Hypothesis / aims of study
Spinal cord injury (SCI) eliminates voluntary control of voiding, leading initially to areflexic bladder (spinal shock) and urinary retention. However, a few months later, detrusor overactivity (DO) appears, which causes urinary incontinence and affects quality of life (QoL). In order to reduce DO, we usually use some medications including anticholinergics or beta-3 agonists. Another treatment strategies including intradetrusor botulinum toxin A injection or neuromodulation are available these days to overcome DO. However, a few decades ago, we had no treatment strategies except for antimuscarinics and how to treat these antimuscarinics-refractory DO was the severe problem. In that era, we hypothesized that bladder overdistention (OD) in the period of spinal shock may prevent the recovery of involuntary bladder contraction, which may reduce the emergence of DO and prevent urinary incontinence. Although the preliminary results of bladder OD were reported , the long-term outcome of bladder OD is still unclear. Therefore, in the present study, we examined the long-term effect of bladder OD in the period of spinal shock on lower urinary tract storage function in patients with complete spinal cord injuries through urodynamic studies.
Study design, materials and methods
We included 31 patients managed with OD (OD group) and 19 patients without OD (non-OD group) during acute bladder-areflexia phase. All patients were confirmed complete paralysis. In non-OD group, regular intermittent catheterization with less than 400 ml of capacity on each occasion was performed at 4-5 times/day. In OD group, once the complete spinal cord lesion was confirmed at the end of the first week after admission, regular intermittent catheterization was discontinued and bladder OD was started. In this group, intermittent catheterization was performed 2 times/day with 600-1000ml urine volume on each occasion. These managements were continued until self-catheterization was initiated. Median OD periods were 21 days. Lower urinary tract function was evaluated through urodynamic studies in 1-, 3- and 5-years after spinal cord injury. Qualiveen-30 was used for the evaluation of QoL.
The maximum cystometric capacity (MCC) was not significantly different between OD and non-OD group at 1-, 3-, 5-years after SCI. However, the maximum bladder pressure (MBP) in OD group was significantly higher than that in non-OD group at 1-, 3-, 5-years after SCI (Fig. 1). In addition, the bladder compliance in OD group was significantly lower than that in non-OD group at 3 years after SCI (Fig. 2). No significant difference was observed in Qualiveen-30 subscores between these two groups. Incidence of DO tended to be higher in OD group than that in non-OD group, but no significant difference was observed. The use rate of anticholinergics in OD group was significantly higher than that in non-OD group at 1-, 3-, 5-years after SCI.
Interpretation of results
MBP was significantly higher and bladder compliance was significantly lower in OD group. These results indicate that lower urinary tract storage function was deteriorated by the bladder OD in the period of spinal shock. As a result, the use rate of antimuscarinics was significantly higher in OD group and the incidence of DO tended to be higher in OD group than that in non-OD group. No significant differences were observed in Qualiveen-30 scores between these two groups. Although the results obtained in this study were contrary to our hypothesis, our results seem to be reasonable to the recent evidences that the bladder OD is one of the risk factors for the emergence of DO.