Bladder outlet obstruction in men with acute urinary retention: an urodynamic study

Rom, Maximilian; Waldert, Matthias; Klingler, H. Christoph; Klatte, Tobias

doi:10.1007/s00345-013-1027-1

Cited by 8 publications

(7 citation statements)

References 20 publications

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“…Although urinary retention in men is often considered a result of benign prostatic obstruction, just 60% of the present cohort met the urodynamic criteria for BOO. Our findings are consistent with prior studies that noted just 50–80% of men with urinary retention indeed have BOO . This finding suggests that not all men with urinary retention require surgical de‐obstruction.…”

Section: Discussionsupporting

confidence: 93%

“…Our findings are consistent with prior studies that noted just 50-80% of men with urinary retention indeed have BOO. 13,14 This finding suggests that not all men with urinary retention require surgical deobstruction. In the present series of men with urinary retention, de-obstructive surgery (TURP or open prostatectomy) was offered to just 57% of patients.…”

Section: Discussionmentioning

confidence: 99%

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Urodynamics of men with urinary retention

2017

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In the present cohort, just 60% of men with urinary retention showed urodynamic evidence of bladder outlet obstruction. Depending on how contractility is measured (bladder contractility index vs isometric detrusor pressure), the rate of detrusor underactivity varies. The majority of men with retention had a low detrusor reserve. Given the wide spectrum of urodynamic findings in men with retention, surgical intervention might not be necessary for all. Furthermore, a careful consideration of urodynamics can assist in the selection of optimal treatment.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Urodynamics of men with urinary retention

2017

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“…The DBOO group displayed a stronger inflammatory response at week 1 and 2 post-obstruction compared with the GBoo group; however, the enhanced response was not observed at week 4 post-obstruction. The bladder cannot accommodate a sudden increase in intravesical pressure during acute obstruction (40), which results in the aggravation of inflammation. As indicated by the expression levels of the aforementioned biomarkers, the dBoo group displayed decreased proliferation and increased inflammation at an earlier time point compared with the GBoo group, suggesting that the dBoo group may have experienced bladder function decompensation at an earlier time point.…”

Section: Discussionmentioning

confidence: 99%

Urethral meatus stricture BOO stimulates bladder smooth muscle cell proliferation and pyroptosis via IL‑1β and the SGK1‑NFAT2 signaling pathway

et al. 2020

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Bladder outlet obstruction (Boo), which is primarily caused by benign prostatic hyperplasia, is a common chronic disease. However, previous studies have most commonly investigated Boo using the acute obstruction model. in the present study, a chronic obstruction model was established to investigate the different pathological alterations in the bladder between acute and chronic obstruction. compared with chronic obstruction, acute obstruction led to increased expression of proliferating cell nuclear antigen and interleukin-1β, which are markers of proliferation and inflammation, respectively. Furthermore, increased fibrosis in the bladder at week 2 was observed. Low pressure promoted mice bladder smooth muscle cell (MBSMc) proliferation, and pressure overload inhibited cell proliferation and increased the proportion of dead MBSMCs. Further investigation using serum/glucocorticoid regulated kinase 1 (SGK1) small interfering rnas indicated that low pressure may promote MBSMc proliferation by upregulating SGK1 and nuclear factor of activated T-cell expression levels. Therefore, the present study suggested that acute obstruction led to faster decompensation of bladder function and chronic bladder obstruction displayed an enhanced ability to progress to Boo.

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“…Much of the reported literature on urodynamic nomograms assessing bladder contractility (BCI) and the implications of capacity on outcomes have been reported in men . There are only a handful of publications which have identified the importance of a large capacity bladder and elevated PVR in women undergoing anterior and/or apical POP repair.…”

Section: Discussionmentioning

confidence: 99%

“…Much of the reported literature on urodynamic nomograms assessing bladder contractility (BCI) and the implications of capacity on outcomes have been reported in men. [17][18][19][20][21] There are only a handful of publications which have identified the importance of a large capacity bladder and elevated PVR in women undergoing anterior and/or apical POP repair. In a retrospective study by Lo et al on urodynamic improvements in detrusor underactivity following prolapse repair (n = 49), the authors found a reduction in cystometric capacity from 449 to 377 (P < 0.001) after prolapse repair, and advocate early surgical intervention since the duration of obstruction may adversely increase capacity and result in a state of detrusor decompensation.…”

Section: Discussionmentioning

confidence: 99%

Urodynamic factors associated with the large capacity bladder and incomplete emptying after prolapse repair (2009‐2015)

Dobberfuhl

Shaffer

Goodman

et al. 2019

Neurourology and Urodynamics

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Aims To identify the clinical and urodynamic factors associated with the large capacity bladder and incomplete bladder emptying after prolapse repair. Methods We identified 592 women who underwent anterior and/or apical prolapse repair at our institution from 2009 to 2015. Women were stratified by urodynamic capacity. The primary outcome was incomplete emptying at the longest follow‐up (postvoid residual [PVR] > 200 mL). Data were analyzed in the Statistical Analysis System software. Results Two hundred and sixty‐six women (mean age, 61 years) had preoperative urodynamic tracings available for review. After surgery, there were 519 PVRs in 239 women recorded at up to 2949 days (mean, 396) and nine time points (median, 2; IQR, 1‐3). The receiver operator curve for predicted probability of longest follow‐up PVR greater than 200 mL (area under curve = 0.67) identified the 600 mL cutpoint which defined large capacity bladder. Large capacity bladders (capacity, >600 mL [n=79] vs ≤600 mL, [n=160]) had a mean: detrusor pressure at maximum flow (21 vs 22 cm H2O; P = 0.717), maximum flow rate (19 vs 17 mL/s; P = 0.148), significantly elevated PVR (202 vs 73 mL; P < 0.001), and significantly lower voiding efficiency (VE) (74 vs 82%, P < 0.05). Following prolapse repair, elevated PVR was associated with large capacity (PVR 101 vs 49 mL, P < 0.05). Large bladders had a two‐ to three‐fold risk of longest follow‐up PVR greater than 200 mL (14.3%‐20.3% [capacity, >600 mL] vs 4.1%‐7.0% [capacity, ≤600 mL]). VE was similar after surgery regardless of the capacity (87% vs 88%, P = 0.772). Conclusions The decision to pursue prolapse repair should be individualized and take into account, the bladder capacity and goals for PVR improvement after surgery.

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Bladder outlet obstruction in men with acute urinary retention: an urodynamic study

Cited by 8 publications

References 20 publications

Urodynamics of men with urinary retention

Urodynamics of men with urinary retention

Urethral meatus stricture BOO stimulates bladder smooth muscle cell proliferation and pyroptosis via IL‑1β and the SGK1‑NFAT2 signaling pathway

Urodynamic factors associated with the large capacity bladder and incomplete emptying after prolapse repair (2009‐2015)

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