A common variation in shape is a prominent lobule of splenic tissue that extends medially from the posterior aspect of the spleen to lie in front of the left kidney (Fig. 7.2). Awareness of this variation is important so that it is not mistaken for a left adrenal or renal mass. Splenic clefts are common and usually occur on the lateral or superior diaphragmatic portion of the spleen (Fig. 7.3). They are easily distinguished from a laceration by their well-defined margins and absence of perisplenic hematoma (12).

Wandering spleen is characterized by abnormal splenic mobility, allowing the spleen to lie in an ectopic location (13). The spleen develops within the dorsal mesogastrium; the latter eventually fuses with the peritoneum of the posterior abdominal wall. The portion of mesogastrium and the peritoneum along this line of fusion degenerates. The
spleen is then connected to the stomach by the gastrosplenic ligament and to the body wall in the region of the left kidney by the splenorenal ligament (2). The splenorenal ligament contains the splenic artery. These ligaments allow some mobility of the spleen normally, but they prevent any significant displacement. Wandering spleen is thought to be the result of incomplete fusion of the dorsal mesogastrium to the posterior parietal peritoneum (12,13,14,15). Incomplete ligamentous formation leads to a long mobile vascular pedicle that is predisposed to torsion. As the pancreatic tail is invested by the dorsal mesogastrium and parietal peritoneum, it also may be involved in the torsion.

Affected children usually present between 3 months and 10 years of age, with most patients being younger than 1 year of age (14). There is a spectrum of clinical findings ranging from an asymptomatic palpable abdominal mass or intermittent abdominal pain (secondary to torsion and detorsion of the splenic pedicle) to an acute surgical abdomen (consequent to torsion of the splenic pedicle and vascular compromise).

CT findings of the wandering spleen include absence of splenic tissue in the left upper quadrant and a soft tissue–attenuation mass elsewhere in the abdomen with a shape and enhancement pattern similar to normal spleen (Fig. 7.4) (14,15,16). Associated findings of poor or heterogeneous parenchymal enhancement, ascites, a twisted splenic pedicle, and a whorled appearance of the pancreatic tail and supporting fat indicate superimposed torsion (17,18,19,20) (Fig. 7.5). A thick, enhancing pseudocapsule, representing omental and peritoneal adhesions, has been observed with chronic or intermittent torsion (21).

Complications of splenic torsion include splenic infarction, abscess formation, peritonitis, bowel obstruction,
pancreatitis, and necrosis of the pancreatic tail (14,22). Chronic torsion with venous congestion has been associated with the development of splenomegaly, gastric varices, and hypersplenism (1). Splenopexy is the surgical treatment for wandering spleen; splenectomy is performed for splenic infarction (15).

Accessory spleen is a common anatomic variant and has been found in approximately 15% of children in autopsy series (23). It is thought to result from failure of fusion of some of the embryonic buds of splenic tissue in the dorsal mesogastrium. Accessory spleens are usually found near the splenic hilum, along the course of the splenic vessels, or within the layers of the omentum, but they can occur anywhere in the abdomen (24,25). Because of the close relationship of the developing spleen with the mesonephros and left gonadal anlage, accessory spleens may be found in the scrotum or attached to the left ovary. This condition is termed splenogonadal fusion. Accessory spleens vary from a few millimeters to >5 cm in diameter (25). Most (90%) are solitary; the remaining patients usually have two accessory spleens. More than two splenules are unusual.

Accessory spleens are usually of no clinical significance. However, in patients who have had splenectomies for hematologic diseases (e.g., idiopathic thrombocytopenic purpura and the hemolytic anemias), the accessory splenic tissue can hypertrophy, resulting in recurrent hypersplenism (26). They appear on CT as smooth, round, or ovoid masses with an attenuation and enhancement pattern identical to that of the normal spleen (Fig. 7.6) (24,26,27). Rarely, the accessory spleen twists on its pedicle, presenting as an acute abdomen. When this occurs, CT shows a nonenhancing, hypoattenuating mass with peripheral rim enhancement (28,29,30,31,32). A whorled or twisted appearance of the vascular pedicle can also be seen.

Splenosis is the result of splenic rupture secondary to trauma or surgery with subsequent autotransplantation of splenic tissue. The peritoneal cavity is the most common site of splenosis, but splenic tissue can be found elsewhere in the abdomen or chest. Abdominal splenosis must be differentiated from accessory spleens. A history of splenic trauma or splenectomy supports splenosis, whereas absence of these clinical attributes favors accessory spleen. In addition, the masses in splenosis are distributed throughout the peritoneum and the retroperitoneum, whereas accessory spleens are usually found in the left side of the abdomen near the splenic hilum (33).

Heterotaxy of cardiosplenic syndromes implies a disorganized organ arrangement in the chest or abdomen. There are two main types of heterotaxy: heterotaxy with polysplenia and heterotaxy with asplenia (34).

Splenic tumors in children are more likely to be benign than malignant. Benign neoplasms include hemangioma, littoral cell angioma, peliosis, lymphangioma, hamartoma,
inflammatory pseudotumor, and leiomyoma. They are usually asymptomatic and incidental findings on imaging studies, but they may present as an abdominal mass or with pain secondary to compression of adjacent organs. Thrombocytopenia owing to platelet consumption (Kasabach–Merritt syndrome) and congestive heart failure have been reported in hemangiomas. Benign neoplasms of the spleen vary in size from <1 cm to >15 cm (1).

Hemangioma, although rare, is the most common benign tumor of the spleen (46,47). Most are sporadic, but they may occur as part of systemic disorders, such as Beckwith–Wiedemann and Klippel–Trenaunay–Weber syndromes (48,49). The lesions are composed of endothelial-lined vascular channels filled with red blood cells; they may be single or multiple (46,47). Multiple hemangiomas may be associated with cutaneous and skeletal hemangiomas. On unenhanced CT scans, hemangiomas appear as isoattenuating or hypoattenuating lesions. Curvilinear peripheral calcifications (46,47,50,51,52) and/or coarse internal calcifications may also be noted. On enhanced scans, they demonstrate nodular peripheral enhancement that is isoattenuating with the aorta and show progressive central fill-in over time and then rapid washout (Fig. 7.11) (8,46,47,50,51,52). Small lesions may show early uniform enhancement, whereas large lesions may demonstrate hypoattenuating areas corresponding to fibrosis.

Littoral cell angioma is a rare vascular neoplasm thought to arise in the lining (littoral) cells of the splenic red pulp sinuses. Patients may be asymptomatic or present with splenic enlargement. CT shows multiple lesions of low attenuation (Fig. 7.12).

Peliosis is another vascular disorder characterized by multiple blood-filled cavities (46,53). It usually occurs in conjunction with peliosis hepatis. It has been associated with anabolic steroid use and acquired immunodeficiency syndrome, but it also may be idiopathic. It differs from splenic hemangioma in that the blood-filled spaces lack an endothelial lining. Most commonly, CT scans show multiple hypoattenuating nodules (Fig. 7.13). The nodules may show centripetal enhancement and contain fluid–fluid levels, corresponding to a hematocrit effect (44,46,53). The appearance can be similar to that of hemangioma, but a
history of immunosuppression or drug therapy should suggest peliosis.

Lymphangiomas are congenital malformations of the lymphatic system composed of multiple, endothelial-lined spaces containing lymph and separated by fibrous bands. They most often occur in the neck and axilla, but they may be found in abdominal viscera. They are usually solitary lesions, although they can be multiple or even diffusely replace splenic parenchyma (termed lymphangiomatosis) (46). CT typically demonstrates multiple, thin-walled, fluid-filled cysts surrounded by septations of varying thickness (Fig. 7.14) (46,54,55,56,57). The attenuation of the fluid components ranges from 15 to 35 HU (55,56). Contrast enhancement typically is absent, although occasionally slight enhancement of the septations or cyst wall may be noted.

Hamartomas, also known as splenomas, splenadenomas, or nodular hyperplasia of the spleen, are benign lesions consisting of an anomalous mixture of normal splenic elements with a predominance of red pulp (46,50,58). They usually present as solitary lesions and less often as multiple nodules. They range from <1 cm to 19 cm in diameter (46). On unenhanced CT scans, splenic hamartomas appear as homogeneous isoattenuating or hypoattenuating masses (46,50,59,60,61). After intravenous contrast administration, they show mild to moderate, heterogeneous enhancement and well-defined borders (Fig. 7.15) (46,59,60,61). Speckled calcifications have been reported. Splenic hamartomas have been described in association with tuberous sclerosis (62).

Inflammatory pseudotumors of the spleen are rare benign lesions composed of a fibroblastic stroma and polymorphous inflammatory cells, particularly plasma cells and lymphocytes (63). The cause is unknown, but an infectious or autoimmune origin has been postulated. On unenhanced scans, they appear as well-circumscribed hypoattenuating masses (64,65,66). Peripheral calcification may be seen. After administration of intravenous contrast agent, heterogeneous enhancement is common with the lesion becoming hypoattenuating to normal parenchyma (Fig. 7.16) (64,65,66).

Leiomyoma is a rare benign tumor originating from smooth muscle cells. It has been reported as an isolated finding in adults. In children, it has been associated with ataxia telangiectasia (67). CT scans show a round,
well-demarcated, hypoattenuating mass with peripheral enhancement. CT findings of leiomyoma and the other solid splenic tumors overlap, and final diagnosis requires tissue sampling.

Lymphoma is the most common malignant splenic neoplasm (39). It may be primary, but more often it is associated with systemic disease. Splenic involvement has been reported at staging laparotomy in approximately 33% of children with Hodgkin lymphoma and in about 15% of children with non-Hodgkin lymphoma. The affected spleen may or may not be enlarged, and conversely mild to moderate splenomegaly may be present in patients in whom no tumor is identified in the excised spleen (68). When splenomegaly is marked, however, there is a higher likelihood of lymphomatous involvement. On unenhanced CT, lymphoma may appear isoattenuating or hypoattenuating to adjacent parenchyma. On contrast-enhanced scans, the CT appearance of lymphoma ranges from splenic enlargement alone to solitary or multiple nonenhancing, low-attenuation masses (Fig. 7.17) (44,69). Calcifications in splenic lymphoma have been reported both before and after treatment (8).

Angiosarcoma is a very rare malignant splenic tumor consisting of disorganized anastomosing vascular channels lined by plump atypical endothelial cells with large irregular nuclei and high mitotic rates (46). Early and widespread metastases to liver, lung, bone, and lymph nodes are frequent. On unenhanced CT, angiosarcomas usually appear hypoattenuating. After intravenous contrast administration, the most common appearance is that of a heterogeneously enhancing mass with poorly defined or diffusely infiltrating borders (8,46,70). Scattered punctate calcifications and hypervascular hepatic metastases may also be seen.

Leukemic infiltration of the spleen can be seen during active stages of the disease or during remission. At CT, the spleen is enlarged; the attenuation is similar to that of the normal spleen. Adenopathy may be noted elsewhere in the abdomen.

Langerhans cell histiocytosis is characterized by a proliferation of marrow-derived histiocytes and predominantly involves the skin, bone, bone marrow, reticuloendothelial system, and lungs. CT findings include splenic enlargement or less often, multiple nodules (71,72).

Splenic metastases are rarely diagnosed antemortem, although in postmortem studies, metastatic disease is not infrequent. They occur most commonly from hematogenous spread of tumor. At CT, metastases usually appear as multiple hypoattenuating areas (44). Enhancement may be observed in the periphery of the lesion.

Pyogenic abscesses may be either solitary or multiple. The common inciting organisms are Staphylococcus aureus, streptococcus, and Gram-negative rods, such as Salmonella sp. (73). CT findings of pyogenic abscess are a round or ovoid hypoattenuating lesion. The rim of the abscess may enhance following intravenous contrast medium administration (24,44,73,75). Central enhancement is absent. Intraluminal gas is specific for the diagnosis of abscess, although this is not a common finding. Bacterial abscesses are usually unilocular, although some may be multilocular. Multilocular abscesses are more likely to be fungal than bacterial (76). In the absence of gas, the appearance of splenic abscess may mimic other splenic pathology, including infarct and neoplasm. In these instances, CT can be used to guide percutaneous aspiration for diagnosis and drainage (73).

Fungal abscesses are most likely to be multifocal or miliary. Most occur in immunosuppressed patients, especially those with chronic granulomatous disease, leukemia, or lymphoma. Candida albicans and Aspergillus fumigatus are common causative organisms in this patient population (8,77).

On contrast-enhanced CT, fungal abscesses are small (<2 cm), multiple, well-defined, non-enhancing lesions of low attenuation (Fig. 7.18) (8,77,78,79,80). Central high-attenuation foci creating a bull's eye or wheel-within-a-wheel pattern can occasionally be noted (24). Punctate calcifications have been observed in treated Candida microabscesses and in lesions caused by Histoplasmosis. Abscesses associated with cat-scratch disease caused by Bartonella henselae have an appearance similar to that of fungal abscesses (Fig. 7.19).

Patients with acquired immunodeficiency syndrome (AIDS) also are at increased risk for developing miliary or multifocal abscesses. Pneumocystis carinii is the most common cause of opportunistic infection. Cytomegalovirus and Mycobacterium avium-intracellulare are other frequent organisms. CT findings include splenomegaly, multiple, small hypoattenuating lesions, and punctate, diffuse, or ringlike calcifications (Fig. 7.20) (8,24,81,82,83). Miliary abscesses in the liver, kidneys, pancreas, and lymph nodes; calcified lymph nodes; and pleural and peritoneal effusions can also be seen (8,83,84).

Although unusual, splenic involvement by pancreatitis can occur because of the close anatomic relationships of the spleen and splenic vessels to the pancreatic tail (74). The spectrum of splenic lesions in patients with complicated pancreatitis includes intrasplenic pseudocyst, abscess, hematoma, infarction, rupture, venous thrombosis, and pseudoaneurysm formation (39,74).

Gaucher disease is an autosomal recessive disorder caused by lack of the lysosomal enzyme glucocerebrosidase. As a result, glucocerebrosides accumulate in the cells of the reticuloendothelial system (90). Two major forms of the disease have been described. The less frequent, infantile or neuropathic form leads to progressive central nervous system involvement and death in the first years of life. The more common nonneuropathic form presents with hepatosplenomegaly and bone infarctions. CT findings include a markedly enlarged spleen and multiple hypoattenuating nodules that correspond to circumscribed clusters of Gaucher cells, occasionally associated with areas of fibrosis (72,91). Splenic infarction also may be seen.

Sarcoidosis is a multisystem granulomatous disease of unknown origin. Abdominal disease has been reported in adolescent patients (92,93). CT findings include splenomegaly and hypoattenuating splenic nodules. Coexistent abdominal lymphadenopathy and hepatomegaly may also be noted (94).

The surfaces of the peritoneal cavity, including the abdominal organs contained within them, are lined by
visceral peritoneum (98). These peritoneal reflections or folds divide the peritoneal cavity into a series of communicating spaces. Folds of peritoneum that join and provide support for structures within the peritoneal cavity are termed ligaments. The name of a particular ligament usually refers to the structures that it joins. A fold that connects the small bowel or parts of the colon to the posterior abdominal wall is referred to as a mesentery. A fold that joins the stomach to other intra-abdominal sites is called an omentum. These reflections provide continuity of anatomic planes not only between intraperitoneal structures, but they also extend between intraperitoneal and extraperitoneal structures. The ligaments, omentum, and mesenteries can act as pathways for the spread of pathologic processes within the peritoneal cavity. Intra-abdominal spread of disease along these pathways can occur via hematogenous or lymphatic dissemination or by direct extension. The anatomic distribution of the more common peritoneal ligaments and mesenteries is presented below so that they can be identified on CT.

As noted above, the name of a ligament usually reflects the two major structures that it joins (Fig. 7.24). The major ligaments in the upper abdomen include the following: the falciform, gastrohepatic (also known as lesser omentum), gastrocolic (also known as greater omentum), hepatoduodenal, duodenocolic, gastrosplenic, and splenorenal ligaments. The falciform ligament connects the liver to the anterior abdominal wall. The anatomic distribution of the other ligaments is self-evident by the name of the particular ligament.

A mesentery is a fold of peritoneum connecting either the small bowel or portions of the colon to the posterior abdominal wall. The small bowel mesentery is a large peritoneal reflection that attaches the small bowel to the posterior abdominal wall. The root of the small bowel mesentery extends from the duodenojejunal flexure in the left upper quadrant to the ileocecal junction in the right lower quadrant of the abdomen (96,99,102). The root is narrow, but the mesentery fans out and becomes broader as it descends. The small bowel mesentery can be identified by its main components: the superior mesenteric artery and its branches, the superior mesenteric vein and its tributaries, a varying number of lymph nodes, and perivascular mesenteric fat (Fig. 7.25).

The mesenteries of the transverse and sigmoid colon are referred to as the transverse and sigmoid mesocolon. The transverse mesocolon lies posterior and inferior to the lesser sac, joining the second part of the duodenum

and head of the pancreas to the transverse colon (96,103). This mesentery can be identified by its vessels, which are the middle colic artery and vein (Fig. 7.26). The sigmoid mesocolon extends from the descending colon into the pelvis. It can also be identified by its vessels: the sigmoidal and hemorrhoidal vessels.

The peritoneal cavity is divided into two unequal parts, supramesocolic and inframesocolic compartments, by the transverse mesocolon (104). These compartments are arbitrarily subdivided into a number of subspaces (Figs. 7.27 and 7.28). These subspaces may be affected by pathologic processes arising in any of the structures to which they are closely related. Although these spaces freely interconnect, they often become compartmentalized when infiltrated by inflammatory or neoplastic processes, causing fluid to collect within them.

The natural flow of intraperitoneal fluid is along pathways determined by the mesentery and peritoneal reflections (Fig. 7.30). Abscesses and metastases tend to grow in areas where fluid pools. Fluid within the inframesocolic compartment preferentially flows into the pelvis where it first accumulates in the posterior cul-de-sac and then the lateral perivesical fossae. Fluid in the right infracolic
space flows along the recesses of the small bowel mesentery before pooling at the confluence of the mesentery with the cecum. Subsequently it spills into the cul-de-sac of the pelvis. Fluid in the left infracolic space pools in the sigmoid mesocolon before overflowing into the pelvis.

Once in the pelvis, fluid can flow via the right or left paracolic gutters into the upper abdomen. Flow into the supramesocolic compartment occurs preferentially by way of the right paracolic gutter into the right subhepatic space, particularly the posterior compartment or Morison pouch. From the right subhepatic space, fluid may extend to the right subphrenic space. Direct spread of fluid across the midline to the left subphrenic is prevented by the falciform and coronary ligaments of the liver. Flow along the left paracolic gutter is slower and weaker than along the right paracolic gutter, and cephalad extension of fluid is usually limited by the phrenicocolic ligament (Fig. 7.30) (99).

Peritoneal infection may be localized (abscess) or generalized (peritonitis). Abdominal abscesses in children are usually caused by appendicitis or Crohn disease or they are complications of abdominal or pelvic surgery or trauma. Most patients present with fever, leukocytosis, and abdominal pain, although patients with chronic walled-off abscesses may have fewer clinical signs or symptoms.

When abscess is a clinical consideration, the entire abdomen should be imaged from the diaphragm to the pubic symphysis and abundant oral contrast material should be administered. The CT appearance of peritoneal abscess varies with its age and location. In the early stages of development, an abscess consists of a focal accumulation of neutrophils and thus, it is seen as a soft tissue mass. Later, as it undergoes liquefaction and develops a highly vascularized rim of connective tissue, it is seen as a near-water-attenuation mass surrounded by a higher-attenuation, enhancing rim (Fig. 7.33). Gas is found in slightly more than one third of abscesses and may appear as multiple small bubbles or as an air–fluid level. Occasionally, septations are identified. Ancillary findings include displacement of surrounding structures, obliteration of adjacent fat planes, increased thickness of adjacent muscle or bowel wall, and increased attenuation of mesenteric fat. A calcific density within a low-attenuation right lower quadrant mass is suggestive of appendiceal abscess. Most abscesses are round or oval in shape, but those adjacent to solid organs, such as the liver or spleen, may have a lenticular or crescentic configuration (Fig. 7.33).

CT is a reliable single imaging test for diagnosing intra-abdominal abscess (108). False-positive diagnoses are most often the result of mistaking unopacified bowel loops for an abscess. In equivocal cases, administration of additional oral or rectal contrast medium can help clarify the nature of a fluid collection. Infrequent causes of false-positive diagnoses include necrotic tumor and fluid collections, such as duplication or mesenteric cyst, pseudocyst, loculated ascites, lymphocele, hematoma, biloma, and urinoma. Correlation with clinical history and physical examination or percutaneous needle aspiration usually helps to establish a definitive diagnosis.

Percutaneous drainage has become a widely accepted treatment for abdominal abscesses. Abscesses with superficial gas collections (bubbles or an air–fluid level) have a greater chance of being drained successfully than do abscesses with deep trapped gas (109).

In patients who are without localizing signs and who are clinically suspected of having abdominal abscess, CT or ultrasonography (US) is the imaging procedure of choice. The choice of examination between CT and US depends on the individual clinical situation. The right subphrenic and subhepatic areas are at least as well studied by US as by CT. Thus, for suspected abnormalities in these locations, US can be used the initial procedure to screen for a suspected abscess. Ultrasonography, however, often is hampered by a large amount of bowel gas; it can also be suboptimal in the immediate postoperative period because of the difficulty in imaging the area directly beneath the surgical wound, drainage tubes, and ostomy appliances. Moreover, the left subphrenic area and the lesser sac may be difficult to evaluate by US because of a gas-filled stomach. This is especially true in patients who have had prior splenectomy. Because these areas are readily studied by CT examination, CT is the preferred approach. CT is considered the method of choice when a retroperitoneal abscess is suspected. If an abscess is detected, CT permits planning of the most appropriate approach for percutaneous or surgical drainage. If the CT examination is unequivocally normal, intra-abdominal abscess can be confidently excluded.

Peritonitis is an inflammation of the peritoneal lining. Bacterial peritonitis usually is secondary to perforated appendicitis, rupture of an abdominal viscus caused by trauma or obstruction, or pelvic inflammatory disease. However, it also may occur in children who have impaired immunologic defenses or bacteremia owing to infection elsewhere in the body or an indwelling catheter (95). CT findings of peritonitis include increased attenuation of the peritoneum, mesentery, or omentum; ascites, sometimes containing septations; thickened, enhancing bowel wall (Fig. 7.34); and abscesses. Peritoneal calcifications may be seen following treatment (Fig. 7.35).

Tuberculosis is a rare cause of peritonitis, but it has increased in frequency with the increasing prevalence of the acquired immune deficiency syndrome (AIDS). Tuberculous peritonitis may result from lymphatic or hematogenous spread from distant sites, direct extension from an intra-abdominal organ (kidney or bowel), or rupture of a caseous abdominal lymph node. CT findings include lymphadenopathy, high-attenuation ascites (20 to 45 HU), and thickening and nodularity of the peritoneal surfaces, mesentery, and/or omentum (110,111,112). In infection owing to Mycobacterium tuberculosis, the peritoneal nodules and lymph nodes commonly have central low attenuation, presumably caused by caseation, and an enhancing rim (Fig. 7.36). With Mycobacterium avium-intracellulare infection, the nodes are commonly of soft tissue attenuation (113,114). Other intra-abdominal findings associated with tuberculous peritonitis include splenomegaly, hepatomegaly, and bowel wall thickening.

Intraperitoneal hemorrhage in the pediatric population is usually the result of trauma to the liver, spleen, or mesentery. Less often it results from a bleeding diathesis or rupture of a vascular neoplasm (i.e., hemangioendothelioma). Similar to hemorrhage elsewhere in the body, intraperitoneal hemorrhage has a varied appearance depending on the age and extent of the hemorrhage. Acute hemorrhage may have the same attenuation as circulating blood (45 HU) (Fig. 7.32), but it may also have an attenuation value close to those of water (<20 HU) (115,116). As the hemoglobin is concentrated and the blood clots, the attenuation of the hemorrhage increases (20 to 90 HU) (98,116). Within several days, as clot lysis occurs, the attenuation value of the blood decreases and usually
approaches that of water after 2 to 4 weeks. On occasion, fresh blood confined within a peritoneal space or within a hematoma demonstrates a hematocrit effect, with layering of the heavier sedimented erythrocytes beneath the supernatant serum (116,117).

Acute hemorrhage into the mesentery may produce localized, well-circumscribed, soft tissue–attenuation masses that may or may not displace bowel. With extensive mesenteric involvement, the mesenteric fat shows diffuse high attenuation, obliterating the margins of surrounding vessels.

Intraperitoneal bile accumulation (biloma) is usually a result of traumatic or surgical injury to the biliary tree. Bilomas may be round or oval and usually have low attenuation values (<20 HU). They are commonly found in the right upper quadrant, although they are not limited to this area (118). The CT appearance of biloma is nonspecific and correlation with clinical history, hepatobiliary scintigraphy, and/or needle aspiration is needed to make a definitive diagnosis.

Intra-abdominal urine collections may be the result of urinary tract obstruction or a traumatic or surgical injury to the kidney, ureter, or bladder. Most such collections are found within the retroperitoneum, but they can be intraperitoneal if there has been traumatic or operative disruption of the boundaries between the retroperitoneum and peritoneal cavity. On unenhanced CT scans, urine ascites appears as a low-attenuation fluid collection (<20 HU). The attenuation value increases if the cyst contents contain hemorrhage, proteinaceous material, or cellular debris. A loculated urine collection (urinoma) appears as a hypoattenuating mass with a thin or imperceptible wall. After the administration of intravenous contrast agent, the attenuation value of urine ascites and a urinoma can increase, reflecting opacification of accumulated urine (Fig. 7.37).

Intra-abdominal collections of cerebrospinal fluid (CSF) result when the peritoneal surface fails to absorb this fluid in patients with ventriculoperitoneal shunts. Loculated CSF collections, termed pseudocysts, develop when an inflammatory response, either to the shunt catheter or the draining CSF, causes a localized peritonitis. This in turn leads to the formation of a thin capsule around the CSF or inflammatory adhesions within the mesentery and omentum, walling off the CSF (Fig. 7.38).

Inflammatory processes, such as pancreatitis and Crohn disease, may infiltrate the mesentery. Crohn disease is a chronic granulomatous disease of the bowel. CT findings include bowel wall thickening, mesenteric lymphadenopathy, and fatty mesenteric proliferation (increased amount of fat around separated bowel loops) (Fig. 7.39). Mesenteric abscesses, fistulae, and sinus tracts also may be present.

In acute pancreatitis, the inflammation can extend into the transverse mesocolon, producing streaky or confluent increased attenuation in the mesenteric fat (119). The small bowel mesentery is involved less commonly. Formation of pseudocysts and abscesses and superior mesenteric vein (SMV) thrombosis also may be demonstrated. In acute SMV occlusion, the attenuation of the thrombus is equal to or higher than that of soft tissue. In chronic occlusion, the thrombus has relatively low attenuation and is surrounded by a higher-attenuation wall that sometimes enhances (120) (Fig. 7.40).

Mesenteric edema also can cause increased attenuation of the mesenteric fat (121,122). Associated findings include poor definition of mesenteric vessels and bowel wall thickening (Fig. 7.41). Mesenteric edema can be the result of hypoproteinemia, cirrhosis, congestive heart failure, tricuspid disease, nephrotic syndrome, vasculitis, Budd–Chiari syndrome, and mesenteric venous or lymphatic obstruction.

Infiltrating lipomatosis is a benign lesion that represents widespread overgrowth of normal fatty tissue. CT shows increased accumulation of normal fat. The lesion grows along fascial planes and can infiltrate muscle (Fig. 7.42) (123). When large areas of soft tissue density are present in the lesion or when the lesion invades surrounding tissue, the possibility of a sarcoma must be considered (123).

Segmental infarction of the greater omentum is an uncommon cause of acute abdominal pain, which can mimic acute appendicitis (124,125,126). Most omental infarction occurs on the right side, possibly related to an embryologic variant of the blood supply of the right-sided omentum, predisposing it to venous thrombosis. Omental infarction can be idiopathic or associated with prior surgery, trauma, or omental torsion. CT shows a masslike area of soft tissue attenuation within the omental fat (Fig. 7.43). The margins of the lesion may be well circumscribed or ill defined. It is
characteristically found between the anterior abdominal wall and the transverse or ascending colon.

Castleman disease, also known as angiofollicular lymph node hyperplasia, is a benign idiopathic disorder characterized by lymphadenopathy, producing tumoral-like masses. The hyaline-vascular form is more common and typically involves the mediastinum. The less frequent plasma cell type more often involves the abdomen (127). Intra-abdominal disease may involve the mesentery, retroperitoneum, or both locations and may be localized or widespread. Marked contrast enhancement of enlarged nodal masses is suggestive of the diagnosis (127).

Inflammatory pseudotumor, also known as inflammatory myofibroblastic tumor, is a benign mesenteric mass occurring in the adolescent or young adult population. It is a reactive lesion that contains spindle cells, mature plasma cells, and small lymphocytes. Patients usually present with fever and an abdominal mass; other findings include anemia, thrombocytosis, and polyclonal hypergammaglobulinemia. CT findings are nonspecific and include an infiltrative or well-defined, homogeneous or heterogeneous soft tissue mass (128,129) (Fig. 7.44).

Aggressive fibromatosis, also referred to as abdominal desmoid tumor and intra-abdominal fibromatosis, is a benign proliferative process. Pathologic sectioning shows an unencapsulated, well-circumscribed, mass composed of fibroblasts in collagenous and/or myxoid stroma (129). Prior abdominal surgery is an important risk factor for the development of this lesion. Presenting signs and symptoms include abdominal pain, a palpable mass, small bowel obstruction, bowel perforation, and gastrointestinal bleeding. The CT appearance is that of a homogeneous soft tissue–attenuation or hypoattenuating mass (Fig. 7.45). Some lesions may have a heterogeneous, striate, or whorled appearance (129).

Mesenteric cysts are developmental malformations of the lymphatic system (also referred to as lymphangiomas).
Patients usually present with asymptomatic abdominal masses or low-grade pain, but they can present with acute abdominal pain if the cyst undergoes torsion, rupture, or hemorrhage or obstructs the gastrointestinal tract. Pathologically, the cysts are thin-walled, multilocular lesions, containing either chylous or serous fluid (130,131,132,133). Calcifications in the wall or septa occur but are rare. Mesenteric cysts originate most commonly in the small bowel mesentery, but they may arise in the omentum, mesocolon, and retroperitoneum.

The CT findings of a mesenteric cyst are a well-defined, unilocular or septated, near-water-attenuation mass with thin or imperceptible walls (Fig. 7.46). The cyst contents may have a higher attenuation if they contain proteinaceous or hemorrhagic material (97,131,132). Cysts with large amounts of chylous fluid may show a fat–fluid layer.

Mesenchymal tumors may arise from lymphatic, vascular, neuromuscular, or fatty tissues. Lymphangiomas represent either congenital malformations of the lymphatic system and as discussed above appear as large, thin-walled, usually multiloculated cysts at CT.

Hemangioma is a benign neoplasm composed of proliferating endothelial cells. Most hemangiomas are subcutaneous or cutaneous, but visceral locations, including mesentery, liver, and bowel, can occur (134). They commonly develop within the first few months of life and undergo rapid proliferation and then rapid involution and
regression. The lesions appear as hypoattenuating or isoattenuating masses on unenhanced CT and show marked enhancement after intravenous contrast administration (Fig. 7.47). This enhancement is homogeneous during the proliferative phase and becomes heterogeneous during the phase of involution (134).

Lipomas may be incidental findings. They can be recognized by their homogeneous fat attenuation.

Neurofibromas usually occur in association with neurofibromatosis type I (NF-1). The CT findings range from small, well-circumscribed, discrete masses to large conglomerate plexiform masses surrounding and displacing adjacent structures (Fig. 7.48). The attenuation can be equal to or less than that of adjacent soft tissue structures. Associated nerve root tumors support the diagnosis.

Primary malignant intraperitoneal neoplasms in children include the small, round blue cell tumors, such as rhabdomyosarcoma, neuroblastoma and extraskeletal Ewing sarcoma, ectomesenchymoma (characterized by the presence of both neuroectodermal and mesenchymal tissues) (Fig. 7.49), mesothelioma (Fig. 7.50), malignant fibrous histiocytoma, desmoplastic small round cell
tumor (Fig. 7.51), gastrointestinal stromal tumor, and extragonadal germ cell tumor (135,136,137,138,139,140,141,142). The CT findings of malignant peritoneal tumors range from one or more lobulated soft tissue masses to diffuse irregular thickening of the peritoneum without discrete masses. Other features include heterogeneous enhancement, areas of central low attenuation corresponding to necrosis or hemorrhage, and small foci of calcification. Ancillary findings include intra-abdominal and pelvic adenopathy, bowel dilatation owing to partial obstruction, and ascites (138,139,140). Distant metastases to lungs and liver may be seen.

Lymphoma is the most common malignant neoplasm involving the peritoneal cavity in children. The primary route of spread of lymphoma to the mesentery is lymphatic dissemination (98).

Mesenteric lymphadenopathy is the most common CT manifestation of non-Hodgkin lymphoma. The CT appearance of mesenteric adenopathy ranges from multiple small, well-circumscribed, round or oval masses to large conglomerate masses obscuring adjacent structures (Fig. 7.52) (143). Large conglomerate nodal masses encasing the superior mesenteric artery and veins can produce a sandwichlike appearance (143,144). Calcification can be seen in untreated lymphoma (Fig. 7.52B), but more often it is a posttreatment sequela, following radiation treatment (145).

Extensive lymphomatous infiltration of the peritoneum is uncommon and is referred to as peritoneal lymphomatosis. CT findings consist of diffuse peritoneal thickening, omental caking, and ascites (Fig. 7.53). Associated retroperitoneal and mesenteric adenopathy may be present.

Small mesenteric lymph nodes are not specific for lymphoma. Nonneoplastic causes of lymphadenopathy, such as Crohn disease, giardiasis, tuberculosis, or other mycobacterium infection and AIDS can have a similar appearance.