Wednesday, October 11, 2006
11089

Analysis of the Free Neurovascular Transfer of Latissimus Dorsi Muscle for Treatment of Bladder Acontractility

Milomir Ninkovic, MD, Gustavo Sturtz, MD, and Arnulf Stenzl, MD.

Bladder acontractility or permanent detrusor dysfunction is a debilitating disorder affecting a large number of relatively young people. The underlying abnormality may be due to damage to the detrusor muscle itself, its autonomic nerve supply, the spinal micturition center or the upper motor neuron system. Until now the only treatment available for bladder acontractility due to a lower motor neuron lesion was lifelong intermittent catheterization. Several experimental studies investigating restoration of detrusor function and voluntary bladder emptying by functional electrical stimulation, direct bladder surface stimulation and detrusor myoplasty have been published. Unfortunately, these approaches are not feasible in cases of dysfunction of the spinal micturition center, sacral motor root, pelvic or intramural nerve, or the neuromuscular end plate. Patients and Methods. Thirty four patients with at least 8 months postoperative follow up with ages between 9 and 60 years-old underwent latissimus dorsi detrusor myoplasty (LDDM) between 1995 and 2005 .The causes of detrusor dysfunction were spinal cord injury in 19 patients, spina bifida in 7, idiopathic and other causes in 8 patients. Operative technique. In the pelvis the transferred latissimus dorsi muscle is attached to the the inner surfaces of both ischial bones and insertions of the sacrospinal ligaments, fascial and ligamentous structures. The microvascular anastomosis are done between thoracodorsal and epigatric inferior vessels. Original resting tension of the latissimus dorsi muscle is restored by bladder distention. Approximately three-quarters of the entire bladder surface are covered by latissimus dorsi muscle leaving only the area of trigone with the ureteral orifices and the lateral vesical pedicles uncovered. The thoracodorsal nerve is sutured to the lowest motor branches of the intercostal nerve. Postoperative follow up. The bladder is initially drained with an indwelling catheter and subsequently by intermittent catheterization. At 12 weeks after latissimus dorsi detrusor myoplasty the patients are instructed to void under physiotherapeutic guidance by voluntarily contracting the lower abdominal muscles. After voiding the residual urinary volume is checked by self-catheterization. Catheterization intervals are gradually increased depending on the residual urinary volumes. Results. The long-term urodynamic results of detrusor myoplasty demonstrate its impact on the entire urinary tract. Of the 35 patients voluntary voiding was restored by latissimus dorsi detrusor myoplasty alone in 32, eliminating the need for catheterization to empty the bladder. In 2 patients LDDM had an insufficient or no effect. In one patient occurred late thrombosis and flap necrosis. Three patients needed complimentary urethrotomy. Discussion. LDDM has proved clinically successful in the long term. Following reinnervation and adequate muscle training, the transplanted latissimus dorsi muscle provides sufficient capacity and strength to replace the missing urinary detrusor muscle. Elimination of the need for self-catheterization has led to growing self-confidence among patients and has enabled many of them to return to their usual daily and occupational activities.
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