CHAPTER 92 W. Stuart Reynolds When conservative and medical therapies for detrusor compliance abnormalities fail, few surgical options remain for “refractory” patients. Presently, there are three accepted modalities of surgical treatment: (1) sacral nerve stimulation (sacral neuromodulation [SNM]), (2) injectable bladder neuromodulation with neurotoxins, most notably botulinum toxin (BoTN), and (3) bladder augmentation. Uses, indications, and techniques for these three modalities continue to evolve as experience and understanding of each are gained. Patient selection, therefore, remains an important aspect of determining which surgical option is best for the patient; an appropriate patient evaluation is required. A full patient history is necessary to elucidate the character of urinary symptoms, to evaluate any previous attempts at medical or surgical treatment, and to identify concomitant medical conditions that may influence the success of treatment or provide contraindications to different therapies. In general, a patient who may be considered for surgical treatment of detrusor abnormalities will need to have failed more conservative treatment modalities, and a complete understanding of previous treatments is essential. A thorough physical examination is warranted that focuses on the lower abdomen and pelvis to note any structural abnormalities, including a vaginal speculum examination and bimanual physical examination in women to evaluate for any associated pelvic organ prolapse, as well as a prostate examination in men. Also, inspection and palpation of the lower back and spine can uncover signs of bony abnormality or scars from any previous spine surgery that may suggest a potential neurologic insult. Finally, the extremities should be examined for pedal edema and neurologic or musculoskeletal abnormalities. A bladder or voiding diary can be considered to better quantify the degree of urinary dysfunction, not only for diagnostic purposes but also to serve as a baseline for subsequent posttreatment comparison. Similarly, patient self-reported quality-of-life and symptom severity questionnaires can provide a more objective, comparable picture of the degree of urinary dysfunction. Finally, in any patient who fails conservative or empirical therapy, multichannel urodynamics is warranted to objectively characterize the nature of the urinary dysfunction and to identify any negative or worrisome prognostic factors associated with the voiding complaints, including bladder capacity and compliance, the presence of detrusor overactivity, the magnitude of resting detrusor pressures, and the coordination of detrusor and sphincter function, all of which may have negative implications for renal function. Combining fluoroscopy (“videourodynamics”) can add important information regarding structural abnormalities of the bladder or ureters, including vesicoureteral reflux, bladder morphology, and bladder neck function. Sacral neuromodulation has been available since FDA approval in 1997 (Interstim, Medtronic, Inc, Minneapolis, Minnesota) and is currently indicated for the treatment of urge urinary incontinence, frequency-urgency syndrome, and idiopathic urinary retention. Although the exact mechanism of action of SNM has not been fully determined, it appears to modulate bladder behavior through electrical stimulation of somatic afferent axons in the spinal roots, which in turn modulate voiding and continence reflex pathways in the central nervous system, likely by inhibiting interneuronal transmission in the bladder reflex pathway. With the present configuration, the Interstim device (comprising a battery-powered neurostimulator, an extension cable, and a tined electrical lead) (Fig. 92–1A) is implanted via a staged, two-step process involving initial percutaneous placement of a semipermanent, tined electrical lead within close approximation of the third sacral nerve root (S3) by placement of the lead through the S3 spinal foramen (Fig. 92–1B). This is typically done with fluoroscopic guidance but may be done without. The tined lead is an insulated, electrical stimulation lead with four contact points near the tip and four plastic collapsible projections, which help to anchor the lead to the surrounding tissue. A temporary, external electrical stimulator is attached and a clinical trial period of 1 to 4 weeks ensues, during which the patient evaluates his or her response to therapy. If appropriate benefit occurs (defined as greater than 50% improvement in symptoms), then an implantable pulse generator (IPG) is connected to the previously placed lead and is surgically implanted in the upper buttocks during a second surgical stage procedure. If there is not a significant response, the implanted lead is removed without implanting an IPG. Adjustments to the impulse generator settings can be made with a remote programming device. Interest in and use of BoTN injection into the bladder for treatment of voiding dysfunction have increased over the past several years, although BoTN is not currently FDA approved for use in the genitourinary system. The causative toxin for botulism, produced by the bacterium Clostridium botulinum, may be one of seven distinct toxins depending on the serotype of the organism (BoTN types A, B, C1, D, E, F, and G). Presently, only BoTN A (Botox, Allergan, Irvine, California; or Dysport, Ipsen, Luxembourg) and B (Myobloc or Neurobloc, Elan, Dublin, Ireland) are commercially available for clinical use. BoTN acts by cleaving a specific site (specific to each BoTN serotype) of a protein complex (soluble N-ethylmaleimide-sensitive factor attachment protein receptor [SNARE] complex) responsible for exocytosis of neurotransmitter vesicles from the neuron. In the case of BoTN A, the most well-studied toxin subtype, the specific substrate is the synaptosome-associated protein of 25 kD (SNAP-25), a component of the SNARE complex; this results in inhibition of synaptic release of acetylcholine from the peripheral motor neurons (Fig. 92–2). At therapeutic doses used for the urinary system, BoTN is understood to inhibit the release of acetylcholine from the motor neuron end plant at the neuromuscular junction, inducing paralysis in the affected muscle, or the bladder in the case of bladder injections. Additionally, BoTN may directly inhibit sensory nerve activity and thus modulate bladder sensory input to the central nervous system. In cases of bladder overactivity or diminished bladder compliance, both mechanisms of action are exploited. Presently, no standardized technique or approach to cystoscopic bladder injections of BoTN is used: a wide range of doses have been used, and a number of different injection templates have been followed. In general, however, BoTN can be injected into the wall of the bladder under cystoscopic vision in an outpatient setting, with local or general anesthesia. The effects of BoTN injection are generally immediately apparent, and symptom improvement can be seen after the first day or so of injection. However, the effects are generally short-lived and wear off after approximately 6 months. When more conservative or less invasive measures have failed in the treatment of bladder compliance abnormalities, the most aggressive management option is augmentation cystoplasty. The goal of bladder augmentation is to create a large-capacity, low-pressure (i.e., high-compliance) reservoir for urine storage. Larger volumes of urine may be stored for longer periods of time, which is beneficial for continence, while detrusor pressure remains low, protecting the urinary system upper tracts from dysfunction and ultimately from renal failure. This is generally achieved at the cost of bladder emptying, and many patients are dependent on intermittent catheter bladder drainage after augmentation. Many different techniques have been developed for augmentation cystoplasty employing a variety of different tissues, including segments of detubularized bowel (ileocystoplasty, cecocystoplasty, sigmoid cystoplasty, and gastrocystoplasty), dilated ureter (ureteroplasty), autoaugmentation (removal of the overlying detrusor muscle of the dome of the bladder), and, more recently, biologic substitution using techniques of bioengineered tissue. The most common procedure involves the use of small intestine, specifically the ileum, and because it has been the best characterized, the ensuing discussion focuses on this technique. Efficacy with use of any of the described techniques can be expected in the properly selected patient. Overall, 70% of patients with urgency, frequency, or urge incontinence achieve success with SNM, defined as “a greater than 50% improvement in symptoms.” Furthermore, for many patients, outcomes are durable for longer than 5 years. Among patients treated with BoTN injection, up to 80% of those treated for overactive bladder symptoms will demonstrate symptom improvement, and up to 70% of those with neurogenic detrusor abnormalities will show improvement. Efficacy in general is limited to 6 months because the effects abate at that time. Repeat injection can be performed with similar efficacy anticipated. Among patients undergoing augmentation cystoplasty, improvement in continence can be expected in more than 75%, with 50% or more completely continent. In some reports, this occurs in 95% of patients. Upward of 80% of patients will experience resolution of preoperative urgency. FIGURE 92–1 A. Interstim device (Medtronic, Inc, Minneapolis, Minnesota), composed of a battery-powered, remote-programmable neurostimulator (implantable pulse generator [IPG]), a semipermanent tined electrical lead, and an insulated extension cable. B. Illustration depicting the final position of the four electrical contact points of the stimulation lead in close proximity to the third sacral nerve root (S3) and the four plastic projections or tines embedded in and securing the lead to the tissue overlying the sacral foramen. (Images source: Medtronic, Inc.) FIGURE 92–2 Schematic depicting the molecular action of botulinum toxin. (Adapted with permission from Rowland LP. New Engl J Med 2002;347:382.) Surgical implantation of an SNM device proceeds by a two-stage process: during the first stage, the electrical stimulation lead is percutaneously placed and positioned in close proximity to the S3 nerve root via the S3 foramen; during the second stage, an IPG is surgically implanted in the upper buttocks, after a successful trial of an external device demonstrating clinical effectiveness. For the first stage, percutaneous lead placement, the patient is placed prone on the operative table; the upper thighs, buttocks, and lower back are widely cleansed, and surgical drapes are placed to allow visualization of the buttocks and gluteal crease, as depicted in Fig. 92–3. With the use of fluoroscopy and a metal surgical instrument, the approximate location of the S3 foramen is noted at the skin level (Fig. 92–3D). A 20-gauge foramen needle is inserted at a 60-degree angle to the skin approximately 2 cm cranial to the actual location of the S3 foramen and is directed into the S3 foramen (Fig. 92–4A
Surgical Management of Detrusor Compliance Abnormalities
Roger Dmochowski
Evaluation of Patients
General Introduction to Three Modalities
Surgical Techniques
Sacral Neuromodulation
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
