Fecal Incontinence: From Anatomy to Recent Advances

Abstract

The anatomy and physiology of the pelvic floor are complex. A thorough understanding of the anatomy is required to understand how we attain physiological continence. Fecal incontinence can be a life-altering condition that presents as an inability to maintain voluntary control of the passage of gas, liquid, or solid stool through the anus in patients who previously had control. The key to successfully managing a patient with fecal incontinence is to identify the underlying cause. There have been many prescribed procedures for patients requiring surgical correction to attain continence. However, the results are dismal for many patients. Recent advances have challenged these procedures with higher success rates.

1. Introduction

Fecal incontinence is a worldwide problem. The prevalence of fecal incontinence is difficult to estimate because often, this condition is underreported due to social stigma. The overall reported prevalence of fecal incontinence ranges from 2 to 21%, with a median of 7.7%. There is a significant variation depending on age. The reported prevalence of fecal incontinence is 7% in women younger than thirty, which rises to 22% in their seventh decade. In geriatric patients, its prevalence is reported as high as 25 to 35% of nursing home residents and 10 to 25% of hospitalized patients. Fecal incontinence is the second leading cause of nursing home placement in the geriatric population [1, 2, 3]. Studies have shown no difference in prevalence among males and females [1, 2]. However, this condition markedly impairs quality of life [1].

Let us discuss this topic in detail, starting from the factors that maintain continence to understand better how to diagnose and select treatment options for patients presenting with this disorder. We aim to cover the different types of surgical procedures, but describing every detail is out of the scope of this chapter.

2. Anatomy

2.1 Anatomy of the perineum

The pelvic floor is a complex structure made chiefly of muscles and tendons spanning the pelvic outlet. The majority of this musculotendinous structure comprises the levator ani (Figure 1, comprised of three muscles: iliococcygeus, pubococcygeus, and ischiococcygeus) lying in a symmetrically paired fashion to cover the outlet that maintains a constant tone even with changes in pressure (e.g., voiding, defecation, Valsalva maneuver), and contracts at times of acute rise in pressure (e.g., coughing, sneezing) [3, 4].

Figure 1.

The pelvic floor showing the arrangement of muscle fibers in a male patient.

Understanding this anatomy is essential to know how physiological continence is maintained. The pubococcygeus comprises of further two parts in both males and females. In males, this muscle is split into the pubourethralis and the puborectalis, while in females, this muscle splits into the pubovaginalis and the puborectalis. When talking about fecal continence, it is important to note that the puborectalis serves in part the sphincter complex of the rectum and as a pelvic floor muscle. At rest (i.e., when not defecating or actively contracting the perineum), the ‘puborectalis sling’ (Figure 2) pulls the anorectal junction anteriorly toward the pubis. This sling forms an angulation between the rectum and anal canal, called the anorectal angle [3, 4].

Figure 2.

The puborectalis sling that forms the anorectal angle.

2.2 Anatomy of the external anal sphincter and the internal anal sphincter

The External Anal Sphincter (EAS) is a complex of three sphincter muscles crisscrossing each other. These three muscular loops form an efficient closing mechanism. When only one loop is present, there is continence of solid stools, but not liquid stools or gas. In males, this sphincter complex is preserved in a trilaminar pattern, while in females, the transverse perineii muscle fuses with the EAS in the lower part of the perineum forming a single complex structure [3].

The trilaminar EAS comprises the following structures from in to outwards [5, 6]:

• Deep EAS, which lacks a posterior attachment and is related to the puborectalis.

• Superficial EAS, which is attached to the anococcygeal ligament posteriorly.

• Subcutaneous EAS, which is a circular structure encircling the anal canal, attached to the anococcygeal ligament posteriorly and the perineal body anteriorly.

When performing a digital rectal examination, one can feel the puborectalis sling in the posterior wall of the rectum. The sling forms the junction between the levator ani muscle and the EAS [3].

The Internal Anal Sphincter (IAS) is a fairly simple structure compared to the EAS. The IAS is a continuation of the circular smooth muscle of the rectum, ending 6–8 mm above the junction of the superficial and subcutaneous parts of the EAS with a well-defined and rounded edge [3, 4, 5].

2.3 Blood and nerve supply to the perineum

Understanding how various factors lead to incontinence also requires understanding the vascular and neural supply to the sphincter complex. The pelvic splanchnic nerves accomplish evacuation of the bowel, while the pudendal and the pelvic splanchnic nerves serve to maintain continence [3, 4, 5, 6].

The IAS receives its motor innervation from the parasympathetic fibers of the pelvic splanchnic nerves, which inhibit contraction. In contrast, the sympathetic fibers supplying the IAS induce contraction to maintain continence [3, 4, 5, 6].

The EAS has supply from both the inferior rectal branch of the internal pudendal nerve and the perineal branch of the fourth sacral nerve, with the levator ani supplied by branches of the S4 (S3-S5) nerve root [3, 4, 5, 6].

3. Physiology

3.1 Definition and physiology of continence

Continence derives from the Latin word continere or tenere, which means the ability to retain a bodily discharge voluntarily. The loss of this voluntary ability leads to incontinence. Continence depends on various factors, including anatomical barriers like the pelvis, curvatures of the rectum, and transverse rectal folds, or physiological barriers like the rectal compliance and the rectoanal sensation.

The structural and functional integrity of the pelvic floor, rectum, sigmoid colon, and anus, along with the IAS and EAS, maintain continence in humans. A study has shown that the contributing factors to continence include, in descending order, nerve-induced activity in the IAS (45%), EAS (35%), anal hemorrhoid plexus (15%), and myogenic tone in IAS (10%). The IAS provides the resting tone of the sphincter, i.e., the ‘resting pressure,’ while the EAS provides voluntary control of the sphincter, i.e., the ‘squeeze pressure’ [7]. The hemorrhoidal cushion acts as a mechanical blockade to the exiting stool, contributing to continence [8].

So, when stool reaches the rectum, it gets distended. A reflexive relaxation of the IAS occurs by the process termed Recto Anal Inhibitory Reflex (RAIR) [8]. Sometimes when the person is unable to defecate (i.e., unable to find a ‘safe’ spot to defecate), the rectum relaxes to allow more stool to fit in, i.e., the accommodation reflex. So, RAIR leads to defecation, while accommodation leads to continence. However, this process is also influenced by the content within the rectum (i.e., solid, liquid, or gas), which is identified by the anal mucosa by the sampling reflex. Loose stool often decreases resting and squeeze pressures, leading to loss of physiological continence mechanisms [3, 8].

3.2 Definition and causes of fecal incontinence

A life-altering condition that presents with an inability to maintain voluntary control of the passage of gas, liquid, or solid stool through the anus in patients who previously had control is defined as fecal incontinence [6, 9]. Thus, most patients experience social isolation and decreased quality of life [1, 2].

Mechanisms of incontinence have been broadly classified as follows [2]:

1. Suprasphincteric dysfunction: issues with stool consistency/volume, rectal compliance and motility, defect in rectoanal inhibitory reflex, and altered rectal sensation.

2. Sphincteric dysfunction: disintegration of IAS, age-related changes, trauma (including obstetric events like forceps or vacuum delivery, anal surgery like sphincterotomy, dilatation, hemorrhoidectomy, or fistula surgery), altered EAS integrity.

3. Neurological: pudendal nerve injury, hypogastric nerve (sympathetic) injury, pelvic nerve (parasympathetic) injury, intrinsic nerve (enteric) injury.

4. Congenital: anorectal malformations, spina bifida, isolated sacral agenesis, following surgical treatment for Hirschsprung disease.

5. Central nervous system disorders: cerebrovascular accidents, Parkinson’s disease, multiple sclerosis, spinal cord injury.

6. Secondary causes: dysfunctional autonomic nervous system (e.g., diabetic patients), intestinal disorders, inflammatory bowel disease, pelvic non-intestinal surgery, rectal resection, pelvic radiotherapy, and rectal prolapse.

Case summary: A 17-year-old male had initially undergone surgery for Fournier gangrene with IAS and EAS involvement. A temporary diversion loop colostomy was also made to protect the wound. However, the patient developed anal stenosis late in the course of the disease. It was difficult to admit even a finger in his anus. However, following two settings of V-Y anoplasty, and a series of post-operative anal dilatation, a finger could readily be admitted into his anus. Nevertheless, his anal tone was very weak. What would you do next?

4. Investigations

4.1 History

The following questions need to be addressed when taking a history from a patient with fecal incontinence [3]:

• History of diarrhea/loose stool and fecal urgency.

• Nature of incontinence: Is the patient aware of incontinence episodes, or is it related to stressful situations when they cannot stop even when they try?

• Degree of incontinence:

  • Is the patient incontinent only to solid, liquid, or gas?

  • How frequently does the patient experience these symptoms?

4.2 Physical examination

When examining the patient, check for soiling, erythema of perineal skin, signs indicating previous trauma, and perform a squeeze test on DRE while assessing the symmetry of closure. Also, look for the rectum/anal canal descent by asking the patient to bear down (Valsalva maneuver) and look for the anal wink or anal cutaneous reflex to assess for pudendal injury [2, 3, 6, 9].

4.3 Severity of incontinence

One can use a simple bedside scoring method called the Browning and Parks scale to assess the severity of incontinence [10]. Alternatively, the Cleveland Clinic Florida fecal incontinence (Wexner) scale can also be used [11]. Do note that leakage of solid stool is considered more severe than leakage of liquid stool or gas. Also, none of these scales will consider defecation frequency, i.e., they may underestimate incontinence in patients with lower defecation frequency.

The Browning and Parks scale assigns four categories to incontinence. Normal patients are assigned to Category 1. Those with difficulty in controlling flatus and diarrhea are assigned to Category 2. Patients with no control of diarrhea and those without control of solid stool are assigned to Categories 3 and 4, respectively [10].

4.4 Tests for incontinence

Let us discuss some commonly used tests for fecal incontinence. Basic investigations include stool and blood tests to identify commonly treatable causes. This can be followed up with a sigmoidoscopy or colonoscopy to check for any mass lesions that may lead to incontinence. Endoscopic ultrasound (EUS) can also help demonstrate lesions in the IAS and EAS, including disruptions and atrophy. An alternative to patients who do not tolerate sigmoidoscopy or colonoscopy may be evaluated using MRI defecography scans or endoanal MRI [3, 6, 12].

Among more specific tests, anorectal manometry is the most widely available and the best tool that tests defects in sphincter function, anal reflexes, rectal sensory function, and compliance. It is also used to assess defecatory function by the expulsion of a rectal balloon, saline continence test, and measurement of rectoanal pressures during straining [3, 6].

Rectal sensitivity is tested by a rectal balloon inflated with incremental volumes. The first detectable sensation is the rectal sensory threshold, which occurs with 30–60 mL of air or fluid. A defecation sensation or urgency occurs with 60–160 mL of air or fluid (defecatory desire volume). Pain occurs with more than 270 mL of air or fluid, with the maximum tolerable volume ranging from 160 to 70 mL of air or fluid. This adaptability of the rectum is calculated by changing rectal pressure during the distention of the balloon with air or fluid [3, 6].

Another test to assess for dyssynergia is the balloon expulsion test. A normal subject can expel a 50 mL balloon filled with water within a minute, but this is impaired when there is a lack of neural coordination. Other tests to identify neural injury include pudendal nerve terminal motor latency testing and electromyography (EMG) [3, 6].

5. Treatment

Once incontinence and its severity have been defined, treatment is started. There are multiple goals of treatment. Firstly, identify underlying disorders and treat them, for example, diarrhea, inflammatory bowel disease, and modification of existing medications used by the patient. Some patients benefit from adding fiber to the diet, while others benefit from including loperamide in their treatment regimen. The use of biofeedback training can also improve symptoms in some patients. EMG feedback devices are available to assist patients with this process. Surgery and other treatment modalities are only advised once a significant sphincter defect is identified or medical therapy fails. Let us discuss some of these treatment modalities in detail [3, 6, 8, 13].

5.1 Surgical options

Since the success rate of surgeries is low, multiple options exist for treating incontinence. These include but are not limited to [1, 2, 3, 6, 8, 9, 10, 11, 13, 14]:

• Restoration and improvement of residual sphincter function

  This can involve correcting a defective external anal sphincter, sphincteroplasty, correcting a defective pelvic floor, correction of anorectal deformities, Sacral Nerve Stimulation (SNS), or Posterior Tibial Nerve Stimulation (PTNS).

• Increasing the outlet resistance of the anal sphincter

  This can involve augmentation of the anal sphincter and anal cushions (anal bulking agents), anal encirclement (Thiersch procedure), non-dynamic graciloplasty.

• Dynamic sphincter replacement

  This involves the use of artificial anal sphincters or a dynamic graciloplasty.

• Fecal diversion

  This is done when surgery is contraindicated for sphincter repair, i.e., fecal diversion via colostomy and ileostomy.

5.2 Creating a stoma for incontinence

The indications for forming a stoma for incontinence include [3]:

• An injury to the cloaca;

• An associated rectovaginal fistula;

• In the presence of Crohn’s disease;

• A history of radiotherapy.

The absolute contraindication for surgery is gross pudendal neuropathy in women. Pudendal neuropathy is evaluated by checking for perianal numbness and examination findings of a lack of sphincter contraction in the bend of the ‘U’ of the divided anal sphincter [3].

6. Recent advances in treatment

6.1 Anal bulking

This procedure was started by Shafik in 1993 by injecting polytetrafluoroethylene into the submucosa. This was then developed by Kumar et al. in 1998 to glutaraldehyde cross-linked collagen (GAX). Currently, there are multiple options, like the bioplastic, silicone-based beads, carbon-coated zirconium beads (Durasphere), autologous fat, calcium hydroxylapatite (Coaptite), Zuidex, Permacol, and even stem cells. The principle behind all these bulking agents is to provide the cushion effect (as provided by the anal cushion). So, patients with failed conservative management and a structurally intact but weak anal sphincter complex benefit from these agents [14, 15, 16].

Recent advances in these agents include using Polyacrylonitrile (Hyexpan) cylinders that inflate by absorbing water. The volume of these implants increases by up to 750%, which has shown much promise in providing continence to these patients [9, 14, 15, 16]. Another recent advance uses a magnetic anal sphincter augmentation device (FENIX MAS). This device has been shown to significantly reduce weekly incontinent episodes and weekly incontinent days in a 5-year study [17].

6.2 Sacral nerve modulation

Approved by the FDA in 2011, multiple studies have shown a 50% reduction in incontinent episodes per week over 12 weeks in at least 50% of patients [18, 19]. The efficacy of this device was demonstrated first by Wexner et al., and a long-term follow-up of 3 years has shown an 86% success rate (n = 83) [20].

6.3 Clamping devices

An experimental treatment has been proposed by Han et al. with the use of prototype clamping devices that reform the anorectal angle. This helps improve continence even in the absence of a sphincter complex [21].

7. Conclusion

Fecal incontinence is a lifestyle-altering disease process. Many treatment modalities can be used to achieve continence in incontinent patients. Some of the newer modalities have shown better outcomes compared to surgical treatment. A good selection of the patient with adequate pre-operative workup is essential for a favorable outcome.

Acknowledgments

The authors do not have any acknowledgments to make.

Conflict of interest

The authors declare no conflict of interest.