Department of Colorectal Surgery
An adequate control mechanism for stool and urine provides a fundamental quality of life allowing for a conscious selection of the appropriate timing, location and privacy for voiding and moving the bowels. Continence is the result of a balanced interaction between the anal sphincter complex (“plug”), stool consistency, the rectal reservoir function, and neurological function. Disease processes or structural defects that alter any of these aspects can lead to fecal incontinence.
Fecal incontinence is defined as the involuntary loss of rectal contents (feces, gas) through the anal canal and the inability to postpone an evacuation until socially convenient. While fecal control is often thought to be synonymous with normal sphincter muscles, other factors are equally important. Hence, fecal incontinence has to be considered to be the common final pathway symptom of multiple independent etiologies.
Consequences of incontinence (both fecal and urinary) are significant at different levels:
(1) patient may develop secondary medical morbidities, e.g., skin maceration, urinary tract infections, decubitus ulcers, etc.
(2) there are substantial direct and indirect financial expenses to the patients (e.g. diapers, clothes, loss of productivity), the employers (days off), insurances (health care cost, unemployment, etc).
(3) impact on quality of life (self-esteem, embarrassment, shame, depression, need to organize life around easy access to bathroom, avoidance of enjoyable activities, etc).
Unfortunately, our knowledge about anorectal and continence physiology and pathophysiology remains limited in many aspects. This not only results in a poor ability to correlate subjective and objective parameters or to predict outcomes, but also in a striking absence of standardization of definitions and quantitation of fecal incontinence. Even though there are scoring systems that are commonly used (e.g. Wexner/CCF incontinence score; Fecal Incontinence Quality of Life (FIQL) score), these often do no include physiologic components to accurately reflect the clinical severity. Most are based on a subjective patient-reported assessment of severity and frequency.
In the US, the Cleveland Clinic Florida (Wexner) fecal incontinence score remains the most commonly used score because of its easiness: the sum of 5 parameters is determined that are scored on a scale from 0 (=absent) to 4 (daily) frequency of incontinence to gas, liquid, solid, of need to wear pad, and of lifestyle changes. A score of 0 means perfect control, a score of 20 complete incontinence. Unfortunately, the patient’s coping mechanisms are not taken into consideration: e.g. a hypothetical completely incontinent patient who spends the whole time on the toilet would not report incontinence to gas, liquid or formed stool, would not need a diaper, and therefore would only have a “daily impact on his quality of life”, i.e. a score of 4 (instead of the more appropriate score of 20).
Primary symptoms of fecal incontinence include a worsening lack of control for different rectal components, i.e. solid stool, liquid/semi-formed stool, gas. Descriptive terms are commonly used to differentiate the degree of incontinence: staining < soilage < seepage < accidents. It is important to recognize individual variations in response to daytime/nighttime, activity, or food intake. Patients may deny any events at all, but report a reduced sensation for arriving stool, a reduced urge-suppressing capacity, and hence a dramatically shortened maximal deferability (time to bathroom).
Secondary symptoms of fecal incontinence are the result of leaking stool and include pruritus ani, perianal skin irritation, urinary tract infections etc. On occasion, the patients may report these symptoms as chief complaint, instead of acknowledging the lack of control as such.
Depending on the etiology, fecal incontinence may have associated symptoms which need to be carefully assessed: urinary incontinence, vaginal bulging (rectocele, cystocele), prolapse (hemorrhoidal, mucosal, full-thickness rectal), altered bowel habits.
A vast number of etiologies have been associated with the development of fecal incontinence, including traumatic injury, degenerative and functional conditions, tumors, inflammatory diseases, or congenital/acquired malformations. By far the most common causes, however, are obstetric injury (often decades before onset of symptoms), anorectal surgeries (hemorrhoidectomy, fistulotomy, sphincterotomy), altered bowel habits (IBS, IBD, diet intolerance, constipation with overflow incontinence), or a status post colo-anal or ileo-anal reconstruction.
Fecal incontinence is very common but because of its taboo nature difficult to assess. Estimated prevalence rates are only available for selected subsets of the population and show a wide variability depending on the method of assessment and target population. International population-based studies suggested a prevalence of 0.4–18%; a telephone survey in the
Physiology and pathophysiology
Successful management of patients with fecal incontinence depends not only on a fundamental knowledge about etiologies, but requires a good understanding of the underlying mechanisms and the intricate interaction of different components that contribute to achieving fecal control:
(1) Plug function: structures and functions need to be in place to create sufficient outlet resistance against the intrarectal pressure of the feces at rest, against increased intra-abdominal pressure, during a peristaltic wave, or during physical stress/activity:
a. Puborectalis sling and external anal sphincter (EAS): striated muscles with slow-twitch, fatigue-resistant muscle fibers. They are innervated by the inferior branch of the pudendal nerve (S3–S4), contribute to about 20–30% of anal resting tone, and provide the voluntary sphincter contraction (squeeze pressure) with roughly a doubling of the resting pressure. Puborectalis dysfunction results in complete incontinence, EAS dysfunction in impaired voluntary control.
b. Internal anal sphincter (IAS): smooth muscle (continuation of the muscularis propria of the rectum), which has an autonomic innervation and contributes to 55% of the resting tone of the anal canal. IAS dysfunction is associated with impaired fine tuning of fecal control.
c. Hemorrhoidal cushions: their expansion provides the fine seal of the anal canal and can contribute to up to 15–25% of the overall control.
d. Configuration of anal canal: The effectiveness of the plug mechanism not only depends on the absolute number of the pressure values, but is a function of the length of the high-pressure zone and its radial translation of force. Focal defects (e.g. keyhole deformity after previous anorectal surgery) can therefore result in significant symptoms despite a seemingly normal pressure profile.
(2) Stool quality and propulsive force:
a. Formed stool is easier to control than liquids or gas.
b. Extent of gas production: increases the force, increases the awareness and self-consciousness.
c. Increased axial propulsive forces (diarrhea, IBS, etc) increase the challenge to the sphincter complex.
(3) Rectal capacity: an adequate low-pressure space allows for accumulation and storage of feces until an evacuation is desired:
a. Overall size of reservoir.
b. Distensibility, as measured and expressed by “rectal compliance”.
c. Configuration of post-surgical neo-reservoir (e.g. J-pouch vs. straight anastomosis).
An impaired reservoir function is commonly seen after previous rectal surgery (e.g. LAR), pelvic radiation, and in the presence of tumors, strictures, or ongoing inflammation.
(4) Neurologic sensory or motor function:
a. Central nervous system: conscious (awareness) and subconscious networking of information from and to the anorectum are necessary for adequate control. Possible central neurologic deficits include: focal defects (stroke, tumor, trauma, multiple sclerosis) or diffuse brain damage (dementia, multiple sclerosis, infection, drug-induced).
b. Intact peripheral nerve function is needed to allow for transmission of the nerve input to the muscle complex, and transmission of sensoriceptor information (rectal pressure, sphincter pressure). Peripheral neuropathy may be localized (parity-induced pudendal neuropathy, pelvic radiation), or have a diffuse pattern (diabetes mellitus, drug-induced).
c. Functional dysfunction: visceral hypersensitivity (IBS).
In every patient, a thorough history should be obtained to define the complaints and their impact, possible triggering factors or events and the time interval to the onset of symptoms. All past treatments and treatment failures as well as the current management have to be described. Further explored should be underlying diseases (diabetes, stroke, etc), current medications, the dynamics of bowel movements, and associated symptoms. Additional tools to define the severity of the fecal incontinence are the administration of quality of life instruments (incontinence score, FIQL).
The clinical exam includes a visual inspection, an educated digital rectal exam (sphincter integrity, sphincter tone, compensatory auxiliary muscle contraction, length of anal canal, rectocele, palpable mass), as well as at least a local visualization of the anorectum. A colonic evaluation should be done according to national guidelines. More objective data can be obtained from anophysiology studies, but the results have to be interpreted with caution in the context of all other factors. Anophysiology studies commonly include:
(1) anorectal ultrasound to assess the presence or absence of a sphincter defect or structural alteration.
(2) manometry including anorectal sensation and determination of the rectal compliance in order to assess the muscle strength and the reservoir function.
(3) determination of the pudendal nerve terminal motor latency (PTNML) to look for pudendal neuropathy as a prognostic parameter.
Depending on the presentation, other steps might be appropriate to evaluate more complex pelvic floor dysfunction, e.g. defecating proctogram or dynamic MRI, urodynamics, or a gynecological evaluation.
(1) Nonoperative treatment
Management of patients with fecal incontinence invariably includes non-operative measures. Dietary changes are intended to identify and avoid foods that cause diarrhea or urgency. Supplementary fibers with limited fluid intake may help to thicken the stool but the increased stool volume may be counterproductive with weak sphincter function. Bowel habit training is important to develop regularity. Supportive measures include application of barrier creams to the perianal skin. The stool load may be reduced through rectal washouts (scheduled enemas). Medications are introduced as needed to slow down the bowels (anti-diarrheal medications), bind bile acids, or to reduce the reflectory sphincter relaxation. Physical therapy and biofeedback training have an important role, even if the objective effect is difficult to document. Yet, it is simple, cheap, and without adverse physical effects, and aims at improving contraction and coordination of the pelvic floor muscles in response to rectal distention.
(2) Operative Treatment
Surgical options are explored in patients with significant fecal incontinence that is refractory to conservative management. Even relatively mild forms may be approached surgically if an obvious and correctable deformity is present and lends itself to a correction (e.g. cloaca-like deformity, keyhole deformity, prolapse, ectropion).
Various operative approaches are available. Their applicability depends on the individual findings, symptoms and a clear definition of treatment goals and priorities.
a. Restoration and improvement of residual sphincter function:
- Sphincter repair (sphincteroplasty) is a rational approach if a segmental sphincter defect is identified. The short-term results are generally good, the long-term function, however, may deteriorate over time.
- Correction of visible deformities (anus, rectum).
- Sacral nerve stimulation: A temporary electrode is implanted, followed by a definitive implantation of the stimulator if the patient shows a good response to the test period. While the exact mechanism of this technique is not yet completely understood, SNS is believed to restimulate a dysfunctional, but anatomically intact anal sphincter muscle (in conjunction with effects on the rectal sensation). The role is rapidly evolving; the indications and settings are subject to ongoing research.
b. Replacement/imitation of the sphincter or its function:
- Narrowing of anal canal to increase the outlet resistance without any dynamic component:
- Thiersch and related procedures with placement of anal encirclement.
- radiofrequency ablation (“Secca procedure“) to create a controlled scar and stricturing of the anal canal.
- Nondynamic graciloplasty: the non-stimulated wrap of gracilis muscle around the anal canal (“bio-Thiersch”) has limited indications because of the high risk of complications and a lack of functionality.
- Implantation/injection of implantable microballoons, carbon-coated beads, autologous fat, silicone, collagen.
- Dynamic sphincter replacement:
- Implantation of artificial bowel sphincter: this is the only approach that provides a true functional/dynamic solution with excellent results; its limitations are related to the risk of infection and device erosion. The technique should therefore be limited to surgeons with the respective expertise.
- Dynamic graciloplasty: compared to the non-stimulated graciloplasty, a pulse generator device is implanted: the continued electrical stimulation of the muscle aims at converting the fast-twitch, fatigable gracilis muscle to a slow-twitch, fatigue-resistant muscle.
c. Fecal diversion:
If other therapies have failed or if comorbidities preclude a more aggressive or time-consuming therapy, the creation of a diverting colostomy remains a predictable alternative. Even if it does not restore continence in a strict sense, it allows to regain control on the waste management and permits resumption of a normal personal and social life style. The patient’s satisfaction will depend on wether the stoma is well-constructed and at an appropriate site.
d. Rarely used tools:
- Malone antegrade continence enema (MACE): a surgery is performed to create an appendicostomy or a continent access colostomy. A catheter may be introduced in scheduled intervals to reduce the fecal load of the colon/rectum by means of timed washouts of the whole colon. Despite convincing concept, the patients typically complain of persistent leakage of residual colonic fluid for several hours following the irrigation.
The text is based on the respective chapters in: A.M. Kaiser, The McGraw-Hill Manual of Colorectal Surgery,
Detailed references are available upon request.