The Musculo-Elastic Theory of anorectal function and dysfunction
PETER PETROS (*) - MICHAEL SWASH (**)
(*) Royal Perth Hospital, University of Western Australia
(**) Dept of Neurology, The Royal London Hospital, London, UK
Abstract:The Musculoelastic Theory of anorectal function and dysfunction states "Anorectal dysfunction in the female is mainly caused by
lax suspensory ligaments inactivating anorectal muscle forces". Anorectal closure. The rectovaginal fascia inserts into perineal body, levator
plate (LP) and the uterosacral ligaments . Contraction of levator plate stiffens rectovaginal fascia and both walls of rectum. Contraction of
longitudinal muscle of the anus (LMA) against the uterosacral ligaments stretches the rectum around a contracted puborectalis muscle, to create
the anorectal angle and closure. Defaecation. Puborectalis relaxes. Posteriorly acting LMA/LP vectors open out the anorectal angle; forward
contraction of the pubococcygeus vector stiffens the perineal body, and anterior wall of anus; the rectum empties.
Pathogenesis. Is similar to that described by the Integral Theory 1 for urinary incontinence: damaged ligaments decrease the force of opening
and closure vectors. Surgery according to this theory. Reinforcement of damaged ligaments with precisely implanted polypropylene tapes
restores structure and function.
Key words: Fecal incontinence, Constipation, Ligament laxity, Connective tissue, Anatomy, Integral Theory.
EXISTING CONCEPTS FOR NORMAL ANORECTAL
The mechanics of defecation and fecal continence are poorly understood. Valvular theories for continence 2 rely on raised intra-abdominal pressure to force the anterior wall of the rectum downwards to close off the anorectal junction. Such theories are not consistent with EMG and radiological data which suggest a striated muscle sphincteric mechanism.3
It has been demonstrated that puborectalis and external anal sphincter muscles contract during effort, indicating a role for both in fecal continence.4 The internal anal sphincter is also said to be important for feces continence.5 The mechanism of defecation is even more poorly understood. According to one description,3 feces enter the anal canal, stimulate stretch receptors and produce the urge to defecate. The internal and external anal sphincters relax, decreasing the pressure within the anus.
The rectum contracts and with the assistance of raised intraabdominal pressure (Valsalva) expels the feces. Shafik 6 suggested an active muscular mechanism for anorectal opening and closure. In his proposal, during straining, the puborectalis, acting as the upper part of a triple loop system, contracts to close off the anal canal. No role is assigned by Shafik for levator plate contraction during anorectal closure. According to Shafik, during defecation, the puborectalis muscle relaxes, the levator plate contracts, and the "suspensory sling" lifts upwards to open out the anorectal canal prior to evacuation by rectal detrusor contraction.
MAJOR EXISTING HYPOTHESES FOR CAUSATION OF FECAL INCONTINENCE (FI)
Major hypotheses advanced for fecal incontinence causation include damage to the external anal sphincter (EAS), stretch-related pudendal nerve damage 7 and internal anal sphincter (IAS) injury.5
These causes are by no means exhaustive. Bharucha,8 in a recent review article quoted the following causes: Anal sphincter weakness Injury: obstetric trauma; Related to surgical procedures (e.g., hemorrhoidectomy internal sphincterotomy, fistulotomy, anorectal infection); Nontraumatic: scleroderma, internal sphincter thinning of unknown cause; Neuropathy stretch injury: obstetric trauma, diabetes mellitus; Anatomical disturbances of pelvic floor: fistula, rectal prolapse, descending perineum syndrome; Inflammatory conditions: Crohn's disease, ulcerative colitis, radiation proctitis; Central nervous system disease: dementia, stroke, brain tumors, spinal cord lesions, multiple system atrophy (Shy Drager's syndrome), multiple sclerosis; Diarrhea: Irritable Bowel Syndrome, postcholecystectomy diarrhea.
The majority of the above "causes" would appear to implicate either the external or internal anal sphincter in causation, or a disturbance of the stretch receptors or their cortical control paths. The Muculo-Elastic Theory concerns mainly the "idiopathic group". Like the nerve damage theory,7 the Musculo-Elastic Theory attributes bowel and bladder dysfunction to muscle insufficiency. Unlike the nerve damage theory,7 such muscle insufficiency is deemed mainly consequent upon laxity of the suspensory ligaments (*), the effective anchoring points of the closure muscles of urethra and anorectum. (*) and so it is potentially reversible with ligament repair.
THE COMMON CAUSATIVE RELATIONSHIP BETWEEN ANORECTAL DYSFUNCTION AND OTHER PELVIC SYMPTOMS
In a study published in 1999,9 simultaneous cure of urinary
stress and idiopathic fecal incontinence was observed
in a group of 25 patients following a midurethral sling procedure
performed for cure of stress incontinence. This operation
created a collagenous pubourethral neoligament; only
connective tissue was repaired. Normal internal anal sphincters
were found in 72% of these patients, and normal external
anal sphincters in 100%.9 Three patients from this group
subsequently reported recurrence of their fecal incontinence
simultaneously with occurrence of vaginal vault prolapse
and posterior zone bladder symptoms (Fig.
Repair of the prolapse with a posterior sling in the position of the uterosacral ligaments (USL) cured the prolapse, the urinary and the feces incontinence.9
Three hypotheses followed naturally from that study.
- Both pubourethral and uterosacral ligaments were essential for anorectal closure.
- The same muscles acting against these ligaments for bladder/urethral closure 1 were most likely also involved in anorectal closure.
- Damaged connective tissue was most likely a major
cause of both urinary and idiopathic fecal incontinence, as
only connective tissue was repaired.
According to this theory, co-ordinated muscle forces acting against competent suspensory ligaments selectively open or close the anorectal tube. It is damage to these ligaments and their fascial attachments which cause continence and evacuation problems.
THE KEY LIGAMENTS OF THE PELVIC FLOOR (Figs. 2, 3)
The Pubourethral Ligament (PUL)
The pubourethral ligament (PUL) originates from the lower end of the posterior surface of the pubic symphysis, and descends like a fan to insert medially into the midurethra and laterally into the pubococcygeus muscle.11, 12
PUL is the effective anchoring point for m.pubococcygeus and levator plate. The Arcus Tendineus Fascia Pelvis (ATFP) The ATFP arises just superior to the pubourethral ligament (PUL), and inserts into the ischial spine.
The vagina is suspended across the ATFPs. The muscle forces (arrows, Fig. 3) , tension the ATFP and vagina. The Uterosacral (USL) and Cardinal Ligaments The uterosacral ligaments (USL) suspend the cervix and apex of the vagina. USL is the effective anchoring point for the longitudinal muscle of the anus 'LMA' 13, 14 and through its attachments to the rectovaginal fascia, levator plate 'LP' (Fig. 3) .
The cardinal ligaments "CL", insert into the anterior portion of cervical ring, and they attach the cervix laterally to the pelvic wall. The perineal body (PB) is approximately 4 cm long, and it occupies half the posterior vaginal wall. Its components are similar to ligaments, collagen, elastin, smooth muscle blood vessels nerves, but it also has striated muscle, being attached to all the superficial and deep perineal muscles.
THE MUSCLES OF THE PELVIC FLOOR (Figs.
There are 3 layers of muscles (Fig. 2) .
Upper layer. The anterior part of pubococcygeus muscle (PCM) inserts into the lateral part of the distal vagina, and contracts forwards against PUL and the perineal body (PB).1 The levator plate complex (LP) inserts into the posterior wall of the rectum, and it stretches the organs backwards.1 It acts against PUL, USL, and PB (Fig. 3).
Middle layer. The longitudinal muscle of the anus (LMA) connects levator plate, pubococcygeus and puborectalis to the external anal sphincter.13, 14 It creates a downward vector, which acts against USL, (Fig 3).
The puborectalis muscle (PRM) originates just medially to PCM. It is closely applied to the lateral walls of the rectum and inserts into its posterior wall. As well as its pivotal role in anorectal closure, the puborectalis muscle is the voluntary muscle activated during 'squeezing' when it elevates the whole levator plate (LP) and also, rectum, vagina and bladder (see X rays, study No 1, in this issue).
Lower (anchoring) layer. The perineal body is the key anchoring point for contraction of bulbocavernosus and the external anal sphincter (EAS). The deep transverse perinei stabilizes the perineal body laterally. As well as being a sphincter in its own right, the EAS is the tensor of the perineal body and principal insertion point of the longitudinal muscle of the anus. The bulbocavernosus stretches and anchors the perineal body. Between EAS and the coccyx is the postanal plate, a tendinous structure which also contains striated muscle. It is proposed that the internal anal sphincter' role is limited to creating water and air-tight closure. A new dynamic musculoelastic sphincter for anorectal closure (Fig. 3).
A new dynamic musculoelastic sphincter for anorectal closure (Fig. 3).
The backward/downward muscle forces ('LP/LMA' arrows) stretch the rectum and rectovaginal fascia (RVF) around a contracted puborectalis muscle (PRM) to create the anorectal angle, and anorectal closure. Contraction of the forward force ('PCM' arrow) and perineal membrane muscles, tension and stabilize the perineal body (PB) and anterior wall of anus. Contraction of the external anal sphincter (EAS) creates a firm anchoring point for LMA, constricts the lower end of the anal canal, and tensions the perineal body. A similar mechanism closes urethra and bladder neck (Fig. 3).
Opening (defecation). With reference to Fig. 3, PRM relaxes. Anorectal stretch and volume receptors initiate a defecation reflex. Levator plate (LP) contraction stretches the posterior rectal wall backwards to full extension against the perineal body, and uterosacral ligament (USL). LMA (downward vector) contracts against the uterosacral ligament 'USL', to open out the tensioned posterior wall and anorectal angle (broken lines, Fig. 3).
Forward contraction by pubococcygeus 'PCM' 'splints' the perineal body and anterior anal wall to convert the anus to a semi-rigid tube. This "semi-rigidity" allows the posterior anal wall to be firmly pulled open, broken lines. This action reduces the internal resistance of the tube, facilitating the expulsion of feces during rectal contraction. A similar mechanism opens out the posterior wall of the urethra during micturition.1 During defecation, we hypothesize that at least initially, EAS must contract for LMA contraction to open out the anorectal angle (broken lines, Fig. 3).
EAS then relaxes once the fecal bolus reaches the lower part of the anus, whereupon LP contraction would stretch the rectum up over the bolus, facilitating evacuation.
Voluntary puborectalis muscle 'PRM' contraction stretches the anus and rectum like a trampoline, to support the feces bolus, relieving its pressure on the stretch receptors. This decreases the afferent stimuli to the cortex, and so prevents the activation of the defecation reflex.
The role of collagen in anorectal dysfunction. The pelvic
muscles contract against pelvic ligaments to open or close
the anal canal. The main structural element of the pelvic
ligaments is collagen.
Collagen may stretch or weaken with age or childbirth (circles, Fig. 4), or it may be congenitally weak.15
A muscle requires a firm insertion point to contract efficiently. As the suspensory ligaments are the effective insertion points of all three directional forces (arrows, Fig. 3), both closure (continence) and opening (defecation) may be compromised.
This explains how FI and "constipation" may co-exist in the same patient. Childbirth may cause dislocation of the collagenous "glue" connecting the mucosa to the anal serosa. Mucosal prolapse or anterior wall intussusception may cause a "motor" type of fecal incontinence by causing a constant stimulation of nerve receptors in the anal mucosa. The effect of age and pregnancy on connective tissue Age-related degenerations of connective tissue superimposed on childbirth damage explain the late onset of feces incontinence (FI) in most patients. Connective tissue in the pelvis is hormonally sensitive 16 and loses elasticity with age 17 and childbirth.
This may explain the incidence of FI during pregnancy (hormonal depolymerization of collagen), after childbirth (connective tissue damage), and in old age (connective tissue degeneration). Cure of nulliparous females by reinforcing the pubourethral ligament with a midurethral polypropylene sling 9 further supports a connective tissue hypothesis, in this instance, genetic ligamentous laxity. A relationship between genetic connective tissue dysfunction and stress incontinence has been previously described.15
Fecal incontinence With reference to Fig. 3, the pubourethral (PUL) and uterosacral (USL) ligaments are the effective anchoring points for backward muscle force, levator plate (LP), and USL for the downward muscle force, longitudinal muscle of the anus (LMA). Laxity in either ligament may invalidate anorectal closure by the 2 directional muscle forces, LP and LMA (arrows, Fig. 3).
Minor degrees of inadequate closure may lead to leakage of wind; greater degrees to liquid or solid feces incontinence. Clearly a severely damaged external anal sphincter muscle may also cause FI. This is a different type of FI to that proposed by this theory, and will not be cured by using implanted tapes to repair damaged suspensory ligaments, Fig. 5 .
In addition to weakening its direct sphincter effect, a damaged EAS would invalidate the rotation of rectum around anus required to create the anorectal angle and watertight closure. Bowel emptying disorders With reference to Fig. 3, laxity in the suspensory ligaments, may weaken the forces stretching open the posterior anorectal wall (downward/backward arrows, 'LP/ LMA'), so the canal may not be fully stretched open during defecation.
Laxity or rupture of the rectovaginal fascia (rectocoele) or perineal body may also prevent the levator plate from stretching the rectal wall into a semi-rigid structure. Inability to open out the tube may vastly increase the intraluminal resistance to feces evacuation, given that the resistance within a tube varies inversely with the 4th power of the radius, Poiseuille's law. All this may lead to bowel emptying difficulties, which may lead to straining, which may further damage the connective tissue, if not the nerve supply of the organ.
The patient interprets this evacuation disorder as "constipation". The feces may bulge into the vaginal cavity. In some instances the patient may need to "manually assist" evacuation by pressure on the perineal body, or the posterior vaginal wall. In this context, the role of the perineal body (PB) is very important. Not only does the PB occupy 50% of the posterior vaginal wall, it is the main anchoring point of the rectovaginal fascia, and therefore, levator plate, (Fig. 3), both critically important for the rectal stretching which precedes evacuation. Mucosal prolapse and intussusception with reference to Fig. 4, there is a close interconnection between the uterosacral ligaments and rectovaginal and prerectal fascia.
The uterosacral ligaments suspend the fascial attachments of vagina and anterior rectal wall. Laxity in the uterosacral ligaments may cause sagging of the anterior rectal walls. Inability to empty may cause straining, and this, in turn, may cause intussusception of the anterior rectal wall. Abendstein has reported a high rate of surgical cure of anterior rectal intussusception with a posterior polypropylene sling (n = 48) plus repair of rectovaginal fascia and perineal body, validated by post-operative evacuating proctography (Part 2, study No 12).
Diagnosis of the site of ligamentous damage is made
using the pictorial algorithm (Fig.
As fecal incontinence may be caused by connective tissue damage in either the anterior or posterior zone, the presence of associated urinary and other symptoms (Fig. 1), helps designate the zone of damage. The site of damage may be confirmed by vaginal examination. Even minor degrees of damage may cause FI, or other pelvic floor symptoms.
New pelvic floor exercises adding squatting exercises18 and more recently, sitting on a rubber "fitball" instead of a chair to strengthen the slow-twitch muscles, have demonstrated an up to 78% improvement in patients with abnormal bowel symptoms such as constipation. The anatomical principle underlying these exercises is that strengthening a muscle also strengthens its ligamentous (or tendinous) insertion points. Clearly such techniques are contraindicated in patients with significant organ prolapse.
Based on the Diagnostic Algorithm (Fig. 1) and clinical examination, polypropylene tapes are inserted to re-inforce damaged ligaments, Fig. 5.
In addition to previous data9 greater than 80% improvement for patients with FI has been noted by Hocking (Study 9), Petros & Richardson (Studies No10 & 11), and Abendstein (Study No 12).
The theory predicts that lax ligamentous insertion points may cause suboptimal muscle contraction, and therefore inability to open or close the anorectal tube. According to Popper's deductive criteria,10 an essential "next step" in the validation of this theory is the objective demonstration of the directional muscle vector forces, and their ligamentous anchoring points, during anorectal closure and opening (defecation) using X ray video or other dynamic imaging methods; then to directly test the hypothesis prospectively in patients with idiopathic fecal incontinence by surgically implanting polypropylene tapes to reinforce the anterior and posterior suspensory ligaments.
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Competing interests: None.
Prof. Peter Petros,