Management of Common Anorectal Disorders
1.0 Introduction/General Considerations
Anorectal disorders include a diverse group of pathologic conditions that are
the cause of significant patient discomfort and disability. Amongst the most
common conditions requiring evaluation, hemorrhoids alone account for almost
2 million ambulatory care visits each year in the United States(1).
Luckily, most anorectal disorders seen in practice can be managed in the office
without any surgical treatment. Despite this, serious disorders like inflammatory
bowel disease and malignancies always need to be kept in mind and considered
in the differential diagnosis when evaluating the patient with an anal complaint.
In addition, problems in these last few centimeters of the gastrointestinal
tract have a major effect on overall quality of life. Serious associated morbidities,
leading to diminished function, may occur secondary to both incorrect or delayed
diagnosed or inappropriate treatment. Although non-operative management is often
the initial treatment, surgical options always need to be a component of the
armamentarium for dealing with these diverse processes. Thus surgeons need to
be aware of all aspects of approaching the patient with anorectal pathology,
as ultimate recovery and function depend on accurate and proper evaluation and
management.
2.0 General Anatomy of the Anorectal Region
The anal canal is approximately 5 cm in length. It begins a few centimeters
above the dentate line and extends down to the anal verge. The histology of
the anal canal at its proximal end is transitional epithelium. (Figure
1) It begins where the columnar epithelium of the rectum ends. The transitional
epithelium extends down to the dentate line where the stratified squamous epithelium
begins. Stratified squamous then extends to the anal verge where the true skin
begins, complete with hair follicles and sebaceous glands. The dentate line
is clearly visible 1 – 2 cm above the anal verge in the middle of the
anal canal. It appears as a series of peaks and valleys highlighted by a purplish/blue
appearance from the underlying blood vessels. Each valley has an opening or
anal crypt that connects to an anal gland. These glands secrete mucous into
the anus. A thorough understanding of the anatomy provides insight into the
associated pathological processes that occur in this region. For example, cryptoglandular
infections are the source of perirectal or perianal abscesses and fistulae.
Innervation of the lower anal canal below the dentate line and perianal skin
is via somatic nerves. Thus, lesions in this area such as abscesses, thrombosed
external hemorrhoids and anal fissures can be extremely painful. Innervation
of the upper anal canal is via autonomic nerves. Lesions in this area such as
anal malignancies and internal hemorrhoids are not usually painful, allowing
procedures such as band placement of internal hemorrhoids to be possible.
Just beneath the hemorrhoidal plexus lies the sphincter complex. Two muscle
groups make up the anal sphincter mechanism. The internal sphincter is the innermost
muscle. It is smooth, involuntary muscle and is primarily responsible for the
resting tone of the anal canal and control of flatus. The external sphincter
muscle is skeletal, voluntary muscle and is primarily responsible for control
of feces. Division of the internal sphincter muscle for treatment of fissures
or fistulae is usually well tolerated and does not lead to significant problems
with incontinence. Division of the external sphincter muscle, however, can lead
to debilitating incontinence to solid stool and is strongly discouraged (2,3).
3.0 Hemorrhoids
3.1 Introduction
Hemorrhoids, also called piles, is a term that refers to the normal circumferentially
located submucosal vascular beds above and below the anal canal. As they are
an essential part of a normal state, the presence of these hemorrhoids does
not mean a pathologic change is present. In the normal state they act to maintain
anal continence, especially when there is increased pressure in the anal canal
during coughing, straining, or sneezing. To have hemorrhoidal disease, changes
that lead to bleeding, thrombosis, prolapse and possible rectal pain need to
be present. Hemorrhoidal disease occurs when the increased anal pressure is
prolonged such as during pregnancy or with severe constipation. It can also
occur with diarrhea, aging, or due to hereditary factors.
3.2 Etiology/ Epidemiology
The term “hemorrhoids” is often misused and therefore prevalence
estimates are often not accurate. Estimates range from prevalence in the United
States being as high as 80% (4) to estimates that over 50%
of the population will have developed hemorrhoidal disease by the time they
are 50 years of age (5). Both men and women are equally affected4.
Symptoms increase with age, with peak incidence being between 45 and 65 years
old (6). Other predisposing factors include pregnancy, chronic
straining and increased abdominal pressure (7). Although an
associated family history has been suggested, it may simply reflect an increased
familial trend in seeking treatment.
3.3 Relevant Anatomy/Physiology
Hemorrhoids are classically located in three columns, including right anterior,
right posterior, and left lateral. (Figure 2) More commonly,
these three columns are obscured by edema, clot, and many times are not found
in these exact locations. The more important discrimination is between internal
and external disease. Internal hemorrhoids are located proximal to the dentate
line, though often found protruding distal to it, and are covered with mucosa
with an autonomic nerve innervation. External hemorrhoids originate distal to
the dentate line, are covered with modified squamous epithelium and have somatic
innervation. Because of this difference in innervation, external hemorrhoids
are more often painful than their internal counterparts. Factors described above,
including chronic straining, will disrupt the anal canal and vascular engorgement
ensues. It is also important to make note that rectal varices associated with
portal hypertension are not hemorrhoids, and are beyond the scope of this text.
Hemorrhoids are classified first in external and internal hemorrhoids. Internal
ones are then classified as to the degree of prolapse during straining, which
aid as a guide to appropriate treatment. First-degree do not descend below the
dentate line; second-degree will protrude on straining, but have spontaneous
reduction; third-degree internal hemorrhoids protrude and require manual reduction
to return to the anal canal; and fourth-degree hemorrhoids protrude beyond the
anal verge and are unable to be reduced.
3.4 Diagnosis
Symptoms of hemorrhoidal disease differ for internal and external hemorrhoids.
Most patients with internal hemorrhoids will come in with the symptom of rectal
bleeding. This bleeding is most commonly painless, bright red, and often noted
when causing additional trauma to the tissues, including during a bowel movement
or during the use of tissue paper. Bleeding is associated with internal hemorrhoids
as they are covered with mucosa. External hemorrhoids do not bleed as often,
as they are covered with anoderm, but can present when they become thrombosed:
severe pain that is acute in onset and constant in nature. (Figure
3) This pain typical peaks after the third or fourth day and will then slowly
subside. Another presenting symptom includes “feeling a small mass”
around the anus. This represents a prolapse and can either be present intermittently
or continuously. As many rectal diseases are associated with bleeding, a thorough
history and physical exam is necessary with important factors being protrusion,
bowel movement patterns, anti-coagulation history and immunosuppression. Examination
should include a good visual external examination including digital rectal examination
to palpate for masses, fissures or fluctuance. Circumferential internal examination
with the anoscope to evaluate the mucosa and evaluate for signs of proctitis
or other concomitant disease should also be performed. (Figure
4) Having the patient perform the valsalva maneuver will aid in assessment
of the degree of protrusion. Emphasis should be placed on identifying the dentate
line and determining the origin of the hemorrhoidal tissue to delineate internal
versus external disease. Further evaluation such as a rigid proctoscopy, sigmoidoscopy
or colonoscopy, if available, may be warranted if no obvious diagnosis can be
made. The differential diagnosis should include anorectal tumors or polyps,
hypertrophied papillae, abscesses, fissures, inflammatory bowel disease, rectal
prolapse, condylomata and other sexually transmitted diseases.
3.5. Management
Treatment for external hemorrhoids is often only sought for pain associated
with thrombosis. The treatment should be guided towards relieving this pain.
As stated before, pain typically peaks after the third or fourth day and will
then slowly subside and this should be considered in deciding upon treatment.
Oral analgesics, sitz baths, bulking agents and/or stool softeners, cold cloths
or ice applied directly to the hemorrhoid are initial treatments3. Increasing
the amount of roughage or fiber (approximately 30g/day) and fluid in the diet
will help alleviate constipation and decrease the pressure in the anal canal,
and is recommended for all patients with any type of hemorrhoidal disease. Surgical
excision can shorten the length of recovery and is recommended when severe symptoms
are present and the patient presents within the period of still increasing pain.
Excision can be performed in the office with use of local anesthetics like xylocaine
containing epinephrine. Excision should include removing the thrombus and leaving
the skin open or closure of the overlying anoderm. Skin tags associated with
external hemorrhoids are often asymptomatic, but if needed can be removed by
simple excision using scissors or electrocautery with, again, local anesthetics.
Other reasons for excision of external disease include large symptomatic piles
that provide difficulty with hygiene or repeated flares.
Internal hemorrhoids can again initially be treated with conservative therapy
and surgery should only be reserved for severe cases. Conservative therapy includes
the therapies described above with addition of usage of hydrocortisone suppositories.
Such therapy is most effective in grade I and II internal hemorrhoids. If these
therapies do not work, use of rubber band ligation, sclerotherapy and photocoagulation
can be used. All three procedures can be performed in the office. Sclerotherapy
involves injecting sclerosants (such as morrhuate sodium, 5% phenol in olive
oil, and hypertonic saline) with a 30-gauge needle. This will then cause an
intense inflammatory reaction that leads to destruction of redundant submucosal
tissue. Although not performed as much as in the past, it may be effective when
other therapies are not available or in the patient taking anticoagulation medication.
Rubber-band ligation, originally described by Barron in 1936, is performed with
a hemorrhoidal ligator, such as the McGivney dilator (8). A
latex rubber ring is placed over the tip of the instrument. Typically, the drum
is loaded with two latex bands for each hemorrhoid to ensure ligation of the
hemorrhoid if a band breaks or slides off. The instrument tip and rubber band
are placed over the hemorrhoid, and a grasping forceps is used to pull the hemorrhoidal
tissue through the drum, positioning the rubber band at the base of the hemorrhoid.
(Figure 5) Prior to placement of the band, the patient
should be asked if any discomfort is felt. This may indicate that the tissue
is too close to the somatically innervated tissue near the dentate line. If
extreme pain is felt after the band is applied, the ligature should be removed
immediately by grasping the band with a crypt hook and cutting it. Band ligation
causes the hemorrhoid to become ischemic and slough off within 7 days or so.
Although we recommend placement of a single band on the initial setting to ensure
tolerance, multiple applications can be performed within a subsequent 2 to 4-week
interval. Ligation of multiple hemorrhoids can be performed, but this will increase
the overall discomfort. Complete relief of symptoms can be achieved in approximately
80% of patients. Rubber band ligation is not to be used for external hemorrhoids.
Photocoagulation, first described by Neiger in 1979, uses a Tungsten halogen
lamp which generates heat and destroys the mucosa and submucosa at a depth of
3mm within the application site. This technique is not any more effective then
the other two therapies, but adds cost.
In severe cases or if other more conservative therapies fail, surgical excision
is necessary. Hemorrhoidectomy is performed with the intent to remove the pathologic
tissue and restore the anal canal to normal function. These procedures can be
performed under a general, spinal, or caudal anesthetic. The addition of local
anesthetics such as lidocaine and marcaine with epinephrine promotes hemostasis
and decreases immediate post-operative pain, and can, in most patients, be used
as the sole agent. Several different techniques have been described and no gold
standard is present. One of the most common techniques used is the Ferguson
technique which closes the defect after removal of the tissue (9).
First a clear identification of the internal sphincter muscle is necessary.
The hemorrhoid should then be lifted off this muscle to ensure that the muscle
is not injured and the entire hemorrhoid complex is removed. An incision is
made with a dissecting scissors or electrocautery in a ‘V’ shape
in the anoderm and is carried proximally to the apex of the hemorrhoidal plexus.
The plane just above the sphincter muscle is relatively bloodless. If a significant
amount of bleeding is encountered, this usually means the hemorrhoidal vessels
are being divided rather than being elevated off the muscles. Once at the apex,
a clamp is placed across the hemorrhoidal vessel pedicle and suture ligated.
This suture is tied in place and then used to close the defect in a running,
interlocking fashion to achieve adequate hemostasis. It is safe to remove up
to three columns of hemorrhoidal tissue at a single operation. Yet removing
all three columns requires thorough knowledge of both the anatomy and excellent
technique, as it increases the risk for fecal incontinence and anal stricturing.
Care should be made to leave at least 1 cm of anoderm between the removed columns
to avoid resultant stricturing of the anal canal.
Newer technologies include the use of a neodymium laser and tissue dissectors/sealants
such as the Ligasure®, Harmonic Scalpel®, and Enseal® device. Another
technique used for prolapsed hemorrhoids is the circular stapler. This device
is transanally placed with a circular purse-string suture located 3-4 cm above
the dentate line. A 33-mm stapling device is also placed transanally, facilitating
circumferential excision of the distal rectal mucosa and a “pexy”
of the sub-luxated tissues back to their native location. Overall operative
time, length of hospital stay and outcomes including recurrence and complication
rates have been equivalent to the standard hemorrhoidectomy. Although difficult
to quantify the “total cost” which encompasses hospital stay, medication
usage, complication rate and return to function, the peri-operative cost for
usage of such stapler is 30% higher (10). The use of the circular
stapler is contraindicated in patients with a fixed external hemorrhoid or anal
stenosis, although there are reports of its use in isolated thrombosed disease.
3.6 Complications
Although post-operative pain is not really a complication, it is the most frequent
problem encountered after surgery. The most effective method of management is
the use of frequent nonsteroidal anti-inflammatory drugs (NSAIDs), sitz baths
for spasm, and attempt to minimize narcotic medications. Other early complications
include bleeding, itching, urinary retention and fecal impaction, and itching
(11). All these complications are minor and can be corrected
with conservative management. Late complications include fecal impaction, secondary
bleeding, wound infection, anal fissure, and incontinence. These late complications
are very uncommon and should be treated accordingly. The most feared complication
is fecal incontinence, but even when present, 50% of the patients will report
resolution of soiling by six weeks (12).
Many types of patients will be seen with this condition, including patients
with immunosuppression or human immunodeficiency virus (HIV). Besides the use
of universal precautions, no differences in wound healing is seen, except in
the patient with end-stage AIDS, although efforts should be placed on optimizing
initial non-operative management (13).
4.0 Anorectal Abscess and Anal Fistula
4.1 Introduction
An anorectal abscess is essentially a “boil” of the perianal/perirectal
region, with the purulent collection developing as the acute manifestation,
and the anal fistula resulting as a consequence of this initial infection. A
fistula is defined as an abnormal communication between any two epithelial-lined
surfaces, with an anorectal fistula specifically being a communication with
the rectum or anal canal and the perianal skin. These two entities are then
similar disease processes along a continual timeline, with the fistula being
the chronic state.
4.2 Etiology/Epidemiology
The etiology of these abscesses is thought to be cryptoglandular in approximately
80% with the remaining 20% being from trauma, HIV, cancer, or inflammatory bowel
disease (14). These very common infectious processes develop
when there is an obstruction of an anal crypt at the dentate line in the anal
canal. The anal gland emptying into that crypt then becomes infected and, depending
on the exact location of the infection, a perianal or perirectal abscess arises.
Such an abscess is either drained surgically or drains spontaneously. If the
opening to the anal crypt does not heal completely, this becomes the internal
opening of a fistulous tract that drains through the external opening on the
anus or buttock where the abscess originally drained. The incidence of fistula
formation ranges from 25% to 50% if all four types of abscesses are included
(15). Patients of all ages can be affected by this disease
with the peak incidence being around 20 to 40 years old. Men are more commonly
affected than women.
4.3 Relevant Anatomy/Physiology
Pelvic floor anatomy is essential to comprehend this disease. The pelvic floor
muscles and surrounding musculature create 4 potential spaces, including the
perianal, the ischiorectal, the intersphincteric, and the supralevator space.
The abscesses are classified by their location in the potential anorectal spaces
in the pelvis: perianal (most common), ischiorectal, intersphincteric, and supralevator
(least common). With the intersphincteric, ischiorectal, or supralevator spaces
a horseshoe abscess should be considered. This abscess starts in the midline
posterior crypt, extends through the deep post-anal space and bilaterally to
both ischiorectal fossae. (Figure 6) It should be thought
of especially when initial drainage fails to heal symptoms or when patients
complain of a deep-seated pain. Fistulas are classified according to their involvement
of the sphincter muscles. An intersphincteric fistula lies superficially, coursing
between the internal and external sphincter muscles. The external opening is
very close to the anal opening and usually very little of the internal sphincter
muscle is involved in the tract. Both a transphincteric fistula and a suprasphincteric
fistula traverse both the internal and external sphincter muscles. The opening
for these fistulas is lateral on the buttock and farther away from the anus
than an intersphincteric fistula. Whereas the transphincteric fistula often
crosses both sphincter muscles at the same level, the suprasphincteric fistula
starts out at the dentate line and then travels superiorly in the intersphincteric
space before going above the sphincter complex and out to the skin through the
ischiorectal fossae. Extrasphincteric fistulas pass above the levator ani, outside
the sphincter complex, and are often a result of trauma or other diseases like
diverticulitis, cancer, trauma, or inflammatory bowel disease. A prediction
of the fistula course can be made by considering Goodsall’s rule, which
is based on an imaginary transverse line drawn across the anal verge. It states
that a fistula with an external opening posterior to this line has an origin
in the posterior midline crypt. A fistula with an external opening anterior
to this plain will have a radially oriented fistula tract. Also, if the secondary
(external) opening is more than 3 cm from the anal verge, a more complicated
cephalad extension, or inflammatory bowel disease origin is possible.
4.4 Diagnosis
Common presenting symptoms for abscesses include pain, swelling and other general
signs of an infection, including fever, especially in ischiorectal and supralevator
abscesses. The pain is classically severe in the perianal or perirectal region,
and mostly gradual in onset (over the course of 2 to 3 days). Pain is not often
associated with fistulas, where drainage and occasional bleeding is more common.
On examination, a tender fluctuant mass can be seen if a perianal abscess is
present. Less dramatic cutaneous findings are noted with abscesses located at
the other above mentioned planes. If the patient can tolerate it, a digital
rectal and vaginal exam should be performed to evaluate for internal anal canal
or lower rectal involvement. Unfortunately, patients with intersphincteric,
supralevator and deep post-anal space abscesses may have a paucity of findings
other than tenderness with digital rectal examination. Careful examination for
any type of ischemic changes of either skin or underlying tissues should be
done as life-threatening necrotizing infections, although rare, may be present.
Examination for a fistula opening should be performed by looking for a small
area of heaped up granulation tissue with pus in the punctuate opening. The
fistula can often be felt as a cord like structure leading to the anal sphincter.
If anoscopy can be performed, one can try to find the internal opening, which
would be at the dentate line and have granulation tissue as well; however, this
is rarely possible outside of the operating room. Further consideration needs
to be taken in patients with a history of such abscesses or fistulas and in
patients with inflammatory bowel disease, as more extensive disease than preliminary
evaluation deems may be present. In such cases, endorectal ultrasound, CT or
MRI, if available might provide additional information.
4.5. Management
A simple abscess without a fistula can be incised, drained and the wound left
open for continued drainage. (Figure 7) An elliptical
or cruciate incision is often preferred. Packing of the wound is not necessary
although most physicians will pack initially, for hemostatic purposes. Perianal
and ischiorectal abscesses can be drained in the office with the aid of local
anesthetics. If the abscess is large, the patient is febrile, or other types
of abscesses are suspected (i.e., supralevator, deep postanal space, horseshoe
abscess) it is best performed, if possible, in the operating room under regional
or general anesthetics. A proper incision and drainage is performed with the
buttocks spread apart and secured by taping to the operating table. We prefer
the prone position for optimal visualization. The area is prepped with betadine
and draped. Local anesthetic is occasionally ineffective due to the presence
of pus, and the patient, if awake, should be tested prior to incision. An incision
is made in a cruciate fashion over the point of maximal fluctuance. One or two
corners of the skin flaps may be excised to keep the cavity open for drainage.
The abscess cavity is probed with a hemostat and all septations are divided.
The cavity may be irrigated with betadine and normal saline and packed loosely
with gauze. The most common error in performing an incision and drainage is
to make the opening too small, causing inadequate drainage and persistent infection.
In addition, for large abscesses, the incision should be placed closer to the
anal verge if possible to keep any resultant fistula tract as short as possible.
In the case of a horseshoe abscess, drainage of the offending crypt, as well
as lateral incisions over the abscess cavity in the ischiorectal fossae should
be made and tracts should be curetted. These incisions and tracts can be kept
open with a Penrose drain. Intersphincteric abscesses should be drained through
the rectum, which involves opening and blunt separation of the internal anal
sphincter muscle. Ischiorectal abscesses should be drained though the ischiorectal
fossa. Any packing can be removed by the patient the following morning. Wound
care at home should be with twice daily washings with clean water. If possible,
the patient should soak in a warm bath once or twice a day. This will relieve
discomfort and hasten healing. Antibiotics are not needed following drainage,
unless marked cellulitis, immunosuppression, valvular heart disease, signs of
systemic infection, or diabetes exist (16). Those patients
with supralevator abscesses commonly have from a pelvic source and may need
drainage from the abdominal route. Those patients with a cryptoglandular source
arising from an intersphincteric abscess extension should be drained into the
rectum; while those with a cryptoglandular source arising from an ischiorectal
extension should be drained to the perineal skin. This is to avoid, as much
as possible, a complex fistula tract.
A fistula is best treated in the operating room with light sedation and local
anesthesia. Positioning is as described above for incision and drainage of an
abscess. The internal opening is identified by placing a probe through the external
opening. If the fistula is intersphincteric and very little of the internal
sphincter muscle is involved, the skin and muscle overlying the tract can be
divided safely with minimal risk of fecal incontinence. (Figure
8) The edges of the fistula are sutured in a marsupialization fashion with
a running stitch of chromic or vicryl consistency. If, however, the fistula
is found to be trans- or suprasphincteric, division of the external sphincter
muscle is discouraged if it involves more than one-third of the thickness of
the sphincter complex, as it will likely cause fecal incontinence. The fistulous
tract should then be cleaned out with a currette and a loose string (suture,
vessel loop) placed through the tract and secured in place. This is called a
Seton and will allow persistent drainage of pus until the fistulous tract can
epithelialize and heal. (Figure 9) Cutting Setons that
are tightened repeatedly over the course of many weeks are discouraged as they
are extremely painful and do not decrease the risk of incontinence. Long-term
outcomes for trans- and suprasphincteric fistulae are not as good as for intersphincteric
fistulae. The former often persist for many months and require repeat examinations
in the operating room with repeated cleaning of the fistulous tract. Newer treatments
include injection of a fibrin glue substance or placement of a collagen plug
in attempts to close the internal opening. The long-term success rate of these
modalities is often less than 50% (17). Further surgical therapy
may involve closure of the internal opening through the use of mucosally-based
advancement flaps, diversion stoma, or in severe cases, proctectomy.
4.6 Complications
Post-operative complications include recurrence of the abscess or fistula. This
occurs in about 37% to 50% of patients (18). Performing a
fistulotomy at the time of abscess drainage may decrease the rate of recurrent
abscess and fistula to 1.8% (19), but increases the risk of
incontinence. Recurrence often occurs from failure to identify the offending
crypt or tract. In patients with abscesses, the physician should always consider
diagnoses such as perianal hidradenitis suppurativa, inflammatory bowel disease,
or HIV infection. Fecal incontinence is an uncommon but feared complication.
The use of a Seton in complicated fistulas decreases this complication.
5.0 Anal Fissure
5.1 Introduction
Anal fissures are common problems that cause severe patient discomfort. A fissure
is basically a linear tear in the anal mucosa which extends distally from the
dentate line to the anal verge. Analogous to a “split lip” of the
anus, every time a patient has a bowel movement, the anal mucosa will be stretched
and the fissure reopened. A fissure can sometimes heal by itself, but due to
recurrent injury by the mechanism described above, and often the associated
increased contraction of the internal anal sphincter, it becomes a chronic problem.
5.2 Etiology/Epidemiology
The etiology for anal fissures is not completely understood. Some type of initial
trauma is necessary with subsequent failure of healing. This initial insult
is often a hard bowel movement and history of constipation, although severe
diarrhea can also be an associated condition as well. Other diseases like Crohn’s
disease, HIV or previous surgery should also be considered. Failure of healing
is thought to be secondary to internal anal sphincter hypertonicity and subsequent
relative decreased blood supply (20). These lesions are often
encountered in patients between 30 to 50 years old, with the incidence the same
in both sexes (21). They are most commonly found in the posterior,
with the next most prevalent site being the anterior midline, where it is more
common in women (10-20%) than in men (1-10%) (22). When fissures
are found laterally, syphilis, tuberculosis, occult abscesses, carcinoma, acquired
immunodeficiency syndrome (AIDS) or inflammatory bowel disease should be considered
as causes. Chronic fissures can be also associated with findings of hypertrophied
anal papillae, sentinel tags, visible sphincter muscle fibers. (Figure
10) Finally, polyps, hemorrhoids and other concomitant disease are often
present.
5.3 Relevant Anatomy/Physiology
Fissures are often sharply demarcated and granulation tissue can be noted. As
stated, chronic fissures can be fibrotic and can form a sentinel pile. As the
posterior midline is the most poorly perfused area of the anal canal, most occur
in this area in both sexes. Increased internal sphincter pressure can decrease
blood flow even further and is thought to contribute to a chronic fissure. In
a person with an anal fissure, the internal anal sphincter goes into spasm,
and this hypertonicity of the muscle results in pain. The external sphincter
is under voluntary control. However, it differs from all other voluntary skeletal
muscles in that it maintains a constant tonic contraction at rest (approximately
15% of the resting pressure), but is not thought to contribute to the chronicity
of the fissure.
5.4 Diagnosis
A thorough history is not only essential, but can often make the diagnosis alone
in this disease. Patients will describe a sharp pain that is initiated by a
bowel movement. The pain will last for a few minutes to several hours. Other
complaints will be bright red bleeding after a bowel movement that is most commonly
described as streaking the stool or on the toilet paper with wiping, although
it can occur throughout the day. If a sentinel pile is present, some tenderness
to palpation can be present. On examination spreading of the buttocks is often
enough to see the fissure and no anoscopic exam is necessary in the acute setting.
Digital rectal examination can often palpate these fissures, although local
anesthetics are recommended due to the severe pain associated with such an exam.
It is the authors’ preference to diagnose and begin treatment (often without
digital examination or anoscopy) and bring the patient back in 2-4 weeks for
a more thorough examination when the patient is less symptomatic.
5.5. Management
Again conservative management is the first option in treatment. Medical management
includes oral analgesics, sitz baths, bulking agents and/or stool softeners,
increased hydration and topical anesthetics. Other topical therapies include
the use of nitrate creams like 0.2% glyceryl trinitrate cream bid or tid to
reduce internal sphincter tonicity (23). They also have a
vasodilatory effect and cause increased perfusion. Side effects of these preparations
include burning and headaches in 25-50%. Calcium channel blockers like diltiazem
either topically or orally can also be used by the same type of mechanism (24).
A more invasive treatment is the injection of Botulinum toxin A (20-40IU) into
the internal sphincter muscle. Similar results have been obtained with only
mild complications of hematoma, thrombosis and infection at the injection site
(25).
If the fissure fails to heal after medical treatment, surgical intervention
is often necessary. Although many procedures have been reported, the lateral
internal sphincterotomy (LIS) is the most commonly performed. This procedure
involves division of the internal anal sphincter muscle to the level of the
proximal extent of the fissure or the dentate line through either a closed or
open procedure. (Figure 11) This relieves the symptoms
in over 98% of patients and has very low recurrence rate (26).
The procedure can be performed under local anesthetics in the operating room
with very minimal complication risk. Fecal incontinence has been reported in
1-40%, although the majority of these are transient and often to flatus alone.
Other surgical approaches include posterior internal sphincterotomy and manual
anal dilation which are each associated with higher complication rates of a
keyhole defect and fecal incontinence (>50%), respectively (27).
5.6 Complications
Post-operative complications from a LIS include bleeding, fistula, infection
and abscess formation. These are very uncommon and occur in less then 1% of
the cases. Fecal incontinence again is a feared complication, but again occurs
in 1-40% of the cases (28), with the vast majority of these
patients improving within 6 weeks.
6.0 Sexually Transmitted Diseases
6.1 Introduction
Common sexually transmitted diseases causing anorectal problems include Human
Papilloma Virus (HPV), Human Immunodeficiency Virus (HIV), and Chlamydia trachomatis
(Lymphogranuloma Venereum).
6.2 Etiology/Epidemiology
The Human Papilloma Virus is transmitted via sexual contact with infected persons.
HPV types 6, 11, 16, and 18 are most commonly associated with perianal condylomata.
Types 16 and 18 have been associated with anal dysplasia, intraepithelial neoplasia,
and invasive squamous cell carcinoma (29). It can be asymptomatic
with no visible lesions so an infected individual may not know he or she has
the virus. In a sexually active population, the prevalence of DNA of the HPV
is around 50 percent. The virus can cause anal symptoms and lesions even in
those individuals who do not practice anal receptive intercourse. Infection
occurs when there is trauma to the epithelium. The virus then enters the basal
cell layer and proliferates. Mature virus particles then move to the superficial
epithelial layers. Papillomas or warts develop when there is hyperplasia of
these epithelial cells as well as hyperplasia of the stroma supporting the epithelium.
These lesions are then called condylomata acuminata.
Co-infection with HIV may alter the severity and manifestations of other sexually
transmitted diseases. Patients infected with the HIV can have common anorectal
problems such as hemorrhoids, abscesses and fistulae. Patients who have progressed
to have the Acquired Immunodeficiency Syndrome (AIDS) are prone to getting idiopathic
AIDS-related anal ulcers. Anal fissures secondary to HIV tend to be off the
midline, deeper involvement of the muscle, and extend higher in the anal canal.
HPV infection in HIV patients is more aggressive with a greater propensity for
dysplastic and neoplastic changes (30). Other anorectal manifestations
of HIV include opportunistic infections resulting in diarrheal disease. Nonspecific
proctitis with no identifiable pathogenic agent has been noted in up to 26%
of patients infected with HIV.
Lymphogranuloma Venereum (LGV) is caused by the intracellular bacterium Chlamydia
trachomatis, serovars L1-L3. (Non-LGV serovars D – K are less virulent).
Chlamydial infections are transmitted to the anorectum via anorectal or oral-anal
intercourse. LGV is characterized by aggressive ulceration of the perianal,
anal and rectal areas. It can also present as perianal abscesses, fistulae or
stricturing. Rectal involvement causes proctitis with associated severe rectal
pain and discharge. Lymphadenopathy can occur in the iliac, inguinal, femoral
and perirectal nodal basins and are often the hallmark of the diagnosis.
6.3 Relevant Anatomy/Physiology
Lesion will be noted around the anal area, but certain diseases can be seen
higher in the lower rectum, approximately 10 to 15 cm from the anal verge. Besides
knowing the general anatomy of the anorectal area as described previously, an
anatomical understanding of the inguinal and perineal area is helpful. No such
anatomy will be specified here, but an understanding of inguinal lymph nodes
and external sexual organs is essential in managing sexually transmitted diseases.
A thorough oral exam is also recommended, as concomitant infection may be present.
6.4 Diagnosis
Symptoms with HPV include pruritus, growths, drainage, difficulty keeping the
area clean, bleeding, and pain. Physical examination reveals fleshy papilliform
lesions of varying sizes that can occur individually or as a carpet of lesions.
(Figure 12) In 10% of patients, only intra-anal lesions
are present. Anoscopy can be performed to assess for lesions in the anal canal,
but is generally not performed until the external lesions have completely resolved
or while in the operating room. There is always concern that the virus may be
introduced into new and proximal areas by instrumentation. However some say
that anoscopy is mandatory because treatment of perianal lesions will be unsuccessful
if intra-anal lesions are not treated concomitantly (30).
AIDS is associated with a number of diseases as it decreases the host immunity.
One of the most common anorectal diseases is AIDS related anal ulcers. They
are extremely painful lesions, proximal in the anal canal, often above the dentate
line. They are broad-based, deep ulcers with destruction of sphincter planes,
leaving mucosal bridges.
Up to 15% of individuals affected with LGV are asymptomatic. If symptomatic
they may present with rectal pain, tenesmus, and fever. Occasionally mucosal
ulcerations are seen. Inguinal lymphadenopathy may be present. Diagnosis of
LGV is dependent on proper specimen collection, namely using a cotton swab,
and transporting to the lab on a special medium kept refrigerated until inoculation
onto culture plates. Gram stain showing polymorphonuclear leukocytes but no
gonococci can be presumed to be chlamydia.
6.5. Management
Treatment for HPV involves destruction of the warty lesions. If the lesions
are few and not internal, this is best accomplished in the clinic setting. There
are several different topical treatments. Podofilox 0.5 % gel can be applied
twice daily for three days, then no treatment for four days. This cycle is repeated
for up to one month, but care should be noted as this should not be applied
in the anal canal. Cryotherapy with liquid nitrogen can be used as a single
application on a cotton swab with care being taken to avoid touching normal
skin. Patients are advised to return in three weeks time for repeat treatment
if necessary. Trichloroacetic acid can also be used in a similar fashion, and
unlike podofilox, can be used in the anal canal. For lesions that are large,
in a carpet on the anus, or in the internal anal canal, electrodessication with
cautery or laser in the operating room is optimal if available. The patient
is positioned as described previously for treatment of anal abscesses. Local
anesthetic is injected. The cautery pen is used to desiccate the warts. The
eschar is removed after this is done. Postoperative pain from this procedure
can be severe and patients should be advised to soak in a warm bath, if available,
several times a day.
Recurrence is high for anal warts, particularly in immunocompromised patients
such as those with HIV. Frequent examinations (every three to six months) should
be performed until the warts are cleared. As stated before, HPV serotypes 16
and 18 can cause dysplastic transformation of the epithelium, which is a precursor
lesion to anal squamous cell carcinoma. The risk of anal squamous cell carcinoma
in the HIV positive individual with HPV is several times that of the non-HIV
positive individual. Therefore, HIV positive patients should be monitored even
more closely (every three months) for wart persistence or recurrence.
Anal ulcer associated with AIDS can be treated with intralesional injection
of steroids (methlyprednisolone 80 – 160 mg in 1 cc of 0.25% bupivicaine)
if available. They respond well to antiretroviral therapy and resolve spontaneously
when the CD4 count is above 2001.
Treatment of LGV involves doxycyline 100 mg orally twice a day for 21 days.
Erythromycin 500 mg orally four times a day for 21 days is a second line agent
if doxycycline is not available. For patients with HIV and LGV, treatment may
need to last several months.
6.6 Complications
Complications with sexually transmitted diseases, in general, involve transmittal
to other individuals. A speedy diagnosis is therefore essential. Even though
patients might not have any visible lesions with these types of diseases, they
still need to be aware of high potential for transmission. After treatment of
the lesions mentioned above, the area may swell significantly. Skin may be sloughed
off following treatment, but scarring is uncommon. Untreated sexually transmitted
diseases may result in rectovaginal or rectovesical fistulae, abscesses, and
rectal strictures. As many of these diseases are treated with prescribed antibiotics,
anti-virals and ani-fungals, side effects and possible allergies need to be
kept in mind. Finally, as stated, dysplastic changes associated with HPV infection
may ultimately lead to a higher risk of anal cancer.
7.0 Pruritus Ani
7.1 Introduction
Pruritus ani or anal itching is an extremely common problem and is associated
with a wide range of mechanical, dermatologic, infectious, systemic and other
conditions. Regardless of the etiology, the itch/scratch cycle is an important
contributor to the problem. This cycle becomes self-propagating and results
in chronic pathologic changes that persist even if the initiating factor is
removed.
7.2 Etiology/Epidemiology
Pruritis ani has many etiologies. It can indicate the presence of an infection,
including pinworms and fungal, poor hygiene or the presence of a fissure. In
children, it is most often associated with pinworm, which can be acquired from
either fecal-oral route or by sexual contact. However, in adults, a multitude
of conditions can lead to the development of pruritis ani. Medications (i.e.
colchicine, prolonged steroids), dermatological conditions (psoriasis), infection
(candida, cornybacterium), anorectal conditions (fissures, fistulas), diabetes,
blood dyscrasias, caffeine and other methylxanthine use are common inciting
conditions. Unfortunately, in many cases, no identifiable source is discovered.
Overall, pruritis ani is more common in males than females.
7.3 Relevant Anatomy/Physiology
Pruritus ani is the itching and irritation of the skin at the anal verge and
surrounding anal margin skin. Due to the irritation and subsequent scratching,
erythema and swelling will be noted at this area.
7.4 Diagnosis
Patients will present with extreme anal itching and continued scratching to
this area. Examination often demonstrates excoriation and irritation due to
repeated scratching with small linear “tears” in the perianal skin
extending radially from the anal verge. When pruritus ani becomes chronic, the
perianal area becomes thickened, lichenified and appears white with fine fissures.
(Figure 13) Pinworms are diagnosed by applying clear
tape to the perianal area in the early morning before the patient has washed
or wiped the area and then applying it to a microscope slide. Using a microscope
pinworm eggs can be identified. Patients should undergo a thorough examination
to exclude other anorectal conditions which could be contributing to the symptoms.
In addition, examination with a Wood’s lamp, fungal scrapes, culture,
stool studies and even biopsy of the perianal skin can all provide valuable
information into the underlying etiology.
7.5. Management
The most important step in treatment is recognizing the underlying cause and
treating the source of the itching. Hygiene and taking sitz baths after every
bowel movement helps cleanse this area, but care should be to thoroughly dry
the area. We often instruct our patients to use a hair dryer instead of causing
extensive abrasions with a towel. Placing a cotton ball at the outside of the
anal verge to collect any sweat or seepage, and using dusting powders other
than corn starch can also be used to keep the area dry and decrease itching.
Dietary adjustment such as avoiding or even limiting caffeine can be effective.
Avoidance of detergent soaps should be a first step. General antihistamines
can be used to decrease itching, but long term treatment with these should be
avoided. In addition, topical steroids may be necessary to decrease the erythema
and swelling, but should be used with caution, for a limited time, once other
sources have been excluded (31).
Pinworm infestation may be treated with pyrantel pamoate (Antiminth), 1 g as
a single oral dose and a repeat dose in two weeks, or mebendazole (Vermox),
100 mg as a single oral dose, with a repeat dose in two weeks if necessary
Mycotic infections with dermatophytes Trichophyton rubrum, Trichophyton mentagrophytes
or Epidermophyton floccosum, or Candida species can cause perianal itching and
treatment with topical imidazole derivatives, such as miconazole (Monistat)
or clotrimazole (Lotrimin), is usually effective.
7.6 Complications
Complications occur due to excessive cleaning, especially with brushes. Such
cleaning aggravates the skin and exacerbates the condition with eventually excoriating
the skin. This are is also very sensitive to soaps and perfumes and cause an
increased itching with increased local trauma as a consequence. Again as treatment
includes prescribed antifungals, side effects and allergies need to be kept
in mind.
8.0 Conclusion
Anorectal disorders are a common group of diseases seen in the office practice.
Advances have been made in understanding the pathogenesis of theses diseases.
Each of the disorders described can be distinguished by a thorough history and
performing a complete exam. By following the symptoms discussed and checking
for exams findings stated, an effective treatment should be able to be found,
whether it is medical or surgical.
Lionel R. Brounts, M.D.*, Laura Goetz, M.D.+, Scott R. Steele, M.D.*
*Department of Surgery, Madigan Army Medical Center, Tacoma, Washington. +Division
of Colon and Rectal Surgery, University of California, San Francisco
Corresponding author:
Scott R. Steele, MD, FACS
Department of Surgery
Madigan Army Medical Center
Fort Lewis, WA 98431
Phone: (253) 968-2200
Fax: (253) 968-0232; 968-5900
Email: harkersteele@mac.com
References
1. Burt CW, Schappert SM. Ambulatory care visits to physician
offices, hospital outpatient departments, and emergency departments: United
States, 1999-2000. National Center for Health Statistics. Vital Health
Stat. 2004. 13(157)
2. Abcarian, H., Alexander-Williams J. Christiansen J., et al.,
Benign anorectal disease: definition, characterization and analysis of treatment.
Am J Gastroenterol, 1994. 89(8 Suppl): p. S182-93
3. Kumar, D., Perianal and anorectal conditions. Br
J Hosp Med, 1996. 55(8): p. 464-67
4. Hussain JN. Hemorrhoids.
Prim Care, 1999. 26(1): p35-51
5. Orlay G. Haemorrhoids-a review. Aust Fam Physician,
2003. 32: p523-26
6. Johanson JF, Sonnenberg A. The prevalence of hemorrhoids
and chronic constipation: an epidemiological study. Gastroenterology, 1990.
98: p380–86
7. Haas PA, Fox TA, Haas G. The pathogenesis of hemorrhoids.
Dis Colon Rectum, 1984. 27: p442–50
8. Barron J. Office ligation of internal hemorrhoids.
Am J Surg, 1963. 105: p563-70
9. Ferguson J, Heaton J. Closed hemorrhoidectomy. Dis
Colon Rectum, 1959, 2: p176-79
10. Ho Y. Cheong S. Tsang C.Seown-Choen F. Stapled
hemorrhoidectomy: cost and effectiveness: randomized control trial including
incontinence scoring, anorectal manometry and endo-anal ultrasound measures
at up to 3 months. Dis Colon Rectum, 2000. 43: p1666-75
11. Pfenninger J. Modern
treatments for internal hemorrhoids: Scalpel surgery is now rarely needed.
British Medical Journal, 1997. 314(7089): p1211-12.
12. Roe A, Bartolo D, Vellacott K, et al. Submucosal vs.
ligation excision hemorrhoidectomy: a comparison of anal stenosis, anal sphincter
manometry, and post-operative pain function. Br J Surg, 1987. 74: p948-51
13. Hewitt W, Sohol T, Fleshner P, et al. Should
HIV status alter indication for
hemorrhoidectomy? Dis Colon Rectum, 1996. 39: p615-18
14. Seow-Choen F, Nicholls RJ. Anal fistula. Br J
Surg, 1992. 79: p197-205
15. Read DR, Abcarian H: A prospective survey of 474 patients
with anorectal abscess. Dis Colon Rectum, 1979. 22: p566-68
16. Corman ML. Anorectal abscess and anal fistula.
Colon and Rectal Surgery. Philadelphia, JB Lippincott, 1993. p 133-87
17. Hyman, N., Anorectal
abscess and fistula. Prim Care, 1999. 26(1): p. 69-80
18. Fazio V. Complex anal fistulae. Gastroenterol
Clin North Am, 1987. 16: p93-114
19. Ramanujam PS, Prasad ML, Abcarian H, et al. Perianal
abscesses and fistulas: A study of 1023 patients. Dis Colon Rectum, 1984.
27: p593-97
20. Lund JN, Scholefield JH. Aetiology
and treatment of anal fissure. Br J Surg, 1996. 83: p1335–44
21. Hancock BD. Anal fissures and fistulas. BMJ, 1992.
304: p904-07
22. Notoras MJ. Anal fissure and stenosis. Surg Clin
North Am, 1988. 68: p1427-40.
23. Gorfine SR. Topical nitroglycerin therapy for anal
fissures and ulcers [Letter]. N Engl J Med, 1995. 333: p1156-57
24. Carapeti EA, Kamm MA, Evans BK, et al. Topical
diltiazem and bethanecol decrease anal sphincter pressure without side effects.
Gut, 1999. 45: p719-22
25. Brisinda G, Maria G, Bentivoglio AR, et al. A
comparison of injections of botulinum toxin and topical nitroglycerin ointment
for the treatment of chronic anal fissure. N Engl J Med, 1999. 341:
p65–69
26. Argov S, Levandovsky O. Open
lateral sphincterotomy is still the best treatment for chronic anal fissure.
Am J Surg, 2000. 179: p201-02
27. Konsten J, Baeten CG. Hemorrhoidectomy
vs. Lord’s method: 17-year follow-up of a prospective randomized trial.
Dis Colon Rectum, 2000. 43: p503-6.
28. Hyman, N. Incontinence
after lateral internal sphincterotomy: a prospective study and quality of life
assessment. Dis Colon Rectum, 2004. 47: p35-38
29. Brown DR, Fife KH. Human papillomavirus infections
of the genital tract. Med Clin North Am, 1990. 74: p1455-85
30. Modesto VL, Gottesman L. Sexually transmitted diseases
and anal manifestations of AIDS. Surg Clin North Am, 1994. 74: p1433-64
31. Stolz E, Vuzevski VD, van der Stek J. General perianal
skin problems. Neth J Med, 1990. 37(Suppl 1): pS43-6
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