Doppler Sonography of the Spleen

Franke, Doris; Deeg, Karl-Heinz

doi:10.1007/978-3-319-03506-2_7

Doris Franke⁴ &
Karl-Heinz Deeg⁵

1786 Accesses
1 Citations

Abstract

Although the spleen is highly vascularised, the rate of focal lesions is far less frequent than in other abdominal organs, such as the liver or kidneys, possibly due to protective factors from the phagocytic and immunological competence of the spleen. Common pathological findings like splenic cysts, infarction or trauma can be diagnosed by ultrasonography with a high sensitivity and specificity. Other pathologies of the spleen such as focal splenic lesions are often unspecific and need further diagnostic evaluation.

In this chapter on Doppler sonography of the spleen in infants and children, the main indications, normal findings and the most common splenic pathologies in children are described. Special subsections deal with the ultrasound assessment of splenic involvement in infectious diseases, benign and malignant focal lesions, vascular pathologies (splenic aneurysms, infarction, peliosis), congenital alterations (wandering spleen, splenunculi, polysplenia) and trauma.

Access provided by Autonomous University of Puebla. Download chapter PDF

Ultrasonography of the pediatric spleen: a pictorial essay

Article 16 November 2018

The Spleen

Abdominal Ultrasound—Liver, Spleen and Biliary Tree

Keywords

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

7.1 Introduction

The spleen may be affected in a wide variety of diseases in children. Nevertheless, it is an often neglected organ in diagnostic imaging as primary splenic lesions are rare.

Focal and diffuse alterations of the splenic parenchyma rarely originate from splenic diseases, but represent mostly secondary involvement of the spleen in systemic diseases. The spleen is the largest single lymphatic organ of the body. It has a diaphragmatic and a visceral surface.

Within the spleen two different functional and morphological systems are combined: the red pulp and the white pulp. The red pulp is building extensive vascular sinusoids with phagocytic, haematopoietic and, in humans less importantly, blood pooling functions. The white pulp is consisting of lymph follicles with immunological activities. In newborns and early infancy, the red pulp predominates. Later, the white pulp increases with the child’s growth and immunological stimuli. However, with ultrasonography (US), no differentiation of red and white pulp is possible.

Although the spleen is highly vascularised, the rate of focal lesions is far less frequent than in other abdominal organs such as the liver or kidneys, possibly due to protective factors from the phagocytic and immunological competence of the spleen. Common pathological findings such as splenic cysts, infarction or trauma can be diagnosed by ultrasonography with a high sensitivity and specificity. Other pathologies of the spleen such as focal splenic lesions are often unspecific and need further diagnostic evaluation (Bachmann and Görg 2004; Sivit and Siegel 2002).

7.2 Normal Findings

7.2.1 Embryology and Vascular Anatomy of the Spleen

The spleen originates from the dorsal mesogastrium in the fifth embryonic week and is lobulated in embryonic life. It is protected by the 9th through the 11th rib. The visceral peritoneum forms the splenic capsule and adheres to the gastrosplenic and splenorenal ligaments as well as to the greater omentum. The splenic artery is the biggest branch (diameter up to 0.5 cm in adolescents and adults) (Fig. 7.1) (Görg 2011) of the coeliac trunk. The splenic artery can be displayed by colour-coded Doppler sonography along its entire, in older patients often serpentinous, course (Fig. 7.2a, b). Branches of the splenic artery supply the corpus and tail of the pancreas (Aa. pancreaticae magnae and dorsales), the fundus and great curvature of the stomach and the major omentum until the splenic artery reaches the spleen. Here, the splenic artery divides into several branches at the splenic hilus and divides within the spleen into segmental, subsegmental and subsubsegmental arteries, which extend into the splenic capsule (Fig. 7.3).

The splenic vein drains the blood from the spleen in 2–6 branches at the hilus and forms, together with the superior mesenteric vein, the portal vein at the splenoportal confluence. The inferior mesenteric vein is the biggest vein which drains into the splenic vein (variance of 30 % into the superior mesenteric vein). Furthermore, the left gastric vein, the small gastric veins (Vv. gastricae breves) and the gastroepiploic veins drain into the splenic vein. The inflow of the inferior mesenteric vein into the proximal pancreatic part of the splenic vein can only rarely be visualised by ultrasonography.

7.2.2 Ultrasonographic Approach

The easiest approach for visualisation of the splenic vessels is a transverse section through the upper abdomen. The artery runs at the superior border of the pancreas, usually localised more cranially than the vein. The middle portion of the artery can also be shown in longitudinal sections through the upper abdomen with the transducer slightly angled to the left side (Fig. 7.4a–f). The artery is always neighboured by the splenic vein, which can be imaged behind the pancreatic corpus and tail in transverse and longitudinal sections (Fig. 7.5a–d). Using B-mode ultrasonography (US) alone, both vessels cannot be exactly distinguished. With the help of the different Doppler techniques (colour or spectral Doppler), however, artery and vein can easily be differentiated. From the left lateral intercostal approach, the splenic hilus and the intrasplenic vessels can be demonstrated (Fig. 7.6a, b).

The investigation of the spleen can be performed non-fasting and without special preparation in the supine position or lying on the right side.

Transducers: The appropriate transducer frequency has to be chosen depending on the age/size of the patient and the indication. In neonates, infants and for the detection of smaller focal lesions, high-resolution linear transducers up to 15 MHz are optimal (Fig. 7.7a, b). Older children, especially obese adolescents, are best investigated with a curved array transducer <6 MHz, followed by an additional approach with a high-frequency transducer in order to detect smaller lesions, discontinuation of the splenic surface in cases of trauma and superficial minor vascular pathologies, which may not be detected with low-frequency curved array scanning (Fig. 7.9).

7.2.2.1 Colour and Pulsed Doppler Sonography (CDS and PW-DS)

Using colour-coded Doppler sonography (CDS) in a transverse mid-abdominal section, the flow in the splenic artery behind the pancreas can be displayed blue as the flow is directed away from the transducer (Fig. 7.4b, d). This translates into a negative flow in the splenic artery in pulsed waved (synonym: spectral) Doppler sonography (PW-DS) behind the pancreatic body (Fig. 7.4c, f) and a positive flow after the artery has passed the pancreatic tail (Fig. 7.4e).

In the splenic vein, however, the flow behind the body of the pancreas is directed towards the transducer and is therefore displayed red (Fig. 7.5b). Pulsed Doppler shows a forward flow displayed above the baseline (Fig. 7.5c). Similar to the flow in the portal vein, a nearly continuous positive flow with small undulations can be seen (Figs. 7.5c and 7.8).

The main indications for Doppler sonography (DS) of the spleen are listed in Table 7.1.

Table 7.1 Main indications for Doppler sonography (DS) of the spleen

Full size table

7.3 Splenic Trauma

The spleen is often injured in accidents, although it is shielded by the ribs of the left hemithorax, which usually protects the spleen from laceration. Enlarged spleens which tower below the costal arch are extremely vulnerable. In blunt abdominal trauma, injury of the spleen must always be ruled out as the spleen is the most common injured abdominal organ accounting for up to 45 % of all visceral injuries (Tataria et al. 2007). An enlarged spleen is far more at risk of being injured after blunt abdominal trauma. Sonographic signs of possible spleen injury are free abdominal fluid with internal echoes, splenomegaly, reduced respiratory movement, inhomogeneous texture of the spleen, subcapsular haematoma, anechoic lacerations within the parenchyma or disruption of the splenic capsule (Hofmann 2005) (Figs. 7.9a–d and 7.10a, b). In many emergency rooms, a FAST (focal abdominal sonography for trauma) protocol with scanning of the four abdominal quadrants for free fluid, as a sign for haemoperitoneum, is done and later followed by a complete and detailed US investigation after deciding on surgical or conservative therapy for a trauma patient. However, in a study by Richards in 2002, 12 % of children with abdominal injury had no free fluid. Contusions, lacerations, ruptures, fractures, subcapsular and perisplenic haematoma (Figs. 7.9b and 7.10a) of the spleen may be distinguished. Haemoperitoneum and active bleeding are the most likely indications for surgical intervention. Due to the thicker splenic capsule in children, operations in splenic trauma are less frequently compared to adults. In paediatric patients, haemodynamic stability is the most important determinant for conservative treatment. Following trauma, splenic healing can rapidly be observed. This was experienced in the last decades of predominately successful conservative management of splenic injuries. Because of devastating post-splenectomy infections with encapsulated bacteria such as Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae, splenectomy should be avoided whenever possible.

Long-term sequelae of splenic injury may be scarring of parts of the spleen, development of posttraumatic pseudocysts, polysplenia and calcification (Fig. 7.11). In 15–30 % of patients, a two-phase delayed splenic rupture may be expected within 2 weeks. Delayed complications, such as splenic abscesses and pseudoaneurysms of the splenic artery and its branches, have been observed (Lynn et al. 2009). To detect complications, a short follow-up by B-mode sonography and CDS should be scheduled (Goletti et al. 1996). In cases of suspected splenic injury, CDS with low flow settings and a low wall filter should be used (Fig. 7.12a). If a high-frequency curved array probe is used, power Doppler is especially helpful for the diagnosis of focal hypoperfusion of the organ (Fig. 7.12b). Areas without perfusion can be distinguished from the surrounding normal vascularised parenchyma. Lacerations are displayed as focal hypoechoic lesions. Power Doppler reveals missing perfusion, often in a triangular shape. Acute posttraumatic injury and lacerations of the spleen may not be visualised with B-mode due to diffuse swelling of the organ. In the detection of traumatic splenic injury, CEUS (contrast-enhanced ultrasonography) is much more sensitive than mere B-mode and Doppler US alone (see Sect. 7.8, Fig. 7.13; Manetta et al. 2009; Weskott 2013).

7.4 Focal Lesions of the Spleen

7.4.1 Introduction

Focal lesions of the spleen are rare (0.2 %, Bachmann and Görg 2005; Chen 2005; Görg 2011). Bachmann et al. described 98 adult patients with focal lesions and classified them as avascular, hypovascular, isovascular, hypervascular and arteriovenous “high flow”, using the surrounding splenic tissue as in vivo reference. Most of the focal splenic lesions (68.4 %) were avascular, 15.3 % appeared hypovascular, 8.2 % isovascular, 5.1 % hypervascular and in 3.1 % an arteriovenous “high-flow” pattern was found. Alongside the diagnosis of intrasplenic pseudoaneurysm, the practical utility of CDS in differentially diagnosing focal spleen lesions is low (Bachmann and Görg 2005). However, US has a role in the detection and follow-up of focal lesions. Cystic and solid lesions are distinguishable in B-mode scanning.

7.4.2 Benign Splenic Lesions

7.4.2.1 Cystic Lesions

Cystic lesions are most commonly dysontogenetic (simple cysts) followed by non-epithelialised pseudocysts (synonym: secondary cyst) and parasitic cysts (hydatid cyst, usually caused by Echinococcus granulosus).

Congenital, dysontogenetic cysts (synonyms: simple cyst, real cyst, epidermoidal cyst, primary cyst) are usually anechoic, round and solitary. They usually show a hyperechogenic epithelial lining at their borders to the splenic parenchyma (Fig. 7.14a, b), a dorsal acoustic enhancement and only occasionally thin septa.

Secondary cysts are diagnosed following trauma, infection or infarction. They are mostly not completely round; multiple and intraluminal septa are present more frequently. Doppler sonography shows no signals within cysts (Fig. 7.15a, b). The difference between a primary and a secondary cyst depends mainly on the presence of an epithelial wall surrounding the cyst. The differentiation is not always reliable with US.

The intracystic fluid of secondary cysts may have an increased echogenicity due to cholesterol crystals, inflammatory debris or haemorrhage. Parietal calcifications are more common in pseudocysts. Surgical enucleation of large cysts may be necessary, but procedures should always be organ preserving (Czauderna et al. 2006). Complications of nonparasitic splenic cysts include intracystic haemorrhage, rupture, peritonitis and hypersplenism (Czauderna et al. 2006).

Echinococcal parasitic infections have to be considered in the differential diagnosis of cystic lesions of the spleen, although splenic involvement is rarer than hepatic or pulmonary manifestations (Fig. 7.16). Splenic echinococcal involvement is reported only in 0.9–8 % of patients, usually in infants with multi-organ disease.

Isolated splenic parasitic cysts are even rarer. In early stages of echinococcal infection, a hyperperfused rim may be seen with DS. Hydatid sand, daughter cysts and infolded membranes may be visible within the cyst, but they can also appear purely cystic or solid. In later stages, calcifications may occur (Dilli et al. 2011). Another cause of parasitic cysts is porcine tapeworm (Taenia solium) infections (Benter et al. 2011).

Lymphangiomas consist of multiple vascular canals filled with lymphatic fluid. Therefore, they have a hypo- or anechoic, pluriseptate appearance with possible debris or calcification inside (Fig. 7.17a, b). Usually, no vessels can be detected inside lymphangiomas. In rare cases however, vessels can be seen within the septae of a lymphangioma. Lymphangiomas grow slowly. They may appear single or multiple (Paterson et al. 1999), mostly with a multicystic, “honeycomb” appearance, rarely like a solid tumour or a solitary cyst. Unlike haemangiomas, the capsule and trabeculae of the spleen, where lymphatic tissue is concentrated, are often involved. The clinical manifestation may range from a small incidental lesion to a large multicystic abdominal mass requiring surgical intervention (Abbott et al. 2004). In lymphangiomatosis, multiple organs are involved, most often the liver, mediastinum, axilla, neck and retroperitoneum.

7.4.2.2 Solid Lesions

Solid lesions show echoes within the lesions and may show perfusion in CDS and pulsed Doppler sonography. In CDS two-thirds of focal splenic lesions appear to be avascular (Bachmann and Görg 2005). The importance of imaging solid splenic lesions is to differentiate them from malignant lesions. For all imaging modalities (US, CT, MRI, CEUS), a definite differential diagnosis of solid splenic focal lesions is difficult.

Although rare, the most frequent benign solid splenic lesions are haemangiomas.

Haemangiomas usually appear hyperechogenic and in CDS often without signals (Taibbi et al. 2012). Their appearance in the spleen is non-specific on B-mode and CDS. Depending on the vessel size inside the haemangioma, capillary and cavernous types can be distinguished. The cavernous type has a combination of solid and cystic components and appears more sponge-like. Haemangiomas may occur solitary or multiple and are found more frequently in association with Klippel-Trénaunay-Weber, Turner or Beckwith-Wiedemann syndromes. Splenic haemangiomas are usually asymptomatic, but complications include bleeding, rupture and Kasabach-Merritt syndrome, a life-threatening consumptive coagulopathy due to disseminated intravascular coagulation starting in the abnormal haemangioma vessels with thrombocytopenia and anaemia (Peddhu et al. 2004). Most lesions are small and found incidentally in asymptomatic patients (Abbott et al. 2004); calcifications may occur.

CDS may reveal flow within the haemangioma; however, splenic haemangiomas often do not show the typical rim enhancement with centripetal inflow into the centre of the lesion as seen in hepatic haemangiomas especially in contrast-enhanced ultrasonography (CEUS) (Taibbi et al. 2012). Capillary haemangiomas and hamartomas seem to be the most likely diagnosis in hyperechogenic lesions, but in all cases a careful ultrasonographic follow-up is warranted (Görg et al. 2006). Even pathological differentiation of hamartomas from haemangiomas may be difficult in the individual case (Abbott et al. 2004).

Hamartomas (splenoma, splenadenoma or “FNH of the spleen”) are non-neoplastic lesions, which are composed of different splenic components apart from the white pulp. The hamartoma/splenoma was first described by the pathologist von Rokitansky in 1861. It consists of irregular red pulp with sinusoidal-like vessel structures and fibrous tissue (Günter 2005; Hartmann et al. 2008; Abramowsky et al. 2004), therefore also called “focal nodular hyperplasia (FNH) of the spleen”. They are typically solitary and asymptomatic; calcifications can be found. Their size varies up to 20 cm (Hartmann et al. 2008) and splenomegaly is usually present. CDS may depict hypervascularity with multiple intralesional colour flow signals distributed in a radial fashion (Görg and Schwerk 1994 and Peddhu et al. 2004). Hamartomas are usually well-described nodular lesions, which tend to compress the adjacent parenchyma. Calcification secondary to ischaemia or haemorrhage is rare.

Mostly the discovery of a hamartoma/splenoma is incidental; in one case out of 170 described, a spontaneous rupture occurred (Günter 2005). Hamartomas are thought to be congenital in origin, and splenic hamartomas have been associated with further hamartomas in other organs such as in patients with tuberous sclerosis or Wiskott-Aldrich-like syndromes (Abbott et al. 2004). However, the aetiopathology remains unclear.

Haemangioendotheliomas are benign vascular tumours with sometimes significant morbidity (organ enlargement, Kasabach-Merritt syndrome and congestive heart failure). The US appearance in the spleen is non-specific; they are mostly described as hypoechoic. Anechoic areas may represent intralesional necrosis compared to the normal splenic parenchyma. Haemangioendotheliomas are hypovascularised in CDS. Calcifications are not a specific feature.

More rare benign manifestations of focal splenic lesions are lipomas and angiomyolipomas (Fig. 7.18).

Littoral cell angioma of the spleen is a rare vascular tumour seen at any age with no gender predisposition. Originally, littoral cell angiomas were thought to be benign, but also malignant features have been described (Abbott et al. 2004). Splenomegaly is almost always present. Littoral cell angioma originates from the red pulp sinuses. In US, lesions are usually multiple. They may have the same echogenicity as the spleen or may be hyper- or hypoechoic. They may be innumerable and confluent, then appearing diffusely with heterogeneous echotexture of the spleen.

Langerhans cell histiocytosis with proliferation of bone marrow-derived histiocytes causes diffuse or focal hypoechoic nodules in the spleen, which vanish after therapy (Paterson et al. 1999) (Fig. 7.19a–c).

7.4.3 Malignant Manifestations in the Spleen

In children and adults, the most frequent malignant manifestations in the spleen are lymphomas (Fig. 7.20a), which may be diffuse, nodular (with small size <3 cm and large size >3 cm) or bulky with extremely large and inhomogeneous lesions. Lymphomas of low malignancy present in B-mode US diffuse or with small nodules, whereas highly malignant lymphomas tend to have larger nodules or bulky disease (Weskott 2012; Benter et al. 2011). The echogenicity of the lesions may be hypoechoic or more rarely (<10 %, Görg 2011) hyperechoic. Doppler US may depict increased vascularity within the lesions (Fig. 7.21); however, there are no reliable differential diagnostic signs. In children with known lymphoma, hypoechoic focal splenic lesions are highly suspicious of being of malignant origin because of the low incidence of focal lesions in the spleen. Thus, the incidental finding of a focal hypoechoic lesion within the spleen should also be suspicious of being a lymphoma.

Contrast-enhanced US (CEUS) is more helpful than Doppler sonography in distinguishing benign from malignant splenic lesions (Fig. 7.21b) (Sutherland et al. 2011; von Herbay et al. 2009; Stang et al. 2011; Chiavaroli et al. 2011). Splenic lymphomas may show iso-, hyper- or hypoenhancement in the early phase of CEUS. In the late phase, all lesions demonstrated rapid wash-out after 60 s (von Herbay et al. 2009). Splenomegaly is usually associated. Normal texture and size of the spleen do not rule out lymphoma manifestation within the spleen. Calcification may occur after chemotherapy.

In the differential diagnosis of malignant focal splenic lesions, angiosarcomas, leiomyosarcomas (Fig. 7.22) and metastases from other paediatric tumours have to be considered. All of these tumours of the spleen are extremely rare.

Angiosarcoma is the most common non-lymphatic, aggressively malignant splenic tumour, usually diagnosed incidentally in older adults (Hartmann et al. 2008; Neuhauser et al. 2000). Unlike hepatic angiosarcoma, primary angiosarcoma of the spleen has no association with exposure to carcinogens.

The spleen is an uncommon organ for metastasis. Most metastases are hypoechoic, but occasionally also hyperechoic lesions with a “target sign” may be found (necrotic anechoic centre and hyperechoic rim). Splenic metastases are usually accompanied by a splenomegaly.

7.5 Vascular Pathologies

7.5.1 Splenic Aneurysms

Splenic vein aneurysms have rarely been reported in children and adults. They may occur during the course of systemic infections. Tolgonay reported spontaneous resolution of a splenic vein aneurysm in a patient with leukaemia (Tolgonay et al. 1998). After appropriate chemotherapy, the spleen diminished in size, and this decrease was accompanied by regression of the aneurysm. Colour Doppler sonography enables the noninvasive detection, diagnosis and follow-up of splenic vein or artery aneurysms.

7.5.2 Splenic Pseudoaneurysms

Pseudoaneurysms may occur after traumatic injury (Safavi et al. 2011). Although rare, traumatic splenic artery pseudoaneurysms can be life threatening. Yardeni presented a 10-year-old boy with a large splenic artery pseudoaneurysm. The pseudoaneurysm was successfully angiographically embolised, and subsequent abdominal CT demonstrated successful resolution of the pseudoaneurysm with a small residual splenic cyst (Yardeni et al. 2004). Unlike splenic artery pseudoaneurysms in adult patients, the severity of the splenic injury does not have predictive value for development of splenic artery pseudoaneurysm in children. Abdominal pain is the most frequent symptom of splenic artery pseudoaneurysm, but some children are asymptomatic at the time of diagnosis. Therefore, the possibility of splenic artery pseudoaneurysm should be ruled out even in the asymptomatic child with mild splenic injury.

As pseudoaneurysms may expand in a splenic haematoma and cause delayed splenic rupture, early diagnosis and treatment are crucial. Abdominal sonography may show free intraperitoneal fluid and an enlarged spleen with a heterogeneous area occupying parts of the organ (Fitoz et al. 2001).

Colour Doppler sonography may show flow within the lesions suggesting pseudoaneurysms.

Pulsed Doppler demonstrates turbulent arterial flow with high-flow amplitude.

In children with posttraumatic splenic pseudoaneurysm, spontaneous thrombosis is reported (Raghavan et al. 2004).

7.5.3 Splenic Infarction

Splenic infarction frequently occurs in patients with myeloproliferative diseases, endocarditis with cardiac emboli, storage disorders such as Gaucher disease and sickle cell anaemia. Various sonographic patterns of splenic infarction exist, but little is known about tumour-associated splenic infarction in cancer patients. In cancer patients with splenic infarction, an acute complete infarction is the most common pattern. It is caused predominantly by a hypercoagulable state and is associated with an extremely short survival rate (Görg et al. 2004). Özcan et al. (2006) described an 11-year-old girl with splenic infarction. The coeliac trunk and common hepatic artery were patent, whereas the splenic artery could not be visualised. Multiple collaterals were found at the splenic hilus region. The diagnosis of splenic artery occlusion was made. Massive gastric bleeding from submucosal gastric collateral vessels, secondary to the splenic artery occlusion, has been reported.

On CDS, identification of prominent collateral vasculature in the peripancreatic region and splenic hilus may be a clue to the diagnosis.

Splenic infarction may be associated with left upper quadrant abdominal pain, fever, chills, nausea, vomiting, pleuritic chest pain and left shoulder pain.

Splenic infarctions impose as triangular subcapsular hypoechoic lesions without perfusion (Fig. 7.23). The branches of the splenic artery are noncommunicating end arteries; therefore, sudden occlusion always leads to infarction. CDS or power Doppler shows absence of colour signals in the affected area, suggesting a lack of perfusion.

Splenic infarction has a high tendency to complete healing or the development of chronic infarction.

Chronic infarction develops in 17.5 % of patients with infarctions. It occurs predominantly in patients with sickle cell anaemia and myeloproliferative disease (Görg and Zugmaier 2003).

Two types of chronic infarction can be discerned (Görg and Zugmaier 2003):

Type I morphology can predominantly be found in homozygous sickle cell anaemia. It is sonographically characterised by a small or normal-sized spleen with diffuse, enhanced echogenicity and foci with diminished echogenicity.
Type II morphology is predominantly found in myeloproliferative diseases. It is characterised by an enlarged spleen with a homogeneous echotexture and solitary, triangular or hyperechoic splenic foci near the surface of the spleen. With colour-coded Doppler sonography, chronic infarcts are characterised by reduced flow signals or the absence of flow (Görg and Zugmaier 2003). Spontaneous splenic ruptures can complicate chronic infarcts in 21 %.

A functional hypo- or asplenia (“autosplenectomy”) may result after multiple splenic infarctions; after bone marrow transplantation, amyloidosis, radiation or associated with autoimmune diseases such as coeliac disease with a reduced size, isoechoic or hyperechoic parenchyma and presence of Howell-Jolly-bodies in the erythrocytes.

Colour Doppler sonography (CDS) revealed an absent flow in 17 %, a hilar flow in 71 % and hilar and parenchymal vascularisation in 12 % of patients with hypo-/asplenia in a study by Görg et al. (2003).

7.5.4 Peliosis

Peliosis is a rare condition of the reticuloendothelial system with multiple blood and thrombi-filled spaces, most often within the liver or in conjunction with hepatic and splenic manifestation. The appearance in US may be hyper- or hypoechogenic with various enhancement patterns after applying contrast media. Calcifications are not described. Peliosis of the spleen is nearly always secondary to an extrasplenic disease (Hartmann et al. 2008) and may be associated with disseminated tuberculosis, HIV, haematological malignancies, transplantation, anabolic hormones and steroid therapy (Paterson et al. 1999; Abbott et al. 2004). Aetiology and pathogenesis of peliosis are poorly understood. If peliotic lesions are located close to the capsule, rupture and life-threatening bleeding with fatal outcomes have been reported (Shimono et al. 1998; Benjamin and Shunk 1978). Fine-needle biopsy should therefore be avoided; the definite diagnosis and therapy is usually made with splenectomy. In CDS, peliosis appears as hypervascularised, blood-filled nodules or cysts with a size up to 1 cm.

7.5.5 Flow in the Splenic Vessels in Congestive Conditions

Splenomegaly is a common sign in congestive conditions, mostly due to chronic liver cirrhosis or portal hypertension after portal vein thrombosis. Bolognesi reported in 2012 that an estimation of the congestion in patients with right heart or congestive failure is possible by evaluation of the splenic pulsatility index and its relation to the hepatic vein diameter.

7.5.6 Flow in the Splenic Vessels in Portal Hypertension

Due to congestion in portal hypertension, splenomegaly is present in most of the children. The splenic vein and artery may increase in diameter and the course of the vessels may be more serpentine (Figs. 7.24 and 7.27c). Normally, the flow in the splenic vein is directed from the spleen to the liver. In portal hypertension however, flow in the splenic vein may either be reversed (Fig. 7.25) or biphasic with flow into portosystemic shunts (Barakat et al. 1998) (Fig. 7.26).

The development of variceal collateral flow at the splenic hilus is characterised by multiple echofree areas at the splenic hilus (Fig. 7.27a). Colour Doppler shows flow within the echofree areas characterising them as dilated veins (Fig. 7.27b, d, e). Pulsed-wave Doppler reveals the flow pattern and velocity.

Further details concerning the flow in the splenic, mesenteric and portal vein are described in the section on liver circulation and portal hypertension.

7.5.7 Thrombosis of the Portal Venous System after Splenectomy

Post-splenectomy thrombosis of the portal vein, mesenteric vein and splenic vein occurs in about 5 % of all patients after splenectomy. Possible risk factors are thrombocytosis and thrombophilic disorders (Stamou et al. 2006).

Age, gender, type or length of the operation and use of preoperative and postoperative thrombosis prophylaxis with low molecular weight heparin did not prove to be significant factors in the occurrence of post-splenectomy thrombosis (Stamou et al. 2006).

After laparoscopic splenectomy, thrombosis of the portal vein and its tributaries occurs more often (18.9 %) (Romano et al. 2006). In 8 % the thrombus extended from the splenic vein to occlude the portal axis. This complication was symptomatic in 11 %, whereas in the rest of the cases, the thrombosis was diagnosed incidentally in asymptomatic patients. Thrombosis occurred even as late as 2 months after splenectomy. Splenomegaly was the only significant factor predictive of thrombosis. Only those patients who were detected early with portal or splenic vein thrombosis had recanalisation of the veins with anticoagulant therapy (Brink et al. 2003). Patients with splenomegaly, who underwent laparoscopic splenectomy, are at special risk of thrombosis of the portal system and should undergo strict imaging surveillance and aggressive anticoagulation therapy (Romano et al. 2006).

Colour Doppler and pulsed-wave Doppler are able to show missing flow in the superior mesenteric vein, the splenic vein and the portal vein (Brink et al. 2003).

7.6 Splenic Involvement in Infectious Diseases

Various infectious diseases cause splenomegaly and usually no distinct morphological or vascular patterns help in the differential diagnosis. However, in Epstein-Barr virus infection, the increase in the splenic volume is especially rapid and marked (Fig. 7.28a, b). In rare cases spontaneous rupture of the organ may appear (Fig. 7.28a). 2D image shows a linear- or triangular-shaped zone of decreased echogenicity (Fig. 7.28a). Colour Doppler or power Doppler reveals the perfusion of the organ. At the site of rupture, no flow can be shown (Fig. 7.28b). Splenomegaly may be sudden and reversible in acute infections and sustained in chronic infections. Other causes of splenomegaly are infections with malaria with a homogenous enlarged spleen (Fig. 7.29a, b). Colour Doppler reveals increased vascularity. Power Doppler demonstrates good perfusion of the organ with no lack of focal perfusion. Pulsed Doppler reveals normal arterial and venous flow.

Cat-scratch disease is caused by infections with Bartonella henselae after bites or scratches from cats and dogs and is common in children (Weinspach et al. 2010). About 50 % of cats are seropositive; cat flees are thought to transmit Bartonella henselae. Immunologically compromised children especially may develop systemic manifestations with multiple small abscesses in the spleen or liver; otherwise the clinical course is usually benign and self- limiting within a few months. Typically, regional lymphadenopathy is present (Fig. 7.30); other non-specific signs are abdominal lymphadenopathy, hepatosplenomegaly and fever. The enlarged lymph nodes are oval shaped and perfused by hilar vessels (Fig. 7.30).

Abscesses within the spleen resemble those in the liver and may occur solitary or multiple and are usually ill defined. Possibly due to the immunological competence of the spleen, abscesses in the spleen are far less frequent than in the liver, especially in nontropical countries (Fotiadis et al. 2008). Abscesses may be secondary to trauma, ischaemic infarcts or following infections. Gram-negative bacteria by haematogenic seeding are more common than gram-positive. Amoebic abscesses can be seen in certain epidemiological conditions. Especially, children with haemoglobinopathies and immunologically compromised children, such as patients with congenital or acquired immunodeficiency, intake of immunosuppressive medication, diabetes mellitus or chronic granulomatous disease (Fig. 7.31a, b), are at risk. In phases of neutropenia, the lesions and the hypervascularised rim zone around the abscess, which can be demonstrated by CDS, may transiently disappear. Usually the abscesses are hypoechogenic and may contain echogenic internal debris or gas bubbles (Fig. 7.31a) (Sutherland et al. 2010); later on calcification can develop. Colour Doppler usually shows no internal vessels in the abscess (Fig. 7.31b).

Postinfectious granuloma within the splenic parenchyma may be seen as multiple hyperechoic lesions after tuberculosis, histoplasmosis, mycobacterium avium and Pneumocystis carinii infection, especially in patients with acquired immune deficiency syndrome (Benter et al. 2011). These miliary lesions may calcify. Isolated splenic tuberculosis is extremely rare (Zhan et al. 2010).

Splenic lesions in visceral leishmaniasis (kala-azar) appear as multiple, small, hypoechogenic spots within the splenic parenchyma and are associated with hepatosplenomegaly (Saxena et al. 2011). In endemic countries, visceral leishmaniasis is an important differential diagnosis in diffuse splenic lesions.

In disseminated mycotic infections, especially found in immunologically compromised patients with lesions of the mucosal barriers, broad spectrum antibiotic treatment, chemotherapy and indwelling catheters, the spleen may be affected as well as the liver and, less frequently, the kidneys (Fig. 7.32). Mostly multiple small echogenic lesions with variable appearance are found; Candida albicans, Cryptococcus neoformans and Aspergillus spp. are the infectious agents. Ultrasonography is valuable in detection and follow-up of lesions. 2D images can show either hyperechoic or hypoechoic lesions which show no Doppler flow within the lesions.

7.7 Congenital Splenic Alterations

7.7.1 Wandering Spleen

A wandering spleen is a rare clinical entity resulting from congenital maldevelopment or acquired laxity of the spleen’s suspensory splenogastric and the splenorenal ligaments (Ayaz et al. 2012; Danaci et al. 2000; Paterson et al. 1999).

Torsion of a wandering spleen is a rare cause of abdominal pain in children and has been described in increased frequency in children with prune belly syndrome with deficient abdominal muscles (Teramoto et al. 1981). The most common presentation is acute abdominal pain, although signs and symptoms vary widely. Due to the risk of splenic infarction, rapid and accurate diagnosis is essential (Fig. 7.33e) (Di Crosta et al. 2009). The right decubitus position can help to identify the migration of the spleen (Chen et al. 2012). A rare complication is haemoperitoneum caused by acute splenic torsion of a wandering spleen (Lopez-Tomassetti Fernandez et al. 2006).

Wandering spleen and splenic torsion can be diagnosed by Doppler ultrasound (Fig. 7.33c, e) (Romero and Barksdale 2003). Confirmatory findings would include absence of the spleen in its normal location and demonstration of a splenic mass elsewhere in the abdomen or pelvis (Fig. 7.33).

Beside the location, the size and echogenicity of the spleen are investigated. Torsion of the spleen may be characterised by an increase in size of the organ and a change in echogenicity. The grey-scale US shows the displaced spleen as a homogeneous, hypoechoic mass suggestive of an enlarged, ectopic spleen in the central abdomen (Fig. 7.33a, b) (Danaci et al. 2000).

Spectral analysis and CDS demonstrate a normal vascular branching pattern and high diastolic flow due to low resistance in the vascular bed. The parenchymal resistance index of the mass is similar to that of the native spleen (Vural et al. 1999).

The aim of colour Doppler is the demonstration of normal or abnormal internal arteries and vessels. Complete torsion is characterised by a lack of demonstrable flow within the splenic parenchyma either on colour flow images or power Doppler (Fig. 7.33e) (Danaci et al. 2000; Nemcek and Miller 1991).

Pulsed Doppler may show pathological flow profiles in the arteries and veins. If torsion occurs, firstly, the peak flow falls in the splenic vein, then the diastolic forward flow in the splenic artery is decreased, due to an increase in the peripheral resistance (Nemcek and Miller 1991).

If no flow can be shown with colour or power Doppler, diagnosis of suspected torsion can be confirmed by contrast-enhanced ultrasonography (CEUS) (Fig. 7.33f). Treatment options include splenopexy or splenectomy.

7.7.2 Accessory Spleens (Splenunculi)

Accessory spleens are common (10–30 %). They may be solitary or multiple and usually don’t measure more than 4 cm (Fig. 7.34). They are most often located at the hilus region (Paterson et al. 1999; Peddhu et al. 2004; Elsayes et al. 2005). They have the same echogenicity and echotexture as the main spleen and are capable of hypertrophy. They may vary from a few millimetres to several centimetres in size and range from 1 to 6 in number. Intrapancreatic splenunculi are rare, but accessory spleens may be found anywhere in the abdomen.

7.7.3 Splenosis

After traumatic injury of the spleen, a diffuse spreading of splenic parenchyma in the abdominal cavity, called splenosis, may occur. Splenosis may protect children from bacterial infections after splenectomy. The nodules may mimic lymphomas or metastases (Ksiadzyna 2011).

7.7.4 Polysplenia

In patients with polysplenia, there is more than one hilus (Fig. 7.35) and multiple splenic nodules. Polysplenia may accompany congenital heart disease. In children with situs inversus and/or heterotaxy syndrome, the spleen is located on the right side usually together with the stomach as both originate from the dorsal mesogastrium. The anatomy of the splenic vessels vary according to specialities of the liver anatomy (e.g. horizontal or butterfly liver with central hilus) and anatomical variations of the great abdominal vessels, including vascular signs of malrotation in half of the patients with malposition or rotation of the superior mesenteric vein around the superior mesenteric artery.

7.8 The Role of Contrast-Enhanced US (CEUS) in Splenic Lesions

Contrast-enhanced ultrasonography (CEUS) has been suggested as a useful tool in characterising incidentally detected splenic lesions (Chiavaroli et al. 2011; Sutherland et al. 2011). Up to now, it is off-label use even for use in extrahepatic indications in adults.

CEUS with second-generation contrast agents has been shown to improve the differentiation between benign and malignant splenic tumours (Stang et al. 2011) and to improve visualisation of splenic metastasis (Neesse et al. 2010).

Most splenic haemangiomas showed isoenhancement after intravenous contrast agents, one-third had a hypoenhancement and 11 % a wash-out; only a minority of the haemangiomas showed a peripheral globular rim enhancement and centripetal fill-in as typically seen in liver haemangiomas (Taibbi et al. 2012).

Rim enhancement may be seen in pyogenic splenic abscesses (Weskott 2013; Paterson et al. 1999). In patients with splenic trauma, CEUS is more sensitive in detecting splenic lesions than conventional US and CDS (Weskott 2013) and may be used as a follow-up imaging technique after interventions of splenic trauma (Dormagen et al. 2011).

Abbreviations

CDS:: Colour-coded Doppler sonography
CEUS:: Contrast-enhanced US
DS:: Doppler sonography
IVC:: Inferior vena cava
PH:: Portal hypertension
PRF:: Pulse repetition frequency (synonym: pulse repetition rate, velocity range, scale)
PW-DS:: Pulsed-wave Doppler sonography
RI:: Resistive index (synonym: resistance index, Pourcelot index)
TAV:: Time average velocity (cm/s)
US:: Ultrasonography
Ved:: End-diastolic velocity
Vs:: Peak systolic velocity

References

Abbott RM, Levy AD, Aguilera NS, Gorospe L, Thompson WM (2004) Primary vascular neoplasms of the spleen: radiologic-pathologic correlation. Radiographics 24:1137–1163
Article PubMed Google Scholar
Abramowsky C, Alvarado C, Wyly JB, Ricketts R (2004) “Hamartoma” of the spleen (splenoma) in children. Pediatr Dev Pathol 7:231–236
Article PubMed Google Scholar
Ayaz UY, Dilli A, Ayaz S, Api A (2012) Wandering spleen in a child with symptoms of acute abdomen: ultrasonographic diagnosis. Case report. Med Ultrason 14:64–66
PubMed Google Scholar
Bachmann C, Görg C (2004) The value of B-mode and colour Doppler sonography in the diagnosis of focal splenic lesions. Ultraschall Med 25:444–447
Article CAS PubMed Google Scholar
Bachmann C, Görg C (2005) Color Doppler sonographic findings in focal spleen lesions. Eur J Radiol 56:386–390
Article PubMed Google Scholar
Barakat M, Hassan A et al (1998) Intrasplenic venous flow patterns demonstrated by Doppler ultrasound in patients with portal hypertension. Br J Radiol 71:384–387
Article CAS PubMed Google Scholar
Benjamin DR, Shunk B (1978) A fatal case of peliosis of the liver and spleen. Am J Dis Child 132:207–208
CAS PubMed Google Scholar
Benter T, Klühs L, Teichgräber U (2011) Sonography off the spleen. J Ultrasound Med 30:1281–1293
PubMed Google Scholar
Bolognesi M, Quaglio C, Bombonato G, Gaiani S, Pesce P, Bizotto P, Favaretto E, Gatta A, Sacerdoti D (2012) Splenic Doppler impedance indices estimate splenic congestion in patients with right-sided or congestive heart failure. Ultrasound Med Biol 38:21–27
Article PubMed Google Scholar
Brink JS, Brown AK et al (2003) Portal vein thrombosis after laparoscopy-assisted splenectomy and cholecystectomy. J Pediatr Surg 38:644–647
Article PubMed Google Scholar
Chen MJ, Huang MJ, Chang WH, Wang TE, Wang HY, Chu CH, Lin SC, Shih SC (2005) Ultrasonography of splenic abnormalities. World J Gastroenterol 11(26):4061–4066.
Google Scholar
Chen JW, Yeh DM, Peng SH, Chen GS, Tseng YH, Lin CW, Tyan YS, Tsao TF (2012) Sonographic diagnosis of a subclinical wandering spleen: role of the decubitus position. J Ultrasound Med 31(3):483–487
PubMed Google Scholar
Chiavaroli R, Grima P, Tundo P (2011) Characterization of nontraumatic focal splenic lesions using contrast-enhanced sonography. J Clin Ultrasound 39:310–315
Article PubMed Google Scholar
Czauderna P, Vajda P, Schaarschmidt K, Kalman A, Jainsch M, Englis A, Lewicki K, Verebely T, Koltai J, Petersons A, Pinter AB (2006) Nonparasitic splenic cysts in children: a multicentric study. Eur J Pediatr Surg 16:415–419
Article CAS PubMed Google Scholar
Danaci M, Belet U et al (2000) Power Doppler sonographic diagnosis of torsion in a wandering spleen. J Clin Ultrasound 28:246–248
Article CAS PubMed Google Scholar
Di Crosta I, Inserra A, Gil CP, Pisani M, Ponticelli A (2009) Abdominal pain and wandering spleen in young children: the importance of an early diagnosis. J Surg 44:1446–1449
Google Scholar
Dilli A, Tatar IG, Ayaz UY, Hekimoglu B (2011) Isolated splenic hydatid disease. Case Rep Med. doi:10.1155/2011/763895
Google Scholar
Dormagen J, Meyerdierks O, Gaarder C, Naess P, Sandvik L, Klow NE (2011) Contrast-enhanced ultrasound of the injured spleen after embolization—comparison with computed tomography. Ultraschall Med 32:485–491
Article CAS PubMed Google Scholar
Elsayes KM, Narra VR, Mukundan G, Lewis JS Jr, Menias CO, Heiken JP (2005) MR imaging of the spleen: spectrum of abnormalities. Radiographics 2:967–982
Article Google Scholar
Fitoz S, Atasoy C et al (2001) Post-traumatic intrasplenic pseudoaneurysms with delayed rupture: color Doppler sonographic and CT findings. J Clin Ultrasound 29:102–104
Article CAS PubMed Google Scholar
Fotiadis C, Lavranos G, Patapis P, Karatzas G (2008) Abscesses of the spleen: report of three cases. World J Gastroenterol 14:3088–3091
Article PubMed Central PubMed Google Scholar
Goletti O, Ghiselli G et al (1996) Intrasplenic posttraumatic pseudoaneurysm: echo color Doppler diagnosis. J Trauma 41:542–554
Article CAS PubMed Google Scholar
Görg C (2011) The spleen. In: Schmidt G, Greiner L, Nürnberg D (eds) Sonografische Differential diagnose,2nd Auflage. Thieme Verlag, Stuttgart
Google Scholar
Görg C, Schwerk WB (1994) Color Doppler imaging of focal splenic masses. Eur J Radiol 18:214–219
Article Google Scholar
Görg C, Zugmaier G (2003) Chronic recurring infarction of the spleen: sonographic patterns and complications. Ultraschall Med 24:245–249
Article PubMed Google Scholar
Görg C, Eichkorn M, Zugmaier G (2003) The small spleen: sonographic patterns of the functional hyposplenia or asplenia. J Clin Ultrasound 31:152–155
Article PubMed Google Scholar
Görg C, Seifart U et al (2004) Acute, complete splenic infarction in cancer patient is associated with a fatal outcome. Abdom Imaging 29:224–227
Article PubMed Google Scholar
Görg C, Görg K, Bert T, Barth P (2006) Colour Doppler ultrasound patterns and clinical follow-up of incidentally found hypoechoic, vascular tumors of the spleen: evidence for a benign tumor. Br J Radiol 79:319–325
Article PubMed Google Scholar
Günter E (2005) Sonoquiz. Endo Heute 18:77–79
Article Google Scholar
Hartmann M, Marx A, Geißinger E, Müller-Hermelink HK, Rüdiger T (2008) Vaskuläre Tumoren der Milz. Pathologe 29:129–135
Article CAS PubMed Google Scholar
Hofmann V (2005) Chapter 9: Milz. In: Hofmann V, Deeg KH, Hoyer PF (eds) Ultraschalldiagnostik in Pädiatrie und Kinderchirurgie, 3rd edn. Thieme, Stuttgart/New York, p 323–336
Google Scholar
Ksiadzyna D (2011) A case report of abdominal splenosis – a practical mini-review for a gastroenterologist. J Gastrointestin Liver Dis 20:321–324
PubMed Google Scholar
Lopez-Tomassetti Fernandez EM, Arteaga Gonzalez I et al (2006) An unusual case of hemoperitoneum owing to acute splenic torsion in a child with immunoglobulin deficiency. J Postgrad Med 52:41–42
CAS PubMed Google Scholar
Lynn KN, Werder GM, Callaghan RM, Sullivan AN, Jafri ZH, Bloom DA (2009) Pediatric blunt splenic trauma: a comprehensive review. Pediatr Radiol 39:904–916
Article PubMed Google Scholar
Manetta R, Pistoia ML, Bultrini C, Stavroulis E, Di Cesare E, Masciocchi C (2009) Ultrasound enhanced with sulphur-hexafluoride-filled microbubbles agent (SonoVue) in the follow-up of mild liver and spleen trauma. Radiol Med 114:771–779
Article CAS PubMed Google Scholar
Neesse A, Huth J, Kunsch S, MIchl P, Bert T, Tebbe JJ, Gress TM, Görg C (2010) Contrast-enhanced ultrasound pattern of splenic metastases – a retrospective study in 32 patients. Ultraschall Med 31:264–269
Article CAS PubMed Google Scholar
Nemcek AA Jr, Miller F (1991) Acute torsion of a wandering spleen: diagnosis by CT and duplex Doppler and colour Doppler sonography. AJR AM J Roentgenol 157:307–309
Article PubMed Google Scholar
Neuhauser TS, Derringer GA, Thompson LDR, Fanburg-Smith JC, Mittinen M, Saarist A, Abbondanzo SL (2000) Splenic angiosarcoma: a clinicopathological and immunophenotypic study of 28 cases. Mod Pathol 13:978–987
Article CAS PubMed Google Scholar
Özcan H, Yagmurlu B et al (2006) Asymptomatic splenic artery occlusion in a child: incidental detection with Doppler ultrasonography. Diagn Interv Radiol 12:68–69
PubMed Google Scholar
Paterson A, Frush DP, Donelly LF, Foss JN, O’Hara SM, Bisset GS (1999) A pattern-oriented approach to splenic imaging in infants and children. Radiographics 19:1465–1485
Article CAS PubMed Google Scholar
Peddhu P, Shah M, Sidhu PS (2004) Splenic abnormalities: a comparative review of ultrasound, microbubble-enhanced ultrasound and computed tomography. Clin Radiol 59:777–792
Article Google Scholar
Raghavan A, Wong CK et al (2004) Spontaneous occlusion of post-traumatic splenic pseudoaneurysm: report of two cases in children. Pediatr Radiol 34:355–357
Article PubMed Google Scholar
Richards JR, Knopf NA, Wang L et al (2002) Blunt abdominal trauma in children: evaluation with emergency US. Radiology 222:749–754
Article PubMed Google Scholar
Romano F, Caprotti R et al (2006) Elective laparoscopic splenectomy and thrombosis of the spleno-portal axis: a prospective study with ecocolordoppler ultrasound. Surg Laparosc Endosc Percutan Tech 16:4–7
Article PubMed Google Scholar
Romero JR, Barksdale EM Jr (2003) Wandering spleen: a rare cause of abdominal pain. Pediatr Emerg Care 19:412–414
Article PubMed Google Scholar
Safavi A, Beaudry P, Jamieson D, Murphy JJ (2011) Traumatic pseudoaneurysms of the liver and spleen in children: is routine screening warranted? J Pediatr Surg 46:938–941
Article PubMed Google Scholar
Saxena AK, Sodhi KS, Narayanan S, Singhi S, Khandelwal N (2011) Splenic lesions in visceral leishmaniasis. Indian J Pediatr 78:753–754
Article PubMed Google Scholar
Shimono T, Yamaoka T, Nishimura K, Naya M, Hojo M, Yamamoto E, Mukaihara S, Hayakawa K (1998) Peliosis of the spleen: splenic rupture with intraperitoneal hemorrhage. Abdom Imaging 23:201–202
Article CAS PubMed Google Scholar
Sivit CS, Siegel MJ (2002) Spleen and peritoneal cavity. In: Siegel M (ed) Pediatric sonography, 3rd edn. Lippincott, Williams & Wilkins, Philadelphia, pp 305–336
Google Scholar
Stamou KM, Toutouzas KG et al (2006) Prospective study of the incidence and risk factors of postsplenectomy thrombosis of the portal, mesenteric and splenic veins. Arch Surg 141:663–669
Article PubMed Google Scholar
Stang A, Keles H, Hentschke S, von Seydewitz CU, Dahlke J, Habermann C, Wessling J (2011) Incidentally detected splenic lesions in ultrasound: does contrast-enhanced ultrasonography improve the differentiation of benign hemangioma/hamartoma from malignant lesions? Ultraschall Med 32:582–592
Article CAS PubMed Google Scholar
Sutherland T, Temple F, Hennessy O, Lee W-K (2010) Abdomen’s forgotten organ: sonography and CT of focal splenic lesions. J Med Imaging Radiat Oncol 54:120–128
Article CAS PubMed Google Scholar
Sutherland T, Temple F, Galvin A, Hennessy O (2011) Contrast-enhanced ultrasound of the spleen: an introduction and pictorial essay. Insights Imaging 2:515–524
Article PubMed Central PubMed Google Scholar
Taibbi A, Bartolotta TV, Matranga D, Midiri M, Lagalla R (2012) Splenic hemangiomas: contrast-enhanced sonographic findings. J Ultrasound Med 31:543–553
PubMed Google Scholar
Tataria M, Nance ML, Holmes JH et al (2007) Pediatric blunt abdominal injury: age is irrelevant and delayed operation is not detrimental. J Trauma 63:608–614
Article PubMed Google Scholar
Teramoto R, Opas LM, Andrassy R (1981) Splenic torsion with prune belly syndrome. J Pediatr 98:91–92
Article CAS PubMed Google Scholar
Tolgonay G, Ozbek SS et al (1998) Regression of splenic vein aneurysm following resolution of splenomegaly. J Clin Ultrasound 26:98–102
Article CAS PubMed Google Scholar
von Herbay A, Barreiros AP, Ignee A et al (2009) Contrast-enhanced ultrasonography with SonoVue. Differentiation between benign and malignant lesions of the spleen. J Ultrasound Med 28:421
Google Scholar
Vural M, Kacar S et al (1999) Symptomatic wandering accessory spleen in the pelvis: sonographic findings. J Clin Ultrasound 27:534–536
Article CAS PubMed Google Scholar
Weinspach S, Tenenbaum T, Schönberger S, Schaper J, Engers R, Rueggeberg J, MacKenzie CR, Wolf A, Mayatepek E, Schroten H (2010) Cat scratch disease – heterogeneous in clinical presentation: five unusual cases of an infection caused by Bartonella henselae. Klin Padiatr 222:73–78
Article CAS PubMed Google Scholar
Weskott HP (2012) Ultrasound in the diagnostic management of malignant lymphomas. Radiologe 52(4):347–359.
Google Scholar
Weskott HP (ed) (2013) Contrast enhanced ultrasound. Uni-Med, Bremen
Google Scholar
Yardeni D, Polley TZ Jr et al (2004) Splenic artery embolization for post-traumatic splenic artery pseudoaneurysm in children. J Trauma 57:404–407
Article PubMed Google Scholar
Zhan F, Wang CJ, Lin JZ, Zhong PJ, Qiu WZ, Lin HH, Liu YH, Zhao ZJ (2010) Isolated splenic tuberculosis: a case report. World J Gastrointest Pathophysiol 1:109–111
Article PubMed Central PubMed Google Scholar

Download references

Author information

Authors and Affiliations

Department of Paediatric Kidney, Liver and Metabolic Diseases, Children’s Hospital, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany
Doris Franke
Clinic for Children and Adolescents, Sozialstiftung Bamberg, Buger Straße 80, 96049, Bamberg, Germany
Karl-Heinz Deeg

Authors

Doris Franke
View author publications
You can also search for this author in PubMed Google Scholar
Karl-Heinz Deeg
View author publications
You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Doris Franke .

Rights and permissions

Reprints and permissions

Copyright information

About this chapter

Cite this chapter

Franke, D., Deeg, KH. (2015). Doppler Sonography of the Spleen. In: Doppler Sonography in Infancy and Childhood. Springer, Cham. https://doi.org/10.1007/978-3-319-03506-2_7

Download citation

DOI: https://doi.org/10.1007/978-3-319-03506-2_7
Published: 19 February 2014
Publisher Name: Springer, Cham
Print ISBN: 978-3-319-03505-5
Online ISBN: 978-3-319-03506-2
eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics