asymptomatic wandering spleen can even be located in the right side of the pelvis, mimick-
Spleen
933
ing a pelvic tumor. CT and MR reveal an absent spleen in its usual location and a splenic-sized tumor inferiorly. Contrast enhancement detects a vascular pedicle. A wandering spleen can be diagnosed with sequential liver-spleen scintig- raphy and with In-111-leukocyte scintigraphy.
An occasional such wandering spleen is associ- ated with dilated feeding vessels within lax lig- aments. Lax suspensory ligaments predispose a wandering spleen to splenic torsion and has even caused splenic flexure volvulus. Splenic torsion is a rare cause of an acute abdomen;
at times contrast enhanced imaging reveals a partly nonenhancing spleen due to ischemia (2).
Accessory Spleen
The term accessory spleen is used to designate additional separate splenic tissue believed to be congenital in origin. It is a common condition, with most accessory spleens located near the splenic hilum, some even being intrapancreatic in location where they can mimic a pancreatic tumor. Although most are relatively fixed in position, an occasional one fits the criteria of a wandering spleen, such as an intrascrotal paratesticular accessory spleen. Similar to a main spleen, cysts can also develop in an acces- sory spleen. In a setting of splenomegaly an accessory spleen will also enlarge. Thus an accessory spleen enlarges secondary to portal hypertension. Torsion of an accessory spleen vascular pedicle can result in vascular compro- mise and progress to ischemia and infarction.
An accessory spleen is detected by computed tomography (CT), ultrasonography (US), MRI, and scintigraphy. On noncontrast CT it mimics enlarged lymph nodes, but after contrast it enhances similar to the spleen. Color Doppler US also suggests the diagnosis. Accessory spleens have the same MR signal intensity as normal spleen parenchyma on all sequences.
A Tc-99m–sulfur colloid scan shows uptake similar to the spleen. Occasionally such uptake results in confusion. Thus after a splenectomy somatostatin receptor scintigraphy reveals uptake in an accessory spleen.
Asplenia and Polysplenia
The terms asplenia and polysplenia are descrip- tive only, and associated abnormalities are
common. These conditions are part of the het- erotaxy syndrome (discussed in Chapter 14).
Splenogonadal Fusion
Splenogonadal fusion in males is discussed in Chapter 13. This rare congenital anomaly is associated with orofacial and extremity abnor- malities. Imaging detects a tumor in the lower abdomen, with radiocolloid spleen scintigraphy and single photon emission computed tomog- raphy (SPECT) showing uptake similar to splenic tissue.
Gaucher’s Disease
Gaucher’s disease is an autosomal-recessive storage disorder caused by a defect in the lyso- somal enzyme b-glucosidase, an enzyme needed to degrade sphingolipids. About 40 mutations of the b-glucosidase gene have been identified, with clinical disease variability depending on the specific type of gene mutation involved. Its hallmark is pathologic storage of glycolipid in mononuclear phagocytes, with a tissue reaction to these lipid-engorged macrophages, or Gaucher cells, probably leading to further organ damage. The diagnosis is made by showing decreased acid b-glucosidase activ- ity in peripheral blood leukocytes. A histologic diagnosis is not necessary in most patients.
Genotyping is available and does detect most carriers, but the variable phenotypic expressiv- ity limits the use of genotyping as a practical tool.
Gaucher’s disease is subdivided into three types based on the presence or absence of neu- rologic involvement: type 1, nonneuronopathic;
type 2, severe neuronopathic; and type 3, a chronic, less severe neuronopathic form similar to type 1, but with more severe, systemic mani- festations.A rare neonatal form leads to hydrops fetalis.
The disease involves multiple organs but
varies considerably in its clinical expressivity
and severity. Typically, splenomegaly, bone
lesions, and eventually central neurologic
involvement become evident. These patients are
at increased risk of developing lymphoprolifer-
ative disorders, including non-Hodgkin’s
lymphoma.
Moderate-to-severe splenomegaly due to reticuloendothelial hypertrophy and hyperpla- sia is a common and often the only imaging finding. Hepatomegaly generally is not a pro- minent feature. A number of CT and US tech- niques have been developed to measure splenic volume. These are useful in patients with Gaucher’s disease who often undergo serial follow-up studies. Follow-up of splenic volume changes are best obtained using the same imaging modality.
A minority of patients have well-defined homogeneous hypodense nodules scattered throughout the spleen. Ultrasonography shows variable echogenicity in these nodules. An irreg- ular, inhomogeneous appearance is seen if these nodules become confluent. Of interest is that splenectomized patients tend to develop retroperitoneal or periportal lym- phadenopathy. Magnetic resonance imaging also identifies splenic nodules in some of these patients, with these nodules being isointense on T1- and hypointense on T2-weighted images.
Also, MR detects splenic infarcts in these patients.
These patients have decreased plasma levels of low-density lipoproteins. Technetium-99m–
low-density lipoprotein scintigraphy shows that these proteins are taken up by the spleen, bone marrow, and liver reticuloendothelial system (3). Such serial studies appear of value in follow-up after therapy.
Splenectomy and heterotopic splenic auto- transplantation have been used to treat hyper- splenism. Partial splenectomy often leads to enlargement of the splenic remnant. It is not clear if such enlargement is due to splenic tissue regeneration or continued glycolipid deposition or both.
An occasional patient with massive splenomegaly develops a splenic abscess.
Thalassemia
Hypersplenism can be corrected in children with thalassemia by partial or total surgical splenectomy. An alternative is partial splenic embolization. After embolization the spleen decreases in size and fewer transfusions are necessary.
Hereditary Spherocytosis
Patients with hereditary spherocytosis have hemolysis, either compensated or leading to anemia, and are at increased risk for biliru- binate gallstones, erythroid aplasia, and hemolytic crises.
Therapy consists of splenectomy, although partial splenic embolization is an option (4).
Niemann-Pick Disease
Niemann-Pick type C disease is an autosomal- recessive lipid storage disorder, leading to an accumulation of syringomyelin and choles- terol in the brain, liver, and spleen. Most affected patients develop neurologic symptoms.
Isolated nodular splenomegaly develops in this condition.
Sickle Cell Disease
Patients with sickle cell disease are at risk for splenic infection, abscess, acute splenic seques- tration crisis, hypersplenism, and splenic infarc- tion. Most acute infarctions involve only a portion of the spleen, although total splenic infarction does develop. During an acute sequestration crisis the hematocrit drops and spleen enlarges, at times massively. Computed tomography identifies multiple hypodense foci in the spleen. Multiple episodes of focal splenic infarction eventually result in a small spleen, at times containing calcifications.
In patients homozygous for this condition MRI reveals a signal void on T2-weighted sequences due to a combination of iron deposi- tion and superimposed calcifications (iron overload is discussed in Chapter 7). These patients have impairment of splenic reticulo- endothelial function; scintigraphy with Tc- 99m–sulfur colloid reveals nonvisualization of the spleen.
Patients with sickle cell disease develop
round intrasplenic nodules, shown to represent
functioning splenic tissue; this tissue is hypo-
dense on CT, hypoechoic on US, appears as
normal spleen on MRI, and manifests uptake of
Tc-99m–sulfur colloid. Imaging thus allows dis-
tinguishing these nodules from abscesses and
infarcts.
Trauma
In the United States, the initial triage of trauma patients classifies them into those who are unstable and require immediate surgery or stable; the latter patients generally undergo contrast-enhanced CT, with a decision for surgery, angiographic therapy, or conservative management based on CT findings. Quite often splenic trauma is only one element of multisys- tem trauma, and the decision for a specific therapy is modified accordingly. Intravenous contrast is necessary for adequate CT evalua- tion. Using splenic arteriography as a gold stan- dard, in 78 hemodynamically stable patients CT achieved an 81% sensitivity and 84% specificity in predicting the need for splenic therapy (5). In general, US is believed to be not as sensitive in detecting the extent of injury.
A number of injury severity schemes based on contrast-enhanced CT have been developed.
Some use the degree of splenic laceration and devascularization as a classification guide.
Both in adults and children these schemes have had limited success in guiding therapy.
A splenic injury classification scale, devised by the American Association for the Surgery of Trauma, is outlined in Table 15.1. In general, the injury severity score best correlates with outcome.
Some patients managed conservatively develop delayed complications, including
splenic or subphrenic abscess, bleeding from a (pseudo)aneurysm, or splenic rupture. Whether routine follow-up CT is warranted in these patients is controversial. Follow-up CT in other- wise asymptomatic patients does not appear to be routinely warranted. Whether US follow-up, including color Doppler, is warranted is not clear.
Blunt abdominal trauma can result in pseudoaneurysms and a splenic arteriovenous fistula; some of these fistulas resolve spontaneously.
Hematoma
A hematoma can be subcapsular or intra- parenchymal in location or, with rupture of the capsule, even perisplenic.
With noncontrast CT, intrasplenic hema- tomas range from hypodense to hyperdense (density-time variations are discussed in Chapter 14). Contrast-enhanced CT reveals a hematoma as a nonperfused region surrounded by contrast-enhancing normal parenchyma. A subcapsular hematoma tends to have a crescent shape, while perisplenic ones are more irregu- lar. Multiple episodes of spontaneous splenic bleeding can eventually result in a CT “onion skin” appearance.
A recent hematoma has a complex US appear- ance, and clotted blood in a hematoma can be
Table 15.1. Surgical splenic injury scale
Grade* Type of injury
I Hematoma Subcapsular,<10% of surface
Laceration Capsular,<1cm in parenchymal depth
II Hematoma Subcapsular, 10–50% of surface
Parenchymal,<5cm in diameter
Laceration Parenchymal, 1–3 cm in depth, trabecular vessels not involved III Hematoma Subcapsular,>50% of surface or expanding Ruptured
Parenchymal,>5cm in diameter or expanding
Laceration Parenchymal,>3cm in depth or involving trabecular vessels
IV Laceration Segmental or hilar vessels involved in devascularization (>25% of spleen)
V Laceration Shattered spleen
Vascular Hilar injury with devascularized spleen
* Advanced one grade for multiple injuries, up to grade III.
Source: Modified from Moore et al. (6).
isoechoic to splenic tissue. Thus a perisplenic hematoma may simply blend into the spleen until it liquifies later on. In time, a hematoma gradually becomes anechoic.
Most hematomas eventually resolve; an occa- sional one becomes infected and requires drainage. Some evolve into nonepithelial cysts.
Splenic hematomas can be drained percuta- neously, although some recur. Gallium-67 sub- traction scintigraphy is useful if an infected splenic hematoma is suspected.
Laceration/Rupture
Splenic laceration is usually associated with intraperitoneal hemorrhage; occasionally splenic injury also leads to extraperitoneal hem- orrhage into the anterior pararenal space (7).
Although uncommon, delayed splenic rupture does occur after trauma. Occasionally even a minor splenic laceration leads to hemor- rhage days later, at times massively. This topic is difficult to place in proper perspective because splenic rupture has been reported even years after prior injury.
Splenic rupture after minor trauma should lead to a search for underlying disease. In Western countries the leading cause of sponta- neous splenic rupture is infectious mononucle- osis. Rupture is a recognized complication in patients with malaria. Rarely, spontaneous splenic rupture occurs in patients with HIV/AIDS, acute leukemia, sickle cell disease, amyloidosis, hepatitis virus infection, and even Salmonella enteritidis infection (8).
Splenomegaly due to such entities as Wilson’s disease predisposes to rupture. Rupture of a splenic cyst after minor trauma can result in an acute abdomen. Splenic rupture is a complica- tion of various interventional procedures, such as colonoscopy, extracorporeal shock-wave lithotripsy, and even after insertion of an implantable defibrillator using a left subcostal approach.
Precontrast CT of a laceration is seen as an irregular, hypodense defect (Fig. 15.1).
Post–intravenous contrast, a laceration is better defined by surrounding contrast-enhancing normal splenic parenchyma; an adjacent subcapsular or extrasplenic hematoma is often present. With active arterial bleeding at the time of study, contrast CT can identify extravasation.
Avulsion
Most splenic avulsions are secondary to major trauma. Avulsion has occurred, however, sec- ondary to colonoscopy and even in a patient with hyperemesis.
Therapy
The overall trend is to manage conservatively hemodynamically stable patients with splenic injury, generally detected by CT, and with no other indication for laparotomy. Conservative management tends to be unsuccessful if a trau- matic pseudoaneurysm or frank extravasation is detected on an initial CT examination; these patients should be treated with early surgical or endovascular therapy. Some of these patients undergo splenic arteriography and, if contrast extravasation is detected, splenic artery embolization is performed. Transcatheter arte- rial embolization therapy performed in trauma patients with angiographically evident contrast extravasation, arterial disruption, or major arte- riovenous fistula is successful in over 90% of these patients.
Computed tomography identifies a splenic artery pseudoaneurysms as contrast blush;
arteriography confirms this finding, and a majority of these aneurysms can be successfully embolized.
A subtotal splenectomy, with preservation of the upper splenic pole supplied by splenogastric
Figure 15.1. Splenic laceration. Ascites is also present.
vessels, was performed in patients with severe splenic injuries (9). Partial laparoscopic splenectomy following splenic trauma is also feasible.
A preexisting diseased (enlarged) spleen is more prone to laceration/rupture than a normal spleen and patients with such a spleen probably undergo a higher rate of splenectomy than those with a normal-size spleen. Conservative management, however, can be successful in stable patients with trauma to a diseased spleen.
At times heterotopic splenic autotransplanta- tion is performed after abdominal trauma requiring total splenectomy. Whether the auto- transplanted splenic tissue is functioning can be evaluated with red blood cell scintigraphy.
Follow-up US in children with blunt splenic trauma found that the time to healing is related to injury severity (10); sequelae include an occa- sional splenic cyst.
Torsion/Volvulus
Occasionally a wandering spleen twists on its axis on either an acute or chronic basis, a con- dition occurring in both children and adults.
Torsion can be suggested in the appropriate clinical setting if the spleen is not in its usual right upper quadrant location (the condition is really a volvulus, although the term torsion is often used interchangeably in the literature).
When acute, the sudden onset of abdominal pain suggests an acute abdomen. On a more chronic basis, few symptoms are elicited and the condition is often detected incidentally when an abnormal lower abdominal or even pelvic tumor is detected and the splenic fossa empty.
Imaging suggests the diagnosis. Computed tomography reveals a hypodense spleen, at times still showing postcontrast peripheral enhancement. Ultrasonography detects a hypo- echoic solid spleen, and Doppler US reveals absent blood flow, confirming the diagnosis.
Torsion and infarction also develop in an accessory spleen, especially if it has a long vas- cular pedicle. A number of these rare events occur in children.
Laparoscopic splenopexy of a mobile spleen has been performed (11).
Splenosis
Acquired splenic tissue outside the spleen, such as ectopic implantation from prior trauma, is termed splenosis, thus distinguishing it from an accessory spleen, which is a congenital condi- tion. Splenosis tends to present with multiple nodules; accessory spleens, on the other hand, are few in number. Splenosis involves the peri- toneum, retroperitoneal tissues, thoracic cavity, and even subcutaneous abdominal wall tissues (Fig. 15.2). It can develop years after splenec- tomy. Even intrahepatic splenosis has been reported (12). One patient developed cerebral splenosis 15 years after splenectomy (13).
Splenosis can become quite large, even mimicking an adjacent neoplasm. Most of these splenic nodules have a smooth outline. If sufficiently large, splenosis is imaged by CT, US, MRI, and scintigraphy. Ultrasonography reveals homogeneous echogenicity.
Splenosis should be differentiated from polysplenia.
Splenomegaly
The definition of an abnormally enlarged spleen (splenomegaly) is arbitrary. One definition used by ultrasonographers is a spleen that deviates by
Figure 15.2. Splenosis.The patient had a splenectomy as a child due to trauma. Computed tomography (CT) reveals left upper quadrant soft tissue nodules. Serial studies showed no change.(Courtesy of Patrick Fultz, M.D., University of Rochester.)
either one or two standard deviations from a group of “normal” spleens using the US splenic volume index.
Etiologies of splenomegaly are legion. Some radiologists subdivide splenomegaly into mod- erate versus massive, with the correspondingly most likely associated etiologies (Fig. 15.3). The most common causes of massive splenomegaly are myelofibrosis, lymphoma, and late-stage leukemia, although these entities are also encountered with lesser splenic enlargement.
Splenomegaly is common in patients with portal hypertension. A rare cause of hepato- splenomegaly is systemic mastocytosis.
Infection/Inflammation
Most splenic infections are hematogenous in origin, although in some patients no primary focus of infection can be determined.
Small, focal, hypodense nodules scattered in the spleen on arterial phase CT images suggest an infection. A finding of such a “spotted spleen,” however, is also seen with some neo-
plasms, especially lymphoma, and noninfec- tious inflammatory conditions such as sarcoid (14).
Abscess
Splenic abscesses are not common. Most develop in a setting of systemic infection, trauma, diabetes, malignancy, or some hemato- logic disorder. Splenic flexure fistulas in colonic Crohn’s disease can involve the spleen and result in abscesses. Some left renal abscesses also involve the spleen. Likewise, a splenic abscess is a complication of a nephrectomy, especially if a nephrectomy is performed for xanthogranulo- matous pyelonephritis. Common pathogens encountered are Staphylococcus and Streptococ-
cus species and Escherichia coli. An occasionalabscess contains Clostridium perfringens or other clostridial species.
Clinical signs and symptoms are nonspecific and include fever, pain, and left upper quadrant tenderness. Splenomegaly is usually present.
Undiagnosed, splenic abscesses result in a high mortality rate.
Imaging should suggest the diagnosis (Fig.
15.4). In some patients a chest radiograph reveals a left pleural effusion. Most splenic abscesses are solitary. Computed tomography shows a hypodense region surrounded by
Figure 15.3. Massive splenomegaly secondary to myelofibrosis.Figure 15.4. Splenic abscess detected by CT. It was of unknown etiology.
a contrast-enhancing rim. Gas within an abscess implies gas-forming bacteria; gas is only rarely secondary to an enteric fistula. A ruptured splenic abscess, however, has led to a pneumoperitoneum.
Most splenic abscesses have a slight hetero- geneous MR appearance on precontrast images.
Peripheral ring enhancement is common on postcontrast images.
Once imaging suggests a splenic abscess, culture of aspirated material should identify the infectious agent. Traditionally splenic abscesses have been treated by splenectomy, although they are amenable to percutaneous drainage, gener- ally under US guidance, and percutaneous drainage has replaced splenectomy in a number of institutions.
Hydatid Disease
Hydatid disease is discussed in more detail in Chapter 7.Although most echinococcal cysts are located in either the liver or the lungs, an occa- sional cyst develops in the spleen, kidneys, bones, heart, or peritoneum. Usually splenic involvement is also associated with other disease, at times being recurrent. Rupture of a splenic echinococcal cyst results in peritoneal dissemination of cyst content.
Cyst wall calcifications develop in about half of splenic echinococcal cysts. Most have a well- demarcated outline; some are multiloculated
(Fig. 15.5). Postcontrast CT reveals little contrast enhancement in the cyst wall.
Other splenic cysts, including the rare lym- phangioma, are in the differential diagnosis.
Tuberculosis
Splenic tuberculosis is rare. Silent splenic involvement is found in some patients with disseminated tuberculosis. Typically multiple small, hypodense lesions are scattered through- out the spleen. No calcification is evident during an acute infection but develop with healing.
The imaging appearance is nonspecific and is similar to that seen with a number of other infections and some lymphomas. Computed tomography revealed multiple, round or oval, hypodense tumors (Fig. 15.6). Ultrasonography of diffuse involvement reveals numerous hyperechoic foci. They are hypointense on T1- weighted images and often heterogeneous on T2-weighted images. They do not enhance with contrast but tend to have a slight rim enhance- ment postcontrast. Splenic tuberculosis is often associated with extraperitoneal adenopathy, with the nodes having peripheral contrast enhancement.
The less common isolated tuberculoma mimics a splenic abscess.
Tuberculous splenic abscesses are photopenic with Tc-99m-sulfur colloid scintigraphy; these abscesses, however, have increased uptake during gallium-67 scintigraphy.
Figure 15.5. Isolated splenic hydatid disease. Contrast-enhanced CT through upper (A) and lower (B) poles reveals a large cystic nonenhancing structure. A daughter cyst is evident in A. (Source: Polat P, Kantarci M, Alper F, Suma S, Koruyucu MB, Okur A. Hydatid disease from head to toe. RadioGraphics 2003;23:475–494, with permission from the Radiological Society of North America.)
A B
fever, sweating, fatigue, and joint pain, with osteoarthritic involvement being the most prevalent complication (15). Abdominal com- plaints were not common.
Calcifications in splenic brucellosis have an irregular and mottled appearance. Of interest is that with most infections calcifications imply disease inactivity within that nidus; brucellosis is unique in that active infection can be present even in a calcified nidus.
Cat-Scratch Disease (Bartonella Infection)
Bartonella henselae infection is related to
contact with cats and is the presumed cause of cat-scratch disease. If disseminated, this infec- tion leads to focal multinodular liver and splenic granulomas.
The splenic granulomas eventually calcify, often having a coarse appearance.
Infectious Mononucleosis (Epstein-Barr Virus Infection)
While splenomegaly is common in patients with infectious mononucleosis, in the occasional patient with disproportionate splenomegaly an underlying hematologic malignancy or a storage disorder such as Gaucher’s disease should be considered.
Some physicians believe that early splenec- tomy is indicated in a setting of splenic rupture complicating infectious mononucleosis, and most patients with spontaneous splenic rupture undergo splenectomy, although a nonoperative approach is feasible in selected patients. Even with initial nonoperative management, some eventually require a splenectomy.
Metabolic and Related Disorders
Hypersplenism
Hypersplenism, or increased splenic hemolysis, is a manifestation of several disorders, such as thrombocytopenic purpura and Gaucher’s disease. Transcatheter splenic artery emboliza- tion is effective therapy for hypersplenism.
Candidiasis
A Candida sp. splenic abscess in the absence of immunocompromise is rare. Both pre- and postcontrast CT aid in detecting these multiple, often small abscesses. They tend to be hypo- dense. A typical US appearance is that of a bull’s-eye, a finding that is neither specific nor always seen. These abscesses appear hypointense on T1- and hyperintense on T2- weighted images. They do not enhance postcontrast.
If large enough, these abscesses are amenable to percutaneous drainage.
Histoplasmosis
Multiple small, punctate intrasplenic calcifi- cations develop in patients with past histoplas- mosis infection. Tuberculosis shows similar findings. In both entities calcifications are indicative of inactive disease.
Imaging readily detects these granulomas.
Brucellosis
Human brucellosis is caused by Brucella
abortus, B. suis, B. canis, and B. melitensis. Thelatter is considered to be the most virulent.
Among patients with brucellosis from Beirut,
Lebanon, the main presenting symptoms were
Figure 15.6. Splenic tuberculosis in an HIV-positive man. Con- trast-enhanced CT shows marked splenomegaly and numerous poorly enhancing nodules throughout the spleen. Enlarged retroperitoneal nodes were also identified. (Courtesy of Patrick Fultz, M.D., University of Rochester.)Platelets, white blood count, and liver function tests improve significantly after such emboliza- tion. Fever, abdominal pain, pleural effusion, and ascites are transient phenomena after splenic embolization.
Partial splenic embolization can be therapeu- tic in cirrhotic patients with hypersplenism.
Residual spleen volumes remain stable in those with infarction rates >80%; on the other hand, in patients with lower infarction rates spleen volume tends to increase. The ideal splenic volume to be embolized is not clear and proba- bly varies depending on disease and age. For instance, children with hypersplenism undergo- ing 30% to 40% splenic volume embolization have lower morbidity compared with those undergoing more extensive splenic emboliza- tion (16); all maintained a platelet count above baseline.
Hyposplenism
The classic example of decreased splenic func- tion is in sickle cell disease. For unknown reasons patients with celiac disease also develop hyposplenism. Decreased splenic function is detected by the presence of abnormal red blood cells and by finding decreased splenic uptake on a Tc-99m–sulfur colloid scan.
Hyposplenism increases the risk of infec- tion and predisposes to spontaneous splenic rupture.
Extramedullary Hematopoiesis
Extramedullary hematopoiesis is most common in patients with congenital hemolytic anemias.
Most foci occur in the liver and spleen but are too small to identify with imaging. If large enough, CT reveals a homogeneous hypodense tumor, suggesting an infection or neoplasm.
Iron Overload
Similar to the liver, MRI of the spleen detects relatively low levels of splenic iron overload, but for meaningful results stringent equipment cal- ibration is necessary. Iron overload is difficult to quantify but is occasionally useful in adults with suspected posttransfusion iron overload.
In children after autologous bone marrow transplantation, MRI detects earlier iron over- load in the liver than in the spleen.
Amyloidosis
Splenic involvement occurs in both primary and secondary amyloidosis. Diffuse rather than focal splenic involvement is more common.
Abnormal regions tend to be hypodense on CT.
Some foci calcify. Arterial phase CT in a patient with primary liver and spleen amyloidosis revealed lack of contrast enhancement (17); the spleen was hypointense on T2-weighted MR images.
Systemic amyloidosis is associated with hyposplenism. Among patients with suspected liver amyloidosis, a liver-spleen scan is quite sensitive in detecting decreased splenic activity and can suggest disease even before abnormal red blood cells are detected in a peripheral smear.
An amyloid spleen predisposes to a sponta- neous splenic rupture.
Sarcoidosis
Splenic abnormalities are present in roughly half of patients with sarcoidosis, with splenic involvement usually being asymptomatic and overshadowed by other organ involvement.
The most common abdominal manifestation of sarcoidosis is hepatosplenomegaly, although marked splenic enlargement is rare. Less often seen are splenic nodules (18), an appearance called spotted spleen. Usually these splenic nodules are larger than their counterparts in the liver. They are not specific to sarcoidosis and are also found with some malignancies and infec- tions. Punctate calcifications develop in some sarcoid spleens; these calcifications are readily identified by imaging and are similar to those seen with histoplasmosis and tuberculosis.
Chest radiography is normal in some patients with splenic sarcoidosis.
Computed tomography reveals sarcoid nodules to be hypodense to splenic parenchyma and hypointense on MRI; they are best identi- fied on T2-weighted fat-suppressed images and on immediate contrast-enhanced images.
Ultrasonography reveals solid, hypoechoic foci.
Extraperitoneal adenopathy is common.
Computed tomography also often detects an
increased number of normal-sized lymph
nodes.
Virus-Associated Hemophagocytic Syndrome
Virus-associated hemophagocytic syndrome consists of erythrocyte and other blood element phagocytosis in multiple organs, including the spleen. Magnetic resonance imaging in a patient with acute lymphocytic leukemia and virus-associated hemophagocytic syndrome revealed multiple, round splenic signal voids believed to represent hemosiderin deposits (19).
Tumors
Nonneoplastic
Inflammatory Tumor
The term inflammatory tumor, also called
inflammatory pseudotumor and inflammatory myofibroblastic tumor,describes a focal inflammatory and reactive response in the spleen. The etiology of these rare tumors is unknown. They consist of a discrete encapsu- lated tumor containing a mixture of spindle cells suggesting myofibroblasts, inflammation, fibrosis, and necrosis.
They vary considerably in size and number.
Some are quite large. They contain a mix of solid and cystic components. Computed tomography reveals a heterogeneous tumor. A central scar is suggested in some. They enhance less than normal spleen on early phase CT, but delayed enhancement is evident on later phases. They are heterogeneous and hypo- to isointense to splenic parenchyma on T1- and hypo- to hyper- intense on T2-weighted MR images. Similar to CT, delayed enhancement is evident post- gadolinium. Their overall appearance is non- specific and a preoperative diagnosis is difficult;
the differential includes a malignancy.
A number of patients with an eventually diag- nosed splenic inflammatory tumor have under- gone a splenectomy.
Hemangioma
Some authors classify splenic hemangiomas under neoplasms, together with angiomas
and angiosarcomas. Although imaging findings overlap somewhat for these entities, patho- genetically hemangiomas are generally consid- ered to be development anomalies and probably should be classified under hamartomas, but they have a sufficiently unique imaging appear- ance that they are discussed separately; keep in mind that an occasional splenic hemangioma exhibits sarcomatoid changes.
Splenic hemangiomas range from single to multiple. Multiple hemangiomas occur in the Klippel-Trénaunay-Weber syndrome. Heman- gioma complications include hemorrhage and rupture. One infant with splenic heman- giomatosis had life-threatening thrombocy- topenia, anemia and intravascular coagulopathy (Kasabach-Merritt syndrome) (20); whether these tumors indeed represented heman- giomatosis or a hemangioendothelioma is not clear.
Similar to liver hemangiomas, CT shows a low-density tumor with a peripheral hypervas- cular contrast-enhancing rim. Unlike in the liver, however, splenic hemangiomas less often show progressive central enhancement (Fig.
15.7).
Gray-scale US reveals hemangiomas as well- marginated, homogeneous and hyperechoic tumors (Fig. 15.8).
Figure 15.7. Presumed splenic hemangioma. Early contrast- enhanced CT image reveals a hypodense tumor. Delayed views showed that this tumor fills in from the periphery and becomes nearly isodense with the spleen. A similar tumor was present on CT images 19 months previously. (Courtesy of Patrick Fultz, M.D., University of Rochester.)
A majority of splenic hemangiomas are hyperintense on T2-weighted MRI relative to the spleen; similar to liver hemangiomas, dynamic MRA reveals progressive centripetal enhance- ment in most, with eventual uniform enhance- ment. They differ from liver hemangiomas in achieving earlier homogeneous contrast enhancement rather than exhibiting gradual enhancement from the periphery inward.
A Tc-99m–red blood cell scan shows a typical hemangioma as a photopenic lesion during perfusion and on early blood pool images, with
subsequent filling-in on delayed images.
Technetium-99m–human serum albumin (HSA) reveals radiotracer accumulation within a hemangioma.
With a suspected hemangioma in an asymp- tomatic patient serial US is useful to evaluate any change.
Peliosis
Splenic peliosis is considerably less common than peliosis hepatis. Peliosis has developed in
Figure 15.8. Splenic hemangiomatosis in a 6-year-old boy. Pre- contrast (A) and intravenous contrast-enhanced (B) CT reveals multiple nonenhancing cysts in the spleen. C: Ultrasonography identifies hyperechoic foci in the spleen. (Courtesy of Luann Teschmacher, M.D., University of Rochester.)C A
B
splenic hamartomas and in splenic parenchyma (21). Splenic peliosis can result in spontaneous splenic rupture, probably due to minor trauma.
The imaging appearance of splenic peliosis is similar to that seen in the liver. Computed tomography reveals hypodense tumors.
Hamartoma
The rare splenic hamartoma, or splenoma, is believed to be congenital in origin. Two types occur: white pulp, composed of aberrant lym- phoid tissue, and red pulp, composed mostly of sinuses. Often a mix of both is found. A histopathologic differentiation from lymphoma is possible with most of these tumors. Most are detected incidentally. An occasional one is asso- ciated with thrombocytopenia or pancytopenia.
The CT appearance is similar to that seen with hamartomas in other locations. They range from homogeneous to heterogeneous. Most do not contain calcifications. Some have a cystic component. They tend to be isodense to splenic tissue. Some exhibit prolonged contrast enhan- cement. US reveals a well-marginated and some- what hypoechoic tumor, at times containing multiple punctate foci, probably representing necrosis.
Most hamartomas are isointense on T1- and hyperintense on T2-weighted images. They have heterogeneous early postcontrast enhancement, often enhancing more uniformly on delayed images. Some hamartomas, however, have an enhancement pattern similar to hemangiomas.
Prolonged enhancement on postcontrast CT and MR images differentiates these lesions from most malignancies. Aside from necrotic regions, angiography reveals them to be hypervascular.
Most hamartoma have similar uptake of Tc-99m-HSA to hemangiomas. Radiocolloid uptake is less within the tumor than in a normal spleen.
Cysts
Pathologically, most splenic cysts can be divided into epithelial-lined cysts, which are develop- mental in origin, and nonepithelial cysts, which are mostly sequelae of a prior hematoma. Radi- ologists often refer to both types as simple
cysts, which is a descriptive term. Except forechinococcal cysts, infections rarely result in a splenic cyst.
A simple cyst, either developmental or post- traumatic, has a well-defined wall, consists of fluid density, and does not enhance post- contrast. Some cysts contain septa. Hemor- rhage into a simple cyst or the presence of cholesterol crystals result in hyperechoic fluid.
Calcifications eventually develop in some cyst walls.
A large splenic cyst is one of the causes of splenomegaly.
Simple cysts have been treated by laparo- scopic spleen-preserving surgery.
Epithelial Cysts
Most developmental cysts, also called epider-
moid cysts, mesothelial cysts, primary cysts, and true cysts, probably represent sequelae ofmesothelial cell remnants trapped in splenic tissue. Several familial splenic cysts are reported. Some authors classify hemangiomas and cystic lymphangiomas as true cysts.
These cysts tend to be asymptomatic until trauma, at times minor, leads to hemorrhage and an increase in cyst size and then rupture.
At times infection or compression of adjacent structures reveals its presence. Most are unilocular.
Prenatal US identified a splenic cyst at 31 weeks’ gestation (22); the cyst had sponta- neously regressed when the infant was 7 months of age.
Nonepithelial Cysts
The majority of cysts encountered in the West are posttraumatic; these do not have an epithe- lial lining and are also called pseudocysts,
hemorrhagic cysts, and serosal cysts. At timesprior hematoma-inducing trauma was relatively minor and is not remembered. Eventually a hematoma evolves into a nonepithelial cyst con- taining serous fluid.
Pancreatic Pseudocyst
Some cysts originating in an adjacent structure
involve the spleen to the extent that imaging will
suggest a splenic origin. For example, a pancre-
atic pseudocyst (also called a false cyst) arising
from the tail of the pancreas can extend into the
spleen and appear intrasplenic. Also in the dif-
ferential is an abscess and a cystic or necrotic neoplasm.
These cysts can be drained percutaneously.
Lymphangioma
Splenic lymphangiomatosis consists of multiple endothelial-lined cysts; it is a rare tumor. Some are associated with splenomegaly or hyper- splenism. Most are discovered incidentally. Not uncommonly, liver and other site lymphan- giomas are also identified.
Imaging typically shows a multilocular cyst or multiple thin-walled cysts, most often sub- capsular in location. An occasional one contains curvilinear calcifications. They are hypodense and do not enhance with postcontrast CT. Occa- sionally diffuse lymphangiomatosis appears on postcontrast CT as a mottled spleen. They are hyperintense on T2-weighted images, except that cyst septa, consisting of fibrous connective tissue, appear hypointense.
Hydatid disease is in the differential diagno- sis of a cystic lymphangioma.
Whether these patients should be treated (resection or embolization) or whether observation is appropriate depends on symptomatology.
Neoplasms
Angioma/Angiosarcoma
An angioma is an unusual splenic tumor that is difficult to classify. This rare, benign vascular tumor is composed of anastomosing vascular channels containing papillary projections.
Littoral cell angiomas are rare neoplasms origi- nating from cell lining sinuses (littoral cells) rather than larger vessels and have chara- cteristic immunohistochemical properties. For unknown reason, anemia or thrombocytopenia develops in some patients. These tumors range from a focal tumor, to a miliary pattern, to ones replacing most of the spleen. Most are benign, although a littoral cell angiosarcoma also occurs. Littoral cell angiomas are hypodense rel- ative to normal spleen tissue (23); dynamic CT reveals progressive and homogeneous contrast enhancement to the point that they resemble normal splenic parenchyma.
A primary angiosarcoma is a rare but highly malignant splenic neoplasm. It can involve accessory spleens. Splenomegaly is not uncom- mon and spontaneous splenic rupture does occur with angiosarcomas. Imaging of some of these tumors suggests abscesses.
Only a few MR findings of primary splenic angiosarcomas are reported. One was hypoin- tense both on T1- and T2-weighted images, which differentiates it from most hemangiomas (24); intratumoral hemorrhage and necrosis were evident. Postgadolinium imaging revealed heterogeneous enhancement.
Lymphoma
The most common focal splenic tumor is malignant lymphoma. Most primary splenic lymphomas appear as a large, solitary tumor;
multifocal tumors are less common. These tumors tend to enhance less than splenic parenchyma on postcontrast CT. Only an occa- sional one shows rim enhancement (Fig. 15.9).
The majority of primary lymphomas are hypo- echoic on US.
Splenomegaly is common but not universal with splenic involvement by lymphoma. Con- versely, splenomegaly may be due to some other underlying disorder. Calcifications are unusual, but have developed in both untreated and, more often, treated lymphoma. Large necrotic nodules mimic an abscess (Fig. 15.10).
Aside from splenomegaly, splenic involve- ment by systemic lymphoma tends to be missed by imaging. In particular, diffuse lymphoma- tous infiltration is difficult to detect. To put splenic involvement by systemic lymphoma in perspective, among 680 patients with malignant lymphoma, US revealed abnormal splenic texture in only 15% (25); among these, about one third each were Hodgkin’s disease, low- grade non-Hodgkin’s lymphoma, and high- grade non-Hodgkin’s lymphoma.
The US appearance of lymphoma involving
the spleen varies considerably (25): diffuse
involvement in 37%, small nodular in 39%, large
nodular in 23%, and bulky in 2%. High-grade
non-Hodgkin’s lymphomas were either large
nodular or small nodular, while low-grade non-
Hodgkin’s lymphomas and Hodgkin’s disease
were either diffuse or had a small nodular
pattern.
Contrast-enhanced MR reveals diffuse splenic infiltration to have immediate heteroge- neous enhancement, becoming isointense on delayed views. Focal lymphoma is hypointense on immediate postcontrast images.
Leukemia
Diffuse leukemic infiltration of the spleen results in a homogeneously enhancing en- larged spleen. Associated lymphadenopathy is common.
Laparoscopic splenectomy is feasible in patients with leukemia and Hodgkin’s lymphoma.
Plasmacytoma/Multiple Myeloma
The rare primary splenic plasmacytoma most often presents with splenomegaly. Some of these patients develop disease progression after splenectomy but in an atypical fashion for multiple myelomas.
Metastases
An isolated metastasis to the spleen is not common. Presumably most abnormal cells are destroyed in the spleen. Colon, lung, ovarian, and other cancers result in multiple metastases, generally late in the course and most metastases
Figure 15.9. Solitary lymphoma. A: Transverse contrast-enhanced CT identifies a hypodense tumor with rim enhancement (arrow).B: The tumor is hypoechoic on longitudinal US (arrows). (Source: Dachman AH, Buck JL, Krishnan J, Aguilera NS, Buetow PC. Primary non-Hodgkin’s splenic lymphoma. Clin Radiol 1998;53:137–142, with permission from the Royal College of Radiologists.)
A B
Figure 15.10. Splenic lymphoma. A: Splenomegaly is present (white arrows). Mottled gas (arrowheads) outlines nodules (curved arrows) in a necrotic cavity. B: The necrotic cavity is better identified on contrast-enhanced CT. A gas-fluid level is present in an irreg- ular, nodular cavity. (Source: Dachman AH, Buck JL, Krishnan J, Aguilera NS, Buetow PC.Primary non-Hodgkin’s splenic lymphoma.Clin Radiol 1998;53:137–142, with permission from the Royal College of Radiologists.)
A B
are small. At times a necrotic metastasis mimics a cyst. Only an occasional melanoma is encountered.
Calcifications develop in an occasional slow- growing tumor. Most metastases are hypodense on CT and are isointense on precontrast MR images; the exception is a melanoma, which often has a heterogeneous appearance.
Metastases appear hypointense on immediate postcontrast MR images, becoming isointense on delayed images.
Diffuse splenic metastases can be missed by CT. Thus a diffuse metastatic seminoma was not detected by CT but was evident on FDG-PET (26).
Other Neoplasms
The rare cystadenocarcinoma probably arises from embryonic rests or mesothelium.
Splenic leiomyosarcomas are very rare.
Calcifications
Some of the conditions associated with splenic calcifications (Fig. 15.11) are listed in Table 15.2.
Hepatosplenic silicosis leads to calcifications in both the liver and spleen, and occasionally
even eggshell-like calcified lymph nodes. Con- ventional radiographs reveal numerous calcified nodules, which are better identified by CT.
Biopsy reveals birefringent particles within the nodules.
Vascular Disorders
Portal Hypertension
Idiopathic portal hypertension, or Banti’s disease, consists of anemia, splenomegaly, and portal hypertension. It is a distinct entity differ- ing from liver cirrhosis-associated portal hyper- tension in both its histopathology and portal hemodynamics.
Splenomegaly is common in portal hyper- tension. Regardless of etiology, the interrela- tionship between portal hemodynamics and splenomegaly is complex and poorly under- stood. A rare cause of portal hypertension but entailing a normal-size spleen is a splenic arte- riovenous fistula; contrast-enhanced imaging or Doppler US should be diagnostic of a fistula.
Duplex Doppler US appears useful in differ- entiating between congestive splenomegaly as seen in patients with liver cirrhosis and splenomegaly due to various myelo- and lym-
Figure 15.11. Extensive splenic calcifications detected by CT(arrow). Either tuberculosis or histoplasmosis can produce these changes. (Courtesy of Algidas Basevicius, M.D., Kaunas Medical University, Kaunas, Lithuania.)
Table 15.2. Conditions associated with splenic calcifications Posttraumatic cyst
Infection/inflammation Tuberculosis Histoplasmosis Brucellosis Hydatid cyst Healed abscess Atherosclerosis Hemangioma Neoplasm Infarcts Sickle cell disease Silicosis Thorotrast
phoproliferative disorders; the maximum portal flow velocity in patients with proliferative dis- ordersis normal, but is reduced in those with congestive splenomegaly.
Leukopenia and thrombocytopenia develop in patients with cirrhosis, portal hypertension, and hypersplenism. In this clinical setting, patients with a superimposed hepatocellular carcinoma undergoing transcatheter hepatic arterial embolization also underwent partial splenic embolization and infarction (27); the leukopenia and thrombocytopenia were cor- rected in a majority of patients if more than 50% of their spleens were infarcted.
Infarction
Vascular emboli result in focal splenic infarc- tion, at times multiple. Splenic artery thrombo- sis is associated with total splenic infarction.
Rarely, a splenic infarct occurs in a setting of congestive splenomegaly or pancreatitis, at times together with splenic vein thrombosis and possibly other infarctions. The risk of infarction is increased in a setting of portal hypertension.
Rarer causes of splenic infarction include sys- temic mast cell disease (28) and celiac disease (29); the latter is also associated with splenic venous thrombosis.
Occasionally intrasplenic gas bubbles are detected after a major infarct; they develop even without an infection.
An infarct is a common cause of a focal splenic tumor. A typical infarct is wedge-shaped and located adjacent to the splenic capsule. Less often an infarct has a round or nodular outline.
Computed tomography reveals lack of contrast enhancement. Occasionally a neoplasm has a similar appearance. The rare total splenic infarction shows only peripheral contrast enhancement, presumably secondary to a cap- sular artery supply. Nevertheless, the lack of splenic contrast enhancement is not pathogno- monic of a total infarction; a more common cause is severe hypotension.
Initially after an infarct, US reveals a hypoe- choic tumor. Later, scarring results in a gradual hyperechoic appearance. Similar to CT, infarcts are identified on delayed postcontrast MRI as hypointense wedge-shaped regions adjacent to the capsule.
Immunosuppression
Abnormal CT scans in HIV patients should not be routinely ascribed to AIDS; a second disease, consisting of either superimposed infection or a neoplasm is most often responsible for abnor- mal findings.
Hepatosplenic abscesses are not uncommon in AIDS patients, often being secondary to unusual organisms. Most are small and multi- ple. An US “snowstorm” appearance is found with some opportunistic liver and spleen infec- tions, reflecting fibrosis or a fibrinous exudate.
Abdominal US with a 3.5-MHz transducer will miss small abscesses in these patients; a 5-MHz transducer should identify more abscesses.
Similar to other patients, splenic tuberculous abscesses in immunocompetent patients are hypodense on CT and hypoechoic on US.
Examination and Surgical Complications
Splenectomy
Compared to an open splenectomy, in both adults and children a laparoscopic splenectomy requires a longer operative time but the patient’s overall hospital stay is shorter. Most laparo- scopic splenectomies are performed for a normal-sized or moderately enlarged spleen, although a laparoscopic approach is feasible in a patient with marked splenomegaly. Some surgeons believe that if the spleen is enlarged, preoperative splenic artery embolization makes laparoscopic splenectomy easier (30).
Following splenectomy, residual splenic tissue can be identified with In-111–labeled autologous platelet SPECT.
An increased risk for postsplenectomy infection is well known. Splenectomy results in depressed phagocytosis and a decrease in serum levels of immunoglobulin M (IgM). The consequences of splenectomy are not trivial, especially in children and in those undergoing splenectomy as part of lymphoma therapy. This risk tends to lessen after several years.
A subphrenic abscess is a recognized compli-
cation after splenectomy, developing either
shortly after surgery or, less commonly, on a
delayed basis. Computed tomography should detect a subphrenic abscess, but keep in mind that an occasional abscess mimics an intact spleen. Image-guided drainage is generally the treatment of choice, with surgery reserved for multiseptated abscesses or if percutaneous drainage fails.
Thorotrast
Thorotrast deposits can be visualized in the spleen with conventional radiography and CT.
The spleen tends to be atrophic.
A Thorotrast-induced angiosarcoma is rare in the spleen, with most occurring in the liver.
The effect of prior Thorotrast use is discussed further in Chapter 7.
References
1. Lieberman S, Libson E, Maly B, Lebensart P, Ben-Yehuda D, Bloom AI. Imaging-guided percutaneous splenic biopsy using a 20- or 22-gauge cutting-edge core biopsy needle for the diagnosis of malignant lymphoma. AJR 2003;181:1025–1027.
2. Deux JF, Salomon L, Barrier A, Callard P, Bazot M. Acute torsion of wandering spleen: MRI findings. AJR 2004;182:1607–1608.
3. Lorberboym M, Vallabhajosula S, Lipszyc H, Pastores G.
Scintigraphic evaluation of Tc-99m-low-density lipo- protein (LDL) distribution in patients with Gaucher disease. Clin Genet 1997;52:7–11.
4. Kimura F, Ito H, Shimizu H, et al. Partial splenic embolization for the treatment of hereditary spherocy- tosis. AJR 2003;181:1021–1024.
5. Shanmuganathan K, Mirvis SE, Boyd-Kranis R, Takada T, Scalea TM. Nonsurgical management of blunt splenic injury: use of CT criteria to select patients for splenic arteriography and potential endovascular therapy.
Radiology 2000;217:75–82.
6. Moore EE, Cogbill TH, Jurkovich GJ, Shackford SR, Malangoni MA, Champion HR. Organ injury scaling:
spleen and liver (1994 revision). J Trauma 1995;38:
323–324.
7. Sivit CJ, Frazier AA, Eichelberger MR. Prevalence and distribution of extraperitoneal hemorrhage associated with splenic injury in infants and children. AJR 1999;172:1015–1017.
8. Kimpel M, Zander T, Dux M. [Spontaneous occult splenic rupture after Salmonella enteritidis infection.]
[German] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 2001;173:380–381.
9. Resende V, Petroianu A. Subtotal splenectomy for treat- ment of severe splenic injuries. J Trauma 1998;44:
933–935.
10. Emery KH, Babcock DS, Borgman AS, Garcia VF. Splenic injury diagnosed with CT: US follow-up and healing rate in children and adolescents. Radiology 1999;212:
515–518.
11. Bittar I, Cohen Solal JL, Cabanis P. [Volvulus of the mobile spleen. Conservative laparoscopic treatment.]
[French] Presse Med 2001;30:1005–1006.
12. Hierholzer J, Fuchs H, Menzel B. [Intrahepatic spleno- sis.] [German] Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 2001;173:769–771.
13. Rickert CH, Maasjosthusmann U, Probst-Cousin S, August C, Gullotta F. A unique case of cerebral spleen.
Am J Surg Pathol 1998;22:894–896.
14. Warshauer DM, Molina PL, Worawattanakul S. The spotted spleen: CT and clinical correlation in a tertiary care center. J Comput Assist Tomogr 1998;22:694–
702.
15. Tohme A, Hammoud A, el Rassi B, Germanos-Haddad M, Ghayad E. [Human brucellosis. Retrospective studies of 63 cases in Lebanon.] [French] Presse Med 2001;
30:1339–1343.
16. Harned RK 2nd, Thompson HR, Kumpe DA, Narkewicz MR, Sokol RJ. Partial splenic embolization in five chil- dren with hypersplenism: effects of reduced-volume embolization on efficacy and morbidity. Radiology 1998;209:803–806.
17. Monzawa S, Tsukamoto T, Omata K, Hosoda K, Araki T, Sugimura K. A case with primary amyloidosis of the liver and spleen: radiologic findings. Eur J Radiol 2002;41:237–241.
18. Thanos L, Zormpala A, Brountzos E, Nikita A, Kelekis D.
Nodular hepatic and splenic sarcoidosis in a patient with normal chest radiograph. Eur J Radiol 2002;41:10–11.
19. Zilkha A, Madan V, Leonidas JC, Valderrama E. Liver and spleen MRI findings in virus-associated hemophagocytic syndrome in a patient with acute lymphocytic leukemia. Pediatr Radiol 1998;28:920–
922.
20. Schulz AS, Urban J, Gessler P, Behnisch W, Kohne E, Heymer B. Anaemia, thrombocytopenia and coagu- lopathy due to occult diffuse infantile haemangiomato- sis of spleen and pancreas. Eur J Pediatr 1999;158:
379–383.
21. Lam KY, Yip KH, Peh WC. Splenic vascular lesions:
unusual features and a review of the literature. [Review]
Aust N Z J Surg 1999;69:422–425.
22. Yilmazer YC, Erden A. Complete regression of a congenital splenic cyst. J Clin Ultrasound 1998;26:223–
224.
23. Levy AD, Abbott RM, Abbondanzo SL. Littoral cell angioma of the spleen: CT features with clinicopatho- logic comparison. Radiology 2004;230:485–490.
24. Imaoka I, Sugimura K, Furukawa M, Kuroda S, Yasui K.
Computed tomography and MR findings of splenic angiosarcoma. Radiat Med 1999;17:67–70.
25. Gorg C, Weide R, Schwerk WB. Malignant splenic lym- phoma: sonographic patterns, diagnosis and follow-up.
Clin Radiol 1997;52:535–540.
26. Lenzo NP, Moschilla G, Patrikeos A. Diffuse splenic metastases from seminoma visualized on FDG PET. AJR 2004;183:525–527.
27. Han MJ, Zhao HG, Ren K, Zhao DC, Xu K, Zhang XT.
Partial splenic embolization for hypersplenism
concomitant with or after arterial embolization of hepatocellular carcinoma in 30 patients. Cardiovasc Intervent Radiol 1997;20:125–127.
28. Maruyama H, Sugihara S, Ishihara K, et al. Systemic mast cell disease with splenic infarction: a case report.
Pathol Int 1998;48:403–411.
29. Andres E, Pflumio F, Knab MC, et al. [Splenic thrombosis and celiac disease: a fortuitous association?] [French]
Presse Med 2000;29:1933–1934.
30. Poulin EC, Mamazza J. Laparoscopic splenectomy:
lessons from the learning curve. Can J Surg 1998;41:
28–36.
