The neurogenic bladder: medical treatment

Abstract

Neurogenic bladder sphincter dysfunction (NBSD) can cause severe and irreversible renal damage and bladder-wall destruction years before incontinence becomes an issue. Therefore, the first step in adequate management is to recognize early the bladder at risk for upper- and lower-tract deterioration and to start adequate medical treatment proactively. Clean intermittent catheterization combined with anticholinergics (oral or intravesical) is the standard therapy for NBSD. Early institution of such treatment can prevent both renal damage and secondary bladder-wall changes, thereby potentially improving long-term outcomes. In children with severe side effects or with insufficient suppression of detrusor overactivity despite maximal dosage of oral oxybutynin, intravesical instillation is an effective alternative. Intravesical instillation eliminates systemic side effects by reducing the first-pass metabolism and, compared with oral oxybutynin, intravesical oxybutynin is a more potent and long-acting detrusor suppressor. There is growing evidence that with early adequate treatment, kidneys are saved and normal bladder growth can be achieved in children so they will no longer need surgical bladder augmentation to achieve safe urinary continence in adolescence and adulthood.

Fig. 1

Classification of the neurogenic bladder, with four subtypes (a–d) according to dysfunctional activities of sphincter and detrusor. For each subtype, clinical implications if untreated and principles of management are summarized

Fig. 2

Suppression of detrusor hyperactivity with resolution of reflux by nonsurgical management. Illustrative patient with high-risk neurogenic bladder sphincter dysfunction (NBSD) (type B), urodynamically showing early unsafe filling pressures (A) with high-grade reflux (a) and urosepsis before treatment. Under clean intermittent catheterization (CIC) plus oxybutynin, the unsafe high-pressure bladder was converted into a safe low-pressure reservoir with good capacity and disappearance of the reflux at control cystography 3 months later (b). Severe systemic side effects, making continuation of oral oxybutynin impossible, disappeared after switching to intravesical oxybutynin. Further urodynamic evaluations (B: after first intravesical administration; C: after 4 months) documented adequate suppression of detrusor hyperactivity (modified from [40]). Long-term (currently 13 years) continuation of CIC and intravesical oxybutynin has resulted in a safe and adequate capacity bladder with social continence for the patient