Fig. 2.1
A 69-year-old man with bladder cancer. (a) Axial US image of the bladder shows a lumen protruding mass (arrows) in the right lateral wall of the bladder. (b) Early-phase contrast-enhanced CT image demonstrates strong enhancing, nodular lesion (arrow) within the bladder. Note low attenuation of urine in the bladder with excreted contrast in the bladder lumen. (c) Maximum-intensity-projection image of bladder mass (arrow) with contrast material filled in the bladder lumen. (d) Nephrogenic phase contrast-enhanced CT image demonstrates obscured tumor contour due to excreted contrast to the bladder lumen. (e) Cystoscopic photograph shows papillary mass fungating into the bladder
Discrete bladder mass and nodule are findings of bladder TCCs. This lesion shows early enhancement after contrast injection (within 60 s) when the lesion is surrounded by low-attenuated urine. However, filling defect in delayed-phase image is also helpful in the detection of tumor when the nodule is large (Fig.2.1c). For this reason, focal hyperenhancement of the bladder urothelium should be considered as bladder TCCs. In other words, early-phase images are more important for detection of bladder TCCs because subtle lesion is more difficult to detect in delayed-phase images due to contrast material excreted to the bladder lumen. As a result, when patients suspected with bladder malignancy undergo contrast-enhanced CT, early-phase image should be obtained before contrast excretes to the bladder.
Presence of ureteral obstruction is observed when tumor invades the bladder muscle. Perivesical fat infiltration is seen when tumor extends to perivesical fat (Fig. 2.2) [17]. Calcification of bladder wall associated with bladder wall thickening should be suspected as malignancy, and further evaluation should be done. But, calcification can also be seen as sequelae of previous infections, bacilli Calmette Guérin (BCG) therapy.
Fig. 2.2
A 74-year-old man with bladder cancer. Contrast-enhanced axial CT image of the bladder shows iso-attenuated mass (large arrow) in the posterior wall of the bladder. Note calcification in the mass (small arrows) and perivesical infiltration (arrowheads)
2.2.1.2 MRI
MR imaging is known to allow more accurate staging of bladder TCCs than CT due to high soft tissue contrast [18]. MR imaging is better in assessing both muscle invasion and extravesical invasion in bladder TCCs. In addition, MR imaging has no radiation. In the evaluation of bladder TCCs, high spatial resolution is needed. For this purpose, phased-array external surface coil, thin section, and large matrix are needed. Twenty-eight to 32 cm axial field of view (FOV) is sufficient to evaluate bladder and adjacent structures. Optimal echo time (60–80 ms) is crucial for high contrast-to-noise ratio, which is important in evaluating bladder wall invasion depth with tumor [19].
Axial T1-weighted images are useful in detecting perivesical tumor infiltration. On T1-weighted images, urine in the bladder shows low signal intensity, bladder wall shows iso-signal intensity, and perivesical fat shows high signal intensity. On T2-weighted images, urine has high signal intensity and bladder wall shows low signal intensity.
With instructing patients to void 2 h before MR, optimal bladder distension can be achieved [20]. When the bladder is underdistended, small tumors cannot be detected due to thickening of bladder muscle. An overdistended bladder may cause obscuring of flat bladder TCCs. Bowel peristalsis causes artifact; this can be reduced with administering an intramuscular antiperistaltic agent and using anterior saturation bands. With swapping phase and frequency-encoding direction, motion artifact can also be reduced [13]. Chemical shift artifact is misregistration of spatial information caused by the difference of resonant frequencies of fat and water. This occurs in the interface of water and fat [21]. This artifact is seen in frequency-encoding direction and appears as low- and high-signal bands along the water-fat interface perpendicular to face-encoding direction. The pixel width of this artifact gets wide as field strength increases. This bandlike artifact can hinder detection of bladder wall tumor. To reduce this artifact, the increase of bandwidth and changing direction of frequency-encoding direction are needed [22]. T2-weighted images are obtained in three orthogonal planes. High-resolution images with plane perpendicular to the bladder mass are most crucial in the evaluation of muscle invasion depth and perivesical extension [18]. When the tumor does not invade bladder muscle, low signal intensity of muscle is not interrupted on T2-weighted image. When the tumor invades bladder muscle, low signal intensity of muscle is interrupted by the tumor. When tumor extends to extravesical fat or organ, this can also be seen MR imaging (Fig. 2.3).
Fig. 2.3
A 57-year-old man with bladder cancer. (a) Sagittal T2-weighted MR image of tumor shows large mass with the bladder wall thickening (arrow). Perivesical stranding (small arrows) was confirmed to tumor spread at histopathologic examination. (b) Sagittal T1-weighted MR image shows mass in the bladder (arrow). Mass shows iso-signal intensity with adjacent muscle. (c) Sagittal contrast-enhanced T1-weighted MR image reveals enhancing mass in the bladder (arrow). Perivesical tumor spread is seen (small arrows)
With multiplanar imaging, MR imaging can minimize partial volume averaging and allow accurate evaluation of bladder muscle invasion with tumor. Coronal images are useful in evaluating bladder lateral wall and dome. Sagittal images are useful in detecting lesions in the anterior and posterior wall [13].
Recently, 3D sequence MR imaging is feasible. Compared to 2D sequence, 3D sequence offers shorter acquisition time, volumetric coverage without interslice gaps, and higher signal-to-noise ratio [19]. With this technique, single-breath-hold imaging acquisition is possible.
The bladder wall does not show early enhancement on the gadolinium-enhanced images. In the early phase (20 s after intravenous contrast injection), bladder TCCs show more enhancement than adjacent bladder muscle [23]. The bladder TCCs, mucosal, and submucosa have early enhancement, but bladder muscle shows late enhancement (60 s) [18]. Bladder TCCs show as filling defect in delayed (>5 min) image, but small lesion can be obscured due to contrast material in the bladder.
The bladder TCCs with increased cellular density show increased signal intensity on diffusion-weighted images and reduced signal intensity on apparent diffusion coefficient (ADC) maps [24]. Changes of signal intensity on diffusion-weighted images are more useful than ADC measurement, because there can be interobserver variation in ADC values in the bladder tumor in relatively thin bladder wall [25]. Diffusion-weighted image in bladder TCCs has shown improved differentiation of bladder TCCs from bladder muscle layer [26–29].
2.2.1.3 Staging
The clinical stage of the bladder cancer is determined by the depth of invasion of bladder wall by the tumor. The clinical staging, with using CT or MR imaging, often underestimates tumor extent. CT is standard imaging modality for preoperative staging. The accuracy of contrast-enhanced CT in the local staging of bladder TCCs is 40–60 % [30, 31]. The accuracy of contrast-enhanced MR imaging is 52–93 % [18, 32–35]. Microscopic perivesical spread (T3a) is not detectable in CT or MR imaging. Macroscopic perivesical disease (T3b) can be diagnosed at CT or MRI. However, perivesical edema or inflammation especially after bladder cancer treatment can mimic perivesical tumor spread. The TNM classification of the renal pelvis and ureter is tabulated in Table 2.1 [36].
Table 2.1
TNM classification of the bladder TCC
Stage | Findings |
|---|---|
Tx | Primary tumor cannot be assessed |
T0 | No evidence of primary tumor |
Ta | Papillary noninvasive carcinoma |
Tis | Carcinoma in situ |
T1 | Tumor invades subepithelial connective tissue |
T2 | Tumor invades muscularis propria |
T2a | Tumor invades the superficial muscularis propria (inner half) |
T2b | Tumor invades the deep muscularis propria (outer half) |
T3 | Tumor invades perivesical tissue |
T3a | Tumor invades perivesical tissue microscopically |
T3b | Tumor invades perivesical tissue macroscopically (extravesical mass) |
T4 | Tumor invades any of the following: prostatic stroma, seminal vesicles, uterus, vagina, pelvic wall, abdominal wall |
T4a | Tumor invades prostatic stroma, uterus, vagina |
T4b | Tumor invades pelvic wall, abdominal wall |
Nx | Regional lymph nodes cannot be assessed |
N0 | No regional lymph node metastasis |
N1 | Single regional lymph node metastasis in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node) |
N2 | Multiple regional lymph node metastases in the true pelvis (hypogastric, obturator, external iliac, or presacral lymph node) |
N3 | Lymph node metastases to the common iliac lymph nodes |
M0 | No distant metastasis |
M1 | Distant metastasis |
2.2.2 Transitional Cell Carcinoma: Kidney and Ureter
Upper urinary tract TCCs occur in the sixth and seventh decades of life and have male predominance [37]. TCCs are common in the urinary bladder, and 5 % of urothelial tumors arise from the renal pelvis or ureter, and they account for 10 % of tumors of the upper urinary tract [38, 39]. Smoking, chemical carcinogens (aniline, benzidine, aromatic amine, azo dyes), analgesic abuse, cyclophosphamide, and heavy caffeine consumption increased risk of TCCs [38, 40].
Upper urinary TCCs are histologically similar to bladder TCCs [41]. Low-grade tumors have superficial, papillary appearance with broad base, are usually small and slowly growing, and have good prognosis [42]. High-grade tumors are less common, pedunculated or diffusely infiltrating, and more aggressive [43].
Synchronous bilateral TCCs occur in 1–2 % of renal TCCs and 2–9 % of ureteral TCCs, and 11–13 % of upper urinary tract TCCs develop metachronous upper urinary tract TCCs [37]. About 50 % of upper urinary tract TCCs will develop bladder TCCs after surgical treatment [38, 44]. Two percent of bladder TCCs have synchronous upper urinary tract TCCs and 6 % will have metachronous upper tract tumor [45].
2.2.2.1 Intravenous Urography and Retrograde Pyelography
TCCs from the upper urinary tract are usually diagnosed with intravenous urography (IVU) in the patients with hematuria. These days, CT urography gradually replaces the IVU the noninvasive methods of choice in the diagnosis of TCCs from the upper urinary tract. The TCCs from the upper urinary tracts are well visualized. Calcifications can be seen in precontrast radiograph in 2–7 % of tumors, and they can be confused as urinary stone [37].
TCCs from renal pelvicalyceal system can be seen as a filling defect in IVU. These filling defects can be single or multiple and smooth, irregular, or stippled (Fig. 2.4). Contrast material dispersed in the papillary mass is shown as stippled appearance in IVU. This finding also can be seen in benign lesions such as blood clot and fungus ball. Some TCCs can show stricture-like lesions; these findings can be misinterpreted as renal tuberculosis [40]. When tumors obstruct renal infundibulum, affected calyx is not visualized in IVU and this is calyceal amputation. When calyx is not seen in IVU, we call it “phantom calyx” (Fig. 2.5).
Fig. 2.4
A 51-year-old woman with papillary transitional cell carcinoma in the left renal pelvis. (a) IVU shows irregular filling defects in the pelvis of the left kidney (arrow). Note the surface of the lesion has mottled and streaky appearances suggesting papillary nature of the lesion (stipple sign). (b) US of the left kidney shows lumen protruding mass in the left renal pelvis (arrow). Note adjacent hydronephrosis. (c, d) Contrast-enhanced CT scans show a mass in dilated left renal pelvis (arrows)
Fig. 2.5
A 54-year-old man with papillary transitional cell carcinoma in the left renal infundibulum. Upper polar calyx is not seen in IVU due to obstruction of infundibulum (phantom calyx)
TCCs from the ureter are seen as single or multiple filling defects. Stippling or proximal obstruction can be seen. When there are long-standing obstructions due to ureteric tumor, contrast excretion can be poor, and it may be hard to evaluate ureteric lesion. When this happens, contrast-enhanced CT or retrograde pyelography (RGP) can be done for further evaluation.
Retrograde pyelography is performed during cystoscopy, for further evaluation when upper urinary tract lesions are not well visualized during IVU or when patients are allergic to contrast materials. Although RGU is more invasive compared with IVU, it can aid confirmation of lesion detected in IVU and help biopsy or brushing during ureteroscopic examination.
Renal TCCs are irregular papillary or nodular mass in RGU (Fig. 2.6). Amputated calyx can be seen when TCCs invade and obstruct renal infundibulum. When tumor fills and distends calyx, we call it “oncocalyx.”
Fig. 2.6
An 84-year-old man with transitional cell carcinoma. (a) RGP shows a papillary filling defect in the right renal pelvis with amputation of the lower calyceal infundibulum (arrows). (b) Contrast-enhanced CT shows mass with irregular surface (arrow) in dilated renal pelvis in the left kidney
Ureteral TCCs are usually seen as polypoid filling defect with proximal dilatation. Circumferential or eccentric ureteric strictures can be seen in TCC and sometimes they can be confused with benign strictures. In malignant stricture, there are usually ureteric fixation and nontapering margin [37]. In RGP, dilatation of the ureter distal to ureteral mass is seen, and this is called “goblet” sign (Fig. 2.7).
Fig. 2.7
An 88-year-old man with ureter transitional cell carcinoma. RGP shows a filling defect in the left midureter. Note smooth concavity of the ureter just beneath the tumor, which is “goblet sign” (arrows)
2.2.2.2 CT
CT is useful in the diagnosis of upper urinary tract TCCs. With CT urography, a small renal pelvis mass and urinary tract mass can be detected. CT urography is superior to IVU in that urothelium, renal parenchyma, and adjacent tissue can be evaluated at a time.
There have been multiple different CT urography protocols: single-bolus technique, split-bolus technique, and triple-bolus technique. Among them single-bolus technique is most commonly used in practice. In single-bolus technique, precontrast scan is acquired from kidney to symphysis pubis. After that one bolus of contrast is injected and early, parenchymal, and excretory phase scan is acquired [46]. The advantage of this technique over the other technique (split-bolus and triple-bolus technique) is that it can provide optimal opacification and distension of the renal pelvis and ureter. In addition, small renal cell carcinomas can be more easily detected compared with other technique. The major disadvantage of this technique is increased radiation dose due to multiple imaging phases. In split-bolus technique, contrast injection is divided into two sessions and imaging is acquired in combined nephrogenic and excretory phase. The advantage of this technique is decreased radiation due to reduced imaging phase [47, 48]. However, there are some questions about the optimal opacification of distal ureter due to half dose of contrast for excreted contrast [47, 48]. Triple-bolus technique splits dose of contrast into three boluses and acquires combined early-nephrogenic phase [49]. With this technique, the radiation dose can be reduced, but the opacification and distension of ureter are also questionable in this technique. In addition, detectability of small renal lesion (such as small renal cell carcinoma) can be decreased.
In performing CT urography, ancillary techniques, such as abdominal compression, intravenous (IV) saline, IV furosemide, and prone positioning, should be considered [46]. Abdominal compression is done for opacification of proximal urinary tract. But, the usefulness is in doubt [50]. IV saline injection is suggested in some studies to distend distal ureters [50]. IV diuretic injection improves distension and opacification of ureter [5]. But there are some difficulties in IV injection of diuretics in daily practice, because of allergy or hypotension.
Single-bolus technique is most commonly used because of optimal distension of the ureter and higher sensitivity in the detection of renal mass [46]. To decrease beam-hardening artifact, which can interfere detection of small lesions, delayed images after 5 min are recommended [51]. When there is obstruction, more delayed image acquisition for excretory phase is needed.
Renal TCCs are seen as filling defect renal pelvis wall thickening in the excretory phase (Fig. 2.4). Other findings are pelvicalyceal irregularity, oncocalyx, or obstructed calyx (Fig. 2.6). Early TCCs are separated from renal parenchyma. Advanced TCCs extend to renal parenchyma. Sometimes renal TCCs have mass-like appearance, mimicking centrally located renal cell carcinoma (RCC) (Fig. 2.8). Imaging features for renal TCCs are as follows: mass epicenter in the renal pelvis or calyx, presence of focal filling defect in collecting system, reniform contour preservation, mainly solid feature, homogeneous attenuation, moderate enhancement, and extension of tumor to ureteropelvic junction.
Fig. 2.8
A 77-year-old man with transitional cell carcinoma in the renal pelvis invading renal parenchyma. Contrast-enhanced CT shows extensive parenchymal invasion (arrows) of the left kidney. Note, the left kidney conserves reniform contour and mass shows homogeneous and solid feature
Ureteral thickening is the most common manifestation of ureteral TCCs (Fig. 2.9) [50]. To detect thickening of ureter in ureter TCCs, meticulous check of all three phase is needed because subtle urothelial thickening can be seen in all three phases. Not only irregular and eccentric but also circumferential and smooth wall thickening can be seen in ureteral TCCs [52]. TCCs show early enhancement so early phase is important phase in the detection of ureteral TCCs (Fig. 2.10) [52]. Enhancement pattern is usually focal and eccentric. Care should be taken for evaluation of ureteral enhancement because this can also be seen in inflammatory lesions [53]. Calcification can be seen ureteral TCCS. Calcification is usually located eccentrically or in the wall. This should be differentiated urinary stone which is located in the central lumen of ureter. Periureteral fat stranding can be seen in urinary TCCs. Usually cancer-related periureteral fat stranding is persistent after treatment; this is differential point from inflammation-related periureteral fat stranding. Filling defects are findings of ureteral TCCs. But, when mass size is small, sometimes it is difficult to detect tumor in excretory phase due to beam-hardening artifact. Some of these lesions can be seen in the early or nephrogenic phase [54]. Ureteral TCCs can accompany hydronephrosis or hydroureter. Dilatation of proximal ureter can be seen even when ureteral TCCs are no visible. So when there is ureteral dilatation proximal to suspected stricture without definite mass, ureteroscopic examination should be done not to miss small ureteral TCCs [52].
Fig. 2.9
Transitional cell carcinoma of the distal ureter in a 77-year-old man. Coronal reformation image of contrast-enhanced CT shows irregular wall thickening of the right midureter (arrows)
Fig. 2.10
Transitional cell carcinoma of the distal ureter in a 73-year-old man. Contrast-enhanced CT shows an enhancing soft tissue lesion (arrow) in the right distal ureter. Note non-opacification of both external iliac veins, indicating that this image is early phase after contrast injection
2.2.2.3 MRI
MR imaging is infrequently used in the evaluation of upper urinary tract TCCs. Generally, MR imaging is less commonly used compared with CT urography due to more time for acquiring image and more motion-related artifacts. However, when the patients have a contraindication to CT contrast agent, MRI can be an option. MR imaging has high soft tissue contrast, is independent to renal function, and allows multiplanar imaging.
TCC shows lower-signal intensity than urine in T2-weighted images and tumors are well visualized. In gadolinium contrast-enhanced images, TCCs show moderate enhancement (Fig. 2.11) [55]. MR urography is used in the evaluation of the upper urinary tract. At MR urography, ureteric TCCs are shown as irregular mass. Sometimes differentiation between stone and small TCCs is difficult in MR urography. Usually ureter stone has sharp margin but ureter TCCs usually have irregular margins.
Fig. 2.11
An 82-year-old man with transitional cell carcinoma of the renal pelvis. (a) T2-weighted MR image shows hypointense mass in the left renal pelvis (arrow). Mass is confined to the renal pelvis. (b) T1-weighted MR image shows iso-attenuated mass in the left renal pelvis (arrow). (c) Contrast-enhanced T1-weighted image shows relatively less enhancement compared with renal parenchyma (arrow)
2.2.2.4 Staging
The TNM classification of the renal pelvis and ureter is tabulated in Table 2.2 [36].
Table 2.2
TNM classification of the renal pelvis and ureter TCC
Stage | Findings |
|---|---|
Tx | Primary tumor cannot be assessed |
T0 | No evidence of primary tumor |
Ta | Papillary noninvasive carcinoma |
Tis | Carcinoma in situ |
T1 | Tumor invades subepithelial connective tissue |
T2 | Tumor invades the muscularis |
T3 | Renal pelvis: tumor invades beyond muscularis into peripelvic fat or the renal parenchyma |
Ureter: tumor invades beyond muscularis into periureteric fat | |
T4 | Tumor invades adjacent organs or through the kidney into the perinephric fat |
Nx | Regional lymph nodes cannot be assessed |
N0 | No regional lymph node metastasis |
N1 | Metastasis in a single lymph node, ≤2 cm in greatest dimension |
N2 | Metastasis in a single lymph node, >2 cm but not >5 cm in greatest dimension; or multiple lymph nodes, none >5 cm in greatest dimension |
N3 | Metastasis in a lymph node, >5 cm in greatest dimension |
M0 | No distant metastasis |
M1 | Distant metastasis |
2.3 Nonurothelial Tumors
2.3.1 Squamous Cell Carcinoma
Squamous cell carcinoma consists less than 5 % of bladder tumors [1]. Symptoms are gross hematuria and irritation during voiding. Risk factors are nonbilharzial region residency, cyclophosphamide, intravesical BCG, smoking, bladder stone, or chronic infection. Paraplegic patients usually have both bladder stone and infection [1, 56]. Tumors are high grade and locally aggressive with muscle invasion [57]. They usually occur at the trigone and bladder lateral wall and diverticula [58]. Metastases are present in 10 % of cases at diagnosis and involve the regional lymph node, bone, lung, and bowel [59]. Muscle invasion is present in 80 %, and extravesical invasion is extensive [60]. Prognosis is generally poor because it presents with advanced stage. Death is usually from local failure, with metastasis (8–10 %) [61].
Bladder squamous cell carcinoma has nonspecific imaging findings. Tumors show focal or diffuse bladder wall thickening or single enhancing bladder mass (Fig. 2.12) [60]. Diverticular squamous cell carcinomas are soft tissue masses and occasionally surface calcification may coexist [58]. Bladder squamous cell carcinoma shows sessile growth pattern compared to papillary growth pattern of TCCs. Bladder wall thickening or calcification can be seen.
Fig. 2.12
A 72-year-old man with squamous cell carcinoma of the bladder. Contrast-enhanced CT shows diffuse bladder wall thickening with mass formation in the posterior wall of the bladder (asterisk). Note perivesical infiltration (arrows), which was histologically confirmed to tumor spread
2.3.2 Adenocarcinoma
Adenocarcinoma is a uncommon bladder neoplasm (less than 2 %) [1]. It can be classified as primary (nonurachal and urachal) and secondary. The mean age of diagnosis is 60 years, and urachal cancer occurs 10 years earlier. Nonurachal adenocarcinoma has male predominance, but urachal adenocarcinoma has equal prevalence in men and women. Hematuria and irritation are common symptoms. In 25 % mucous secreted in urine [62]. Umbilical discharge can be seen in urachal cancer.
Bladder adenocarcinoma is associated with bladder exstrophy and persistent urachus. Other risk factors are chronic mucosal irritation associated with intestinal metaplasia, urinary diversion, and pelvic lipomatosis associated with cystitis glandularis.
Metastatic adenocarcinoma of the bladder is more common than primary bladder adenocarcinoma. Adenocarcinoma is most common histologic type of secondary bladder neoplasms. Primary sites include direct invasion from colon, prostate, rectum, and pelvic tumors [63]. Hematogenous metastases from the stomach, breast, and lung are less common. Differentiation of primary and secondary bladder adenocarcinomas is important in deciding treatment plan. When bladder metastases occur, usually there are locally invasive primary malignancies.
Although urine cytology is useful, sensitivity is limited when tumor is located beneath mucosal layer. At cystoscopy, adenocarcinoma is usually single nodular lesion occurring at bladder base (58–67 %) and urachus. Primary adenocarcinoma is histologically same with colon adenocarcinoma, and it is difficult to distinguish primary adenocarcinoma from metastatic adenocarcinoma, even with special stain [63].
Nonurachal adenocarcinoma shows diffuse bladder wall thickening at CT (75 %) and stranding of surrounding fat (88 %) [64]. Distant metastases (38 %), lymph node metastasis (25 %), rectus muscle invasion (25 %), and peritoneal seeding were observed.
Urachus is a midline remnant of the cloaca and allantois. It is located extraperitoneally and is bounded by the transverse fascia and parietal peritoneum. This area is called “Retzius space” [65]. In fetal life, urachus is regressed to a fibrous band and becomes medial umbilical ligament. This extend anterior dome of the bladder to umbilicus. Incomplete regression of the urachus causes four anomalies: urachal sinus, patent urachus, urachal diverticulum, and urachal cyst. Among them, urachal cyst is the most common (30 %) [66]. Most urachal tumors are adenocarcinomas (90 %). Because urachal remnant is lined by transitional epithelium, the suggested pathogenesis is metaplasia of urachal mucosa into columnar epithelium and malignant transformation [65]. In urachal cancer, mucin stain is positive [62]. Urachal cancer has male predominance and occurs between 40 and 79 years old [65, 67]. Common symptoms are hematuria, dysuria, abdominal pain, suprapubic mass, and discharge from the umbilicus [17, 68].
In IVU or cystography, urachal adenocarcinoma is seen as a filling defect or extrinsic compression in the dome of the bladder. Tumor can be detected with ultrasound (US) as a fluid-filled, mixed echogenic solid mass with or without calcification adjacent to abdominal wall. But these imaging findings are nonspecific.
CT and MR imaging are more accurate imaging modalities for evaluation of both local staging and distant metastases. CT feature is a midline mass anterior superior to the dome of the bladder with mixed solid and cystic appearance (Fig. 2.13) [65]. The cystic component is mucin. Peripheral punctate or stippled or curvilinear calcification is present in 50–70 %, and they are considered pathognomonic for urachal carcinoma [65, 68–70]. Urachal adenocarcinoma is outside of the bladder in 88 % [70]. In contrast to bladder TCCs, extravesical tumor spread is common (Fig. 2.14). Bladder wall invasion is present in 92 % and metastases are present in 48 % [70, 71]. Pseudomyxoma peritonei rarely occurs.
Fig. 2.13
A 57-year-old man with adenocarcinoma of the bladder. Contrast-enhanced CT shows well-enhancing mass (arrow) in the anterior wall of the bladder. There are irregularities in the outer margin of the tumor indicating perivesical tumor extension
Fig. 2.14
A 62-year-old woman with urachal adenocarcinoma. Contrast-enhanced CT scan shows a mixed cystic and solid midline mass with punctate calcification anterocranial to the bladder (arrows)
MR imaging is the best technique for evaluation of urachal adenocarcinoma. On T2-weighted images, there are focal high-signal-intensity lesions suggestive of mucin [65]. On T1-weighted images, tumor shows iso-signal intensity and enhances with contrast material.
2.3.3 Small Cell Tumors
Small cell bladder tumor is a rare tumor (0.5 % of bladder tumor) [72, 73]. This tumor is an aggressive tumor with advanced stage at diagnosis. Presenting symptom is hematuria (88 %) and patients usually have smoking history (65 %). Patient’s age has a wide range (20–90 years old); there is male predominance (male-female = 3-5:1) [72, 73].
Small cell bladder tumor arises from neuroendocrine cells. They are sheets of small cells with round hyperchromatic nuclei, sparse cytoplasm, and mitotic figure in histology. Majority have mixed tumor histology.
Cystoscopically, tumors are large and polypoid or nodular with ulcerative surface, mimicking other high-grade bladder cancer. The most common site is the lateral bladder wall [73]. On CT images, tumor has wall invasion, central necrosis, or cystic change (Fig. 2.15). Mass size is from 3 to 8 cm [74]. Calcification is not common. Tumor shows patchy enhancement unlike bladder TCCs [74]. Metastases occur rapidly, and the metastatic sites are the peritoneum, liver, bone, lung, and lymph nodes (66 %) [1].
Fig. 2.15
Small cell carcinoma of the bladder in a 65-year-old woman. Contrast-enhanced CT scan shows broad-based, large mass (arrow), which is not distinguishable from other bladder tumors. Note perivesical infiltration
2.3.4 Lymphoma
Lymphoma involvement of the bladder is much more often secondary rather than primary. Secondary involvement of the bladder is present in 10–25 % of lymphoma patients [75]. In secondary lymphoma, lymphadenopathy in abdomen and pelvis is usually found. It is common in middle-aged women with nonspecific urinary symptom (hematuria or mass effect). The cell type is B-cell mucosa-associated lymphoid tissue type or diffuse large B-cell type [75]. Hodgkin lymphoma is rare.
Imaging findings are well-defined bladder masses without infiltration (Fig. 2.16) [17]. They can mimic TCCs and cannot be differentiated from other primary bladder masses [76].
Fig. 2.16
Non-Hodgkin lymphoma of the bladder in a 49-year-old woman. Contrast-enhanced CT scan shows a homogeneously enhancing diffuse bladder wall thickening (arrows). Note enlargement of the uterus suggesting lymphoma involvement (asterisk)
2.3.5 Leiomyoma
Bladder leiomyoma is a benign mass arising from the smooth muscle of the bladder and the most common benign bladder tumor [76]. Histologically, leiomyoma is noninfiltrative smooth muscle tumors lacking mitotic activity, cellular atypia, and necrosis. It is more common in women [77]. Two third of them grow externally, one third internally, and rarely grow intramurally [78]. Most are small and asymptomatic and discovered incidentally. Most of them have no symptoms, but sometimes, pressure from mass, urinary obstruction, hesitancy, dribbling, and hematuria can occur [79]. Although it is a benign tumor without malignant potential, histologic evaluation is needed to exclude possibility of well-differentiated leiomyosarcoma. They are benign and grow noninvasively and focal excision of the mass is the treatment of choice. However, sometimes they can recur after surgical treatment. At cystoscopy, leiomyoma is covered with normal bladder mucosa. They are well-circumscribed, solid, homogeneous, and smooth mass from the bladder wall. Cystic components indicate degeneration. MR imaging is superior to CT in characterizing leiomyoma, demonstrating the submucosal origin of the tumor and the preservation of the muscle layer.
Imaging findings of bladder are similar to those of uterine myoma. On T1-weighted image, they show iso-signal intensity, and on T2-weighted image, they show low signal intensity (Fig. 2.17). They can show heterogeneous high signal intensity on T2-weighted image if there are degeneration [79]. They show variable enhancement on contrast-enhanced image, with degenerated areas lacking enhancement [17]. A pedunculated luminal leiomyoma can be differentiated from bladder TCCs in that it has low signal intensity on T2-weighted images. A preoperative suggestion of leiomyoma is invaluable in alerting the surgeon to benign and preventing radical cystectomy.
Fig. 2.17
Leiomyoma of the bladder in a 52-year-old man. (a) Contrast-enhanced CT images show a homogeneously enhancing, soft mass in the lower abdomen (arrow). (b) T2-weighted MR image shows low-signal-intensity mass from the posterior wall of the bladder (arrow). (c) T1-weighted MR images shows intermediate signal intensity mass (arrow). (d) Contrast-enhanced T1-weighted image shows strong enhancement of the mass (arrow)
2.4 Pathologic Consideration
2.4.1 Urothelial Tumors
2.4.1.1 Papillary Urothelial Lesion
Urothelial Papilloma
Pathologically, urothelial papilloma is exophytic papillary mass lined by benign, normal-looking urothelium with normal thickness (Fig. 2.18). Urothelial lining shows normal polarity, and umbrella layer is well developed. Cytologic atypia is absent or minimal. Branching of papillary architecture is minimal. Papillary core of urothelial papilloma is thin and slender, but occasionally is edematous. Most urothelial papillomas are solitary.
Fig. 2.18
Urothelial papilloma has fibrovascular core lined by normal-looking urothelium with normal thickness. Umbrella layer is well defined
Inverted Papilloma
Inverted papilloma is benign urothelial tumor showing inverted growth pattern. Grossly inverted papilloma is small polypoid lesion with smooth surface. Microscopically inverted papilloma reveals invagination of urothelium into submucosa with cord or trabecular pattern (Fig. 2.19). Cytologic atypia of the urothelium is absent or minimal.
Fig. 2.19
Inverted papilloma shows endophytic growth of normal-looking urothelium with trabecular architecture. Overlying urothelium is normal
Papillary Urothelial Neoplasm of Low Malignant Potential
Papillary urothelial neoplasm of low malignant potential resembles urothelial papilloma but shows increased thickness of urothelial layers with minimal or no cytologic atypia (Fig. 2.20). The polarity of the urothelium is preserved, and the umbrella layer is often normally present. Papillary core is thin and delicate. Branching and complexity of papillae are limited.
Fig. 2.20
(a) Papillary urothelial neoplasm of low malignant potential has papillary architecture with mildly increased branching and hyperplastic urothelial lining. (b) Urothelial layer is increased, but cytologic atypia is minimal
Low-Grade Papillary Urothelial Carcinoma
Low-grade papillary urothelial carcinoma shows architectural disorganization and low-grade cytologic atypia. Grossly, this tumor is solitary or multiple exophytic papillary mass. Microscopically low-grade papillary urothelial carcinoma reveals more complex papillary architecture with thickened urothelial layers. Tumor cells also show loss of polarity with mild cytologic atypia and nuclear size variations (Fig. 2.21). But there is no marked nuclear pleomorphism. Mitotic figures are relatively rare.
Fig. 2.21
(a) Low-grade papillary urothelial carcinoma shows more complex papillary architectures and thickening of urothelial layer with frequent branching and fusion of papillae. (b) Mild cytologic atypia and some mitotic figures are found
High-Grade Papillary Urothelial Carcinoma
High-grade papillary urothelial carcinoma shows more complex architecture than low-grade papillary urothelial carcinoma. Tumor cells commonly show higher degree of nuclear atypia such as nuclear pleomorphism, hyperchromasia, and nuclear enlargement (Fig. 2.22). Mitoses are frequently observed. Tumor cells frequently reveal discohesion and denudation. High-grade papillary urothelial carcinoma can be admixed with low-grade area.
Fig. 2.22
(a) High-grade papillary urothelial carcinoma shows complex papillary architecture with occasional large atypical nuclei. (b) High-power view reveals prominent nuclear pleomorphism and frequent mitotic figures
2.4.1.2 Fat Urothelial Lesion
Urothelial Dysplasia
Urothelial dysplasia is a premalignant lesion with poor reproducibility [80–82]. Microscopically, urothelial layer shows loss of polarity and cytologic atypia, but those are not enough to make diagnosis of urothelial carcinoma in situ (Fig. 2.23) [81, 82].
