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Surg Clin N Am 82 (2002) 1273–1290

Fecal incontinence
Susan Congilosi Parker, MD*, Amy Thorsen, MD
Division of Colon and Rectal Surgery, School of Medicine,
University of Minnesota, 393 Dunlap Street N, Suite 500,
St. Paul, MN 55104, USA

Fecal incontinence is a common problem not frequently discussed


between patients and their physicians. More appropriately termed anal
incontinence, it encompasses the inability to control the passage of flatus,
liquid, or solid stool. What may seem like a minor inconvenience to the
physician may be extremely distressing to the patient; the incontinent
patient may experience social isolation, feelings of inadequacy and low
self-esteem, and sexual dysfunction in addition to the physical symptoms
of recurrent genitourinary infections and perianal skin breakdown [1].
Community-based studies reveal a 2.2% prevalence of anal incontinence;
30% of these patients are over the age of 65, and 63% are female [2]. By
understanding the anatomic and physiologic mechanisms of fecal inconti-
nence, the surgeon can appropriately evaluate and treat her patient with
medical or surgical therapy.

Anatomy and physiology of anal continence


Fecal continence depends on the interplay of normal anal sphincter and
pelvic floor function; rectal compliance, capacity, and sensation; colonic
transit and stool consistency; and central nervous system function. An alter-
ation in one or more of these factors can have a positive or negative effect on
continence. Etiologies of fecal incontinence are listed in Box 1.
The pelvic floor musculature and sphincter complex consists of the leva-
tor ani, the puborectalis, and the internal and external anal sphincters. The
levators, also known as the iliococcygeus and pubococcygeus muscles, arise
from the obturator fascia, pubic bone and ischial spine. Their fibers travel
posteriorly, inferiorly, and medially until they decussate with fibers from the

* Division of Colon and Rectal Surgery, University of Minnesota, 393 Dunlap Street N,
Suite 500, St. Paul, MN 55104.
E-mail address: scongilosi@colonrectal.org (S. Congilosi).

0039-6109/02/$ - see front matter Ó 2002, Elsevier Science (USA). All rights reserved.
PII: S 0 0 3 9 - 6 1 0 9 ( 0 2 ) 0 0 0 6 1 - 0
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Box 1 Causes of fecal incontinence


Aging
Congenital anorectal anomalies
Diarrheal states
Infectious diarrhea
Inflammatory bowel disease
Short-gut syndrome
Laxative abuse
Radiation enteritis
Neurologic conditions
Congenital anomalies
Dementia, stroke
Diabetes
Multiple sclerosis
Neoplasms of brain, spinal cord
Pelvic floor denervation
Chronic straining at stool
Descending perineum syndrome,
Multiple pelvic organ prolapse
Rectal prolapse
Vaginal delivery
Overflow incontinence
Impaction
Encopresis
Rectal neoplasms
Trauma
Accidental injury
Anorectal surgery (eg, fistulotomy)
Obstetrical injury

Adapted from Mado RD, Williams JG, Caushaj PF. Fecal incontinence. Current
concepts. N Engl J Med 1992;326(15):1002–1007; with permission.

opposite side to form the anococcygeal raphe and attachments to the coccyx
and lower sacrum. Medial to the levators and anterior to the anococcygeal
raphe is the levator hiatus. The lower rectum, vagina, and urethra pass
through this hiatus and are bound together by a dense fascia. During defe-
cation, the levator ani contract and cause a dilating effect on the pelvic vis-
cera [3]. Inferior to the levators, the puborectalis muscle originates from the
back of the pubis and runs posteriorly to form a second U-shaped sling
behind the rectum. Through tonic contraction, the puborectalis angulates
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the anorectal junction to approximately 90 degrees at rest, and allows


straightening by relaxing during defecation [4]. The levator ani and pubor-
ectalis muscles receive innervation superiorly from branches of sacral ner-
ves S2-4 [5]. Along its inferior surface, the puborectalis may also receive
branches from the pudendal nerve [6]. Changes in normal pelvic floor func-
tion can result from central or peripheral nerve insults, and common causes
are spinal injuries, perineal descent, vaginal delivery, rectal prolapse, and
chronic straining.
The internal anal sphincter (IAS) consists of a thickening of the circular
smooth muscle of the rectum as it joins the anal canal. Shorter in length
than the external sphincter, it ends approximately 8 mm to 12 mm inferior
to the dentate line [7]. At rest, the internal sphincter provides 80% of sphinc-
ter tone [8]. A normal IAS will relax in response to rectal distention, but sub-
sequently regain tone during rectal accommodation [9]. The internal
sphincter receives both sympathetic innervation from the hypogastric plexus
and parasympathetic innervation from S1-3 [10–12].
The external anal sphincter (EAS) is a striated circular muscle which sur-
rounds the entire anal canal. The EAS also contributes to resting sphincter
tone [13]. Through normal involuntary reflex pathways, the external sphinc-
ter will contract in response to rectal distension, increased intra-abdominal
pressure, and change from a supine to upright position [10,14,15]. Voluntary
contraction can be performed for 40 to 60 seconds until the EAS fatigues
[16]. The external sphincter receives innervation primarily via the inferior
rectal branch of the pudendal nerve, and up to a third of patients may
receive additional innervation from a separate branch of S4 [6]. The puden-
dal nerve arises from sacral plexus nerve fibers (S2–4), exits the pelvis
through the greater sciatic foramen, crosses the ischial spine, and travels
in Alcock’s canal toward the ischial tuberosity. Direct internal and external
sphincter injury leading to incontinence can result from obstetric, operative,
penetrating, or pelvic trauma. Poor sphincter function may result from
interruption of spinal and central pathways from congenital, acquired, or
traumatic CNS defects, or from peripheral nerve injury or neuropathy.
Changes in rectal capacity and sensation can also affect continence. The
compliant rectum can maintain low intraluminal pressures as fecal volume
increases [17]. This normal elasticity can be lost in patients with ulcerative
colitis, radiation proctitis, and neorectums secondary to sphincter-saving
procedures, resulting in high intraluminal pressures, urgency, and inconti-
nence [18–20]. The sensation of rectal distension is most likely mediated
by stretch receptors in the puborectalis and levator ani muscles [21]. In con-
trast, the anal canal epithelium hosts multiple pain, touch, cold, pressure,
and friction receptors that detect the nature of rectal contents [22]. Neuro-
pathies, spinal cord malformations, perineal descent, fecal impaction, and
encopresis may alter normal sensory thresholds [23]. CNS disturbances,
such as dementia, stroke, and encephalopathies, may prevent the patient’s
appreciation of rectal distention [24].
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Finally, conditions leading to increased stool volume may overcome the


normal storage capacity of the sigmoid and rectum and lead to incontinence.
Liquid stool may result from malabsorption, infectious and inflammatory
colitis, and irritable bowel syndrome. In fact, stool consistency may be the
most important factor influencing fecal incontinence [25].

Evaluation
A detailed history and physical exam will often reveal the etiology and
severity of incontinence. The addition of anorectal physiology testing may
confirm clinical judgment or expose unsuspected deficits. Laboratory evalu-
ation can also quantify the severity of the physiologic defect and is often
used to prognosticate the rate of success of a proposed treatment plan.

History
A history of fecal incontinence may be difficult to obtain from an embar-
rassed patient. The onset of symptoms and any relationship to a change in
bowel habits should be assessed. The degree of incontinence (flatus, liquid,
or solid stool), frequency of episodes, and their effects on the patient’s qual-
ity of life will document present function and determine whether more
aggressive therapies are indicated. As previously discussed, gastrointestinal
diseases such as infectious colitis, inflammatory bowel disease, and irritable
bowel syndrome may cause or exacerbate fecal incontinence, and previous
pelvic radiation resulting in proctitis may cause rectal bleeding, tenesmus,
and leakage. Neurologic diseases associated with loss of control include con-
genital spinal cord abnormalities, spinal trauma, and multiple sclerosis. A
history of diabetes may indicate pelvic floor neuropathy as a possible etiol-
ogy of incontinence [26].
Injuries to the anal sphincters may go unnoticed until other factors exac-
erbate the physiologic defect; thus a history of prior anorectal surgery or
perineal trauma is extremely relevant. Anorectal procedures treating hemor-
rhoidal disease, fistulas, and fissures may cause occult sphincter injury.
Some degree of incontinence may be noted in up to 45% of patients under-
going fistula surgery [27]. Nielson et al [28] demonstrated a 65% incidence of
sphincter defects on anal ultrasound after sphincter stretch for fissure-in-
ano. Varying rates of impaired control have been reported after lateral inter-
nal sphincterotomy, possibly related to technique [29] or sphincterotomy
length [30].
A detailed obstetric history may be extremely revealing in the female
patient. In addition to the number of vaginal deliveries, a history of
increased birth weight, episiotomy use, instrumented delivery, and pro-
longed labor should be noted. Clinically recognized sphincter disruption
is noted in up to a quarter of all childbirths, and ultrasound studies
reveal an additional 11% incidence of unsuspected sphincter injuries [31].
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Independent risk factors for sphincter disruption include midline episiotomy


[32], clinicians with higher episiotomy usage [33], and forceps delivery [34].
An active second stage of labor that exceeds one hour may increase the risk
of pelvic floor denervation in primiparas [35].

Physical examination
A focused physical exam is performed not only to identify obvious
defects, but also to differentiate incontinence from fecal soiling due to poor
hygiene, prolapse, or fistulous disease. Inspection of the perianal skin may
reveal excoriation, scars from previous surgeries or episiotomies, a patulous
anus, or an obvious cloacae. A ‘‘keyhole deformity,’’ resulting from a pos-
terior midline sphincterotomy or fistulotomy, may cause fecal leakage as
opposed to true incontinence. Prolapsing hemorrhoids, mucosa, or full
thickness prolapse may be elicited by valsalva. The presence of an anal wink
should be assessed on each side to determine whether normal anocutaneous
reflexes are intact.
On digital exam, any masses or palpable defects are noted. The presence
of impacted stool suggests fecal overflow as the mechanism of incontinence.
Resting and squeezing sphincter tone should be assessed subjectively.
Puborectalis contraction can be felt posteriorly just above the external
sphincter. A bidigital exam can be performed to appreciate perineal body
width or detect a rectovaginal fistula. Anoscopy will reveal hemorrhoids
or fistulas, and flexible sigmoidoscopy can exclude the presence of masses
or inflammatory conditions which may lead to incontinence. A complete
colonoscopy should be considered in the patient who reports a change in
bowel habits. If the diagnosis of incontinence is in doubt, the ability of the
patient to retain a 100 cc water enema can be easily assessed in the office.

Anorectal physiology testing


Not all patients require laboratory assessment; patients with altered
bowel function or minor degrees of incontinence may respond well to med-
ical management. Physiology testing will define anatomic defects, quantify
anal sphincter function, and identify neurologic deficits. Laboratory stud-
ies include endoanal ultrasound, anal manometry, pudendal nerve latency
testing, and occasionally defecography.
When performed by an experienced clinician, endoanal ultrasound
approaches 100% sensitivity and specificity in identifying internal and exter-
nal sphincter defects [36,37]. A 15 mm diameter probe with a 360 degree
rotating 10 mHz transducer is used to image the sphincters at several levels
in the anal canal. The internal anal sphincter is imaged as the hypoechoic
ring closest to the transducer, surrounded by a hyperechoic ring represent-
ing the external anal sphincter. Lateral breaks in the internal sphincter may
be seen after sphincterotomy or hemorrhoidectomy. Obstetrical trauma
resulting in sphincter injury may appear as anterior disruptions of both the
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external anal sphincter muscle and internal anal sphincter muscle on ultra-
sound. The degree of muscle separation can be measured, and perineal body
length can be assessed by applying pressure on the posterior vaginal wall.
This maneuver may also aid in identifying the presence and location of a
rectovaginal fistula. Endosonographic sphincter abnormalities are seen in
up to 90% of women whose sole risk factor for fecal incontinence is obstetric
trauma [38,39].
Anal manometry quantifies functional deficits in the internal and external
sphincters and tests for the presence of normal anorectal reflexes. Using
either a microballoon, or a water-perfused or solid-state transducer, resting
and squeeze pressures are measured throughout the length of the anal canal.
In the relaxed patient, resting pressures mainly reflect internal sphincter
function, whereas squeeze pressures represent voluntary external sphincter
contraction. Normal values of both resting and squeeze pressures vary
among patient populations; lower pressures are found in women and with
advancing age [40–42]. Given the wide range of normal pressures and the
variety of factors involved with anal continence, absolute values predicting
incontinence are difficult to define. Although manometry cannot differenti-
ate a sphincter injury from a neurogenic deficit [43], it can confirm neuro-
genic dysfunction in patients with intact sphincters and normal pudendal
nerve terminal motor latencies [44].
Rectal sensory testing includes volumetric measurements of first detect-
able sensation, sensation of fullness, and maximal tolerated volume by bal-
loon distention. Hypersensitivity can be seen with inflammatory conditions
and poor rectal compliance. Blunted rectal sensation—found in patients
with diabetes [45], multiple sclerosis [46], and megarectum [47]—may lead
to overflow incontinence. Several studies indicate that successful biofeed-
back therapy for fecal incontinence may be attributed to improvements in
rectal sensation [48–51].
The pudendal nerve, containing fibers from sacral nerves S2–4, provides
motor innervation to the external sphincter and receives sensory informa-
tion from the perineum. Pudendal nerve terminal motor latency (PNTML)
measures the conduction time to external sphincter contraction after nerve
stimulation at the level of the ischial spine. The nerve may be difficult to
identify in obese patients and with technician inexperience. Prolonged laten-
cies may be associated with obstetric injury, perineal descent, prolapse, and
medical neuropathies. Pudendal neuropathy is observed in up to 70% of
patients with fecal incontinence, and in over 50% of patients with sphincter
injury [52]. Controversy exists as to whether prolonged PNTML predicts
poor outcome following sphincteroplasty [53–57].
Defecography evaluates rectal emptying of contrast material under fluo-
roscopy. Incontinent patients are often observed to have a more obtuse ano-
rectal angle on defecography [58]. This study may reveal internal or external
prolapse not appreciated on exam, or a poorly emptying rectocele contribu-
ting to incontinence associated with sphincter dysfunction.
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The necessity and value of anorectal physiology testing has been debated
in the literature. In a prospective study, Liberman et al demonstrated a 10%
change in management when physiologic evaluation (endosonography,
manometry, and PNTML) was performed after clinical assessment. Trans-
anal ultrasound was found to be the study most likely to alter the clinical
treatment plan. Endosonography may reveal unsuspected sphincter injuries
in patients thought to have neurogenic incontinence, or a lack of a signifi-
cant anatomic pathology in patients with suspected sphincter disruption
[59]. Although pudendal neuropathy may not affect the decision to correct
a sphincter defect, the knowledge of its presence will assist in counseling
patients on functional expectations. Anorectal physiology testing has also
been demonstrated to be useful in evaluating patients with severe perineal
trauma prior to colostomy takedown [60].

Medical management
Most patients with fecal incontinence will benefit from an initial attempt
at medical management of their problem. Regardless of the etiology of the
incontinence, patients with mild to moderate symptoms may improve
enough to delay or preclude surgical options, and patients with severe symp-
toms may obtain a degree of improvement while undergoing further testing
or awaiting surgery. Medical management consists of dietary manipulation,
use of antidiarrheals, bowel management regimens, and biofeedback.

Dietary measures
Dietary manipulation refers to the initial common-sense counseling of the
patient regarding diarrhea-inducing foods, possible sources of food intoler-
ance, and the addition of bulk-producing agents to the diet. Foods associ-
ated with diarrhea include alcohol, caffeine, fruit juices, prunes, licorice,
and some vegetables such as beans, broccoli, cauliflower and cabbage. Com-
mon sources of food intolerance are lactose and gluten. A daily food diary is
the most useful method to pinpoint offending foods, as personal recollection
is often faulty. Although this aspect of treating fecal incontinence is more
trial and error and less science, the use of increased dietary fiber to increase
stool bulk is well accepted [61]. The patient should slowly increase the daily
fiber intake, seeking a goal of at least 20 to 25 grams a day and ideally 30
grams a day. The varieties of methycellulose and psyllium products now
available over the counter in powder, granule, and pill form make this an
achievable goal.

Antidiarrheals
The most commonly used antidiarrheals are adsorbents and opium deriv-
atives. Adsorbents, such as Kaopectate (Pharmacia & Upjohn, Peapack,
1280 S.C. Parker, A. Thorsen / Surg Clin N Am 82 (2002) 1273–1290

NJ) are most useful for mild degrees of incontinence and act, as the name
suggests, by absorbing excess fluid in stool. Opium derivatives range from
the over-the-counter loperamide (Imodium, McNeil Consumer Healthcare,
Fort Washington, PA) to the more potent prescription alternatives of diphe-
noxylate hydrochloride (Lomotil, Searle, Chicago, IL), codeine, and tincture
of opium. Low-dose amitriptyline (20 mg daily), a tricyclic antidepressant
with anticholinergic and serotoninergic properties, also improves fecal
incontinence symptoms, but it is unclear if it acts mainly by decreasing
colonic transit or by altering rectal motor contractions [62]. In our practice,
loperamide is the most commonly used drug for moderate to severe in-
continence. Loperamide combines multiple actions—slowing colonic
transit, increasing fluid absorption, and inhibiting mucous secretion—with
a lower abuse potential than other opium derivatives. Loperamide is also
the only antidiarrheal that acts as a sphincter agonist, increasing anal
sphincter pressure [63]. The best use of these medications is prophylactically
with a regularly scheduled dose to avoid or decrease episodes of inconti-
nence.
Inherent in any discussion of diarrhea and fecal incontinence is consider-
ation of the patient with irritable bowel syndrome (IBS). Irritable bowel
syndrome is unlikely to be the sole source of incontinence, but the combi-
nation of the diarrheal form of IBS with a mildly compromised anal sphinc-
ter can result in a debilitating problem. Medical management, particularly
the use of bulking agents, as already outlined, is appropriate for these
patients. The variable nature of IBS can make prophylactic use of anti-
diarrheals problematic. Alosetron (Lotronex, Glaxo Smithkline, Uxbridge,
Middlesex, UK), a serotonin type 3 receptor antagonist, is effective for
women with diarrhea-predominant irritable bowel syndrome but was with-
drawn from the market in 2001 due to episodes of ischemic colitis [64,65].
Reintroduction of this or similar serotonin modulating drugs may offer
therapeutic benefits in the future.
A final category of medications that are not strictly antidiarrheals but
may have the desired effect are the bile salt binders cholestyramine and
colestipol. These resins treat bile acid diarrhea by binding with bile salts
in the small intestine, but also alter the absorption of fat-soluble vitamins
and certain medications (digoxin, warfarin, thiazides). Appropriate patients
are those who relate a change in bowel consistency to the timing of a chol-
ecystectomy or those suspected of having altered small bowel reabsorption
of bile salts, which occurs by passive diffusion throughout the gut but by
active transport in the terminal ileum.
A recent area of interest is the use of topical agents such as phenylephrine
to increase internal anal sphincter contraction and increase resting tone
[66]. Although 10% topical phenylephrine was not successful in an initial
randomized, controlled trial, the use of a topical agent remains an intriguing
option that may eventually prove useful for the treatment of minor perineal
soiling associated with decreased resting tone.
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Bowel management
The goal of an effective bowel management program is to allow the
patient to produce a complete bowel movement at a scheduled time by using
an individualized combination of dietary measures, laxatives, suppositories,
enemas, or digitization. This approach to bowel dysfunction, commonly
used by spinal-cord injury patients, is also applicable to patients with less
complete neurologic disorders (multiple sclerosis, diabetes), congenital dis-
orders (imperforate anus, spina bifida), decreased rectal sensation, or incom-
plete evacuation. Patient compliance is essential for success and daily care is
typical [67]. In a telephone survey of 171 adults with spinal-cord injuries for
a mean of 8.9 years, the most common bowel regimen was a chemical rectal
stimulant (in 39% of subjects) [68]. If bowel management becomes arduous,
particularly for the spinal cord injury patient, a stoma can greatly decrease
the time spent on bowel care and provide greater independence [69].
Adult patients with overflow incontinence and pediatric patients with
encopresis present with complaints of fecal incontinence due to the constant
seepage of stool from a full rectum. Treatment of both patients begins with a
complete colonic cleansing. The first step is rectal disimpaction, either man-
ually or with enemas, followed by use of a cathartic such as a polyethylene
glycol colonic prep (Nulytely, Braintree Laboratories, Inc, Braintree, MA).
Once the colon is empty, the patient uses a regimen of laxatives and daily
attempts at defecation after meals, often aided by suppositories or enemas,
to avoid recurrent constipation. Use of a polyethylene glycol laxative devel-
oped for daily use (Miralax, Braintree Laboratories Inc., Braintree, MA)
can simplify a laborious regimen [70]. Other options to consider in patients
with evacuation difficulties who fail bowel regimens include retrograde
enemas and the antegrade colonic enema (ACE) procedure [71,72].

Biofeedback
Biofeedback therapy is best applied to motivated patients with some abil-
ity to voluntarily contract the external anal sphincter, even if the muscle is
partially disrupted, and intact rectal sensation. Over the course of three to
five weekly sessions, a trained biofeedback therapist works with the patient,
teaching basic concepts of anatomy and physiology and instructing the
patient in appropriate exercises to improve external anal sphincter strength,
improve rectal sensory thresholds, and enhance coordination of external
anal sphincter function in response to rectal distention. Overall success rates
of 64% to 89% are reported, and biofeedback can enhance function after
sphincteroplasty [73,74]. Despite its use since 1974, the mechanism of suc-
cess is unclear, therapists apply varying treatment protocols and instrumen-
tation, and long-term results are infrequently reported [73,75]. Nevertheless,
the advantages of biofeedback—that it is safe, effective, and does not pre-
clude other treatments—seem to outweigh its limitations.
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Surgical treatments
Surgical therapy for fecal incontinence is considered in patients with anat-
omic abnormalities and with severe incontinence refractory to medical man-
agement. Hemorrhoids or anal fistula leading to fecal soiling should be
treated appropriately. Rectal prolapse may be corrected with a perineal or
abdominal approach. Sphincter injuries are usually first repaired with over-
lapping sphincteroplasty. Innovative techniques, such as stimulated gracilo-
plasty, artificial bowel sphincter, and sacral nerve stimulation, are usually
reserved for patients with complex anatomic defects, neurogenic inconti-
nence, or failure from other therapies. Fecal diversion may be appropriate
and acceptable in selected patients.

Sphincteroplasty
Originally described by Parks [76], overlapping sphincteroplasty is the
most common delayed procedure used to treat traumatic sphincter disrup-
tion. With the patient in the prone jackknife position, a curvilinear incision
is made in the perineal body over the anterior injury. Anterior vaginal and
posterior anodermal flaps are created, and the sphincter muscle is dissected
laterally on each side of the defect. Sphincter mobilization is not carried pos-
terior to the midlateral line to avoid pudendal nerve injury. The anterior
scar is divided in the middle, but not excised, to aid in suture fixation. The
muscle flaps are then overlapped to form a snug anal opening; the repair is
then secured with 2-0 absorbable mattress sutures. An anterior levatoro-
plasty is sometimes added to lengthen the anal canal. The skin is loosely
reapproximated in a manner to increase perineal body length and allow
adequate drainage of the repair.
The success of overlapping sphincteroplasty is reported to be between
70% and 90% [77–80]. Almost two thirds of these patients will have good
to excellent results; a small minority of patients will have worse function.
Poor preoperative continence (incontinence of solid stool) [81] and previous
repairs [82] may be predictive of poorer postoperative continence levels.
Advanced age [79,80,83], fecal diversion [80,84,85], or bowel confinement
[86] do not appear to affect results. It is controversial whether the presence
of unilateral or bilateral pudendal neuropathy affects the outcome of sphinc-
teroplasty [53,54,77,81,87–89].
In the acute setting, a recognized sphincter injury may be primarily
repaired. Obstetric injuries are traditionally repaired in an end-to-end man-
ner at the time of disruption. Up to three quarters of these repairs will con-
tinue to have external sphincter disruption on postoperative endoanal
ultrasound, however [31]. Sultan et al used overlapping sphincteroplasty
to repair acute obstetric injuries; only 15% of patients had a persistent exter-
nal sphincter defect on follow-up ultrasound at three months [90]. It is
unclear whether this change in repair technique prevents patients from
having symptomatic incontinence in the future.
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The management of nonoperative traumatic injuries, such as open pelvic


fractures and perineal impalement injuries, depends on the overall stability
of the patient. Commonly associated with motorcycle accidents, mortality
rates as high as 32% to 58% have been observed with pelviperineal trauma
[91]. Up to 80% of survivors suffer the complication of pelvic sepsis [92].
Hence the standard approach consists of achieving hemodynamic stability,
followed by diverting colostomy, distal stump washout, and presacral drain-
age. Sphincter repair may be performed electively when other acute issues
are resolved. Repair at the time of injury may be considered in the stable
patient with isolated perineal trauma [93]. Most patients will experience
good to excellent continence after delayed repair. Preoperative anorectal
physiology testing may detect occult defects and improve the likelihood of
successful repair [77].

Innovative treatments for fecal incontinence


Innovative treatments for fecal incontinence are typically applied to the
patient whose only other option is a stoma because traditional methods have
failed or are inadequate to handle an extensive traumatic or neurogenic
injury. Additionally, only about half of the patients having an initial suc-
cessful result from biofeedback or anterior sphincteroplasty retain that func-
tional result for three or more years [75,88,94]. Options include the artificial
anal sphincter, dynamic graciloplasty, and sacral stimulation, although
other treatments are on the horizon.

Dynamic graciloplasty
The dynamic graciloplasty and the artificial anal sphincter are both
advanced variations of anal encirclement for fecal incontinence. The earliest
and simplest version of anal encirclement was the use of silver wire, de-
scribed by Thiersch. Dynamic graciloplasty combines transposition of the
gracilis muscle with electrical stimulation via an implantable pulse genera-
tor. The gracilis muscle is preferred because it has a proximal neurovascular
bundle and it can be tunneled under the skin in the proximal thigh and
wrapped around the anal canal. Applying electrical stimulation to the gra-
cilis muscle allows conversion of the fast-twitch, fatigable leg muscle to a
slow-twitch, fatigue resistant muscle that more closely resembles an anal
sphincter. Baeten first reported the use of electrical stimulation with a gra-
cilis muscle wrap for fecal incontinence in 1988 and subsequently reported a
72% continence rate [95,96]. The latest report from a multicenter trial found
a 63% success rate, with success defined as a 50% improvement in inconti-
nent events, and operative morbidity was high [97]. Use of dynamic gracilo-
plasty is limited to Canada and Europe because FDA approval is not being
sought in this country. Total anorectal reconstruction with dynamic gracilo-
plasty is reported but with a high morbidity [98,99].
1284 S.C. Parker, A. Thorsen / Surg Clin N Am 82 (2002) 1273–1290

Artificial bowel sphincter


In our practice, the artificial anal sphincter (Acticon bowel sphincter,
American Medical Systems, Minnetonka, MN) has supplanted use of the
dynamic graciloplasty, because the two procedures are applicable to many
of the same patients. Several features of the artificial bowel sphincter make
it a more attractive option than the complex dynamic graciloplasty proce-
dure: it is placed in a single operation, the device is operational six weeks
after placement without the need for muscle conditioning, and a painful
muscle transposition is avoided.
The artificial anal sphincter currently in use is a modification of an arti-
ficial urinary sphincter (AMS 800, American Medical Systems). It is an
implantable device composed of a silicone elastomer that maintains conti-
nence via a fluid-filled cuff that surrounds and compresses the anal canal.
The patient controls the device via a pump placed in the scrotum or labia.
Squeezing the pump 9 to 12 times forces the fluid from the cuff into a reser-
voir balloon, which is implanted in the space of Retzius. This deflates the
cuff and opens the anal canal, allowing the passage of stool. The cuff then
automatically slowly reinflates and occludes the anal canal providing conti-
nence until defecation is again desired.
Christiansen and Lorentzen first reported implantation of an artificial
anal sphincter for fecal incontinence in 1987 [100]. Since then, several groups
have reported their experience with the AMS 800 and later modifications of
the device [101–106]. Infections occurred in 15% to 25% of patients, 20% of
patients were explanted, and final success rates were often over 70%. Com-
plications could be successfully treated without major morbidity.
A multicenter clinical trial of the artificial anal sphincter at 19 sites in
the United States, Canada, and Europe ended in 2000 [107]: 112 patients
were implanted (86 females) and followed a common protocol consisting
of quality-of-life questionnaire, incontinence scoring, and physiology
testing at six months and one year. At one year after implantation 75
patients (67%) had a functioning device and 3 were lost to follow-up. The
infection rate was 25%, and 46% of implanted patients (51 of 112) had
revisional surgery: 41 (37%) had devices explanted and 7 were successfully
reimplanted.
In this study a successful clinical result was defined as a decrease in the
fecal incontinence score (FISS) of at least 24 points (score range 0–120),
indicating a drop of at least two levels. For example, a patient incontinent
of liquid and solid stool daily before surgery could report several inconti-
nent events a month, but not weekly incontinence, to be judged a clinical
success. To qualify for the study patients had a FISS of at least 88 or a
stoma. At one-year follow-up, the mean FISS score had dropped from
105 (incontinent to liquids and solids daily) to 48 (incontinent to seepage). A
valid criticism of this study is the use of a scoring system instead of diary
data that may have more accurately reflected a change in continence, but suc-
cessful patients nonetheless saw a dramatic drop in their scores.
S.C. Parker, A. Thorsen / Surg Clin N Am 82 (2002) 1273–1290 1285

The artificial bowel sphincter (Acticon, American Medical Systems)


received approval from the Food and Drug Administration (FDA) in
December of 2001 for use on adults with intractable fecal incontinence. Sur-
geons who participated in the FDA trial and others who have undergone
subsequent training perform the surgery at a limited number of sites in this
country.

Sacral stimulation
Sacral nerve stimulation, like the artificial anal sphincter, was initially
devised for urinary incontinence. Matzel, in 1995, introduced the use of
sacral stimulation to treat patients with functional but not anatomic deficits
of the anal sphincter muscle [108]. The procedure entails placing an elec-
trode in a sacral foramen (S2, 3, or 4), to stimulate the nerve roots. The
desired effect is maximum contraction of pelvic muscles with minimal stim-
ulation of the fibers to the lower extremity. Once the optimal site is selected,
the lead is connected to a temporary external pulse generator for a test pe-
riod of stimulation, currently three weeks. If function improves adequately
at the end of the test period, implantation of a permanent pulse generator
is performed. Both the initial operation for placement of the lead and the
subsequent placement of the pulse generator are well tolerated procedures
done under light sedation.
The indications for sacral stimulation are quickly being expanded due to
the low morbidity of the procedure, promising results obtained on a wide
variety of urology patients, and findings indicating that the stimulation
effect is not confined to the striated muscle [109]. Although stimulation of
the efferent motor nerves does seem to result in an increase in anal canal
pressure due to contraction of the anal sphincter muscles, conversion of
muscle fibers similar to that obtained with dynamic graciloplasty may also
occur [108]. Sacral stimulation may modulate sacral reflexes and sacral para-
sympathetic nerves, thereby altering rectal compliance, anal canal resting
tone, and rectal sensitivity [109]. The initial assumption that a patient
needs an intact sphincter and pudendal nerve is already being challenged.
An international multicenter trial evaluating the use of sacral stimulation
for fecal incontinence will help define the patient population for this novel
treatment.

Summary
The treatment of fecal incontinence is particularly gratifying because the
loss of fecal control has a devastating effect on a patient’s lifestyle. One must
consider the myriad factors that influence bowel control to properly diag-
nose and treat each patient. Physiology testing, particularly the use of ultra-
sound, is essential when treatment extends beyond dietary and medical
management. Recent reports suggest that the success of typical treatments
1286 S.C. Parker, A. Thorsen / Surg Clin N Am 82 (2002) 1273–1290

may diminish with time. This may indicate a greater need in the future for
innovative options such as the artificial bowel sphincter or sacral stimulation.

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