Incomplete bladder emptying in patients with stroke: is detrusor external sphincter dyssynergia a potential cause?

OBJECTIVES

To delineate the frequency, clinical risk factors, and urodynamic mechanisms of incomplete bladder emptying (IBE) among patients with recent stroke.

DESIGN

Retrospective study.

SETTING

Inpatient setting in the rehabilitation ward of a university hospital.

PARTICIPANTS

All patients with acute stroke admitted for rehabilitation between January and December 2005, excluding those with a history of lower-urinary tract symptoms and urologic diseases. Eighty-two patients (42 women and 40 men; mean age, 65.5 y) were included.

INTERVENTIONS

Not applicable.

MAIN OUTCOME MEASURES

We measured postvoid residual (PVRs) by catheterization or by using an ultrasonic bladder scanner. Twenty-five patients (30.5%) had IBE with PVRs greater than 100 mL on 2 consecutive days. Patients with IBE were evaluated by a urologist and subsequently underwent urodynamic studies.

RESULTS

The presence of IBE was significantly associated with urinary tract infection (P<.001) and aphasia (P=.046). The presence of IBE was not related to sex, stroke location, nature of stroke (hemorrhagic or ischemic), history of diabetes mellitus, or previous stroke. Urodynamic studies done on 22 patients with IBE revealed acontractile detrusor in 8 patients (36%) and detrusor underactivity in 3 (14%). Eleven patients (50%) had detrusor-external sphincter dyssynergia (DESD) combined with normative detrusor function (5 patients) or detrusor hyperactivity (6 patients); all but 1 of these patients had a supratentorial lesion. The presence of DESD was associated with a longer onset-to-evaluation interval (P=.018) [corrected] and spasticity of the stroke-affected lower limb (P=.02). [corrected] Diabetes mellitus was associated with the presence of acontractile detrusor or detrusor underactivity (P=.03).

CONCLUSIONS

IBE is common among patients with stroke and is caused by decreased detrusor contractility or DESD. Spasticity of the external urethral sphincter is a possible pathophysiologic mechanism of DESD.