JOURNAL ARTICLE

Therapeutic satisfaction and dissatisfaction in patients with spinal cord lesions and detrusor sphincter dyssynergia who received detrusor botulinum toxin a injection

Hann-Chorng Kuo
Urology 2008, 72 (5): 1056-60
18533231

OBJECTIVES: To investigate satisfaction in terms of quality-of-life (QOL) improvement among patients with spinal cord lesions and detrusor sphincter dyssynergia treated with botulinum toxin A (BoNT-A) injections to the detrusor for urinary incontinence and bladder dysfunction.

METHODS: A total of 50 patients with spinal cord lesion and detrusor sphincter dyssynergia were treated with BoNT-A injections (200 U) into the urinary bladder detrusor muscle. The urodynamic parameters, QOL scores, and general satisfaction with the treatment were assessed.

RESULTS: Overall satisfactory results were perceived by 78% of patients who received detrusor BoNT-A injections. The maximal bladder capacity had increased significantly (221 +/- 107 vs 432 +/- 115 mL, P = .000), detrusor pressure decreased (43.5 +/- 21.1 vs 12.6 +/- 10.7 cm H(2)O, P = .000), and postvoid residual urine volume increased (121 +/- 107 vs 325 +/- 123 mL, P = .000) by 3 months after BoNT-A treatment. Patients had significant improvement in QOL indexes (Urogenital Distress Inventory 6-item short form 11.7 +/- 2.3 vs 4.1 +/- 2.1, P = .01; and Incontinence Impact Questionnaire, 7-item short form 16.3 +/- 3.5 vs 11.7 +/- 4.1, P = .03) after BoNT-A treatment. Decreases in incontinence grade and urgency episodes contributed the most to satisfaction, and increased difficulty in urination and the need for catheterization contributed to dissatisfaction. Of the 50 patients, 25 (50%) received repeated BoNT-A injections; 4 patients finally decided to undergo augmentation enterocystoplasty because they desired permanent corrections and did not wish to receive repeated injections.

CONCLUSIONS: The patient satisfaction rate was 78%, and QOL improved among these patients after detrusor BoNT-A injections for urinary incontinence and bladder dysfunction.

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