Chapter 7.3
Fecal and Urinary Incontinence:
Epidemiology and Etiology
Dana R. Sands and Minda Neimark
As more is understood about the function of the pelvic floor, colorectal surgeons, urogynecologists, and urologists will find themselves working together to treat women with complex mixed forms of incontinence and pelvic organ prolapse. No longer should these issues be addressed in isola- tion. Several population-based studies have been conducted to ascertain the true incidence of isolated fecal and urinary incontinence. The incidence of dual incontinence is much less studied. The evolution of the concept of the pelvic floor as one functional unit with both anterior and posterior com- ponents has led physicians treating patients with isolated incontinence to search for evidence of dual incontinence. This has allowed us to provide more comprehensive medical care for our patients.
Fecal Incontinence
Epidemiology and Etiology
Fecal incontinence represents a significant public health concern. It is esti- mated that over 400 million dollars per year are spent on adult diapers in the United States (1). The prevalence of fecal incontinence is grossly under- estimated due to the social stigma associated with the condition and the reluctance of both patient and physician to discuss these problems. The problem extends beyond geographic borders and stretches worldwide.
Several studies from various countries have estimated the prevalence of fecal incontinence in the general population to be between 1.4% and 12.7%
(Table 7.3-1). This range reported after meta-analysis of over 26 000 people underscores the difficulty in fully assessing the magnitude of the problem.
The etiology of fecal incontinence can be classified into two groups:
patients with normal pelvic floor function and those with abnormal pelvic floor function. Initially, it is important to rule out pseudoincontinence as the cause of the patient’s symptoms. Pseudoincontinence results from perineal soiling that can be related to poor hygiene, prolapsing hemorrhoids, anal
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fistula, or dermatologic conditions. Overflow incontinence is another cause for fecal incontinence. It often is seen in the elderly and is associated with fecal impaction. Fecal incontinence with normal pelvic floor function can result from persistent liquid stool, causing diarrhea and urgency, or may be related to systemic illnesses including diabetes, multiple sclerosis, sclero- derma, or dementia. Acquired fecal incontinence related to pelvic floor dys- function can be subdivided further into etiologies related to sphincter injury and those related to denervation injury. The most common cause of sphinc- ter injury in otherwise healthy women is obstetric trauma. The true inci- dence of sphincter injury and subsequent fecal incontinence is difficult to assess because the symptom presentation often is delayed. Sangalli et al.
(10) contacted over 200 women 13 years after obstetric related anal sphinc- ter trauma. Fecal incontinence was noted in 11.5% and 25% of women with third- and fourth-degree lacerations, respectively. In the subgroup of women with fourth-degree lacerations, subsequent vaginal delivery was associated with a higher prevalence of severe incontinence. Ryhammer and colleagues (11) assessed the long-term effect of vaginal delivery on anorec- tal function in a group of normal perimenopausal women. Increasing parity correlated with increased perineal descent, decreased anal mucosa sensi- tivity, and prolonged pudendal nerve terminal motor latency (PNTML).
They concluded that repeated vaginal deliveries had a long-term adverse effect on anorectal physiology and function.
Trauma to the anal sphincters is not limited to obstetric causes. Surgical treatment of anal fistulae fissures and hemorrhoids can all lead to varying degrees of incontinence (12). In a prospective study of 50 patients who underwent fistulectomy, hemorrhoidectomy, or sphincterotomy, Felt- Bersma and colleagues (13) found a 46% incidence of anal sphincter defects. Thirty percent of these patients had symptoms of fecal inconti- nence, whereas 70% had occult sphincter defects. The implications for future continence in the subgroup with occult injuries are unknown. The largely abandoned Lord technique for the treatment of hemorrhoidal disease, consisting of anal dilatation, has been reported to have associated Table 7.3-1. Prevalence of fecal incontinence in various countries.
Country Year Study Size (N) Prevalence
United Kingdom (2) 2001 2 818 3%
Nigeria (3) 2002 3 963 6.96%
Australia (4) 2002 660 9%
United Kingdom (5) 2002 10 116 1.40%
New Zealand (6) 2001 717 12.70%
United Arab Emirates (7) 2001 450 11.30%
Switzerland (8) 2001 984 4.40%
United States (9) 1995 6 959 2.20%
incontinence rates as high as 52% in the long term (14). The presence of a rectal prolapse also can lead to incontinence secondary to the chronic dilatation of the anal sphincters and traction injury to the pudendal nerves, resulting in pudendal neuropathy, although the physiology here is complex with a mixture of sphincter damage, altered mucosal sensitivity, disabled anorectal sampling, and rectoanal incoordination, as well as fundamental alteration in the rectoanal inhibitory reflex (15). Neuropathic injury to the pelvic floor will be addressed further in this chapter. Female sex, previous anorectal surgery, and previous vaginal delivery are all risk factors for the development of fecal incontinence related to pelvic floor dysfunction.
Urinary Incontinence
Urinary incontinence (UI), defined as the involuntary loss of urine suffi- cient to be a social or hygiene problem, is a newly recognized health issue affecting millions of people worldwide (16). Urinary incontinence in the elderly is a major cause of disability and dependency, imposing a significant financial burden on both the patient and society as a whole. In 1995, the total estimated expense of UI was $26.3 billion, or $3565 per individual aged 65 and older with urinary incontinence (17).
Urinary incontinence, a generalized term, encompasses several etiologies of incontinence including stress incontinence, overactive bladder (OAB), mixed incontinence (stress and OAB), and overflow incontinence. Each condition of incontinence is characterized not only by distinct symptoms, but also by overlapping symptoms requiring investigative studies to define the etiology of the patient’s UI. The following are etiologies of UI defined by International Continence Society (ICS) classification:
Stress Incontinence (SUI): urine loss coincident with an increase in intra- abdominal pressure in the absence of a detrusor contraction or over- distended bladder.
Overactive bladder (OAB): a term used to encompass a range of irritative bladder filling and storage symptoms. For this chapter, the term OAB will be used to define involuntary loss of urine associated with involuntary or uninhibited detrusor contractions documented by cystometry. Terms used to clinically define this condition are detrusor hyperreflexia or detrusor instability. Other terms that are used clinically, but have not been defined by the ICS, are motor urge incontinence and sensory urge incontinence.
Mixed incontinence is combined SUI and OAB.
Overflow Incontinence is defined as involuntary loss of urine associated with over distension of the bladder.
Epidemiology
The epidemiology of UI includes incidence, prevalence, types of inconti- nence, as well as associated risk factors such as age, gender, and medical ill- nesses (see Table 7.3-2). Although there recently has been an increased awareness of UI among physicians and the public, it still remains an under- reported health condition due to the ongoing perception as a socially embarrassing condition. It has been estimated that almost 40% of women who experience urinary incontinence endure the condition for a year or more before consulting a doctor. In addition, although studies have been conducted in an attempt to determine the true prevalence of urinary incon- tinence, they have produced only estimates due to differences in method- ology, as well as variations in the definitions of UI.
Urinary incontinence incidence is defined as the number of new cases over a certain period of time. The incidence of UI reported in the literature is limited due to factors such as dropouts by migration, noncompliance, and death. Elving (18) reported an increase in the incidence of urinary inconti- nence in women between the ages of 45 and 59 years.
Sex and Age
Urinary incontinence has been demonstrated to be more prevalent in women than in men, with prevalence ranging from 4.5% to 53% in women and 1.6% to 24% in men. This chapter will address only the epidemiology
Table 7.3-2. Risk factors associated with UI.
Age Gender Medical illness Cerebrovascular events
Parkinson’s Multiple sclerosis Pulmonary disease
Chronic bronchitis
Chronic obstructive pulmonary disease Diabetes
Connective tissue disease Congenital
Spina bifida Medications
Thiazides Oral estrogen Body mass index Previous pelvic surgery Childbirth
Menopause Smoking
of UI in the female patient. It is well documented that UI increases with age.The lifetime risk of undergoing a single operation for prolapse or incon- tinence by age 80 is 11.1% (19). A recent survey showed that 12.5% of women less than 80 years of age, 19% of women between 80 and 89 years of age, and 31.1% of women greater than 90 years of age reported daily UI (20). It has been demonstrated that functional urethral length—an impor- tant component of the continence mechanism—is affected by age and estro- gen status. This is due to a decrease in both urethral vascularity and smooth and skeletal muscle, both of which are estrogen dependent. This has been made evident by studies demonstrating that the use of local estrogen improves incontinence symptoms.
Urinary incontinence is a very common condition in the nursing home setting, where it is the number one reason for admission to a nursing home, with an estimated prevalence as high as 70% (21).
Types of Incontinence
Stress incontinence—reportedly occurring in 49% of all women—is more predominant than OAB, which occurs in approximately 22% of women.
Mixed incontinence is reported to occur in 47% of the female population.
Reported symptoms have been shown to be a poor diagnostic tool for UI.
Therefore, urodynamics should be performed prior to initiating treatment, especially when surgical treatment is considered (22).
Stress urinary incontinence results when there is loss of support to the bladder neck failing to maintain a watertight seal under conditions of increased intra-abdominal pressure. When the bladder neck can no longer maintain a seal at rest, the condition is called intrinsic sphincter deficiency (ISD)—a more severe form of stress incontinence.
Overactive bladder (OAB) has been popularized recently as a term for the condition encompassing a range of irritative bladder filling and storage symptoms. It includes urinary frequency, urgency, and urge incontinence, singly or in combination. Urgency is a strong desire to void accompanied by a fear of leakage. Frequency represents the need to urinate on an abnor- mally frequent basis—more than eight times per day or more than two times per night (nocturia). Urge incontinence refers to the symptom of urine loss preceded by a strong sense of urgency. Detrusor instability is the term used when loss of urine secondary to a spontaneous or provoked involuntary detrusor contraction is demonstrated during cystometry. If the uninhibited detrusor contractions are due to a neurologic etiology, such as multiple sclerosis or Parkinson’s disease, then the term detrusor hyper- reflexia is used. Complaints of bladder dysfunction may be the initial symptom of a neurologic lesion. In fact, 20% to 30% of patients with mul- tiple sclerosis or Parkinson’s disease will have bladder dysfunction com- plaints prior to a diagnosis of their primary neurological disease.
Race
The distribution of incontinence types differs between racial groups. It is theorized that these differences in distribution are due to genetic factors and lifestyle. In a recent study evaluating the prevalence of UI amongst first-degree relatives, there was a three-fold prevalence of UI amongst first- degree relatives of index female patients presenting with UI (23). It has been demonstrated that white postmenopausal women are more likely to report UI than black postmenopausal women (32% vs. 18%) (18). In a study of 200 women who had undergone multichannel urodynamic evalu- ation, white women were more likely to have a diagnosis of stress urinary incontinence than black women (61% vs. 27%). In addition, 56% of black women were more likely to have OAB, compared with 28% of white women (24). A recent study by Mattox and Bhatia (25) evaluated the preva- lence of UI among white and Hispanic women with similar age, gravity, and parity. Hispanic women were more likely to have stress incontinence than white women (30% vs. 16%), and white women were more likely to have OAB than Hispanic women (44% vs. 27%).
Dual Incontinence
Epidemiology
After comparison of the etiology and relative risk factors for the develop- ment of isolated fecal and urinary incontinence, there is no surprise that these two afflictions frequently coexist. Dual incontinence is grossly under- diagnosed. In a population-based study from Minnesota, over 1 500 people over the age of 50 responded to a questionnaire related to fecal and urinary incontinence (26). Here, 5.4% and 9.4% of men and women, respectively, suffered from combined fecal and urinary incontinence.Among people with fecal incontinence, the prevalence of concurrent urinary incontinence was 51.1% in men and 59.6% in women. In the younger age groups, the inci- dence of combined incontinence in women was twice as high as in men.
These incidences are much higher than those previously reported by Nakanishi (27), who found the prevalence to be 53/1 000 in a community- based review.
Lacima and colleagues (28) investigated the incidence of coexisting fecal incontinence in a subgroup of patients being treated in a urodynamic hos- pital unit. After interviewing 900 consecutive patients suffering from urinary incontinence, they found the incidence of dual incontinence to be 8.7%. The urodynamic evaluation of this group revealed stress incontinence in 42%, detrusor instability in 11%, mixed incontinence in 37%, voiding dis- order in 3%, and no urodynamically detectable abnormality in 6%. A history of vaginal delivery and chronic straining was more frequent in the group of patients with dual incontinence. In a similar review, Meschia et al.
(29) investigated the prevalence of fecal incontinence in 881 women being treated for urinary incontinence or pelvic organ prolapse. Twenty percent of their patients suffered from fecal incontinence. Of the patients with urinary incontinence, 24% had coexistent fecal incontinence, and indepen- dently, the women with urinary incontinence were more likely to report their symptoms of fecal incontinence than those being treated for pelvic organ prolapse alone. Alnaif and Drutz (30) noted, however, that dual incontinence exists even in the nulliparous population of teenage girls in Canada. In a survey of 332 teenage girls, the prevalence of urinary inconti- nence symptoms was 17%, where 38% had minor symptoms of fecal incon- tinence (usually to gas), and 3% had major symptoms of fecal incontinence.
Of interest, with the exception of the one woman who suffered from enure- sis, none of the women with fecal or urinary incontinence symptoms had sought medical attention or felt that the symptoms were abnormal.
The experience at the Cleveland Clinic Florida again points to a high inci- dence of dual incontinence (31). In a group of patients who were treated surgically for fecal incontinence, the incidence of concomitant urinary incontinence was 54%, and 64% of patients treated surgically for rectal pro- lapse had associated urinary incontinence. These numbers are much higher than the general population, pointing to a common pathophysiology for urinary and fecal incontinence involving pelvic floor dysfunction.
Damage to the Pelvic Floor
Obstetrics
The pelvis traditionally has been separated into three compartments: the anterior containing the bladder, the middle compartment, which is occu- pied by the uterus and vagina, and the posterior compartment occupied by the rectum and anus. Because all three compartments share similar inner- vation and muscular support, it is logical to assume that damage to the nerves and muscles of the pelvic floor can lead to pelvic floor dysfunction and urinary and/or fecal incontinence. This concept of the pelvic floor as a single functional unit is gaining acceptance by physicians who address dys- function of the pelvis resulting in incontinence, urinary or fecal. The patho- physiology behind fecal and urinary incontinence is thought to be the result of a combination of factors including childbirth, connective tissue disorders, pelvic neuropathies, congenital factors, pelvic surgery, and miscellaneous factors such as obesity, respiratory disorders, occupational and recreational stress, and hypoestrogenism. This is important for a physician to understand because it is traditionally thought that most of the damage that occurs to the pelvis is iatrogenic.
As stated previously, there are many factors contributing to damage of the pelvic floor. Obstetrical injury is thought to be the principal factor con-
tributing to the development of incontinence. It has been well established that a vaginal delivery—notably the first—is associated strongly with the future development of urinary and fecal incontinence. Approximately 40%
of women who undergo a vaginal delivery will at some point develop urinary and/or fecal incontinence. It also has been shown that women who undergo elective cesarean section without previous labor have fewer com- plaints of these symptoms. This would indicate there has been little to no damage sustained by that mode of delivery. Instrumental vaginal deliveries with forceps have been shown to be responsible for a greater decrease in intra-anal pressure and a greater incidence of weak pelvic floor muscula- ture compared with vaginal delivery without forceps. This determination was based on objective data including physical examination and urody- namics (32).
Pelvic floor dysfunction caused by obstetrical injury is related to damage of the anatomical support or denervation injury of the pudendal nerve. The event of a vaginal delivery results in dilation and stretching of the pelvic floor, connective tissue supports including the perineal body, and the muscles of the anal sphincter. Episiotomy and occult damage to the exter- nal anal sphincter (EAS) as evidenced by endoanal ultrasound reveals many unsuspected defects of both the internal and external anal sphincters following vaginal delivery. Sultan et al. (33) used endoanal ultrasonography to evaluate the sphincter morphology in 202 women before and after delivery and six weeks postpartum. Thirty-five percent of the primiparous and 44% of the multiparous patients had anal sphincter disruptions after delivery.
There are multiple studies that have found childbirth, particularly with a vaginal delivery, to be associated with the development of pelvic neu- ropathies either by direct compression or stretching of the nerve. The pudendal nerve innervates the pelvic floor muscles, as well as the anal and the external striated urethral sphincter, as the nerve travels along the pelvic sidewall. Specifically, the inferior hemorrhoidal branches innervate the EAS and the perineal branches of the pudendal nerve innervate the peri- urethral sphincter. The site of damage to the pudendal nerve determines the extent of dysfunction to the various muscles it innervates (34,35).
Snooks et al. (36) demonstrated slowed conduction of the perineal nerve in those patients with stress urinary incontinence. The type of obstetrical event that results in a neuropathy has been evaluated in studies assessing pudendal nerve function. Tetzschner and colleagues (37) demonstrated an increase in terminal motor latency of the pudendal nerve (PTML) in women who underwent a vaginal delivery. In a recent study, PTML record- ings were compared in women beyond 34 weeks gestation who either deliv- ered vaginally or by elective Caesarean section. Terminal motor latency of the pudendal nerve values were significantly more prolonged in those women who had a vaginal delivery when compared with women who had an elective Caesarean section, either in primipara or multipara, and women
who had a Caesarean section after the onset of labor also had prolongation of PTML (38,39).
Pelvic Surgery
Pelvic surgery—especially radical pelvic surgery with extensive dissection—
can lead to pelvic floor dysfunction. Several studies have shown that a major cause of pelvic morbidity after radical surgery for gynecologic cancer is damage to the pelvic nerve plexus. Bladder dysfunction after pelvic surgery from either blunt or sharp dissection has been attributed to damage to the autonomic nerves: the sacral splanchnic (parasympathetic), hypogastric (sympathetic), and the pelvic autonomic nerve plexus.
Surgical repair of pelvic organ prolapse when performed through the vaginal route has been shown to result in damage to the pudendal nerve and its perineal branch because the perineal branch supplies the anterior vaginal wall. Women evaluated up to 32 months postoperatively who under- went vaginal reconstruction and had a suboptimal outcome of their pro- lapse determined by physical examination demonstrated a neuropathy documented by an increase in the PTML of the perineal branch of the pudendal nerve (40). It also has been demonstrated that vaginal dissection can worsen preexisting perineal neuropathy in patients with pelvic relax- ation and stress incontinence. Benson and McClellan (41) found that pelvic floor surgery involving vaginal dissection with or without needle ure- thropexy in patients with pelvic floor relaxation or urinary incontinence resulted in further deterioration of nerve function based on terminal motor latency studies of both the perineal and inferior rectal branches of the pudendal nerve six weeks following surgery.
Menopause
Epidemiologic studies have demonstrated a higher prevalence of UI in postmenopausal women. This most likely is due to a combination of lower urinary tract changes that occur in the postmenopausal woman, as well as the higher incidence of medical illnesses that have been associated with UI.
Urethral function is affected by age. Maximal urethral pressure and func- tional urethral length increase from infancy to early adulthood, and then decrease with advancing age. It also has been shown that the pelvic floor, bladder, and vagina are estrogen-dependent. Because normal urethral func- tion is dependent on estrogen, further decrease in functional length occurs after menopause because of estrogen deficiency, contributing to the devel- opment of UI.
Surgical Outcome for Combined Fecal and Urinary Incontinence
There are limited data available on combined surgery for urinary and fecal incontinence. Advantages to performing a combined procedure as com- pared with several surgeries include lower cost, fewer in-hospital days, and only one exposure to general anesthesia. In addition, a single combined surgery would ideally decrease the amount of trauma to the pelvic floor, thus decreasing the potential for neuropathy. Halverson and colleagues (42) reported surgical outcomes in patients who underwent sphincteroplasty alone versus sphincteroplasty and urogynecologic surgery, including trans- vaginal hysterectomy, vaginal prolapse repair, and urethropexy. There were no significant differences in terms of surgical success, morbidity, or mor- tality between the two groups. There was also no significant difference in limitation—physically, socially, or sexually—between the two groups. In addition, 92% of the patients were satisfied that their double incontinence was repaired at the same time. Silvis and colleagues (43) evaluated the overall benefit of performing a rectovaginovesicopexy for 25 women with combined fecal and urinary incontinence. In this small series, constipation was improved in 78%, fecal incontinence in 69%, and urinary incontinence in 50%, based on defecography, physical examination, and mailed response questionnaires.
Ross (44) evaluated 46 women who had UI and fecal incontinence treated surgically by laparoscopic Burch colposuspension and overlapping sphincteroplasty. At one year postoperatively, 89% were objectively dry and 82% had no reported fecal incontinence. Sacral nerve stimulation has been shown to be successful for UI, urge incontinence, and detrusor instability (see Chapter 7.4). New data regarding sacral nerve stimulation for com- bined treatment of fecal and urinary incontinence are now being analyzed and are awaited. Perhaps the most convincing evidence for a similar neu- ropathic etiology for fecal and urinary incontinence has been the success associated with sacral nerve stimulation. Initially used for the treatment of urinary incontinence, patients with concomitant fecal incontinence soon noted improvement in both symptoms. Early and mid-term results have shown sacral nerve stimulation to be beneficial in the treatment of complex forms of incontinence (45,46).
Conclusions
The true epidemiology of combined urinary and fecal incontinence is diffi- cult to assess. The social stigma associated with these conditions has made it difficult for physicians to adequately identify affected patients. As we learn more about the function of the pelvic floor and recognize the common
etiology of both anterior and posterior compartment dysfunction, we will offer better and more comprehensive care to our patients.
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1261–7.
Editorial Commentary
Dr. Dana Sands (an alumnus in the Department of Colorectal Surgery at Cleveland Clinic Florida) and Dr. Minda Neimark (an alumnus of the Section of Urogynecology at Cleveland Clinic Florida) work closely together on a routine basis to address mixed fecal and urinary incontinence.
They have brought to this book their collective wisdom and have helped us to recognize a fact often overlooked by colorectal surgeons, specifically that urinary incontinence may well coexist with fecal incontinence and that the treatment of one condition may exacerbate the other. Their work together has highlighted the fact that prior to any intervention for one type of incon- tinence the other type of incontinence should be assessed with whatever
tests are appropriate and if appropriate, simultaneously treated to prevent such exacerbation. I think that the very high incidence of dual incontinence may be striking to many readers along with the fact that both etiologies can often be successfully simultaneously addressed. Their contribution repre- sents the future of pelvic floor physiologic evaluation and treatment. It is important for coloproctologists to understand that we should work as a team with our urogynecology colleagues to ensure proper evaluation and treatment in these patients.
SW
