Purpose:An ill-defined proportion of patients undergoing urethroplasty fail to experience improvement in lower urinary tract symptoms (LUTS) despite being stricture-free. We aim to identify the incidence, associations and causes of “LUTS failure” after urethroplasty.Materials and Methods:Patients undergoing urethroplasty over a 6-year period were offered enrollment in a prospective study examining urinary function after urethroplasty. Patients were assessed preoperatively and 6 months postoperatively using the International Prostate Symptom Score (IPSS) and cystoscopy. “LUTS failure” was defined as ≤3-point improvement in IPSS despite an anatomically successful urethroplasty. Multivariable logistic regression was utilized to evaluate the association between patient factors and “LUTS failure.”Results:Of 365 patients meeting inclusion criteria, mean postoperative IPSS (20.3 vs. 5.4, p <0.0001) and median urinary quality of life (UQOL; 5 vs. 1; p <0.0001) were significantly improved. Despite being stricture-free, 7.7% of patients reported “LUTS failure” and 10.1% reported UQOL nonresponse. On multivariable logistic regression, increasing age (OR 1.04, 95% CI 1.01–1.06; p=0.006) and hypospadias (OR 18.2, 95% CI 2.1–156.0; p=0.008) were associated with “LUTS failure,” while stricture location (p=0.76), length (p=0.14), previous urethroplasty (p=0.96), failed endoscopic treatment (p=0.17), type of urethroplasty (p=0.93) and other etiologies were not. Qualitatively, the most likely causes of “LUTS failure” were detrusor underactivity (39.3%), overactivity (21.4%), pelvic floor dysfunction (21.4%) or benign prostatic hyperplasia (14.3%). Only increasing age was associated with UQOL nonresponse (OR 1.03, 95% CI 1.01–1.07; p=0.02).Conclusions:While many patients experience improved voiding function after urethroplasty, 7.7% experience “LUTS failure” and 10.1% report UQOL nonresponse. Both occurrences are independently associated with increasing patient age and most commonly related to detrusor underactivity.
all of the following subsets: bulbar UP (p< 0.01), penile UP (p[ 0.03), bulbar onlay graft UP (p[ 0.03), penile onlay graft UP (p[ 0.3) and bulbar EPA (p< 0.01). There were too few ventral graft procedures to compare dorsal vs. ventral onlay.CONCLUSIONS: Post-UP PVD and EjD are associated, supporting the theory of a common etiology. The association persists whether the UP is in the penile or bulbar urethra, suggesting that BS damage is not the primary cause. The association persists whether the bulbar UP is done with a graft vs EPA, suggesting that graft placement is not the cause; but we were unable to compare dorsal vs. ventral graft. By exclusion, these symptoms may be due to a loss of elasticity that is inherent to any UP (with or without a graft) or due to a neurologic cause.
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