Filling defects in the bladder must be differentiated from contour defects. A filling defect is an area of incomplete opacification on computed tomography (CT), excretory urography, or cystography and denotes something lying free within the bladder lumen. Examples include calculi, blood clots, and foreign bodies. Contour defects are mural or mucosal lesions that alter the contour of the contrast-filled bladder; examples include urothelial tumors, metaplastic and inflammatory masses, and wall thickening from any cause.

On excretory urography, a blood clot usually appears as an irregular, mobile filling defect, but occasionally may appear fixed in position and therefore may not be distinguishable from a tumor. Clots in the bladder may have a vermiform or wormlike appearance if bleeding has occurred in the upper urinary tract and a clot has formed in the ureter. Ultrasound shows that the blood clot is quite echogenic, unlike a bladder tumor, which often has an echogenicity similar to the bladder wall or other soft tissue. CT may help to distinguish a blood clot from a tumor by demonstrating the typical high attenuation of blood on enhanced images (60 to 80 Hounsfield units [HU]), and is useful to exclude a radiolucent stone. On occasion, a clot may be so large as to essentially fill the bladder (Fig. 15.1).

Foreign bodies within the bladder are most commonly inserted by the patient. Among other items, pens, pencils, matches, wire, tubing, and string can be seen within the bladder lumen. Foreign bodies may also be iatrogenic (e.g., broken or shorn catheter fragments) or may result from penetrating trauma (e.g., bullets). A rare complication of bladder catheterization is the introduction of pubic hairs into the bladder. These may become encrusted with calcium.

Mucosal edema around one ureteral orifice is most often caused by a stone impacted at the ureterovesical junction, but may also be due to the recent passage of such a stone. Focal mucosal edema may also result from bladder irritation by extravesical conditions such as acute appendicitis, Crohn disease, or sigmoid diverticulitis. Another cause of focal edema is an indwelling catheter, whose tip may irritate the bladder wall, typically near the dome. Generalized bullous edema may accompany acute cystitis secondary to infectious or inflammatory (irritative) etiologies.

Cystography shows the irregularity of the bladder wall produced by focal edema as a contour defect. Either ultrasound or CT may show an extravesical cause for localized bladder edema, such as an appendiceal abscess or other bowel disease. If no localized extravesical mass is seen, focal thickening may indicate a bladder tumor. On CT, the attenuation of the edematous bladder mucosa is only slightly less than that of soft tissue and presents as a contour defect of the bladder wall. CT is unlikely to distinguish edema from other causes of bladder wall thickening, including infiltrating bladder tumor.

Virtually all acute infections of the bladder can, if severe, result in diffuse bullous edema of the urothelium, leading to a nodular irregular contour of the bladder on imaging studies. In many instances, this acute pattern will resolve in a matter of days and the bladder will return to its normal smooth appearance. However, severe infections can progress to a chronic phase, in which the bladder capacity is significantly reduced by fibrosis and contraction of the bladder wall. Identical appearing chronic cystitis occurs with many of the inflammatory (irritative) processes discussed later in this chapter.

Acute cystitis is present when more than 100,000 bacteria are present in 1 mL of urine. Most bacteria causing cystitis enter the bladder through the urethra. Escherichia coli is the most commonly encountered organism, but other common agents include species of Staphylococcus, Streptococcus, Proteus, Pseudomonas, Aerobacter, and Candida. Tuberculosis typically infects the bladder by descent down the ureter from a granulomatous focus in one or both kidneys.

Several factors contribute to a natural resistance of the bladder to infection. These include resistance of the bladder mucosa, the washing of organisms out of the bladder by normal voiding, trapping of organisms entering the bladder through the urethra by mucous secretion of the periurethral glands, and the bactericidal effect of prostatic secretions. Bladder infection is almost invariably the result of interference with one or more of these factors. For example, infection is more common when the bladder mucosa has been damaged by trauma, stone, or tumor; when outlet obstruction prevents bacteria from being completely washed out; and when bladder catheterization or instrumentation introduces infection by bypassing the protective mechanisms of the urethra and prostate. Acute cystitis can present with varying degrees of severity. In women, associated hemorrhage is common.

Acute cystitis usually responds well to antibiotic therapy and in uncomplicated cases does not progress to chronic disease. Although cystitis may recur two or three times a year in sexually active women, more frequent recurrence of acute cystitis and cases that are resistant to antibiotic therapy suggest an underlying cause. In such cases, imaging of the entire urinary tract and cystoscopic evaluation of the bladder are indicated to exclude causes such as urinary stone disease, bladder diverticulum, colovesical fistula, and perivesical abscess.

Cystitis due to tuberculosis is an interstitial process initially associated with mucosal edema and later progressing to bladder wall thickening and fibrotic contraction with reduced bladder capacity and a predisposition to vesicoureteral reflux. Rarely, there can be associated calcification of the bladder wall.

Emphysematous cystitis is a rare condition nearly always found in diabetic or immunocompromised patients. This is a true infectious cystitis most often due to E. coli, which ferments glucose to produce carbon dioxide and hydrogen. This gas is initially formed in the bladder wall and subsequently transgresses the mucosa into the lumen of the bladder. Emphysematous cystitis is associated with the same type of irritative symptoms as any other acute bladder infection. Gas within the lumen but not in the bladder wall is usually the result of catheterization or instrumentation in which air is introduced during the procedure. It may also be caused by a fistula between the bladder and the colon, small bowel, or vagina. Only rarely is such a finding caused by cystitis alone.

In patients with emphysematous cystitis, the plain film typically shows gas within the bladder and irregular streaky radiolucencies within the bladder wall (Fig. 15.2). Air within the bladder lumen should not be mistaken for rectal air. Air within the bladder conforms to the bladder shape, that is, ovoid with the long axis horizontal (like an egg on its side) and in central position low in the pelvis (Fig. 15.3). Gas within the rectum has a vertical orientation,
and the rectal folds often may be recognized. A lateral radiograph often distinguishes the anterior position of the bladder from the posterior location of the rectum. CT clearly shows the mural and luminal locations of the gas (Fig. 15.4).

Emphysematous cystitis nearly always responds rapidly to appropriate antibiotic therapy and control of underlying diseases such as diabetes. It does not progress to a chronic condition.

Schistosomiasis (Bilharzia) is one of the most common parasitic infections in the world, but is especially prevalent in the Nile Valley. Only Schistosoma hematobium affects the urinary tract. The definitive host is a human, and the intermediate host is a freshwater snail. Because the disease typically involves the intestines and bladder, eggs escape the human host in the feces and urine. These eggs, when deposited in fresh water, hatch into miricidia, which infest snails, develop, and emerge as cercariae. These cercariae infect humans directly through the skin, when humans are wading into or swimming in infested waters. After the skin is penetrated, they enter peripheral capillaries, drain to the lung, squeeze through the alveolar capillaries, and enter the systemic circulation. The cercariae that survive enter the mesenteric arteries and, hence, pass through the portal venous system. They develop into adolescent flukes in the portal blood and then migrate against the flow in the portal system using two suckers, which they alternately attach to the wall of a vein. They eventually reach the smallest venules in the wall of the bladder, probably through the hemorrhoidal plexus. From there, millions of eggs enter the urine, or are trapped in the bladder walls where they die, producing a severe granulomatous reaction. The granulomas calcify, causing linear streaks of calcium in the bladder wall. Large conglomerations of eggs in the bladder wall produce masses known as bilharzioma, which may also eventually calcify.

The clinical presentation of patients with schistosomiasis is typically hematuria. In initial stages, the bladder mucosa is edematous and hemorrhagic. Later, the bladder becomes fibrotic with a reduced volume and calcified wall. Cystoscopic examination is mandatory to exclude squamous cell carcinoma of the bladder, which has a markedly increased incidence in patients with schistosomiasis. Biopsy may be necessary to distinguish bilharzioma from carcinoma, although carcinoma usually presents as a later complication. Schistosomiasis rarely affects the kidneys or collecting systems, except by obstruction due to bladder disease or involvement of the distal ureter.

As the disease progresses, plain-film radiography may show dense calcification of the bladder wall or bladder stones (Fig. 15.5). Calcification of the distal ureter may also be seen, but is rarely present without bladder involvement. A bladder tumor should be suspected when follow-up studies show absence of wall calcification in areas that were previously calcified (Fig. 15.6). Although there are other causes of bladder calcification, including tuberculosis, radiation cystitis, alkaline-encrusted cystitis, and, rarely, bladder cancer, none is as common or as dramatic as schistosomiasis. The
ureterovesical junction may be partially obstructed by the changes in the bladder wall, resulting in ureteral dilation. Schistosomiasis may also affect the prostate and urethra. The disease is destructive and results in urethral fistula formation, producing a pattern similar to that seen with advanced tuberculosis. Fistulae may drain into the perineum, scrotum, suprapubic skin, or buttocks.

CT is more sensitive than plain radiographs in visualizing faint calcifications in the walls of the ureters and bladder in patients with suspected schistosomiasis (Fig. 15.7).

Candidiasis of the bladder, typically seen in poorly controlled diabetic patients, causes fermentation of sugars in the urine, forming gas in the bladder lumen. It may also present as a fungus ball in the lumen. These fungus balls may be single or multiple and are seen as laminated, gas-containing filling defects within the bladder.

Bladder diverticula may occur as a result of bladder outlet obstruction, or rarely, a congenital deficiency in bladder musculature adjacent to the ureterovesical junction (Fig. 15.19). The latter is termed a Hutch diverticulum and is commonly associated with ipsilateral vesicoureteral reflux. Bladder diverticula are not infrequently encountered in adults, usually being acquired and resulting from functional or mechanical bladder outlet obstructions (the former due to neurogenic bladders and the latter often due to prostatic enlargement). Bladder diverticula due to outlet obstruction are rare in children but may occur in the clinical setting of urethral valves. Neurogenic dysfunction of the bladder is another cause of multiple diverticula in children.

Multiple bladder diverticula are common, usually arising from the lateral walls and rarely arising near the bladder dome. A widenecked diverticulum empties readily, but a narrow-necked diverticulum empties slowly and is more likely to have residual urine. A large bladder diverticulum may displace the bladder to the opposite side and may be larger than the bladder. In such cases, the bladder is identified on CT by its thickened wall, whereas the diverticulum has a smooth thin wall.

There may be a higher incidence of tumor in bladder diverticula than in the bladder lumen itself, explained by stasis of carcinogen-laden urine in the diverticulum. There is a tendency for such tumors to spread outside the bladder more rapidly than bladder lumen tumors because the walls of false diverticula consist only of urothelium protruding between muscle bundles and are not surrounded by detrusor muscle.

Ultrasound is effective in the assessment of bladder diverticula. Echo-free outpouchings from the bladder are readily seen (Fig. 15.20), and filling defects within a diverticulum such as stones or tumors also are visible. Tumors within a diverticulum may present as soft-tissue masses in the diverticulum or only as thickening of the diverticulum wall, whereas stones may produce typical shadowing. The tumor may on occasion obstruct the mouth of the diverticulum. In such cases, the diverticulum will not be opacified on cystography or other contrast-enhanced studies (Fig. 15.21).

CT is an excellent method of assessing bladder diverticula (Fig. 15.22). Stones are easily seen on unenhanced CT images as highattenuation filling defects, whereas a tumor presents as a soft-tissue mass arising from the diverticulum wall and protruding into the contrast medium-filled diverticulum (Fig. 15.23). MRI is also useful in evaluating tumors arising in bladder diverticula (Fig. 15.24).

Patients with herniation of the bladder into or through the inguinal canal present with swelling in the groin or scrotum that increases as the urinary bladder fills and subsides as the patient voids. Bladder herniation most commonly is paraperitoneal in location, with the bladder remaining extraperitoneal and medial to a true inguinal hernia sac. Herniation of the bladder also can be within a true hernia sac or can occur totally extraperitoneally with the peritoneum remaining in the abdomen. The bladder also may herniate through the femoral canal into the thigh or through various incisional hernias.

Bladder herniation can occur in varying degrees and can usually be easily seen when the bladder is filled with contrast medium during cystography (Fig. 15.25) although an upright film is occasionally necessary to make the diagnosis. Bladder herniation may occasionally be seen as an incidental finding on CT and is usually easy to detect when the bladder lumen contains contrast material (Fig. 15.26). However, in some cases this condition may be quite subtle (Fig. 15.27).

A cystocele is defined as prolapse of the bladder into the anterior portion of the vagina and is seen radiographically as descent of the bladder below the symphysis pubis. A cystocele results from laxity of the pelvic floor muscles and is usually only one component of pelvic floor dysfunction, which may include a cystocele, hypermobile bladder neck, vaginal vault prolapse, rectocele, enterocele, sigmoidocele, or rectoanal intussusception. Conditions that predispose to pelvic floor dysfunction include multiparity, obesity, prior pelvic surgery, excessive straining, connective tissue disorders, neuropathy, and advancing age. MRI is useful for evaluating the pelvic floor without the need for bladder or rectal opacification.

Various conditions in the pelvis extrinsic to the bladder can cause an impression on the bladder wall, can circumferentially compress the bladder, or can deviate the bladder to one side.

Displacement or compression of the bladder implies a pelvic mass. Common lesions that may indent the bladder include enlarged pelvic lymph nodes, tumors arising from the colon, reproductive organs, or mesenchymal tissues, presacral teratomas, iliac artery aneurysms, bladder diverticula, hematomas (Fig. 15.32), and abscesses. An anterior meningomyelocele behind the bladder can deviate the bladder anteriorly. These masses are usually accompanied by pathognomonic changes in the sacrum, including a wellcorticated concavity on one side of the sacrum and deviation of the sacrum to the contralateral side (scimitar sacrum). Other cystic lesions that can indent the bladder from behind include seminal vesicle and müllerian duct cysts.

Circumferential compression of the bladder results in a configuration commonly known as a “teardrop” or “pear-shaped” bladder. Processes that can surround the bladder include the normal variant of a narrow pelvis with prominent iliopsoas muscles such as can be found in young male patients. Diffuse pelvic hematoma, another cause of teardrop bladder, is nearly always seen in the setting of recent surgery or trauma (Fig. 15.33), although spontaneous bleeding can occur in patients with bleeding diatheses or on anticoagulation therapy.

Another condition resulting in bladder compression is pelvic lipomatosis. This results from a proliferation of mature, unencapsulated fat within the pelvis. No etiology for this condition has been identified. Radiographically, plain films may show a lucency in the pelvis corresponding to the increased fat. The distal ureters are medially deviated, but the mid ureters may be laterally displaced due to the elevation of the lower urinary tract. Additionally, the ureters may be obstructed in severe cases. On barium enema, the rectosigmoid colon is straightened and narrowed. The excess pelvic fat responsible for compressing the colon and bladder can be easily confirmed with CT (Fig. 15.34).

Bilateral pelvic lymph node enlargement due to metastatic disease may also result in a teardrop or vertical configuration of the bladder (Fig. 15.35). This is usually found in patients with lymphoma. Other tumors that drain to the pelvic lymph nodes, such as prostate cancers, do not typically produce bulky lymph node metastases. Other causes of teardrop bladder include development of bilateral external iliac artery aneurysms, massive venous collaterals in the pelvis in patients with inferior vena cava obstruction, retroperitoneal fibrosis occurring deep in the pelvis, and lymphoceles that form after pelvic lymph node dissection.