Hypothesis / aims of study
Cystometric assessment of bladder function is a crucial component of clinical evaluation for patients suffering from lower urinary tract symptoms and urinary incontinence. Recent findings of Think Dry trial of geriatric population (1) add to a growing body of evidence on diagnostic superiority of cystometry in the standing position over seated or supine positions for detecting detrusor overactivity (DO), even at similar filling rates and bladder volumes. Because standing posture triggers a homeostatic rise in heart rate and abdominal (splanchnic) vasoconstriction (2) and causes orthostatic anti-diuresis, we hypothesize that increased bladder sensitivity for DO in standing posture results from reduced bladder perfusion lowering the bladder compliance, necessary for dampening peristaltic waves propelling smaller urine boluses from ureter to bladder in the standing position. We reviewed available literature to support this hypothesis and validate the need for future physiologic investigation.
Study design, materials and methods
We collated published clinical evidence on the effect of posture on blood pressure and urine production to obtain mechanistic insights into diagnostic superiority of standing cystometry to detect DO. Sagittal MRI scans illustrate urine bolus and urine column in ureters.
Results
Upright posture activates sympathetic nervous outflow to counteract the pooling of blood in dependent tissues, which triggers reflexive rise in heart rate and splanchnic vasoconstriction to raise diastolic blood pressure (2) and lower urine production. These changes result in reduced bladder perfusion and lower bladder compliance. Reduced compliance may potentiate DO via two distinct mechanisms. First, reduced compliance will increase bladder pressure in response to filling, even when performed at similar rates 50mL/min to seated cystometry (1). This could lead to increased activation of neurogenic and myogenic signaling triggering DO. Further, a less compliant bladder wall when distended is also less likely to dampen compression waves transmitted to bladder from ureter and smaller urine boluses produced due to orthostatic anti-diuresis require compression waves of higher amplitude for ureteral peristalsis. As opposed to standing cystometry, 2-6-fold higher rate of endogenous urine production in supine or sitting cystometry (3) causes coalescence of larger urine boluses into column in ureter (shown in scan) and enables urine propulsion in ureter without peristalsis to a well-perfused and a highly compliant bladder wall. The reduction of ureteral peristalsis in supine posture reduces the strain on distended bladder wall imposed from ~25 % higher endogenous urine volume produced during sitting cystometry (3) vs standing cystometry.
Interpretation of results
A large body of clinical evidence implicates that increased sensitivity of standing cystometry for diagnosing DO stems from bladder hypoperfusion and lower bladder compliance in standing posture increasing bladder sensitivity to high amplitude compression waves propelling smaller urine boluses in the standing position. A well-studied epidemiologic association between hypertension, and atherosclerosis with DO reinforces the link between bladder hypoperfusion and DO. Therefore, to minimize the need for repeat invasive cystometry, patients who are able should be encouraged to undergo standing cystometry. For those unable to stand, fluid restriction, utilization of hypotonic instillate, or administration of an anti-diuretic medication may raise the likelihood of DO detection in standing cystometry. Further studies are needed to directly validate these findings and support their clinical significance.