Location

Moultrie, GA

Start Date

17-4-2026 12:00 PM

End Date

17-4-2026 1:00 PM

Description

Background:

Chronic lower urinary tract dysfunction can lead to progressive structural remodeling of the urinary bladder, such as detrusor hypertrophy and mucosal trabeculation. Bladder diverticula, defined as mucosal outpouching through the detrusor muscle, may develop in response to sustained elevations in intravesical pressure or impaired bladder emptying. These diverticula facilitate urinary stasis and increase the risk of complications, including infection, calculi formation, urinary retention, and, less frequently, malignant transformation. Identification of gross anatomic changes offers important insights into the long-term sequelae of chronic bladder dysfunction.

Methods:

Routine pelvic dissection was conducted during anatomical laboratory instruction. Gross examination of the urinary bladder and adjacent structures was performed and documented with photographs. Histologic evaluation, imaging correlation, and urodynamic data were not available. Clinical records were also inaccessible.

Results:

A 92-year-old male cadaver with a reported history of vascular dementia demonstrated severe bladder trabeculation and a large, broad-based bladder diverticulum. Multiple calculi were identified within the diverticular cavity. A suprapubic catheter tract was observed entering the diverticulum rather than the primary bladder lumen. The prostate appeared grossly non-enlarged.

Conclusions:

These findings illustrate advanced structural bladder remodeling associated with chronic urinary dysfunction. The coexistence of severe trabeculation, diverticulum formation, and intradiverticular calculi suggests prolonged urinary stasis and altered bladder emptying dynamics. Although benign prostatic obstruction is commonly implicated in acquired diverticula, the absence of gross prostatic enlargement in this specimen raises consideration of alternative contributors, including neurologic mechanisms of lower urinary tract dysfunction. This case highlights the value of cadaveric pathology in demonstrating the structural consequences of chronic bladder dysfunction.

Embargo Period

5-28-2026

COinS
 
Apr 17th, 12:00 PM Apr 17th, 1:00 PM

Severe Bladder Trabeculation with Large Diverticulum and Calculi in a Male Cadaver: Gross Findings and Etiological Considerations

Moultrie, GA

Background:

Chronic lower urinary tract dysfunction can lead to progressive structural remodeling of the urinary bladder, such as detrusor hypertrophy and mucosal trabeculation. Bladder diverticula, defined as mucosal outpouching through the detrusor muscle, may develop in response to sustained elevations in intravesical pressure or impaired bladder emptying. These diverticula facilitate urinary stasis and increase the risk of complications, including infection, calculi formation, urinary retention, and, less frequently, malignant transformation. Identification of gross anatomic changes offers important insights into the long-term sequelae of chronic bladder dysfunction.

Methods:

Routine pelvic dissection was conducted during anatomical laboratory instruction. Gross examination of the urinary bladder and adjacent structures was performed and documented with photographs. Histologic evaluation, imaging correlation, and urodynamic data were not available. Clinical records were also inaccessible.

Results:

A 92-year-old male cadaver with a reported history of vascular dementia demonstrated severe bladder trabeculation and a large, broad-based bladder diverticulum. Multiple calculi were identified within the diverticular cavity. A suprapubic catheter tract was observed entering the diverticulum rather than the primary bladder lumen. The prostate appeared grossly non-enlarged.

Conclusions:

These findings illustrate advanced structural bladder remodeling associated with chronic urinary dysfunction. The coexistence of severe trabeculation, diverticulum formation, and intradiverticular calculi suggests prolonged urinary stasis and altered bladder emptying dynamics. Although benign prostatic obstruction is commonly implicated in acquired diverticula, the absence of gross prostatic enlargement in this specimen raises consideration of alternative contributors, including neurologic mechanisms of lower urinary tract dysfunction. This case highlights the value of cadaveric pathology in demonstrating the structural consequences of chronic bladder dysfunction.