Anal Incontinence



Anal Incontinence


Mikio A. Nihira

Okechukwu A. Ibeanu



INTRODUCTION

Defecation is normally a private function, which is performed at socially acceptable times chosen by the individual. Bowel control is learned in early childhood, and failure of bowel control may be associated with loss of independence, reduced self-esteem, social isolation, a sense of inadequacy or helplessness, and clinical depression.


EPIDEMIOLOGY AND ETIOLOGICAL FACTORS

The incidence and prevalence of anal incontinence (AI) is difficult to estimate. Surveys report widely differing figures. Sampling biases may result in significant underestimation in some populations and overestimation in others. For example, embarrassment may cause anally incontinent individuals to deny their symptoms in self-reporting surveys. On the other hand, surveys in which people over the age of 65 are represented by nursing home occupants may overestimate the prevalence in geriatric populations (1). Similarly, the reported prevalence of AI in younger, obstetric populations is suspected to be underestimated because a proportion of these patients may have injuries that go unrecognized, or these individuals experience transient fecal incontinence. Lastly, a standardized definition of AI does not exist. Currently, the reported prevalence varies according to the definition used. In several papers, “fecal incontinence” refers to the exclusive loss of feces, while the term “anal incontinence” is used for incontinence inclusive of flatus and stool (1). In addition, the threshold for the frequency of incontinence varies. Some surveys include individuals who admit to any anal incontinence in the past 1 year, while other surveys focus only on individuals who report incontinence of liquid or solid stool in the past month. Data collection methods also affect the quality of information obtained. Although face-to-face interviews offer the greatest potential for accurate data collection, some individuals are uncomfortable disclosing private information to a live examiner. Conversely, paper questionnaires can be difficult to complete for impaired patients.

Macmillan et al (1) performed a systematic literature review on the prevalence of AI (including flatal incontinence) and fecal incontinence in community-dwelling individuals. These investigators retrieved 1,517 articles and identified 16 that fit their inclusion and exclusion criteria. Overall, these studies estimate the prevalence of AI to be 2% to 24% and the prevalence of fecal incontinence to be 0.4% to 18%. Only 3 of the 16 studies employed a design that minimized significant sources of bias; these studies focused on fecal incontinence and had a much smaller prevalence variation than the other 13. The estimated prevalence of fecal incontinence in these particular trials ranged from 11% to 15%.

Fecal incontinence has a multifactorial etiology, and in gynecologic practice, the majority of patients with AI have obstetric trauma as the principal cause of their symptoms. Many of these women have anal sphincter defects (2). However, patients typically present years after the presumed obstetrical insult, which implies that compensatory continence mechanisms degrade with time.

Sultan et al (3) reported that 35% of a group of primiparous women who were demonstrated to have had intact sphincters antepartum had sphincter defects observed on endoanal ultrasound 6 weeks after vaginal delivery. More concerning was their observation that 13% of the primiparous women developed fecal incontinence or fecal urgency after delivery. Pretlove et al (4) followed a cohort of postpartum patients and found that 61% of patients with recognized sphincter defects were symptomatic
postpartum. The patients were not stratified according to parity or age. Faltin et al (5) performed immediate postpartum endoanal ultrasound in 150 primiparous women. They identified clinically undetected anal sphincter tears in 42 of 150 women (28%). In a postal questionnaire 3 months postpartum or more, fecal incontinence was reported by 22 women (15%). The odds ratio of those who had clinically undetected sphincter tears was 8.8 for the development of fecal incontinence.

In addition to sphincter defects, vaginal delivery is associated with pudendal neuropathy, particularly during a prolonged or difficult second stage of delivery. A proposed mechanism of injury is that nerve damage results from traction or compression. This damage may develop into impaired rectal evacuation with the need to strain, perineal descent, and subsequent fecal and urinary incontinence. Other common conditions seen by an obstetrician-gynecologist that are associated with fecal incontinence are presented in Table 22.1.

While there is no universally accepted scoring system for AI at present, several scoring systems have been described and used in different trials. These include the Cleveland Clinic Florida Fecal Incontinence Scale (Wexner) (6), Fecal Incontinence Severity Index (FISI) (7), Fecal Incontinence Quality of Life Score (FIQL) (8), Gastrointestinal Quality of Life Index (GIQLI) (9), as well as non-disease-specific instruments such as the Short Form-36 (10).


PATHOPHYSIOLOGY

The detailed pathophysiology and evaluation of AI are covered in Chapters 20 and 21.








TABLE 22.1 General Causes of Anal Incontinence Encountered by the Gynecologist















Obstetric trauma


Injury to the sphincter
Injury to the levator ani
Pudendal neuropathy (stretch injury)


Pelvic organ prolapse


Descending perineal syndrome


Anorectal surgical trauma


Sphincter disruption
Sphincter dilatation


Functional etiologies


Fecal impaction
Diarrhea


The maintenance of fecal incontinence involves complex interaction between higher centers (frontal cortex) and intact neural pathways between the spinal cord and pelvic muscles and sphincters. These, together with several other physiologic mechanisms, work to result in bowel control, allowing defecation to occur voluntarily at socially acceptable times. Degeneration or injury at any of these levels can result in fecal incontinence; hence there are a variety of etiological factors (Tables 22.2 and 22.3).

Specifically, obstetric-related fecal incontinence can result from pudendal nerve damage by compression or stretching, in addition to physical disruption of the anal sphincter mechanism from perineal lacerations. Postmenopausal estrogen deficiency may also affect levator muscle and pelvic floor strength.


CLINICAL EVALUATION

The goal of the evaluation process is to understand the specific pathophysiology in the individual patient in an effort to identify any easily treatable contributing condition and develop an appropriate treatment plan. Thorough assessment begins with a detailed history and physical examination. Prior instrumented deliveries, gastrointestinal disease, and neurological history should be noted. Levator strength should be assessed, as well as the presence of pelvic or rectal prolapse, hemorrhoids, fistulas, and any abnormal or absent reflexes or sensation. A focused neurological examination is essential as well as an appropriate assessment of any suspected diarrheal disease.









TABLE 22.2 Factors That Contribute to the Continence of Stool and Flatus















Colonic factors


Normal stool consistency and volume
Normal colonic accommodation and capacity


Muscular factors


Intact anal sphincters and resting anal tone


Neurologic factors


Normal mentation and social behavior
Intact levator muscle innervation
Intact external sphincter mechanism
Normal anal sensory mechanism (sampling)


Anorectal factors


Normal rectal capacity and compliance
Intact anal seal of the vascular cushions


Investigative tools for the evaluation of AI include anorectal manometry, endoanal ultrasound, defecography, endoscopy, and pudendal nerve latency tests; a description of these tests can be found in Chapter 21.


PREVENTION

Because obstetrical trauma is the most common etiology of AI in women, prevention should be focused on the management of labor and delivery. There is an association between sphincter disruption and episiotomy (both midline and mediolateral). When episiotomy must be performed for obstetrical indications, the mediolateral approach should be preferred in an effort to avoid direct injury to the anal sphincters (11). There is also a well-established association between operative delivery using forceps and anal sphincter trauma. Avoidance of episiotomy and use of vacuum-assisted vaginal delivery (as opposed to forceps) when operative delivery is indicated, as well as maintaining a low threshold for cesarean delivery for labor dystocia, may be protective (12).


MANAGEMENT

Before embarking on an extensive work-up and committing to specific treatments for AI, it is prudent to identify and address any gastrointestinal conditions that may contribute to fecal incontinence.

Treatments for AI include medical therapy, behavioral therapy in the form of biofeedback therapy, and surgery. A significant issue in the management of AI is the differing opinion on what constitutes successful treatment. This is due to a lack of consistent outcome measures. The use of post-treatment questionnaires in some studies relies on vague and subjective quantification such as “improved,” while in other studies there is variation in the inclusiveness of the definition of incontinence with respect to gas, liquid, or solid stool.


NONSURGICAL THERAPY


Dietary Modification

The initial approach to conservative treatment of AI is to manipulate and improve the consistency and volume of bowel movements by increasing dietary fiber intake to generate well-formed stools. Formed stool is easier to control than liquid stool, which tends to seep out from the incompetent anal sphincter and produces soiling. Fiber supplements are easily available without prescription. Dosage should be titrated to stool consistency by the patient. The use of bulking agents should be monitored in the elderly because excessive use can predispose such patients to fecal impaction, especially if fluid intake is inadequate. A common side effect of high fiber consumption is increased flatus. The avoidance of highly spiced foods and bowel irritants like pepper and caffeine, lactose, beer, and some citrus fruits, all of which may produce diarrhea, can improve continence for many patients.


Pharmacotherapy

In addition to dietary manipulation, constipating agents can be useful in patients with chronic loose stools, which are hard to control.

Loperamide is a popular drug that reduces bowel motility, hence increasing stool transit time.
A 4-mg dose before meals has been demonstrated to improve continence (13). The main side effect is constipation, which is usually better tolerated than AI. A balance between continence and constipation can usually be achieved with careful dose titration and with attention to the precise timing of administration.








TABLE 22.3 Differential Diagnosis of Anal Incontinence












































































































Anatomic derangements


Developmental (congenital abnormalities)



Traumatic (obstetric trauma, hemorrhoidectomy, anal sphincterotomy, or dilatation)



Fistula, rectal prolapse, sequelae of inflammatory bowel disease


Neurologic disorders


Central nervous system process




Dementia, sedation, mental retardation




Stroke, brain tumor, spinal cord lesion, multiple sclerosis




Tabes dorsalis



Peripheral nervous system process




Cauda equina lesions




Polyneuropathies




Diabetes mellitus, toxic neuropathy




Shy-Drager syndrome



Traumatic neuropathy




Obstetric trauma




Perineal descent



Altered rectal sensation (unknown lesion)




Fecal impaction




Delayed sensation syndrome




Skeletal myopathies




Myasthenia gravis




Muscular dystrophies


Smooth muscle dysfunction


Abnormal rectal compliance




Proctitis due to inflammatory bowel disease, radiation




Rectal ischemia



Internal anal sphincter weakness




Radiation proctitis




Diabetes mellitus




Childhood encopresis


Modified from Johanson JF, Lafferty J. Epidemiology of fecal incontinence: the silent affliction. Am J Gastroenterol 1996;91:33-36, with permission.


Codeine phosphate may also be used to induce constipation in divided daily doses of 30 to 120 mg. It can cause drowsiness. Lomotil (codeine with diphenoxylate and atropine) is a good alternative, but anticholinergic side effects may limit its use (14).

Fecal incontinence secondary to fecal impaction or constipation should be treated with laxatives. Again, caution must be used in elderly patients, because excessive use can cause diarrhea and electrolyte imbalances. The goal of this therapy is to clear hard stool and maintain predictable, regular bowel evacuations, leaving the rectum empty between bowel movements.

Alpha-adrenergic agonists theoretically appeared promising as a means of increasing the resting tone of the internal anal sphincter, but unfortunately a preparation of topical phenylephrine was disappointing in clinical practice (14).

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jul 24, 2016 | Posted by in UROLOGY | Comments Off on Anal Incontinence

Full access? Get Clinical Tree

Get Clinical Tree app for offline access