STRUCTURAL BASIS OF GERIATRIC VOIDING DYSFUNCTION .4. BLADDER OUTLET OBSTRUCTION

Several aspects of the pathogenesis of voiding dysfunction in bladder outlet obstruction remain unresolved. The structural basis of obstruct ive versus nonobstructive dysfunction was investigated in a prospectiv e ultrastructural/urodynamic study of 35 elderly subjects of comparabl e age. Detrusor structure was examined by electron microscopy, with bl inded clinical and urodynamic information. Seven detrusor specimens we re segregated by a distinctive myohypertrophy, structural pattern, whi ch 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 p lus some elastic fibers, in the markedly widened spaces between indivi dual muscle cells and abundant profiles characteristic of enlarged, hy pertrophic muscle cells. Superimposed degeneration of muscle cells and axons in 6 specimens matched those of 5 men and 1 woman who had impai red detrusor contractility. In 3 specimens there were also abundant pr otrusion junctions and ultra-close abutments; these matched those of 2 men and 1 woman with obstruction plus detrusor overactivity. Observat ions on the degree of bladder trabeculation in the entire population o f 35 subjects are presented. It is concluded that bladder outlet obstr uction is associated with changes in detrusor structure that can accou nt for the resultant voiding dysfunction. Features of the myohypertrop hy pattern, with or without superimposed degeneration, can explain ove rall weakness of the obstructed detrusor despite hypertrophy of its ce lls. Protrusion junctions and abutments probably mediate electrical co upling of muscle cells leading to involuntary contractions in the over active (unstable) obstructed detrusor. Excessive deposits of elastic f ibers (hyperelastosis) between widely separated muscle cells and in in terstitium are suggested as the probable structural basis for increase d bladder distensibility and chronic retention.