Fecal incontinence is one of the most psychologically and socially debilitating conditions in an otherwise healthy individual. It can lead to social isolation, loss of self-esteem and self-confidence, and depression. This article is devoted to the problem of fecal incontinence in the adult female patient. 
In 2015, summaries of the epidemiology, pathophysiology, classification, and treatment of fecal incontinence were published from the 2013 National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Workshop
Fecal incontinence has many etiologies. One or a combination of several factors can lead to the inability to control passage of stool or flatus. Congenital abnormalities such as spina bifida and myelomeningocele with resultant spinal cord damage can result in fecal incontinence. Inflammatory bowel disease may lead to decreased compliance of the rectum and may manifest as fecal urgency, frequency, soilage, or incontinence. Anal surgery, such as hemorrhoidectomy and sphincterotomy, has been associated with internal sphincter injury and subsequent urgency and incontinence. 
Medical conditions that may result in fecal incontinence include diabetes mellitus, stroke, spinal cord trauma, and degenerative disorders of the nervous system. These conditions may alter normal sensation, feedback, or function of the complex mechanism of anal continence. The patient’s ambulatory status is also important when considering the etiology of the disorder. Wheelchair-bound patients and those who are dependent on others for access to bathroom facilities may have episodes of functional incontinence, yet have completely normal anorectal function.
Vaginal delivery is widely accepted as the most common predisposing factor to fecal incontinence in an otherwise young and healthy woman.  Vaginal delivery may result in internal or external anal sphincter disruption, or may cause more subtle damage to the pudendal nerve through overstretching and/or prolonged compression and ischemia.
Many studies support the theory that mechanical sphincter disruption contributes to fecal incontinence.  Abramowitz and colleagues found a de novo sphincter defect rate of 16.7% after vaginal delivery (14% with external, 1.7% internal, and 1% both). The overall anal incontinence rate was 9%, and 45% of these women had identifiable sphincter defects on anal endosonography. 
In addition, inadequate repairs of obstetric sphincter injuries may contribute to delayed symptoms of fecal incontinence. In a study of 34 women who sustained third-degree obstetric anal sphincter tears and 88 matched controls, Sultan et al found that approximately half the women (47%) who sustained a third-degree tear experienced some impairment of anal continence despite a primary repair. Anal pressures were significantly lower, but pudendal nerve terminal motor latency measurements were not different. They relate the cause as a persistent mechanical sphincter disruption rather than pudendal nerve damage. 
Similarly, Nielsen et al found that 13 of 24 (54%) patients who underwent primary repair for sphincter disruption at the time of delivery demonstrated external sphincter defects at 3- and 12-month follow-up. Tetzschner et al found that 18 of 94 (19%) of women who sustained obstetric anal sphincter rupture had fecal incontinence shortly after delivery.  A follow-up study by the same group demonstrated that 30 of 72 (42%) women who had sustained an obstetric anal sphincter rupture had fecal incontinence at 2-4 years postpartum.  Factors that are significantly associated with an increased risk of third-degree obstetric sphincter tears are primiparity, occiput posterior presentation, use of forceps, fetal weight greater than 4000 g, perineal tears, episiotomy, and prolonged second stage of labor.
Pudendal nerve injury may also be a mechanism in fecal incontinence. The pudendal nerve innervates the external anal sphincter muscle, anal canal skin, and coordinates reflex pathways. Evidence of neurologic damage from the forces of labor is illustrated in a study by Fynes et al, who evaluated anorectal physiology in women undergoing cesarean delivery at different stages of labor. They found that anorectal function was unaltered in women undergoing cesarean delivery early in labor. In women with advanced cervical dilation (>8 cm) at the time of cesarean delivery, they found delayed pudendal nerve terminal motor latency (PNTML) and reduced anal squeeze pressures. 
In the Tetzschner study of women who sustained obstetric anal sphincter rupture during vaginal delivery, postpartum fecal incontinence was also associated with delayed PNTML of greater than 2.0 milliseconds.  This type of neurologic injury was confirmed in a recent large study. In 923 patients with fecal incontinence (745 women), 56% demonstrated pudendal neuropathy (38% were unilateral). Neuropathy was associated with decreased anal resting tone and squeeze pressures.  Similarly, Allen et al found that 80% of patients had electromyelogram (EMG) evidence of nerve damage after their first vaginal delivery, particularly if they had a long second stage of labor or delivered larger infants
Successive vaginal deliveries increase the risk of developing fecal incontinence. Sultan et al demonstrated that 35% of primiparous women and 44% of multiparous women had sphincter disruption after delivery but were asymptomatic. In this same study, 13% of primiparous patients and 23% of multiparous patients undergoing vaginal delivery complained of fecal incontinence or fecal urgency at 6 weeks postpartum. Symptoms are worse if a patient has had damage to the sphincter in a prior delivery or was symptomatic with anal incontinence previously. Ryhammer et al found a significant long-term association between the number of vaginal deliveries and several anorectal parameters in perimenopausal women. They noted lower perineal position at rest, increased perineal descent with maximal straining, decreased anal sensibility to electrical stimulus, and prolonged latency in pudendal nerves to be associated with increasing parity. 
In recent years, national attention has been focused on the risks and benefits of cesarean delivery prior to labor and its impact on pelvic floor health. However, the literature is divided as to whether cesarean delivery is protective against fecal incontinence.
In a population-based Oregon study from 2009 of 5,491 primiparous women, nearly half (45.2%) experienced a new onset of at least 1 symptom of fecal incontinence in the survey period of 3-6 months after delivery. Among these women with fecal incontinence, 46% reported incontinence of flatus only, 22.8% were incontinent of liquid stool and 18% were incontinent of solid stool. Vaginal delivery was associated with a greater risk of fecal incontinence compared with cesarean section (OR=1.45). However, vaginal delivery without laceration of instrument assistance did not increase the risk of fecal incontinence over cesarean. Interestingly, cesarean was not completely protective against fecal incontinence given that 38% of women who delivered by cesarean without labor or pushing reported new onset symptoms of fecal incontinence
Fecal Incontinence Workup
Surgical repair for fecal incontinence is usually an elective procedure. Evaluation and treatment of anemia, infection, or other abnormalities indicated by findings from a complete blood cell count should be initiated prior to surgical repair.
A pregnancy test should be performed at or near the time of surgery on every female patient who may be pregnant.
The standard diagnostic imaging study for the anal sphincters is transanal or endoanal ultrasonography. Much of the early work on endoanal ultrasonography was performed at St. Marks Hospital in the United Kingdom by Law, Burnett, and Sultan et al. Multiple reports have qualified ultrasonography as the criterion standard in the diagnostic evaluation of the anal sphincters.
Ultrasonography allows the provider to perform a real-time, 360-degree evaluation of both the internal and external anal sphincters. Sensitivity and specificity of ultrasonography findings are 98-100% for the external anal sphincter and 95.5% for the internal anal sphincter. Burnett et al have shown that 90% of women presenting with anal incontinence and a history of a vaginal delivery had ultrasonographic evidence of damage to the external anal sphincter, internal anal sphincter, or both.
Endoanal ultrasonography is performed in the left lateral or lithotomy position. The lithotomy position in females allows for the evaluation of other pelvic support defects.
Traditionally, 3 regions of the rectum are evaluated ultrasonographically. The areas of focus are distal, where only the external anal sphincter is observed (first image below); at the level where both the internal and external anal sphincters can be observed in the mid anal canal (second image below); and proximal at the level of the levators (pubococcygeus) (third image below).
Treatment & Management
Conservative treatment options for fecal incontinence include bulking agents and biofeedback. After history and physical examination findings have helped exclude systemic disease and local anal pathology as the source of the patient’s problem, the provider can initiate treatment.
The goal of medical therapy is to reduce stool frequency and improve stool consistency. A regular bowel regimen including daily laxatives should be established. If impacted, manual disimpaction and a daily tap-water enema may help prevent reaccumulation. The etiology of diarrhea should be diagnosed and treatment initiated. Mild incontinence can often be improved by initiating simple conservative measures. For patients with infrequent, low volume stools, bulking agents are helpful, as formed stools are easier to control than liquid stools. Methylcellulose (Citrucel) or psyllium (Metamucil, Fiberall, Hydrocil) can be taken daily. Additional firming of the stool can be obtained by restricting fluid with intake of the bulking agent. This may be helpful therapy in the patient who has incontinence of soft stool or liquid stool.
In patients with diarrhea due to noninfectious etiologies or with reduced rectal compliance due to radiation proctitis or inflammatory bowel disease, agents that slow the motility of the gut may be helpful. Loperamide hydrochloride increases gut transit time, allowing for increased absorption of water from the volume of stool. This results in a firmer, more easily controlled stool. The maximum daily dosage is 16 mg. The usual dose regimen is 2-4 mg twice or three times daily to control symptoms. An additional benefit of the opiate derivative loperamide (Imodium) is that it increases internal anal sphincter tone and may improve rectal compliance. Diphenoxylate hydrochloride/atropine (Lomotil) has also been used; however, diphenoxylate hydrochloride can cause dependence and is a schedule V medication under the Controlled Substance Act.
Biofeedback is a safe, minimally invasive behavioral technique that uses auditory or visual feedback to reeducate the pelvic floor musculature. Although many different therapies have been used, several studies that have demonstrated a significant improvement in fecal incontinence by treatment with biofeedback. [52, 53] Other data, including a recent Cochrane review, does not provide clear evidence of therapeutic benefit.  The most commonly used techniques are rectal sensitivity training and anal sphincter strength training.
During rectal sensitivity training, a rectal balloon is gradually distended with air or water and the patient is asked to report first sensation of rectal filling. Once this threshold volume is determined, repeated reinflations of the balloon are performed with the objective being to teach the patient to feel the distension at progressively lower volumes. The rationale is that some patients are found to have high threshold volumes and if the patient detects stool arriving sooner, there is more possibility to either find a toilet or use an anal squeeze, or both. Conversely, the same technique has also be used to teach the patient to tolerate progressively larger volumes in those with urgency and a hypersensitive rectum. 
Biofeedback techniques have also been used to demonstrate anal sphincter pressures or activity to the patient, thereby enabling teaching of anal sphincter exercises and giving feedback on performance and progress. This can be achieved by using EMG skin electrodes, manometric pressures, intra-anal EMG, or anal ultrasonography. The patient is encouraged, by seeing or hearing the signal, to enhance squeeze strength and endurance. There is no consensus on an optimum exercise regimen for use at home between sessions, nor on the number of squeezes, frequency of exercises, or treatment duration. Different authors may describe very different programs. 
Biofeedback requires some rectal sensation and the ability to voluntarily contract the sphincter. It appears to be effective for neurogenic and idiopathic anal incontinence and for incontinence related to disruption of anal sphincters  , but a recent Cochrane review did not demonstrate conclusive therapeutic benefits. Biofeedback’s success seems to depend on improving rectal sensation, because manometric studies have not shown consistent improved sphincter pressure. Personal units are now available (without prescription) for home use after initial clinical instruction. They use a vaginally placed, air-filled sensor that provides information on force and duration of contractions. Results from biofeedback can diminish over time, but home devices provide the patient the opportunity for a prolonged course of therapy and intermittent reeducation in a private setting.
In a 2012 randomized, double-blind study, 3 months of treatment with transcutaneous electrical tibial nerve stimulation (TENS) was not significantly better than sham treatment in improving the number of incontinence and urgency episodes in 144 patients with fecal incontinence.
Once medical therapy has been maximized, minimally invasive and surgical therapies may be considered. In select patients, injectable materials may provide improvement in anal sphincter function.
Several reports have described injection of various materials to augment the function of the internal anal sphincter. Injectable silicone has been shown to be effective. In a study of 82 patients with severe fecal incontinence and a low anal resting pressure caused by internal anal sphincter dysfunction, patients were randomized to silicone injection into the intersphincteric space and internal anal sphincter with (Group A, n = 42) or without (Group B, n = 40) guidance by endoanal ultrasonography. Results show that fecal incontinence improved significantly in both groups with up to 12 months of follow-up but to a greater extent in the group in whom injection was ultrasonographically guided. No serious complications occurred. 
Results with carbon-coated microbeads have been less promising. In a pilot study of 33 patients, the submucosal injection of carbon-coated microbeads improved minor fecal incontinence by increasing anal pressure but did not significantly improve quality of life.  Experience with collagen injections has been more limited.
Several surgical procedures are performed for the treatment of anal incontinence. The type of procedure used is based on the patient history, physical examination findings, and results of diagnostic evaluation. The current philosophy in pelvic reconstructive surgery is restoration of normal anatomy. Usually, sphincter complex defects are secondary to obstetric injury, fistula repair, or lateral internal sphincterotomy. The standard procedure for anal incontinence due to anal sphincter disruption is the anterior overlapping sphincteroplasty. This procedure was first proposed by Parks et al in 1971 and modified by Slade et al in 1977.
Anterior sphincteroplasty consists of dissecting out the external anal sphincter, dividing the scar tissue in the midline, and then overlapping the scar so that muscle is approximated to muscle as closely as possible. The surgery can be performed with the patient in the prone jackknife position or the dorsal lithotomy position. Controversy exists as to the need to identify and plicate the internal anal sphincter. Its value in the continence mechanism has been discussed. Several postoperative studies have demonstrated improvement in resting and squeeze pressures, which suggest that either the internal sphincter was plicated intentionally or that the internal anal sphincter was also unintentionally plicated in the process of overlapping the scar mass. In an older study, Fang and colleagues suggest not separating the internal from the external anal sphincters; however, they do not discuss the reasoning for this. 
Several other studies have performed ultrasonography of the sphincters postoperatively, yet few specifically mention the condition of the internal sphincter. Briel et al compared 2 groups of patients who underwent surgical repair. One group had surgical repair of only the external sphincter between 1973 and 1989. The second group underwent surgical repair consisting of restoration of the rectovaginal septum, perineal body, and repair of the external and internal sphincters. These patients had surgical repair between 1989 and 1994. They found that the more complex repair conferred no advantage. The measured outcome focused on anal continence, which was restored or improved in 63% and 68%, respectively. 
For the internal anal sphincter repair, the surgical approach requires dissection along the intersphincteric plane and identification of the internal anal sphincter. The sphincter is then dissected free from the rectal mucosa and mobilized. The surgical technique varies depending on the bulk of scar tissue. The scar tissue is either divided or left intact as the sphincter is plicated.
Abou-Zeid performed isolated internal sphincter repair in 8 patients with ultrasonographically proven defects of the internal anal sphincter. All patients had anal incontinence of varying degrees. All had undergone a prior surgical procedure, such as hemorrhoidectomy or sphincterotomy, and had developed symptoms subsequently. All patients underwent preoperative ultrasonography, and 6 patients underwent postoperative endoanal ultrasonography to document internal sphincter anatomy. Continence scores improved in all patients, and 2 patients achieved complete continence.  The small numbers of this cases series are encouraging, but do not allow for definitive conclusions.