Introduction

Webster’s dictionary defines continence as “the abil-ity to retain a bodily discharge voluntarily”. Theword has its origins from the Latin continere ortenere, which means “to hold”. The anorectum is thecaudal end of the gastrointestinal tract, and isresponsible for fecal continence and defecation. Inhumans, defecation is a viscero somatic reflex that isoften preceded by several attempts to preserve conti-nence. Any attempt at managing anorectal disordersrequires a clear understanding of the anatomy andthe integrated physiologic mechanisms responsiblefor maintaining continence.

Embryology

The primitive gut is formed during the third week ofgestation. The anorectal region in humans derivesfrom four separate embryological structures: thehindgut, the cloaca, the proctodeum, and the analtubercles [1]. The hindgut forms the distal third ofthe transverse colon, the descending colon, the sig-moid, the rectum, and the upper part of the analcanal to the level of the anal valves [2]. The end of thehindgut enters into the cloaca, an endoderm-linedcavity that is in direct contact with the surface ecto-derm. The cloaca is initially a single tube that is sub-sequently separated by caudad migration of theurorectal septum into anterior urogenital and poste-rior intestinal passages. During the 10th week ofdevelopment, the external anal sphincter is formedfrom the posterior cloaca as the descent of the uro-genital septum becomes complete. By the 12th week,the internal anal sphincter is formed from a thick-ened extension of rectal circular muscle [3]. Theproctodeal portion of the cloacal membrane disinte-grates to form the anal tubercles that join posteriorlyand migrate ventrally to encircle a depression,known as the anal dimple or proctodeum. The analtubercles join the urorectal septum and genital tuber-cles to form the perineal body, completing the sepa-

ration between the rectum and the urogenital tract.The upper portion of the anal canal is derived fromendoderm and is supplied by the inferior mesentericartery, which supplies the hindgut. The lower third ofthe anal canal has ectodermal origins and is suppliedby the rectal arteries, which are branches of the inter-nal pudendal artery [2].

Anatomy

Pelvic Floor

The pelvic floor is a dome-shaped muscular sheet [4]that predominantly contains striated muscle and hasmidline defects enclosing the bladder, the uterus, andthe rectum. These defects are closed by connectivetissue anterior to the urethra, anterior to the rectum(i.e., the perineal body), and posterior to the rectum(i.e., the postanal plate). Together with the viscera (i.e.,the bladder and anorectum), the pelvic floor is respon-sible for storing and evacuating urine and stool.

The levator ani and the coccygeus muscle com-prise the two muscular components of the pelvicfloor or pelvic diaphragm. The muscles that consti-tute the levator ani complex are the puborectalis, thepubococcygeus, and the ileococcygeus. These mus-cles originate at different levels of the pubic bone, thearcus tendineus fascia pelvis (condensation of theobturator internus muscle fascia), and the ischialspine. These muscles are inserted at the level of therectum, the anococcygeal raphe (levator plate), andthe coccyx (Fig. 1).

It is unclear whether the puborectalis should beregarded as a component of the levator ani complexor the external anal sphincter. Based on developmen-tal evidence, innervation, and histological studies,the puborectalis appears distinct from the majorityof the levator ani [1]. On the other hand, the pub-orectalis and external sphincter complex are inner-vated by separate nerves originating from S2–4 (seebelow), suggesting phylogenetic differences betweenthese two muscles [5].

Anatomy and Physiology of Continence

Adil E. Bharucha, Roberta E. Blandon

1

Rectum and Anal Canal

The rectum is 15- to 20-cm long and extends from therecto sigmoid junction at the level of third sacral ver-tebra to the anal orifice (Fig. 2). The upper and lower

rectums are separated by a horizontal fold. Theupper rectum is derived from the embryological hindgut, generally contains feces, and can distend towardthe peritoneal cavity [7]. The lower part, derivedfrom the cloaca, is surrounded by condensed extraperitoneal connective tissue and is generally empty

4 A.E. Bharucha, R.E. Blandon

Fig. 1. Pelvic view of the levator ani de-monstrating its four main components:puborectalis, pubococcygeus, iliococ-cygeus, and coccygeus. Reprinted withpermission from [6]

Fig. 2. Diagram of a coronal section ofthe rectum, anal canal, and adjacentstructures. The pelvic barrier includesthe anal sphincters and the pelvic floormuscles. Reprinted with permissionfrom [8]

Chapter 1 Anatomy and Physiology of Continence

in normal subjects, except during defecation. Inhumans, there are fewer enteric ganglia in the rectumcompared with the colon and very few ganglia in theanal sphincter [9, 10].

The anal canal is an anteroposterior slit, with itslateral walls in close contact. The literature describesa longer (approximately 4.0–4.5 cm) “surgical” or “cli-nical” anal canal and a shorter (approximately 2.0 cm)“anatomical” or “embryological” anal canal. The analvalves and the distal end of the ampullary part of therectum mark the proximal margin of the “short” and“long” anal canal, respectively. The proximal 10 mmof the anal canal is lined by columnar, rectal-typemucosa. The next 15 mm (which includes the valves)is lined by stratified, or a modified columnar, epithe-lium. Distal to that is about 10 mm of thick, nonhairy, stratified epithelium (i.e., the pecten). Themost distal 5–10 mm is lined by hairy skin.

The anal canal is surrounded by the internal andexternal anal sphincters. The internal sphincter is athickened extension of the circular smooth musclelayer surrounding the colon that contains discretemuscle bundles separated by large septa [11]. In therectum, the interstitial cells of Cajal (ICC) are organ-ized in dense networks along the submucosal andmyenteric borders. In the internal anal sphincter, theICCs are located along the periphery of the musclebundles within the circular layer.

The external sphincter is composed of superficial,subcutaneous, and deep portions; the deep portionblends with the puborectalis [7]. In men, this trilam-inar pattern is preserved around the sphincter cir-cumference. In contrast, the anterior portion of theexternal sphincter in women is a single muscle bun-dle. External sphincter fibers are circumferentiallyoriented, very small, and separated by profuse con-nective tissue [12].

Nerve Supply to the Pelvic Floor

Autonomic Innervation

The anorectum and pelvic floor are supplied by sym-pathetic, parasympathetic, and somatic fibers [13].Sympathetic pre ganglionic fibers originate from thelowest thoracic ganglion in the paravertebral sympa-thetic chain and join branches from the aortic plexusto form the superior hypogastric plexus. Because thesuperior hypogastric plexus is not a single nerve, thealternative term for this plexus, i.e., “presacralnerve”, should be avoided. The superior hypogastricplexus provides branches to the uteric and ovarian(or testicular) plexus, and divides into right and lefthypogastric nerves. The hypogastric nerves unitewith preganglionic parasympathetic fibers originat-

ing from ventral rami of the second, the third, andoften the fourth sacral nerves to form the inferiorhypogastric plexus, which is located posterior to theurinary bladder. The inferior hypogastric plexusgives rise to the middle rectal plexus, the vesicalplexus, the prostatic plexus, and the uterovaginalplexus. The nerve supply to the rectum and analcanal is derived from the superior, middle, and infe-rior rectal plexus. Parasympathetic fibers in the supe-rior and middle rectal plexuses synapse with post-ganglionic neurons in the myenteric plexus in therectal wall. In addition, ascending fibers from theinferior hypogastric plexus travel via superiorhypogastric and aortic plexuses to reach the inferiormesenteric plexus, ultimately innervating thedescending and sigmoid colon. After entering thecolon, these fibers form the ascending colonic nerves,traveling cephalad in the plane of the myentericplexus to supply a variable portion of the left colon.

Sacral parasympathetic pathways to the colonhave excitatory and inhibitory components [14].Excitatory pathways play an important role incolonic propulsive activity, especially during defeca-tion. In other species (e.g., guinea pig), feces trans-port may be entirely organized by the enteric nervoussystem; spinal and supraspinal reflexes are alsoinvolved in the process [15]. Inhibitory pathwaysallow colonic volume to adapt to its contents, andthey also mediate descending inhibition that initiatescolonic relaxation ahead of a fecal bolus.

Somatic Motor Innervation

Cortical mapping with transcranial magnetic stimu-lation suggests that rectal and anal responses arebilaterally represented on the superior motor cortex,i.e., Brodmann area 4 [16]. There are subtle differ-ences in the degree of bilateral hemispheric repre-sentation between subjects. Motor neurons in Onuf’snucleus, which is located in the sacral spinal cord,innervate the external anal and urethral sphincters.Though they supply striated muscles under volun-tary control, these motor neurons are smaller thanusual α-motor neurons and resemble autonomicmotor neurons [17]; however, the conduction veloci-ty in pudendal nerve fibers is comparable with that ofperipheral nerves. In contrast to other somatic motorneurons in the spinal cord, these neurons are rela-tively spared in amyotrophic lateral sclerosis but areaffected in Shy-Dräger syndrome [18, 19]. Somaticbranches originating from Onuf’s nucleus travel inthe pudendal nerve, the muscular branches, and thecoccygeal plexus. The pudendal nerve branches intoinferior rectal and perineal and posterior scrotalnerves. The inferior rectal nerve conveys motor

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fibers to the external anal sphincter and sensoryinput from the lower anal canal and the skin aroundthe anus. The perineal nerve divides into posteriorscrotal (or labial) branches and muscular branches.The posterior scrotal branches innervate the skin,while muscular branches are distributed to the trans-verse perinei, the bulbospongiosus, the ischiocaver-nosus, the urethral sphincter, the anterior part of theexternal anal sphincter, and the levator ani.

Motor fibers of the right and left pudendal nerveshave overlapping distributions within the externalanal sphincter. Sherrington observed that stimula-tion of the right pudendal nerve caused circumferen-tial contraction of the external anal sphincter [20].Conversely, tonic external sphincter activity, sphinc-ter inhibition during colonic distention, and thecutaneo anal reflex were not affected by sectioningeither pudendal nerve.

The nerve supply to the puborectalis has been thesubject of controversy. The early literature based ondissections by several workers suggested that thepuborectalis was innervated from below by thepudendal nerve, or jointly by the inferior rectal andperineal branches of the pudendal nerve. Therefore,the puborectalis was regarded as being derived notfrom the levator ani but from the external analsphincter. However, an electrophysiological studythat preoperative stimulation of the sacral nervesabove the pelvic floor invariably (i.e., 19 of 20 exper-iments) resulted in electromyogram (EMG) activityin the ipsilateral puborectalis, but not in the externalanal sphincter [5]. Gross dissection studies inhumans, rats, and squirrel monkeys demonstratethat the anal sphincter and levator ani muscle areinnervated by separate nerves [21–23].

Somatic Sensory Innervation

Rectal distention is perceived as a more localizedsensation of rectal fullness, interpreted by the patientas a desire to pass wind or motion. Colonic disten-sion, on the other hand, causes ill-defined discomfortand eventually pain. The anal canal responds to dis-tention and to innocuous mucosal proximo distalmechanical shearing stimuli [24]. In addition tomucosal nerve endings, there are also low threshold,slowly adapting mechanoreceptors in the guinea pigrectum. These intraganglionic laminar endings(IGLEs) detect mechanical deformation of the myen-teric ganglia [25, 26]. The anal canal is lined bynumerous free and organized nerve endings (i.e.,Meissner’s corpuscles, Krause end-bulbs, Golgi-Maz-zoni bodies, and genital corpuscles), perhapsexplaining why it is exquisitely sensitive to lighttouch, pain, and temperature. Sensory traffic is con-

veyed by unmyelinated small C fibers and larger Aδmyelinated fibers that have slow and fast conductionvelocities, respectively [27].

Animal models and clinicopathological findings inhumans suggest that pelvic nerves traveling to thesacral segments are more important for conveyingnon–noxious and noxious colonic sensations thanare lumbar colonic (sympathetic) nerves [12, 28–30].There are more afferent neurons supplying the colonin the sacral, compared with lumbar segments in thecat, i.e., 7,500 versus 4,500 neurons [31, 32]. However,the number of spinal visceral afferent neurons is rel-atively small, i.e., only 2.5% or less of the total num-ber of spinal afferent neurons supply skin and deepsomatic structures [33].

In general, sacral afferents may be better suited forconveying afferent information than are lumbarafferents, as they are more likely to lack resting activ-ity and respond to pressure increments with a widerrange of discharge frequency [34, 35]. Janig and Mor-rison identified three different classes ofmechanosensitive visceral afferents in the cat colon[33]. Tonic afferents fired throughout colonic disten-tion and accurately encoded the intensity of disten-tion between 20 and 100 mmHg. Phasic colonicafferents generally discharged at the onset and occa-sionally at the cessation of a distention stimulus.Tonic afferents were predominantly unmyelinated,slowly conducting C fibers, while most phasic affer-ents were faster-conducting myelinated Aδ fibers.The afferents innervating the anal canal responded toshearing stimuli, but not colonic or anal distention.

Two different theories have been proposed toexplain visceral pain perception. Proponents of thespecificity theory suggested that pain was a distinctsensory modality, mediated by sequential activationof visceral nociceptors and central pain-specific neu-rons in the spinal dorsal horn. However, in the catcolon, Janig and Koltzenburg found no afferent fibersthat were selectively activated by noxious stimuli,arguing against the specificity theory. The alternativehypothesis for pain perception, i.e., pattern or inten-sity theory, attributes pain perception to spatial andtemporal patterns of impulses generated in non spe-cific visceral afferent neurons [24]. However, electro-physiological studies of visceral afferent fibers inother organs, including the colon, have documentedhigh-threshold visceral afferent fibers that onlyrespond to noxious mechanical stimuli. Subsequent-ly, Cervero and Janig reconciled these opposing con-cepts in a convergence model wherein input fromlow- and high-threshold mechanoreceptors convergeon spinothalamic and other ascending tract cells[36]. Physiological processes are generally accompa-nied by low- level activity, mediation of regulatoryreflexes, and transmission of nonpainful sensations.

6 A.E. Bharucha, R.E. Blandon

Chapter 1 Anatomy and Physiology of Continence

High-intensity stimuli increase firing of low-thresh-old afferents and also activate high-threshold affer-ents, thereby activating nociceptive pathways andtriggering pain [36].

More than 90% of all unmyelinated pelvic affer-ents are silent, being activated by electrical stimula-tion, but not even by extreme noxious stimuli [33].Silent afferents can respond to chemical stimuli ortissue irritation, becoming responsive to eveninnocuous mechanical stimuli after sensitization[37]. These neurophysiological changes are de-tectable within minutes after tissue irritation, arelikely to persist for the duration of irritation, andhave been implicated in explaining visceral hyper-sensitivity.

Anal Sphincter Tone and Reflexes

Internal Anal Sphincter

The internal sphincter is primarily responsible forensuring that the anal canal is closed at rest [14, 38].The other contributors to anal resting tone includethe external anal sphincter, the anal mucosal folds,and the puborectalis muscle. Penninckx et al. [39]estimated that anal resting tone was generated bynerve-induced activity in the internal sphincter (45%of anal resting tone), myogenic tone in the internalsphincter (10%), the external sphincter (35%), andthe anal hemorrhoidal plexus (15%). These figuresshould be regarded as estimates, because they wereobtained, in part, from complex studies in which analresting pressure was sequentially recorded beforesurgery (i.e., abdomino perineal resection), aftercurarization, and in the resected specimen beforeand after verapamil. Moreover, the relative contribu-tions of these factors to anal resting tone are influ-enced by several factors, including the size of theprobe and the location at which pressure was meas-ured.

Frenckner and Ihre investigated the contributionof myogenic tone and the extrinsic (sympathetic andparasympathetic) nerves to anal resting tone byassessing anal pressure at rest and in response to rec-tal distention under baseline conditions after lowspinal anesthesia (L5–S1), and after high spinal anes-thesia (T6–T12) [38]. A separate study assessed analpressures before and after pudendal nerve blockade.The decline in anal resting pressure was significantlygreater after high (32±3.2 mm Hg) than low (11±7.1mm Hg) anesthesia or after pudendal nerve blockade(10±3.9 mmHg), suggesting there is a tonic excitatorysympathetic discharge to the internal anal sphincterin humans. However, the anal pressure during rectaldistention was similar among the three groups, sug-

gesting that this excitatory sympathetic dischargedoes not contribute to anal pressure during rectal dis-tention. Conversely, sympathetic stimulation eitherevoked internal anal sphincter relaxation, [40, 41] orcontraction followed by relaxation [42].

Anal resting pressure is not stationary but variesduring the day. In addition to spontaneous relax-ation of the internal sphincter, circadian variationsthat are dependent on the sleep/wake cycle and ultra-dian (~20 to 40 min in length) rhythms that are inde-pendent of the sleep/awake cycle have also beendescribed [43].

Anal relaxation induced by rectal distention [i.e.,the recto anal inhibitory reflex (RAIR)] is mediatedby intrinsic nerves. This reflex is absent inHirschsprung’s disease. The extrinsic nerves are notessential for the reflex, as it is preserved in patientswith cauda equina lesions or after spinal cord tran-section. However, extrinsic nerves may modulate thereflex, as relaxation is more pronounced and pro-longed in children with sacral agenesis [44]. Therecto anal inhibitory reflex is probably mediated bynitric oxide (NO); morphological studies reveal anefferent descending nitrergic rectoanal pathway [45].Other nonadrenergic/noncholinergic neurotransmit-ters, i.e., vasoactive intestinal peptide (VIP) andadenosine triphosphate (ATP), may also participatein the RAIR [46, 47].

External Anal Sphincter

Though resting sphincter tone is predominantlyattributed to the internal anal sphincter, studiesunder general anesthesia or after pudendal nerveblock suggest the external anal sphincter generallyaccounts for ~25% up to 50% of resting anal tone.When continence is threatened, the external sphinc-ter contracts to augment anal tone, preserving conti-nence. This “squeeze” response may be voluntary, orit may be induced by increased intra-abdominalpressure [48] or by merely moving a finger across theanal canal lining [49]. Conversely, the externalsphincter relaxes during defecation.

The only other striated muscles that display rest-ing activity are the puborectalis, the external urethralsphincter, the cricopharyngeus, and the laryngealabductors. Resting or tonic activity depends on themonosynaptic reflex drive, perhaps explaining whyresting anal sphincter tone is reduced, but voluntarycontraction of the external sphincter is preserved intabes dorsalis [50]. The fiber distribution also favorstonic activity; type 1 (i.e., fatigue-resistant, slowtwitch) fibers predominate in the human analsphincter [12], while cats and rabbits predominantlycontain type 2 or fast-twitch muscle fibers [51].

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Puborectalis

The tonically active puborectalis muscle maintainsthe resting anorectal angle. Moreover, puborectaliscontraction during a sudden rise in abdominal pres-sure reduces the anorectal angle, thus preservingcontinence. As noted earlier, electrophysiologicalstimulation studies in humans suggest this muscle issupplied, strictly ipsilaterally, by branches originat-ing from the sacral plexus above the pelvic floor [5].Disruption of the puborectalis inevitably causes sig-nificant incontinence, underscoring the importanceof this muscle in maintaining continence.

Sacral Reflexes

The pelvic floor striated muscles contract reflexly inresponse to stimulation of perineal skin, (i.e., asomatosomatic reflex) or anal mucosa (i.e., a viscero-somatic reflex). The cutaneoanal reflex is elicited byscratching or pricking the perianal skin and involvesthe pudendal nerves and S4 roots. Sacral reflexes alsoregulate anal sphincter tone during micturition.Thus, electrical activity of the internal anal sphincterincreases during urinary bladder emptying inhumans, returning to normal after micturition [53].Conversely, the external anal sphincter relaxes dur-ing micturition in humans, cats, and dogs.

Mechanisms of Continence and Defecation

The mechanisms that maintain fecal continenceinclude anatomical factors (i.e., the pelvic barrier, the

rectal curvatures, and the transverse rectal folds),recto anal sensation, and rectal compliance. Stool isoften transferred into the rectum by colonic high-amplitude-propagated contractions, which oftenoccur after awakening or meals [54]. Denny-Brownand Robertson observed that rectal distentionevoked rectal contraction and anal sphincter relax-ation, facilitating evacuation [28]. The pelvic floor,particularly the puborectalis, also generally relaxesduring defecation (Fig. 3). Simultaneous assessmentsof intrarectal pressures and pelvic floor activity (bymanometry, EMG, or imaging) reveal that increasedintra rectal pressure and anal relaxation are requiredfor normal defecation. However, the relative contri-butions of increased intra-abdominal pressure gen-erated by voluntary effort [55] and rectal contraction[56] to the “propulsive” force during defecation areunclear, partly because a barostat rather than amanometry is necessary to optimally characterizerectal contractions, which are of relatively low ampli-tude. Current concepts suggest that minimal strain-ing to initiate defecation is not abnormal, becausemany asymptomatic subjects strain to initiate defe-cation [57]. However, excessive straining, and partic-ularly a Valsalva maneuver, may impede evacuationbecause while a Valsalva maneuver may increaseintrarectal pressure, the pelvic floor muscles alsocontract, increasing outlet resistance [58]. Thus, it isnecessary to assess the balance between these twosometimes opposing forces by measuring the netrecto anal force during evacuation [59]. One possibil-ity is that the relative contributions of voluntaryeffort and rectal contraction to defecation vary,depending on the circumstances prior to defecation.For example, the voluntary effort may range from

8 A.E. Bharucha, R.E. Blandon

Fig. 3. Sagittal dynamic magnetic resonance images of normal puborectalis relaxation (left panel, subject 1) and puborectal-is contraction (arrow, right panel, subject 2) during rectal evacuation. In both subjects, evacuation was associated with per-ineal descent (2.6 cm in subject 1; 1.7 cm in subject 2) and opening of the anorectal junction. During evacuation, the anorec-tal angle increased by 36° in subject 1 and declined by 10° in subject 2. Reprinted with permission from [52]

Rest Evacuation Rest Evacuation

Chapter 1 Anatomy and Physiology of Continence

being negligible when stool is soft to considerablewhen stool is hard and situated in the upper rectum.

If defecation is inconvenient, it can generally bepostponed. The rectal contractile response to disten-tion normally subsides as the rectum accommodatesor relaxes. The external sphincter and/or puborectal-is can be contracted voluntarily. This contractileresponse requires the ability to perceive stool in therectum and perhaps also in the anal canal. Indeed,the anal sphincter may also relax independently ofrectal distention, allowing the anal epithelium toperiodically “sample” and ascertain whether rectalcontents are gas, liquid, or stool [60].

These mechanisms underscore that defecation isan integrated somato visceral reflex. Indeed, the cen-tral nervous system plays a greater role in regulatinganorectal sensomotor functions compared with otherregions of the gastrointestinal tract. The elaboratesomatic defecation response depends on centersabove the lumbo sacral cord, and probably craniad tothe spinal cord itself. However, Garry observed thatcolonic stimulation in cats induced colonic contrac-tion and anal relaxation, even after destruction of thelumbo sacral cord, and concluded that the gut“seems not to have wholly surrendered its independ-ence” [61].

Pharmacological Considerations

In contrast to non sphincteric regions, sympatheticnerves excite while parasympathetic nerves inhibitthe sphincters. The internal anal sphincter has denseadrenergic innervation in humans and monkeys. It isalso more sensitive to adrenergic compared withcholinergic agonists [62]. Cholinergic agonists eithercontracted or relaxed internal anal sphincter strips inhumans.

Anal administration of exogenous nitrates (i.e.,0.2% glyceryl trinitrate) has been extensively testedand widely used to treat anal fissures, as these areoften associated with increased anal resting tone[63]. Topical calcium-channel blockers (e.g., 0.2%nifedipine or 2% diltiazem) are probably moreeffective than nitrates for treating anal fissures, witha lower incidence of side effects. Bethanecol andbotulinum toxin have also been used to treat analfissures.

The beneficial effects of loperamide in fecal incon-tinence may be attributable not only to a reduction ofdiarrhea, but also to an increase of anal resting tone[64]. The α1 adrenoreceptor agonist phenylephrineapplied to the anal canal increased anal resting pres-sure by 33% in healthy subjects and incontinentpatients [65]. However, phenylephrine did not signif-icantly improve incontinence scores or resting anal

pressure compared with placebo in a randomizeddouble-blind placebo-controlled crossover study of36 patients with fecal incontinence [66].

Surgical Considerations

From a therapeutic perspective, an understanding ofanatomy is particularly important for managing analfistulae, preventing nerve injury during surgical dis-section, and understanding the consequences of rec-tal resection. Left-sided colectomy may result inpostoperative colonic transit delays in the unresectedsegment; this likely represents parasympathetic den-ervation, as ascending intramural fibers travel in aretrograde manner from the pelvis to the ascendingcolon. The sigmoid colon and rectum are also sup-plied by descending fibers that run along the inferiormesenteric artery. These nerves may be disruptedduring a low anterior resection, leaving a denervatedsegment that may be short or long depending onwhether the dissection line includes the origin of theinferior mesenteric artery [67]. A long denervatedsegment is more likely to be associated with non-propagated colonic pressure waves and delayedcolonic transit than is a short denervated segment. Inaddition to colonic denervation, a low anterior resec-tion may damage the anal sphincter and reduce rec-tal compliance [68]; in contrast to anal sphincterinjury, rectal compliance may recover with time [69].Defecation may also be affected after surgical sectionof pelvic nerves in humans [70, 71].

Denonvilliers’ fascia is intimately adherent to theanterior mesorectal fat but only loosely adherent tothe seminal vesicles. During anterior rectal dissec-tion, the deep parasympathetic nerves situated in thenarrow space between the rectum and the prostateand seminal vesicles may be damaged, leading toimpotence [72]. For benign disease, most surgeonswill tend to stay posterior to Denonvilliers’ fascia inan attempt to protect the pelvic nerves. For malig-nant disease, the choice is less straightforward,because dissection behind rather than in front of thefascia may, in theory, be associated with incompleteresection and/or local recurrence.

Because vaginal delivery can damage the analsphincters and the pudendal nerve, up to 10% ofwomen develop fecal incontinence after a vaginaldelivery [73]. The incidence of post partum fecalincontinence is considerably higher (i.e., 15–59%) inwomen who sustain a third-degree (i.e., anal sphinc-ter disruption) or a fourth-degree tear (i.e., a third-degree tear with anal epithelial disruption) [74, 75].The only prospective study that imaged the analsphincters before and after vaginal delivery demon-strated that anal sphincter defects and pudendal

9

nerve injury after vaginal delivery were often clini-cally occult and that forceps delivery was the onlyindependent factor associated with anal sphincterdamage during vaginal delivery [76]. A CochraneReview concluded that restrictive episiotomy policieswere beneficial (i.e., less posterior perineal trauma,less suturing, and fewer complications) comparedwith routine episiotomy policies [77]. However, thereis an increased risk of anterior perineal trauma withrestrictive episiotomy. Both the external and internalanal sphincters may be damaged during a severe per-ineal laceration. When possible, lacerations thatrequire complex repair should be carried out in theoperating room, under regional or general anesthe-sia, with appropriate instruments, adequate light,and an assistant [78]. A randomized controlled studydemonstrated that compared with end-to-end repair,primary overlapping repair of external anal sphincterdefects was associated with a significantly lower inci-dence of fecal incontinence, fecal urgency, and per-ineal pain at 12 months [79]. Though some expertshave suggested that both the internal and externalanal sphincters be repaired, there are no trials com-paring concurrent repair of the internal and externalanal sphincters to repair of the external sphincteralone after obstetric injury [80, 81].

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11

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12 A.E. Bharucha, R.E. Blandon

The comprehensive overview of the anatomy andphysiology of faecal continence by Drs. Bharuchaand Blandon provides an excellent summary of whatis increasingly acknowledged to be a highly complexarea of human biology. Readers should also directtheir attention to Table 1 in Chapter 4 in this book.Historically, both research and clinical interest havefocused on the role of the anal sphincter complex inthe maintenance of continence and the physiologicalchanges within the sphincters and pelvic floor associ-ated with defecation. This is perhaps not surprisingbecause of both the relative inaccessibility to study ofthe colorectum itself and the lack of appropriatephysiological tools to assess function. However, it isbecoming increasingly recognised, principallythrough the efforts of the Mayo Clinic group [1–3],our own group [4–6], and that of others [7, 8], thatthe contribution of normal rectal sensorimotor andbiomechanical function may be equally crucial to themaintenance of continence, as evident from recentstudies showing loss of rectal reservoir function asso-ciated with hypersensitivity, hypocompliance, hyper-contractility, and hyperreactivity in faecal inconti-nence [1–8]. Conversely, an appreciation thatimpaired sensation (hyposensitivity) and hypercom-pliance may underlie (notably, passive) incontinencein a proportion of patients is also gaining momen-tum [9–14]. Introduction of the barostat and stan-dardised protocols for its use has facilitated thisgreater understanding of rectal and colonic dynam-ics, both in health and in disturbed bowel function [2,8, 13]. Evaluation of colorectal motor function,though still primarily restricted to the research set-ting, can now be reproducibly determined by a vari-ety of techniques, including the use of long cathetersplaced either antegrade [15, 16] or retrograde [17, 18]to assess pancolonic motility; other, less invasive,methods to assess colonic contractility and transitwill soon be available [19]. Furthermore, the associa-tion between cerebral activity and bowel function cannow also be studied, and carefully constructed proto-cols employing techniques such as functional mag-netic resonance imaging (f-MRI), the assessment of

cortical evoked potential, etc. [20–24], will provideessential knowledge concerning the brain–gut axis.

Development and use of these physiological toolshas confirmed the importance of suprasphinctericcomponents to continence and defecation. Neverthe-less, the pelvic floor and anal sphincters are “the finalcommon path”, and, certainly in the surgical setting,represent a frequent source of disturbed function.There is no doubt that anal sphincteric disruption isthe main pathogenic mechanism in acquired faecalincontinence, but levator ani failure, including thatof the puborectalis, is increasingly recognised to beof aetiological importance [2, 25, 26]. Nevertheless,failure to study and address those other componentsfundamental to continence will, not surprisingly,lead to poor outcomes following intervention direct-ed solely at sphincteric dysfunction. We recentlydemonstrated how assessment of rectal sensorimotorfunction can direct surgery for both incontinence(rectal “augmentation” with or without electricallystimulated gracilis neosphincter for urgency, associ-ated with rectal hypersensitivity, low rectal compli-ance and exaggerated motor activity [4]) and consti-pation (vertical rectal reduction for megarectumassociated with hyposensitivity and excessive com-pliance [27]), with functional success associated withnormalisation of pathophysiology. It remainsunclear exactly how sacral nerve stimulation (SNS)may improve both colonic motility (in cases of iner-tia [28]) and continence (in incontinence [29]), but itis apparent that the primary effect is certainly not onsphincteric function [30, 31]. Effects on rectal senso-rimotor activity are not consistent [30–32], and itmay be that we simply do not have the right tools tomeasure the physiologically significant effects of SNS(possibly central or spinal [21]) and, ultimately, topredict in whom the technique has a good chance ofpositive effect [29].

Intuitively, anal sensation must be integral to nor-mal continence. It was first systematically assessedby Duthie and Gairns in 1960 [33], since when itsmeasurement and significance has been somewhatquestioned [34]. It may be, however, that it is the

Invited Commentary

Peter J. Lunniss, S. Mark Scott

methodology with which we are currently assessinganal sensation (usually electrostimulation) that isimperfect, as the multitude and density of nerve end-ings subserving different sensations within the analtransitional zone beg a more influential role. Equally,one may argue that the key to normal anal motorfunction is the conjoined longitudinal muscle of theanal canal. In the foetus, this structure is thicker thanthe internal sphincter. As it descends between theinternal sphincter and the true intersphincteric space(medial to the external sphincter), it sends exten-sions medially across the internal sphincter to helpsupport the submucosa of the anal canal (notably theanal cushions), laterally and variably across theexternal sphincter into the ischiorectal fossa andpelvic side wall fascia, and caudally to insert into theperianal skin [35]. It is, indeed, the anatomy of theselateral and distal extensions that define the compo-nents of the external sphincter. Not only does suchan arrangement provide a supporting meshwork forthe other sphincter components, but the differentialresponses to neurotransmitters compared with theinternal sphincter [36] begs a more active functionalrole, its contraction flattening the anal cushions,shortening and widening the anal canal, and evertingthe anal orifice during defecation [37]. Thinning, lossof muscle and fragmentation associated with ageing[38], and perhaps in a more accelerated way, in sub-jects with pelvic floor weakness and prolapse, areundoubtedly of significance. Another important con-sideration was highlighted by the discovery of nona-drenergic, noncholinergic (NANC) fibres subservinginternal anal sphincter contraction, mediatedthrough the neurotransmitter nitric oxide [36, 39,40]. This heralded both the acknowledgement of thesuperspecialised function of this distal continuationof the gut circular muscle and the advent of“reversible chemical sphincterotomy” [41] to reduceresting tone, as well as (less successful) attempts ataugmenting sphincter tone with topical sympath-omimetic agents [42].

Further study is merited concerning the role ofcoordinated colorectoanal activity in normal conti-nence and defecation. It is clear that entry of stool orgas into the rectum initiates a series of events(including elicitation of reflexes), the consequencesof which may or may not be consciously perceived.Investigation of these reflexes may shed further lighton our understanding of the pathophysiology ofincontinence. For example, several parameters ofthe rectoanal inhibitory reflex (RAIR) may be quan-tified, and the RAIR has been shown to be attenuat-ed in patients with faecal leakage [43–45]. The sig-nificance of the rectoanal contractile reflex requiresfurther research, particularly its relation to con-scious perception of anorectal distension [3, 46–48].

Although the gross anatomy of the musculature ofthe anal canal is well known, the same cannot be saidof innervation of the pelvic floor and anorectum.Readers will be already highly familiar with thedebate concerning the influence of pudendal neu-ropathy on continence and defecation, its measure-ment, and usefulness in directing therapy or advisingon prognosis following (especially surgical) interven-tion. Cadaveric studies have demonstrated threevariations in pudendal nerve anatomy [49, 50], andits innervation of the levator ani group of musclesremains controversial. In addition, how much vari-ability and asymmetry there is in external analsphincter innervation has not been explored untilrecently [51]. There is now, however, growing aware-ness that the concept of lateral dominance—asym-metry in the neural contribution of a bilaterallyinnervated midline structure—applies to pudendalnerve innervation [52–54]. This may be particularlyimportant in that damage to the dominant nerve,sustained through whatever injurious mechanism(e.g. traction injury), may leave the individual moresusceptible to dysfunction of those structures inner-vated by the pudendal nerve with resultant inconti-nence. In a similar vein, autonomic innervation tothe pelvic viscera remains poorly studied, particular-ly with reference to the exact neuroanatomy of affer-ent pathways. Consequently, there remains consider-able inconsistency in the literature when describingthe correct neurological nomenclature of afferentneurones and pathways to the rectum. However, sig-nificant advances are being made: Drs. Bharucha andBlandon have highlighted the finding of rectal intra-ganglionic laminar endings (rIGLEs) in the guineapig rectum that serve as slowly adapting mechanore-ceptors [55], and other molecular mechanismsinvolved in mechanosensory transduction have alsobeen identified. For example, rectal sensory nervefibres expressing the transient receptor potentialvanilloid 1 (TRPV1) receptor, which is believed to beinvolved in neuronal signalling, have been found tobe increased in patients with urge faecal incontinenceassociated with rectal hypersensitivity [56]. Theresults of further study of both somatic and auto-nomic innervation may go some way to help resolverecurrent angst and sometimes anger at clinical andresearch meetings!

One other point that deserves consideration is thatfaecal incontinence and “constipation” frequentlycoexist. This perhaps underscores the importance of“normal” defecation to the preservation of conti-nence, in that passive (overflow) faecal leakage, orpostdefecation incontinence, may occur as a conse-quence of incomplete rectal emptying secondary to a“mechanical” (i.e. anatomical, such as large recto-cele, intussusception, megarectum etc.) or “function-

14 P.J. Lunniss, S.M. Scott

Chapter 1 Anatomy and Physiology of Continence · Invited Commentary

al” outlet obstruction (e.g. pelvic floor dyssynergia,poor defecatory dynamics, nonrelaxing pelvic flooretc.). As such, a comprehension of the normalprocess of defecation should be considered funda-mental to the clinical management of patients withfaecal incontinence.

Finally, the complexity of these two biologicalfunctions (continence and defecation), which we alltake for granted until something goes wrong, meansthat the risk factors contributing towards disturbedfunction are often multifactorial and that interven-tions, especially surgical, that aim to restore primari-ly anatomy and thus, hopefully, function, are notassociated with outcomes that are always satisfactoryto the patient. As professionals involved in healthdelivery, emphasis on research must continue andexpand as the basis for effective, targeted and indi-vidualised treatment.

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16 P.J. Lunniss, S.M. Scott