Neurovesical dysfunction in children after treating pelvic neoplasms
Version of Record online: 23 JUL 2003
Volume 92, Issue 3, pages 289–292, August 2003
How to Cite
Mosiello, G., Gatti, C., De Gennaro, M., Capitanucci, M.L., Silveri, M., Inserra, A., Milano, G.M., De Laurentis, C. and Boglino, C. (2003), Neurovesical dysfunction in children after treating pelvic neoplasms. BJU International, 92: 289–292. doi: 10.1046/j.1464-410X.2003.04326.x
- Issue online: 23 JUL 2003
- Version of Record online: 23 JUL 2003
- Accepted for publication 11 April 2003
- pelvic neoplasm;
- vesical dysfunction;
To evaluate 10 years of experience, and thus define the occurrence and causes, of neurogenic lower urinary tract dysfunction in children with pelvic neoplasms treated by surgery.
PATIENTS AND METHODS
From 1991 to 2000, 33 children were operated by the same surgeons for pelvic neoplasms; 11 were analysed, comprising four each with sacrococcygeal teratoma (ST) and ganglioneuroma, and one each with yolk sac tumour (YST), neuroblastoma and myofibroblastic bladder sarcoma (MBS). The other patients were not assessed because eight had died or were in severe progression, three were treated by bladder substitution and the others were lost to follow-up or refused a urological evaluation. All 11 children were evaluated at ≥ 6 months after surgery with a questionnaire about bowel and voiding habits, a neurological and orthopaedic assessment, a noninvasive urodynamic study, renal ultrasonography and spinal and pelvic magnetic resonance imaging (MRI). All patients with signs of bladder dysfunction were evaluated by a pressure-flow study. The results were analysed for surgical approach and anatomical involvement, i.e. group A, extensive surgery for complete tumour excision in the sacral area (ST and YST); group B, surgery for tumour resection in the paraspinal ganglia area (neuroblastoma and ganglioneuroma); and group C, bladder tumour with partial bladder resection (MBS).
Eight patients had signs or symptoms related to bladder sphincter dysfunction. One child refused the invasive urodynamic evaluation, leaving seven for analysis (two each ST and ganglioneuroma, one each YST, neuroblastoma and MBS). The urodynamic findings were normal in three children. On spinal and pelvic MRI a presacral lipoma with syringomyelia was discovered in one child with ST. Eight children had bladder dysfunction and two had no neurogenic damage (which was only in sacral tumours); in one child it was related to an upper motor neurone lesion from spinal dysraphism and in the other to a lower motor neurone lesion from surgical injury to the splanchnic nerves. Patients operated for paraspinal tumours had more bladder dysfunction but no signs of neurogenic damage, as did the patient with partial bladder resection. However in Group B, there may have been a transient or incomplete nerve injury in one patient.
Deficits of parasympathetic, sympathetic and somatic innervation of the bladder and the urethra may occur in children after surgery for pelvic neoplasms, related to minor or major surgical trauma. In ST, a tethered cord may be associated with mixed neurogenic damage. Knowledge of bladder dysfunction in anorectal malformations, spinal dysraphism, etc. and the clinical protocol used in these patients also seemed to be useful for understanding the development of voiding dysfunction in patients with neoplasm.