Fecal Incontinence and Rectal Prolapse

Techniques of Colorectal Surgery

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Fecal Incontinence and ~ectal Prolapse

Michael M. Henry, M.B., F.R.C.S.*

Rectal prolapse and fecal incontinence can be considered as two end points in the spectrum of pelvic floor disorders (Table 1), the descending perineum syndrome and mucosal prolapse representing the less severe manifestations of these disorders. Although rectal prolapse and fecal incontinence are both well-recognized sequelae of the aging process, functional disorders of the anorectum are increasingly diagnosed in much younger age groups. The last decade has seen a substantial renaissance in the study and management of these disorders combining the academic and scientific talents of proctologists, physiologists, and neurologists.

PHYSIOLOGIC CONSIDERATIONS OF CONTINENCE AND DEFECATION It would be naive to assume that fecal continence is the consequence of a single process. Probably, it is achieved by means of a complex series of factors controlled by spinal and local nerve pathways that can at the same time be regulated by the conscious will. The role of the anal sphincters remains partly uncertain. The fact that the internal sphincter cannot be considered to playa major role is suggested by the fact that only a minor loss of function, if any, occurs subsequent to anal dilatation or anal sphincterotomy. Similarly, division of the external sphincter ring usually is safe provided the deeper section of muscle, namely the puborectalis, is left intact. The puborectalis is generally considered one of the major muscks of anorectal continence, its contraction causing acute angulation between the upper anal canal and lower rectum-the anorectal angle. The precise mechanism and significance of this angle remains in doubt. Parks '4 believed that the angle facilitates a flap valve mechanism, whereby rises in intraabdominal pressure cause the anterior rectal wall to "snap shut" over the upper anal canal, thus excluding the lu'men of the anus from rectal contents. However, Bartolo and associates could not demonstrate any such movement of the anterior rectal wall in a radiological study in a group of subjects performing the Valsalva maneuver. l It can be disputed, however, whether performing the Valsalva maneuver *Consultant Surgeon, Central Middlesex Hospital, London; Director and Honorary Consultant Surgeon, Sir Alan Parks Physiology Unit, St. Mark's Hospital, London; and Senior Lecturer. Academic Surgical Unit, St Mary's Hospital, London

Surgical Clinics of North America-Vol. 68, No.6, December 1988

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Table 1. Spectrum of Pelvic Floor Disorders Descending perineum syndrome Anterior rectal mucosal prolapse Solitary rectal ulcer syndrome Obstructed defecation syndrome Perineal pain syndrome Complete rectal prolapse Urinary incontinence Fecal incontinence

exactly reproduces the protective mechanism operating when intra-abdominal pressure rises such as to threaten anorectal continence. It is quite possible that anorectal angulation contributes to continence in a very simple way analogous to the means by which the water supply to the end of the hosepipe can be interrupted simply by kinking the pipe. The puborectalis and external anal sphincter muscles display the property of continuous electric tone, an observation not seen in most skeletal muscles. This function is a direct consequence of a spinal reflex" and as such can be abolished if the afferent limb of the reflex is destroyed, as seen, for example, in tabes dorsalis, and also if the efferent limb is affected by lower motor-neuron lesions such as cauda equina trauma or tumor. The sensation of a full rectum is important to continence because the individual is alerted to the need for defecation. Decreased awareness of rectal filling is seen in patients with spinal injury, stroke, or dementia, and such patients develop fecal impaction, with inevitable disturbances of anorectal function. The discrimination between flatus and feces is said to be achieved by means of the locally mediated reflex whereby rectal distention causes inhibition of internal sphincter contraction. 5 By this means, a small sample of rectal contents enters the anal canal to make contact with the numerous sensory receptors at the dentate line. If feces are detected, vigorous contraction of the external sphincter propels the sample back to the rectum until such time as defecation can proceed. 6 If defecation is to occur satisfactorily, it is important that the electric tone maintaining pelvic floor contraction be interrupted. This is achieved reflexly in response to "bearing down." The anorectal angle is thereby rendered increasingly oblique so that the anus and rectum virtually remain at 180 degrees to each other. Some authorities believe that rectal emptying is facilitated by means of a peristaltic wave in the rectum. However, this observation has rarely been made in the laboratory when rectal pressures have been monitored except under conditions whereby the rectum has been artificially stimulated by means of an irritant suppository. Probably, the rectum fills by sigmoid peristalsis, and the rectum subsequently empties by simple raising of the intra-abdominal pressure, passage through the anus itself being facilitated by reflex inhibition of the internal sphincter (as well as the external sphincter). At the completion of the defecatory act, there is a rapid return of electric tone to the pelvic floor to restore the anorectal angle. 17

FECAL INCONTINENCE Many factors may disturb the mechanisms of anorectal continence, and the degree of functional disturbance can range from minor soiling to devastating and incapacitating degrees of incontinence. It has become increasingly clear to clinicians over the last decade that this is a common condition, with an estimated prevalence of at least 4.2:1000 rising to more than 10:1000 in the over-65-year age group.21

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It should be stated that incontinence can occur in the presence of morphologically normal anal sphincters and pelvic floor if these should be overwhelmed by excessive stool of loose consistency. Hence, patients with inflammatory bowel disease or diarrhea of bacterial origin are frequently incontinent; in patients with colitis, this is frequently the most distressing symptom. Minor Incontinence This problem can be defined as the occasional soiling of underwear, incontinence to flatus, or both. This clinical state can be the consequence of minor anal disorders such as skin tags or prolapsing hemorrhoids, which can lead to breakdown of local hygiene. Incontinence to flatus is seen in conditions where the internal anal sphincter is rendered deficient, such as rectal prolapse and following anal stretch. These patients are at particular risk of incontinence during bouts of diarrhea, and it is important to inquire into whether incontinence is related to stool consistency. Treatment is usually simple, consisting either of the management or prevention of diarrhea with suitable constipating agents or the treatment of the local anal condition, such as excision of anal tags or hemorrhoidectomy. Major Incontinence The unheralded and frequent passage per anum of fully formed stool is clearly much more disruptive to the patient's attempts to maintain normal life. Such patients are understandably greatly distressed by their condition. Etiology. Any trauma that disrupts the pelvic floor and dislocates the anorectal angle will cause major incontinence. This may be seen after severe bony fractures of the pelvis or impalement injury or after fistula surgery. Research conducted in the physiology unit at St. Mark's Hospital, London, has implicated neurologic damage as a major factor in fecal incontinence. 15 Such injury can be sustained as a consequence of obstructed defecation with excessive straining8 or, more commonly, be associated with direct damage to the pudendal nerves during traumatic vaginal delivery?O For example, a prolonged second stage of labor, the application of forceps, multiparity, and high birth-weight infants all can contribute to neurologic injury, which in turn can cause pelvic floor failure. Patients who have sustained such injury may retain full continence as a consequence of their internal sphincter and of work hypertrophy in the remaining normal external sphincter fibers. However, if such patients later should be subjected to either fistula surgery or anal dilatation, this may be sufficient to convert them "overnight" into incontinent and profoundly dissatisfied patients. Other lower motor-neuron lesions, such as cauda equina tumor, may lead to incontinence, but in our experience at St. Mark's Hospital, these cases are rare. As mentioned earlier, other generalized neurologic disorders such as stroke, multiple sclerosis, and dementia may lead to incontinence partly as a consequence of fecal impaction and partly because suprasegmental and cortical control is disturbed. These higher control mechanisms of continence have not been comprehensively investigated as yet, and the understanding of their true role is incomplete. Clinical Features. A full history and examination should be carried out as would be anticipated in any patient with rectal symptoms. Sigmoidoscopy and perhaps radiologic studies should be considered to enable the exclusion of inflammatory bowel disease or neoplasm. Digital examination may well establish the diagnosis if a poor resting tone (internal sphincter) with or without poor squeeze tone (external sphincter) is discovered. Absence of the anal reflex to clinical testing is indicative of neurologic injury to the external sphincter. 7 Wherever there is doubt about the true status of anal sphincter function, physiological testing should always be considered. 9 Complex neurophysiological study is not always mandatory; often, a

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simple manometric assessment of anal canal function is sufficient for a decision on which to base management. Treatment. By definition, major incontinence causes serious problems for the patient, and frequently serious measures have to be instituted to improve function, as it is unlikely that simple conservative measures will produce satisfactory longterm results. Having said this, I must note that some authorities claim good results from biofeedback techniques,19 but once de nervation damage has been established, it seems unlikely that the remaining muscle fibers can be educated to recover normal function. Biofeedback techniques undoubtedly can be expected to have great value for incontinence of lesser degrees, where work hypertrophy in the remaining healthy muscle could be encouraged. The late Sir Alan Parks 14 devised the operation of postanal repair as an attempt to restore anorectal function by a combination of causing decreased obliqUity of the anorectal angle, increasing the length of the anal canal, and elevating the pelvic floor. In fact, there is little evidence that any of these other than the change in the length of the canal actually takes place as a consequence of surgery. Nevertheless, there is no doubt that many patients are improved by this procedure,lO and some show improved physiological parameters,3 possibly secondary to an improved mechanical advantage of the muscle fibers. In the United States, the surgical procedure most favored is that of the gracilis sling transposition. 16 This operation is technically much more complex than postanal repair and does not restore function with functioning muscle fibers, but it may help by surrounding the anus with unyielding fibrous tissue, a policy similar to that adopted in the Thiersch operation for the treatment of rectal prolapse.

RECTAL PROLAPSE Etiology There is no general agreement or any single theory that can satisfactorily account for this condition, but a number of observations that may be relevant should be considered. Ripstein lB commented that there is a failure of structures surrounding the rectum to provide adequate support, thus resulting in an unstable situation. However, there is no evidence that such a primary defect exists; rather, the physical changes encountered in the surrounding tissues are most likely to be secondary effects caused by traction of the prolapsing rectum. At the time of operation, an abnormally deep pouch between the rectum and the vagina may be observed in patients with prolapse. Moschcowitz12 claimed that such an anatomic abnormality predisposes to the development of herniation of the pouch of Douglas through a defect in the endopelvic fascia onto the anterior rectal wall and subsequently into the rectal lumen. Again, there is no evidence that these are not secondary rather than primary events. Broden and Snellman2 studied the dynamics of the initiation of rectal prolapse by cine radiographic techniques. Lateral films were taken during defecation by patients with rectal prolapse in whom the pelvic anatomy had been outlined by contrast medium in the vagina and rectum. It was found that in all cases, prolapse was initiated by intussusception of the rectum at a level 6 to 8 cm from the anal verge. Electrophysiological studies of the pelvic floor in patients with rectal prolapse have shown that the muscles in many patients are denervated. 13 A possible etiology could be that as a consequence of denervation, the anorectal angle is disrupted, thus favoring prolapse of the anterior rectal wall into the anal canal. This sets up an intussuscepting process that results eventually in complete extrusion of the rectum through the anal canal.

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Clinical Features The complaint of prolapse, which can be either permanent or, alternatively, only a feature of defecation, is frequently superseded by the complaint of fecal incontinence, which is a frequent accompaniment. Occasionally, the prolapse is painful and may present as an emergency with strangulation or rupture. On the other hand, sometimes the patient is totally unaware of the prolapse, which may be noted during routine examination. Sometimes, prolapse is suspected but cannot be demonstrated given the constraints of the examination couch. In these circumstances, the prolapse might be diagnosable with the patient straining in the squatting position or, alternatively, dUring evacuation proctography. Treatment In the young, a conservative approach should be adopted wherever appropriate, as most evidence suggests that the condition resolves spontaneously. Hence, injection sclerotherapy or other local measures to the rectal mucosa in conjunction with measures to improve bowel function should be the initial lines of management. If these fail, surgery might be necessary. Ideally, perineal procedures are preferred to abdominopelvic operations, because the former are less likely to interfere with the autonomic nerves serving sexual function or to cause sterility in the female by instigating pelvic fibrosis. In older age groups, there is usually little to be gained by medical measures alone, so wherever possible, surgical treatment should be recommended, as this is the only effective means of controlling prolapse of any significant degree. A large number of operations have been described, but the most favorable procedures in terms of recurrence rates would be those that involve perirectal implantation. The Wells operation 22 is a procedure whereby the rectum is tethered to the hollow of the sacrum by means of a strip of polyvinyl alcohol sponge. The midpoint of a rectangle of sponge is sutured to the anterior surface of the sacrum, creating two Haps that are then sutured to the anterior aspect of the rectum in such a way that it is nearly completely encircled by material. Similarly, a more favored operation in the U. S. is that described by RipsteinlB whereby TeHon mesh is used to encircle the anterior hemicircumference of the rectum, with the two lateral Haps being sutured to the presacral fascia, as described in the next article. Both operations have found general favor, with low recurrence rates and low mortality rates. However, they are both abdominal operations, and for this reason, some surgeons prefer the operation described by Delorme,4 in which the predominant rectal mucosa is excised per anus. This procedure, although less invasive, does in most series have higher recurrence rates.

SUMMARY The majority of patients who suffer from full-thickness prolapse can be treated successfully and safely. The small proportion who remain incontinent of feces after correction of prolapse may at a later date be helped by postanal repair. If dietary indiscretion and abnormal patterns of defecation are major etiologic factors in this condition, then measures to improve dietary and defecatory habits must be instituted mainly to prevent further problems after the deformity has been cured surgically. There seems no doubt that follOWing rectopexy there is an increased tendency to constipation.

REFERENCES 1. Bartolo DCC, Roe AM, Locke-Edmunds JC, et al: Flap valve theory of anorectal continence. Br J Surg 73:1012-1014, 1986

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2. Broden B, Snellman B: Procidentia of the rectum studied with cineradiography: a contribution to the discussion of causative mechanism. Dis Colon Rectum 11:330-347, 1968 3. Browning GGP, Parks AG: Postanal repair for neuropathic faecal incontinence: correlation of clinical result and anal canal pressures. Br J Surg 70:101-104, 1983 4. Christensen J, Kirkegaard P: Delorme's operation for complete rectal prolapse. Br J Surg 68:537-538, 1981 5. Denny Brown D, Robertson EG: An investigation of the nervous control of defecation. Brain 58:256-310, 1935 6. Duthie HI, Bennett RC: The relation of sensation in the anal canal to the functional anal sphincter: a possible factor in anal incontinence. Gut 4:179-182, 1963 7. Henry MM, Swash M: Assessment of pelvic floor disorders and incontinence by electrophysiological recording of the anal reflex. Lancet 1:1290-1291, 1978 8. Henry MM, Parks AG, Swash M: The pelvic floor musculature in the descending perineum syndrome. Br J Surg 69:470-472, 1982 9. Henry MM, Snooks SJ, Barnes PRH, et al: Investigation of disorders of the anorectum and colon. Ann Roy Coll Surg Engl 67:355-360, 1985 10. Henry MM, Simson JON: Results of postanal repair: a retrospective study. Br J Surg 72(Suppl):S17-S19, 1985 11. Melzack J, Porter NH: Studies of the reflex activity of the external sphincter ani in spinal man. Paraplegia 1:277-296, 1964 12. Moschcowitz AV: The pathogenesis, anatomy and cure of prolapse of the rectum. Surg Gynecol Obstet 15:7-21, 1912 13. Neill ME, Parks AG, Swash M: Physiological studies of the anal sphincter musculature in faecal incontinence and rectal prolapse. Br J Surg 68:531-536, 1981 14. Parks AG: Anorectal incontinence. Proc Roy Soc Med 68:681-690, 1975 15. Parks AG, Swash M, Urich H: Sphincter denervation in anorectal incontinence and rectal prolapse. Gut 18:656-665, 1977 16. Pickrell K: Construction of a rectal sphincter in restoration of anal continence by transplanting the gracilis muscle. Ann Surg 135:853-859, 1952 17. Porter NH: A physiological study of the pelvic floor in rectal prolapse. Ann Roy Coll Surg Engl 31:379-404, 1962 18. Ripstein CB: Treatment of massive rectal prolapse. Am J Surg 83:68-71, 1952 19. Schuster MM: Biofeedback for fecal incontinence. JAM A 238:2595-2596, 1977 20. Snooks SJ, Swash M, Henry MM, et al: Injury to innervation of pelVic floor sphincter musculature in childbirth. Lancet 2:546-550, 1984 21. Thomas TM, Egan M, Walgrove A, et al: The prevalence offecal and double incontinence. Community Med 6:216-220, 1984 22. Wells C: New operation for rectal prolapse. Proc Roy Soc Med 52:602-603, 1959 The Sir Alan Parks Physiology Unit St. Mark's Hospital City Road London ECIV 2PS