[Voiding dysfunction after surgical resection of deeply infiltrating endometriosis: pathophysiology and management].

Autonomic nerve (sympathic and parasympathic) damage plays a crucial role in the aetiology of bladder dysfunction that occurs after resection of deeply infiltrating endometriosis (uterosacral ligaments, colorectal bowel, rectovaginal wall). This review presents an overview of the pathophysiology and management of voiding dysfunction that occur after this kind of surgery. The rate of significant post-voiding residual volume and/or hypoactive bladder after colorectal resection for endometriosis ranges from 15 to 20%. This rate seems to be higher (up to 30%) after proximal utero-sacral ligaments resection. This is explained by the location of the inferior hypogastric plexus at the proximal portion of the utero-sacral ligaments. Urodynamics investigations show non specific hypoactive bladder and altered uroflowmetry. Concerning treatment, further controlled studies are needed to assess the hypothetical usefulness of parasympathomimetic and prokinetic agents for hypoactive bladder occurring after pelvic autonomic denervation. Neuromodulation is a successful treatment for patients with refractory lower urinary tract dysfunction. However, there is no controlled study that focused on its efficacy in voiding dysfunction after radical pelvic surgery. Overall, the main objective of the treatment is to avoid the complications of post-voiding residue (such as infection) and of abdominal pushing effort (deterioration of perineal tissues). Therefore, self catheterization should be recommended when this postoperative complication occurs. An understanding of the location of the autonomic pelvic network should help prevent iatrogenic injury through the adoption of surgical techniques, such as nerve sparing, that reduce postoperative autonomic dysfunction.