Fecal incontinence is reported in 3% of community-dwelling individuals but increases with increasing age, reaching a prevalence of 54% in nursing-home residents. This association with increasing age predicts an overall increase in patients suffering fecal incontinence as the population ages. Most authors agree that the true prevalence of this condition is underestimated in the current scientific literature due to under reporting related to embarrassment. Fecal incontinence has tremendous psychosocial and economic implications for individuals as the loss of such a basic function is emotionally devastating and can lead to poor self-esteem, depression, social isolation, and decreased quality of life. It is not surprising that fecal incontinence is the second leading reason for nursing-home placement, even though fewer than one-third of individuals with this condition seek medical attention.

Among women seeking benign gynecologic care, 28% report fecal incontinence, which supports most epidemiologic studies identification of female gender as an independent risk factor for developing fecal incontinence. This increased prevalence among women is felt to reflect a risk factor unique to women, parturition. The differential diagnosis of fecal incontinence is complex, including systemic, pharmacologic, neurological, anatomical, and functional factors, and in a given individual the etiology is frequently multifactorial. Anatomic and structural causes of fecal incontinence are usually due to obstetric or surgical trauma. Direct damage or de-innervation of the internal anal sphincter (IAS), external anal sphincter (EAS), and the puborectalis can result in varying degrees of fecal incontinence. Those with impaired resting tone from a defective IAS tend to complain of passive incontinence (incontinence at rest), which is worse during sleep because of decreased EAS activity. An inability to respond to sudden distention and to suppress defecation is often seen with external sphincter dysfunction. External and internal sphincter dysfunction often results in incontinence of liquid stool. Incontinence of solid stool is usually seen with widening of the anorectal angle from damage to the puborectalis muscles. Damage to the anal cushions usually causes minor soiling. Other anatomic and structural abnormalities associated with fecal incontinence include obstructive disorders such as pelvic organ prolapse, descending perineum syndrome, anismus, and intussusception; fistulas from diverticulitis, inflammatory bowel disease, cancer, or surgical trauma; and decreased rectal compliance from inflammatory bowel disease, cancer, and radiation. Decreased compliance results in higher intraluminal pressures with smaller volumes of stool, poor storage capacity, urgency, and incontinence.

The overlapping sphincteroplasty is specifically indicated for women with injured EASs, and consequently, effective use of this repair requires a surgeon to have a thorough understanding of all the factors contributing to fecal incontinence in a given patient. This means that the reconstructive surgeon must have a complete knowledge of normal and pathological anorectal function, and utilize this knowledge in working up the patient to determine the factors contributing to fecal incontinence. In a woman with fecal incontinence, the integrity of the anal sphincter should be assessed
by anorectal exam, and then confirmed with endoanal ultrasonography. Endoanal ultrasonography helps to distinguish the anatomy of the EAS and distinguish the location of the defects as well as allowing assessment of the IAS. However, its utility is limited to assessment of anatomy, and the function of the sphincter is equally as important. De-innervation of the EAS due to stretch injury of the pudendal nerve is common in women after vaginal delivery, and studies show that the overlapping sphincteroplasty is less effective in women with a concurrent pudendal neuropathy. Proper preoperative counseling of patients regarding postoperative expectations of continence, therefore requires an assessment of pudendal nerve function. Judging voluntary contraction of the EAS on physical exam provides useful information, although many surgeons also assess nerve function using Pudendal Terminal Nerve Latency testing.

The surgical field in an overlapping sphincteroplasty is contaminated, but trying to limit the amount of stool in the field can decrease the degree of contamination. A bowel prep can be useful toward this end, provided that it is not too aggressive or given too late, as in these circumstances the patient may present for surgery with runny diarrhea. We usually use magnesium citrate, and a Fleets enema the morning of surgery.

The patient should be positioned in lithotomy or modified lithotomy position. Either regional anesthesia or general anesthesia is appropriate. Antibiotic prophylaxis with a second generation cephalosporin or metronidazole is recommended, although there is minimal data to show its efficacy. A risk assessment for deep venous thromboembolism is also indicated and prophylaxis for thromboembolism is usually indicated due to the lithotomy position and length of the surgery. Submucosal infiltration with injectable lidocaine with epinephrine simplifies postoperative pain and assists dissection and hemostasis. A Foley catheter should be placed during the surgery to drain the bladder. Following is a brief description of the surgical procedure used (see also video: Overlapping Sphincteroplasty).

The surgical approach begins with a transverse incision in the posterior fourchette from 4 to 8 o’clock (Figure 38.1). This incision is then extended bilaterally in a semilunar fashion. The incision should extend sufficiently on to the perineum to provide access to the lateral aspects of the EAS. The transverse incision is then joined by a midline longitudinal incision in the epithelium of the posterior vaginal wall. This incision is carried approximately half of the vaginal length. The vaginal epithelium is then dissected off the underlying tissue in the plane between the mucosa and the vaginal muscularis or rectovaginal septum. This dissection is facilitated by using sharp dissection combined with countertraction provided by Allis clamps, a self-retaining retractor, or by using a finger behind the vaginal mucosa. This technique of dissecting the posterior vaginal wall is further described in Chapter 37. For the overlapping sphincteroplasty, the extent of the dissection only needs to include the distal posterior wall, as the goal is to provide access to the perineal body (Figure 38.2).

Once the perineal body is exposed, the surgeon begins the dissection of the EAS. The goal of the dissection is to isolate the scarred ends of the ruptured EAS so that they can be reapproximated. Depending on how the torn sphincter healed, the EAS may be in a U configuration with scar tissue on the ends, or it may be a donut with the anterior portion limited to scar tissue. Preoperative endoanal ultrasonography is helpful to determine which configuration is present. In the case of the U configuration, the scarred ends are dissected individually, while in the donut configuration the scarred anterior portion is divided first to allow the dissection of the distal scarred ends.

Regardless of the anatomy, the dissection is facilitated by the use of a muscle stimulator to identify the functional portion of the EAS. We use a Péna muscle stimulator to stimulate the muscle through the skin at 3 and 9 o’clock. This not only confirms the location of the EAS, but also demonstrates the contractile portion of the EAS. The stimulator is useful throughout the dissection to insure that the dissection is proceeding as planned.

Once the location of the EAS ends are confirmed, the scarred end is grasped with an Allis clamp, which provides traction so that the sphincter can be dissected away for the surrounding tissue. Skin hooks or Allis clamps on the perineal skin provide the countertraction to permit this dissection (Figure 38.3

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