Fecal incontinence is a symptom of bowel dysfunction where patients lose the ability to control gas or stool passage. Although its incidence is not high and it does not directly threaten life, it causes physical and mental distress, severely disrupting normal life and work.

bubble_chart Etiology

There are many factors that affect normal bowel function, including stool consistency, rectal capacity, anorectal sensation and reflexes, anal canal tension, and the integrity of the nervous system controlling the puborectalis muscle and external anal sphincter. Any disruption to the balance of these mechanisms can lead to fecal incontinence. Clinically, fecal incontinence can be caused by sphincter injury, colonic diseases, neurological disorders, congenital conditions, and other diseases.

(1) Trauma

The primary cause is sphincter injury, most commonly due to anorectal surgery or obstetric trauma. High anal fistula surgery, in particular, can damage the anorectal region and sphincter muscles, as can third-degree perineal tears during childbirth. Domestic reports indicate that 72.5% (65/95) of adult fecal incontinence cases result from improper surgical or therapeutic methods. Birmingham (1978–1990) reported 334 cases of fecal incontinence, including 57 cases due to surgical trauma (24 from anal fistulas) and 122 cases from obstetric trauma. Additionally, improper surgical management of internal hemorrhoids, anal fissures, rectal prolapse, or rectal tumors, as well as external trauma, drug injections, burns, frostbite disease, etc., can also lead to fecal incontinence.

(2) Anal and intestinal diseases

The most common causes are rectal tumors and inflammatory diseases. Birmingham (1975–1980) reported 341 cases of fecal incontinence, including 104 cases of intestinal cancer, 70 cases of inflammatory bowel disease, and 40 cases of rectal prolapse. Rectal tumor infiltration can destroy the sphincter, while ulcerative colitis and Crohn’s disease cause chronic rectal inflammation and prolonged diarrhea. Complete rectal prolapse can lead to anal laxity and pudendal nerve traction damage, accounting for 127 cases.

Conditions such as central nervous system diseases, spina bifida, spinal meningocele, spinal and sacral nerve injury, infections, spinal tumors, congenital anorectal malformations, and anorectal nerve dysfunction can all result in fecal incontinence.

bubble_chart Clinical Manifestations

Depending on the degree of incontinence, it can be divided into complete incontinence and incomplete incontinence: ① Complete incontinence: The anus cannot control the discharge of solid stool, loose stool, or gas; ② Incomplete incontinence: Only solid stool can be controlled, while loose stool and gas cannot be controlled. According to the severity of incontinence, it can be classified into 3 grades.

Grade I: Occasional fecal soiling of underwear.

Grade II: Inability to control feces, with frequent soiling of underwear due to fistula disease, accompanied by gas incontinence.

Grade III: Complete incontinence.

Patients cannot voluntarily control defecation or passing gas. In cases of complete incontinence, feces naturally leak out, soiling underwear, and during sleep, feces discharge soils bedding. The anal and perineal areas are often moist, with perianal skin erosion, pain, cutaneous pruritus, and eczematous changes. In cases of incomplete incontinence, there is no incontinence with solid stool, but control is lost with loose stool or diarrhea.

bubble_chart Diagnosis

(1) Medical History

It is necessary to inquire about the causes of fecal incontinence, the initial symptoms, the current severity of incontinence, and any history of surgery, radiation, or injury in the anorectal area. Bowel habits, frequency of defecation, and stool consistency should be noted, as well as any history of neurological, metabolic, or urinary system diseases.

In cases of complete incontinence, the anus often appears open and round upon visual inspection, or there may be deformities, defects, or scars. Feces or intestinal fluid may be discharged from the anus, and the perianal skin may show eczematous changes. When the buttocks are manually spread apart, the anal canal is completely relaxed and round. Sometimes, partial defects or scars in the anal canal may allow visualization of the rectal lumen through the round opening.

In cases of incomplete incontinence, the anus does not close tightly, and fecal contamination may occur around the anus during diarrhea.

(3) Digital Rectal Examination

The anus is lax, and the contraction of the sphincter and anorectal ring is either weak or completely absent during anal canal contraction. If caused by injury, scar tissue may be palpable in the anal area. In cases of incomplete incontinence, the digital examination may reveal weakened sphincter contraction.

(4) Endoscopy

Proctoscopy can reveal any deformities in the anal canal, the condition of the anal skin and mucous membrane, and the degree of anal closure. Fiberoptic colonoscopy can detect conditions such as colitis, Crohn's disease, polyps, or cancer. Rigid sigmoidoscopy can be used to observe the presence of complete rectal prolapse.

(5) Defecography

This X-ray barium examination can assess the morphological and functional dynamics of the anal sphincter, anal canal, and rectum, determining the presence and severity of incontinence. The involuntary leakage of a large amount of barium is a sign of incontinence.

(6) Anal Manometry

This test can detect abnormalities in the internal and external sphincters and the puborectalis muscle. It evaluates the anorectal inhibitory reflex, baseline pressure, contraction pressure, and rectal capacity for distension. Incontinence patients typically exhibit reduced baseline and contraction pressures in the anal canal, loss of internal sphincter reflex relaxation, and decreased rectal distension tolerance.

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This can determine the functional range of the sphincter, distinguishing between voluntary and involuntary muscles, and assessing the extent of nerve injury and recovery.

(8) Anal Ultrasound (AUS) Examination

In recent years, anal ultrasound has been used to clearly visualize the submucosal layer of the anorectum, the internal and external sphincters, and surrounding tissues, aiding in the diagnosis of fecal incontinence and detecting sphincter damage. Yang (1993) used AUS to examine 38 cases of fecal incontinence, finding sphincter defects in 17 out of 23 cases (74%). All these patients had a history of perianal, anorectal, or vaginal surgery. Among 15 cases, 6 (40%) had no history of trauma, and routine physical examinations failed to detect sphincter defects, which were only confirmed after AUS. Thus, this examination is particularly valuable for diagnosing fecal incontinence.

bubble_chart Treatment Measures

The treatment of fecal incontinence should be based on the underlying cause and the extent of injury, employing different therapeutic approaches. If fecal incontinence is secondary to another condition, the primary disease must be treated, such as central nervous system disorders, metabolic diseases, or anorectal diseases. Treating the primary condition may cure or improve fecal incontinence in some cases.

(1) Non-surgical Therapy

1. Promoting Bowel Movements: Treat colonic and rectal inflammation to ensure normal stool consistency, avoiding diarrhea and constipation. Refrain from consuming irritating foods and opt for high-fiber diets.

2. Anal Sphincter Exercises: Improve the voluntary contraction ability of the external sphincter, puborectalis muscle, and levator ani muscle to enhance anal function.

3. Electrical Stimulation: Commonly used for neurogenic fecal incontinence.

Caldwell (1963) placed stimulating electrodes within the external sphincter. Hopkinson (1966) and Macleod (1979) used plugs and electromyography to stimulate the sphincter and pelvic floor muscles, inducing regular contractions and sensory feedback, both of which can improve anal function.

(2) Surgical Therapy

Surgical treatment is necessary for cases involving local defects due to surgical injury, obstetric trauma, or external force injury to the sphincter, congenital diseases, or post-resection of the anal sphincter after rectal cancer surgery. Procedures include sphincter repair, rectovaginal sphincter repair, sphincter plication, skin graft tube formation, and sphincteroplasty.

1. Anal Sphincter Repair Objective: Separate and suture the scar tissue at both ends of the severed sphincter. This is often used for recent injuries where at least half of the sphincter retains function. If the wound is infected, repair should be performed within 6–12 months to prevent muscle atrophy. Delayed treatment may lead to sphincter atrophy and fibrosis, complicating surgical identification and suturing, thereby affecting outcomes. Method: Make a semicircular incision 1–2 cm outside the scar, incise the skin and subcutaneous tissue, and appropriately separate the severed ends of the sphincter from the scar tissue. Remove the scar tissue but leave a small amount of fibrous tissue at the sphincter ends for suturing. Separate the internal sphincter from the external sphincter along the intersphincteric space and further dissect the levator ani muscle upward, taking care not to injure the mucous membrane. Use two tissue forceps to grasp the severed ends of the internal and external sphincters, cross-testing their mobility and tension. After confirming suitability, insert a 1.5–2 cm diameter anoscope into the anus and retest sphincter tension. Suture the internal and external sphincters end-to-end or overlap them with silk sutures. Remove the anoscope after suturing, then close the subcutaneous tissue and skin. Postoperatively, bowel movements should be controlled for 3–4 days, followed by sitz baths and wound care to maintain cleanliness. Marti (1990) analyzed 401 cases of sphincter repair from seven authors in the literature, reporting a success rate of 90%.

2. Sphincter Plication Indicated for cases of sphincter laxity.

(1) Anterior Anal Sphincter Plication: Make a semicircular incision 1–2 cm anterior to the anus along the anal margin. Reflect the skin and subcutaneous tissue backward to cover the anus. Lift the skin flap to expose a triangular space between the bilateral external sphincters and the internal sphincter. Suture the bilateral external sphincters with silk sutures to close the gap, tightening the anal canal, and finally suture the skin.

(2) Intravaginal Sphincter Plication: Since the incision is farther from the anus, the risk of infection is lower. Make a circular incision on the posterior vaginal wall, dissect upward to expose the anterior portion of the external sphincter, lift the sphincter, and plicate it with silk sutures to tighten it. Insert a finger into the anal canal to test tension. Suture the levator ani muscle at the upper end of the wound and finally close the posterior vaginal wall.

(3) Parks' postanal pelvic floor repair: Suitable for patients with persistent incontinence or spontaneous incontinence after rectal prolapse fixation. A curved incision is made posterior to the anal verge, followed by subcutaneous dissection to separate the internal and external sphincters of the anorectum. The internal sphincter and anal canal are pulled forward, and dissection is continued upward above the puborectalis muscle to fully expose the bilateral iliococcygeus and pubococcygeus muscles. The bilateral muscles are sutured intermittently, with particular emphasis on securely suturing the puborectalis muscle to shorten it, thereby advancing the anorectal angle and restoring its normal position. The external sphincter is also sutured and shortened, followed by wound closure and drainage placement. Since this procedure inherently causes outlet narrowing, excessive straining during defecation may rupture the repair site. Therefore, postoperative bowel movements should avoid straining, and laxatives may be used if necessary. Parks et al. (1971) reported 183 cases, with complete restoration of anal continence achieved in 72%, improvement in 12%, and no improvement in 16%.

3. Skin Graft Anal Canaloplasty Applicable for anal canal skin defects and mucosal ectropion causing fecal incontinence. A pedicle skin graft is transplanted into the anal canal, such as the S-shaped skin graft anal canaloplasty.

Surgical Method: Assume the lithotomy position. Make a circular incision along the edge of the everted mucosa, separate it from the surrounding tissue, and excise the excess mucosa. Make an S-shaped incision centered on the anal canal to create two skin flaps, upper and lower. The upper flap is shifted to the right side of the anal canal, and the lower flap to the left. The inner edges of the flaps are sutured to the mucosa, and the mucosal edges can be fully sutured to the flaps.

4. Sphincteroplasty Currently, the gracilis or gluteus maximus muscle is often transplanted around the anal canal to replace or reinforce sphincter function. This is suitable for cases of complete sphincter destruction, congenital absence of the sphincter, or those unsuitable for sphincter repair.

⑴ Gracilis Muscle Transplantation Sphincteroplasty: First, assume the supine position. Make a 5–8 cm longitudinal incision along the gracilis muscle on the inner thigh, incise the fascia to expose the gracilis muscle, and dissect upward to the neurovascular bundle. Make a 3–4 cm longitudinal incision on the inner knee to locate the gracilis muscle and dissect upward to connect with the upper incision. Make a 3–4 cm oblique incision at the tibial tuberosity to locate the insertion point of the gracilis muscle, and cut it at the periosteum of the tendon insertion. Then, pull the gracilis muscle out through the upper thigh incision, wrap it in saline gauze, and set aside for later use.

Switch to the lithotomy position. Make incisions at the anterior and posterior midline of the anus, 2 cm from the anal margin. Use long forceps to create two subcutaneous tunnels around both sides of the anus, connecting the anterior and posterior incisions. Then, make a 2–3 cm incision on the opposite side near the pubic tubercle and create a subcutaneous tunnel connecting it to the anterior anal incision. Pull the gracilis muscle out through the upper thigh incision, dissect it upward, and pass the muscle bundle through the tunnel to the anterior anal incision. Wrap it around one side of the anus to the posterior, then around the opposite side to the anterior, and pull it out through the pubic tubercle incision. The gracilis muscle is thus wrapped around the anus, tightened to maximally constrict the anus, and the tendon is fixed to the periosteum of the pubic tubercle. Finally, suture all incisions.

Generally, standing with legs adducted can control defecation, while squatting relaxes the anus. However, individual variations are significant, and it may take time to master bowel control. Tianjin Binjiang Hospital (1982) reported postoperative results for 57 adults: excellent in 24 cases (normal bowel function), good in 25 cases (solid stool fully controlled but not loose stool, no need for pads), fair in 5 cases (frequent fecal soiling or requiring pads), and ineffective in 3 cases (no sensation of defecation, constant fecal leakage, requiring constant use of pads).

Recently, dynamic graciloplasty has been proposed for fecal incontinence, where an electrode is implanted post-gracilis muscle transplantation to stimulate the muscle for sustained contraction. Electrical stimulation increases resistance, gradually transforming muscle fibers from type II (fatigue-prone) to type I (fatigue-resistant). The stimulator's switch is controlled externally by a magnet to facilitate defecation. Recent clinical evidence shows long-term electrical stimulation can maintain tension in the transplanted gracilis muscle, restoring bowel control. Cavina reported 47 cases of coloanal anastomosis with neosphincter stimulation after abdominoperineal resection. In 40 cases followed for over 4 years, 65% had good control, 22% fair, and 13% incontinence. However, the stimulator is expensive, prone to infection, and long-term efficacy requires further follow-up.

⑵ Gluteus Maximus Transplantation Sphincteroplasty: A pedicled gluteus maximus muscle bundle is wrapped around the anal canal to replace the sphincter, as in the Chestwood (1903) procedure. A 3 cm wide muscle strip is dissected from each gluteus maximus, with the distal end cut and the proximal end remaining attached to the sacrococcygeal region. The strips are crossed behind the anal canal, wrapped around it, and sutured anteriorly, though results are less satisfactory.

Chittendon (1930), Mclanahan (1941), von Rapport (1952), Dittertow, Grim (1983), and Schmidt (1986) successively applied this surgical procedure.

From 1986 to 1991, Shanghai Renji Hospital treated 8 cases of anal incontinence caused by various reasons using the pedicled gluteus maximus muscle to reconstruct the anal sphincter. Follow-up results showed good outcomes.

The surgical method is divided into two steps during the initial stage [first stage].

Step 1: Under continuous epidural anesthesia, the patient is placed in the left or right lateral position. Routine disinfection of the ipsilateral buttock and lower limb is performed, followed by draping. An "L"-shaped incision is made on the lateral side of the ipsilateral thigh and buttock. The subcutaneous tissue and fascia are incised to expose the gluteus maximus muscle belly. A pedicled gluteus maximus muscle bundle, 4 cm wide, is isolated along with the upper half of the vastus lateralis muscle bundle to maintain its length (care must be taken during dissection to avoid injury to the sciatic nerve and major blood vessels). The nerve supply and blood supply to the pedicled muscle bundle are preserved. The freed gluteus maximus muscle bundle is pulled through a skin tunnel at the ipsilateral ischial tuberosity to the perineum, and the thigh and buttock skin are sutured.

Step 2: The patient is placed in the lithotomy position. The intestinal cavity is routinely irrigated, and the skin is disinfected. A crescent-shaped incision is made on the medial side of each ischial tuberosity to expose the bursa of the ischial tuberosity. Through these two incisions, a subcutaneous tunnel is created anteriorly to the perineum and posteriorly to the level of the coccyx and ischial spine. Care must be taken to avoid puncturing the rectal wall and anal canal during the creation of the subcutaneous tunnel. The freed pedicled gluteus maximus muscle is passed around the lower end of the rectum through the subcutaneous tunnel and maintained at a certain tension. The freed gluteus maximus muscle bundle is fixed and sutured to the bursa of both ischial tuberosities. The skin is sutured, and drainage must be placed.

Various surgical methods for treating anal incontinence caused by congenital or traumatic factors have failed to achieve satisfactory results, leading many scholars to advocate for abdominal colostomy. As early as 1952, Pickrell reported using pedicled neurovascular gracilis muscle transplantation for anal sphincteroplasty to treat fecal incontinence, with the main advantage being stronger muscle strength, allowing contraction of the anal canal when the thigh is flexed. In 1982, Proshian proposed using the gluteus maximus muscle to reconstruct the anal sphincter, as its muscle strength is superior to that of the gracilis muscle. Since 1983, Renji Hospital has adopted the pedicled neurovascular gluteus maximus muscle to reconstruct the anal sphincter, initially applied in radical surgery for rectal cancer (Miles), and later using the same method for cases of anal incontinence. All cases achieved good results without severe infection. The transferred pedicled neurovascular gluteus maximus muscle bundle did not undergo fibrosis due to infection, which is a critical factor in ensuring the muscle bundle functions as a sphincter. Therefore, infection prevention is key to surgical success. To effectively prevent infection and ensure surgical success, strict adherence to aseptic techniques during surgery is essential, along with thorough preoperative preparation, including nutritional support to improve the patient's constitution and adequate bowel preparation, such as bowel cleansing and the use of intestinal antibiotics.