Treatment Options for NDO
Treatment options for NDO include, for failure to empty: behavioral modification (ie, pelvic floor exercises), clean intermittent catheterization (CIC), botulinum toxin A injection into the sphincter, suprapubic catheter, indwelling catheter, sphincterotomy, urethral stent, and urinary diversion. For failure to store, treatment options include: behavioral therapy (ie, diet and fluid intake, timed voiding), antimuscarinics, beta3-agonist, botulinum toxin A injections into the detrusor, indwelling catheter, and reconstruction.
Behavioral therapy. Treatment includes behavioral therapy that may be combined with antimuscarinics.33 Behavioral modifications comprise moderating fluid intake, reducing or eliminating caffeine, pelvic floor muscle exercises, biofeedback, timed voiding, toileting assistance, bladder education/retraining, and weight loss.
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Pharmacologic approaches. These include the oral antimuscarinic/anticholinergic agents listed previously. The beta3-agonist mirabegron as well as some other agents also may be tried; however, none of these pharmacologic agents are approved for NDO.
Botulinum toxin. This approach may be appropriate for some patients with NDO (see Patient-Clinician Video C with Dr. Chancellor).
OnabotulinumtoxinA. Two phase 3 randomized, placebo-controlled, pivotal studies in patients with incontinence due to detrusor overactivity associated with a neurologic condition (eg, spinal cord injury or multiple sclerosis) who were either spontaneously voiding or using catheterization found that onaBoNTA significantly reduced weekly incontinence episodes and increased incontinence QoL.34,35
OnaBoNTA at a dose of 200 U in 135 patients (Figure 2) and 300 U in 132 patients decreased mean urinary incontinence at week 6 by 21 and 23 episodes per week, respectively, vs. 9 episodes per week in 149 patients on placebo (each dose P<0.001). Also, maximum cystometric capacity, maximum detrusor pressure during the first involuntary detrusor contraction (PdetmaxIDC), and Incontinence-Quality of Life (I-QoL) score were significantly improved over values in the placebo group (each dose P<0.001).34
In patients with multiple sclerosis (n=154) or spinal cord injury (n=121), at week 6, onaBoNTA 200 U and 300 U significantly reduced UI episodes per week (-21.8 and -19.4, respectively) vs. placebo (-13.2; P<0.01); onaBoNTA benefit was observed by the first posttreatment study visit at week 2. Improvements in maximum cystometric capacity, PdetmaxIDC, and I-QoL total score at week 6 were significantly greater with both onaBoNTA doses than with placebo (P<0.001).35 The approved dose of onaBoNTA is 200 U.
The most frequent AEs were UTI, urinary retention, hematuria, fatigue, and insomnia.34,35 With regard to retention, clinicians should keep in mind:
- The need for CIC is temporary.
- If CIC must be used, it does not mean that all voids involve CIC.
- The risk of CIC at 100 U for OAB is ~5%.
- The risk of CIC at 200 U for NDO is ~20%.
- If a patient has neurogenic bladder dysfunction and is spontaneously voiding, consider using the 100 U dose to decrease the risk of postinjection need for CIC.
AbobotulinumtoxinA. A study of the efficacy and dose dependency of aboBoNTA in 13 men and 9 women with NDO who received successive doses injected repeatedly into the bladder showed a constant effect following 4 injections. Both doses—500 U (in 12 patients) and 1000 U (in 10 patients)—showed similar duration and efficacy, which was slightly better, although nonsignificant, with 1000 U.36
