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approaches including LIFT, with healing rates that range between
57% and 100%. Changes in bowel continence have been reported in
up to 35% of patients treated with the procedure.
Other Continence Preserving Procedures
Synthetic and biologic materials such as fibrin glue and fistula plugs
were once promising additions to the armamentarium of fistula
treatment. Their general principle is obliteration of the internal
opening and fistula tract. Their primary benefit was a minimal risk
profile, as they pose no risk to continence, are easily repeated in the
case of recurrence, and do not preclude subsequent surgical management. However, more recent evaluations reveal low success rates, so
the procedures as standalone procedures have been relatively aban-
FIG. 7 Mucosal (Martin’s) advancement flap. A longitudinal incision is made
over the strictured area in the anal canal. Proximal rectal and anal mucosa
are then undermined through a transverse incision starting at the proximal
end of a previously made longitudinalincision. The flap is then sutured to
the distal edge of the internal anal sphincter, leaving open the most distal
aspect of the wound. (From Liberman H, Thorson AG. How I do it: anal steno-
sis.Am J Surg.2000;179:325.)
the base (proximal end) of the flap is wide, at least two to three times
the width of the apex. The trapezoidal-shaped flap is typically 2 to
4 cm long to allow for tension-free closure caudal to the level of the
original internal opening. Care should be taken to avoid excessive
handling of the flap, which can result in hematoma formation and
tissue compromise. The fistula tract is debrided with a curette, and
the external opening is widened to allow for drainage. Absorbable
suture is used to close the internal opening, and the integrity of the
closure is tested with injection of hydrogen peroxide at the external
opening. The tip of the flap with the internal opening is excised,
and the flap is gently pulled distally over the internal opening to the
dentate line, but not below it, to prevent ectropion formation. Wound
edges are reapproximated with interrupted absorbable suture.
Fistula healing after endorectal advancement flap repair is
reported in 66% to 87% of patients with cryptoglandular disease.
Factors associated with failure include prior radiation, Crohn’s disease, active proctitis, prior abscess drainage, rectovaginal fistula,
smoking, malignancy, obesity, and having more than one prior
attempted fistula repair. An endorectal advancement flap may be
repeated after a failed flap procedure or performed after other failed
doned. The use of fistula plugs or biologic mesh has been described
to augment the success of the LIFT repair however evidence that this
leads to superior results is limited.
Minimally invasive approaches to anal fistulas that use endoscopic or laser closure techniques such as video-assisted anal fistula
treatment (VAAFT), fistula laser closure (FiLaC), and endoscopic
clipping using an over-the-scope clip (OTSC) device have been
described in small, single-institution series with limited follow-up
and various degrees of industry support. Although short-term healing appears comparable to LIFT and endorectal advancement flap
repairs, long-term results are unavailable. All of these techniques
require specialized equipment and expertise, and their use is generally not recommended at this time.
S u g g e S t e d R e a d i n g S
Browder LK, Sweet S, Kaiser AM. Modified Hanley procedure for manage-
ment of complex horseshoe fistulae. Tech Coloproctol. 2009;13(4):301–306.
Bubbers EJ, Cologne KG. Management of complex anal fistulas. Clin Colon
Rectal Surg. 2016;29(1):43–49.
Emile SH, Khan SM, Adejumo A, Koroye O. Ligation of intersphincteric fistu-
la tract (LIFT) in treatment of anal fistula: An updated systematic review,
meta-analysis, and meta-regression of the predictors of failure. Surgery.
2020;167(2):484–492.
Gosselink MP, van Onkelen RS, Schouten WR. The cryptoglandular theory
revisited. Colorectal Dis. 2015;17:1041–1043.
Jacob TJ, Perakath B, Keighley MR. Surgical intervention for anorectal fistula.
Cochrane Database Syst Rev. 2010;5:CD006319.
Vogel JD, Johnson EK, Morris AM, et al. Clinical practice guideline for the
management of anorectal abscess, fistula-in-ano, and rectovaginal fistula.
Dis Colon Rectum. 2016;59(12):1117–1133.
Anal Stenosis
Chassidy Grimes, MD, and Dana Hayden, MD
BACKGROUND
Anal stenosis is a narrowing of the anal canal. The narrowing can be
anatomic, in which normally pliable anal mucosa is replaced with
fibrotic tissue. This scarring can be isolated or circumferential and
can vary in length. The narrowing can also be functional as a result
of a hypertonic internal sphincter. The causes of anatomic stenosis
can be further subdivided into congenital, primary, and secondary
causes (Box 1). The most common cause of secondary stenosis is surgery, most likely occurring after multiquadrant hemorrhoidectomy
when large areas of anoderm are removed. The literature cites that
up to 87% of cases are secondary to hemorrhoidectomy (Liberman
& Thorson, 2000; Katdare & Ricciardi, 2010; Khubchandani, 1994).
Stenosis may also result after procedures such as low anorectal
anastomosis or fistulectomy (Chiarelli et al., 2018). This chapter
focuses on the diagnosis and management of anatomic secondary
anal stenosis.
DIAGNOSIS
The diagnosis of anal stenosis is largely clinical, taking into consideration the patient’s surgical and medical history as well as physical
examination findings. The patient will often present with complaints
such as constipation, obstipation, painful bowel movements, bleeding, and small-caliber stools (Farid et al., 2010; Chiarelli et al., 2018).
Alternatively, they can have diarrhea caused by chronic laxative
use or overflow from subsequent upstream rectal dilation. It is
recommended that an anorectal examination be performed under
anesthesia to both minimize patient discomfort as well as distinguish

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BOX 1 Causes of Anatomic Stenosis
Congenital
Imperforate anus
Anal atresia
Primary
Senile
Secondary
Postsurgical
Laxative abuse
Inflammatory bowel diseases (Crohn’s disease)
Radiotherapy
Tuberculosis
Sexually transmitted infections
Trauma
Chronic diarrhea
Malignancy
TABLE 1 Grading of Anal Stenosis
Severity Level of Stenosis
Mild: Anal canal can be exam-
ined by a lubricated index
finger or medium HillFerguson retractor.
Moderate: Forceful dilation
is required to insert a
lubricated index finger or
medium Hill-Ferguson
retractor.
Severe: Forceful dilation is
required to insert a lubricated little finger or small
Hill-Ferguson retractor.
between a functional and anatomic cause of stenosis. Under anesthesia, the internal sphincter will relax, leading to resolution of
the stenosis if it is functional. With true scarring and stricture, the
stenosis will remain regardless of muscle relaxation. Anoscopy and
proctoscopy can be useful in determining the extent of stenosis and
assess the health of the rectal mucosa (Liberman & Thorson, 2000;
Katdare & Ricciardi, 2010). It is important to look for any firm tissue,
ulcerations, or outgrowths within or surrounding the area of stenosis and biopsy when appropriate to rule out malignancy as a cause.
Grading of anal stenosis proposed by Milson and Mazier is based on
severity and level of involvement within the anal canal (Table 1). This
classification may help guide the next steps in management (Milsom
& Mazier, 1986).
Low: Involvement at least
0.5 cm distal to the dentate
line
Middle: Involvement 0.5 cm
distal and proximal to the
dentate line
High: Involvement 0.5 cm
above the dentate line
the patient at home with a finger or a small plastic dilator. Dilation
may be considered controversial given the risk of incontinence, as it
may lead to hematoma formation within the intersphincteric space
causing further scarring (Khubchandani, 1994). Although there are
associated risks, some patients respond well to dilation. It should
be considered particularly in cases of Crohn’s disease and radiation
therapy where large perineal surgical operations are not advised
(Kashkooli et al., 2015; Liberman & Thorson, 2000; Lightner et al.,
2020). Most cases of mild and moderate stenosis can be managed
conservatively. For cases of severe stenosis, it is still recommended
to begin with medical management, although patients are likely to
require surgery (Brisinda et al., 2009).
Operative Management
Surgical management is considered in cases of moderate to severe
stenosis or for those patients who failed medical management. There
is a wide variety of options for surgical management. In cases of anastomotic stricture, a step-up approach should be considered. Initially,
dilation can be performed, followed by circular stapler resection
or stricturoplasty, and then finally transabdominal resection of the
anastomosis with repeat anastomosis as the last option (Kraenzler et
al., 2017). For other anatomic strictures, anoplasty is the treatment
of choice. The overall goal of anoplasty is to divide the stricture and
deliver more pliable, healthy anoderm into the area without tension,
thereby relieving the stenosis. This can be done with a variety of
surgical techniques.
Stricturoplasty
Stricturoplasty involves release of the stricture. The stricture is
divided longitudinally and closed transversely. This method can
provide symptom relief for the patient but can lead to subsequent
scarring and recurrent stenosis (Duieb et al., 2009; Katdare & Ricciardi, 2010).
Mucosal Advancement Flaps
During mucosal advancement flaps, the scar is excised and if there
is also scarring of the underlying sphincter, a sphincterotomy is performed (Fig. 1). A transverse incision is made at the dentate line, and
the rectal mucosa is undermined and advanced to the distal edge of
the internal sphincter to cover the defect (Rakhmanine et al., 2002).
The external portion of the wound is left open. Although there is a
small risk of mucosal ectropion, this is a good option for midlevel
stenosis because of minimal complications and symptom relief
(Casadesus et al., 2007).
Y-V Advancement Flap
This technique begins with a Y-shaped incision at the area of
stricture, and then it is carried on to the perianal skin, creating
a V (Fig. 2). The V portion of the incision is taken down to the
MANAGEMENT
Nonoperative Management
Management of anal stenosis depends on severity of stenosis and
the patient’s symptoms. It is generally accepted to start with conservative measures. This involves management with a high-fiber
diet, adequate hydration, and stool softeners. In addition, gradual
manual anal dilation can be performed. The initial dilation can be
performed under anesthesia with subsequent serial dilation done by
FIG. 1 Mucosal advancement flap. (From Fleshman JW. Fissure-in-anoand anal
stenosis. In: Beck DE, Wexner SD, eds:Fundamentals of Anorectal Surgery,ed 2.
London: Saunders; 1998.)

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FIG. 2 Y-V advancement flap. (From Fleshman JW. Fissure-in-anoand anal
stenosis. In: Beck DE, Wexner SD, eds:Fundamentals of Anorectal Surgery,ed 2.
London: Saunders; 1998.)
subcutaneous tissue, which contains the blood supply to the flap
(Gingold & Arvanitis, 1986; Liberman & Thorson, 2000). The apex
of the V is advanced into the anal canal and affixed to the internal
sphincter and rectal mucosa. This technique can be done bilaterally
but is not considered adequate for coverage of a stenosis >25% circumference of the anal canal (Brisinda et al., 2009).
V-Y Advancement Flap
An initial vertical incision is created to incise the scar tissue (Fig. 3).
A V-shaped incision is then made with the apex lying on the perianal
skin. Similar to the Y-V flap, the V is carried down to the subcutaneous tissue. The broad-based portion is advanced and affixed to
the dentate line with the final Y-shaped incision. This technique is
useful for the management of low, severe anal stenosis (Angelchik
et al., 1993).
House Flap
The initial incision is longitudinal and created from the dentate line to
the area of stenosis (Fig. 4). Two transverse incisions of equal width are
then created on both ends of the longitudinal incision. A house-shaped
flap is then created with the width of the base matching the width of
the transverse incisions and is carried down to subcutaneous tissue
with the apex overlying the perianal skin. It is then advanced into the
anal canal to cover the defect and sutured in place (Christensen et
al., 1992). This technique is useful for stenoses that extend from the
dentate line onto perianal skin. It also avoids the narrow apex involved
in Y-V advancement flaps, which are subject to ischemia (Alver et al.,
2008; Casadesus et al., 2007). House flaps can be performed bilaterally
and cover large areas of stenosis (Chiarelli et al., 2018).
FIG. 3 V-Y flap. (From Fleshman JW. Fissure-in-anoand anal stenosis. In:
Beck DE, Wexner SD, eds:Fundamentals of Anorectal Surgery,ed 2. London:
Saunders; 1998.)
Diamond-Shaped and U-Shaped Flap
For a diamond-shaped flap, the scar is incised with a vertical incision
that is carried on to perianal skin to make a diamond shape (Fig.5).
FIG. 4 House flap. (From Fleshman JW. Fissure-in-anoand anal stenosis. In:
Beck DE, Wexner SD, eds:Fundamentals of Anorectal Surgery,ed 2. London:
Saunders; 1998.)

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The flap is advanced into the anal canal and sutured (Liberman &
Thorson, 2000). The U-shaped flap is performed in similar fashion
(Fig. 6). It is useful for management of strictures with associated
mucosal ectropion, but the donor site is not closed, making it a less
desirable technique (Brisinda et al., 2009).
Rotational S Flap
This technique is used is cases of extensive and circumferential anal
stenosis that require excision of a large amount of skin (Handaya &
Sunardi, 2019) . An S-shaped incision is created, with the midportion
carried down to the dentate line transversely (Fig. 7). The wide portions of the S are then rotated down to the dentate line and sutured.
One limitation of the S flap is that it does not release the stricture as
effectively as the previously described advancement flaps (Brisinda
et al., 2009).
POSTOPERATIVE CARE AND
COMPLICATIONS
The majority of these procedures can be performed in an outpatient
setting but may require admission depending on the extent of dissection or surgeon preference. Postoperative care typically involves
adequate pain control, a strict bowel regimen that ensures soft stools,
and sitz baths or showers to keep the wounds clean (Chiarelli et al.,
2018). Complications include wound infection, flap ischemia, fecal
incontinence, failure to correct stenosis, recurrent stenosis, and
ectropion (Brisinda et al., 2009; Casadesus et al., 2007). Complication rates are relatively low, and good patient satisfaction has been
demonstrated with diamond, Y-V, and house flaps (Farid et al., 2010).
SELECTION OF SURGICAL TECHNIQUE
Given the multitude of options, Duieb et al. described an algorithmic
intraoperative approach to deciding which technique to use. First, an
FIG. 5 Diamond flap. (From Fleshman JW. Fissure-in-anoand anal stenosis. In:
Beck DE, Wexner SD, eds:Fundamentals of Anorectal Surgery,ed 2. London:
Saunders; 1998.)
initial longitudinal incision through the stricture is created, assessing
FIG. 6 U flap. (From Fleshman JW. Fissure-in-anoand anal stenosis. In: Beck DE, Wexner SD, eds:Fundamentals of Anorectal Surgery,ed 2. London: Saunders; 1998.)
FIG. 7 Rotational flap. (From
Fleshman JW. Fissure-in-anoand
anal stenosis. In: Beck DE, Wexner
SD, eds:Fundamentals of Anorectal
Surgery,ed 2. London: Saunders;
1998.)

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for a sphincter component, and sphincterotomy is performed when
necessary. Next, primary transverse closure is attempted if there
is no tension. If excessive tension is present, then a Y incision is
created via extension of the initial longitudinal incision, and a Y-V
flap is attempted. If there is continued tension, the Y incision is
extended to create a diamond flap. Even though low complication
rates were reported, this approach was only performed in a small
subset of patients and by only one surgeon (Duieb et al., 2009). It
does not consider the different patterns and extent of stenosis and
is solely based on tension. Farid et al. reported on 60 patients with
anal stenosis. They demonstrated that house flap reconstruction
achieved greater anal caliber while maintaining continence and
significantly improved quality of life when compared with Y-V and
diamond-shaped flaps (Farid et al., 2010). In conclusion, there is
no clear consensus on which technique is superior. Selection of
approach is ultimately based on surgeon experience and should be
individualized based on surgical history and anatomy, taking into
consideration the benefits and limitations noted with each of the
procedures.
S u g g e S t e d R e a d i n g S
Alver O, Ersoy YE, Aydemir I, etal. Use of “house” advancement flap in ano-
rectal diseases. World J Surg. 2008;32(10):2281–2286.
Angelchik PD, Harm BA, Starling JR. Repair of anal stricture and mucosal
ectropion with Y-V or pedicle flap anoplasty. Am J Surg. 1993;166(1):55–
59.
Brisinda G, Vanella S, Cadeddu F, et al. Surgical treatment of anal stenosis.
World J Gastroenterol. 2009;15(16):1921.
Casadesus D, Villasana LE, Diaz H, etal. Treatment of anal stenosis: A 5-year
review. ANZ J Surg. 2007;77(7):557–559.
Chiarelli M, Guttadauro A, Maternini M, etal. The clinical and therapeutic
approach to anal stenosis. Annali Italiani Di Chirurgia. 2018;89:237–241.
Christensen MA, Pitsch RM, Cali RL, Blatchford GJ, Thorson AG.
House” advancement pedicle flap for anal stenosis. Dis Colon Rectum.
1992;35(2):201–203.
Duieb Z, Appu S, Hung K, Nguyen H. Anal stenosis: Use of an algorithm to
provide a tension-free anoplasty. ANZ J Surg. 2009;80(5):337–340.
Farid M, Youssef M, El Nakeeb A, Fikry A, El Awady S, Morshed M.
Comparative Study of the House Advancement Flap, Rhomboid Flap, and
Y-V Anoplasty in Treatment of Anal Stenosis: A Prospective Randomized
Study. Dis Colon Rectum. 2010;53(5):790–797.
Gingold BS, Arvanitis M. Y-V anoplasty for treatment of anal stricture. Surg
Gynecol Obstet. 1986;162(3):241–242.
Handaya Y, Sunardi M. Bilateral rotational S Flap technique for preventing
restenosis in patients with severe circular anal stenosis: A review of 2
Cases. Ann Coloproctol. 2019;35(4):221–224.
Kashkooli S, Samanta S, Rouhani M, Akbarzadeh S, Saibil F. Bougie dilators:
Simple, safe and cost-effective treatment for Crohn’s-related fibrotic anal
strictures. Can J Surg. 2015;58(5):347–348.
Katdare MV, Ricciardi R. Anal stenosis. Surg Clin North Am. 2010;90(1):137–
145.
Khubchandani IT. Anal stenosis. Surg Clin North Am. 1994;74(6):1353–1360.
Kraenzler A, Maggiori L, Pittet O, Alyami MS, Prost à la Denise J, Panis Y.
Anastomotic stenosis after coloanal, colorectal and ileoanal anastomosis:
What is the best management? Colorectal Dis. 2017;19(2):O90–O96.
Liberman H, Thorson AG. Anal stenosis. Am J Surg. 2000;179(4):325–329.
Lightner AL, Click B, Yamamoto T, Spinelli A, Kotze P. Management of isolated
anal strictures in Crohn’s disease. Dis Colon Rectum. 2020;63(12):1639–1647.
Milsom JW, Mazier WP. Classification and management of postsurgical anal
stenosis. Surg Gynecol Obstetr. 1986;163(1):60–64.
Rakhmanine M, Rosen L, Khubchandani I, Stasik J, Riether RD. Lateral
mucosal advancement anoplasty for anal stricture. Brit J Surg.
2002;89(11):1423–1424.
Management of
Pruritus Ani
Matthew D. Price, MD, and Chady Atallah, MD
DEFINITION
Pruritus ani is a dermatologic condition characterized by an itching
or burning sensation of the perianal region. Although this condition
can be seen in any age group, patients often present in their third to
fifth decade of life after having attempted multiple over-the-counter
or home remedies with little success. Pruritus ani affects 1% to 5% of
the population with a male-to-female ratio of 4:1. Primary idiopathic
anal pruritus is responsible 50% to 90% of the time. Secondary causes
include infections or infestations, dermatologic inflammatory diseases, premalignant and malignant neoplasms, and benign anorectal
or systemic diseases (Box 1).
ETIOLOGY
Primary/Idiopathic Pruritus Ani
Primary or idiopathic pruritus ani is diagnosed after all secondary causes have been ruled out and no pathologic etiology can be
identified. Fecal soilage, moisture, and various nonspecific offending agents are thought to act as triggers. C-fibers, a class of nonmyelinated nerve fibers found in the somatic sensory system, are
believed to play a key role. Scratching to relieve the itch is known to
cause further excoriation and inflammation, which leads to further
stimulation of nerve fibers. This process is known as the itch-scratch
cycle. A key step in treating this condition is breaking the itch-scratch
cycle. Additionally, increased levels of histamine, bradykinin, and
kallikrein have been associated with the condition.
Certain foods have been associated with primary/idiopathic pruritus ani including coffee, caffeinated beverages, citrus fruits, chocolate, alcoholic beverages, tomatoes, and spicy foods (Box 2). These
foods have been shown to alter bowel habits and can act as irritants
to the perianal skin.
Secondary Pruritus Ani
Infectious
Fungal infections, particularly Candida, are relatively common
causes of pruritus ani with an estimated frequency of 10% to 43%.
Similar to most fungal infections, these usually occur in moist or
sweaty environments such as skin folds in elderly or obese patients.
Immunosuppressed patients or patients taking antibiotics are more
prone to developing Candida-related anal pruritus. Antifungal powder, good hygiene, and keeping the affected areas dry are important
steps in treatment. Oral antifungals can be used in cases of severe
infections. Several case reports have associated streptococci and
Corynebacterium minutissimum with pruritus ani, but they are found
much less commonly than fungal infections.
Sexually transmitted diseases are common causes, particularly in
patients practicing anoreceptive intercourse. Neisseria gonorrhoeae,
Chlamydia trachomatis, Treponema pallidum, herpes, Molluscum
contagiosum, and Condyloma acuminatum have all been implicated.

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BOX 1 Causes of Secondary Pruritus Ani
Infectious
Bacterial infection (Staphylococcus, Streptococcus, Erythrasma)
Sexually transmitted infection (Gonococcus, Chlamydia)
Fungal infection (Candida, dermatophytes)
Parasites (pinworms, scabies)
Viral infection (Herpes virus, Condylomata, Molluscum)
Dermatologic
Contact dermatitis
Atopic dermatitis
Perianal psoriasis
Lichen sclerosus
Seborrheic dermatitis
Anorectal
Hemorrhoids (external, prolapsing internal)
Fistula-in-ano
Anal fissures
Hidradenitis suppurativa
Fecal incontinence
Perianal Crohn’s disease
Skin tags
Chronic diarrhea
Pilonidal disease
Malignant
Anal canal cancer
Anal margin cancer
Rectal cancer
Bowen’s disease
Extramammary Paget’s disease
Systemic Disease
Diabetes mellitus
Leukemia
Lymphoma
Chronic renal failure
Iron-deficiency anemia
Hyperthyroidism
Hyperbilirubinemia
BOX 2 Food Products That Contribute
to Pruritus Ani
Caffeine-containing products (colas, coffee, tea, energy drinks)
Citrus fruits and vegetables
Carbonated beverages
Chocolate
Tomato
Beer
Spicy and acidic foods
Refined carbohydrates
Nuts
at night, resulting in local irritation. Oral albendazole is used for
treatment.
Dermatologic
Eczema, or atopic dermatitis, is the most common dermatologic condition responsible for anal pruritus. It is usually an allergic response
to a wide variety of inciting agents including laundry detergents or
topical creams. Identifying the inciting factor can be difficult, but
eliminating exposure is key to treatment.
Psoriasis can cause anal pruritus, although it more commonly
affects extensor surfaces of the extremities. Several series show that
4% to 8% of patients presenting with pruritus ani have psoriasis.
Treatment of psoriatic anal pruritus involves topical steroids for brief
symptomatic improvement followed by maintenance topical calcipotriene, salicylic acid, or ultraviolet light.
Other less common dermatologic causes of pruritus ani include
lichen sclerosus, seborrheic dermatitis, lichen planus, and lichen
simplex chronicus.
Anorectal Diseases
Benign anorectal conditions such as external and internal hemorrhoids, anal fissures, fistulae, hidradenitis suppurativa, perianal
Crohn’s disease, anal skin tags, and pilonidal disease are commonly
found in patients with pruritus ani. Management of the specific condition is associated with improvement in pruritus.
Malignant or premalignant anorectal processes can result in pruritus ani and should be considered at presentation including cancers
of the anal canal, anal margin, or even the lower rectum. Bowen’s
disease (perianal squamous cell carcinoma in situ) and Paget’s
disease (cutaneous adenocarcinoma in situ) are the most common
premalignant lesions. If Paget’s disease of the anal canal is discovered,
further endoscopic evaluation of the colon is needed to rule out an
underlying carcinoma.
Miscellaneous
Other causes of anal pruritus include radiation-induced perianal
dermatitis from cancer treatments, systemic diseases including uremic or cholestatic pruritus, and excessive moisture of the perianal
skin from urinary incontinence or vaginal discharge. Treatment is
dependent on the specific condition.
EVALUATION AND DIAGNOSIS
History
Evaluation of a patient presenting with anal pruritus begins with
a thorough history and physical examination. Patients can present
with a range of symptoms from mild irritation to severe, unrelenting
pain. Timing of symptoms can vary from worsening pruritus with
bowel movements to persistent pruritus throughout the day, or even
nocturnal symptoms. Bleeding can be present, though anything more
than spotting on toilet paper would warrant further workup for other
pathologies. Symptoms can be longstanding or recent onset. Patients
usually present to a specialist after having trialed several forms of treatment either on their own or as directed by their previous providers.
A patient’s bowel and cleansing habits should be discussed, including bowel frequency, diarrhea, anal incontinence, excessive wiping,
scented soaps, or prepared wipes. Sexual history should be ascertained.
Dietary habits should also be assessed for potential triggers (see Box 2).
Parasitic perianal infections are rare including pinworm (Entero-
bius vericularis), scabies (Sarcoptes scabiei), and pediculosis pubis.
Nocturnal pruritus ani in children is characteristic of pinworm
infections. The nematodes of the pinworm usually reside in the large
Physical
Physical examination begins with inspection of the perianal area,
perineum, and genitalia. Physical findings can range from completely normal to severe widespread excoriations. The Washington
Criteria has often been used to stage the appearance of perianal skin
according to severity of disease and should be documented with each
encounter to track treatment response (Table 1). Secondary causes

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TABLE 1 Washington Hospital Staging Criteria
Stage 0 Normal-appearing perianal skin
Stage I Erythematous and inflamed perianal skin
Stage II White, lichenified perianal skin
Stage III Lichenified skin with coarse ridges and ulceration
must be ruled out with anoscopy, and when indicated cultures or
biopsies should be taken. Indications for biopsy include any nonhealing wounds, ulcerations, or lesions suspicious for malignancy.
Microbiologic testing should be pursued based on clinical suspicion.
Any perianal drainage should be sent for bacterial and viral culture.
Patients with diarrhea should have their stool cultured and evaluated
for ova or parasites. Flexible sigmoidoscopy and colonoscopy with
biopsies should be performed whenever inflammatory bowel disease
or malignancy remain on the differential.
MANAGEMENT
Initial treatment of pruritus ani should be directed toward treatment
of any secondary causes identified. Once secondary causes have been
treated, symptom relief, healing of impaired skin, and prevention of
further damage should be the goals. It is important to inform patients
early on that there will likely be a period of trial and error as an
instant cure is unlikely.
Education and Lifestyle Modifications
Patients should be instructed to not scratch the area so as to begin
to break the “itch-scratch cycle” and prevent further excoriation and
irritation. As poor anal hygiene is a known trigger, time should be
spent educating on proper anal hygiene including gentle cleansing
of the perianal area with water and unscented soaps followed by cool
air-drying or dabbing with toilet paper after each bowel movement.
Scented soaps and prepared “baby wipes” should be avoided. The
anal region should be kept dry. This can be achieved by placing a
cotton ball in the gluteal fold after cleansing. Overzealous hygiene
with aggressive scrubbing should be cautioned against as this too can
lead to further excoriation and worsen the cycle. Though uncommon
in the United States, bidets followed by patting dry the area with
unscented toilet paper has been shown to be an effective method of
maintaining good anal hygiene. If chronic diarrhea impedes proper
perianal hygiene, fiber supplements or stool bulking agents should
be prescribed.
Loose-fitting clothing should be used to allow for natural aeration. Home and over-the-counter remedies should be discontinued
when initiating a stepwise treatment to rule out possible confounding factors. Dietary modifications should be made to avoid foods that
have shown to be associated with the condition, including caffeine,
spicy and acidic foods, chocolate, tomatoes, and carbonated beverages (see Box 2).
Medical
Following initiation of lifestyle modifications, topical agents can be
used for further treatment and symptom management. Hydrophobic
barrier creams that include zinc oxide such as Calmoseptine, Desitin,
and Balmex are helpful to allow for healing and long-term prevention. Antihistamines, both topical and systemic, have been shown to
decrease nocturnal itching. Topical capsaicin, a component of chili
peppers, has been shown to suppress the histamine-mediated itchscratch response. Topical steroids can be considered once infectious
causes have been ruled out. Topical cortisone cream is effective in
relieving pruritic symptoms, however long-term use is associated
with atrophy of the skin, thus treatment is usually limited to 2-week
periods. Though steroids are rarely curative, they can be effective in
breaking the itch-scratch cycle and allow time for the skin to heal.
Lack of clinical and symptomatic improvement within 2 weeks of
full lifestyle modification and topical therapy warrants further evaluation for missed secondary causes. Other treatments that have been
studied, though with limited data, include topical tacrolimus ointment for 4 weeks leading to decreased itch intensity and frequency.
Intradermal and subcutaneous injection of the perianal region with
methylene blue has shown resolution of symptoms in 20% to 88%
of patients. Methylene blue is thought to destroy sensory nerve
endings resulting in hypoesthesia of the perianal region. Initial trials
of methylene blue were complicated by several patients developing
full-thickness skin necrosis, though the technique has since been
modified. Patients should be counseled that the methylene blue will
often permanently color the treated area blue.
S u g g e S t e d R e a d i n g S
Ansari P. Pruritus Ani. Clin Colon Rectal Surg. 2016;29(1):38–42.
Kim JH, Kim DH, Lee YP. Long-term follow-up of intradermal injection of
methylene blue for intractable, idiopathic pruritus ani. Tech Coloproctol.
2019;23:143–149.
Ortega AE, Delgadillo X. Idiopathic pruritus ani and acute perianal dermati-
tis. Clin Colon Rectal Surg. 2019;32(5):327–332.
Siddiqi S, Vijay V, Ward M, Mahendran R, Warren S. Pruritus ani. Ann R Coll
Surg Engl. 2008;90(6):457–463.
Surgical Management
of Fecal Incontinence
Sarah Stringfield, MD, and Alessandro Fichera, MD
INTRODUCTION
Fecal incontinence (FI) is defined as the uncontrolled passage of
feces or gas over at least 1 month’s duration in an individual who
had previously maintained control. Fecal incontinence is a common condition, affecting up to 11% of men and 26% of women
older than 50 years of age. It is the second leading reason for
admission to nursing homes and is present in up to 50% of institutionalized patients. True prevalence may be even higher, as social
stigma surrounding incontinence likely limits reporting. Fecal
incontinence has a profound negative impact on quality of life and
generates a substantial financial and logistical burden to healthcare
and society.
Continence depends on the complex relationship between the
anal sphincter and pelvic floor musculature, rectal reservoir function,
stool consistency, and neurologic function. Conditions that alter any
of these factors may result in FI. General categories of causes of FI
include structural abnormalities, functional disorders, neurologic
etiologies, and congenital malformations (Table 1). In women, the

314 SURGICAL MANAGEMENT OF FECAL INCONTINENCE
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TABLE 1 Causes of Fecal Incontinence
Category Examples
Acquired structural
abnormalities
Functional disorders Diarrhea
Neurologic disorders Pudendal neuropathy
Congenital disorders Imperforate anus
leading cause is obstetric injury. Treatment is challenging and must
be individualized to each patient based on the underlying cause.
Obstetric injury
History of anorectal surgery
Rectal or hemorrhoidal prolapse
Anal or rectal fistula
Sphincter-sparing rectal resection
Trauma
Inflammatory bowel disease
Irritable bowel disease
Hypersecretory tumors
Fecal impaction (paradoxical diarrhea)
Radiation proctitis
Physical disabilities
Psychiatric disorders
Spinal injury or surgery
Multiple sclerosis
Dementia
Central nervous system disorder
Spina bifida
Cloacal defect
DIAGNOSTIC EVALUATION
A variety of diagnostic tests can be performed to help determine the
cause of the patient’s fecal incontinence and quantify the severity of
their symptoms (Table 2). Patients presenting with FI require a thor-
ough history and physical examination. Direct and specific questions
must be asked to understand the type and extent of incontinence.
This can include awareness of continence episodes (urge vs. passive
incontinence), timing and frequency of symptoms, stool characteristics and habits, and other associated symptoms such as prolapse,
drainage, and urinary or sexual dysfunction. A detailed obstetric
and surgical history is essential. Underlying disease processes such as
diabetes, stroke, inflammatory bowel disease, or certain medications
may contribute to FI.
A thorough anorectal physical examination should be performed.
Essential components of the examination include assessing the anal
sphincter tone and pelvic accessory muscles at rest as well as during
squeeze and Valsalva maneuvers. The patient should be evaluated
for the presence of pelvic organ prolapse, masses, perianal skin irritation, hemorrhoids, fissures, and fistulas.
There are many validated patient-reported scoring systems
that can be used to quantify the severity of fecal incontinence. A
commonly used system is the Cleveland Clinic Florida Fecal Incontinence Score (Wexner scale), which assesses the frequency of five
parameters (incontinence to solid stool, liquid stool, gas, wears a pad,
and lifestyle alteration) and sums it into an aggregate score. Additional scoring instruments include the Fecal Incontinence Severity
index, Fecal Incontinence Quality of Life score, and the St. Mark’s
Incontinence score. All scoring systems emphasize different symptoms and may be limited by the subjectivity of the reporting, failure
to include coping mechanisms, and lack of objective physiologic test
TABLE 2 Diagnostic Evaluation and Workup
Study Components and Examples
Patient history Awareness of incontinence episodes
Timing and frequency of episodes
Stool characteristics
Stool habits
Other associated symptoms (pro-
lapse, drainage, urinary or sexual
dysfunction)
Obstetric and surgical history
Medications
Underlying diseases
Physical examination Sphincter tone at rest and squeeze
Pelvic accessory muscles during
squeeze and Valsalva
Anatomic abnormalities: prolapse,
masses, hemorrhoids, fissure,
fistulas
Perianal skin irritation
Patient-reported scoring
systems
Endoanal ultrasound Sphincter integrity
Anorectal physiology Manometry
Defecography Prolapse
data. Although the scoring systems provide a useful way to quantify
severity of incontinence, they do not have the ability to accurately
predict outcomes.
Objective testing predominantly assesses sphincter integrity
and anorectal function. Endoanal ultrasound is the most sensitive
means to confirm whether a sphincter defect is present in patients
with suspected sphincter injury and determine the size of the defect.
Ultrasound can identify defects in both internal and external anal
sphincters (Fig. 1). Anorectal physiology testing includes manometry, anorectal sensation, volume tolerance, and compliance, and it
helps define the elements of dysfunction. Although findings do not
consistently correlate with the severity of FI or predict outcomes,
this type of testing can help define the elements of dysfunction and
guide management. Pudendal nerve terminal motor latency and
electromyography may be useful in select circumstances. Defecography, either with MRI or fluoroscopy, may be useful in cases of
pelvic organ prolapse to visualize positional instability and identify
involved pelvic compartments. Colonoscopy should be performed
in patients with bleeding, those with a change in bowel habits, and
those who meet national screening guidelines.
Cleveland Clinic Florida Fecal
Incontinence score
Fecal Incontinence Severity index
Fecal Incontinence Quality of Life
score
St. Mark’s Incontinence score
Anorectal sensation
Volume tolerance
Compliance
Electromyography
Rectocele/enterocele
Positional instability

ANORECTAL 315
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EAS
A
FIG. 1 Endoanal ultrasound evaluation of anal sphincters. (A) Intact sphincter complex. (B) Approximately 110-degree anterior sphincter defect.
IAS, Internal anal sphincter (dark ring) ; EAS, external anal sphincter (white ring).
NONOPERATIVE MANAGEMENT
Medical Management
Initial management of FI for all patients, regardless of etiology,
should be nonoperative. The goal is to control symptoms and attempt
to correct any modifiable factors contributing to the patient’s presentation. Up to 20% to 50% of patients can improve after starting
medical management and lifestyle changes, which avoids surgery
in many patients. Initial steps include optimizing stool consistency,
slowing bowel motility, and minimizing the average stool load in the
rectum, particularly before sleeping or leaving home. These changes
can often be accomplished with habit changes and dietary modifications as well as pharmacologic and bowel management interventions.
Common foods that promote urgency or diarrhea should be avoided.
This includes caffeine, sugar replacements, and lactose. Dietary fiber
supplementation may improve stool consistency in patients with
diarrhea, prevent seepage, and promote complete evacuation. Antidiarrheal medications such as loperamide and diphenoxylate-atropine
can also help thicken stools and decrease frequency. Cholestyramine
can be helpful in patients with bile acid diarrhea, usually those with a
history of cholecystectomy or terminal ileal resection. Irritable bowel
syndrome can be treated with tricyclic antidepressants and drugs
such as alosetron or eluxadoline. Bowel management programs start
with patient education regarding regularity and timing of bowel
movements in relation to the gastrocolic reflex. Timing meals and
reducing stool load in accordance with planned events or sleeping
can prevent episodes of incontinence in these situations. Scheduled
enemas can reduce stool load and are therapeutic in patients with
fecal impaction and overflow incontinence. Incontinence pads and
barrier creams for perianal skin care are useful adjunctive treatments.
IAS
EAS
IAS
B
TABLE 3 Surgical Targets and Options
Goal Options
Correction of
anatomic
abnormalities
Enhancement
of sphincter
function
Sphincter replace-
ment or support
Diversion Colostomy
Reduction of fecal
load
any adverse side effects, and it should be offered to any patient who
may be a candidate.
Overlapping sphincteroplasty
Prolapse repair
Fistula repair
Hemorrhoid treatment/excision
Cloaca or keyhole deformity repair
Sacral nerve stimulation
Radiofrequency energy administration
Injection of bulking agents
Tibial nerve stimulation
Artificial bowel sphincter
Implantation of magnetic anal sphincter
Graciloplasty
Cerclage (Thiersch procedure)
Pelvic sling system
Ileostomy
Antegrade continence enema
Biofeedback
In patients with some degree of preserved voluntary sphincter
contraction, pelvic floor physical therapy and biofeedback therapy
can improve symptoms. The sessions focus on strengthening and
re-coordinating the pelvic floor and sphincter function in response
to rectal distension. The patient is monitored during the biofeedback sessions and counseled on appropriate muscle contraction,
relaxation, abdominal pressure, and breathing techniques. Subjective
benefits have been noted in up to 64% to 89% of patients who participate in the therapy. Long-term results and objective benefits are less
clearly defined. The approach is simple, noninvasive, and without
SURGICAL MANAGEMENT
Patients who fail medical management may be offered a surgical
option. There are many options for surgical interventions, and the
approach typically depends on the etiology of the incontinence,
severity of the symptoms, and several patient factors (Table 3). The
initial approach should typically correct any anatomic abnormalities
that may be contributing to incontinence, as restoration of normal anatomy may normalize function. This can include rectal or
hemorrhoidal prolapse, rectovaginal or anal fistulas, and cloacal or
keyhole deformities. If symptoms persist, then incontinence-specific
approaches may be considered. While many incontinence-specific

316 SURGICAL MANAGEMENT OF FECAL INCONTINENCE
Median sacral crest
hypogastric plexus
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options exist, many are not frequently used or require medical
devices that have been taken off the market. The most common and
efficacious surgical interventions include sacral nerve stimulation,
sphincteroplasty, and fecal diversion.
Sacral Nerve Stimulation
Sacral nerve stimulation (SNS) is a technology initially developed
for urinary incontinence but was demonstrated to have benefits
for FI as well. The device stimulates the S3 nerve root by delivering
mild electrical pulses. The exact mechanism by which it improves
urinary and fecal incontinence is not fully understood. SNS has been
approved by the US Food and Drug Administration (FDA) for use in
treatment of FI in the United States since 2011 and can be performed
in most patients with FI. Patients with sphincter defects up to 120
degrees can see a reduction in severity and frequency of FI episodes
with implantation of SNS.
The procedure is performed in two stages. During the first stage,
a tined lead is placed under fluoroscopic guidance along the S3 nerve
root (Figs. 2 and 3). The procedure is performed under monitored
anesthesia care or general anesthetic with a short-acting paralytic
agent. The patient is placed prone, and exposure of the buttocks and
feet are maintained to visualize motor responses. Access to the S3
foramen is obtained with a hollow needle under fluoroscopic guidance. Appropriate needle placement is confirmed by stimulating the
needle with an electrical impulse and confirming appropriate motor
response. Motor responses of S3 stimulation include pelvic bellows
and ipsilateral big toe plantarflexion. Using Seldinger technique, a
wire and subsequently a tined lead is placed through the S3 foramen
and along the S3 nerve root. The lead is tunneled laterally to a subcutaneous pocket and coupled with an external wire. The external
wire is tunneled out of the skin several centimeters removed from
the subcutaneous pocket and coupled with an external battery pack.
The external wire and battery pack are bandaged, and the patient is
instructed to avoid showering during the trial period.
During a 2-week trial period, the patient keeps a diary of incontinence symptoms and compares it to a diary kept before implantation of the SNS. Lead settings are modified in the outpatient setting
until the patient has maximum benefit with minimal discomfort. If
the patient sees a benefit, typically 50% or greater reduction in the
number of incontinence episodes, then the second stage of the procedure is performed. The patient is positioned in the same way. The
external wire is uncoupled from the tined lead and removed. The
lateral subcutaneous pocket is opened, and the permanent device is
connected to the tined lead and implanted. If the patient does not see
a reduction in incontinence symptoms or does not tolerate the device
during the trial period, then the lead and external wire are removed
during the second phase.
Patients now have the option of having a rechargeable battery or a
larger, non-rechargeable battery pack placed that lasts approximately
SNS device
implantation
Tined lead
Electrodes
Pudendal nerve
Inferior
Posterior femoral
cutaneous nerve
Perineal nerve
Sciatic nerve
Iliac crest
Sigmoid
colon
(outline)
S3
L3
L4
Rectum
Rectum
L5
S1
S2
S3
S3
S4
S4
Dorsal sacral
foramina
Lateral sacral crest
Ischial spine
Uterus
Coccyx
Bladder
Vagina
FIG. 2 Sacral nerve stimulator placement and anatomy. (From Hull T. Posterior Pelvic Floor Abnormalities. Philadelphia: Elsevier; 2011).
Anus
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