The aim of this study is to characterize and evaluate patients with a videourodynamic study (VUDS) diagnosis of bladder outlet obstruction (BOO) who have a normal contemporaneous uroflowmetry, which is termed “high flow bladder outlet obstruction (HF BOO).”

This was a retrospective review of an ongoing database of patients evaluated for refractory lower urinary tract symptoms (LUTS) at a tertiary care center who underwent VUDS. A urodynamic diagnosis of bladder outlet obstruction considered the bladder outlet obstruction index (BOOI), the bladder contractility index (BCI), the shape and duration of the detrusor contraction, and the appearance of the urethra at voiding cystourethrography. 

Patients were diagnosed with definite BOO if the BOOI was > 40, and presumed BOO if they had a sustained detrusor contraction < 40 cm H2O in men and < 20 cm H2O in women with a contemporaneous Qmax < 12 ml/s during pressure-flow study and radiographic evidence of urethral obstruction. Patients were diagnosed with HF BOO if they had a BOOI > 40 with a contemporaneous pressure-flow or free-flow uroflowmetry Qmax > 12 mL/s. Patients with incomplete data or erroneous urodynamic tracings were excluded. Pressure-flow and free-flow mean values were compared between those with definite BOO, presumed BOO, and HF BOO via a single factor ANOVA with post-hoc Tukey’s HSD test. For patients with HF BOO, post-treatment free-flow values were compared between those treated conservatively and surgically.

The dataset consisted of 422 patients as of March 20, 2021 who underwent VUDS. There were 123 patients (113 males, 10 females) who were diagnosed with definite BOO, and 116 patients (106 males, 10 females) diagnosed with presumed BOO. An additional 34 patients with VUDS proven BOO (27 males, 7 females) were diagnosed with HF BOO. Seven HF BOO patients, all male, were lost to follow up. Table 1 depicts mean values for pressure-flow and free-flow metrics for presumed BOO, definite BOO, and HF BOO patients. Of note, HF BOO patients had the highest pressure-flow and free-flow Qmax, voided volumes, and BCI. However, the BOOI was greatest in definite BOO, followed by HF BOO and presumed BOO. 

15 HF BOO patients (12 males, 3 females) had conservative treatment with monitoring for symptom progression or medications, with an average decrease in Qmax of 2.9 mL/s. 12 HF BOO patients (8 males, 4 females) underwent surgical treatment, with an overall improvement in Qmax of 5 mL/s (Table 2).

Based on our results and two published studies, the prevalence of HF BOO patients ranged from 7% to 22%. HF BOO patients had a greater Qmax, voided volume, and BCI compared to presumed and definite BOO patients, and a lower BOOI than definite BOO patients (Table 1). This suggests that HF BOO patients have stronger detrusor contractions than both the definite and presumed cohorts. Taken together, the data suggests that HF BOO patients are a distinct diagnostic entity and sheds light on why they can be easily misdiagnosed. Furthermore, after treatment, Qmax improved only in those who underwent surgery (Table 2). This suggests surgery may be a more effective treatment than conservative therapies in HF BOO, especially when considering the decrease in Qmax observed in the conservatively treated patients over time.

HF BOO was documented in 22% of patients with VUDS proven BOO. If this data can be replicated, it suggests that approximately 1 in 5 patients will be mis-diagnosed as not having BOO based on screening free-flow uroflowmetry. This may lead to inappropriate treatment. We are encouraged by our observations of an increase in Qmax and the decrease in post-void residual urine in our sub-set of HF BOO patients who underwent surgery. However, the clinical implications of HF BOO have not been well described and need further evaluation in order to improve the current diagnostic and treatment algorithm for BOO.