Introduction
The ability to control evacuation, as discussed in Chapter 1, is guaranteed by many factors. These include intact anal sphincter mechanism, compliant reservoir, effi- cient evacuation, stool volume and consistency, intes- tinal motility, pelvic floor structural integrity, cortical awareness, cognitive function, mobility and access to facilities. Normal defecation is a process of integrated somatovisceral responses, which involve coordinated colo-recto-anal function [1]. Incontinence occurs when one or more of these mechanisms are impaired and the remaining mechanisms are unable to compen- sate. Although integrity of the sphincteric mechanism plays a major part, there are other important aspects, such as stool volume and consistency, colonic transit, rectal compliance and sensation, anorectal sensation and anorectal reflexes [2]. In this chapter, all these aspects are discussed separately, but in the majority of cases (80% according to Rao et al. [3]), the cause of faecal incontinence (FI) is multifactorial [4, 5].
Suprasphincteric Dysfunction
Stool Consistency/Volume and Gastrointestinal Transit The consistency of the faeces and the rate at which they are introduced into the rectum may play a role in determining incontinence. Liquid stools rapidly delivered to the rectum are able to determine urgency and incontinence even in normal subjects [6]. Many patients with idiopathic FI have chronic diarrhoea, often secondary to irritable bowel syn- drome (IBS). In these subjects, sigmoid pressures and sigmoid motility index are usually higher than in the normal population.
Rectal Compliance and Motility
The rectum is a muscular tube composed of a contin- uous layer of longitudinal muscle that interlaces with
the underlying circular muscle. This unique muscle arrangement enables the rectum to serve both as a reservoir and as a pump for emptying stools [7]. A normally distensible rectum is able to maintain low intraluminal pressures despite large volume [8]. If this capacity deteriorates, a smaller quantity of faeces will result in higher pressure, causing urgency and eventually incontinence. This mechanism is clearly evident in patients with ulcerative colitis [9, 10], radi- ation proctitis [11] or after sphincter-saving opera- tions [12, 13]. Decreased compliance has been noted in many patients with FI [14–17]. However, it is not clear whether this fact always represents a cause or whether it may be a consequence of incontinence itself. Rasmussen et al. [16], having found no differ- ences in rectal compliance between patients with idiopathic or traumatic incontinence, postulated that decreased rectal compliance is likely a consequence of an incompetent anal sphincter and not the cause of incontinence itself.
Rectoanal Inhibitory Reflex
Rectoanal inhibitory reflex (RAIR) enables rectal contents to come into contact with the epithelium of the upper anal canal, where there is a high concen- tration of free and organised sensory nerve endings [18]. The mechanism is guaranteed by concomitant rectal contraction and internal anal sphincter (IAS) relaxation. At the same time, there is a reflex external anal sphincter (EAS) contraction that prevents acci- dents. This sampling mechanism occurs several times per hour [19] and allows an accurate distinc- tion between flatus, liquid and solid faces, and for these reasons it has a role in the fine adjustment of continence, allowing the individual to choose whether to retain or discharge their rectal contents. It is likely that minor degrees of sensory impairment are not by themselves causative of incontinence in patients with otherwise normal anorectal function [20]. However, if the sampling mechanism is defec- tive and sphincter function is poor, the patient may
Pathophysiology of Faecal Incontinence
Luigi Zorcolo, David C.C. Bartolo
3
be completely unaware of impending incontinence, especially if anal sensation is also reduced [21, 22]. In one of our studies [23], it was noticed that sampling, considered as the moment in which rectal and upper anal pressure are equal, occurred spontaneously in only 33% of incontinent patients compared with 89%
of controls (p<0.05). These findings confirmed that an impaired sampling mechanism plays an impor- tant role in incontinent patients.
Rectal Sensation
The contribution of altered rectal sensation, either in terms of hyposensitivity or hypersensitivity, to disor- ders of defecation is becoming increasingly recog- nised [24, 25]. The rectum itself does not have pro- prioceptors; these are located in the levators, pub- orectalis (PR) and anal sphincters [26] and subserve the sensation of distension and stretch of the rectal wall. These sensations travel along the pudendal nerve to S2, S3and S4roots [27]. The pudendal nerve is a mixed nerve that is the main nerve responsible of innervation of the anorectal wall and sphincteric complex. Its course through the pelvic floor makes it vulnerable to stretch injury, especially during vaginal delivery. Many cases of FI in the presence of a mor- phologically intact sphincter are related to impaired evacuation and disturbed sensation of the rectum due to intrinsic neuropathy [28–30].
The aetiology of rectal hyposensitivity is unclear, although there is limited evidence to support the role of pelvic nerve injury and abnormal toilet behaviour [25]. More frequently, it is associated with diseases such as altered mental conditions (i.e. dementia;
stroke; encephalopathy) and sensory neuropathy (i.e.
diabetes; spina bifida; meningocele) [31–34]. Rectal hyposensitivity is more often related to constipation, but it can also be the cause of passive incontinence.
Despite a normal or borderline sphincter function, blunted anorectal sensation with impaired EAS con- traction during the sampling reflex may result in soil- ing [35]. This is what typically happens in institu- tionalised elderly people in whom reduced rectal sen- sation and poor rectal motility often determine faecal impaction with overflow incontinence secondary to continuous elicitation of the anorectal reflex. Overall, high conscious rectal sensory threshold is probably the primary cause of incontinence in about one third of patients [36].
Rectal hypersensitivity is also a frequent mano- metric finding in patients with FI and acts as an inde- pendent trigger of urgency [1, 37, 38]. Chan et al. [1]
found this anomaly in 44% of their patients with urge incontinence. They noticed that when sphincteric dysfunction was associated with rectal hypersensitiv-
ity, patients had a significantly increased stool fre- quency and urgency, a greater use of pads and more lifestyle restrictions compared with patients with iso- lated sphincter dysfunction. The same authors, utilis- ing a prolonged rectosigmoid manometry, investi- gated rectosigmoid motor function, demonstrating that rectal hypersensitivity is often associated with an exaggerated rectosigmoid contractile activity [24].
Rectal hypersensitivity is generally the effect of impaired relaxation properties of the rectum [16, 39, 40]. Other mechanisms have been advocated, such as sensitisation of the extrinsic peripheral pathways [41] or central afferent mechanisms [42], low-grade inflammation [43] and abnormalities in perceptual and behavioural processes causing a state of height- ened vigilance and focused selective attention [44, 45].
Sphincteric Dysfunction
Internal Anal Sphincter Integrity
The IAS is a circular smooth muscle that is responsi- ble for 50–85% of the resting tone [46–48]. Its con- tinuous maximum contraction is due to both intrin- sic myogenic and extrinsic autonomic neurogenic properties [48, 49]. With age, resting pressure pro- gressively decreases because of gradual degeneration of the muscular fibres [50]. Primary degeneration of IAS with atrophy was identified by Vaizey et al. in a group of 45 patients (ten men), and this was the only demonstrable cause of passive incontinence [51].
Structural damage of this muscle is often secondary to anorectal trauma or anal surgery. Several studies have shown that IAS injuries occur in up to 35% of women during childbirth, but in these cases, there is usually an associated damage of the EAS [52].
In these conditions resting tone is low, and EAS contraction may not be sufficient to avoid involun- tary loss of gas or liquid stools, and passive inconti- nence may occur.
More frequently, the IAS appears to be anatomi- cally intact but still unable to maintain a continuous contraction. This has been noticed in about 25% of patients with idiopathic incontinence [53]. With manometric and electromyographic (EMG) studies, we previously noticed that in 92% of patients with neurogenic incontinence, there was a median of four episodes of IAS EMG silence per hour, each lasting a median of 90 s, not associated with sampling mech- anism. This phenomenon was not recorded in the control group [54]. These findings have no clear interpretation, but they probably reflect the func- tional and histological disturbances of the IAS relat- ed to neurogenic damage.
Puborectalis, Anorectal Angle, External Anal Sphincter Integrity
Despite the fact that the PR and EAS have somewhat different innervations (see Chapter 1), they act as an indivisible unit, and for this reason, the PR is now considered as the deepest part of external sphincter.
These muscles form together the triple loop system described by Shafik [55]. Unlike the other skeletal muscles, which are usually inactive at rest, these muscles maintain a continuous unconscious resting tone [56]. This can be explained by the fact that they are also rich in type I fibres, which are responsible for tonic contractile activity [57, 58].
The PR and the anorectal angle (ARA) due to its U-shaped sling contribute to maintaining gross fae- cal continence. It has been postulated that this result is guaranteed by a flap-valve mechanism in which the anterior rectal wall occludes the upper anal canal [59, 60]. However, a study performed by us questioned this theory and suggested that, rather, the PR func- tions by sphincteric occlusion of the anal canal [61].
To demonstrate this, anal and rectal pressures were measured simultaneously together with EAS and PR EMG and synchronously superimposed on an image intensifier displaying the rectum outlined by barium.
In this way, we studied 13 subjects at rest and during a Valsalva manoeuvre, and we noticed that there was a significant rise in rectal and sphincter pressures and EAS and PR EMG. In a further 13 patients, Val- salva manoeuvres were performed during proctogra- phy alone. In all subjects, the anterior rectal wall was always clearly separated from the upper sphincter despite a maximal effort and a rectum filled with suf- ficient liquid to produce a desire to defecate.
The involvement of a flap-valve mechanism has also been hypothesised by Bannister et al. [62]. In fact, they noticed that in the normal population, the pressure gradient between rectum and anus is the reverse of that which would be found if an anterior rectal flap valve maintained continence. Instead, they suggested that continence is normally maintained by a reflex contraction of the EAS.
The EAS response to stimuli (such as increased intra-abdominal pressure, rectal distension or anal dilatation) is contraction. In normal conditions, this can be voluntarily sustained for 40–60 s, a period of time which is generally sufficient for the rectum to accommodate [63]. Inability to voluntary activate the EAS for a sufficient period, as happens when the sphincter has been injured during a vaginal delivery, is the commonest cause of urge incontinence in the Western world. Cumulative injuries may occur and often are associated with a decline in pudendal nerve conduction [64]. Such damage has also been noticed after late caesarean deliveries [65]. Less frequently,
the sphincter appears morphologically intact but still is unable to provide good contraction because of iso- lated neurological impairment [66].
Conclusions
FI is a complex problem, and its pathophysiology is often multifactorial, involving both suprasphincteric and sphincteric dysfunction. Many aspects are still unclear and require further studies. Hopefully, a bet- ter understanding of neurophysiological mecha- nisms will be the key to correctly assessing these dif- ficult patients and to choosing the right treatment.
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Although this chapter by Drs. Zorcolo and Bartolo on the pathophysiology of anal incontinence is quite thorough, I would like to emphasize several points that affect the management of incontinent patients.
The role of transit disorders, which is explained in this chapter, is particularly important in the patho- physiology of anal incontinence. Whereas we are used to having patients consult for diarrhea who, in fact, have anal incontinence (unvoiced symptom), we now frequently receive patients consulting for anal incontinence associated with unrecognized diarrhea. This “clinical impression” is confirmed by objective data. We recently published an article on the frequency of transit disorders (diarrhea or con- stipation) in anal incontinence in 287 consecutive patients in a tertiary care center [1]. One hundred and thirty-four patients (47%) had a transit disorder associated with anal incontinence: 70 patients (24%) had constipation and 64 (22%) had diarrhea. Even if transit orders were not the only cause of anal incon- tinence, treating this disorder cured or improved incontinence in 62% of cases [1]. When managing an incontinent patient, transit disorders must first be investigated before any specific tests are per- formed for incontinence. Treatment of transit disor- ders improves incontinence in more than half the patients, and no further investigations are required.
Indeed, if specific treatment for anal incontinence is proposed (sacral nerve stimulation or artificial bowel sphincter, for example) without first taking into account transit disorders, the risk of failure is high.
The active or passive nature of anal incontinence is valuable clinical information that should be sys- tematically determined in incontinent patients. As the authors mentioned, active anal incontinence sug- gests external anal sphincter defects and/or altered colorectal function (noncompliant, hypersensitive rectum, increased rectosigmoid contractility).
Although passive anal incontinence may suggest internal anal sphincter defects, as mentioned by Zor- colo and Bartolo, in our experience, it is more fre- quently due to incomplete rectal emptying, which
should be managed by suggesting medical treatment to improve emptying at the first intention.
Finally, it is also important to add some informa- tion about the neurological control of continence because of (1) the frequency of neurological lesions causing anal incontinence, and (2) the development of treatments such as sacral nerve stimulation that may improve rectosphincter function by modulating its neurological control. As with vesicoureteral func- tion, neurological control of anorectal function has a specific segmentary spinal organization. This organ- ization results in the automatic emission of stools in paraplegic patients. However, in healthy subjects, anal continence and defecation seem to be, as with urinary continence and micturition, controlled by the cerebral cortex. Different studies based on regis- tered somatosensory evoked potentials or functional imaging have shown that primary and secondary somesthetic areas responsible for spatial discrimina- tion are activated after anal and rectal stimulation [2, 3].
Other areas involved in affect and attention, such as the insula, anterior cingular cortex, and prefrontal cortex, are also activated, especially after rectal stim- ulation. Chronic sacral nerve stimulation seems to modify certain cerebral areas involved in conscious- ness and attention to the feeling of needing to evacu- ate [4]. As with micturition, there seems to be a supraspinal command center located in the brain- stem, probably in a pontic structure near the center for micturition (M center). Thus, a real command center, capable of modifying sphincter tone, has been located in the locus coeruleus [5]. In humans, patients with brainstem lesions have been found to have modified anorectal motricity [6]. This suggests that center(s) in the brainstem (locus coeruleus?) could be similar to that for micturition, responsible for coordination of the sympathetic, parasympathet- ic, and somatic systems innervating the anorectal nerve apparatus. Thus, the(se) center(s) would coor- dinate “harmonious” defecation (rectal contraction, relaxation of the internal and external sphincters resulting in opening of the anal canal). The brain- stem center of micturition could be controlled by
Invited Commentary
Anne-Marie Leroi
cortical areas in the frontal lobe. Indeed, anorectal functional anomalies have been described in patients with frontal lobe lesions [7].
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