DOI: 10.1148/rg.266065126
RadioGraphics 2006;26:1847-1868
Inflammatory and Nonneoplastic Bladder Masses: Radiologic-Pathologic Correlation1
Jade J. Wong-You–Cheong, MD,
Paula J. Woodward, MD,
Maria A. Manning, MD and
Charles J. Davis, MD
1 From the Department of Diagnostic Radiology, University of Maryland School of Medicine, 22 S Greene St, Baltimore, MD 21201-1595 (J.J.W.); and Departments of Radiologic Pathology (P.J.W., M.A.M.) and Genitourinary Pathology (C.J.D.), Armed Forces Institute of Pathology, Washington, DC. Received July 5, 2006; revision requested August 2 and received August 24; accepted August 24. All authors have no financial relationships to disclose.
Address correspondence to J.J.W. (e-mail: jwong{at}umm.edu).
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Abstract
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Although the vast majority of bladder tumors are epithelial neoplasms, a variety of nonneoplastic disorders can cause either focal bladder masses or diffuse mural thickening and mimic malignancy. Some of these entities are rare and poorly understood such as inflammatory pseudotumor, which produces ulcerated, bleeding polypoid bladder masses. These masses may be large and have an extravesical component. Bladder endometriosis manifests as submucosal masses with characteristic magnetic resonance imaging features consisting of hemorrhagic foci and reactive fibrosis. Nephrogenic adenoma has no typical features, and pathologic evaluation is required for diagnosis. Although imaging features of malacoplakia are also nonspecific, characteristic Michaelis-Gutmann bodies are found at pathologic evaluation. The various types of cystitis (cystitis cystica, cystitis glandularis, and eosinophilic cystitis) require pathologic diagnosis. Bladder infection with tuberculosis and schistosomiasis produces nonspecific bladder wall thickening and ulceration in the acute phase and should be suspected in patients who are immunocompromised or from countries where these infections are common. The diagnosis of chemotherapy cystitis and radiation cystitis should be clinically evident, but imaging may be used to determine severity and to assess complications. Extrinsic inflammatory diseases such as Crohn disease and diverticulitis may be associated with fistulas to the bladder and focal bladder wall abnormality. The extravesical findings allow the diagnosis to be made easily. Finally, extrinsic masses arising from the prostate or distal ureter may cause filling defects, which can be confused with intrinsic bladder masses.
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LEARNING OBJECTIVES FOR TEST 6
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After reading this article and taking the test, the reader will be able to:
- Describe a group of inflammatory and nonneoplastic disorders that can cause focal bladder masses or diffuse bladder wall thickening and might be misdiagnosed as malignancy.
- Outline the pathogenesis and risk factors for these disorders.
- Discuss the imaging characteristics and distinguishing features of these entities.
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Introduction
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Pathologic conditions of the bladder can manifest as a focal bladder mass or diffuse wall thickening. Focal masses may be neoplastic or may develop secondary to congenital, inflammatory, idiopathic, or infectious sources. Clinical, macroscopic, and radiologic findings for these masses may overlap; thus, histologic evaluation is required. Some of these entities, such as inflammatory pseudotumor, endometriosis, Crohn disease, and filling defects such as ureteroceles, have radiologic features suggestive of the diagnosis and may be first suspected by the radiologist.
Diffuse bladder wall thickening can develop secondary to many nonneoplastic conditions, including infection with bacteria or adenovirus; schistosomiasis; tuberculosis; inflammatory conditions such as cystitis cystica, cystitis glandularis, or eosinophilic cystitis; and exposure to chemotherapy (particularly with cyclophosphamide) or irradiation. Although the radiologic characteristics of these disorders are less specific, radiologic evaluation is still of value.
These various conditions may affect different portions of the bladder wall, so it is important to be familiar with its histologic layers. The bladder wall consists of four layers (Fig 1). The lumen is lined by uroepithelium, which comprises three to seven layers of stratified flat cells. These cells are flexible and can change shape from cuboidal to flattened as the bladder distends, hence the term transitional epithelium. The second layer underneath the epithelium is the lamina propria, which is very vascular. Deep to the lamina propria is the third layer, which consists of bundles of smooth detrusor muscle (muscularis propria). The detrusor muscle is a complex network of interlacing smooth muscle fibers. The inner and outer muscle fibers tend to be oriented in a longitudinal fashion, but distinct layers are usually not discernible. Fibers from the detrusor muscle merge with the prostatic capsule or anterior vagina and pelvic floor muscles. A fourth adventitial layer is formed by connective tissue. A serosal covering, formed by the peritoneum, is present only over the bladder dome. The bladder is suspended within the extraperitoneal space and is surrounded by pelvic fat.
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Figure 1. Normal bladder wall. Diagram shows the urothelium (a), lamina propria (b), muscularis propria (detrusor muscle) (c), and adventitia (d). (Reprinted, with permission, from reference 1).
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Herein, we review a diverse group of nonneoplastic disorders with inflammatory, idiopathic, and infectious causes that manifest as focal bladder masses or diffuse bladder wall thickening. The article describes and illustrates the clinical, pathologic, and radiologic features of these conditions, with emphasis on radiologic-pathologic correlation. Acute bacterial cystitis from infection will not be discussed.
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Inflammatory Pseudotumor (Pseudosarcomatous Fibromyxoid Tumor)
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An inflammatory pseudotumor is a nonneoplastic proliferation of myofibroblastic spindle cells and inflammatory cells with myxoid components. Patients present most commonly with an ulcerating bleeding mass, hematuria, and voiding symptoms. Other signs and symptoms include fever and iron deficiency anemia. This condition is more common in adults, with the mean age at diagnosis reported to be 38 years, with a range of 15–74 years (2). Inflammatory pseudotumors also occur in children, and one case in a neonate has been reported (3). The condition may have male predominance, as the male-to-female ratio was 11:6 in one series of 17 patients (2).
Inflammatory pseudotumor is an interesting entity that has been reported in every organ of the body. Within the bladder, the lesion is locally aggressive and may mimic malignancy clinically, at cystoscopy, and at imaging. At histologic analysis, the lesions are distinct and show loosely packed spindle cells within a myxoid matrix. The pathogenesis of inflammatory pseudotumor is not clear; some have postulated that the lesion develops in response to infection, inflammation, or malignancy, but the causative relationship had not been proved (4). Accordingly, some authors prefer the name pseudosarcomatous fibromyxoid tumor, which is more accurate and also describes the histologic findings (5). Inflammatory pseudotumor, unlike urothelial carcinoma, has no association with smoking (5). Lesions are varied in size, ranging from 2 to 8 cm in diameter, and have an edematous surface and a gel-like consistency at cystoscopy (6,7). Even though these lesions are locally aggressive, with an invasive growth pattern, inflammatory pseudotumors fail to progress after resection.
At imaging evaluation, inflammatory pseudotumor usually appears as a single bladder mass, which may be exophytic or polypoid (Fig 2) and which may be ulcerated. Intramural solid and cystic variants may also occur (Fig 3). These masses tend to spare the trigone; however, large lesions may invade through the bladder and may have a substantial extravesical component (Fig 4), making differentiation from a malignant process impossible.
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Figure 2a. Polypoid inflammatory pseudotumor. (a–c) Coronal T1-weighted (a), gadolinium-enhanced fat-suppressed T1-weighted (b), and T2-weighted (c) magnetic resonance (MR) images show an enhancing polypoid mass projecting into the bladder lumen (arrow). (d) Photograph of the cut, resected specimen shows a glistening surface, with adjacent thickening of the bladder wall.
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Figure 2b. Polypoid inflammatory pseudotumor. (a–c) Coronal T1-weighted (a), gadolinium-enhanced fat-suppressed T1-weighted (b), and T2-weighted (c) magnetic resonance (MR) images show an enhancing polypoid mass projecting into the bladder lumen (arrow). (d) Photograph of the cut, resected specimen shows a glistening surface, with adjacent thickening of the bladder wall.
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Figure 2c. Polypoid inflammatory pseudotumor. (a–c) Coronal T1-weighted (a), gadolinium-enhanced fat-suppressed T1-weighted (b), and T2-weighted (c) magnetic resonance (MR) images show an enhancing polypoid mass projecting into the bladder lumen (arrow). (d) Photograph of the cut, resected specimen shows a glistening surface, with adjacent thickening of the bladder wall.
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Figure 2d. Polypoid inflammatory pseudotumor. (a–c) Coronal T1-weighted (a), gadolinium-enhanced fat-suppressed T1-weighted (b), and T2-weighted (c) magnetic resonance (MR) images show an enhancing polypoid mass projecting into the bladder lumen (arrow). (d) Photograph of the cut, resected specimen shows a glistening surface, with adjacent thickening of the bladder wall.
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Figure 3. Cystic inflammatory pseudotumor. Axial contrast material–enhanced computed tomographic (CT) image shows a predominantly cystic mass (arrow) arising from the anterior bladder wall. * = bladder lumen.
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Figure 4a. Invasive inflammatory pseudotumor. Transverse ultrasonographic (US) (a), axial contrast-enhanced CT (b), and axial gadolinium-enhanced fat-suppressed T1-weighted MR (c) images show a large, lobulated mass arising from the lateral wall of the bladder with significant extravesicular extension (arrows).
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Figure 4b. Invasive inflammatory pseudotumor. Transverse ultrasonographic (US) (a), axial contrast-enhanced CT (b), and axial gadolinium-enhanced fat-suppressed T1-weighted MR (c) images show a large, lobulated mass arising from the lateral wall of the bladder with significant extravesicular extension (arrows).
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Figure 4c. Invasive inflammatory pseudotumor. Transverse ultrasonographic (US) (a), axial contrast-enhanced CT (b), and axial gadolinium-enhanced fat-suppressed T1-weighted MR (c) images show a large, lobulated mass arising from the lateral wall of the bladder with significant extravesicular extension (arrows).
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On CT and MR images, inflammatory pseudotumors demonstrate enhancement (Figs 2, 4), and at color Doppler US, these lesions may show internal vascularity 
(7). On T2-weighted MR images, inflammatory pseudotumor may appear heterogeneous, with a central hyperintense component surrounded by a low-signal-intensity periphery (Fig 5); after administration of contrast material, the periphery enhances while the central region enhances poorly (7).
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Figure 5. Inflammatory pseudotumor. Axial T2-weighted MR image shows a lobulated polypoid mass arising from the anterior wall of the bladder with central hyperintensity (*) and low peripheral signal intensity (arrowhead).
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The central region of an inflammatory pseudotumor consists of necrotic tissue, and the periphery comprises fascicles of spindle cells in edematous stroma with myxoid components, vessels, and inflammatory cells (Fig 6). This structure may produce the pattern of ringlike enhancement observed on CT and MR images that may be suggestive of the diagnosis, but histologic confirmation is essential (7). In young adults, the presence of luminal clot surrounding an enhancing bladder mass may also suggest this diagnosis (4).
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Figure 6. Inflammatory pseudotumor. Photomicrograph (original magnification, x100; hematoxylin-eosin [H-E] stain) shows uniform, elongated spindle cells within a background of myxoid stroma. These cells are loosely packed, a feature that helps differentiate this lesion from a smooth muscle tumor, which has a densely packed, cellular stroma.
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Treatment may consist of surgery, a regimen of high-dose steroids, radiation therapy, or conservative management. Because imaging features may overlap, it is critical that the pathologist distinguish inflammatory pseudotumor from rhabdomyosarcoma and myxoid leiomyosarcoma to prevent unnecessary radical surgery.
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Endometriosis
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The urinary tract is not usually involved by endometriosis; however, when it is, the bladder is the most common site, with a reported prevalence of 1%–15% in women with endometriosis (8–10). Bladder endometriosis can occur spontaneously after direct implantation of endometrium or following pelvic surgery. Bladder endometriosis has been reported in only premenopausal women (5). The ectopic endometrium responds to circulating hormones during the menstrual cycle, although in a less predictable fashion than uterine endometrium. Cyclic hematuria is highly suggestive of bladder endometriosis, but it occurs in only 20% of cases (9). Patients may have cyclic pain, dysuria, urgency, and pain, or they may be entirely asymptomatic.
Endometriosis can occur in several forms: cystic ovarian endometriotic masses, superficial endometriosis, or deeply infiltrating endometriosis with endometrial deposits or implants more than 5 mm deep into the peritoneum. Bladder endometriosis is deeply infiltrating (8) (Fig 7). Bladder implants typically occur at the vesicouterine pouch. These masses can grow through the muscle into the submucosa, producing an obtuse bulge into the bladder lumen. Less frequently, endometriosis can grow through the mucosa and produce a polypoid mass (11). A confluent area of endometriosis can develop between the bladder and uterus and obliterate the vesicouterine pouch (11). Small superficial serosal implants may also occur. Most endometriotic lesions are found in the posterior wall of the bladder above the trigone or at the dome (8,10,12).
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Figure 7. Endometriosis. Photomicrograph (original magnification, x100; H-E stain) shows endometrial glands (arrows) surrounded by endometrial stromal cells, deep within the muscularis propria of the bladder.
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There are three main theories regarding the pathogenesis of bladder endometriosis. The first and most widely accepted theory is that endometriosis develops in the bladder because of retrograde menstruation, which seeds the surface of the bladder serosa. Spread of endometrium to distant sites may also occur during surgery, such as cesarean section. The other theories postulate that bladder endometriosis arises due to metaplasia of mullerian remnants or direct extension from anterior uterine adenomyosis (12).
Bladder endometriosis can occur in several locations. Superficial and deeply infiltrating lesions are much more common in dependent sites in the peritoneal cavity, such as the posterior Douglas cul-de-sac, rather than the anterior vesicouterine pouch (8). Endometriosis of the detrusor muscle is believed to result from trapping of endometrial cells in the anterior cul-de-sac with a resultant inflammatory response and fibrosis, which then obliterates this space (12). Typically, bladder endometriosis is inseparable from the anterior uterus, but it does not usually result from direct extension of adenomyosis. In addition, bladder endometriosis has not been observed in retroverted uteri because of the absence of a dependent vesicouterine pouch.
The bladder may also be the site of involvement by endocervicosis and endosalpingiosis, conditions that represent ectopic cervical and tubal epithelium, respectively. These entities are usually grouped with endometriosis and are collectively referred to as mullerianosis (13).
At cystoscopy, endometriosis typically appears as bluish or reddish-brown submucosal masses. Bleeding may occur from the surface of the masses, which range in size from 2 to 4 cm (13,14). Endometriotic masses may grow into the bladder lumen and mimic a polypoid neoplasm (13).
Characteristic histologic features are endometrial glands and stroma with hemosiderin-laden macrophages from repeated hemorrhage (Fig 7). Fibrosis may be an accompanying feature. Malignant transformation of endometriosis to adenocarcinoma of the endometrioid and clear cell types is rare (15).
Imaging features can be nonspecific, with the location of the lesions being more helpful than their imaging appearances at US, CT, and excretory urography (Fig 8). Endometriotic bladder masses are posterior and may be inseparable from the anterior aspect of the uterus. Images may show a nonspecific filling defect, typically located posteriorly in the bladder, with variable protrusion into the lumen (16,17). Transvaginal US has been found to be useful in demonstrating the depth of endometriotic lesions in the bladder wall and the continuity of bladder endometriosis to adenomyosis in the anterior myometrium if present (14).
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Figure 8a. Endometriosis. (a) Right posterior oblique view of the bladder obtained during intravenous urography shows an irregular, rounded filling defect along the posterior dome. (b) Longitudinal US image shows a solid homogeneous, hypoechoic mass protruding into the bladder lumen.
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Figure 8b. Endometriosis. (a) Right posterior oblique view of the bladder obtained during intravenous urography shows an irregular, rounded filling defect along the posterior dome. (b) Longitudinal US image shows a solid homogeneous, hypoechoic mass protruding into the bladder lumen.
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MR imaging is superior to other imaging modalities because of higher contrast resolution, delineation of bladder wall layers, tissue characterization, and multiplanar capability. The typical MR imaging features of bladder endometriosis are hemorrhagic foci with high signal intensity (representing blood) on fat-suppressed and non–fat-suppressed T1-weighted images (11). Such foci may occur in areas of fibrosis, which are dark on T1- and T2-weighted images (Fig 9) (11,16). Bladder endometriosis may also have high signal intensity on T2-weighted images. In a series of 16 patients with endometriosis of the bladder, all patients had fibrotic lesions that contained high-signal-intensity foci on T1- and T2-weighted images (11). When imaging findings were correlated with surgical results, MR imaging was reported to have a high specificity of 98.9% and a high negative predictive value of 98.9%, with a moderate sensitivity of 88% and an accuracy of 97.9% (11). The authors reported that the main limitation of MR imaging was in delineating the relationship of endometriotic masses to the ureteral orifice, a limitation that has surgical implications.
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Figure 9a. Endometriosis. (a, b) Axial T1-weighted (a) and fat-suppressed T1-weighted (b) MR images show high-signal-intensity foci (arrow) within a soft-tissue mass in the vesicouterine space, projecting into the bladder lumen. (c) Axial T2-weighted MR image shows the lesion is predominantly low signal intensity (arrow), a finding consistent with fibrosis. (d) Axial gadolinium-enhanced fat-suppressed T1-weighted image shows homogeneous enhancement of the lesion (arrow).
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Figure 9b. Endometriosis. (a, b) Axial T1-weighted (a) and fat-suppressed T1-weighted (b) MR images show high-signal-intensity foci (arrow) within a soft-tissue mass in the vesicouterine space, projecting into the bladder lumen. (c) Axial T2-weighted MR image shows the lesion is predominantly low signal intensity (arrow), a finding consistent with fibrosis. (d) Axial gadolinium-enhanced fat-suppressed T1-weighted image shows homogeneous enhancement of the lesion (arrow).
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Figure 9c. Endometriosis. (a, b) Axial T1-weighted (a) and fat-suppressed T1-weighted (b) MR images show high-signal-intensity foci (arrow) within a soft-tissue mass in the vesicouterine space, projecting into the bladder lumen. (c) Axial T2-weighted MR image shows the lesion is predominantly low signal intensity (arrow), a finding consistent with fibrosis. (d) Axial gadolinium-enhanced fat-suppressed T1-weighted image shows homogeneous enhancement of the lesion (arrow).
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Figure 9d. Endometriosis. (a, b) Axial T1-weighted (a) and fat-suppressed T1-weighted (b) MR images show high-signal-intensity foci (arrow) within a soft-tissue mass in the vesicouterine space, projecting into the bladder lumen. (c) Axial T2-weighted MR image shows the lesion is predominantly low signal intensity (arrow), a finding consistent with fibrosis. (d) Axial gadolinium-enhanced fat-suppressed T1-weighted image shows homogeneous enhancement of the lesion (arrow).
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Endometriotic masses enhance, either homogeneously or peripherally, with contrast material (Fig 9) (16). Bladder endometriosis is rarely isolated, and in the majority of patients, other foci of endometriosis are present in the pelvis (10).
Treatment of symptomatic bladder endometriosis consists of partial cystectomy.
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Nephrogenic Adenoma
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Despite its name, a nephrogenic adenoma is not a neoplastic mass but rather a benign reactive process that occurs in the urothelium. Chronic irritation by calculi, infection, injury, or previous surgery incites metaplasia of the urothelium, which develops papillary and tubular growths. A typical case might be a patient with a history of undergoing repeated biopsies for urothelial carcinoma, with the reparative process causing a nephrogenic adenoma. Nephrogenic adenomas involve the lamina propria but spare the muscle layer. Irritative voiding symptoms or hematuria are the most common symptoms (18,19). Patient age ranges from 26 to 80 years; men are three times more likely than women to develop nephrogenic adenoma (19).
At cystoscopy, a nephrogenic adenoma may resemble urothelial carcinoma or chronic cystitis with multiple polypoid or single sessile growths (18). It can occur in diverticula or at sites of previous surgery. Imaging studies reveal polypoid or sessile masses within the bladder or irregular mucosa, all of which are nonspecific findings (Fig 10); the diagnosis can be made only with a histologic evaluation (18,20). At histologic analysis, the adenoma resembles immature urothelial or metanephric structures (Fig 11) (5).
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Figure 10. Nephrogenic adenoma. Anteroposterior view of the bladder obtained during intravenous urography shows an irregular lobulated filling defect at the base of the bladder. Pathologic evaluation showed urothelial carcinoma with an adjacent nephrogenic adenoma.
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Figure 11. Nephrogenic adenoma. Photomicrograph (original magnification, x150; H-E stain) of a bladder biopsy specimen shows a background of chronic inflammatory cells with tubules lined by cuboidal (straight arrow) or teardrop-shaped (curved arrow) cells. Note the papillations (arrowheads) on the luminal surface.
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Optimal treatment is endoscopic resection. Although nephrogenic adenomas recur in up to 63% of cases, they are not premalignant (19). Bladder surveillance is required.
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Malacoplakia
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The term malacoplakia signifies soft plaque. Malacoplakia is a rare chronic granulomatous condition that can affect any organ, with the urinary tract being the most common system involved. Within the urinary tract, the bladder is the most frequently affected organ, with 40% of patients with malacoplakia having bladder involvement and 16% renal involvement (21). The disease is found predominantly in women, with a female-to-male ratio of 4:1 (21). Patients of any age may develop malacoplakia, but the peak occurrence is in middle age. The disease is more common in patients with diabetes mellitus or in immunocompromised individuals, such as those with autoimmune diseases, those with acquired immunodeficiency syndrome, or recent transplant recipients.
Presenting symptoms include gross hematuria and signs of urinary tract infection such as hesitancy, dysuria, and frequency. Patients may have variable proteinuria, as well as leukocytes and erythrocytes in their urine. Malacoplakia is highly associated with Escherichia coli infection (21), but infection alone is not thought to be causative. The pathogenesis of malacoplakia is mainly thought to involve impaired host defenses and defective phagocytosis. There is an underlying decreased cyclic guanosine monophosphate/cyclic adenosine monophosphate (cGMP/cAMP) ratio (22). Bacteria ingested by the macrophages are destroyed but not completely digested. They persist in the phagolysosomes and become mineralized, resulting in the pathognomonic calcified intracellular inclusions, the Michaelis-Gutmann bodies (Fig 12) (23).
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Figure 12. Malacoplakia. Photomicrograph (original magnification, x150; H-E stain) shows the classic target or bull’s-eye appearance of Michaelis-Gutmann bodies (arrows), which represent calcified intracellular inclusions within large histiocytes.
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Malacoplakia begins in the submucosa with overlying normal or hyperplastic epithelium, later followed by mucosal ulceration. Its appearance at cystoscopy varies, ranging from soft, flat yellow-brown plaques to nodules, papillary lesions, hemorrhagic masses, and necrotic ulcerations. The size of the lesions can range from a few millimeters to several centimeters. Plaques can extend into the distal ureters.
Imaging characteristics of malacoplakia are likewise varied. There may be multiple, polypoid, vascular, solid masses or circumferential wall thickening (Fig 13), associated with vesicoureteric reflux and dilatation of the upper urinary tract (24). Malacoplakia may be extremely aggressive, invading the perivesical space (Fig 14), and it can even cause bone destruction (25). Ring-shaped bladder calcification representing adherent calculi has been described after treatment (26). A less common radiologic manifestation is that of a predominantly retrovesical mass involving the uterus or an extravesical anterior mass (27).
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Figure 13a. Malacoplakia. (a) Axial CT image shows marked circumferential bladder wall thickening. (b) Photograph of the cut, resected specimen shows a friable, hemorrhagic mucosal surface and dramatic wall thickening.
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Figure 13b. Malacoplakia. (a) Axial CT image shows marked circumferential bladder wall thickening. (b) Photograph of the cut, resected specimen shows a friable, hemorrhagic mucosal surface and dramatic wall thickening.
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Figure 14a. Malacoplakia. Axial CT images through the upper (a) and lower (b) pelvis show a large, irregularly enhancing mass (arrows in a), which is contiguous with the bladder. Note the diffuse thickening of the bladder wall (arrow in b).
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Figure 14b. Malacoplakia. Axial CT images through the upper (a) and lower (b) pelvis show a large, irregularly enhancing mass (arrows in a), which is contiguous with the bladder. Note the diffuse thickening of the bladder wall (arrow in b).
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Given the nonspecific cystoscopic and imaging appearances of malacoplakia that may simulate those of neoplasms, biopsy is essential for appropriate conservative management. Treatment regimens include antibiotics, ascorbic acid, and a cholinergic agonist.
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Cystitis Cystica and Cystitis Glandularis
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Cystitis cystica and cystitis glandularis are common chronic reactive inflammatory disorders, which occur in the setting of chronic irritation (23). Metaplasia of the urothelium is incited by irritants such as infection, calculi, outlet obstruction, or even tumor (28). The urothelium then proliferates into buds (nests of von Brunn), which grow down into the connective tissue beneath the epithelium in the lamina propria. The buds then differentiate into cystic deposits of cystitis cystica or into intestinal columnar mucin-secreting glands (goblet cells) resulting in cystitis glandularis (Fig 15) (13). The histologic features of both cystitis cystica and cystitis glandularis are usually present, rather than either in its pure form. Mucin may be extravasated into the stroma and may cause these entities to be misdiagnosed as adenocarcinoma (13). Florid proliferation results in nodular masses in the lamina propria. Atypia and muscle invasion are not features and, if present, should suggest the diagnosis of adenocarcinoma.
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Figure 15. Cystitis cystica and cystitis glandularis. Photomicrograph (original magnification, x150; H-E stain) shows nests of von Brunn with cystic changes (straight arrow), typical of cystitis cystica, and mucin-filled goblet cell metaplasia (curved arrow), typical of cystitis glandularis.
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Cystitis glandularis also occurs in association with pelvic lipomatosis and is believed to result from bladder obstruction and chronic infection. Bladder exstrophy is also associated with diffuse cystitis glandularis. Although there are reports of adenocarcinoma developing in cystitis glandularis of the intestinal type only, the association is rare (13,28). However, patients with this condition should be closely monitored.
Cystitis glandularis and cystitis cystica can occur at any age, and there is reported prevalence of 2.4% in children with urinary tract infections (29). A slight male predominance is reported. Symptoms are those of chronic irritation, such as frequency, dysuria, urgency, and hematuria. In rare cases, mucus may be secreted in the urine.
At cystoscopy, the mucosa usually has a cobblestone pattern. In addition, cystitis glandularis may develop into a papillary or polypoid mass (Fig 16), a form that mimics carcinoma, with a predilection for the bladder neck and trigone (30,31). In young patients, their age should raise the suspicion that the lesion might be nonneoplastic, but biopsy is necessary for a definitive diagnosis.
Masses from cystitis cystica and cystitis glandularis vary in number and size and manifest as filling defects at urography (Fig 17) (30–32). A hypervascular polypoid mass has been observed on CT and MR images, with low signal intensity reported with T1-weighted sequences. On T2-weighted images, the lesion was predominantly low in signal intensity with a central branching high-signal-intensity pattern. The hyperintense area showed the most contrast enhancement and corresponded to the vascular stalk (33). The muscle layer should be intact, a feature that distinguishes cystitis cystica and cystitis glandularis from urothelial carcinoma.
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Figure 17. Cystitis cystica and cystitis glandularis. Oblique view of the bladder obtained during intravenous urography shows a lobulated contour of the bladder, with a nodular filling defect (arrow).
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Treatment consists of removing the source of irritation and surgical excision of the area of inflammation or cystectomy in rare severe cases. These patients should be monitored carefully because of the possible association with adenocarcinoma.
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Eosinophilic Cystitis
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Eosinophilic cystitis is another rare chronic inflammatory disease of the bladder, with only 83 reported cases in adults (34). It is characterized by an infiltrate of eosinophils into the bladder wall and associated with variable degrees of fibrosis and muscle necrosis (34). Eosinophilic cystitis can occur in patients with atopy, with peripheral eosinophilia, or after bladder surgery. Whether it represents a distinct entity has been questioned, as eosinophilic infiltrates are also seen with other conditions and the list of associated disorders is long: adverse reactions to drugs and food, parasitic or nonparasitic urinary tract infection, urothelial carcinoma, autoimmune disorders, and eosinophilic enteritis (5,34). Eosinophilic cystitis may be idiopathic, as no cause is found in 29% of adult patients (34). It is postulated that an antigen-antibody response occurs in the bladder and attracts eosinophils, which provoke an inflammatory response. In both adults and children, there is a slight male predominance, with a ratio of 1.3:1 reported for adults. The age distribution is wide, with a mean age of 41.6–48 years (34,35).
Hematuria (macroscopic or microscopic) and frequency are the most common presenting symptoms (35). Other clinical features include irritative voiding symptoms such as dysuria and pain, as well as urinary retention. Five percent of patients may be asymptomatic, for whom eosinophilic cystitis is diagnosed incidentally at biopsy during surveillance for urothelial carcinoma, for example (36). Peripheral eosinophilia is found in 0%–43% of cases and positive urine cultures in 26% (34–36). Impaired renal function is not uncommon (34).
At cystoscopy, all patients with eosinophilic cystitis have erythema (36). Other manifestations are polypoid, velvety, or ulcerative lesions and bladder mass or edema in 17% of cases (36). At histologic analysis, there is transmural inflammation, with the most intense inflammatory change found in the lamina propria. The inflammation is typified by eosinophilic predominance with edema. Muscle necrosis may occur, leading to fibrosis and a contracted bladder (34).
At radiologic evaluation, single masses are observed more frequently than multiple bladder masses and may be sessile (Fig 18) (34,36). The bladder wall may appear normal or thickened (37). A cystic variant with an enhancing wall may be seen (Fig 19). MR imaging shows a mass that is hyperintense relative to muscle with T1-weighted sequences, isointense with T2-weighted sequences, and enhanced after intravenous administration of contrast material (Fig 18). In the fibrotic stage, the bladder is small and contracted, and there may be resultant hydronephrosis. Since clinical and imaging features overlap with those of other disorders, particularly neoplasm which may coexist with eosinophilic cystitis, biopsy is needed for both children and adults (36).
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Figure 18a. Eosinophilic cystitis. (a) Sagittal T1-weighted MR image shows a single, sessile mass (arrow) arising from the posterior bladder wall; the mass is mildly hyperintense relative to muscle. (b) Sagittal gadolinium-enhanced fat-suppressed MR image shows enhancement of the mass (arrow) and the adjacent bladder wall.
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Figure 18b. Eosinophilic cystitis. (a) Sagittal T1-weighted MR image shows a single, sessile mass (arrow) arising from the posterior bladder wall; the mass is mildly hyperintense relative to muscle. (b) Sagittal gadolinium-enhanced fat-suppressed MR image shows enhancement of the mass (arrow) and the adjacent bladder wall.
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Figure 19a. Cystic eosinophilic cystitis. (a, b) Axial (a) and sagittal reconstructed (b) contrast-enhanced CT images show a thick-walled cystic mass (arrow) arising from the anterior dome of the bladder. (c) Intraoperative photograph, with the bladder wall retracted (arrowheads), shows the mass (arrow) protruding into the lumen. (d) Photograph of the cut specimen shows a circumferentially thickened wall, as seen on the CT images. (e) Photomicrograph (original magnification, x120; H-E stain) shows an intense infiltration of eosinophils deep within the muscularis propria (*).
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Figure 19b. Cystic eosinophilic cystitis. (a, b) Axial (a) and sagittal reconstructed (b) contrast-enhanced CT images show a thick-walled cystic mass (arrow) arising from the anterior dome of the bladder. (c) Intraoperative photograph, with the bladder wall retracted (arrowheads), shows the mass (arrow) protruding into the lumen. (d) Photograph of the cut specimen shows a circumferentially thickened wall, as seen on the CT images. (e) Photomicrograph (original magnification, x120; H-E stain) shows an intense infiltration of eosinophils deep within the muscularis propria (*).
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Figure 19c. Cystic eosinophilic cystitis. (a, b) Axial (a) and sagittal reconstructed (b) contrast-enhanced CT images show a thick-walled cystic mass (arrow) arising from the anterior dome of the bladder. (c) Intraoperative photograph, with the bladder wall retracted (arrowheads), shows the mass (arrow) protruding into the lumen. (d) Photograph of the cut specimen shows a circumferentially thickened wall, as seen on the CT images. (e) Photomicrograph (original magnification, x120; H-E stain) shows an intense infiltration of eosinophils deep within the muscularis propria (*).
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Figure 19d. Cystic eosinophilic cystitis. (a, b) Axial (a) and sagittal reconstructed (b) contrast-enhanced CT images show a thick-walled cystic mass (arrow) arising from the anterior dome of the bladder. (c) Intraoperative photograph, with the bladder wall retracted (arrowheads), shows the mass (arrow) protruding into the lumen. (d) Photograph of the cut specimen shows a circumferentially thickened wall, as seen on the CT images. (e) Photomicrograph (original magnification, x120; H-E stain) shows an intense infiltration of eosinophils deep within the muscularis propria (*).
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Figure 19e. Cystic eosinophilic cystitis. (a, b) Axial (a) and sagittal reconstructed (b) contrast-enhanced CT images show a thick-walled cystic mass (arrow) arising from the anterior dome of the bladder. (c) Intraoperative photograph, with the bladder wall retracted (arrowheads), shows the mass (arrow) protruding into the lumen. (d) Photograph of the cut specimen shows a circumferentially thickened wall, as seen on the CT images. (e) Photomicrograph (original magnification, x120; H-E stain) shows an intense infiltration of eosinophils deep within the muscularis propria (*).
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Typically, eosinophilic cystitis runs a benign, self-limiting course following removal of the etiologic factor, if known. Treatment is conservative initially. Local transurethral resection can be supplemented with a regimen of antihistamines, steroids, nonsteroidal anti-inflammatory drugs, or antibiotics if there is intercurrent infection. A small percentage of patients may require cystectomy for severe, unremitting symptoms and failure to respond to conservative measures (36).
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Tuberculosis
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Tuberculosis of the bladder is an uncommon bladder disease in Western countries, even though the genitourinary tract is the second most frequent site of tuberculosis after the lungs. Worldwide, tuberculosis remains the most common infectious cause of death. Tuberculosis of the urinary tract almost always begins in the upper tracts, with the bladder being secondarily involved. Bladder tuberculosis results directly from infection with Mycobacterium tuberculosis or less often from Bacillus Calmette-Guerin (BCG) treatment for urothelial carcinoma. The diagnosis may be difficult because of nonspecific symptoms, clinical results, and imaging findings.
Symptoms are nonspecific and include dysuria, urgency, frequency, and hematuria. Tuberculosis should be considered in patients with refractory cystitis, with sterile pyuria, or who originate from countries where tuberculosis is more common. Immunocompromised patients with acquired immunodeficiency syndrome or recipients of organ transplants are also at higher risk. Urine culture or cytology may be helpful, but a more rapid and sensitive assay is the polymerase chain reaction performed on urine (38).
At cystoscopy, early features of bladder tuberculosis are cystitis with a thick, chalky, white mucosa; mucosal ulceration; and edema. Later, fibrosis causes a contracted bladder. Characteristic features at biopsy are caseating granulomas and a positive Ziehl-Neelsen stain. Care must be taken during biopsy, as a tuberculous bladder is at increased risk of perforation (38). Necrosis can occur but is rare when bladder tuberculosis is induced by B Calmette-Guerin treatment.
In the acute phase of bladder tuberculosis, sonographic findings include irregular mucosal masses due to coalescing tubercles with ulceration and edema, diffuse wall thickening, and trabeculation (39). At urography, the bladder mucosa is irregular (Fig 20), and there may be ureteral strictures and thickening with obstruction, or a fixed and patulous vesicoureteric junction orifice, resulting in vesicoureteric reflux. In the chronic phase, imaging findings are a thick-walled contracted bladder from fibrosis (40). The diminution of bladder volume accounts for symptoms of frequency. There may be associated calcification in the seminal vesicles, but bladder wall calcification is rare and seen only after healing (32,39,40). Bladder tuberculosis may be complicated by fistulas or sinus tract formation, although these complications are rare and are demonstrated better on CT and MR images.
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Figure 20. Tuberculosis. Anteroposterior view obtained during intravenous urography shows irregularity of the bladder contour (arrowheads). There is also distortion and irregularity of the renal calices (arrows).
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Treatment consists of antituberculous regimens.
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Schistosomiasis
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Bladder schistosomiasis is uncommon in the United States, but it is a major health problem in developing parts of the world, especially Africa, and cases are seen in immigrants to the U.S. (41). Genitourinary tract infection is caused by the Schistosoma haematobium species. The larvae (cercariae) are released from snails into water and penetrate human skin exposed to the infected water. They travel to the lungs and liver of the human host, where they reside until they mature. After maturation, the adult worm pairs travel to the pelvic veins, where oviposition occurs. The eggs are deposited in the bladder wall vessels and incite a granulomatous response that results in polypoid lesions. During this time, eggs are excreted in urine. Adult worms may live for many years after initial infection. Even after the death of the adult worms, large numbers of calcified eggs can be found in the bladder wall (Fig 21) with no viable eggs in the urine (41). The eggs incite a chronic inflammatory response and fibrosis, which is an important predisposing factor for squamous carcinoma.
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Figure 21. Schistosomiasis. Photomicrograph (original magnification, x 200; H-E stain) shows schistosome ova (arrows) surrounded by numerous lymphocytes. These ova are starting to calcify. When extensive numbers of ova are present, calcification can be seen with imaging.
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Symptoms of bladder schistosomiasis are non-specific and are most commonly dysuria, supra-pubic pain, microscopic hematuria, and frequency. There may be some white cells in the urine, in addition to the red cells. The definitive diagnosis is made when eggs are found at urine microscopy. At gross pathologic analysis, the lesions are white and raised in the acute phase, but the polypoid lesions flatten as fibrosis ensues.
Imaging findings mirror the pathologic course. In the acute phase, nodular bladder wall thickening is observed at urography or cross-sectional imaging (Fig 22). There may be ureteral dilatation. The chronic phase is characterized by a contracted, fibrotic, thick-walled bladder with calcifications. These calcifications are typically curvilinear and represent the large numbers of calcified eggs within the bladder wall. Distal ureteral calcification may also be present (Fig 23). A mass may be secondary to inflammation or complicating carcinoma, typically squamous carcinoma.
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Figure 23a. Schistosomiasis. Anteroposterior radiograph (a) and axial CT image (b) of the bladder shows curvilinear calcification in the bladder wall (arrowheads), which also extends to the distal left ureter (arrow). Calcification, representing an abundance of calcified ova, is typically seen in the chronic phase of the infection.
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Figure 23b. Schistosomiasis. Anteroposterior radiograph (a) and axial CT image (b) of the bladder shows curvilinear calcification in the bladder wall (arrowheads), which also extends to the distal left ureter (arrow). Calcification, representing an abundance of calcified ova, is typically seen in the chronic phase of the infection.
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For treatment, patients are given praziquantel, which destroys the adult worms and incites the eggs to hatch. It has no effect on the chronic fibrotic changes in the bladder wall and ureters.
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Crohn Disease
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Bladder involvement in Crohn disease consists of fistulas from inflamed small and large bowel. Crohn disease is the most frequent cause of ileovesical fistula and ileocolovesical fistula (42). Enterovesical fistulas occur in 1.7%–7.7% of patients with Crohn disease and are most often from the ileum (64% of cases) and colon (21%) (42). Fistulas are slightly more common in male patients, with the median patient age being 27 years; patient age ranges from 10 to 76 years (42). The most suggestive symptoms are pneumaturia and fecaluria, which occur in 68% and 28% of patients, respectively (42). Dysuria and recurrent urinary tract infections, pain, and fever are the other most common symptoms (43). Pyuria is present in 100% of cases, and E coli is the most common bacterial infective agent (43).
The bladder is secondarily involved by the adjacent bowel inflammatory lesions. Transmural inflammation and deep fissures cause fistulas between diseased bowel and other viscera such as the bladder. Cystoscopy and CT are the most useful diagnostic tools (42). At cystoscopy, the fistula may be directly visualized, and there may be pus, feces, and bullous edema in the bladder (42). At CT, air within the bladder, focal irregularity of the wall (most commonly on the right side of bladder), and tethering of thickened adjacent bowel are the usual findings (Fig 24) (42,44). The presence of orally administered contrast material in the bladder is diagnostic of a fistula between the bowel and bladder. Hydronephrosis may also be present. Other signs of pelvic Crohn disease, such as fibrofatty proliferation, infiltration of fat, phlegmon, and lymphadenopathy, should also be present. The diagnosis of a fistula may also be made with fluoroscopic studies of the bowel or bladder, such as a small bowel series or cystography, respectively (Fig 24).
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Figure 24a. Crohn disease with a fistula to the bladder. (a) Contrast-enhanced, coronal CT reformation shows wall thickening of the distal small bowel (straight arrow) and the adjacent bladder (curved arrow). (b) Collimated radiograph obtained during a small bowel contrast study shows an enterovesical fistula (curved arrow), extending from the abnormal segment of the ileum to the bladder (arrow).
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Figure 24b. Crohn disease with a fistula to the bladder. (a) Contrast-enhanced, coronal CT reformation shows wall thickening of the distal small bowel (straight arrow) and the adjacent bladder (curved arrow). (b) Collimated radiograph obtained during a small bowel contrast study shows an enterovesical fistula (curved arrow), extending from the abnormal segment of the ileum to the bladder (arrow).
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Treatment consists of surgery, with resection of the abnormal segment of bowel and closure of the bladder defect. The value of medical therapy has not yet been established.
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Diverticulitis
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Colovesical fistulas and cystitis are not uncommon complications of diverticulitis. Patients present with pneumaturia, pain, fever, pyuria, and fecaluria. CT is more sensitive than cystography or contrast enema studies (44). Imaging findings include bladder wall thickening with gas in the bladder lumen and adjacent inflamed colon with diverticula and pericolonic fat stranding (Fig 25). Such fistulas typically occur on the left wall of the bladder. The use of rectal or oral contrast agents will opacify the bladder and help confirm the diagnosis, assuming the contrast material was not excreted by the kidneys.
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Figure 25a. Diverticulitis with a fistula to the bladder. (a) Axial CT image shows diffuse wall thickening of the sigmoid colon with an adjacent focal, thick-walled, gas-containing abscess (arrowhead). (b) Coronal CT reformation shows the abscess (arrowhead) immediately adjacent to the bladder. A fistula has formed with gas within the bladder lumen, as well as diffuse bladder wall thickening (arrow).
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Figure 25b. Diverticulitis with a fistula to the bladder. (a) Axial CT image shows diffuse wall thickening of the sigmoid colon with an adjacent focal, thick-walled, gas-containing abscess (arrowhead). (b) Coronal CT reformation shows the abscess (arrowhead) immediately adjacent to the bladder. A fistula has formed with gas within the bladder lumen, as well as diffuse bladder wall thickening (arrow).
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Definitive treatment consists of surgical excision of the fistulous tract and diseased segment of bowel.
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Radiation and Chemotherapy Cystitis
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Severe hemorrhagic cystitis may develop after chemotherapy or irradiation of the bladder. Chemotherapy-related cystitis occurs from systemic or local chemotherapy. Radiation injury may result from external, interstitial, or intracavitary radiation therapy for bladder or other pelvic malignancy, and the effects may be acute or delayed.
In the acute phase of radiation and chemotherapy cystitis, there is a hemorrhagic cystitis secondary to denudation of the urothelium, which then becomes covered with fibrinous exudates (23). Patients may have minor symptoms related to voiding difficulty or gross hematuria, dysuria, frequency, and urinary retention. The most severe radiation injuries cause bladder necrosis, incontinence, and fistula formation. Hyperemia, petechiae, hemorrhage, and ulceration may be visible at cystoscopy. At histologic analysis, there is cellular atypia, with mild to moderate nuclear pleomorphism but no mitoses (45). The epithelial proliferation may be so marked as to be confused with invasive cancer in the lamina propria (45). At imaging, there is an abnormal bladder wall with focal or diffuse irregular thickening (Fig 26), spasticity, and decreased distensibility. Hypervascularity in the wall and bleeding vessels result in intraluminal clot, visible at US or CT (46,47). MR imaging may show inflammation and edema as high signal intensity with T2-weighted sequences and can enable the bladder wall to be distinguished from clot (47).
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Figure 26a. Chemotherapy cystitis from cyclophosphamide. (a) Longitudinal US image shows diffuse wall thickening (arrows). (b) Axial contrast-enhanced CT image shows enhancement of the mucosal surface (arrow), as well as diffuse wall thickening. The hyperemic mucosa may ulcerate and cause significant hematuria.
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Figure 26b. Chemotherapy cystitis from cyclophosphamide. (a) Longitudinal US image shows diffuse wall thickening (arrows). (b) Axial contrast-enhanced CT image shows enhancement of the mucosal surface (arrow), as well as diffuse wall thickening. The hyperemic mucosa may ulcerate and cause significant hematuria.
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Beyond 1 year, chronic radiation effects result from an obliterative endarteritis in the lamina propria, followed by ischemic changes and interstitial fibrosis. Symptoms are mostly related to the contracted bladder and consist of frequency, urgency, dysuria, hematuria, and incontinence. Pneumaturia and fecaluria are highly suggestive of a fistula. At imaging, a small fibrosed bladder with a thick wall and resultant hydronephrosis are seen. Calcification may be seen in rare cases (Fig 27). Other evidence of previous irradiation includes fatty replacement of the pelvic musculature and widening of the presacral space (Fig 27). Gas within the bladder is indicative of a fistula. Complex fistulas may ensue (Fig 28).
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Figure 27. Radiation cystitis, chronic changes. Axial CT image shows focal thickening and calcification of the right posterior bladder wall (straight arrow). There is subtle widening of the presacral space (curved arrow) and fatty infiltration of the pelvic musculature (arrowheads).
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Figure 28a. Radiation cystitis with fistula. (a) Collimated anteroposterior view of the bladder obtained during cystography shows a fistulous communication between the bladder and perivesical space (arrow). (b) Axial CT image obtained after cystography helps confirm the presence of contrast material posterolateral to the bladder (arrow). Note the radiation changes within the bones. * = Foley catheter balloon.
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Figure 28b. Radiation cystitis with fistula. (a) Collimated anteroposterior view of the bladder obtained during cystography shows a fistulous communication between the bladder and perivesical space (arrow). (b) Axial CT image obtained after cystography helps confirm the presence of contrast material posterolateral to the bladder (arrow). Note the radiation changes within the bones. * = Foley catheter balloon.
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Treatment is supportive, with blood transfusions and bladder irrigation with instillation of various agents such as alum, silver nitrate, and formalin. Pelvic vascular embolization may be required, and hyperbaric oxygen has been shown to be helpful (46,48). For patients with intractable symptoms, urinary tract diversion or cystectomy may be the last option.
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Extrinsic Masses Causing Bladder Filling Defects
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In addition to the conditions previously described, a number of other entities can protrude into the bladder and mimic a bladder mass. These entities include extrinsic masses of prostatic, uterine (Fig 29), and ovarian origin; ureteroceles, extramedullary hematopoiesis; urachal cysts; paraganglionic tissue; hamartomas; amyloidosis; and vascular malformations (5).
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Figure 29a. Cervical cancer invading the posterior wall of the bladder. Axial contrast-enhanced CT (a) and sagittal T2-weighted MR (b) images show a large, irregular cervical mass invading the posterior wall of the bladder (straight arrow). There is uterine obstruction with hematometros (curved arrow in b).
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Figure 29b. Cervical cancer invading the posterior wall of the bladder. Axial contrast-enhanced CT (a) and sagittal T2-weighted MR (b) images show a large, irregular cervical mass invading the posterior wall of the bladder (straight arrow). There is uterine obstruction with hematometros (curved arrow in b).
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An enlarged prostate gland may protrude into the bladder base and simulate a mass arising from the bladder at imaging. The enlargement is more commonly benign than malignant: Malignant lesions are more irregular (Fig 30). Benign prostatic hyperplasia is common and its prevalence increases with patient age, but it is not an indication for imaging. However, an enlarged median lobe of the prostate that bulges into the base of the bladder may be incidentally seen and needs to be distinguished from an intrinsic bladder mass (Fig 31). At CT or US, the site of origin of the mass is more diagnostic than its appearance. At MR imaging, however, benign prostatic hyperplasia has a characteristic appearance, consisting of round nodules of varying sizes that have high signal intensity with T2-weighted sequences, as well as a variable amount of low-signal-intensity fibrosis (49) (Fig 32). The relative proportion of nodules to stromal reaction depends on the degree of stromal versus glandular hyperplasia.
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Figure 30a. Prostate cancer. Anteroposterior view of the bladder obtained during intravenous urography (a) and axial unenhanced CT scan (b) show an irregular, nodular filling defect in the base of the bladder (arrow). Histologic evaluation showed prostatic adenocarcinoma.
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Figure 30b. Prostate cancer. Anteroposterior view of the bladder obtained during intravenous urography (a) and axial unenhanced CT scan (b) show an irregular, nodular filling defect in the base of the bladder (arrow). Histologic evaluation showed prostatic adenocarcinoma.
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Figure 31. Benign prostatic hypertrophy. Axial CT image shows a large, smooth, lobular mass bulging into the base of the bladder (arrow). Despite its large size, this "mass" proved to be benign hypertrophy of the prostate.
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Figure 32a. Benign prostatic hypertrophy. Sagittal (a) and coronal (b) T2-weighted MR images show the central portion of the prostate gland protruding into the bladder base (arrow). In this case, the gland is predominantly low signal intensity, a finding that indicates it contains a larger amount of stromal rather than glandular hyperplasia.
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Figure 32b. Benign prostatic hypertrophy. Sagittal (a) and coronal (b) T2-weighted MR images show the central portion of the prostate gland protruding into the bladder base (arrow). In this case, the gland is predominantly low signal intensity, a finding that indicates it contains a larger amount of stromal rather than glandular hyperplasia.
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Ureteroceles are another common entity that causes bladder filling defects. They are secondary to congenital obstruction of the ureteral meatus, resulting in saccular dilatation of the intramural course of the ureter. The ureterocele may be associated with a duplicated (80% of cases) or single collecting system and may insert into the bladder ("orthotopic" insertion in 17%–35% of cases) or into an ectopic site such as the urethra or vagina. One in 4000 children have an ureterocele, and there is a 4–7:1 female-to-male ratio. Approximately 10% of ureteroceles are bilateral (50).
Patients may be asymptomatic, but when symptoms are manifested, they are varied and relate to vesicoureteric junction obstruction and reflux. Symptoms and signs include urinary tract infection, urosepsis, frequency, hematuria, pain, urinary retention, and stone disease. At cystoscopy, the wall of the ureterocele is smooth and covered by normal epithelium. The wall of the ureterocele consists of one layer of ureteral epithelium and one of bladder urothelium, with intervening connective tissue and muscle (50).
Imaging features of ureteroceles are characteristic of the entity. At sonography, the classic appearance is a fluid-filled intraluminal lesion arising from the wall of bladder. The ureterocele is contiguous with the ureter, and an associated ureteral jet helps confirm the diagnosis (Fig 33). Associated duplicated or dilated upper tracts may be present. A ureterocele is a smooth filling defect of variable size, depending on whether it is collapsed or distended at urography, with a radiolucent rim referred to as the "cobra sign" (Fig 34). At CT or MR imaging, the ureterocele is a round fluid-filled lesion. CT or MR urography allows a more comprehensive evaluation of the urinary tract (Fig 35).
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Figure 33a. Ureterocele. (a) Longitudinal gray-scale US image shows an anechoic cystic structure (arrow) at the ureteral orifice. (b) Transverse color Doppler US image shows an ureteral jet, a finding that confirms the cyst is an ureterocele.
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Figure 33b. Ureterocele. (a) Longitudinal gray-scale US image shows an anechoic cystic structure (arrow) at the ureteral orifice. (b) Transverse color Doppler US image shows an ureteral jet, a finding that confirms the cyst is an ureterocele.
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Figure 34. Left posterior oblique radiograph of the bladder shows a contrast material–filled ureter that creates a smooth filling defect within the bladder. As the ureter prolapses into the bladder, the combined walls of the ureter and bladder create a radiolucent rim, the so-called cobra sign (arrow).
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Figure 35a. (a) Axial contrast-enhanced CT image shows a contrast material–filled ureterocele (straight arrow) and a dilated, distal left ureter (curved arrow). (b) Coronal three-dimensional CT uro-gram shows the ureterocele (arrow) and dilated left ureter to excellent advantage.
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Figure 35b. (a) Axial contrast-enhanced CT image shows a contrast material–filled ureterocele (straight arrow) and a dilated, distal left ureter (curved arrow). (b) Coronal three-dimensional CT uro-gram shows the ureterocele (arrow) and dilated left ureter to excellent advantage.
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Management depends on symptoms, but treatment usually consists of surgical unroofing of the ureterocele and control of infection.
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Conclusions
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The discovery of a focal bladder mass usually requires pathologic evaluation. Although bladder neoplasms are common, there are a number of nonneoplastic and inflammatory disorders that can manifest as a focal bladder mass and mimic malignancy. Some of these entities, such as inflammatory pseudotumor, endometriosis, Crohn disease, diverticulitis, ureterocele, and benign prostatic hyperplasia, have radiologic features highly suggestive of the diagnosis and should be recognized by the radiologist to prevent unnecessary radical surgery. Diffuse bladder wall thickening has a longer list of differential diagnoses, and clinical and pathologic correlation is required.
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Footnotes
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Abbreviations: H-E = hematoxylin-eosin
The opinions and assertions contained herein are the private views of the authors and are not to be construed as official nor as representing the views of the Department of Defense.
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References
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Abstract
LEARNING OBJECTIVES FOR TEST...
