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232
Fig. 12.1 Anal ssure
Fig. 12.2 Atypical ssure with skin changes, broad base, and lateral
location. (Courtesy of Sam Atallah, MD)
tion [2]. Chronic ssures are persistent, long-lasting ssures
that continue for more than 6weeks. In particular, the persistently high internal sphincter tone leads to chronicity of ssures, and they can cause pain even after a local anesthetic is
applied [1]. Chronic ssures may be found at an outpatient
clinic examination, although examination and visualization
V. L. Tsikitis and S. Marecik
Fig. 12.3 Acute ssure with clear edges and no signs of chronicity of
sphincter hypertrophy. (Courtesy of Richard P.Billingham, MD)
may be difcult due to pain and internal sphincter spasm.
Inspection classically reveals indurated edges, visible
sphincter muscle at the base, associated hypertrophic papilla
proximally, and a sentinel tag distally (Fig.12.3).
It is speculated that the lack of normal activity of nitric
oxide synthase (NOS) is responsible for the chronicity of
long-standing ssures. One study aimed to compare the presence of NOS in patients with and without chronic anal ssures. Internal sphincter biopsies were taken from patients
with chronic anal ssures at the time of lateral internal
sphincterotomy and from patients that were undergoing
abdominoperineal resections that acted as the control group.
Internal sphincter specimens from patients with chronic ssures contained little or no NOS compared to the internal
sphincters from the abdominoperineal resection specimens
[5]. In addition, the increased internal sphincter tone associated with anal ssures is thought to cause local ischemia
which prevents the ssure from healing. When the topography of the inferior rectal arteries was examined using postmortem angiography, the anoderm is supplied by the inferior
rectal arteries after traversing the internal sphincter, and it
clearly illustrated that the arterial perfusion is inversely
related to the pressure of the internal sphincter [6]. High
tonicity of the internal sphincter muscle will lead to lower
perfusion of the anal canal, suggesting the ssure represents
a nonhealing ischemic ulcer. Likewise, cadaver studies have
demonstrated a paucity of arterioles in the posterior midline
of the anal canal, also explaining the propensity for the posterior location of ssures [7, 8].
Anal ssures can also occur in women during labor and
delivery due to shear forces and local trauma. In fact, 11% of
chronic ssures are associated with difcult or instrumented
deliveries and are most common in the anterior midline [3].
Interestingly, these chronic ssures are not associated with
12 Anal Fissure andAnal Stenosis
233
increased sphincter tone, but normal or even low pressures. It
is important to distinguish the etiology of chronic ssures, so
treatment is appropriately tailored [9].
Medical/Pharmaceutical Treatment
Topical Agents
First-line treatment of anal ssures consists of conservative
medical treatment including stool softeners, psyllium ber
and other bulking agents, sitz baths, and the application of
topical analgesics such as lidocaine gel for pain control.
Most studies show healing rates of 16–31% in acute and
chronic ssures with conservative management [3]. The
application of local lidocaine does not increase ssure
healing rates when compared to placebo; however, lidocaine
can provide symptomatic pain relief [4, 10]. In addition,
maintenance therapy with ber decreases the risk of ssure
recurrence [11].
The goal of medical treatment of anal ssures is to
decrease the internal sphincter tone and allow healing.
Topical nitrate use leads to healing of chronic anal ssures in
about 50% of patients and demonstrates a 13.5% improvement in healing over placebo; however, recurrence rates are
high [4]. In particular, close to 50% of the patients who had
their ssures healed with nitrates will experience a recurrence. Commonly used topical nitrates include isosorbide
dinitrate and glyceryl trinitrate. However, these nitrates are
rarely used today due to their unpleasant side effects, primarily headaches [3, 4].
Application of topical calcium channel blockers including nifedipine and diltiazem has been associated with healing close to 90% of chronic anal ssures [12]. In addition, a
double-blinded, multicenter, randomized trial comparing the
application of nifedipine (treatment group) to hydrocortisone
and lidocaine (control group) found that the nifedipine treatment healed acute ssures within 21days in 95% of patients
compared to 50% in the control group [13]. In this study,
anal manometry conrmed that nifedipine decreased the
resting anal pressure by 30% compared to the control group
[13]. Data suggest that the cure rate of anal ssures is higher
with three times’ daily application of calcium channel blockers and with a 3-month treatment duration [14].
Botulinum Toxin Injection
When conservative management with topical ointment fails,
a second-line treatment still under the medical management
umbrella is the injection of botulinum toxin (Botox).
Interestingly, Botox injection has better results when used as
a second-line treatment [3, 15]. Treatment with Botox has
healing rates ranging from 27% to 96% [3]. The most common side effect related to Botox injection is temporary
incontinence, particularly to atus, that can occur in up to
18% of patients [3]. Multiple dosages (ranging from 20 to
100 international units (IU) or more) have been described,
and varied injection sites have been proposed [3, 4]. One
advantage of Botox injection over topical nitrates and calcium channel blockers is that it does not require a frequent
application schedule and does not cause similar unpleasant
side effects [4, 16]. However, its efcacy is questionable
with one meta-analysis showing that Botox injection had no
signicant advantage over nitrate topical application or placebo [10]. Another meta-analysis comparing Botox to
sphincterotomy reported that Botox has lower healing rates
but also lower rates of incontinence [17].
A Cochrane review of 77 studies and 5031 participants
showed that nitrates are marginally more efcacious than
placebo (48% healed versus 35%) in healing ssures [18].
Botulinum toxin injections and calcium channel blockers
were equivalent to nitrates in efcacy but had fewer side
effects [18]. No arms of medical therapy compared favorably
to surgical treatment; however, they all carry a lower risk of
permanent incontinence [10, 18].
Operative Treatment
Anal dilation is possibly the oldest treatment for anal ssures
and is only mentioned here for historic purposes. There is
substantial variance in the surgical technique with a wide
range of outcomes. A 2011 Cochrane review examining
seven randomized controlled trials comparing anal dilation
to sphincterotomy reported that anal dilation was less effective and resulted in higher rates of incontinence (OR: 4.03,
95% CI: 2.04–7.46) [19]. More recently pneumatic balloon
dilation has been described for anal ssure therapy. In one
study, a 40-mm-diameter and 60-mm-long anal balloon was
inserted into the anal canal after adequate lubrication and
was positioned with 10mm protruding from the anus. The
balloon was rapidly inated to a 20 psi pressure (1.4atm)
and maintained in situ for 6 min. The balloon was then
deated and removed. The ssure-healing rates were 83.3
percent in the pneumatic balloon dilatation and 92 percent in
the lateral internal sphincterotomy group. At anal manometry, mean resting pressure decrements obtained after pneumatic balloon dilatation and lateral internal sphincterotomy
were 30.5 and 34.3 percent, respectively. At 24-month follow- up, the incidence of incontinence, irrespective of severity, was 0 percent in the pneumatic balloon dilatation group
and 16 percent in the lateral internal sphincterotomy group
(P<0.0001) [20].
Lateral Internal Sphincterotomy (LIS)
Lateral internal sphincterotomy (LIS) is considered the gold
standard for treatment of chronic anal ssures with multiple
randomized studies showing its superior effectiveness in
234
V. L. Tsikitis and S. Marecik
treating the symptomatology when compared to conservative
medical management [21–32]. LIS has healing rates of
88–100%, but it can be associated with incontinence rates of
8–30% [4]. This incontinence can be transient (less than
2months) or prolonged (over 2months) in 3–7% of patients
[3]. However, these incontinence rates are reported with traditional LIS, when the sphincterotomy is carried up to the
dentate line. Such a traditional sphincterotomy has a lower
rate of recurrence and a higher risk of permanent incontinence when compared to the “tailored” sphincterotomy [33],
which is dened as a sphincterotomy to the apex of the ssure. The “tailored” sphincterotomy has been shown to preserve more of the sphincter and lowers incontinence rates
[19, 34]. Older randomized trials comparing traditional and
tailored sphincterotomy showed statistically higher healing
rates with the traditional technique, with relatively similar
reported incidences of minor incontinence (<3% incontinence rate) [35, 36]. Accordingly, the tailored sphincterotomy is as the preferred surgical approach which provides
symptom relief and decreased risk of permanent incontinence. LIS may be considered as rst-line surgical treatment
in patients without prior obstetrical injury, inammatory
bowel disease, prior anorectal operations, or sphincter weakness [4]. In particular, patients with chronic anal ssures and
without underlying fecal incontinence may benet from LIS
as the rst line of treatment.
Technique
LIS is performed with either an open or closed technique. In
the open technique, an incision is made distal to the dentate
line exposing the intersphincteric groove. The surgeon then
elevates and divides the internal sphincter muscle to the
height of the ssure and closes the wound with an absorbable
stitch. In the closed technique, the intersphincteric groove is
not exposed but delineated. A narrow-bladed scalpel, at
side adjacent to the muscle, is introduced through the skin in
either right- or left-lateral position of the intersphincteric
groove, and the tip is advanced submucosally to the dentate
line. The sharp edge of the knife is turned toward the internal
sphincter muscle, and the muscle is divided, releasing the
tension and creating a palpable defect. The skin opening can
be left open or closed with a chromic stitch. In a recent
Cochrane review comparing the open and closed techniques,
no difference in outcomes including persistence of the ssure or fecal incontinence was demonstrated between the
two techniques (Figs.12.4 and 12.5) [19].
Outcomes
Reported recurrence rates range from 0% to 15% after LIS,
which are usually attributed to insufcient length of the division of the internal sphincter muscle [3]. LIS can be repeated
and offered as a treatment of recurrent ssures and performed
on the contralateral side of a prior sphincterotomy site [4].
There is a paucity of data regarding recurrent ssures after
LIS.A recent study including 57 patients evaluated repeated
LIS for recurrent ssures with a mean follow-up of
12.5±4.2years. They reported a 98% healing rate and a 4%
minor incontinence rate including incontinence to atus and
seepage. The authors used the modied Cleveland Clinic
Incontinence Questionnaire to report patients’ symptoms,
and 2 female patients out of 57 reported varied incontinence
to atus and seepage [37]. Overall, one should consider LIS
as the standard surgical treatment for chronic anal ssures
with increased sphincter tone when medical management
has failed.
Local Advancement Flaps
Local advancement aps are the rst line of surgical treatment for chronic anal ssures associated with normal or low
anal pressures. These patients are usually female patients
that have developed ssures after a prolonged and difcult
vaginal delivery. These aps are usually anocutaneous aps
(dermal V-Y or house ap) which have been described using
a variety of techniques (see below in the “Anal Stenosis”
segment). Giordano etal. demonstrated a 98% healing rate
after anorectal advancement ap surgery independent of
anal tonicity [38]. At a 6-month follow-up, there was no
reported ssure recurrence or fecal incontinence [38].
Interestingly, the authors reported a 6% rate of ssure formation at a new site [38]. A smaller study showed similar
successful results after local advancement ap surgery for
ssures in the setting of hypotonicity with a median followup of 7months [39].
Anocutaneous aps have been combined with sphincterotomy or Botox injection to simultaneously address the
chronic nonhealing wound and the underlying sphincter
hypertonicity [4]. One randomized study allocated 50 patients
to receive LIS, 50 patients to receive V-Y advancement ap,
and 50 patients to receive a combination of LIS and V-Y ap
(see diagram in “Anal Stenosis” segment). At the 1-year follow-up, healing rates for patients who received LIS, V-Y
advancement ap, and a combination of LIS and V-Y ap
were 84%, 48%, and 94% (p= 0.001), and recurrence rates
were 4%, 22%, and 2% (p=0.01), respectively [40].
Fissurotomy andFissurectomy
Fissurotomy and ssurectomy are not considered standard
treatment options for anal ssure. Chronic ssures frequently
present with subcutaneous tracts that extend distally from the
chronic ssure to the sentinel tag. Fissurotomy involves
incising and dividing that tract to expose the chronic underlying cavity and release the perianal skin, resulting in widening of the anal canal. The wound remains open to heal by
secondary intention. One prospective trial of 109 patients
undergoing ssurotomy had resolution of symptoms in 98%
of patients, with the other 2% requiring subsequent sphinc-
a
12 Anal Fissure andAnal Stenosis
235
b
c
Fig. 12.4 Closed lateral sphincterotomy. (a). Location of the intersphincteric groove. (b). Insertion of the knife blade in the intersphincteric plane.
(c). Lateral to medial division of the internal anal sphincter (inset: medial to lateral division of the muscle)
terotomy [41]. In contrast, ssurectomy is dened as the
excision of the chronic ssure wound with excision of the
sentinel pile, if present. In a recent Cochrane review on operative procedures for ssure in ano, the authors commented
on two studies which compared ssurectomy with sphincter-
otomy [19]. These studies comprised of total of 162 patients
and found that sphincterotomy was signicantly less likely
to result in treatment failure compared to ssurectomy (OR
8.07 [1.42–45.84]). One of the two studies concluded that
ssurectomy is not a procedure of choice because of its asso-
236
V. L. Tsikitis and S. Marecik
ab
c
Fig. 12.5 Open lateral internal sphincterotomy. (a). Radial skin incision distal to the dentate line exposing the intersphincteric groove. (b).
Elevation and division of the internal sphincter. (c). Primary wound closure
ciated recurrence risk (3%) and the high rate of incontinence
(6%) [42]. Another study reported that ssurectomy, in combination with isosorbide dinitrate cream, resulted in 100%
healing within 10 weeks without recurrence and without
incontinence complaints [43]. A third study showed that ssurectomy with concurrent Botox injection led to 100%
improvement of symptoms with objective wound healing in
93% of patients [44].
eases. Fissures in Crohn’s patients usually present as deep,
painful ulcerations and are treated with Crohn’s medical
therapies. Crohn’s ssures are rarely treated surgically
because of perceived poor wound healing that may lead to
signicant perianal deformity and potentially to incontinence. Multidisciplinary care is instrumental in addressing
anorectal Crohn’s pathology, and optimal medical management may lead to resolution in more than half of the
cases [45, 46]. Treatment of atypical ssures associated
with sexually transmitted diseases is dictated by identify-
Atypical Fissures
ing the causative organism after a biopsy of the ssure.
HIV-related ssures are the most commonly encountered
Atypical ssures are most commonly seen in patients with
Crohn’s disease and patients with sexually transmitted dis-
and may present either as deep, broad-based ulcers or as
typical appearing ssures. These ssures are not associated
12 Anal Fissure andAnal Stenosis
237
with internal sphincter hypertonicity. Short-term successful
treatment options include surgical debridement and intralesional steroid injection; however, in the long term, optimizing antiretroviral therapy is instrumental for improving
symptomatology [47].
Anal Fissure, Conclusion
Anal ssures are common and can be effectively treated with
conservative medical management. When ssure symptomatology is long-standing (more than 6 weeks), topical calcium channel blockers in combination with sitz baths and the
use of psyllium ber or other bulking agents are the rst lines
of treatment. Botulinum toxin injection can be added when
medical management fails to provide a resolution of symptoms. LIS is considered the standard surgical treatment for
chronic anal ssures with a hypertonic internal sphincter and
can be considered rst-line treatment for patients that have
no underlying fecal incontinence. Advancement aps remain
an option for patients with symptomatic chronic anal ssures
with associated hypotonicity and/or compromised
continence.
Anal Stenosis
Incidence andCauses
Post-hemorrhoidectomy (secondary) anal stenosis or stricture
is present in 1.5–4% of cases with some recent reports quoting even higher incidence of 19% [53–55]. Hemorrhoidectomy
accounts for approximately 90% of all anal stenosis cases
[41, 42]. One of the more common scenarios occurs during
excessive removal of acute, swollen, and partially necrotic
grade IV hemorrhoids while failing to preserve adequate anoderm. Secondary anal stenosis following a pull-through procedure can occur in up to 16% of cases and occurs most often
following mucosectomy and/or anastomotic dehiscence [56,
57]. Pull-through procedures or sagittal anorectoplasties per-
formed on children in order to treat congenital anal stenosis
can lead to secondary anastomotic anal stenosis [58, 59].
Stapling procedures for hemorrhoids (PPH) have also been
associated with scarring and stenosis in the area of the anorectal junction [60]. Finally, Crohn’s disease can lead to stricture formation at many levels [61, 62], often with transmural
disease frequently involving the internal sphincter. Stricture
at the anorectal junction occurs when deep ssures of the rectal mucosa converge at the anorectal ring. More distal strictures of the anal canal are related to ssuring and stulizing
disease involving the anus and perianal region or simply from
chronic inammation caused by chronic diarrhea. The potential causes of anal stenosis are summarized in Table12.1.
Introduction, Denition, andTypes
Anal stenosis is an uncommon but potentially serious condition characterized by abnormal narrowing of the anorectal
junction, anal canal, or the anal margin. It occurs when the
physiologic capacity of the anal canal is lost and the pliable
tissues are replaced with brotic connective tissue [48]. This
leads to an abnormally tight and inelastic anal canal and can
also involve the internal anal sphincter [49]. Anal stenosis
commonly results from the loss of anodermal coverage distal
to the dentate line and less frequently can occur in the proximal anal canal [50].
Anal stenosis can be classied as congenital, primary, or
secondary [51]. Congenital stenosis is related to developmental abnormalities, which are frequently associated with
imperforate anus, anal atresia, or Hirschsprung disease.
Conversely, primary stenosis occurs later in life and is
related to rare involutional (senile) changes. Lastly, secondary anal stenosis is the most common presentation.
Historically, it has been connected to an improperly performed surgical hemorrhoidectomy, in particular a now
almost abandoned technique proposed by Whitehead [52].
Anal stenosis can also, however, be encountered after any
anorectal procedure or disease process resulting in repetitive trauma or excessive destruction of anoderm and hemorrhoidal tissue.
Symptoms
Symptoms of anal stenosis include difcult, painful, or
incomplete evacuation, fecal impaction, constipation,
decrease in stool caliber, tenesmus, bleeding, overow diarrhea, fecal seepage, and incontinence.
Evaluation
Initial diagnosis of anal stenosis can frequently be made in
the ofce during physical examination, although anatomic
ndings may not directly correlate with the severity of patient
symptoms. Findings can reveal narrowing of the anal opening
with common circumferential ssure formation [51].
However, the true extent and severity of the stenosis often has
to be investigated and identied with the patient under anesthesia to avoid unnecessary pain or discomfort. An exam
under anesthesia will also enable the physician to differentiate between the anatomical and functional cause of the stenosis and allow for biopsy of any suspicious lesions [63].
Relaxation of the anus during anesthesia is characteristic for
functional stenosis, while the persistence of stricture points to
anatomical stenosis caused by the scarring of the anoderm
and potentially the underlying internal sphincter. A thorough
238
V. L. Tsikitis and S. Marecik
Table 12.1 Potential causes of anal stenosis
Anorectal procedure
Hemorrhoidectomy
Excision and fulguration of condylomas
Wide local excision of Paget’s and
Bowen’s disease
Transanal excision of anorectal polyp or
cancer
Sphincteroplasty
Anastomotic type
Coloanal
Ileal pouch anal anastomosis
Mucosectomy
Pull-through for Hirschsprung’s disease
Inammatory bowel
disease
Involving lower rectum, anal canal, and
anal verge
Trauma
Chronic laxative use
Fissure(s)
Being a result and/or a reason
Radiation
Suppurative processes
Complex abscess/stula
Hidradenitis
Infectious
Sexually transmitted diseases
Tuberculosis
Neoplastic
Congenital
Table 12.2 Classication of anal stenosis
Severity Location Extent
Mild: Exam can be
completed with a nger
or medium HillFerguson retractor
Moderate: Dilation
needed to examine with
a nger or medium
Hill-Ferguson retractor
Severe: Unable to
examine with little
nger or small
Hill-Ferguson retractor,
unless forcefully dilated
Low: At least
0.5cm distal to
the dentate line
Mid: Within
0.5cm distal
and proximal to
the dentate line
High: At least
0.5cm proximal
to the dentate
line
Localized: One level
or quadrant of the
anal canal
Diffuse: More than
one level or quadrant
Circumferential:
Entire circumference
evaluation of the anorectum will allow for determination of
the degree, extent, and level of the stricture, circumferential
distribution of brosis, and any sphincter involvement.
Classication
Based on the above ndings, the severity of stricture can be
classied and appropriate treatment chosen. The most commonly used Milsom and Mazier classication is presented in
Table12.2 [50]. This classication divides the stenosis into
mild, moderate, and severe and low (65% of patients), midlevel (18.5% of patients), and high (8.5% of patients). In
addition, stenosis can be “diaphragmatic” (after inammatory bowel disease, characterized by a thin strip of constrictor tissue), “ringlike” (annular, lesions <2cm), or “tubular”
(length>2cm).
Treatment
The treatment of anal stenosis is based on patient symptoms
and varies depending on the severity, location, and cause of
the stenosis. Inammatory and infectious etiology should
always be treated with appropriate medical therapy rst.
Nonoperative Treatment
This option is typically used for patients with mild and occasionally moderate stenosis (as an initial step) and is based on
dietary modications, stool softeners, and “bulking therapy”
with dietary ber supplementation [49]. Assuring that the
stool is soft enough to pass through the stenosis, it allows for
the natural, repetitive stretch of the anal canal by a fecal
bolus. At a minimum, this can prevent further stricture formation. In many cases, this therapy is successful and can
lead to effective widening of the anal canal lumen [64].
If the bulking therapy is not successful, or the patient
experiences a signicant amount of pain during elimination,
digital or mechanical dilation can be performed [51]. This
can be attempted in the ofce with the use of local anesthetic
gel and a set of Hegar dilators, followed by at-home dilations. Alternatively, the patient can undergo the rst dilation
under anesthesia (with digital, Hegar, or pneumatic technique), followed by regular gradual dilations at home. A set
of metal or plastic dilators can be acquired for between $15
and $100. Historically, candles or other similarly shaped
household objects have also been used.
Any dilation under anesthesia should be performed carefully and follow two main principles. The rst is to allow for
only minimal trauma to the already strictured anoderm and
to avoid creation of deep ssures. The second principle
requires no disruption of the underlying internal sphincter
muscle. If the dilation procedure cannot meet the above principles, it should be avoided, and the patient should be advised
of other corrective techniques described later in the text.
Aggressive dilation with deep ssure creation and trauma
to the internal sphincter will likely lead to a brief improvement in symptoms. However, in the long term, it will also
lead to worsening of the anoderm and sphincter brosis [51].
Dilations can be successfully performed in patients with
Crohn’s disease, postradiation stenosis, or anastomotic strictures [49]. They are routinely used following pull-through
procedures for Hirschsprung’s disease in children [65]. It is
important to identify any anastomotic strictures as early as
12 Anal Fissure andAnal Stenosis
239
possible. In fact, it is the author’s routine practice to check
for them during the rectal exam within the rst 2weeks after
surgery. Early recognition of not-yet brotic strictures allows
for early, frequent digital dilations in the ofce or home,
thereby avoiding the need for forceful mechanical dilation
later.
Dilations of chronic and brotic strictures require compliant and highly motivated patients. Approximately half of
patients with anal Crohn’s stenosis will respond to medical
therapy and dilations, while the other half will require proctectomy or proximal diversion [66, 67]. Dilations are more
effective for shorter strictures. Pain related to dilations is a
major factor that can limit the effectiveness of the therapy.
Sphincter damage leading to fecal incontinence is a major
concern after repeated dilations [68]. If the stenosis is refractory to safe dilations, other surgical options should be
considered.
Anal stenosis is often associated with anal ssure disease,
which can be a result of or cause for the stenosis. For this
reason, it is important to rst address the ssure, as described
earlier in this chapter. Lastly, it is important to note that
because many patients initially present relying on laxatives,
enemas, suppositories, and even manual disimpaction
maneuvers, this can lead to additional trauma of the already
stenotic anal canal in the long term [51, 68].
Surgical Treatment
Operative treatment is reserved for severe and persistent
moderate anal stenosis, as well as for rare refractory cases of
mild symptomatic stenosis [49–51, 54, 63, 68]. Sphincter
function evaluation with anorectal manometry and pudendal
nerve motor latency can also be attempted before the surgical
correction if indicated; however, it will not likely change the
course of treatment and may be either painful or difcult to
perform. Endoanal ultrasound is not typically an option.
All corrective cases are performed under general anesthesia or under sedation with local anesthesia allowing for sufcient retraction and exposure of the anal area. The main
challenge is to provide the initial access to the strictured anal
canal, which will frequently require using a small-size HillFerguson retractor. Often, a gentle pneumatic or Hegar dilation is necessary to open the lumen. Any suspicious areas
should be biopsied to rule out malignancy since chronic
wounds have a higher propensity for malignant transformation. The extent and radial distribution of the scar should also
be ascertained since further treatment will be determined by
these ndings [50]. The internal sphincter involvement, and
its brosis, is evaluated for possible functional stenosis,
which may require lateral internal sphincterotomy [51]. Any
brotic stenosis of the internal sphincter muscle should be
addressed by concomitant sphincterotomy (unilateral or
bilateral) to improve chances of successful outcome [63].
The Lone-Star retractor is frequently used to bring the
anus into the effective operating eld. Release or excision of
the scar tissue enables further access into the anal canal.
Reconstruction of the anodermal defect can then be performed with a fragment of a healthy rectal wall (commonly
referred to as rectal mucosa), anoderm of the anal verge, or
the perianal and gluteal skin including the underlying subcutaneous tissues.
Transverse Closure Following Excision ofScar (With
Possible Sphincterotomy)
For short strictures involving the internal sphincter, an incision or excision of the scar with internal sphincterotomy can
be attempted. This will create a diamond-shape defect.
Transverse closure of this wound can then be attempted, as
long as there is no excessive tension on the tissues [69].
Absorbable and long-lasting 2-0 and 3-0 sutures should be
used (e.g., Vicryl). If there is too much tension on the edges
of the defect, the patient should be considered for a Y-V
advancement ap (see below) [69]. Simple stricture release
without any reconstruction attempt can lead to temporary
improvement in symptoms but will likely result in stricture
recurrence [49].
Rectal Advancement Flap
Advancement of the healthy rectal tissue is primarily
reserved for proximal and mid-anal canal stenosis [70–72]. It
is performed as a modication of Martin’s anoplasty following the incision or excision of the scar and optional concomitant internal sphincterotomy (preferably in the lateral
position) [73]. In the literature, this is described as “rectal
mucosal ap”; however, this term is a misnomer. The ap is
often not created, but rather the rectal wall is stretched to
cover the defect. And if the ap is created, to prevent ischemia of the ap, the dissection should also involve the deeper
tissues, including one or both layers of the muscularis propria of the rectum (potentially including some fragments of
the distal internal sphincter) or even a thin layer of the mesorectal tissue, which can ll in the sphincterotomy defect. One
of the important stipulations of this technique is to advance
the ap only to the level of the intersphincteric groove, thus
preventing mucosal ectropion creation. A potential defect
distal to the intersphincteric groove is usually left open for
secondary healing. Rahkmanine reported very good results
with this technique [74] (Fig.12.6).
Y-V Advancement Flap
This procedure, as with the techniques described below, is
used for mid- and distal anal stenosis [48, 75–77]. It involves
the advancement of the anoderm or the perianal skin into the
anal canal. After gentle dilation of the anus, a small- or
medium-size Hill-Ferguson retractor is used for the expo-
240
b
Flap advancement
Fig. 12.6 Rectal
advancement ap
Sphincterotomy
a
V. L. Tsikitis and S. Marecik
sure. The scar is longitudinally incised or removed, and
concomitant internal sphincterotomy can then be performed.
The vertical limb incision of the Y is extended proximally,
beyond the stenosed area, into the anal canal. Subsequently,
two incisions constituting the oblique limbs of the Y are created, starting at the distal end of the defect and extending
into the anal margin, for a total length of at least 5cm. The
created V ap should include the underlying subdermal tissue. In thinner patients, it can also include the subcutaneous
layer of the external sphincter muscle in order to provide
adequate blood supply and mobility. The ap is then stretched
proximally into the anal canal. The tip of the V ap is
anchored to the internal sphincter and the anal canal mucosa
at the proximal end of the defect. The edges of the ap are
sutured to the corresponding edges of the defect. Longlasting absorbable sutures are used. The V-Y ap can be used
to cover no more than 25% of the anal circumference and can
be performed bilaterally (similar to most advancement aps).
It should be noted that the tip of the ap is prone to ischemia.
Healing rate between 64% and 100% has been reported
(Fig.12.7) [75–78].
V-Y Advancement Flap
This technique involves the creation of a triangular island
ap using the skin, anoderm, and subdermal tissue, with the
proximal base of the ap directly adjacent to the defect from
the scar excision (and potentially the sphincterotomy) [50].
The foundation can also involve the subcutaneous layer of
12 Anal Fissure andAnal Stenosis
Fig. 12.7 Y-V advancement ap
241
Fig. 12.8 V-Y advancement ap
the external sphincter [79]. The tethering of the ap is only
dependent upon its deeper layers, while all edges are free.
The ap is then advanced into the resulting defect and
sutured circumferentially, while the donor site is closed.
This effectively pushes the ap into the anal canal. This
technique was initially developed as the treatment for anal
ectropion but later became an option in treating anal stenosis (Fig.12.8) [80].
Diamond (Rhomboid) Flap
This technique, described by Caplin and Kodner, involves
advancement of the rhomboid skin and subcutaneous
ap into the defect formed by stricturotomy in the distal
anal canal [81]. It can also include the bers of the subcutaneous layer of the external sphincter to increase its
thickness and reach. The ap is moved into the defect,
while attached by its deeper layers which provide the
vascular supply. It is then sutured circumferentially to
the surrounding tissues. The donor site defect is closed,
effectively pushing the ap into the anal canal. Excellent
healing rates after diamond anoplasty have been reported
(Fig.12.9) [76, 78, 81].
House Flap
This technique was rst described by Christensen etal. [82].
The house ap anoplasty involves proximal advancement of
the perianal skin into the area of the stricturotomy, located
distally to the dentate line. The concept is similar to the V-Y
ap or diamond ap techniques; however, the formation of a
wider ap allows for more effective treatment of the stenosis.
In order to accomplish this, the initial longitudinal incision
through the stenosed area is supplemented by two transverse
incisions of equal length at both ends, centered on the longitudinal incision. This may also involve the internal sphincter.
Alternatively, the scar can be excised in the form of a square.
Subsequently, a house-shape ap is created using the adjacent skin and subcutaneous tissue. Occasionally this can
include the subcutaneous layer of the external sphincter for
better vascularity and further reach. The base of the (house)
ap equals the length of the transverse incisions, and the
height of the house walls equals the length of the defect. The
ap is moved into the defect, while only tethered by its
deeper layers, which provide the vascular supply. It is then
sutured circumferentially to the surrounding tissues while
the donor site defect is closed, thus effectively pushing the