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Section VII • Anorectal Physiology Testing 317
anal sphincter mechanism and the physiology of defecation. XXIX. Reversion to normal defecation after
combined excision operation and end colostomy for
rectal cancer.Am J Surg 151:278–284
14. Shafik A (1987) A new concept of the anatomy of the
anal sphincter mechanism and the physiology of defecation. XXVIII. Complete rectal prolapse: a technique
of repair: Coloproctology 9:345–352
15. Shafik A (1984) A new concept of the anatomy of the
anal sphincter mechanism and the physiology of defecation. XX. The pelvic double-sphincter control complex. Theory of pelvic organ continence with clinical
application. Urology 23:611–618
16. Shafik A (1997) Study on the origin of the external
anal, urethral, vaginal and prostatic sphincters. Int
Urogynecol J Pelvic Floor Dysfunct 8:126–129
17. Shafik A (1998) A new concept of the anatomy of the
anal sphincter mechanism and the physiology of defecation. Mass contraction of the pelvic floor muscles.
Int Urogynecol J Pelvic Floor Dysfunct 9:28–32
18. Shafik A (1982) A new concept of the anatomy of the anal
sphincter mechanism and the physiology of defecation.
XVII. Mechanism of defecation. Coloproctology 4:49–54
19. Shafik A (1991) Constipation. Some provocative
thoughts. J Clin Gastroenterol 13:259–267
20. Shafik A (1991) Straining-levator reflex. The description of a new reflex and its clinical significance.
Coloproctology 13:314–319
21. Denny-Brown D,Robertson EG (1935) An investigation
of the nervous control of defecation. Brain 58:256–310
22. Shafik A (1990) A new concept of the anatomy of the
anal sphincter mechanism and the physiology of defecation. XLII. Recto-puborectalis reflex. Coloproctology
12:170–172
23. Shafik A (1993) The recto-levator reflex. The description of a new reflex and its clinical application.
Preliminary report. Clin Physiol Biochem 10:13–17
24. Shafik A (1991) Levator-puborectalis reflex: Its role in
elimination. Pract Gastroenterol 15:28–35
25. Mahieu P, Pringot J, Bodart P (1984) Defecography 1.
Description of a new procedure and results in normal
patients. Gastrointest Radiol 9:247–251
26. Mahieu P, Pringot J, Bodart P (1984) Defecography 2.
Contribution to the diagnosis of defecation disorders.
Gastrointest Radiol 9:253–261
27. Barnes PR, Lennard-Jones JE (1984) Patients with constipation of different types have difficulty in expelling
a balloon from the rectum. Gut 25:562–563
28. Lestar B, Penninckx FM, Kerremans RP (1989)
Defecometry. A new method for determining the
parameters of rectal evacuation. Dis Colon Rectum
32:197–201
29. Shafik A (1991) Straining puborectalis reflex:
Description and significance of a “new” reflex. Anat
Record 229:281–284
30. Shafik A, Khalid AM (1992) Fecoflowmetry in fecal
incontinence. Eur Surg Res 24:61–68
31. Shafik A, Khalid A (1993) Fecoflowmetry: A new
parameter assessing rectal function in normal and
constipated subjects.Dis Colon Rectum 36:32–42
32. Shafik A, Abdel-Moneim K (1992) Fecoflowmetry: A
new parameter assessing rectal function. Int Surg
77:190–194
33. Shafik A, El-Sibai O, El-Gohary H et al (1999) Residual
rectal fluids in normal, constipated and incontinent
subjects. Techn Coloproctol 3:19–21
34. Shafik A,Khaled AM (1991) Rectometry.A new method
assessing rectal function. Coloproctology 13:237–243
35. Shafik A (1992) Rectal neck pressure measurement.
Technique and role in assessment of rectal neck disorders. Coloproctology 14:42–49
36. Shafik A (1992) Water enema test. A parameter for
assessing rectal function. Pract Gastroenterol 16:
24J–24P
37. Shafik A (1992) Fecal leak test. Simple test for assessing
degree of fecal incontinence. Gut [Suppl 2] 37: A25, 302
38. Shafik A, Nour A,Abdel-FattahA (1995) Transcutaneous
electrorectography. Human electrorectogram from surface electrodes. Digestion 56:479–482
39. Shafik A (1997) Deflation reflex.Description and clinical significance. Anat Rec 249:405–408
40. Shafik A, El-Sibai O (2001) Rectal inhibition by inferior rectal nerve stimulation in dogs: Recognition of a
new reflex: The ‘voluntary anorectal inhibition reflex.
Eur J Gastroent Hepatol 13:413–418
41. Shafik A, El-Sibai O (2000) The anocavernosal erectile
dysfunction syndrome. II. Anal fissure and erectile
dysfunction. Int J Import Rcs 12:279-283
42. Shafik A (2001) Injured external anal sphincter in
erectilo dysfunction. Andrologia 33:35-41
SECTION VIII
Treatment Options
for Fecal Incontinence
VIII.1.
Introduction
G.A. Santoro, G. Di Falco
The treatment of incontinence remains somewhat
empirical although considerable advances have
been made in understanding the pathophysiology
of the condition in recent years [1].The purpose of
this section is to characterize this disorder and to
put into perspective the numerous procedures
that have been described for the treatment of this
condition [2–6].
Normal continence depends on cognitive func-
tion, stool volume and consistency,colonic transit,
SIGMOID COLON:
contractions retard
progress of stool
RECTUM:
compliance
and sensation
of urgency
PUBORECTALIS MUSCLE:
phasis contractions and
ano-rectal angle
rectal compliance, anorectal sensation, anorectal
reflexes, and sphincter control (Fig. VIII.1). Anal
incontinence is the inability to control the release
of bowel contents,and it can be partial (liquid and
gas) or complete (solid). It is important to differentiate between minor levels of functional loss and
the clinical state in which there is a serious disruption of normal life. Minor degrees of anal incontinence are defined as the occasional fecal staining
of underwear (fecal leakage or soiling or seepage),
INT. ANAL SPHINCTER M.:
passive barrier
to leakage
POSTERIOR
EXT. ANAL SPHINCTER M.:
phasic contractions
ANTERIOR
Fig. VIII.1. Pelvic floor components
involved in the mechanisms for preserving continence
322 Benign Anorectal Diseases
Table VIII.1. Grading of fecal incontinence according
to Parks [4]
Grade
Parks I Fully continent
Parks II Soiling or incontinence to gas
Parks III Incontinence to liquid stool
Parks IV Incontinence to solid stool
incontinence of flatus, incontinence in the presence of loose stool only, or rectal urgency. These
symptoms are relatively common, especially with
increasing age, and most patients can be satisfactorily managed by nonoperative therapy (diet,
drugs, bowel training, sphincter exercises,
improved hygiene). Major incontinence is defined
as the frequent and inadvertent voiding per anum
of formed stool and represents the most severe
form of fecal incontinence. Several incontinence
severity scales have been described in the last 10
years [4–9]. Parks [4] was one of the first to
describe such a system (Table VIII.1). This system
is very simple, and it is one of the most frequently
utilized. However, it does not take into account the
frequency of symptoms. St. Mark’s incontinence
scoring system proposed by Vaizey et al. [7] measures frequency and consistency and, in addition,
includes questions on the use of pads or plugs,
antidiarrheal medications, interference with daily
activities, and association of incontinence with a
strong urge to defecate (Table VIII.2) [7].
There are many and varied causes of inconti-
nence, and it is important to categorize the etiolo-
gy of incontinence so that an appropriate thera-
peutic approach can be selected (Table VIII.3)
[10]. Diagnosing the cause and assessing the
severity of the condition precede any treatment
[10–12]. Anorectal physiology investigations, such
as endoanal ultrasound [12–18], anal manometry
[19, 20], pudendal nerve terminal motor latency
[21], mucosal electrosensitivity [22], electromyography [23–25], and magnetic resonance [26–27]
help the clinician in determining the nature of the
incontinence. Most patients have acquired anal
incontinence secondary to obstetric laceration
[28–36], previous anorectal surgery (such as fistulotomy or hemorrhoidectomy) [37–40], or trauma
(such as impalement).These injuries are the most
amenable to surgical management,specifically the
anal sphincteroplasty [31–44]. Other causes of
incontinence, such as long-standing prolapse or
third- to fourth-degree hemorrhoids, often
respond to treatment of the primary disorder
alone. More difficult to treat are the neurogenic
injuries, such as those resulting from massive
neuromuscular trauma, myelomeningocele or
demyelinating diseases of the spinal cord, and diabetic neuropathy. A procedure suited to injuries of
this type is to create a neosphincter with the gracilis muscle transposition [45–49] or the artificial
bowel sphincter [50].
Inflammatory condition, such as ulcerative
colitis, Crohn’s colitis, amebic colitis,or radiationinduced proctitis, can cause incontinence by the
diarrhea or because of the decreased compliance
of the rectum secondary to inflammation or scarring, and treatment should be aimed at the primary problem.
Sacral nerve stimulation represents a new
therapeutic approach for the specific group of
patients with idiopathic fecal incontinence in
Table VIII.2. St. Mark’s incontinence score according toVaizey et al.[7]
Clinical condition Never Rarely Sometimes Weekly Daily
Incontinence to solid stool 0 1 2 3 4
Incontinence to liquid stool 0 1 2 3 4
Incontinence to gas 0 1 2 3 4
Alteration in lifestyle 0 1 2 3 4
No Yes
Need to wear a pad or plug 0 2
Taking constipating medicines 0 2
Lack of ability to defer defecation for 15 min 0 4
Section VIII • Treatment Options for Fecal Incontinence 323
Table VIII.3. Etiology of fecal incontinence
Category Mechanism Common causes
Functional Rapid transit Irritable bowel syndrome, inflammatory bowel disease,
tumors
Pelvic floor dyssynergia Idiopathic, spinal cord injury
Psychological Dementia, psychosis, behavioral
Sphincter weakness Sphincter muscle injury Obstetrical trauma, accidental trauma, surgical trauma
Pudendal nerve injury Obstetrical trauma, idiopathic, peripheral neuropathy
Central nervous system injury Spina bifida,spinal cord injury,cerebrovascular accident
Sensory loss Afferent nerve injury Diabetic neuropathy, spinal cord injury
which traditional pelvic repair would not be effective [51–53]. An innovative treatment is radiofrequency energy delivered to the anal sphincter,creating precise submucosal thermal lesions. Over
time, these lesions are resorbed, and the tissue
contracts [54–55]. In patients in whom there is no
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it is impractical to create a neosphincter, a defunctioning stoma is often the best option.
There now follows a critical appraisal of the
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324 Benign Anorectal Diseases
dimensional endoanal sonography in assessing anal
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(2005). Three-dimensional anal endosonography may
improve diagnostic confidence of detecting damage to
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24. Tjandra JJ, Milsom JW, Schroeder T, Fazio VW (1993)
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26. Williams AB, Malouf AJ, Bartram CI et al (2001)
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30. Zetterstrom JP, Mellgren A, Jensen LL et al (1999)
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32. Snooks SJ, Setchell M, Swash M, Henry MM (1984)
Injury to innervation of pelvic floor sphincter musculature in childbirth. Lancet 2:546–550
33. Sultan AH, Kamm MA, Hudson CN et al (1993) Anal
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48. Baeten CGMI, Geerdes BP, Adang EMM et al (1995)
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Section VIII • Treatment Options for Fecal Incontinence 325
(1996) Artificial anal sphincter. Dis Colon Rectum
39:1345–1351
51. Malouf AJ, Vaizey CJ, Nicholls RJ, Kamm M (2000)
Permanent sacral nerve stimulation for fecal incontinence. Ann Surg 232:143–148
52. Ganio E, Ratto C,Masin A et al (2001) Neuromodulation
for fecal incontinence: outcome in 16 patients with
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53. Matzel KE, Kamm MA, Stosser M et al (2004) Sacral
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54. Takahashi T, Garcia-Osogobio S, Valdovinos MA et al
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VIII.2.
Surgical Treatment of Fecal Incontinence
L. Zorcolo, D.C.C. Bartolo
Patients with major fecal incontinence often do
not benefit from medical treatment or biofeedback and thus are proposed for surgery. Different
surgical options are available, the choice of which
depends on the type of incontinence, the severity
of symptoms, and the compliance of the patient.
The efficacy of surgery still remains difficult to
assess, but it is quite evident that none of the operations can guarantee a return to perfect continence. Surgical treatment for fecal incontinence
can be divided in two main groups:
1. Operations to reinforce the existing muscles
• Anterior sphincter repair (ASR)
• Postanal repair
• Total pelvic floor repair
2. Operations to create a neosphincter
• Muscle transposition
Nonstimulated graciloplasty
Gluteoplasty
Dynamic graciloplasty (DGP)
• Artificial bowel sphincter (ABS)
Other surgical options, such as stoma creation
or colonic conduit, can help improve the quality of
life when nothing else can be done.
In this chapter, we will focus on indications,
techniques, and outcomes of the most common
procedures, which are ASR and (less commonly)
postanal repair for the first group,and stimulated
graciloplasty and ABS for the second group. New
procedures, such as sacral nerve modulation and
implantation of sphincteric bulking material, also
aim to improve continence through the existing
muscles. These emerging operations have a very
low morbidity and no mortality and, especially
the former, seem to be valid alternatives to major
procedures. These will be discussed in separate
chapters.
Reinforcement of the Existing
Sphincter
Anterior Sphincter Repair
Obstetric trauma is considered to be the commonest cause of fecal incontinence,and current opinion
based on anal endosonography is that the majority
of these patients have structural sphincter damage
[1]. The first-line treatment for this condition is
ASR. This is a relatively simple operation with low
morbidity. However, its efficacy following recent
longer-term outcome analyses has been recognized
to be substantially less than previously reported.
Patient Selection
This operation should be considered in all incon-
tinent patients with a demonstrable external
sphincter defect, unresponsive to conservative
treatment. Some authors argue that patients with
abnormally prolonged pudendal nerve terminal
motor latency (PNTML), especially if bilaterally
prolonged, are not good candidates for repair
[2–5], but this has not been confirmed by others
[6–9]. There is a general agreement that results
are probably poorer in older patients, in those
with associated evacuatory disorders, and in the
presence of multiple defects. However, none of
these are absolute contraindications to the repair.
328 Benign Anorectal Diseases
Notes on Techniques
Preoperatively,patients receive bowel preparation
with stimulants or osmotic laxatives, antibiotics,
and thromboembolic prophylaxis. Covering stoma
has been demonstrated to be unnecessary [6, 10,
11]. Under general anesthesia, the patient is placed
in a modified lithotomy position and catheterized.
The prone jack-knife position can also be used
and is more popular in North America, but we find
that with the buttocks protruding well beyond the
flexed knees, there is good exposure (Fig. VIII.2).
A curvilinear incision is made in the anterior perineum at the edge of the pigmented anal skin. The
incision is parallel to the anal margin and is
extended for about 180° (Fig. VIII.3). The wound
can be exposed with Gelpi or Lone Starr retractors, and the external sphincter ring is identified
and progressively freed up.
Dissection is initiated in the midline, where
scar tissue is present, and carried out in either
direction, searching for the retracted edges of the
sphincter muscle. Detection of the residual muscle may be facilitated by the use of diathermy.
Once identified, the two ends of the external
sphincter are mobilized from surrounding fat and
from the internal sphincter up to the level of the
levator muscles (Fig. VIII.4). Care must be taken
Fig. VIII.2. Exposure of the operative field in Lloyd-Davies
position. This lady had an extensive EAS scar with disruption
of the perineal body
Fig. VIII.3. A curvilinear incision is made ad the edge of pig-
mentated skin (dotted line)
Fig. VIII.4. The two ends of the external sphincter are freed
up (black arrows)
Section VIII • Treatment Options for Fecal Incontinence 329
Fig. VIII.5. Levatoroplasty with interrupted stitches (white
arrow)
posterolaterally, where the branches of the
pudendal nerve enter the muscle. The scar tissue
found anteriorly must not be excised because it
will be used for the repair. However, it can be
divided in the midline to facilitate mobilization of
the two ends of the sphincter. If the internal anal
sphincter is clearly identified, this can be imbricated separately from the external one, but this
procedure did not appear to offer any benefit [9,
12]. At this stage, a levatorplasty can be added to
tighten the anterior pelvic floor and reconstruct
the perineal body (Fig. VIII.5). In this case, the
levator muscles on each side are approximated
together with interrupted stitches of a slow
absorbable suture [i.e.,2/0 polydioxanone (PDS)].
The finding that levatorplasty improved outcome
has been supported by some series [13–15] but not
by others [4].
Finally, the two ends of the external sphincter
are overlapped by suturing the scar tissue from
one end to the middle part of the opposite sphincter muscle. Usually, 3–5 interrupted mattress
stitches of 2/0 PDS on each side are placed, and
they are tied snugly but not too tightly in order to
avoid muscular ischemia (Fig. VIII.6). When scar
tissue is not clearly evident, the sphincter ring can
be plicated rather than divided and overlapped.
Fig. VIII.6. Overlapping of the two ends of the external
sphincter
Hemostasis must be meticulous.At the end of the
procedure,the wound, which was originally transverse, can be usually closed in an inverted “Y”
fashion, thus increasing the distance between
anus and vagina (Fig. VIII.7). We often leave a
small opening if there is any tension in order to
minimize the risk of infection. Occasionally, it
may be necessary to create an advancement or an
island flap to cover the repair. Postoperatively, the
urinary catheter is kept in situ for 24–36 h, and a
normal diet is reintroduced the day after operation, supplemented with bulking laxatives to optimize stool consistency and avoid straining and
impaction. Bowel confinement and the use of
antidiarrheal drugs have been demonstrated to be
unnecessary and are associated with more complications [16]. Daily wound cleansing is practiced.
Complications
ASR can be considered a relatively simple procedure with low morbidity and no mortality. The
most common complication is wound infection.
In the authors’ experience, this occurred in 24
patients (26%). Five required an examination
under anesthesia while one developed perineal
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