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Pelvic Floor
Vol. 16 No 1 | Autumn 2014
Feature
Faecal incontinence


This article is 5 years old and may no longer reflect current clinical practice.

The management of faecal incontinence in the post-obstetric/pelvic floor patient.

An accepted and standardised definition of faecal incontinence (FI) does not exist, but usually it incorporates the involuntary loss of control of bowel motions, occurring with any level of frequency.1 It usually also includes flatus incontinence, particularly in patient-generated definitions.It can also be further stratified by the type of stool lost and frequency. However, the condition means different things to different patients, all of which can be socially disabling and distressing. Typical symptom complexes include one or several of urgency, post-defaecatory soiling, flatus incontinence, insensate soiling and frank faecal incontinence. While the condition may have an obstetric aetiology, it may not necessarily present in the puerperium. In fact, many patients do not manifest the impact of their historical obstetric trauma until decades later, particularly once postmenopausal. Likewise, patients who manifest early faecal continence disorders following obstetric trauma may not develop a long-standing problem. This underscores the multifactorial nature of the continence mechanism and its disorders.

Mechanism of faecal continence

Normal bowel continence is a multifactorial mechanism, which is important to keep in mind when assessing a patient reporting these symptoms. The mechanism can be considered as five main components:

  1. Stool consistency: even the most normal of anal sphincters can fail in the setting of severe diarrhoea, a point familiar to any individual who has experienced gastroenteritis. This becomes an important area to address in all disorders of bowel continence.
  2. Rectal structure and function: pathology of the rectum may present with alteration of continence, be it inflammatory bowel disease, mucosal or rectal prolapse or neoplasia. Indeed ‘postpartum faecal incontinence’ can be the presenting symptom of a rectal tumour (author’s own experience). Likewise, prolapse-related disorders of the rectum, such as distal rectal atonia and rectocele, can produce a reservoir effect that can predispose to leakage.
  3. Anal sphincter structure and function: this refers to function of both the (involuntary) internal anal sphincter (IAS), and the (voluntary) external anal sphincter (EAS). However, it also refers to pelvic floor activity, ensuring that obstetric-related injuries such as levator muscle avulsion and levator ani denervation are considered.
  4. Local reflexes: local and lower motor neurone reflex activity controls much of the involuntary sphincter activity. An example of a local reflex is the rectoanal inhibitory reflex (RAIR), which is essential to anal ‘sampling’ of rectal contents to distinguish gas from liquid and solid. This can be interrupted by a variety of disorders, including rectal prolapse and following colorectal surgery.
  5. Descending neurological control: normal bowel control, of course, relies on normal upper motor neurone function, from frontal lobe to spinal cord. This is an important factor in continence disorders of those in the highest prevalence group, the elderly.2

Pathophysiology

Approximately 20–25 per cent of primiparous women will experience some early postpartum alteration of faecal continence after vaginal delivery.3-4 For the majority of patients, this consists of flatus incontinence, with the rate of frank FI being less than five per cent.4 Typically this has been ascribed to obstetric anal sphincter trauma, which is not an uncommon event. The incidence of a third- or fourth-degree obstetric anal sphincter tear is around one per cent5, although estimates vary as high as nine per cent.6 However, approximately one-third of women show evidence of occult anal sphincter defects on postpartum endoanal ultrasonography7, although the relevance of these is unclear according to a recent longitudinal study.8 This last point reinforces the fact that, while a significant obstetric tear can cause IAS and EAS damage, several other events in parturition can affect bowel continence. Pudendal neuropathy, direct pelvic floor musculo-aponeurotic injury and endopelvic fascia disruption can all affect bowel continence early in the postpartum period. The risk factors for all of these injuries are well-described – vaginal delivery, primipara, large birthweight, prolonged second stage, forceps delivery, epidural usage and racial group. Therefore a sphincter injury may in reality be a ‘marker’ of some or all of the above possible occult injuries coexisting.

Patient assessment

The first task is to explore the patient’s symptomatology – what does the patient mean by ‘incontinence’? Do they have urgency, post-defaecatory soiling, flatus incontinence, insensate soiling or frank faecal incontinence? Urgency is suggestive of typical EAS injury, whereas flatus incontinence is more likely where there is an IAS injury. Frank FI may suggest a more significant combined injury. Insensate soiling and post-defaecatory soiling may have a sphincteric cause, but may also indicate underlying rectal prolapse or rectocele. There is, of course, overlap within these broad categories and more than one symptom may be present. The symptoms are a guide to diagnosis and treatment options. It is important to establish the frequency and severity of the faecal incontinence and, in particular, how it affects the patient’s ability to carry out their normal daily activities. A comprehensive medical, surgical and obstetric history must be taken, including medication usage.

The information available from physical examination is vital. The anus may be patulous at rest, suggestive of IAS dysfunction. It may also be descended at rest, or the perineum may be obviously ‘ballooned’ outwards. Further excessive descent (>3cm) may be noticed on straining. A rectal prolapse may appear on straining. Digital rectal examination can estimate resting and squeeze activity of the anal sphincter, although this does not necessarily correlate with the results of anal manometry.9 Relative contributions of the puborectalis (PR) muscle and EAS to the anal squeeze function can be noted. Asking the patient to bear down during digital  rectal examination can unmask a non-relaxing PR muscle. The same manoeuvre may reveal uterine prolapse or bring a rectal intussusception down onto the examining finger. The presence or size of a rectocele can also be assessed. Rectal loading may be present as a cause of FI owing to faecal overflow. Rigid proctosigmoidoscopy may reveal a luminal or mucosal abnormality, rectal mucosal prolapse or haemorrhoids.

Conservative management

Before any special tests need to be done, the patient may benefit greatly from conservative management. This falls into three main categories – dietary changes, pelvic floor rehabilitation and medications. These can be remembered as the ‘Three Ls’ – low fibre diet, ‘levator’ exercises and loperamide. Consider the following factors:

  • Patients with FI are generally better off with a firm bowel motion rather than soft. This can be achieved by decreasing dietary fibre, and in some cases eliminating fibre supplementation (for example, proprietary Psyllium-based supplements). With correct dietary advice this is achievable while still maintaining a well-balanced diet. Patients with flatus incontinence should be given advice about wind-promoting foods and which to avoid, and also be encouraged to avoid stimulants such as caffeinated beverages, alcohol, nicotine and artificial sweeteners.
  • Pelvic floor rehabilitation includes sphincter exercises, pelvic floor muscle training and biofeedback. A recent Cochrane review has found a paucity of evidence around which of these is superior in faecal incontinence, and whether they offer any benefit over optimal conservative management.10 A single centre randomised trial of this very question showed a good short-to-medium-term response to optimal conservative management, with no extra benefit derived from the addition of biofeedback or sphincter exercises.11 Excluding this latter study, the overall quality of studies in this area is questionable and, certainly, no detrimental effect has been shown. There is room for further investigation in this area, but pelvic floor rehabilitation continues to be encouraged in the interim.
  • Addressing medications is two-fold – examining whether the patient is on any detrimental medications (for example, laxatives, Metformin) and recommending the use of a constipating agent such as loperamide. The effect of loperamide is dual – firming the stool consistency by delaying colonic transit and also improving the tonic activity of the IAS.12 This can be particularly useful in IAS dysfunction, where the patient may report insensate FI or post-defaecatory soiling. Starting at a very low dose (for example, 1mg daily) can avoid an episode of severe constipation that can diminish patient compliance.

Conservative management also includes general advice about perianal hygiene and skin care, and the use of barrier or protective creams such as zinc-based preparations.

Specialist assessment

If conservative measures fail, specialist assessment in a colorectal pelvic floor clinic is warranted. This consists of a review of the history and examination, and special tests. These include anal sphincter manometry, anal sphincter ultrasound imaging and tests of anorectal function, such as anal sphincter electromyography, pudendal nerve terminal motor latency and rectal balloon volume sensation testing. Complementary to this is defaecating proctography, essentially a bowel-emptying X ray. Transperineal ultrasound is an emerging modality, although it is not mainstream in colorectal practice at this stage. Functional magnetic resonance imaging does not as yet have an established role.

Specific treatment

Overlapping anal sphincter repair (OLSR) still has a place in the management of post-obstetric FI, but its role is decreasing. It is most suited to patients who have symptoms of EAS dysfunction, for example, urgency and frank FI. In particular, these patients who also have evidence of anatomical deficits, such as cloaciform defect, make ideal candidates. Patients who undergo OLSR at a younger age have a more sustained result than those over 50 years old.13 In general, OLSR in the elective setting for post-obstetric FI is not undertaken until the patient is one-to-two years postpartum and has completed their family.

Increasingly, posterior compartment prolapse-related disorders are receiving attention as a cause of FI. A symptomatic rectocele can be treated with good effect and low morbidity with a transanal rectocele repair.14 High-grade internal rectal prolapse is being addressed by way of laparoscopic anterior mesh rectopexy, with significant improvements in faecal incontinence and quality of life.15 FI owing to symptomatic rectal mucosal prolapse, likely part of the pelvic organ prolapse spectrum, responds well to office-based local therapy such as rubber band ligation.

Sacral nerve stimulation (SNS) has changed the landscape of faecal incontinence management over the last decade. The percutaneously-placed, continuous S3 nerve root stimulation has proven significant effects on FI symptoms and quality of life. Initially used after failure of conservative and surgical management, it is gradually moving up the FI treatment algorithm, being employed much earlier in a patient’s treatment in a bid to avoid other unnecessary surgeries. For instance, it has proven efficacy whether the EAS is intact or not, hence lessening the need for EAS repair, particularly in patients over 50 years of age where the long-term benefits of OLSR are unclear. It has the advantage of a ‘test’ phase for two weeks, prior to permanent implantation if the patient responds to treatment. The mechanism of action is not well-understood, but is likely to be via improved anal motor and rectal sensory function, via upper and lower motor neurone-mediated effects.16

Transcutaneous posterior tibial nerve stimulation (PTNS) is an emerging potential alternative to SNS. It has the advantage of not requiring a permanent implant and is applied by the patient themselves in the manner of a TENS machine. It is thought to work by neuromodulating pelvic S3 activity, by peripheral stimulation of the nerve. Despite initially promising reports, its efficacy is not yet proven.17

For a small proportion of patients, the above interventions will either be ineffective or contraindicated. In this situation it may be necessary to consider some form of bowel irrigation treatment (either transanal or antegrade via an ostomy) to avoid soiling accidents. These are often intensive to manage and sometimes ultimately diverting colostomy needs to be considered.

Summary

Faecal incontinence is a multifactorial disorder and there is a move away from a ‘sphincter-centric’ treatment approach. Patients may present several years following an apparent obstetric anal injury and this often reflects a multifactorial failure of the continence mechanism. Optimisation of conservative measures can be very effective. In those who fail these simple measures, there is a range of surgical options, with the potential for significant improvements in continence and quality of life.

References

  1. Macarthur C, Wilson D, Herbison P, Lancashire RJ, Hagen S, Toozs- Hobson P, et al. Faecal incontinence persisting after childbirth: a 12 year longitudinal study. BJOG. 2013 Jan;120(2):169-78; discussion 78-9.
  2. Nelson RL. Epidemiology of fecal incontinence. Gastroenterology. 2004 Jan;126(1 Suppl 1):S3-7.
  3. Fynes M, Donnelly VS, O’Connell PR, O’Herlihy C. Cesarean delivery and anal sphincter injury. Obstet Gynecol. 1998 Oct;92(4 Pt 1):496- 500.
  4. Eason E, Labrecque M, Marcoux S, Mondor M. Anal incontinence after childbirth. CMAJ. 2002 Feb 5;166(3):326-30.
  5. Fernando RJ, Williams, A.A., Adams, E.J. The management of third-and fourth-degree perineal tears. Guideline No 29. London, UK: Royal College of Obstetricians and Gynaecologists; 2007.
  6. Dudding TC, Vaizey CJ, Kamm MA. Obstetric anal sphincter injury: incidence, risk factors, and management. Ann Surg. 2008 Feb;247(2):224-37.
  7. Sultan AH, Kamm MA, Hudson CN, Thomas JM, Bartram CI. Anal-sphincter disruption during vaginal delivery. N Engl J Med. 1993 Dec 23;329(26):1905-11.
  8. Frudinger A, Ballon M, Taylor SA, Halligan S. The natural history of clinically unrecognized anal sphincter tears over 10 years after first vaginal delivery. Obstet Gynecol. 2008 May;111(5):1058-64.
  9. Diamant NE, Kamm MA, Wald A, Whitehead WE. AGA technical review on anorectal testing techniques. Gastroenterology. 1999 Mar;116(3):735-60.
  10. Norton C, Cody JD. Biofeedback and/or sphincter exercises for the treatment of faecal incontinence in adults. Cochrane Database Syst Rev. 2012;7:CD002111.
  11. Norton C, Chelvanayagam S, Wilson-Barnett J, Redfern S, Kamm MA. Randomized controlled trial of biofeedback for fecal incontinence. Gastroenterology. 2003 Nov;125(5):1320-9.
  12. Read M, Read NW, Barber DC, Duthie HL. Effects of loperamide on anal sphincter function in patients complaining of chronic diarrhea with fecal incontinence and urgency. Digest Dis Sci. 1982 1982/09/01;27(9):807-14.
  13. Warner MW, Jones OM, Lindsey I, Cunningham C, Mortensen NJ. Long-term follow-up after anterior sphincter repair: influence of age on functional outcome. Colorectal Dis. 2012 Nov;14(11):1380-8.
  14. Abbas SM, Bissett IP, Neill ME, Macmillan AK, Milne D, Parry BR. Long-term results of the anterior Delorme’s operation in the management of symptomatic rectocele. Dis Colon Rectum. 2005 Feb;48(2):317-22.
  15. van Geluwe B, Wolthuis A, Penninckx F, D’Hoore A. Lessons learned after more than 400 laparoscopic ventral rectopexies. Acta Chir Belg. 2013 Mar-Apr;113(2):103-6.
  16. Carrington EV, Knowles CH. The influence of sacral nerve stimulation on anorectal dysfunction. Colorectal Dis. 2011 Mar;13 Suppl 2:5-9.
  17. Horrocks EJ, Thin N, Thaha MA, Taylor SJ, Norton C, Knowles CH. Systematic review of tibial nerve stimulation to treat faecal incontinence.

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