Intradetrusor Injections Of Onabotulinum Toxin Research Articles

Evaluation of the effect of 100U of Onabotulinum toxin A on detrusor contractility in women with idiopathic OAB: A multicentre prospective study.

AimsIntradetrusor injection of Onabotulinum Toxin A (BTX‐A) is a third‐line treatment for overactive bladder (OAB). Voiding dysfunction and the need for intermittent catheterization are potential complications, consequent to bladder contractility (BC) decrement.Primary aim: to evaluate BC variation after BTX‐A detrusor injection in women with idiopathic OAB.MethodsA prospective multi‐institutional observational study was conducted. Medical history, bladder diary, 24‐h pad test, and invasive urodynamic parameters were recorded before and 4–6 weeks after BTX‐A 100U administration. BC was measured as Modified Projected Isovolumetric Pressure (PIP1), that is, maximum flow rate (Qmax) + detrusor pressure at Qmax (PdetQmax).Continuous variables were expressed as median and interquartile range. We compared continuous variables using Wilcoxon test and proportions between two times with Fisher exact test.ResultsNo changes in PIP1 were observed (p > 0.05) in 45 women enrolled between January 2018 and September 2019. Median age was 54.6 years. At baseline, 91.1% had urge urinary incontinence, with 4.9 ± 2.6 daily pads used and a 24‐h pad test of 205.4 ± 70.8 g. Baseline detrusor contractility was normal in all the patients.Postoperatively, an improvement in the 24‐h pad test (p < 0.01), daily voids (p < 0.01), and nocturia (p < 0.01) occurred. Urodynamics pointed out a significant reduction of detrusor overactivity rate (p < 0.01) and an increase of median maximum cystometric capacity (p < 0.01). No difference was observed in median Qmax (p > 0.05), PdetQmax (p > 0.05), and PVR (p > 0.05). No patient needed postoperative catheterization.ConclusionsThe current series provides evidence that detrusor injection of botulinum toxin is an effective option for treating OAB, without causing voiding dysfunction and BC impairment.

Alkalinized lidocaine solution as a first-line local anesthesia protocol for intradetrusor injection of onabotulinum toxin A: Results from a double-blinded randomized controlled trial.

Local anesthesia protocols for intradetrusor onabotulinum toxin A (BoNTA) injection lack standardization. We aimed to determine if an alkalinized lidocaine solution is more effective than lidocaine only. Patients of both genders aged 18 or above enlisted for intradetrusor BoNTA injection (idiopathic, neurogenic, and bladder pain syndrome) were included in a double-blinded randomized controlled trial after obtaining their informed consent. All participants filled a bladder diary and a urine culture was performed. Subjects were randomized 1:1 to Protocol A (20 ml 2% lidocaine + 10 ml 8.4% sodium bicarbonate) or Protocol B (20 ml 2% lidocaine + 10 ml 0.9% saline solution). A Numeric Rating Scale (0-10) was used to assess the level of pain immediately after the procedure (primary endpoint). Secondary endpoints included pain after 1 h, urinary tract infection, acute urinary retention, and hematuria related to the procedure. A total of 116 patients were randomized. Baseline characteristics (age, sex, indication, and bladder diary parameters) of patients in Group A and B were similar. Pain scores at the end of the procedure were significantly lower with the alkalinized solution (Protocol A and B, respectively, 2.37 ± 0.31 vs. 4.44 ± 0.36, p < .01). No differences were observed 1 h after treatment (Protocol A and B, respectively, 0.54 ± 0.17 vs. 0.69 ± 0.19, p = .487). The only adverse event reported was mild-to-moderate self-limited hematuria in 15.4% of patients. The use of an alkalinized lidocaine solution has proven to be significantly superior to lidocaine only as local anesthesia before intradetrusor BoNTA injection, suggesting that this may be considered a first-line option.

Re: Switch to Abobotulinum Toxin A May be Useful in the Treatment of Neurogenic Detrusor Overactivity when Intradetrusor Injections of Onabotulinum Toxin A Failed.

Re: Switch to Abobotulinum Toxin A May be Useful in the Treatment of Neurogenic Detrusor Overactivity when Intradetrusor Injections of Onabotulinum Toxin A Failed.

Outcomes of intradetrusor onabotulinum toxin A injection in patients with Parkinson's disease.

To assess the safety and efficacy of intradetrusor onabotulinum toxin A injections for the treatment of overactive bladder (OAB) in patients with Parkinson's disease (PD). All PD patients who underwent intradetrusor injections of onabotulinum toxin A (BoNT-A) for storage symptoms between 2010 and 2017 were included in a retrospective study. A 100 U dose of BoNT-A (Botox®, Allergan Irvine, CA) was used for the first injection in all patients. The primary endpoint was clinical success defined as any subjective improvement in OAB symptoms self-assessed by the patients 4 weeks after the injections. Out of 24 patients analyzed, 19 reported improvement of their OAB symptoms 4 weeks after the first injection (79.2%) with complete resolution of urgency urinary incontinence in seven patients (29.1%; P < 0.001). The average post-void residual (PVR) increased significantly after the first injection from 17.6 to 125.3 mL (P < 0.001). Three of the patients had to start clean intermittent catheterization (CIC) after the first injection (12.5%). Out of 49 injections in total, only five caused incomplete bladder emptying requiring the use of CIC (10.2%). Higher pre-injection PVR was significantly associated with both a lower chance of symptomatic improvement (P = 0.04) and a higher risk of incomplete bladder emptying with institution of CIC (P = 0.047). Intradetrusor injections of BoNT-A 100 U appeared as a safe and effective option in PD patients with OAB symptoms and a low PVR before the injection. Higher preoperative PVR was the strongest predictor of both treatment failure and postoperative urinary retention requiring CIC.

Switch to Abobotulinum toxin A may be useful in the treatment of neurogenic detrusor overactivity when intradetrusor injections of Onabotulinum toxin A failed.

To assess the outcomes of switching to a different brand of botulinum toxin A (BTA, from Botox® to Dysport®) in case of failure of intradetrusor injections (IDI) of Botox® in the treatment of neurogenic detrusor overactivity (NDO). The charts of all patients who underwent a switch to IDI of Dysport® after failure of an IDI of Botox® at six departments of neurourology were retrospectively reviewed. The main outcomes of interest were the bladder diary data and four urodynamic parameters: maximum cystometric capacity (MCC), maximum detrusor pressure (PDET max), and volume at first uninhibited detrusor contraction (UDC). Fifty-seven patients were included. After the first injection of Dysport®, no adverse events were reported. A significant decrease in number of urinary incontinence episodes per day was observed in 52.63% of patients (P < 0.001) and all patients experienced a reduction in PDET Max (-8.1 cmH20 on average; P = 0.003). MCC significantly increased by a mean of 41.2 (P = 0.02). The proportion of patients with no UDC increased significantly at week 6 after ATA injections (from 15.79% to 43.9%; P = 0.0002). Hence, 32 patients draw clinical and/or urodynamic benefits from the botulinum toxin switch from (56.14%). After a median follow up of 21 months, 87% of responders to BTA switch were still treated successfully with BTA. Most patients refractory to Botox® (56.14%) draw benefits from the switch to Dysport®.

Long-term real life efficacy of onabotulinum toxin A for the treatment of neurogenic detrusor overactivity in a population using intermittent self-catheterization

Intradetrusor injection of onabotulinum toxin A (IDIBA) is the third-line therapy for patients with neurogenic detrusor overactivity (NDO). There is few evidence of long-term efficacy but no study assessed reasons for failure or abandonment of IDIBA and CISC (clean intermittent self-catheterization) combined strategy. We aimed to assess its long-term outcome in NDO management, and analyze failure and discontinuation. We retrospectively reviewed medical records of patients admitted in our neurourology department between 2001 and 2013. Inclusion criteria were: age > 18, NDO secondary to spinal cord injury (SCI), multiple sclerosis (MS) or myelomeningocele, NDO management associating IDIBA and CISC, failure of a 3-month combination of two anticholinergics and a 3 year follow-up minimum. Patients with bladder surgery were excluded. Clinical, urodynamic and radiologic data before the first injection, six weeks after the first and last injections were analyzed. Primary endpoints were failure (defined by clinical or urodynamic criteria) and abandonment rates at 3, 5 and 7 years. We secondarily analyzed risk factors for failure and discontinuation. During selected period, 292 patients were included, with mean age 40 ± 13.6 years, 58.2% males and mean duration of NDO 10.8 years. Etiologies for NDO were SCI (84.6%), MS (10.6%) and myelomeningocele (3.4%). After 3 years, 219 patients (80.6%) were still treated, 128 (71.1%) and 58 (60.8%) after 5 and 7 years respectively. Failure rates were 12.6%, 22.2% and 28.9% after 3, 5 and 7 years respectively. Discontinuation rate after 7 years was 11.3%. Reasons were: difficulties related to CISC (3.8%), personal convenience (2.7%), pseudobotulism (2.4%), pregnancy (1.03%), pain (1.03%) and prostatic cancer (0.3%). Clinical, urodynamic and radiologic severity criteria of NDO before IDIBA initiation were major risk factors for treatment failure. This is the first long-term follow-up study of patients with NDO treated by IDIBA and CISC. Less than two third of patients were still treated after 7 years. The main reason for abandonment was difficulties with CISC. Choosing the best time for IDIBA initiation could improve the management of these patients. Further studies are needed to determine the impact of initiation timing, and prior oral anti-muscarinics use on long-term efficiency.

Intradetrusor injections of onabotulinum toxin A (Botox®) 300 U or 200 U versus abobotulinum toxin A (Dysport®) 750 U in the management of neurogenic detrusor overactivity: A case control study.

To compare the outcomes of the first intradetrusor injections of abobotulinum toxin 750 U and onabotulinum toxin 200 and 300 U in patients with neurogenic detrusor overactivity (NDO). A retrospective case-control study was conducted including 211 NDO patients treated in three consecutives eras with onabotulinum toxin 300 U (2004-2006; 80 patients), abobotulinum toxin 750 U (2007-2011; 78 patients) or onabotulinum toxin 200 U (2011-2014; 53 patients). Urodynamic and clinical parameters were compared between groups. The primary endpoint was the rates of success defined as the combination of urgency, urinary incontinence, and detrusor overactivity resolution. When comparing abobotulinum toxin to onabotulinum toxin any doses (200 or 300 U; n = 133), success rates were similar (65.4% vs. 55.6%; P = 0.16). Patients treated with abobotulinum toxin 750 U had higher success rate (65.4% vs. 41.5%; P = 0.007) compared to those who received onabotulinum toxin 200 U. In contrast, there were similar success rates in abobotulinum toxin 750 U and onabotulinum toxin 300 U groups (65.4% vs. 65%; P = 0.91) but with a trend towards longer interval between the first and the second injection in the onabotulinum toxin 300 U group (12.4 vs. 9.3 months; P = 0.09). Intradetrusor injections of abobotulinum toxin 750 U for NDO provided better outcomes than injections of onabotulinum toxin 200 U. Success rates of abobotulinum toxin 750 U and onabotulinum toxin 300 U were similar but interval between injections tended to be longer with onabotulinum toxin 300 U. Neurourol. Urodynam. 36:734-739, 2017. © 2016 Wiley Periodicals, Inc.

652 Intradetrusor injections of onabotulinum toxin A (Botox®) 300 u or 200 u versus abobotulinum toxin A (Dysport®) 750 u in the management of neurogenic detrusor overactivity: A case control study

652 Intradetrusor injections of onabotulinum toxin A (Botox®) 300 u or 200 u versus abobotulinum toxin A (Dysport®) 750 u in the management of neurogenic detrusor overactivity: A case control study

Prevention of Urinary Tract Infection for Patients with Neurogenic Bladder

Urinary tract infection is a common problem among patients with neurogenic bladder dysfunction that can be costly and challenging to manage. Current literature on the topic of preventing urinary tract infections in this heterogeneous patient population is challenged by the difficulty in defining urinary tract infections and by the lack of long-term data from controlled randomized studies. New research suggests that intradetrusor injection of onabotulinumtoxin A may be a useful adjunct in preventing urinary tract infections, and further studies are needed to determine if probiotics, bacterial interference, and/or vaccines will prove to be of use in the population.

Current and future drugs for treatment of MS-associated bladder dysfunction

A majority of patients diagnosed with multiple sclerosis (MS) will develop lower urinary tract symptoms (LUTS) during the course of the disease. Even if antimuscarinic (anticholinergic) treatment is currently the mainstay of conservative treatment of neurogenic detrusor overactivity (NDO), including MS-induced NDO, extensive data regarding their effectiveness and safeness are lacking. When antimuscarinic medications fail to prove efficacious, a further option is intradetrusor injections of onabotulinumtoxin A. In several studies, more than half (and up 76%) of the patients treated with onabotulinumtoxin A experienced significant improvement in symptoms or even achieved complete continence. Cannabis extracts have shown some promise but has still not gained wide acceptance as an effective treatment. Over the last few years many new disease-modifying drugs that have been approved and introduced for treatment of MS. These drugs may have effects not only on the MS disease process, but also on the disease symptoms, including LUTS. However, MS is not primarily a bladder disease and treatment of the underlying pathophysiology should be the main goal of treatment. Since most of the urology drugs are targeting LUTS, these drugs should be regarded as “adds on” to treatments modifying the underlying disorder. Considering that most of these drugs have not been studied specifically with respect to efficacy on LUTS, and since they are not without significant side effects, it seems important that if and when they are going to be used for treatment of bladder symptoms should be a joint decision between the neurologist and urologist taking care of the patient.

Onabotulinum Toxin A: A Therapeutic Option for Refractory Neurogenic Detrusor Overactivity and Idiopathic Overactive Bladder

Overactive bladder syndrome affects up to 17% of the American population and adversely impacts quality of life. Antimuscarinic agents have been the primary treatment of neurogenic detrusor overactivity and overactive bladder, but they are often ineffective or poorly tolerated. Onabotulinum toxin A for refractory cases provides an important therapeutic alternative. Indications, use, efficacy and safety data for intradetrusor injection of onabotulinum toxin A will be reviewed.

Phase 3 Efficacy and Tolerability Study of OnabotulinumtoxinA for Urinary Incontinence From Neurogenic Detrusor Overactivity

We assessed the efficacy, safety and effects on quality of life of onabotulinumtoxinA in patients with neurogenic detrusor overactivity. In this 52-week, international, multicenter, double-blind, randomized, placebo controlled trial 416 patients with neurogenic detrusor overactivity and urinary incontinence (14 or more episodes per week) resulting from multiple sclerosis (227) and spinal cord injury (189) were treated with intradetrusor injections of onabotulinumtoxinA (200 or 300 U) or placebo. The primary end point was the change from baseline in the mean number of urinary incontinence episodes per week at week 6. Maximum cystometric capacity, maximum detrusor pressure during the first involuntary detrusor contraction and Incontinence Quality of Life total score were secondary end points. Adverse events were monitored. OnabotulinumtoxinA at a dose of 200 U in 135 patients and 300 U in 132 decreased mean urinary incontinence at week 6 by 21 and 23 episodes per week, respectively, vs 9 episodes per week in 149 on placebo (each dose p<0.001). Also, maximum cystometric capacity, maximum detrusor pressure during the first involuntary detrusor contraction and Incontinence Quality of Life score were significantly improved over values in the placebo group (each dose p<0.001). Median time to patient re-treatment request was greater for onabotulinumtoxinA 200 and 300 U than for placebo (256 and 254 days, respectively, vs 92). The most common adverse events were urinary tract infection and urinary retention. Of patients who did not catheterize at baseline 10% on placebo, 35% on 200 U and 42% on 300 U initiated catheterization due to urinary retention. OnabotulinumtoxinA significantly improved neurogenic detrusor overactivity symptoms vs placebo. Clean intermittent catheterization initiation due to urinary retention appeared to increase in a dose dependent fashion. No clinically relevant benefit in efficacy or duration was identified for the 300 U dose over the 200 U dose.