Your Family Physician

Introduction

Fecal incontinence can be 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 fecal incontinence relating to the adult female patient.

Problem

Anal incontinence is the loss of anal sphincter control leading to the unwanted or untimely release of feces or gas. True anal incontinence must be distinguished from other conditions that lead to stool passing through the anus. Stool seepage that produces soilage of undergarments may result from hemorrhoids, enlarged skin tags, poor hygiene, fistula-in-ano, and rectal mucosal prolapse. Other conditions that result in poor bowel control are inflammatory bowel disease, laxative abuse, parasitic infection, and toxins. Fecal urgency also must be differentiated from fecal incontinence because urgency may be related to medical problems other than anal sphincter disruption.

Frequency

Fecal incontinence is a devastating condition. More than $400 million is spent each year for adult diapers that control urinary and fecal incontinence. It is the second leading cause of admission to long-term care facilities in the United States. Exact data on the prevalence of fecal incontinence are difficult to obtain. This is partly because patients are reluctant to volunteer information about their condition to their health care provider. Johanson and Lafferty found that only 20% of patients mentioned the condition to their physician during a physician visit.

The reported incidence rate in the general population is 1-5%. Nelson and colleagues found a prevalence rate of 2.2% in the general population. In their study, 30% of the individuals were older than 65 years and 63% were women. Johanson and Lafferty observed an overall prevalence rate of 18.4% among individuals seen by primary care physicians. However, in this study, any involuntary loss of stool or soiling was considered to be incontinence, and, therefore, patients with soilage for reasons other than true incontinence may have been included.

Johanson and Lafferty and others have found an increasing prevalence of fecal incontinence associated with advancing age. In individuals younger than 30 years, the prevalence rate was 12.3%, compared to 19.4% in those older than 70 years. The long-term cost of fecal incontinence per patient, secondary to obstetric injury alone, is estimated to be $17,166.

Nygaard and colleagues evaluated the prevalence of anal incontinence 30 years postpartum in 3 groups of women. One group had disruption of the anal sphincter with vaginal delivery, the second group had an episiotomy without disruption of the anal sphincter, and the third group delivered by cesarean. They found no significant difference in the frequency of flatus incontinence among the 3 groups, at a rate of 30-40%. Approximately 58% of the sphincter disruption group had bothersome flatus incontinence, compared to 30% and 15% of the episiotomy and cesarean groups, respectively. The percentage of bothersome fecal incontinence was similar among the 3 groups, at around 20%. Other authors have suggested that anal incontinence affects approximately 10% of adult females.

Etiology

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. Damage to the anal sphincter from vaginal delivery, surgical procedures, inflammatory conditions, and neoplastic processes can contribute to the development of fecal incontinence. Several inflammatory bowel conditions lead to decreased compliance of the rectum and may manifest as fecal urgency, frequency, soilage, or 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.

Childbirth is widely accepted as the most common predisposing factor to fecal incontinence in women. This has led to an incidence of fecal incontinence in women that is 8 times greater compared to men. Childbirth may result in internal or external anal sphincter disruption or more subtle damage to the pudendal nerve through overstretching and/or prolonged compression and ischemia. Abramowitz and colleagues found a de novo sphincter defect rate of 16.7% after vaginal delivery. They also found that 13% of primiparous and 20.6% of multiparous women had new-onset anal incontinence after delivery. Sultan et al demonstrated that 35% of primiparous women and 44% of multiparous women demonstrated 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.

In another study, Sultan et al found that approximately half the women who sustain a third-degree obstetric anal sphincter tear experience some impairment of anal continence despite a primary repair. They relate the cause as a persistent mechanical sphincter disruption rather than pudendal nerve damage. In fact, 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. In a study evaluating urinary and anal incontinence in women with obstetric anal sphincter rupture, Tetzschner et al found that women who had sustained an anal sphincter rupture had a 17% chance of anal incontinence at 3 months, which then increased to 42% at 2-4 years postpartum.

Successive vaginal deliveries increase the risk of developing fecal incontinence if a patient has had damage to the sphincter in a prior delivery or was symptomatic with anal incontinence after a prior delivery. 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. Nelson et al found that age, female sex, poor general health, and physical limitations are predisposing factors to fecal incontinence.

Additional factors that appear to increase risk are primiparity, occiput posterior presentation, use of forceps, fetal weight greater than 4000 g, perineal tears, episiotomy, and prolonged second stage of labor. 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.

Allen et al found that 80% of patients had electromyelogram (EMG) evidence of nerve damage after their first vaginal delivery. Several authors demonstrated lower resting pressures on manometric evaluation and delayed PNTML after a single vaginal delivery. Both Cornes et al and Ryhammer et al demonstrated that anal sensation and sampling are negatively impacted after childbirth.

Age also plays a significant role in the development of fecal incontinence. Haadem et al evaluated 49 continent, healthy women with a mean age of 51 years (range, 20-79 y). Findings from anal manometry studies showed a decrease in maximum anal resting pressure and maximum squeeze pressure that was associated with age. These parameters declined more rapidly after menopause. This same study found that with aging, anal closing pressure (the difference between maximum resting pressure and rectal pressure) is reduced, which is an important determinant of anal continence. Similar findings of decreased anal pressures on manometry results were reported by Bannister et al, who also found that aging resulted in lower rectal volumes needed to inhibit anal sphincter tone.

When evaluating the effects of aging on anorectal sphincters, Laurberg and Swash found no significant changes in resting anal pressure. However, in women older than 50 years, they found that anal canal squeeze pressure was significantly lower compared to that found in younger women. Johanson and Lafferty found that the prevalence rate of fecal incontinence in individuals younger than 30 years was 12.3%, compared to 19.4% in those older than 70 years. Approximately 56% of psychogeriatric patients and 32% of geriatric patients in long-term care facilities are anally incontinent on a regular basis. Increasing age is also associated with slowed pudendal nerve conduction, perineal descent at rest, and decreased anorectal sensory function.

The external anal sphincter has been shown to have a higher concentration of estrogen receptors when compared to rectus muscle in the same patient and when compared to estrogen receptor concentration of external anal sphincter in men. This may play a role in this complex disorder.

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 totally normal anorectal function.

Pathophysiology

Anal continence requires the complex integration of signals among the anal sphincters, puborectalis muscle, and the smooth muscle of the colon and rectum. Anal continence also requires the ability to adequately determine anorectal contents and the ability to access the necessary facilities to evacuate the rectum. Damage at any level in this system may lead to anal incontinence.

As colonic contents are presented to the rectum, the rectum distends. This results in a parasympathetically mediated relaxation of the internal anal sphincter and a contraction of the external anal sphincter. Rectal contents are allowed to come into contact with the very sensitive epithelial lining of the upper anal canal. The contents are then sampled as to their nature, ie, gas, liquid, or solid. Gowers originally described this as the rectal anal inhibitory response (RAIR). The epithelial lining of the upper anal canal has a rich supply of sensory nerve endings, especially in the region of the anal valves. This sampling is described as an equalization of the rectal and upper anal canal pressures.

Miller et al found that sampling occurred spontaneously in 16 of 18 control patients but in only 6 of 18 incontinent patients. It is likely that decreased anorectal sensation and abnormal sampling contribute in the pathogenesis of anal incontinence. Several disease processes can alter sensation of the anoderm and sampling.

If evacuation of the rectum is not appropriate, sympathetically mediated inhibition of the smooth muscle of the rectum and voluntary contraction of external anal sphincter and puborectalis musculature occur. The bolus of material is then pushed back up the rectum into the rectal reservoir. A decrease in the compliance of this rectal reservoir has been associated with fecal urgency and anal incontinence. The exact mechanism of this is unclear, and debate continues as to whether it is a cause or result of anal incontinence.

Contraction of the puborectalis increases the anorectal angle and keeps the bolus of material above the internal anal sphincter until the internal sphincter is able to recover. The anorectal angle is created as the rectum perforates the levator complex. The most medial fibers of the pubococcygeus muscle are referred to as the puborectalis muscle. These fibers create a sling around the rectum. They are fused to the sacrum posteriorly via the levator plate. This creates an anterior displacement of the anal canal as it perforates the pelvic diaphragm. The angle created by a midluminal line in the anal canal above the levators and one below the levators is referred to as the anorectal angle. The anorectal angle varies considerably but averages from 80-105°.

As this complex of muscles contracts and the rectum is pulled forward, the anorectal angle becomes more acute and prevents the bolus of stool from descending further. The contents of the rectum are forced back into the compliant rectal reservoir above the levators, which allows the internal anal sphincter to contract again. The internal anal sphincter is responsible for 50-80% of the resting tone in the rectum. The external sphincter contributes 25-30% of the resting tone, and the anal cushions contribute 15% of the resting tone. Also, the activity to the puborectalis and external anal sphincter, which are capable of generating much stronger contraction but fatigue after 30-60 seconds, is increased.

Any process that interferes with this mechanism, such as trauma from vaginal delivery or insult to the neuromuscular integrity from a variety of causes, can result in a failure of the mechanism to function and lead to anal incontinence.

Presentation

Patients who present for evaluation of fecal incontinence usually have had to overcome extreme embarrassment over their condition prior to their office visit. Care should be given to the manner in which the topic is approached in order to promote an open and comfortable discussion.

Obtain a thorough history, including duration of anal incontinence, type of incontinence experienced, frequency of incontinent episodes, type of stool lost, impact of the disorder on the patient's life, history of associated trauma or surgery, and associated factors such as protective garment use. Review medications and dietary habits to determine if an easily remedied cause exists. A review of systems for systemic medical conditions that contribute to fecal incontinence is important.

Information about the number of vaginal deliveries and the presence of any factors pertaining to those deliveries that may have contributed to the incontinence helps in determining the cause of the incontinence. As previously mentioned, prolonged second stage of labor, forceps delivery, significant tears, and episiotomy, among other causes, are associated with increased risk for anal sphincter disruption and pudendal nerve injury.

Several fecal incontinence surveys attempt to quantify and qualify the severity of fecal incontinence. Two examples are the Fecal Incontinence Quality of Life Scale produced by Rockwood et al and the Fecal Incontinence Questionnaire by Reilly et al. The forms are largely designed as outcome measures and are most useful in a research setting. The benefit to the practitioner not in a research environment is that a great deal of information about patient symptoms and the impact of those symptoms can be obtained in a short period of time.

Patient evaluation begins with a careful history as previously described. Practitioners who routinely perform physical examinations on female patients should be familiar with normal perineal, vaginal, and anal sphincter anatomy. The examination should consist of a visual inspection of the perineal body and anus and a careful inspection of the vaginal epithelium. This is performed to look for skin tags, hemorrhoids, anal fissures, fistulae, and scars that may indicate prior trauma.

Digital rectal examination with the index finger in the rectum and thumb of the same hand or the index finger of the opposite hand in the vagina is mandatory to palpate the anal sphincters, determine perineal body thickness, evaluate anal sphincter and levator tone, and test for perineal body hypermobility. This examination is likely the single most useful and informative part of patient evaluation. Rectal examination is recommended as a routine part of a woman's annual well-woman examination, but it is often deferred. It is mandatory in the evaluation of fecal incontinence and associated pelvic organ prolapse.

As the provider is beginning the rectal examination, resistance is met at the anal verge. A great deal of experience is required on the part of the provider in order to determine the degree of normal resistance. If the examining finger meets little resistance and the anus feels patulous, further questioning about symptoms of anal incontinence can be asked.

While performing the rectal examination, the patient is asked to tighten the sphincter around the examining finger. A circumferential increase in the pressure should be felt. Patients who have a disrupted anal sphincter may have adequate innervation to the existing muscle bellies, and pressure may be felt on the examining finger. Evaluating the nature and location of increases in muscle tone is important. Pressure may be placed on the finger laterally from existing functional muscle, but no or very little pressure may be felt anteriorly. Disruption of the muscle sphincter allows the muscle bellies to retract laterally and posteriorly, similar to the ends of a rubber band that is cut after being placed on gentle stretch. Scar tissue may develop anteriorly between the 2 ends of muscle and, with contraction of the lateral muscle bellies, gives the impression of an intact anal sphincter. Palpation of the muscle can assist in this situation.

The external anal sphincter is palpable as a 1.5-2 cm moderately firm doughnut-shaped mass within the perineal body. If, upon palpation of the perineal body, the examining fingers are not separated by much tissue or the muscle mass is not palpated, damage to the anal sphincter is likely. Palpation from a midline position laterally helps to define where normal muscle exists. Importantly, these findings can be subtle and may require come degree of experience to elicit.

During rectal examination, the tip of the examining finger is gently flexed and traction is placed on the perineal body. The perineal body is normally supported by the perineal membrane (urogenital diaphragm), which originates from the ischiopubic rami bilaterally. The perineal membrane, along with other fascial supports, inhibits the caudad displacement of the perineal body. Birth trauma sufficient enough to result in detachment or tearing of this support also may have resulted in damage to the anal sphincters, and this history finding may prompt further questioning and evaluation.

Indications

Indications for surgical repair for fecal incontinence are largely based on physical findings and the degree to which the patient is symptomatic. Surgical repair of the anal sphincter is not without potential complications and discomfort. Importantly, the physician should counsel the patient about the risks of the procedure and the potential for recurrence.

Examination may reveal a sphincter defect that is discovered in association with other defects in pelvic support. The patient may be asymptomatic or only mildly symptomatic for anal incontinence. Whether surgical repair should be performed in this situation is controversial and must be a decision reached between the patient and the physician. The evidence presented suggesting that age alone is a risk factor for the development of anal incontinence must be factored into the equation if a known anatomic defect is present. Clearly, this type of patient is at increased risk of anal incontinence in the future. Additionally, surgical outcomes of sphincter repair have been shown to be poorer in older women.

Relevant Anatomy

A clear understanding of anatomy is mandatory for any surgical procedure, including surgical procedures of the perineum and anal sphincter. The perineal body is composed of a fusion of several structures. The Denonvilliers fascia is fused, which serves to suspend the perineal body from the sacrum via the endopelvic fascia. The bulbospongiosus and superficial transverse perineum muscles insert onto the perineal body. The bulbospongiosus originates from the pubic rami and inserts into the anterior aspect of the central tendon of the perineum. The superficial transverse perineum muscle originates on the ischial tuberosities and approaches the perineal body from a lateral position. The perineum is innervated by the labial nerve and inferior rectal nerve, which are branches of the pudendal nerve. The external anal sphincter is fused to the perineal body more posteriorly.

The anatomy of the external anal sphincter continues to undergo debate. Some suggest that it composed of 3 parts that are fused, while others maintain that it is composed of 2 more distinct parts. A subcutaneous portion just deeper than the perineal skin, a superficial portion, and a deep portion exist. Some combine the subcutaneous and superficial components into a single component. The separation of these components is indistinct in a surgical repair. The deep portion of the external anal sphincter is fused to the puborectalis muscle of the levator complex, and some even suggest that it is a continuation of it. It receives innervation from the pudendal nerve.

The internal anal sphincter is a continuation of the inner circular smooth muscle of the bowel wall. This musculature thickens over the last 2.5-4 cm of the rectum. The internal anal sphincter lies deep to the external anal sphincter, and an identifiable and surgically important plane exists between them. The internal anal sphincter begins at the level of the levator complex, and its distal extent is just proximal to the subcutaneous portion of the external sphincter. The internal anal sphincter is supplied by the autonomic nervous system. It exists in a state of continuous maximal contraction and provides a barrier to the involuntary loss of stool.

The levator complex is composed of the pubococcygeus, the iliococcygeus, and the coccygeus muscles. The most medial fibers of the pubococcygeus make up the puborectalis. These fibers loop around the posterior aspect of the rectum and create an anterior displacement of the rectum known as the anorectal angle. The pelvic surface of the levator complex is innervated by sacral efferents from S2 through S4. The inferior surface is supplied by the perineal and inferior rectal branches of the pudendal nerve.

Contraindications

Contraindications to surgery for anal incontinence occur when the etiology for incontinence is uncertain; when a nonsurgical therapy, such as medication or diet alteration, would provide relief of symptoms; a woman is pregnant; or when surgical repair would place the patient at risk for complications from other medical conditions.

Source : http://emedicine.medscape.com/article/268674-overview