Poor detrusor contractility and related impaired bladder emptying is a debilitating and irreversible disorder presenting a major medical and social problem. It is estimated that several thousand patients with this disease in the United States depend on clean intermittent catheterization several times a day.¹ The underlying pathology of bladder acontractility may be damage to the detrusor muscle itself, its autonomic nerve supply, or the spinal micturition center. Possible causes include congenial anomalies (eg, myelomeningocele and myelodysplasia), acquired infections, inflammatory or autoimmune diseases, chronic overdistension due to subvesical outlet obstruction, and central or peripheral nerve injuries secondary to trauma or degenerative diseases. The hypoflexic or areflexic bladder characteristically results in urinary retention and overflow incontinence associated with urinary tract infections, stone formation, and vesicoureteral reflux. If left untreated, this condition inevitably leads to impairment of the upper and lower urinary tract.

The main goals in treating patients with neurogenic bladder dysfunction are

Until now, the gold standard treatment has been lifelong clean intermittent catheterization that has reduced renal-related mortality in the past 4 decades but is also associated with serious adverse effects^2–4:

One approach to restore bladder contraction is the so-called sacral neuromodulation that enables a voluntary bladder emptying by electrical stimulation^7,8 but requires an intact spinal cord, micturition center, and spinal roots.⁹ If these conditions are not fulfilled, voluntary micturition can be achieved only by a functional muscle transfer.

The free neurovascular LDM is particularly appropriate for this procedure because it provides a suitable neurovascular pedicle, muscle size, and configuration of muscle fibers that could be initially proved in an experimental model.^10,11 In this procedure, the LDM is partially wrapped around the acontractile bladder with its thoracodorsal nerve coaptated to the lowest branch of the intercostal nerve. After the reinnervation of the LDM, a contraction of the rectus abdominis muscle results in a simultaneous contraction of the transferred latissimus, which leads to an voluntary emptying of the bladder. As the contraction of both muscles then increases the intravesicular pressure, the nerve coaptation enables a synergistic function of both muscles. In 1998, successful clinical applicability of the LDDM for the treatment of bladder acontractility was reported for the first time.¹²

Candidates for LDDM are patients with bladder acontractility that is not ascribed to an upper motor neuron lesion (ie, multiple sclerosis, apoplectic stroke, or spinal trauma above the 12th thoracic vertebra) (Box 1). Main causes of acontractility that indicate the procedure are spinal trauma below Th12, tethered cord syndrome, lumbar hernia of nuclei pulposi, megacystis/bladder outlet obstruction, sacral myelomeningocele, and idiopathic and chronic retention after hysterectomy. Considering the complex procedure, life expectancy should be more than 10 years. There should be no improvement of the bladder dysfunction for at least 1 year. Suitable patients should handle clean intermittent catheterization with safety for at least 1 year and be able to continue performing this catheterization in case of LDDM failure. There should be no signs of infravesical obstruction at urethrocystoscopy.¹³