Structural Basis of Geriatric Voiding Dysfunction. IV. Bladder Outlet Obstruction

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Abstract
Several aspects of the pathogenesis of voiding dysfunction in bladder outlet obstruction remain unresolved. The structural basis of obstructive versus nonobstructive dysfunction was investigated in a prospective ultrastructural/urodynamic study of 35 elderly subjects of comparable age. Detrusor structure was examined by electron microscopy, with blinded clinical and urodynamic information. Seven detrusor specimens were segregated by a distinctive myohypertrophy, structural pattern, which matched with 6 male and 1 female subjects 72 to 96 years old (mean age 83) who had urodynamically proved outlet obstruction. This pattern was characterized by widely separated muscle cells with reduction of intermediate cell junctions, collagenosis, that is abundant collagen plus some elastic fibers, in the markedly widened spaces between individual muscle cells and abundant profiles characteristic of enlarged, hypertrophic muscle cells. Superimposed degeneration of muscle cells and axons in 6 specimens matched those of 5 men and 1 woman who had impaired detrusor contractility. In 3 specimens there were also abundant protrusion junctions and ultra-close abutments; these matched those of 2 men and 1 woman with obstruction plus detrusor overactivity. Observations on the degree of bladder trabeculation in the entire population of 35 subjects are presented. It is concluded that bladder outlet obstruction is associated with changes in detrusor structure that can account for the resultant voiding dysfunction. Features of the myohypertrophy pattern, with or without superimposed degeneration, can explain overall weakness of the obstructed detrusor despite hypertrophy of its cells. Protrusion junctions and abutments probably mediate electrical coupling of muscle cells leading to involuntary contractions in the overactive (unstable) obstructed detrusor. Excessive deposits of elastic fibers (hyperelastosis) between widely separated muscle cells and in interstitium are suggested as the probable structural basis for increased bladder distensibility and chronic retention.