Patients with bladder acontractility caused by lower motor neuron lesion are generally dependent on lifelong clean intermittent catheterization with all of its inherent risks. The functional neurovascular transfer of the latissimus dorsi muscle to the pelvis allows the restoration of voluntary voiding. This article describes the operative technique, indications, preoperative considerations, and postoperative care. The literature is reviewed and the latissimus detrusor myoplasty is compared with other functional muscle transfers to restore voluntary micturition.
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The main goal of the latissimus dorsi detrusor myoplasty is to get patients with bladder acontractility independent from lifelong self-catheterization with its related disadvantages.
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The free neurovascular latissimus dorsi muscle (LDM) is particularly appropriate for the detrusor myoplasty because it provides a suitable neurovascular pedicle, muscle size and configuration of muscle fibers.
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The coaptation of the thoracodorsal nerve to a branch of the intercostal nerve results in a synergistic function of the transferred latissimus muscle and the muscles of the abdominal wall
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The success of the latissimus dorsi detrusor myoplasty (LDDM) is dependent on an excellent cooperation between both surgical disciplines—urology and plastic surgery.
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Introduction
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. 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
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Preservation of upper urinary tract integrity
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Insurance of adequate continence
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Minimization of stone formation and urinary infection
All these therapeutic goals aim to improve patient quality of life and prolong life expectancy.
Catheterization
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 :
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Urinary tract infections; prevalence varies widely in literature (from 12 to 88%).
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Epididymitis
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Epididymo-orchitis
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Urethral trauma and stricture
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Bladder injury
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Urolithiasis
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Deteriorating renal function
In addition, the socioeconomic and psychological burdens of lifelong intermittent catheterization must be considered.
All these disadvantages associated with this procedure emphasize the importance of effective alternative treatment options for the acontractile bladder.
Sacral Neuromodulation
One approach to restore bladder contraction is the so-called sacral neuromodulation that enables a voluntary bladder emptying by electrical stimulation but requires an intact spinal cord, micturition center, and spinal roots. If these conditions are not fulfilled, voluntary micturition can be achieved only by a functional muscle transfer.
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. 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.
Preoperative considerations and assessments
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.
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Bladder acontractility without upper motor neuron lesion
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No indication for neuromodulation
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Life expectancy greater than 10 years
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No improvement of bladder dysfunction longer than 1 year
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Patient should handle clean intermittent catheterization greater than 1 year
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No infravesical obstruction
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Intact 12th intercostal motor nerve
Routine preoperative evaluation includes
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Video-urodynamics
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Diagnostic urethrocystoscopy
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Excretory urography
In addition, electromyography of the lower portion of the rectus abdominis muscle should be performed to confirm an intact 12th intercostal motor nerve for the neural coaptation. In patients with idiopathic cause of the disease, a neurophysiologic assessment of the sacral district, including MRI or CT, is recommended to exclude an upper motor neuron lesion. Preoperative targeted diagnostics are also essential to identify those patients who are eligible for a detrusor myoplasty and those who can also benefit from sacral neuromodulation. Urodynamics are essential to evaluate suspected acontractility. In cases of equivocal urodynamic findings, sacral neuromodulation should be applied to rule out the presence of bladder hypocontractility rather than acontractility. Direct electrostimulation of the sacral nerves may then help identify those patients with hypocontractility who might be candidates for implantation of a permanent device for sacral neuromodulation.
Preoperative considerations and assessments
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.
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Bladder acontractility without upper motor neuron lesion
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No indication for neuromodulation
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Life expectancy greater than 10 years
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No improvement of bladder dysfunction longer than 1 year
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Patient should handle clean intermittent catheterization greater than 1 year
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No infravesical obstruction
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Intact 12th intercostal motor nerve
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