PTU - Polskie Towarzystwo Urologiczne
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Injection of Botulinum Toxin-A (DYSPORT™) for idiopathic detrusor overactivity
Article published in Urologia Polska 2008/61/Supl. 1.


Mariusz Blewniewski, Marek Jeromin, Waldemar Różański
II Klinika Urologii UM, WSS im. M. Kopernika w Łodzi



Botulinum toxin (Dysport™) is produced by the bacteria Clostridium botulinum and is one of the most potent naturally occurring substances known. This toxin is a potent neuromuscular-junction antagonist. Due to this property, Dysport™ has been used in a variety of conditions where Intradetrusor injection with this toxin appears to be highly effective treatment for patients with intractable idiopathic detrusor overactivity.


This videotape shows the technique of intradetrusor injection of BotulinumToxin-A (Dysport™) by using transurethral injection for the treatment of intractable idiopathic detrusor overactivity.

Materials and methods.

All women gave consent to treatment and were informed that the long-term effects were unknown. They were warned about the risk of self-intermittent catheterization post-operatively. This procedure was done under general anesthesia. A prophylactic antibiotic was given. Cystoscopy was performed using 0° telescope and Dysport was injected with 23G. This needle has a working length of 45cm. Dysport is available in 500IU vial and was dissolved in 20-30 ml of saline. The bladder was filled and 500IU for idiopathic detrusor overactivity of Dysport™ was injected. 20-30 separate sites were injected with 1 ml each by using 2 syringes, and the dead space of the needle flushed with normal saline. The Albaran protective stabilizing device prevents the needle being bent when working at the corners.


All women were assessed before and at 2 months and 4 months using a bladder diary and VAS and cystometry only pre-operatively. All the women treated so far have shown a marked improvement in LUTS symptoms.


The transurethral injection is easy to use. The procedure takes <30 minutes and we recommend that to women who have failed to respond to oral anticholinergics