Overactive bladder is an umbrella term that collectively covers several lower urinary tract conditions including urgency incontinence. The International Continence Society defines overactive bladder as “urgency, with or without urgency incontinence, usually with frequency and nocturia, in the absence of pathologic or metabolic factors that would explain these symptoms.”¹ Specific definitions of the various presentations are listed as follows:

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  Urgency—a sudden, compelling desire to pass urine, which is difficult to defer

  
  
• 
  

  Frequency—complaint by the patient that she voids too often by day (generally considered normal to void ≤8 times per day)

  
  
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  Nocturia—complaint that individual has to wake up ≥1 time per night to void

  
  
• 
  

  Urgency incontinence—the complaint of involuntary leakage accompanied by or immediately preceded by urgency

  
  
• 
  

  Detrusor overactivity incontinence—incontinence due to an involuntary detrusor contraction

Overactive bladder is estimated to affect approximately 42.2 million adults in the United States resulting in a $24.9 billion annual cost for treatment.² Typically overactive bladder and urgency incontinence are treated with behavioral and/or pharmacological interventions. Currently there are nine commercially available anticholinergic medications on the market specifically targeted at treating overactive bladder. Newer medications such as beta-3 agonists are an alternative pharmacological intervention. Unfortunately, anticholinergics have a high discontinuation rate due to a variety of factors including, most importantly, lack of efficacy and high side effect profile.³ For those who are refractory to conservative measures, or who have contraindications to pharmacological intervention, there are several surgical alternatives available for treatment including sacral neuromodulation and intravesical botulinum injection. There are also other more invasive, nonreversible surgical interventions such as denervation procedures and augmentation cystoplasty that are briefly included in this chapter.

Sacral nerve stimulation (SNS) delivers nonpainful, mild electrical pulses to the sacral nerves to modulate the reflexes that influence the bladder, sphincter, and pelvic floor to improve or restore normal voiding function. It has been available in the United States as a treatment option for refractory voiding dysfunction since 1997 and in Europe since 1994. Currently over 80,000 implants have been performed worldwide, with recent exponential growth occurring in the United States. Since its inception, the therapy has evolved to a minimally invasive procedure that can be performed as an outpatient under local anesthesia. Current FDA-approved indications for SNS include urinary urgency incontinence, urgency–frequency, and nonobstructive urinary retention. With the performance of more implants worldwide, data suggest a benefit of SNS on other types of pelvic floor dysfunction such as chronic constipation and fecal incontinence.⁴

Mechanism of Action

The exact mechanism of action of SNS in the treatment of voiding dysfunction is not completely understood; however, several theories exist. de Groat demonstrated that sacral preganglionic outflow to the bladder receives inhibitory input from both somatic and visceral afferents.^5-7 In addition to providing important insight into the organization of these inhibitory pathways, de Groat has also shown that stimulation of the somatic afferents in the pudendal nerve induces inhibitory mechanisms of detrusor activity.^8,9

Urgency Incontinence and Urgency/Frequency

SNS may promote bladder storage via afferent pathways that project to the sacral cord and inhibit detrusor activity by the suppression of interneuronal transmission in the bladder reflex pathway.^10-12 It is thought that this inhibition is via the afferent limb of the voiding reflex that would block input into the pontine micturition center (PMC). Blocking input into the PMC would inhibit involuntary detrusor contractions without interference of normal voiding that is mediated via the excitatory efferent pathway from the brain to the sacral parasympathetics.¹³

Nonobstructive Urinary Retention

SNS may promote bladder emptying via inhibition of an overactive guarding reflex (a progressive, involuntary increase in the activity of the external urethral sphincter during bladder filling). Stimulation of the sacral nerves may block excitatory outflow to the urethral sphincter and pelvic floor and thus promote bladder emptying.^14,15 Pudendal afferent stimulation can also facilitate voiding reflexes by inhibiting an overly suppressive guarding reflex. There is also some thought that patients with urinary retention have hypertonicity of the pelvic floor musculature that inhibits pelvic floor and urethral sphincter relaxation resulting in ineffective bladder emptying. SNS allows patients to regain awareness of the pelvic floor muscles and restores voluntary relaxation thus facilitating the voiding reflex.^16,17

Procedure

SNS involves a two-stage procedure. The initial phase is considered the test stimulation period where the patient is allowed to evaluate whether or not the therapy is effective in controlling her symptoms. There are two techniques for performing the test stimulation:

1. 
   

   The first is an office-based procedure termed the percutaneous nerve evaluation (PNE). This involves placing a temporary electrode wire through the S3 sacral foramen under local anesthesia. The location of the S3 foramen may be determined through palpation of bony landmarks or by fluoroscopy (described in more detail later in the chapter). The wire is secured to the skin with tape and connected to an external generator the patient wears for a trial period of three to seven days. If patients have at least 50% improvement in their symptoms during the test phase, they are candidates for chronic implant of the lead and implantable pulse generator (IPG). The advantage of the PNE is that it is an incision-free procedure performed in the office utilizing local anesthesia, and does not require hospitalization. The disadvantage comes from the fact that the wire is not securely anchored in place, and has the propensity to migrate away from the nerve with physical activity. If this happens, it is considered an inadequate trial and the patient may proceed with a staged trial.

   
   
2. 
   

   The second alternative is known as a staged implant introduced by Spinelli et al. in 2003.^18,19 This is typically performed as an outpatient procedure using local anesthesia, intravenous sedation, and intraoperative fluoroscopy. This procedure involves placement of the chronic quadripolar lead wire adjacent to a sacral nerve root (typically S3). The lead is self-anchoring and therefore reduces the potential for migration. The patient goes through a test phase that can last from 7 to 21 days. The advantage of this technique is that it allows for a longer trial period with minimal risk of lead migration. The chronic wire also has four electrodes that can each be trialed as the active electrode to achieve optimal improvement in patients’ symptoms. In addition, during the second stage, or final implant, the previously placed tined lead remains in place and is simply connected to the IPG. This eliminates the chance of variable lead placement from the test and implantation phases. The disadvantage of the staged implant is that it requires two visits to the operating room and may be more costly to the health care system. However, in a prospective study comparing the PNE with the staged implant, there was a significantly higher rate of conversion to implant with the staged procedure versus the PNE (88% vs 46%). Infection rates have not been shown to be higher with the staged implant when compared with the PNE.²⁰

To determine optimal lead placement, both motor and sensory responses are desired (Table 29-1). The motor response is typically seen as a pulling in of the pelvic floor muscles known as a “bellows” response, as well as flexion of the great toe. The typical sensory response is a tapping or vibratory sensation in the vagina, rectum, or perineum. There has been no definitive study to determine which factor is more predictive of success. However, a recent study reported that a positive motor response was more predictive than a sensory response in achieving successful trial stimulation, 95% versus 5%, respectively.²¹

Preoperative

Patient Evaluation

Patients should complete a three- to four-day voiding diary to document baseline symptoms and provide an objective measure to determine efficacy of the trial stimulation. They should also have failed other conservative measures such as biofeedback, bladder retraining, and pharmacological therapies. Typically it is recommended that a patient fail a minimum of two anticholinergics prior to going on SNS. Relative contraindications for SNS therapy include the need for regular MRIs, advanced dementia, and complete spinal cord transection.

Consent

SNS is a very safe procedure; however, as with any surgical intervention, there are always risks. The most common risk associated with SNS is infection. Infection rates have been reported in the range up to 7%.²² Other complications include lead migration as well as pain at the lead or IPG site. Although there is a potential risk of nerve injury, there has never been a report of such an occurrence.

Patient Preparation

Since infection is the most common complication, preventative measures to reduce infection can be beneficial. These include use of an antiseptic scrub the day prior to surgery and the day of surgery, as well as perioperative parenteral antibiotics providing gram-positive coverage. Although there are no comparative studies, most clinicians also recommend oral antibiotics during the staged implant trial period.

Intraoperative

1. 
   

   Patient positioning and anesthesia: For most patients SNS is performed as an outpatient procedure under monitored anesthesia care (MAC) sedation. There are some practitioners who prefer general anesthesia; however, this eliminates the opportunity to determine the patient’s sensory response to stimulation. The patients are placed in the prone position with a pillow under the hips to elevate and flatten the sacrum. Fluoroscopy is used for lead placement; therefore, the patient needs to be positioned on the table so the C-arm of the fluoroscope can obtain a lateral view of the sacrum without interference from the bed post. The buttocks should be gently taped apart to allow for easy visualization of the bellows response without having to place the surgeon’s hand into this part of the surgical field as this may increase risk of contamination and infection. The patient should have a surgical prep that covers the lower back from flank to flank and down to and including the rectum. A sterile towel may be placed over the exposed rectum to keep it separate from the rest of the surgical field, and only exposed during stimulation.

   
   
2. 
   

   Determining the location of the sacral foramina: Both bony landmarks and fluoroscopy can be used to help determine the level of S3. Typically the location of the S3 foramen is 9 cm from the tip of the coccyx at the level of the greater sciatic notch. Location can be confirmed fluoroscopically in the anterior–posterior orientation (Figures 29-1 and 29-2).

   
   
3. 
   

   Needle placement: Local anesthesia is applied to the skin and subcutaneous tissue. The foramen needle (3.5 or 5 in) is placed through the S3 foramen at an approximate 60° angle to the skin, in a slight medial to lateral orientation (along the natural course of the nerve). Stimulation is then delivered to the needle and the motor and sensory responses are noted (Figure 29-3).

   
   
4. 
   

   Placement of the lead wire: Once confirmation of correct placement of the foramen needle is determined, a small 2 to 3 mm incision is made lateral to the needle to accommodate the lead and lead tunneler. A directional guide is passed through the foramen needle and the needle removed. An introducer is placed over the directional guide to a depth where the radio-opaque marker is at the level of the anterior sacrum.

   
   

   The lead wire is then placed through the introducer and the introducer sheath is withdrawn to expose all the electrodes. Each electrode is tested for an appropriate response (Figure 29-4).

   
   

   Once appropriate response is noted, the introducer is removed over the lead wire exposing the tines, which are fixation elements, that allow for the lead to be secured within the thoracolumbar fascia and paraspinous muscles (Figure 29-5). The final placement of the lead is confirmed with fluoroscopy. There are four electrodes on the lead wire: the deepest is the zero electrode and the most superficial is the number three electrode that often times straddles the anterior edge of the sacrum.

   
   

   The lead is then tunneled to the ipsilateral posterior hip and a pocket is created to approximately 1.5 to 2 cm depth in the subcutaneous tissue to allow for housing of either the IPG or temporary extension. If the patient is undergoing a staged implant, the lead wire will be attached to a temporary extension, and that temporary extension is tunneled to the contralateral side with the same tunneling device and attached to an external stimulator.

   
   

   If the patient has a successful staged implant trial as defined by a 50% or greater improvement in symptoms, she will undergo placement of the IPG. If the patient has had a successful PNE, then the lead wire and IPG may be placed at the same surgical setting.

   
   
5. 
   

   Placement of the IPG: The IPG pocket is created in the posterior hip area on the ipsilateral side, approximately 3 to 4 cm below the posterior iliac crest. The depth is taken to approximately 1.5 to 2 cm to allow for some cushioning of the IPG. Once the IPG is placed, the pocket is irrigated and closed in two layers.