Congenital UBD are found rarely; according to results of autopsy of children, the rate is 1:100; they are more often found in boys than in girls and much more often in men than in women. The cause of congenital UBD formation is supposed to be development abnormality or influence of certain congenital factors such as trauma and retention of urine during the antenatal period. The rate of acquired diverticula development correlates with the incidence of diseases which cause infravesical obstruction (benign prostate hyperplasia, urethra stricture, sclerosis of urinary bladder neck, prostate sclerosis, etc.). It was discovered that every fifth patient which had surgery for infravesical obstruction developed UBD; however, only 15 % of those diverticula required surgical treatment [7–9].

The most common classification is dividing diverticula into congenital or true diverticula and acquired or false diverticula. The cause of development of true diverticula as the urinary bladder abnormality is malformation of the urinary bladder wall due to the influence of factors such as a trauma and urine retention during the antenatal period. The rate of acquired or false UBD development correlates with the incidence of diseases which cause infravesical obstruction (benign prostate hyperplasia, urethra stricture, sclerosis of urinary bladder neck, prostate sclerosis, etc.). Development of acquired UBD was observed in every fifth patient which had had surgery for infravesical obstruction.

Apart from the etiology of congenital and acquired UBD, the following criteria are also used for their type division: diverticulum wall containing a complete set of layers or only mucosa, number of diverticula and their size, presence or absence of a sphincter, etc. This classification implies different etiologies of true and false diverticula. The former are considered to be a consequence of dysembryogenesis, and the latter—a result of infravesical obstruction. However, there is a number of works where this classification is subject to valid criticism. The provided evidence includes observations of acquired diverticula that contained a full set of layers characteristic of the bladder wall and of congenital diverticula that consisted only of mucosa. In this case the etiology of acquired and congenital diverticula looks similar—formation of diverticula depends on two factors: congenital, weakness of certain parts of the urinary bladder, and acquired, urinary difficulty.

Anatomical features which before were considered as parameters for UBD classification into congenital and acquired ones, such as different structure of walls of congenital and acquired diverticula, presence of a sphincter in the congenital diverticulum neck, and multiplicity of acquired diverticula, are considered to be invalid by the majority of authors, since congenital and acquired UBD cannot be differentiated from each other at the morphological level [10, 11].

A similar study of the urinary bladder wall revealed that the wall was not developed equally in all parts of the bladder [3]. Noted that “…the urinary bladder has parts, where diverticula are found most often (area of ureteral orifices, the front and the rear walls), that feature a weaker development of muscles…” [3]. As for the sphincter of the diverticulum, the majority of authors deem that it is formed by connivent muscles of detrusor; thus, it cannot be called a true sphincter. Contractions of the detrusor during urination prevent the diverticulum from complete voiding, and residual urine accumulates in it. This caused describing UBD as “urine trap.” In spite of differences in views on UBD etiology, it should be said that up to now division of diverticula into true and false ones is the most common classification.

Thus, UBD can develop both during antenatal and postnatal life; however, the mechanism of their formation is the same: on the one hand, a weakness of certain bladder parts and, on the other hand, an obstruction to the bladder voiding (Figs. 3.1 and 3.2).

In case no symptoms appear, which is typical for the majority of UBD cases, the diverticulum is discovered “accidentally,” nowadays most often during USG examinations. Previously UBD were incidentally discovered during cystoscopy or cystography.

Many authors note that in case of UBD no typical clinical presentations are observed and infravesical obstruction symptoms prevail mostly.

The main UBD symptoms are urinary difficulty (up to complete urine retention), two-stage urination (urine is discharged first from the bladder and then from the diverticulum), or urination with Courvoisier procedure; these symptoms are observed not often.

UBD clinical presentations are induced by complications of this disease, such as overlay of infections and lithogenesis, compression of adjacent organs, hematuria, and ureterohydronephrosis. Vesicoureteral reflux may develop if the diverticulum is located in the area of ureteral orifice when its closing function is affected. Until complications arise, the diverticulum usually remains completely latent [5, 10].

Also the following rarer UBD complications are described: acute urine retention, acute renal failure, and urinary stasis with consequent tumoral degeneration. It is believed that the mucosa of the diverticulum is more subject to metaplasia which results from stasis of urine and a chronic infection. According to data by a number of authors, malignant tumors develop in 3–7 % of UBD [12–17].

In rare cases of UBD, acute abdomen symptoms and presentations similar to acute appendicitis may arise. In the literature, several cases of spontaneous diverticula rupture are described which caused development of urinary peritonitis [18, 19].

The methods used for diverticula visualization and diagnosis confirmation are ultrasonography, ascending and descending cystography, computer-aided tomography, and magnetic resonance imaging [6, 20].

Urinary bladder ultrasonography is one of the leading methods of diverticula diagnostics which displays an echo-free outpouching that protrudes outside the urinary bladder outlines (Figs. 3.3, 3.4, and 3.5).

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