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RECT
AL AND
PARARECTAL
19. Fecal Incontinence 93
20.
Rectal Stricture: Etiology and Management 98
21.
Management of Fecal Impaction 102
22.
Rectal Prolapse 107
23.
Solitary Rectal Ulcer Syndrome 111
24.
Rectocele 114
25.
Rectal Foreign Bodies 118
26.
Diagnosis and Management of Sacral and Retrorectal
Tumors 121
REGION
Management of Rectal Villous Tumors 132
27.
28.
Preoperative Evaluation of the Patient with Rectal
Cancer: Staging and Strategy 135
29.
Cancer of the Rectum: Neoadjuvant Therapy 141
30.
Cancer of the Rectum: Operative Management 146
31.
Local Treatment of Rectal Cancer 152
32.
Locally Recurrent Rectal Cancer: Management and
Follow-up 157
33.
Perineal Hernia 162
2
91
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F
 I
P
. Ronan O’Connell

INTR
ODUCTION AND INCIDENCE
F
ecal incontinence may be dened as the inability to voluntarily con­trol the release of atus or stool until a socially convenient time and place. Fecal continence, which is learned in childhood, is one of the most important social milestones in development, and its loss is a devastating handicap. e prevalence of incontinence varies by gen­der, age, and denition; however, as many as 2% of women regularly experience diculty controlling stool and at least 10% have diculty controlling atus. Incontinence is more common in parous women because childbirth is the most common cause of pelvic oor injury. Menopause also contributes through diminished trophic eects of estrogen on pelvic connective tissues, and symptoms frequently become manifest in the sixth or seventh decade. e overall cost of fecal incontinence to society is unknown, but the magnitude of the problem is illustrated by the fact that fecal incontinence is the second leading reason for admission of elderly persons to nursing homes—a reason more common than dementia. e hidden cost is a reduc­tion in quality of life and lost opportunities resulting from this most embarrassing of symptoms. 
C
AUSES
ecal continence depends on the presence of an intact anal sphinc-
F ter mechanism, coupled with adequate rectal compliance and a nor­mal volume and consistency of stool. A wide variety of anatomic and physiologic factors can alter continence, particularly changes in colonic transit and stool consistency, abnormal rectal physiol­ogy, abnormal anorectal sensation, pelvic oor denervation, and disruption of the integrity and function of the internal and external anal sphincters. In general, the four main causes are (1) abnormal stool volume and consistency; (2) neurologic disorders leading to sphincter weakness; (3) anatomic defects in the anal sphincters; and (4) abnormal rectal physiology. Because these problems oen over­lap, each area must be addressed to ensure accurate diagnosis and eective treatment. 

ASSESSMENT

Many scoring systems have been proposed to categorize the severity of fecal incontinence. e use of such systems is important for accu­rate patient assessment, medicolegal documentation, and objective evaluation of treatment outcomes. Each scoring system has strengths and weaknesses. e ideal system would accurately and reproducibly describe the frequency of incontinent episodes, the degree to which patients are incontinent of gas, liquid, and solid stool, and the eect of incontinence on lifestyle. Two validated scoring systems are widely used: the Cleveland Clinic Continence Score and the St. Mark’s Conti­nence Score. Quality of life scores should be determined independently.
Use of the validated Fecal Incontinence Quality of Life symptom­specic score is helpful because it is the patient’s quality of life that is the most important determinant of the need for intervention.
Evaluation of fecal incontinence begins with a detailed interview that includes a careful medical, surgical, and obstetric history. e timing and type of incontinence should be noted, as well as the use of pads, diapers, or medications. It is important to ascertain the severity of the incontinence, which may vary from soiling to loss of a com­plete bowel movement, and whether the incontinence is primarily associated with urgency and the inability to hold the rectal contents or is passive. Many patients have a combination of symptoms that may include obstructed defecation with incomplete evacuation.
Obtaining a dietary history is important because many patients consume inappropriately high amounts of fermentable ber in the mistaken belief that a “healthy diet” is required for their bowel con­dition. Oen breakfast is omitted, particularly by working mothers, and thus the opportunity to use the gastrocolic reex to ensure a pre­dictable early morning bowel movement is lost.
Physical examination should include exible sigmoidoscopy to rule out neoplastic and inammatory disorders, with further evalua­tion of the small and large bowel as clinically indicated. e perineum is inspected for scars, stulas, and adequacy of the perineal body. e presence of rectal prolapse or perineal descent is appreciated by ask­ing the patient to bear down. Digital examination at rest and with squeeze eort permits qualitative assessment of internal and external sphincter function. e presence and extent of a rectocele or uterine prolapse should be determined.
Endoanal ultrasonography is the best technique currently avail­able to evaluate patients for possible anatomic anal sphincter defects and should be performed in all patients with incontinence. e rela­tionship between the extent of an individual anal sphincter defect and continence is dicult to correlate; however, defects extending to one quadrant (90 degrees) or greater usually contribute signicantly to a patient’s symptoms. Defects in the external anal sphincter (EAS) are associated with urge incontinence, whereas internal anal sphinc­ter (IAS) defects are associated with passive soiling and leakage of mucus. Occult anal stulas and other less common pathologic condi­tions also may be identied using endoanal ultrasound, and three­dimensional imaging may be useful in assessing the extent of injury. In expert hands, transperineal ultrasonography provides detailed anatomic images and may allow dynamic assessment of rectocele, rectal intussusception, and levator ani injury.
Patients considering surgery because of the severity of their incontinence should undergo anorectal physiologic assessment. Anal manometry documents resting and squeeze pressures, indicating IAS and EAS function, respectively. Rectal sensation may be assessed using balloon distention to determine the volume of rst sensation, volume of rst urge, and maximum tolerated volume. Pudendal nerve func­tion may be evaluated noninvasively by determining pudendal nerve terminal motor latency with a glove-mounted electrode; however, the results are not predictive of therapeutic outcome, and the technique is
93
94
Fec
al Incont
Inence
ot routinely performed. Concentric nerve electromyography of the
n EAS can accurately determine the presence of motor neuropathy, and the cliteroanal reex can be used to determine aerent and eerent conduction along the pudendal nerve and its terminal branches. In practice, such investigations are rarely performed.
Defecography provides a dynamic view of rectal function and permits identication of pelvic oor disorders such rectocele or internal intussusception that can contribute to incontinence through obstructed defecation and incomplete evacuation. 
TREA
TMENT
T
reatment should be individualized based on the severity of symp­toms, the patient’s overall condition, and the degree to which the incontinence is aecting the patient’s quality of life.
Medical Management
rue incontinence must be dierentiated from pseudoincontinence,
T soiling of mucus or pus caused by prolapsing hemorrhoids, full-thickness rectal prolapse, or occult stulas. In these instances, therapy is directed at the primary cause. Conservative management is appropriate for true mild incontinence and is focused on optimizing stool consistency and colonic motility. Excess fermentable ber should be excluded from the diet and replaced by ber supplements taken once or twice daily to pro­vide a so, bulky stool. Patients with loose stools should be instructed to take only enough water to dissolve the bulking agent, thus permitting maximal absorption of excess stool water. Judicious use of antidiarrheal agents such as loperamide or diphenoxylate with atropine is appropriate to decrease stool frequency. Frequently, these drugs are most helpful at bedtime or prior to planned social engagements. Loperamide has been shown to increase internal anal sphincter pressure and may help minor degrees of seepage from a lax anus. In some patients, the adult dose of loperamide (2 mg) leads to constipation, and in these circumstances, 1 mg pediatric syrup is useful. Some patients, particularly those with chronic seepage, also may benet from regular emptying of the rectum with a small tap-water enema. 
eedback
Biof
Biofeedback is a dynamic technique that allows a person to learn and respond to physiologic changes in the body. In the case of fecal incon­tinence, patients are trained to improve voluntary anal sphincter contraction, improve rectal sensation, and coordinate squeeze eorts with rectal distention. Biofeedback represents a qualitative improve­ment over simple pelvic oor exercises, such as those popularized by Kegel, because the patient learns to focus eorts upon the appro­priate target, the EAS, rather than the gluteus maximus. Biofeedback is painless, noninvasive, relatively inexpensive, and risk free. Rec­tal sensory training is accomplished by instillation of progressively smaller quantities of air into a rectal balloon.
Requirements for biofeedback therapy include motivation, the ability to follow instructions, and the ability to contract the sphincter muscle to a detectable degree. Specic indications for biofeedback include neu­rogenic fecal incontinence, inability to undergo surgery, and failure of sphincteroplasty. e eects of biofeedback on incontinence are reason­able, with most patients experiencing sustained improvement. 
Surger
Anal Sphincter Repair (Sphincter
Anal sphincter injury is most commonly due to obstetric trauma, with the site of injury in the anterior quadrant of the anus. In other patients,
y
oplasty)
such as those who have had previous anorectal surgery, perineal injury, or pelvic fractures, the site and extent of a suspected sphincter injury may be dicult to determine upon clinical examination, and endorec­tal ultrasonography may be required to dene sphincter anatomy.
Acute anal sphincter injuries, particularly those that occur during childbirth, are best repaired at the time of injury. e repair should be performed under optimal conditions in the operating room, rather than in the labor ward. If an obstetric injury has been missed or the primary repair breaks down, secondary repair should be delayed until local inammation and edema have completely resolved.
Patients undergoing elective anal sphincteroplasty may need to perform full mechanical bowel preparation; however, an enema on the morning of the surgical procedure is usually adequate. Periop­erative broad-spectrum parenteral antibiotics should be prescribed. e operation may be performed with the patient in a lithotomy or prone jackknife position and the buttocks taped apart. Prior to inci­sion, inltration of the operative eld with a 1:100,000 adrenaline solution is helpful and particularly aids in dissection of the rectovagi­nal septum. When the perineum is foreshortened, a curvilinear inci­sion should be made between the anus and vagina; however, if the perineum is of adequate length, a curved incision along the posterior vaginal fourchette is associated with fewer wound healing problems. e use of stay sutures or a Lone Star retractor (CooperSurgical, Inc., Trumbull, Conn.) to retract wound edges is helpful.
Once the incision is made, sharp dissection is required to elevate anorectal and vaginal mucosa from the sphincter complex and associ­ated scar. is process is technically the most dicult part of the pro­cedure, and care is required to avoid “buttonholing” the rectal mucosa. e scar and sphincter mechanism are dissected laterally to the mid­coronal line to a sucient degree to allow overlap of the sphincter ends in the midline. When possible, the IAS should be separately identied and repaired. Excessive posterolateral dissection should be avoided because branches of the pudendal nerve are found in the 3 and 9 o’clock positions and may be damaged inadvertently. Cephalad dissec­tion in the rectovaginal septum continues until the levator ani muscles are identied where they insert along the “white line” on the obturator internus muscle on each side. In cases in which the sphincter muscles are dicult to identify, it is usually possible to identify healthy sphinc­ter in the ischiorectal fossa, away from the area of maximal scarring in the anterior midline, and dissect medially. In most instances, an overlapping sphincteroplasty, as described by Parks, is preferred. e attenuated muscle and scar are divided (preserving the scar to help prevent the suture from tearing through the muscle) and overlapped to recreate a snug anal canal (Fig. 19-1). e repair is then performed with a series of absorbable horizontal mattress sutures. Many surgeons also perform an anterior levatorplasty in an eort to lengthen the anal canal; however, it is a potential cause of dyspareunia.
Occasionally, the area of sphincter injury may show only thin­ning rather than a complete disruption. Under these circumstances, some surgeons prefer to simply plicate the muscle rather than divide it and overlap the ends. Data supporting this approach are limited. e key to a good outcome is to create a high-pressure zone in the anus of 2 cm or longer, and thus repair in depth is important.
lostomy or other fecal diversion is not necessary for the great
A co majority of sphincter repairs but may be considered under special circumstances, such as the failure of previous repair eorts.
One important aspect of sphincter repair aer obstetric injury is re-creation of an adequate perineal body. For routine repairs, vertical closure of the anterior portion of the incision is generally adequate. When more severe injuries are present—for example, with a complete cloacal defect—additional skin can be brought into the area through use of a cruciate incision followed by a Z-plasty closure. Depending on the extent of dissection in the rectovaginal septum, many surgeons insert a closed suction drain and vaginal pack that may be removed the following morning. In this circumstance, a urinary catheter also should be inserted at the end of the procedure.
Postoperative management aer sphincter repair varies consider­ably among surgeons. Narcotic analgesic medications are needed and
RECTAL AND PARARECTAL REGION
95
B
A
C
re best delivered in the postoperative period either by epidural catheter
a or patient-controlled analgesia pump. A regular diet may be resumed and laxatives are prescribed to avoid constipation or fecal impaction in the early postoperative period. Most patients are able to be discharged on the second postoperative morning. Some surgeons instruct their patients to perform a daily tap-water enema for the rst month aer surgery; at a minimum, patients should be instructed to perform an enema in the absence of a spontaneous daily bowel movement.
Between 60% to 80% of patients can expect a good or excellent result aer sphincter repair, although minor defects in control, such as leakage of gas or mild seepage, are common. However, continence may deteriorate over time. Adverse prognostic factors include multi­ple previous failed repairs, severe preoperative incontinence (to solid versus liquid stool), and possibly pudendal neuropathy. 
Postanal Repair
Parks devised a postanal repair for patients with anatomically intact but poorly functioning anal sphincters. e goals of the operation are to lengthen and narrow the anal canal and provide a more acute anorectal angle. e procedure is accomplished via a posterior intersphincteric dis­section and is carried above the rectosacral fascia, which provides access to plicate the puborectalis and external anal sphincter. Results of this pro­cedure have been variable, and evidence suggests that function continues to deteriorate aer surgery. e operation is now rarely performed. 
Anal Encirclement
iersch described the rst anal encirclement procedure for rectal prolapse in 1891. e principle of the technique is to tighten the anal orice with use of a simple subcutaneous suture. During the past 50 years a large number of alternative “sutures” have been described, ranging from wire to synthetic suture to various forms of silicone rub­ber. More recently, dynamic devices have been developed that allow relaxation of the anal canal to facilitate defecation. e articial bowel sphincter (ABS) consists of three components: an inatable cu, a pressure-regulating balloon reservoir, and a patient-activated control
FIGURE 19-1
anal sphincter (A). mattress sutures complete the repair (C). (From Fazio VW, Church JM, Delaney CP, eds. Current Therapy of Colon and Rectal Surgery. 2nd ed.
Philadelphia: Elsevier Mosby; 2005.)
Mobilization of the external
Overlap (B) and horizontal
pump. An appropriately sized cu is selected and positioned outside the EAS. e balloon is implanted in the space of Retzius by means of a short Pfannenstiel incision. e pump is positioned in the labia majora in women and in the scrotum in men. e system is lled with radiopaque uid, and its components are connected to one another by tubing. e cu is le in a deated position postoperatively through use of a deactivating button on the control pump. Provided healing is complete, the cu is activated aer 6 weeks, and under normal cir­cumstances the cu is inated. When the patient wishes to defecate, he or she pumps the uid from the cu. e cu spontaneously rells from the pressure-regulating balloon over 7 to 10 minutes.
e ABS has been used with some success; however, device ero­sion and outlet obstruction have proven to be dicult problems. A magnetic anal sphincter has been developed that consists of approxi­mately 20 individual magnetic beads linked by titanium wires that allow distraction of the magnets when pressure is applied to the anal canal during defecatory eorts (Fig. 19-2). Early results are promis­ing, but device erosion can occur, and longer term data are awaited. 
Muscle Transposition
Transposition of the gracilis muscle to encircle the anal canal as a treatment for fecal incontinence was described by Pickrell in 1952. Although the transposed muscle was meant to serve as a replace­ment sphincter, functional results proved to be poor. Augmentation of “neosphincter” function can be obtained by electrical stimulation of the obturator nerve because it supplies the gracilis muscle, and a stimulated gracilis neosphincter remains a useful option in patients who have lost considerable bulk of the sphincter mechanism, most oen as a consequence of perineal trauma. 
Sacral Ner
l nerve stimulation (SNS) is a novel approach to the treatment of
Sacra
ve Stimulation
fecal incontinence. is technique is similar to that used in urology prac­tice to treat voiding dysfunction, with reports of considerable success.
96
FIGURE 19-2
magnetic anal sphincter after inser
P
atients undergo acute percutaneous nerve testing to conrm pelvic oor contraction and to identify the optimal site of stimulation. e optimal site of stimulation causes maximal pelvic oor contraction with minimal associated contraction of the leg and foot. Once this site is iden­tied (most commonly S3), a temporary lead is secured in position and the patient undergoes test stimulation with an external pulse generator. If the incontinence improves by at least 50%, permanent lead implanta­tion with subcutaneous attachment to an implantable pulse generator is performed. Excellent functional outcomes with minimal morbidity have been reported. Several studies have shown improved quality of life asso­ciated with SNS therapy.
e mechanism of action of SNS for improving fecal incontinence is uncertain; however, data suggest augmentation of sensory aerent pathways and possibly normalizing colonic transit. In this regard, SNS has also been shown to reduce colonic transit time in patients with intractable constipation. e long-term results of SNS are excel­lent without apparent loss of ecacy. Some patients require device reprogramming, perhaps because of tissue reaction around the elec­trodes; however, in most patients, diculties arise only when the bat­tery life expires aer 6 to 8 years. Device replacement is relatively simple. It remains unclear whether SNS or anal sphincteroplasty should be the initial treatment of patients with EAS defects; how­ever, most surgeons recommend sphincter repair for defects aecting more than 25% of the sphincter. 
osterior Tibial Nerve Stimulation
P
A
s with sacral neuromodulation, posterior tibial nerve stimulation has been used by urologists to treat urinary incontinence. Recently, the technique has been investigated with regard to treatment of fecal incontinence. To date, eight studies using dierent neuro­modulatory protocols have been published. Short-term successes range from 30% to 83%. e advantages compared with SNS are that it is minimally invasive and potentially more cost-eective. However, the recent CONFIDeNT multicenter placebo controlled trial of a 12 week course of posterior tibial nerve stimulation found no signicant benet over sham stimulation. 
Fec
al Incont
Intraoperativ
e radiograph showing the position of a
Inence
tion.
Continence Enemas
C
ontinence enemas have long been the standard means of managing continence in patients with spinal cord defects that result in consti­pation and spurious incontinence. Malone developed the antegrade continence enema procedure for children, particularly those with spina bida. In adults, various ileal and colonic access conduits have been devised; however, the problem of stomal stenosis and access dif­culties aect all of them. Retrograde continence enema techniques can be very successful in motivated patients with spinal cord defects, multiple sclerosis, or diabetic neuropathy for whom SNS or antegrade continence enema have proven ineective. 
Stem Cells, Bulking Agents, and Other Techniques
n a number of studies, autologous myoblasts and broblasts have been
I injected into the urinary sphincter for the treatment of stress urinary incontinence with mixed results. Shak was the rst to explore the use of autologous fat cells injected into the external anal sphincter. More recent studies have used fat- and muscle-derived stem cells in the treatment of anal incontinence. Over the short term, results show modest improve­ments, and longer term data are awaited. e use of injectable nonbiode­gradable bulking agents has been disappointing because the ideal agent should be nonreactive, remain in situ, be easy to inject, and be cost­eective. To date, only one randomized trial of dextranomer in stabi­lized hyaluronic acid (Solesta, Q-Med AB, Uppsala, Sweden) has shown promise. Recently a thin, solid, polyacrylonitrile cylinder has been devel­oped (the Gatekeeper, THD, Correggio, Italy). Four to six of these cyl­inders are inserted into the intersphincteric plane, and within 24 hours they become thicker and shorter, with resultant narrowing of the anal canal. Again, long-term results are awaited. Finally, the SECCA device (CJ Medical, Tresilian, Truro, United Kingdom), which uses radiofre­quency energy to cause brosis in the anal canal, has been reported to improve continence. Long-term results with the procedure and compar­ative studies are required before its eectiveness can be judged. 
Fecal Diversion
Patients with severe fecal incontinence who have no therapeutic options should be strongly encouraged to consider a stoma. However, many patients, sometimes including those with debilitating symp­toms, are reluctant to even consider this option. e argument to be made is that of converting an unmanageable perineal stoma into a manageable abdominal one. Patients have unlimited time to make this decision, and referral to an enterostomal therapist, a patient who has undergone an ostomy, or both is invaluable. Patients can predictably expect to regain control of their bowel function and return to normal function in society without the fear of embarrassing accidents.
For most patients, the appropriate choice of stoma is an end­sigmoid colostomy. e stoma site should be marked preoperatively by the enterostomal therapist, taking into consideration patient habitus, scars, and other abdominal wall deformities. Patients with severe associ­ated bowel dysfunction such as slow transit constipation may be better served by an end-ileostomy. e procedure itself can be expeditiously performed using a minilaparotomy, trocar procedure, or laparoscopic techniques. It is important to counsel the patient that a defunctioned rec­tum may continue to produce mucus and that an interval proctectomy might be needed to manage distressing ongoing leakage of mucus. 

CONCLUSIONS

F
ecal incontinence is a distressing condition that is underreported and undertreated. e cause of the incontinence dictates its ther­apy. Although the diagnosis is usually evident from the history and
Candidate for surgery for FI
No immediate
surgical
indication
RECTAL AND PARARECTAL REGION
97
??
Biomaterial injection
Manometry, EMG, MRI, defecography
0–90° <180°
SNS
? MAS
hysical examination, appropriate investigation provides useful
p
Evaluation
EAUS ±
Sphincter
defect
Sphincteroplasty
conrmation and may uncover additional occult disease. Endoanal ultrasonography plays a particularly important role in dening the anatomy of both normal and disrupted anal sphincters.
e treatment of incontinence depends both on its cause and its severity. Mild incontinence is best treated by conservative management and sometimes biofeedback. Direct anal sphincter repair is indicated for more severe incontinence when an anatomic sphincter defect is present. When standard therapy is not appropriate or has failed, SNS should be considered (Fig. 19-3). Use of an ABS device or magnetic anal sphincter is an option when other modalities have failed. Continence enemas are useful, particularly when other modalities of treatment have failed or are deemed inappropriate. e role of injectable agents and other novel therapies remains to be established. Experience with the use of a gracilis neosphincter is limited, but the operation is of value particularly in patients with perineal tissue loss. Fecal diversion remains an excellent solution for the incontinent patient who is not a candidate for standard or salvage therapy or for whom these therapies have failed.
u
S
Engel AF, Kamm MA, Sultan AH, etal. Anterior anal sphincter repair in pa-
Findlay JM, Maxwell-Armstrong C. Posterior tibial nerve stimulation and fae-
S t
g g e
tients with obstetric trauma. Br J Surg. 1994;81:1231–1234.
cal incontinence: a review. Int J Colorectal Dis. 2011;26(3):265–273.
e d
R
e
a d i n g
S
SECCA
>180° or
perineal tissue loss
FIGURE 19-3
Individualized treatment:
• Muscle transpostion
• Artificial sphincter/MAS
• ACE
• Colostomy
• Conservative therapy
Glasgow SC, Lowry AC. Long-term outcomes of anal sphincter re-
pair for fecal incontinence: a systematic review. Dis Colon Rectum. 2012;55:482–490.
Knowles CH, Horrocks EJ, Bremner SA, etal. Percutaneous tibial nerve stimu-
lation versus sham electrical stimulation for the treatment of faecal incon­tinence in adults (CONFIDeNT): a double-blind, multicentre, pragmatic, parallel-group, randomised controlled trial. Lancet. 2015;386:1640–8.
Norton C, Kamm MA. Anal sphincter biofeedback and pelvic oor exercises
for faecal incontinence in adults—a systematic review. Aliment Pharmacol er. 2001;15:1147–1154.
Ratto C, Parello A, Donisi L, etal. Novel bulking agent for faecal incontinence.
Br J Surg. 2011;98:1644–1652.
Rockwood TH, Church JM, Fleshman JW, etal. Fecal Incontinence Quality of
Life Scale: quality of life instrument for patients with fecal incontinence. Dis Colon Rectum. 2000;43:9–16.
Tan E, Ngo NT, Darzi A, etal. Meta-analysis: sacral nerve stimulation versus
conservative therapy in the treatment of faecal incontinence. Int J Colorectal Dis. 2011;26:275–294.
in NN, Horrocks EJ, Hotouras A, et al. Systematic review of the clinical
eectiveness of neuromodulation in the treatment of faecal incontinence. Br J Surg. 2013;100:1430–1447.
Vaizey CJ. Faecal incontinence: standardizing outcome measures. Colorectal
Dis. 2014;16:156–158.
Wong MT, Meurette G, Wyart V, etal. e articial bowel sphincter: a single
institution experience over a decade. Ann Surg. 2011;254:951–956.
operativ incontinence (FI). ACE, Antegrade continence enema; EAUS, endoanal ultrasound; EMG, electromyography; MAS, magnetic anal sphincter; MRI, magnetic resonance imaging; SNS, sacral nerve stimulation.
Alg
orithm for
e treatment of fecal

R
 S: E  M
William Sangster and Da
vid B. Stewart, Sr.

DEFINITION

ectal stricture, or stenosis, is a pathologic narrowing or constriction
A r involving the lumen of the rectum. is narrowing can be the result of an intrinsic process that is occurring within the lumen or wall of the rectum, or it can be secondary to an extrinsic process compressing the rectum. A “clinically relevant” rectal stricture is one that is symptom­atic and not easily dened by measurement of the diameter. However, the condition frequently has been illustrated in terms of the inability to traverse the aected cross-section of rectum with either a rigid procto­scope (12 mm diameter) or a rigid sigmoidoscope (19 mm diameter). 
PRESENT
S
ymptomatic rectal strictures cause obstructive symptoms such as a gradual change in stool caliber or consistency, anorectal bleed­ing, tenesmus, or abdominal distention and discomfort that is oen exacerbated by eating. Some symptomatic rectal strictures that are not treated will eventually cause a complete large bowel obstruction, especially those associated with inammatory bowel disease (IBD), malignancy, and radiation-induced proctitis.
e diagnosis of a rectal stricture is based on history, physical examination, and, occasionally, imaging ndings. e degree of a ste­nosis is best imaged with a water-soluble contrast enema. Computed tomography and magnetic resonance imaging, with or without rectal contrast enhancement, can be helpful in assessing other segments of the alimentary tract or the peritoneal cavity for conditions such as IBD and cancer. 
ATION AND DIAGNOSIS
stricture that has been found incidentally. All strictures require assess­ment before it is safe to recommend observation. e rst step in the assessment is to exclude malignancy. Multiple biopsies, as well as imag­ing with endorectal ultrasound, computed tomography, and magnetic resonance imaging, are usually required to exclude cancer. All strictures should be described in terms of their diameter, their distance from the anal verge, and their length, because shorter strictures are more ame­nable to endoscopic dilatation than are longer benign strictures, which are more likely to require either diversion or resection.
For distal rectal strictures (those <6 cm from the anal verge), dila­tion can be performed digitally or with the assistance of instruments, such as Hegar dilators. Hegar dilators are quite useful because they come in multiple sizes with graded diameters, allowing a gradual dilation that provides a measure of safety against perforation. For more proximal strictures, dilatation with a rigid proctoscope or endoscopic balloon is an option. e success rate of endoscopic dila­tion is variable (88% to 100%) and depends on several factors, includ­ing stricture location (>8 cm from the anal verge being preferable), a shorter stricture (<1 cm), and the absence of any previous radiother­apy. As with Hegar dilators, pneumatic dilatation provides a choice of instruments to accommodate almost any stricture. When pneumatic dilation fails, other techniques include endoscopic electroincision of the stricture or endoscopic stent placement. Currently, stent place­ment for the treatment of benign rectal strictures has only been used in an o-label manner, and it is not approved by the Food and Drug Administration in the United States because of high rates of stent migration. If a stricture cannot be managed endoscopically, resection or fecal diversion is required.

ETIOLOGY

S
trictures of the rectum may develop as a result of multiple causes that can be broadly categorized as benign and malignant. ese causes are listed in Table 20-1. Management depends on the cause of the stric- ture, its distance from the anal verge, and the degree of stenosis. 

BENIGN RECTAL STRICTURES

lthough a variety of benign diseases can produce a rectal stricture,
A most benign strictures are due to an ischemic colorectal anastomosis or IBD. Benign rectal strictures do not need to be treated unless they are symptomatic, at which point several options are available, depend­ing on the nature and severity of the stricture (Fig. 20-1). Patients may be referred to a colorectal surgeon because an unexpected stricture is discovered during a colonoscopy. It is vital that the surgeon under­stand the dierence between a stricture that requires treatment and a
98
Rectal Strictur Disease
lthough rectal strictures related to IBD are usually benign, they are
A oen dicult to manage and thus warrant a separate discussion.
A rectal stricture in Crohn disease has been, and continues to be, a predictor of poor outcome, especially in terms of avoiding a permanent stoma. It has been suggested that the formation of rec­tal strictures in persons with Crohn disease is frequently associated with active disease involving both the rectum and anus, which confers a low probability of preserving per-anal defecation. Patients with a rectal stricture due to Crohn-related proctitis may require multiple surgeries, such as resection with a diverting stoma followed by subse­quent closure of the stoma, or, more commonly, an urgent resection to address a large bowel obstruction followed by an elective comple­tion proctectomy.
In an eort to avoid a resection and a likely permanent stoma, endoscopic balloon dilation has been attempted. For Crohn-related strictures, balloon dilation has a 60% to 70% success rate as dened by
es Related to Inflammatory Bowel
TABLE 20-1: Etiology of Rectal Strictures
Benign Malignant
nastomotic stricture Primary rectal cancer
A
Inammatory bowel disease (e.g.,
Crohn disease/ulcerative colitis)
Radiation Ovarian cancer
Ischemia Prostate cancer
Penetrating injury/foreign
body trauma
Caustic injury Sarcoma
Endometriosis
Pelvic abscess
exually transmitted infections (e.g.,
S
lymphogranuloma venereum)
T
uberculosis
Recurrent rectal cancer
Lymphoma
RECTAL AND PARARECTAL REGION
ean symptom-free interval of 12 to 18 months aer one dilation.
a m
99
However, balloon dilation has a high rate of perforation (approxi­mately 10%), sometimes with devastating consequences. To improve outcomes, some persons have suggested injecting corticosteroids directly into the area of the stricture in conjunction with dilation as a means of impeding collagen cross-linking and theoretically to decrease brosis aer dilation. However, intramural steroid injection was not demonstrated to improve outcomes in a randomized trial by East etal, and thus currently this use of steroids is not a routine practice. In the case of long-standing Crohn-related rectal strictures, biopsies should always be performed to exclude malignancy. Lengthy strictures and those with a greater severity and greater degree of dis­tortion of the rectal wall are more likely to require surgical resection, as are strictures with early and frequent recurrence aer endoscopic dilation.
For rectal strictures that occur in the setting of ulcerative colitis, management options are limited and tend to favor surgical resection, especially considering that removal of the rectum and colon is a cure for this form of IBD. Although rectal strictures related to ulcerative colitis have more frequently been shown to be benign than malig­nant, several scenarios exist in which the diagnosis of malignancy should be especially strongly considered. It has been estimated that if a stricture develops late in the course of the disease (aer approxi­mately 20 years), the probability of the stricture being malignant is as high as 61%. It has also been observed that if the stricture results
Benign anastomotic stricture
Asymptomatic Symptomatic
Monitor
<6 cm from anal verge
Digital/Hegar dilation
Surgical candidate
Recurrent symptomsSuccessful
Re-dilateMonitor Monitor
Recurrent symptoms
>6 cm from anal verge
Rigid proctoscope dilation/
endoscopic balloon dilation
Successful
Unsuitable for surgery
FIGURE 20-1 T
Resection versus stoma
reatment algorithm for benign rectal anastomotic strictures.
Endoscopic stent
placement or other
endoscopic therapy
100
Rect
RictuRe: etiology
al St
and Manage
Malignant Rectal Stricture
Ment
Surgical candidate
Excision ±
neoadjuvant or
adjuvant therapy
FIGURE 20-2
Decompression Palliation
Endoscopic self-expanding
metal stent placement
± (Chemo)radiotherapy
Surgical excision?
T
reatment algorithm for malignant rectal strictures.
in symptoms of a large bowel obstruction, the probability of the stricture being malignant is virtually 100%. Considering that there is a putative surgical cure for ulcerative colitis, and considering the diculties associated with false-negative biopsies of strictures that occur in the setting of ulcerative proctitis, surgical resection should be performed unless the patient is not a candidate for the procedure. Whether that surgery should entail a restorative proctocolectomy or a permanent ileostomy is a complex decision, because the presence of a malignancy in the rectum may warrant the use of radiotherapy, with its potential impact on an ileal pouch–anal anastomosis. 
MALIGNANT RECT
alignant strictures of the rectum are most commonly, and most
M
AL STRICTURES
appropriately, treated with surgical resection. Choices among surgi­cal options include anterior or low anterior resections, an abdomi­noperineal resection, or local excision through a transanal approach (Fig. 20-2). e choice of surgery depends on the size and clinical stage of the cancer, its distance from the anal verge, and the general health of the patient. In general, the endoscopic treatment of malig­nant colorectal strictures has been used in two clinical scenarios: preoperative decompression as a bridge to surgery, and endoscopic decompression for palliation in scenarios in which surgery is not feasible. Endoscopic modalities currently center on self-expanding metal stents and endoscopic laser therapies.
Self-expanding metal stents have been approved for use both in palliation and for preoperative decompression, which, in the latter instance, can serve to convert an indication for urgent surgery into a more elective scenario. Decompression permits mechanical prepa­ration of the large intestine and therefore the potential for avoiding the creation of a stoma. Endoscopic stents are composed of a variety of metal alloys and currently come in varying sizes. Successful stent deployment with improvement in the degree of colonic distention has been demonstrated in up to 80% to 90% of patients, based on the current literature. Stents for proximal rectal strictures appear to be tolerated better than stents for distal rectal strictures because stents placed distally in the rectum may produce tenesmus, rectal pain, and fecal incontinence. Perforation is the most serious complica­tion of endoscopic stenting within the rectum and has been observed to occur at a rate of 5% to 10%. In minor cases, perforation can be
Unsuitable for surgery/
does not desire diversion
Endoscopic self-expanding
metal stent placement or
laser therapy
(Chemo)radiotherapy
or monitor
managed with bowel rest and parenteral antibiotics. Larger perfora­tions may require emergency surgery. e reported stent migration rate and stent occlusion rate due to tumor ingrowth or fecal impac­tion is variable, ranging from 3% to 30%. If obstructive symptoms recur as a result of stent migration or tumor ingrowth, placement of a second stent is an option. Although no set guidelines exist regarding the length of time that an endoscopically placed rectal stent can be safely le in situ, reports have been made of stents remaining in place for up to 5 years without complications.
Laser therapy, which has been utilized for decades, has been found to be most useful in the palliation of obstructions caused by bulky, exophytic tumors. Overall, laser therapy has been shown to achieve successful palliation in 80% to 90% of cases in which it has been used. However, an average of approximately three procedures is required to achieve sucient relief of obstructive symptoms. ere­fore, some persons are attempting to transition to argon beam plasma coagulation, which has been reported to produce results similar to laser therapy. ese results have yet to be conrmed. 
SUMMAR
e management of rectal strictures varies according to their eti-
Th
Y
ology, severity, location, and the health status of the patient. After asymptomatic strictures have been evaluated to exclude cancer, they should be monitored but not necessarily treated. Symptom­atic rectal strictures can be treated endoscopically by dilation or incision, and if these techniques fail, by resection or diversion. Malignant strictures are resected or palliated with use of radia­tion, stenting, or debulking.
S
u
g g e
B
aron TH. Colonic stenting: technique, technology, and outcomes for
malignant and benign disease. Gastrointest Endosc Clin North Am.
2005;15(4):757–771. East JE, Brooker JC, Rutter MD, etal. A pilot study of intrastricture steroid
versus placebo injection aer balloon dilatation of Crohn’s strictures. Clin
Gastroenterol Hepatol. 2007;5(9):1065–1069. Fields S, Rosainz L, Korelitz BI, etal. Rectal strictures in Crohn’s dis-
ease and coexisting perirectal complications. Inflamm Bowel Dis.
2008;14(1):29–31.
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