Chapter 31: Anorectum

The anatomy of the anus and rectum dictates the clinical evaluation and treatment of patients with anorectal disorders (Figure 31–1).

From external to internal, the surface anatomy of the anorectum is comprised of gluteal skin, anoderm, the anal transitional zone, and proximally the rectal mucosa. The gluteal skin includes hair, sebaceous glands, and sweat glands. This area, particularly 3-5 cm of anal margin skin circumferentially around the anus, can commonly become infected with the human papilloma virus resulting in anal condyloma. Anal condyloma can also affect more proximal tissue in the anoderm and lower rectal mucosa. Perianal hidradenitis is also relatively common and develops in the apocrine sweat glands of the perianal skin. Unlike anal condyloma, perianal hidradenitis can only occur in the gluteal skin as there are no sweat glands in the anoderm.

The anoderm begins at the anal verge and ends at the dentate line. Unlike the gluteal skin, the anoderm is devoid of hair and sweat glands. Anal fissures occur in the anoderm and can be associated with a sentinel tag externally and a hypertrophied anal papilla internally (Figure 31–2). Surgical excision of too much anoderm during hemorrhoidectomy or other anorectal surgery can result in anal stenosis.

The anal transitional zone lies between the squamous anoderm and the rectal mucosa. In this zone, squamous, cuboidal, transitional, and columnar epithelium exist with longitudinal ridges called the columns of Morgagni. Between the columns of Morgagni are anal crypts with associated anal glands that open into their bases. Clinically, the anal transitional zone is important for two main reasons. First, the anal transitional zone is the crossover from somatic to visceral innervation and for lymphatic drainage from the inguinal to the pelvic nodes. Lymphatics from the anal canal above the dentate line drain via the superior rectal lymphatics to the inferior mesenteric lymph nodes and laterally to the internal iliac nodes. Below the dentate line, drainage occurs to the inguinal lymph nodes but can occur to the inferior or superior rectal lymph nodes. Second, the anal glands in the crypts are the site of anorectal abscesses and anal fistulas. Anatomically the anal glands in the crypts extend to a variable depth resulting in perianal, intersphincteric, or ischiorectal abscesses when these glands become blocked.

Proximal to the anal transitional zone is the rectal mucosa. Above the dentate line and underlying the rectal mucosa are the vessels that, when abnormally engorged, manifest as internal hemorrhoids. Hemorrhoids are not veins but arteriovenous connections that have pulsatile flow. Patients with bleeding from hemorrhoids can have significant blood loss. Further, internal hemorrhoids are covered by mucosa and because they are above the dentate line, they are viscerally innervated. This is the reason rubber-band ligation of internal hemorrhoids is possible without anesthesia. In contrast, external hemorrhoids are below the dentate line, covered by anoderm and skin. Any surgical intervention on external hemorrhoids requires some type of anesthesia.

Hemorrhoidal vessels are anchored by Treitz’ muscle. When the Treitz’ muscle attachments weaken, internal and external hemorrhoids can prolapse, bleed and cause perianal irritation and discomfort. Internal hemorrhoids can prolapse and can be confused with rectal prolapse. Generally, internal hemorrhoids prolapse in columns occurring in the right anterior, right posterior and left lateral quadrants around the anus. When the anus is examined, these prolapsing columns of internal hemorrhoids appear as radial folds. This is distinguished from the circumferential folds of rectal prolapse.

The rectum extends 12-15 cm proximal to the dentate line. The rectum has three curves that create folds called the valves of Houston. It is supported by the puborectalis and levator muscles that are also called the pelvic floor. In addition, the rectum is fixed posteriorly by presacral (Waldeyer) fascia, laterally by the lateral ligaments, and anteriorly by Denonvilliers fascia. The arterial supply of the anorectum is via the superior, middle and inferior rectal arteries. The superior rectal artery is the terminal branch of the inferior mesenteric artery and descends in the mesorectum. It supplies the upper and middle rectum. The middle rectal arteries arise from the internal iliac arteries and enter the rectum anterolaterally at the level of the pelvic floor musculature. They supply the lower two-thirds of the rectum. Collaterals exist between the middle and superior rectal arteries. The inferior rectal arteries—branches of the internal pudendal arteries—enter posterolaterally, do not anastomose with the blood supply to the middle rectum, and supply the anal sphincters and epithelium.

The venous drainage of the anorectum is via the superior, middle, and inferior rectal veins draining into the portal and systemic systems. The superior rectal veins drain the upper and middle thirds of the rectum and empty into the portal system via the inferior mesenteric vein. The middle rectal veins drain the lower rectum and the upper anal canal into the systemic system via the internal iliac veins. The inferior rectal veins drain the lower anal canal, communicating with the pudendal veins, and draining into the internal iliac veins. Communication between the venous systems allows low rectal cancers to spread via the portal and systemic systems. Lymphatic drainage of the upper and middle rectum is into the inferior mesenteric nodes. Lymph from the lower rectum may drain into the inferior mesenteric system or into lymphatics around the lower rectum that drain into the inguinal nodes and then into periaortic nodes. Below the dentate line, lymphatic drainage occurs primarily to the inguinal nodes but may drain into the inferior mesenteric lymph nodes.

The innervation of the rectum is from both the sympathetic and parasympathetic nervous systems. The sympathetic nerves originate from the lumbar segments L1-3, form the inferior mesenteric plexus, travel through the superior hypogastric plexus, and descend as the hypogastric nerves to the pelvic plexus. The parasympathetic nerves arise from the second, third, and fourth sacral roots and join the hypogastric nerves anterior and lateral to the rectum to form the pelvic plexus. Sympathetic and parasympathetic fibers pass from the pelvic plexus to the rectum and internal anal sphincter (IAS) as well as other pelvic viscera. Injury to these nerves can lead to sexual and bladder dysfunction, and loss of normal defecatory mechanisms.

Beneath the surface anatomy of the anus and rectum are the anal sphincter muscles. The IAS muscle is involuntary and is responsible for anal canal resting tone. The IAS is innervated with sympathetic and parasympathetic fibers. Both are inhibitory and keep the sphincter in a basal state of contraction. The external anal sphincter (EAS) muscle is voluntary and responsible for anal canal squeezing tone. The external sphincters are skeletal muscles innervated by the pudendal nerve with fibers that originate from S2-4. The EAS muscle fuses with the pelvic floor muscles to create a bowl-like muscular support of the lower rectum.

While systemic diseases such as diabetes, scleroderma and multiple sclerosis can affect the anal sphincter muscles, far more common is direct injury to the sphincter muscles from vaginal delivery or surgery. Using transanal ultrasound to evaluate the anal sphincter muscles before and after vaginal delivery it has been demonstrated that approximately one-third of women injure their anal sphincter at the time of delivery. Fortunately, only one-third of these women develop fecal incontinence.

Operative intervention for hemorrhoids, anal fissure, and anal fistula can result in anal sphincter injury. Sphincter injury should not occur during hemorrhoid surgery as hemorrhoidal vessels are superficial to the anal sphincter muscles. Division of the anal sphincter is necessary and curative for anal fissure and for anal fistula treated by fistulotomy. While lateral internal sphincterotomy for anal fissure carries a fecal incontinence rate of less than 0.5%, fistulotomy for complex anal fistulas has a rate of over 50%. For this reason, sphincter-sparing approaches to anal fistulas are now the standard of care for patients with anal fistulas involving a significant amount of anal sphincter muscle.

Anorectal Pain

Pain is one of the most common presenting symptoms of anorectal disorders. The common causes of anorectal pain are shown in Table 31–1. The vast majority of patients have either thrombosed external hemorrhoid, anal fissure, or anorectal abscess. The other causes of anorectal pain are relatively unusual. The etiology of anorectal pain can often be determined with a careful history that is then confirmed with the physical examination.

For patients with anorectal pain, the most important aspects of the patient history are the nature and onset of the pain and any associated symptoms. If the pain is acute in onset (< 1-3 d) and associated with a lump at the anus, a diagnosis of a thrombosed external hemorrhoid is highly likely. If the pain is acute in onset and associated with fever and swelling at the anus, then an anorectal abscess should be suspected. Finally, if the pain is described as a “cut,” “tear,” or “sharp as a knife” and associated with bowel movements, then an anal fissure is the probable cause. Inspection alone will usually confirm the suspected diagnosis as an external hemorrhoid, abscess or cellulitis or anal fissure will be present. It is important to efface the anus by pulling the gluteal cheeks apart in order to identify an anterior or posterior anal fissure that occurs just inside the anal canal. Most patients with anorectal pain cannot tolerate a digital examination and anoscopy but fortunately these evaluations are often unnecessary. If after obtaining a history and carefully inspecting the anus and the diagnosis is still in doubt, an examination under anesthesia may be indicated as small number of patients may have an intersphincteric or supralevator abscess that usually cannot be diagnosed by inspection alone.

Anorectal Bleeding

Bleeding is the most common presenting symptom in patients with anorectal disorders. Common causes of anorectal bleeding are shown in Table 31–2. While a careful history may suggest the etiology of bleeding, patients can tolerate and require a thorough physical examination as well as anoscopy and lower endoscopy. Even if anorectal pathology is identified on physical examination or anoscopy, endoscopic evaluation is always necessary in order to rule out proximal pathology such as polyps or cancer.

In patients with anorectal bleeding, the history can help identify the source of the bleeding by fully characterizing the amount, timing and location of the bleeding. Blood seen just on the toilet paper suggests anal canal pathology whereas blood seen mixed with the stool suggests a more proximal bleeding source. Inspection of the anus may reveal prolapsing hemorrhoids, an anal fissure, an anal fistula, or anal ulcer. Anoscopy is necessary to evaluate for possible internal hemorrhoids and distal proctitis. Flexible sigmoidoscopy is typically recommended for younger patients (< 40 years old) who do not have a family history of colon cancer. Colonoscopy is recommended for patients over age 40 with anorectal bleeding or patients under age 40 who have a family history of colon cancer. While these general guidelines are appropriate for most patients, the choice between flexible sigmoidoscopy and colonoscopy is individualized to each patient’s clinical scenario.

Anorectal Mass

Most anorectal mass lesions are either anal skin tags, a thrombosed external hemorrhoid or a sentinel pile associated with an anal fissure (Table 31–3). In addition to the history, physical examination and anoscopy, most patients with mass lesions need either flexible sigmoidoscopy or colonoscopy depending on their age, diagnosis, and whether or not there is a family history of colon cancer. The unusual tumors such as lipoma and GIST that occur deep to the skin, anoderm, and rectal mucosa are difficult to diagnose preoperatively. These tumors often require additional preoperative anatomic evaluation with transanal ultrasonography and/or pelvic MRI to determine their extent and relationship to the anal sphincter muscles.

Anorectal Discharge

Discharge from the anus is a relatively common complaint and has a wide range of possible etiologies (Table 31–4). The most common causes of anorectal discharge are mucosal prolapse, anal fistula, and fecal leakage. Patients with anal fistula often have a history of perirectal abscess. On examination, the patient should be asked to strain in order to identify mucosal and rectal prolapse. Anal sphincter tone should be assessed during the digital examination. In patients with previous anorectal surgery, careful inspection of the anus is important to identify any anal contour abnormalities (keyhole deformities). In addition to anoscopy, most patients will require lower endoscopy. Patients with fecal leakage or incontinence often require further functional and anatomic studies.

Hemorrhoids are blood vessels in the lower rectum and anal canal. They are not veins but rather arteriovenous connections with pulsatile flow. External hemorrhoids are located below the dentate line and anatomically identified by the presence of anoderm or skin overlying the hemorrhoidal vessel. Due to either diarrhea, constipation, or straining, a hemorrhoidal vessel can become thrombosed with a clot resulting in a painful lump and possibly some bleeding if the clot ruptures through the anoderm. External hemorrhoids typically cause symptoms when they thrombose, prolapse, or cause irritation/hygiene difficulties. Internal hemorrhoids originate from above the dentate line and are covered by mucosa. These blood vessels can become enlarged/engorged (eg, pregnancy) and/or their anchoring muscle, the Treitz muscle, can become weakened (eg, straining, constipation). When either one or both of these circumstances occur, the hemorrhoidal vessels can prolapse into the lumen of the anal canal as well as can prolapse externally. This mechanical prolapse of hemorrhoidal vessels can cause bleeding, irritation, and pressure-like pain.

Internal hemorrhoids can be classified as grade I-IV by their symptoms and degree of prolapse. Grade I hemorrhoids are prominent but do not prolapse. Grade II hemorrhoids prolapse but spontaneously reduce. Grade III hemorrhoids prolapse but require manual reduction. Grade IV hemorrhoids prolapse and cannot be manually reduced. The four-level grading system helps guide the choice of treatment of hemorrhoids.

Signs & Symptoms

Patients with thrombosed external hemorrhoids complain of acute pain and swelling or lump at the anus. Patients with external hemorrhoid skin tags will have more chronic symptoms of prolapsed, “extra skin,” irritation, and difficulty with hygiene after bowel movements. Patients with internal hemorrhoids complain of bleeding, pressure-like pain and prolapse. Patients with bleeding internal hemorrhoids can have significant blood loss and become anemic acutely or chronically. Other than thrombosed external hemorrhoids, patients with hemorrhoids do not complain of sharp pain but rather bleeding, prolapse, irritation, and sometimes a pressure-like pain due to the prolapse. Both external and internal hemorrhoids can become incarcerated and gangrenous resulting in necrosis of skin and mucosa as well as bleeding.

Examination of the patient with a thrombosed external hemorrhoid reveals a purple swelling at the anus consistent with a clot in an external hemorrhoid vessel. Patients with external prolapse and tags reveal chronic protrusion and lumps without acute pain and discoloration. Patients with internal hemorrhoids may reveal nothing externally unless the internal hemorrhoids prolapse externally. Digital evaluation of the rectum can rule out any mass lesions or malignancy but internal hemorrhoids cannot be assessed adequately using digital rectal examination. Anoscopy is necessary to properly evaluate internal hemorrhoids. The examiner asks the patient to push or strain while visualizing each of the three common hemorrhoidal piles in the right anterior, right posterior and left lateral positions within the anal canal. Internal hemorrhoids are present if prolapse or bleeding occurs in any of the three locations visualized during anoscopy. Physical examination alone establishes a diagnosis of hemorrhoids. Further evaluation with laboratory or imaging studies is unnecessary unless there has been significant hemorrhage. All patients should also undergo evaluation of the more proximal colon with flexible sigmoidoscopy or colonoscopy as indicated.

Differential Diagnosis

Since patients and many primary care providers identify any anorectal symptom as being due to hemorrhoids, nearly all patients complain of “hemorrhoids” or will have been told that they have “hemorrhoids.”

Patients with rectal bleeding need to be carefully evaluated not only with anoscopy but also with flexible endoscopy to rule out proximal pathology such as colitis, polyps or cancer. Patients with rectal bleeding, under age 40 and without a family history of colon cancer, can undergo anoscopy and flexible sigmoidoscopy. Patients with rectal bleeding between 40 and 50 years of age need evaluation with anoscopy and flexible sigmoidoscopy or colonoscopy with colonoscopy preferred for most patients. Patients over age 50 with bleeding need to be evaluated with anoscopy and colonoscopy. Finally, all patients with a significant family history of colon cancer should undergo anoscopy and colonoscopy regardless of age. Thus, it is very important in patients with rectal bleeding to evaluate the whole colon in most circumstances in order to rule out malignancy.

In patients with symptoms of prolapse, the surgeon must differentiate hemorrhoidal prolapse from true rectal prolapse. Patients with hemorrhoidal prolapse have prolapsing hemorrhoids in one or more of the standard hemorrhoid locations—right anterior, right posterior, and/or left lateral position. Because the hemorrhoids prolapse in these specific locations, the examiner sees prolapsing mucosa and underlying hemorrhoidal vessels with radial folds between the various prolapsing hemorrhoids. Patients with true rectal prolapse have circumferential prolapse of mucosa and full-thickness rectal wall that results in concentric folds. Patients with full-thickness rectal prolapse have decreased sphincter tone whereas patients with prolapsing hemorrhoids typically have normal to increased sphincter tone.

Treatment of External Hemorrhoids

Patients with chronic tags and external hemorrhoids are treated with reassurance particularly if the tags are small and minimally symptomatic. If they have symptoms of irritation, topical hydrocortisone cream can be helpful. If the external hemorrhoids are causing recurring symptoms of irritation, discomfort, and difficulty with anal hygiene then simple surgical excision may resolve them. If a patient with a thrombosed external hemorrhoid is seen within 3 days of the onset of symptoms then excision of the clot may be beneficial. Excision of the clot in these patients who present early to the surgeon allows for faster resolution of their symptoms. Simple incision of the clot is associated with a higher recurrence rate so if surgical intervention is undertaken it should be complete excision of the hemorrhoidal vessel and clot. Most patients with thrombosed external hemorrhoids seek medical attention after 3 days of symptoms. Surgical excision will not hasten resolution of symptoms in these patients, and management is topical and oral pain medications, stool softeners and laxatives. The clot typically resolves in 2 weeks-2 months. After resolution of their clot, occasionally patients are left with a residual skin tag. Hemorrhoidal disease is common during pregnancy and can be treated postpartum if symptoms persist.

Treatment of Internal Hemorrhoids

Patients with mild to moderate internal hemorrhoids (grades I-II) and constipation are treated with fiber, fluids, and possibly laxatives to improve their bowel habits. For most of these patients this medical treatment to improve their bowel function will resolve their hemorrhoidal symptoms. For patients with “hemorrhoids” and hyperactive bowel function, treatment should be directed at the cause of the diarrhea/multiple bowel movements. These patients should not undergo hemorrhoid surgery. Patients with normal bowel habits and persistent hemorrhoidal symptoms are candidates for a surgical approach.

Surgical Treatment of Hemorrhoids in the Office Setting

Internal hemorrhoids can be treated with in-office procedures such as rubber band ligation, sclerotherapy, and infrared coagulation. Most patients with grades I-III hemorrhoids can be successfully treated with office-based procedures. Of the office-based procedures, rubber band ligation is typically the most effective option.

A. Rubber Band Ligation of Hemorrhoids

Small to moderate-sized symptomatic internal hemorrhoids (grades I-III) can be treated with rubber band ligation. This in-office treatment involves placement of an anoscope then grasping the largest hemorrhoidal pile above the dentate line with a clamp and then using a rubber band ligator to place a rubber band around the “neck” of the hemorrhoid. Because the rubber band is placed above the dentate line, patients can tolerate this procedure without anesthesia and usually do not have significant postprocedure pain. After banding patients have either no symptoms or a mild to moderate pressure sensation that resolves in hours to a day or two. The rubber band is a noose around the hemorrhoid’s “neck,” and the hemorrhoid and rubber band will fall off within 5-10 days resulting in a scar that reduces the hemorrhoid size and degree of prolapse. When this sloughing of the hemorrhoid and rubber band occurs, the patient may experience bleeding that occasionally is severe enough to require an emergent visit. Patients are banded without antibiotics as sepsis after banding is exceedingly uncommon. Since post-banding sepsis presents with urinary retention, fever and increasing pain, any rubber band ligation patient with this constellation of symptoms needs to be evaluated urgently. Treatment of post-banding sepsis requires intravenous antibiotics, band removal, debridement of necrotic tissue and supportive care in an intensive care unit. Banding is usually performed one “pile” at a time but placement of multiple bands at one setting is possible. Postbanding instructions include keeping the stools soft, using pain medication as needed and returning for urgent reevaluation if signs and symptoms of sepsis develop. Rubber band ligation is well-tolerated and quite successful for patients with grades I-III internal hemorrhoids.

B. Sclerotherapy

Sclerotherapy involves using anoscopy to inject a sclerosing agent into the apex of grades I- II internal hemorrhoids. A variety of sclerosing agents have been used with a commonly used option being phenol in oil. Typically, 3-5 mL of sclerosing solution is injected. While the initial success rate approaches that of rubber band ligation, recurrences are common. Complications are unusual but necrosis, rectal perforation, and sepsis have all been reported.

C. Infrared Coagulation

Infrared coagulation involves application of infrared energy directly to the internal hemorrhoids with an infrared coagulation probe. Using anoscopy, the probe is placed on the hemorrhoid for 1-2 seconds which results in coagulation of the hemorrhoid with a decrease in size and blood flow through the hemorrhoid. Recent studies have shown that infrared coagulation is as good as rubber band ligation for patients with grades I-II internal hemorrhoids. Complications are unusual but include bleeding, necrosis, and sepsis.

Surgical Treatment of Internal Hemorrhoids in the Operating Room

Patients with persistent symptoms despite in-office treatment of their hemorrhoids are candidates for surgery in the operating room. Surgery is usually performed only for patients with grades III-IV internal hemorrhoids. In the operating room, surgical treatment of internal hemorrhoids can be by surgical excision, stapled hemorrhoidopexy or doppler-guided ligation.

A. Excisional Hemorrhoidectomy

Classic excisional hemorrhoidectomy is performed either in the lithotomy or prone position. After the induction of anesthesia the hemorrhoidal piles are excised with scissors, cautery or harmonic scalpel. The resulting wounds are closed, partially-closed or left open depending on surgeon preference. Care is taken to excise just the mucosa, submucosa, and hemorrhoids and to avoid injury to the underlying anal sphincter muscle. In addition, care is taken not to excise too much mucosa and anoderm as this could result in anal stenosis. The procedure takes less than an hour and is scheduled as outpatient surgery. Given that the incisions start externally and end in the anal canal/lower rectum, patients can have significant discomfort postoperatively. Adequate pain control, keeping the bowel movements soft and avoiding constipation are all important postoperatively. Early complications after excisional hemorrhoidectomy include bleeding, infection, and urinary retention. The rate of urinary retention can be reduced by limiting the amount of intravenous fluids during surgery. Late complications include anal stenosis and mucosal ectropion and whitehead deformity (circumferential mucosal ectropion). Given its high success rate and low recurrence rate, all other surgical interventions are compared to excisional hemorrhoidectomy to determine their efficacy.

B. Stapled Hemorrhoidopexy

A stapled hemorrhoidopexy is useful for patients with circumferential grade II-III hemorrhoids who fail in-office treatment. The technique involves placement of a purse-string suture 3-4 cm above the dentate line in the submucosal plane. The circular stapler’s anvil is then placed proximal to the purse string suture and the suture is tied drawing the internal hemorrhoids into the circular stapler. The stapler is then closed and fired removing a circumferential strip of internal hemorrhoids. The staple line, 1-2 cm above the dentate line, is inspected and any bleeding oversewn. Thus, the procedure removes a strip of internal hemorrhoids and creates a hemorrhoidopexy at the staple line that reduces hemorrhoidal prolapse. The procedure does not address external hemorrhoids and thus would not be useful for patients with significant external hemorrhoidal disease. Because the procedure’s incision (at the staple line) is above the dentate line, stapled hemorrhoidopexy is associated with less pain and discomfort than traditional excisional hemorrhoidectomy. The results of stapled hemorrhoidopexy have been good and are comparable to excisional hemorrhoidectomy. Complications from stapled hemorrhoidopexy are also comparable to excisional hemorrhoidectomy with the exception of including some unique complications such as recto-vaginal fistula and rectal obstruction. Appropriate patient selection and meticulous surgical technique are required to achieve the best results with stapled hemorrhoidopexy. Thus, stapled hemorrhoidopexy is a good option for grade II-III internal hemorrhoids that are not associated with significant external hemorrhoids.

C. Doppler-Guided Hemorrhoidectomy

Doppler-guided hemorrhoidectomy involves the use of a specially designed anoscope with a doppler probe that allows for precise identification and ligation of the hemorrhoidal vessels. Six to eight hemorrhoidal vessels are identified and suture ligated using the doppler probe to identify the vessels and then confirm the interruption of blood flow after suture ligation. Early results have demonstrated that this technique is comparable to excisional hemorrhoidectomy for grade II-III internal hemorrhoids. The complication profile is also favorable. More experience with the doppler-guided hemorrhoidectomy is necessary in order to adequately evaluate the long-term effectiveness of the procedure.

Prognosis

The successful treatment of external and internal hemorrhoids is related to changing the patient’s bowel habits. Increasing dietary fiber, decreasing constipating foods, introducing exercise, and decreasing time spent on the toilet all decrease the amount of time spent straining in the squatting position. These behavioral modifications are the most important steps in preventing recurrence.

An anal fissure is a tear in the anoderm usually located in the posterior or anterior midline of the anal canal. An anal fissure may be associated with a sentinel tag located at the distal aspect of the anal fissure (anal verge) and/or a hypertrophied anal papilla at the proximal aspect of the fissure. The inciting event causing an anal fissure is thought to be trauma to the anal canal from a hard bowel movement or other cause. This trauma results in a tear that leads to pain and spasm of the internal anal sphincter muscle particularly during and after bowel movements. The spasm results in elevated anal resting pressures that can unfortunately lead to a vicious cycle of further spasm and pain. With elevated resting pressures, the blood flow to the posterior and anterior midline decreases inhibiting healing of the fissure. Fissures are usually classified as either acute with symptoms occurring just over the past month or chronic with symptoms present for greater than 2-3 months. Over 90% of fissures are located in the posterior midline with the rest located in the anterior midline. Given their etiology of spasm and elevated resting pressures resulting in decreased blood flow, chronic anal fissures can be considered “ischemic ulcers” of the anal canal.

Clinical Findings

Patients with an anal fissure complain of sharp pain with or immediately after bowel movements. They may also complain of rectal bleeding and a “hemorrhoid” or sentinel tag. Patients often describe moderate to severe pain like a “knife” or “razor blade” during defecation. Due to the pain, patients fear going to the bathroom that can result in delaying defecation, hardened stool, and additional pain. On inspection of the external anus, there may be a sentinel tag in either the posterior or anterior midline. To visualize the fissure, the examiner needs to evert the anus by pulling the right and left anal margin skin laterally. As the anus is everted, the examiner can carefully inspect the anoderm in the posterior and anterior midline for a tear in the anoderm. Patients with significant pain and spasm may not even tolerate this maneuver. In these patients it is helpful to gently expose the anus and ask the patient to strain to defecate to see if during straining self-eversion of the anus occurs. Due to pain, digital rectal examination, and anoscopy are not performed immediately, but reserved for when the symptoms resolve or the patient is in the operating room. Laboratory and imaging studies are not necessary but flexible endoscopy of some type should be scheduled if it has not been performed recently.

Differential Diagnosis

Classic anal fissures occur in either the posterior (90% +) or anterior (1%-10%) midline. Not all posterior and anterior anal canal tears are anal fissures. Anal canal ulcers can occur from Crohn disease, leukemia, HIV, cancer and infections such as herpes, syphilis, cytomegalovirus, and tuberculosis. These anal canal ulcers mimic anal fissures. A careful history can help identify possible etiologies of an anal ulcer. On the other hand, typical anal fissures are associated with increased sphincter tone so any patient with decreased sphincter tone should be suspected of having an anal canal ulcer rather than a fissure. Further, whenever a “fissure” is located laterally rather than in the posterior or anterior midline, an anal canal ulcer should be suspected. There should be a low threshold to suspect an anal ulcer rather than fissure. In these patients, an examination under anesthesia with biopsy of the ulcer is necessary to rule out an infectious or malignant etiology.

Complications

In addition to causing pain and bleeding, anal fissures can become infected and develop a fissure-fistula complex. This relatively unusual complication is easily treated with a posterior intersphincteric fistulotomy.

Medical Treatment

The pathogenesis of an anal fissure is pain and spasm resulting in increased internal anal sphincter (IAS) muscle pressures, decreased blood flow, and a nonhealing fissure in the anoderm of the anal canal. Treatment is directed at breaking this pain and spasm cycle to relax the internal sphincter muscle, increase blood flow, and allow the fissure to heal. To do this, patients should keep their stools soft with stool softeners and laxatives to avoid further anal canal trauma. In addition, warm baths are recommended to relax the sphincter muscle and allow the fissure to heal. Stool softeners, bulking agents, and sitz baths will heal 90% of anal fissures. Topical ointments can also be prescribed to decrease the anal sphincter pressure. Nitroglycerin ointment (0.2% or 0.4%) or calcium channel blocker ointment (0.2% diltiazem gel) can be used to chemically relax the IAS muscle. Side effects include headache which occurs more frequently after nitroglycerin ointment. Patients who fail this regimen and have a persistent fissure are candidates for surgery or treatment with botulinum toxin. Botulinium toxin injection into the anal sphincter can be successful but is costly and has a higher recurrence rate than surgery. Thus, medical treatment of anal fissures includes stool softeners, bulking agents, warm baths, topical nitroglycerin ointment or diltiazem gel, and possibly botulinum toxin injection. Most patients with acute anal fissures and over 50% of patients with chronic anal fissures are successfully treated without surgery. Patients who fail medical management of their anal fissure should undergo surgical intervention.

Surgical Treatment

Surgical treatment of an anal fissure involves performing a lateral internal sphincterotomy. While the fissure may be biopsied and a sentinel tag or hypertrophied anal papilla excised, the most important part of an operation for anal fissure is directed via a lateral incision at the IAS muscle. In the operating room, a lateral incision is made in the intersphincteric groove between the internal and EAS muscles and a submucosal and intersphincteric dissection is performed in order to clearly identify the IAS muscle. The IAS muscle is then cut the length of the fissure in order to permanently relax the anal canal. After sphincterotomy, relaxation of the anal canal is readily appreciated by the surgeon. This short, outpatient operation has over a 90% success rate and a recurrence rate of less than 10%. Patients often have less pain after surgery. Complications include bleeding, infection, and rarely fecal incontinence (< 0.5%).

Patients who have preexisting fecal leakage or lack increased anal sphincter muscle pressures are poor candidates for lateral internal sphincterotomy which could result in worsening bowel control. These relatively rare patients are better treated with an anal advancement flap that does not involve dividing any sphincter muscle. For a description of the anal advancement flap, see the section on anal stenosis.

An anorectal abscess is one of the three common causes of anorectal pain and is the only cause that usually requires urgent surgical treatment. Most anorectal abscesses have a cryptoglandular etiology. When the anal glands in the crypts of the dentate line become blocked, an anorectal abscess can develop. Because these glands extend a variable depth, the developing abscess can track in various anatomic planes. Abscesses are classified by their anatomic location:—perianal, ischiorectal, intersphincteric, and supralevator (Figure 31–3). Fortunately, most abscesses are perianal or ischiorectal and can be relatively easily identified on physical examination. Intersphincteric and supralevator abscesses are unusual and often are only identified by MRI/CT or examination under anesthesia. Most abscesses are cryptoglandular in etiology but some patients develop abscesses related to another disease process such as Crohn, tuberculosis, and cancer. While many abscesses will heal with simple incision and drainage, some 30%-60% of abscesses will not heal and patients will complain of persistent drainage and recurrent inflammation related to an anal fistula. In these patients, the cryptoglandular source and external surgical drainage site remain connected allowing for passage of mucus and stool through this tract. The location of the abscess, thus, determines the location and tract of the resulting anal fistula. Anal fistulas are classified by their relationship with the anal sphincter muscle—intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric. Due to the frequency of the abscesses that created them, intersphincteric and transsphincteric fistulas are the most common anal fistulas. Suprasphincteric and extrasphincteric fistulas are exceedingly rare. Due to their relationship with the anal sphincter muscle, treatment of anal fistulas should be evaluated and treated by highly specialized surgeons familiar with sphincter-saving techniques in order to avoid complications such as fecal incontinence. Since fistulas occur in 30%-60% of patients after anorectal abscess drainage, patients undergoing abscess drainage should be warned about the possibility of a fistula and should be given appropriate follow-up to insure healing and absence of a persistent fistula tract.

Clinical Findings

Patients with an anorectal abscess complain of acute pain, swelling, and possibly a fever. An occasional patient may complain of leakage of mucus and pus related to the spontaneous drainage of the abscess. For patients with perianal and ischiorectal abscesses, physical examination often reveals erythema, fluctuance, and asymmetry between the right and left perirectal tissues. An occasional patient will present with a symmetric horseshoe abscess cavity circling half or more of the circumference and may have no left-right asymmetry. If a patient has an intersphincteric or supralevator anorectal abscess, there is often none of the above findings on physical examination. Thus, patients with a suspicion of an abscess but no obvious physical examination findings should either be imaged with MRI or taken to the operating room for an examination under anesthesia. Laboratory testing is usually not helpful in patients with an anorectal abscess although frequently these patients will have an elevated white blood cell count. Radiologic studies are also not necessary as the vast majority of anorectal abscesses are obvious on the basis of history and physical examination alone. Some patients with symptoms of an abscess and no physical examination findings may benefit from imaging studies as well as patients with recurrent or complex abscesses such as some patients with Crohn disease. Potential imaging studies include CT, MRI, and anorectal ultrasound. Anorectal ultrasound is not well tolerated in patients with an acute abscess and CT will miss some abscesses. Thus, if an imaging study is necessary, an MRI is the imaging test of choice being able to readily identify complex abscesses and their anatomic extensions.

Patients with an anorectal fistula complain of chronic drainage of mucus and blood, irritation, and usually have an antecedent history of an anorectal abscess. If a patient has persistent drainage 6-8 weeks after abscess drainage, then a fistula should be suspected, and evaluation and treatment for an anal fistula should be initiated. Some patients with anal fistulas will have a relatively remote or no history of an abscess. Physical examination reveals the external opening and often there is a palpable subcutaneous tract between the external opening and the anus. It is important to remember that any nonhealing wound or opening around the anus should be presumed to be a fistula until proven otherwise. Laboratory testing is not necessary in patients with anal fistulas but imaging studies may be useful for recurrent and complex anal fistulas. MRI is the imaging procedure of choice to identify anal fistula tracts, side tracts, and the relationship of the tracts to the anal sphincter muscle. Transanal ultrasonography can also be useful and can be performed intraoperatively using hydrogen peroxide enhancement to highlight the fistula tract.

Differential Diagnosis

The differential diagnosis for patients with anorectal abscess or fistula includes perianal hidradenitis, pilonidal disease, and rarely bartholin gland cyst. On physical examination, it may be difficult to differentiate an anorectal abscess/fistula from complex hidradenitis or pilonidal disease. Further, hidradenitis or pilonidal disease can occur concurrently with an anorectal abscess or fistula. Careful evaluation in the operating room is necessary to determine if an abscess is communicating only with the skin (hidradenitis), only with the midline gluteal cleft (pilonidal disease) or with the anus (fistula). Rare causes of anorectal abscesses and fistulas include tuberculosis, actinomycosis, cancer, and diverticulitis.

Complications

Abscesses can enlarge and spread along various anatomic planes around the anus. Abscesses can form a posteriorly based horseshoe around the anus usually just sparing the anterior perirectal space. Abscesses can also track around just one side of the anus (1/2 horseshoe). While it may be unusual for a single abscess to destroy a significant amount of anorectal tissue and diminish anorectal function, multiple recurrent abscesses can result in destruction of anorectal anatomy and muscle function resulting in a deterioration of anorectal function.

In rare circumstances, an anorectal abscess can result in systemic sepsis. Treatment should include adequate drainage of the abscess, intravenous antibiotics, and supportive intensive care unit care.

Anorectal abscesses can recur after treatment. The reasons for recurrence include inadequate initial drainage (often because deep postanal space was not drained), the presence of a fistula, and Crohn disease. Nearly all patients with recurrent or complex abscesses should be evaluated for Crohn disease.

Anal fistulas should be treated when identified because although they may be minimally symptomatic they can develop into an acute anorectal abscess. Fistulas, too, may recur after treatment due to undiagnosed side tracts or Crohn disease. Crohn disease should be ruled out in all patients with complicated or recurrent anal fistulas.

Treatment of Anorectal Abscesses

Anorectal abscesses are treated by incision and drainage. For the common perianal and ischiorectal abscesses, a cruciate incision is made over the area of fluctuance as close to the anal verge as possible to decrease the length of a fistula tract if one should develop. Frequently it is useful to excise the skin tips of the cruciate incision in order to allow for adequate drainage and insure that the abscess heals from the inside out as premature skin healing could result in a recurrent abscess. When draining an acute abscess, it is very unlikely to be able to identify an internal opening and the course of the fistula tract if one is present. Thus, when draining an abscess either in the office or the operating room, it is important to concentrate effort at insuring that the abscess is adequately drained and worry about a fistula later if it should develop. For the relative rare intersphincteric abscess, transanal drainage is performed. In the operating room, the intersphinteric abscess is palpated within the anal canal and via an anoscope a longitudinal incision is made to drain the abscess internally into the rectum. Supralevator abscesses can also be treated in this way. Alternatively, supralevator abscesses can be drained in the interventional radiology suite using CT-guidance but this may result in an extrasphincteric fistula if the etiology of the abscess is cryptoglandular.

After surgical drainage, only immunocompromised patients or patients with associated sepsis are treated with antibiotics. For large abscesses, placement of a penrose or mushroom-catheter drain may be necessary to insure adequate drainage. After draining a horseshoe abscess posteriorly, it is useful to make counter incisions at the anterior extent of the abscess on both sides of the anus and put looped penrose or vessel-loop drains from the posterior opening to the anterior opening. These drains are left for at least 2-3 weeks and will allow for better drainage of the entire abscess cavity. Finally, follow-up of patients after abscess drainage is important to insure that the abscess completely heals and does not evolve into a persistently draining fistula tract.

Treatment of Anorectal Fistula

Traditionally, anorectal fistulas have been treated by fistulotomy. Fistulotomy is performed one of three ways. The simplest fistulotomy is a single-stage procedure laying open the fistula tract. A two-stage approach is used for fistulas that involve a significant amount of sphincter muscle. The two-stage approach uses a seton which is a suture or vessel loop drain that is tied to itself after placement in the fistula tract. With the two-stage approach, the first step is a partial fistulotomy and seton placement. After healing from this first step, the second step is a completion fistulotomy. A final method of fistulotomy involves placement of a cutting seton and then gradual division of the fistula tract and involved sphincter muscle by tightening of the cutting seton over time. While fistulotomy may still be utilized for subcutaneous, intersphincteric, and low transphincter fistulas (all have little or no muscle involvement), fistulotomy has fallen into disfavor because division of the sphincter muscle during fistulotomy as well as contour deformities associated with fistulotomy can result in fecal incontinence and leakage. Thus, while fistulotomy is a highly successful way to treat subcutaneous and intersphincteric fistulas that involve minimal to no anal sphincter muscle, transsphincteric fistulas are better treated with a sphincter-sparing approach to avoid the complication of fecal incontinence.

Sphincter-sparing treatment approaches for transphincteric anal fistulas include fibrin glue, anal fistula plug, the ligation of the intersphincteric fistula tract (LIFT) procedure, and the rectal advancement flap. Prior to any of these sphincter-sparing procedures, a vessel loop draining seton is placed into the fistula tract, and the tract is allowed to heal around the seton for 3 months. While this seton placement procedure step can be omitted, studies have shown that the success rate of the subsequent definitive sphincter-sparing procedure is higher after seton placement. For the fibrin glue procedure, the seton is removed, the internal opening suture closed and then fibrin glue is instilled via the external opening to seal the tract. The anal fistula plug procedure is done in a similar fashion just using the plug rather than the glue. No incisions are made with either of these procedures which tend to be very well-tolerated by patients. Unfortunately, the success rate is only 60%-70% for fibrin glue and probably even lower for the anal fistula plug. Thus, a number of patients (30%-40%) will fail glue or plug at which time further treatment by repeating the glue or plug or by opting for the more invasive LIFT procedure or rectal advancement flap. The main complications for glue/plug are recurrence and abscess (rare).

The relatively new procedure is called LIFT because it involves ligation of the intersphincteric fistula tract. During this outpatient operation after removal of the seton (if placed previously), an interphincteric groove incision is made and the fistula tract in the intersphincteric space is identified and circumferentially dissected free. This dissection allows for proximal and distal suture ligation and division of the fistula tract within the intersphincteric space. This procedure is well-tolerated, spares the sphincter muscle, and is successful 80% of the time. Complications include recurrence of a simpler intersphincteric fistula and rarely abscess formation.

If the previously mentioned sphincter-sparing techniques are unsuccessful in healing an anal fistula, an anorectal advancement flap can be performed. For patients, this is a significantly more involved operation than the above options as it involves much larger incisions, longer operative time, and longer healing time. In the operating room, patients are placed prone for an anterior internal opening or placed in lithotomy position for a posterior internal opening. A U-shaped flap of mucosa, submucosa, and some underlying sphincter muscle is dissected proximally with the base of the “U” just distal to the internal opening. Once the flap is completely mobilized, the internal opening in the underlying sphincter muscle is closed with one or two figure of eight sutures. The tip of the flap is then excised and the flap is advanced distally to cover the suture closure of the internal opening in the sphincter muscle. The flap is then sutured into place providing a double layer closure of the internal opening. The external opening is enlarged and left open for drainage. Patients undergoing anorectal advancement flap are typically observed overnight to control pain and monitor for anorectal bleeding. If the flap remains in place and heals, the internal opening will be closed, and the rest of the fistula tract will heal. The success rate for the rectal advancement flap procedure is 85%-95% with the higher success rates associated with preoperative seton drainage.

Prognosis

With the exception of Crohn patients who can develop recurring anal abscesses and fistulas, the prognosis with anorectal abscesses and fistulas is excellent. The new sphincter-sparing techniques for anal fistulas do require multiple operations, but that is a small price to pay in order to minimize the occurrence of fecal incontinence which can be over 50% in patients after traditional fistulotomy.

Condylomata acuminata are caused by the human papillomavirus (HPV) and are transmitted primarily by sexual contact. In the United States, condylomata acuminatum is the most common sexually transmitted viral disease. It is the most common anorectal infection of men who have sex with men (MSM) and is particularly prevalent in HIV-positive patients. The disease is not limited to men or women who practice anoreceptive intercourse. In women, the virus may track down from the vagina, and in men, it may track from the base of the scrotum. A recent study found that 16% of asymptomatic heterosexual men tested positive for anal HPV. In addition to causing anal warts, HPV infection is the primary cause of anal dysplasia and anal squamous cell cancer. While HPV strains HPV-6 and HPV-11 cause benign warts, HPV-16 and HPV-18 are the two HPV strains with the highest risk of anal cancer. Despite the high prevalence of HPV infection, most HPV-infected individuals will not develop cancer due to the response of the immune system against the virus. Immunocompromised individuals such as patients with HIV or transplant recipients have an increased HPV-related cancer risk. Recently a vaccine has been developed that prevents cancer, precancer, and most types of warts.

Clinical Findings

Patients with condylomata acuminata present with wart-like growth around the anus and in the anal canal. The presence of warts is associated with discomfort, irritation, and possibly some occasional rectal bleeding. Due to HPV’s high prevalence in MSM and its risk of causing cancer, primary care physicians, infectious disease clinics, and HIV clinics often screen for HPV with anal pap smears. Patients with positive anal pap smears are referred for further evaluation. The appearance of condylomata acuminata and HPV disease can be quite variable. Wart-like growths are typical but flat patches of warty growth can also be seen. Other HPV changes cannot be seen without the assistance of high-resolution anoscopy (HRA). HRA involves applying acetic acid to the anal canal and using a colposcope to look for HPV-related changes in the anoderm and rectal mucosa. Laboratory and radiographic studies are rarely utilized in the evaluation of patients with condylomata acuminata. Thus, evaluation of patients with HPV-related condylomata acuminata requires careful external examination, anoscopy, and possibly HRA to determine the extent of disease.

Differential Diagnosis

Because of the variable appearance of condyloma acuminata, hemorrhoids, skin tags, and fibroepithelial polyps among many other anal skin conditions can mimic condylomata acuminata. Due to the large differential diagnosis for perianal and anal canal skin changes, it is important that a biopsy is taken of all anal canal lesions in order to make an accurate diagnosis.

Prevention

A quadrivalent HPV vaccine against HPV-6, -11, -16, and -18 has been recently developed and has been shown to prevent cancer, precancer, and most types of warts. The vaccine is best given prior to any sexual activity but also has efficacy after the initiation of sexual activity. In uninfected individuals, the efficacy of the vaccine against the development anal dysplasia and anal cancer was 75% whereas in patients with known HPV infections the efficacy was 50%.

Treatment

Condylomata acuminata are treated in the office or the operating room. Significant external disease or any internal anal canal disease is probably best treated in the operating room. Isolated external disease can be safely treated in the office. Condylomata acuminata are treated using a variety of excisional and destructive methods. In the office, anal warts can be excised after injecting local anesthesia or destroyed with bichloroacetic acid, podophyllin, liquid nitrogen, infrared coagulation, or electrocautry. In the operating room, excision and destruction using electrocautery is commonly used. All excised specimens are sent for pathologic analysis. If highly suspicious lesions are excised during an operation, their location should be specified in the case that the pathology is unfavorable, and re-excision is required. Unless a patient has a significant burden of disease, all lesions are either excised or destroyed in the operating room. Some surgeons will use HRA in the office and operating room in order to identify and treat all HPV-related changes. After surgery pain medication and stool softeners are prescribed, and patients are given appropriate follow-up.

Complications and Prognosis

While some bleeding, pain, and rarely infection may occur after excision of condylomata, the most common complication is recurrence. Patients should be informed prior to surgery that the recurrence rate is high (30%-80%) but that often small areas of recurrence can be treated in the office. Patients should also understand that close follow-up is necessary for early detection of recurrence. This close follow-up is important in order to avoid reoperation and the development of malignancy.

A relatively rare variant of condylomata acuminatum is the locally aggressive but benign giant condylomata acuminatum known as a Buschke–Lowenstein tumor. Treatment is radical excision for palliation or cure. In some patients, surgery has been combined with adjuvant chemotherapy and radiation therapy with success.

After excision of condylomata acuminatum patients should be informed of their pathology results. If an area of squamous cell cancer has been excised on the anal margin, re-excision of this area may need to be performed if the margins were positive. If squamous cell cancer has been identified in the anal canal or from an unknown location around the anus, then the patient should be treated with chemoradiation (Nigro protocol). On the other hand, pathologic analysis may not reveal cancer but rather anal intraepithelial neoplasia (AIN). Anal intraepithelial neoplasia is graded from I (most benign) to III (most ominous and closest to cancer). Many surgeons would return to the operating room to reevaluate and excise areas of AIN-III if there is any question about the completeness of excision at the initial operation. In HIV-positive patients, some grade of AIN is a very common finding. Most surgeons would follow patients with higher grades of AIN at more frequent intervals.

The prognosis of patients with condylomata acuminata is excellent as despite the presence of anal warts and HPV, anal cancer is still quite rare. Further, the prognosis of anal cancer is excellent if located on the anal margin and completely excised. Prognosis of anal canal squamous cell cancer is also good as treatment with chemoradiation is very successful for most localized anal canal squamous cell cancers. Salvage abdominoperineal resection for recurrence of squamous cell cancer after chemoradiation is unusual.

Pilonidal disease is a chronic gland infection in the depths of the gluteal cleft. While the glands and resulting pits can occur anywhere along the gluteal cleft, they occur most often in the superior gluteal cleft over the sacrum. The pathogenesis of pilonidal disease is thought to be a process in which the follicles in the midline gluteal cleft get blocked, infected, and then drain leaving open midline pits. In the depths of the gluteal cleft these pits have a vacuum effect on loose hair and hair is literally sucked into these pits. During surgery, tufts of hair can be found in the pits and chronic abscess cavity. Thus, while the hair does not cause pilonidal disease, the presence of hair in the pits and glands acts as a foreign body and causes the infection and drainage to persist. Pilonidal disease usually occurs in men (3:1 male to female ratio) between the ages of 15 and 40 with the peak incidence between 16 and 20 years. Although pilonidal disease is typically chronic with recurrent drainage and inflammation, it often regresses with time and is rare after 40 years of age. The pathogenesis and natural history of pilonidal disease is important to remember when recommending treatment. Given its natural history that involves disease regression with time, conservative treatment, and minimal surgery is recommended for most patients.

Clinical Findings

Patients with pilonidal disease present in three main ways—acute abscess, chronic draining pits or complex, recurrent disease after previous surgery. Patients with an acute pilonidal abscess will have pain and possibly swelling in or along the gluteal cleft. Given the relatively fixed nature of the tissues in this region and how deep a typical pilonidal abscess is located, swelling and cellulitis are often absent, and physical examination often underestimates the size of the abscess. Patients with chronically draining midline pits will have one or more pits in the midline with drainage and recurrent inflammation. Often hair will be seen protruding from the pits. Patients with complex disease after previous surgery such as pilonidal cystectomy will have chronic, nonhealing wounds in the midline of the gluteal cleft. History and physical examination are sufficient to make the diagnosis of pilonidal disease regardless of the type of presentation. Laboratory and imaging studies play no role in the evaluation of patients with pilonidal disease.

Differential Diagnosis

Pilonidal disease occurs in the superior gluteal cleft and is usually relatively easy to diagnose. Pilonidal disease occurring inferior in the gluteal cleft and close to the anus may be difficult to distinguish from an anal fistula. An examination under anesthesia may be required in order to differentiate pilonidal pit and cyst from an anal fistula. Further, pilonidal disease off the midline may mimic hidradentitis. Usually, hidradenitis will occur elsewhere and will not be just limited to the gluteal cleft like pilonidal disease.

Treatment

Patients with an acute abscess related to pilonidal disease should undergo incision and drainage of their abscess. Antibiotics are not necessary unless the patient has significant infection, sepsis, or is immunocompromised. The abscess is nearly always located deep to the midline gluteal cleft. Because incisions in the midline heal poorly, an acute abscess should be drained through a lateral incision at least 2 cm off midline. A generous lateral incision allows for adequate drainage of pus and hair from the pilonidal cyst. Shaving a wide area around the gluteal cleft is important to help prevent further accumulation of hair in the cyst. After abscess drainage, patient should be followed to insure healing, but further operative intervention is usually not necessary.

Patients with chronically draining pilonidal pits should be treated conservatively. The whole gluteal cleft and surrounding gluteal skin should be shaved, and all hair in the pits removed. Patients are instructed to bend over in the shower and allow the water to blast the gluteal cleft to help prevent accumulation of hair in the pits. Patients should undergo repeat shaving and hair removed from the pits every week or 2 until resolution of symptoms. If symptoms recur, conservative treatment with shaving and removal of pit hair should be resumed. Patients with persistent drainage and inflammation despite 2-3 months of conservative treatment are candidates for surgery. Traditionally, surgical treatment of pilonidal disease involved pilonidal cystectomy which meant complete removal of the midline chronic abscess cavity. This procedure is associated with wound breakdown and possible development of a nonhealing midline wound that may in fact be more debilitating than the disease prior to surgery. Given this possibility, midline incisions are absolutely avoided. Rather, a minimally invasive operation entitled lateral incision and pit closure is performed. After a lateral incision is made, the abscess cavity in the midline is accessed via this lateral incision to remove all pus, hair, and granulation tissue. Next, the pits in the midline are excised and the minimal 2-3 mm wounds closed with nylon suture. The lateral incision is left open for drainage. If the excised midline pit wounds heal, the pilonidal disease is eliminated, and the lateral incision will heal readily over 2-4 weeks.

Patients with complex, recurrent pilonidal disease with large, nonhealing midline wounds need complex flap surgery to resolve their symptoms. Many types of flaps have been used to close these wounds and all flaps involving incisions in the midline or that cross the midline are plagued by poor healing in the midline. Due to poor midline healing, the Bascom cleft closure flap procedure that not only avoids the midline but eliminates the gluteal cleft is a very good option for these patients. In this procedure, the open wound is excised and the excision is extended laterally off the midline on one side leaving an asymmetric wound. The skin and subcutaneous tissues of the gluteal cleft and cheek of the opposite side are then mobilized and advanced across the midline to the side with the lateral excision. This flap accomplishes two important goals—the flap closure incision is off the midline facilitating healing (and there is no midline portion of the incision) and the gluteal cleft is eliminated as the cleft is mobilized and advanced to the opposite side. Without a gluteal cleft, further pilonidal disease is unheard of.

Complications & Prognosis

Patients with pilonidal disease are young, active adults, and often desire a quick fix for their symptoms. It is important to counsel patients regarding the natural history of the disease. Patients need to understand the chronic nature of the disease but also that it naturally regresses with time. With understanding, patients will more readily participate in conservative treatment and understand the goals of minimally invasive surgery such as lateral incision and pit closure. Overall, the prognosis of patients with pilonidal disease is excellent.

Anal stenosis is a relatively unusual condition that is most commonly associated with either previous surgery, malignancy, or Crohn disease. Patients often are successful at self-treating their stenosis by keeping their stools soft with stool softeners and laxatives. Complete anal canal obstruction is rare. Identification of the etiology of the anal stenosis is key to successful treatment.

Clinical Findings

Patients with anal stenosis complain of difficult evacuation and possibly rectal bleeding. The history is important to determine the etiology of their symptoms. The most common cause of anal stenois is previous anorectal surgery particularly hemorrhoid surgery. Since stenosis often occurs years to decades after hemorrhoid surgery, patients should be specifically questioned regarding prior anorectal surgery. Patients with anal stenosis related to Crohn disease usually have a relatively long history of anorectal Crohn disease. This may include treatment of abscesses, fistulas, and anal canal ulcers. Patients with malignancy may have a history of anal condyloma but often will have no antecedent history. Physical examination reveals a narrowed anal canal. Digital examination is still possible in patients with a mild anal stenosis. Moderate to severe anal canal stenosis does not allow digital examination. Due to the severity of stenosis, it may be difficult to determine if the stenosis is due to a mass or tumor. Laboratory and imaging studies play no role in the evaluation of patients with anal stenosis. Flexible endoscopy is important in all patients with anal stenosis. In those patients with moderate to severe stenosis, flexible endoscopic evaluation may be impossible prior to treatment and is done after the stenosis is corrected.

Treatment

Mild anal stenosis can be treated with stool softeners and laxatives with good results. Patients with persistent symptoms despite treatment and those patients with moderate to severe stenosis require endoscopic or surgical intervention. Because malignancy is always a possibility even after hemorrhoid surgery or in patients with Crohn disease, a biopsy of the anal canal stenosis is mandatory. Of course any patient diagnosed with malignancy needs treatment specific for the malignancy which usually involves chemoradiation (anal cancer) and possibly surgery (if rectal cancer). For patients without malignancy, the choice of a surgical procedure is dictated by the etiology of the anal stenosis.

Patients with Crohn disease can undergo endoscopic balloon dilatation of their anal stricture or operative anal stricturoplasty. During anal stricturoplasty, longitudinal incisions are made through the stricture at one to three locations around the anal canal. Recurrent stricture can be treated with repeat balloon dilatation or operative anal stricturoplasty.

Patients with postsurgical anal stenosis have a deficiency of anoderm related to their previous operation and subsequent scarring. Due to their deficiency of anoderm, these patients are not appropriate candidates for stricturoplasty but rather are better served with a local advancement flap into the anal canal to correct their anoderm deficiency. Many local advancement flaps have been described and used successfully such as the V-Y, Y-V, and the anal houseflap. During the anal houseflap operation the patient is placed in the prone position and the anal canal is visualized. Standard operative anoscopes will not fit into the anal canal of patients with moderate to severe stenosis and thus use of a nasal speculum is necessary. With the anal canal visualized, the anoderm is divided longitudinally for the length of the strictured anal canal. Transverse incisions are then made at the proximal and distal aspects of this incision converting the incision wound into a rectangular defect. A house-shaped flap of anal margin skin and subcutaneous tissue is developed and advanced into the anal canal. The flap is then sutured into place, and the donor site closed. In some cases, two or three separate houseflaps around the anus are necessary to adequately correct the anal stenosis. Thus, the advancement of anal margin skin into the anal canal corrects the deficiency of anoderm and relieves the anal stenosis.

The results following anal advancement flap treatment of anal canal stenosis are very good. Potential complications include bleeding, infection, flap necrosis, and flap retraction. If an advancement flap fails it can be repeated in another quadrant around the anus.

Pruritus ani is a challenging dermatologic disorder characterized by intense itching of the perianal skin. Diagnosis of this problem is typically not straightforward and, subsequently, patients are seen by a variety of specialists including, gastroenterologists, dermatologists, and colorectal surgeons. The incidence of pruritus ani ranges from 1% to 5% in adults and typically has a male predominance (ratio 4:1).

Pruritus ani is broadly classified either as primary (idiopathic) or secondary. Up to 90% of cases are considered idiopathic while the remaining secondary cases are caused by a variety of local and systemic conditions.

Clinical Findings

Patients typically present with complaints of an unpleasant perianal burning, which usually starts insidiously. As the condition becomes more chronic, this burning is replaced by varying degrees of itching that can become intolerable. Careful history uncovers that symptoms are often more pronounced at night.

Physical findings on examination can be varied. In the early stages the skin may appear normal; however, as the patient continues to scratch, the local inflammation worsens, resulting in erythematous, excoriated, and macerated skin. In the chronic stage, the skin is often lichenified with coarse ridges and ulcerations.

Differential Diagnosis

Identifying the primary etiology of pruritus ani can be very challenging; therefore, a careful history and physical examination is required. Information on diet, medications, synchronous skin conditions, common anorectal disorders, bowel function and stool consistency, as well as prior anorectal procedures should be ascertained. A thorough examination of the perianal skin and anoscopy are essential. Skin scrapings, cultures, and biopsy of suspicious lesions are important adjuncts to elucidate the underlying etiology. The routine use of endoscopy and radiologic studies is unnecessary unless there is a high index of suspicion for a colorectal cause. Some of the established causes of secondary pruritus ani are summarized in Table 31–5.

Treatment

The goal of treatment should be directed toward establishing clean and dry perianal skin that is free of ulcerations. If pruritus is found to be secondary to one of the aforementioned causes then treatment should be directed towards that specific pathology. The management of idiopathic pruritus is more challenging, often requiring intensive patient education and behavior modification. A high-fiber diet should be encouraged while eliminating foods that may precipitate pruritus. If symptoms improve, then these foods may be slowly reintroduced in order to identify the offending product.

Meticulous perianal hygiene should be stressed as the first step in management. Patients should discontinue use of all topical medications and should clean the perineum only with water, avoiding soaps and other potential irritants. In cases of more severe skin excoriation, skin barrier creams may provide symptomatic relief. A brief trial of topical steroids (hydrocortisone 0.5%-1%) is also often a useful adjunct but should not be used for prolonged periods as it results in thinning of the perianal skin. Topical hydrocortisone 1% has been shown in a double-blinded, randomized, placebo-controlled to reduce daily visual analog score (VAS) for severity of itch by 68% and weekly Dermatology Life Quality Index (DLQI) scores by 75%.

In patients with refractory symptoms, topical capsaicin can be considered. A randomized, placebo-controlled, trial comparing topical capsaicin (0.006%) with placebo (1% menthol) in patients with chronic pruritus ani found that of 44 patients, 31 (70%) had relief of their symptoms. Intradermal injection of methylene blue (1%) has also been described with limited success. Skin necrosis from inappropriate infiltration has been described.

Prognosis

The successful identification and treatment of secondary causes of pruritus ani often yields good results. However, relapses can be common with idiopathic pruritus. Every attempt should be made to continue to reinforce patient education.

Proctitis and anusitis are general terms referring to inflammation within the anal canal or rectum secondary to infectious pathogens or inflammatory causes. Sexually transmitted diseases are an increasingly common cause of proctitis with an incidence exceeding 15 million new cases annually in the United States. The differential diagnosis can be quite broad with a variety of bacteria and viruses; therefore, a systematic approach is important. The diagnosis and management of these conditions depends primarily on the underlying etiology.

1. Herpes proctitis

The Herpes Simplex Virus (HSV) is a DNA virus that is the most prevalent STD in the United States. The majority of anogenital infections are caused by the HSV-2 serotype, accounting for approximately 80%-90% of infections. Anorectal infections typically result from autoinoculation or direct contact with infected partners. The virus travels along peripheral nerves and has a variable incubation period (days to weeks). Prodromal symptoms may consist of burning, irritation, fever, and myalgia. This typically escalates to more intense, painful proctitis, and tenesmus. The characteristic lesions are small vesicles with surrounding erythema, which eventually coalesce and rupture forming painful ulcerations. Additionally, patients may develop tender inguinal adenopathy.

Evaluation of the rectum with a proctoscope will demonstrate erythematous and friable mucosa with ulcerations and mucopurulent discharge. Tzank smear of the discharge reveals the characteristic multinucleated giants cells with intranuclear inclusion bodies. Viral cultures of the discharge from these vesicles are also highly positive in acute infections.

HSV infections are usually self-limited in the absence of superimposed bacterial infections; therefore, initial treatments, such as sitz baths and oral analgesics are aimed at controlling symptoms. There is no cure for active infections but Acyclovir, Valacyclovir, and Famciclovir will shorten the duration of symptoms and may be used for suppressive therapy in patients with frequent recurrences.

2. Anorectal syphilis

Syphilis is caused by the spirochete, Treponema pallidum, which typically has an incubation period of 2-6 weeks. This disease was once on the verge of elimination but the incidence has been increasing steadily, especially young black men.

Acute anorectal infection is characterized by a small papule (chancre) on the anal margin or within the anal canal, which eventually ulcerates and may be mistaken for a routine anal fissure. This eventually regresses spontaneously in 3-4 weeks and is followed by a secondary stage 2-10 weeks later. Secondary syphilis may consist of fever, malaise, arthralgia, a maculopapular rash on the palms and soles of the feet, tenesmus, mucoid discharge, rectal pain, and inguinal adenopathy.

There are several methods for diagnosis. Dark-field microscopy will reveal the spirochetes, which have a corkscrew-shaped appearance. Biopsy shows spirochetes on a Warthin–Starry silver stain. There are also two serologic tests, RPR and VDRL.

Treatment consists of a single dose of penicillin intramuscularly in the early phase. If identified later, three doses are given 2 weeks apart.

3. Gonococcal proctitis

Gonococcal proctitis is caused by the organism, Neisseria gonorrhoeae, which is an intracellular gram-negative diplococcus. It is estimated that there are approximately 3 million people infected yearly worldwide; however, there is a large population of asymptomatic carriers. Anorectal infection results from contiguous spread from the genital area in women and from receptive anal intercourse in men.

The incubation period varies but can last up to 2 weeks. Symptoms then include pruritus, tenesmus and a thick, purulent discharge, which can be expressed from the anal crypts. Proctitis of the mid to distal rectum can be identified on proctoscopy. Standard Gram stains of the discharge are generally unreliable; however, culture on Thayer–Martin medium increases the positive yield.

The first-line treatment of anorectal gonorrhea includes a single intramuscular dose of ceftriaxone. Penicillin is no longer recommended given the high rate of resistance. Infected patients and partners should also be treated for concomitant Chlamydia infection, which is very common.

4. Chlamydial proctitis and lymphogranuloma venereum

Chlamydia trachomatis is the most common sexually transmitted infection worldwide and the most frequently reported STD in the United States. This intracellular bacteria has several serotypes that have an incubation period up to 2 weeks. Serotypes D-K are responsible for proctitis and genital infections while serotypes L1-L3 are responsible for lymphogranuloma venereum (LGV).

A large portion of patients will be asymptomatic; however, when present, symptoms of an active anorectal infection include rectal pain, tenesmus, and fever. Similar anorectal complaints are present in patients with LGV but the inguinal adenopathy is often more prominent with large matted nodes with overlying erythema.

Diagnosis of active infections can be challenging with routine culture given the intracellular location of the bacteria. Often patients with suggestive symptoms of proctitis that have a Gram stain demonstrating leukocytes without detectable gonococci are presumed to have a Chlamydia infection and treated accordingly. Cell culture is also possible using a sucrose phosphate media. Treatment consists of a single oral dose of Azithromycin or Doxycycline twice daily for 7 days. Treatment with Doxycycline is extended to 21 days for LGV. Sexual partners should be treated as well to prevent reinfection.

5. Condyloma acuminata

Condyloma acuminata, caused by the human papilloma virus, have a recognizable raised, cauliflower-like appearance and are located on the anal margin, within the anal canal, or surrounding the genitalia. This presents one of the most common STDs in the United States for which consultation with a colorectal surgeon is sought. There are more than 60 subtypes of this latent virus with types 6 and 11 producing benign exophytic lesions. Types 16 and 18 are noted to be more aggressive, often causing lesions with high-grade dysplasia that may progress to cancer if left untreated.

Patients are often asymptomatic but may present with complaints of bleeding, itching, or anal discomfort due to the growths. Once present, there is no way to eradicate the infection surgically. The goal of treatment is to remove the macroscopic burden of disease with excisional biopsies and electrocautery. Recurrences are common; therefore, surveillance of these patients is extremely important. Bichloracetic acid, trichloracetic acid, and Imiquimod are topical agents that have been used with reasonable success.

6. Chancroid

Chancroid is a rare sexually transmitted disease in the United States caused by the gram-negative bacteria, Haemophilus ducreyi. Globally, the incidence is higher in developing countries.

The infection manifests itself days after transmission with painful inguinal adenopathy and erythematous papules around the genitalia that eventually ulcerate. Diagnosis is typically made with routine culture of the fluid from the ulcers. Treatment consists of single doses of Azithromycin (orally) or Ceftriaxone (intramuscularly).

7. Inflammatory proctitis

Inflammatory proctitis refers to a general mild to moderate inflammation of the rectum that is unrelated to an underlying infection or sexually transmitted disease. Symptoms include rectal bleeding, urgency, tenesmus, and often diarrhea. Examination of the rectum is characterized by a continuous erythematous, friable mucosal surface. If applicable, cultures should be taken to elucidate any infectious etiology and biopsies should be taken to rule out Crohn disease.

This condition can be self-limited but persistent cases typically respond to short courses of steroid enemas. Additionally, mesalamine enemas are efficacious. If there is no improvement after a few weeks of treatment, the patient should be reevaluated.

8. Radiation proctitis

Radiation proctitis is an unfortunate byproduct of pelvic irradiation that typically occurs in two phases. Acute injury occurs during or shortly after the administration of pelvic radiation. This is characterized by vascular congestion and friable mucosa. Symptoms include rectal bleeding, urgency, tenesmus, and diarrhea. The late phase of injury occurs months to years after the completion of treatment and is characterized histologically by fibrosis that can manifest clinically with strictures, fistulas to the urinary tract or vagina, and telangiectasias. Symptoms include bleeding, change in bowel habits, recurrent urinary tract infections, and vaginal discharge. Evaluation should include flexible sigmoidoscopy or colonoscopy and biopsy to make the diagnosis and rule out malignancy.

The initial treatment of acute radiation proctitis incorporates medications that manage symptoms, including bulking agents, antidiarrheals, and antispasmodics. Enemas of steroids, mesalamine, or short-chain fatty acids have been shown to improve proctitis as well. Refractory cases can be treated topical application of 4% formalin to the rectal mucosa. Radiation proctitis complicated by fistulas is best managed surgically with interposition of normal, healthy tissues.

Rectovaginal fistulas can be congenital or acquired and are generally characterized by their abnormal connection between the epithelialized mucosal surfaces of the rectum and the vagina. Distal fistulas arising from the anal canal are appropriately termed, anovaginal fistulas. Acquired rectovaginal fistulas are generally caused by obstetric injuries, inflammatory bowel disease, trauma, or infection.

Clinical Findings

A. Symptoms and Signs

The diagnosis of a rectovaginal fistula is typically straightforward based on an accurate history; however, in some instances, patients can be asymptomatic. Commonly, patients will present with complaints of the passage of air or feces from the vagina. The degree of distress often depends of the size of the fistulous opening. With smaller fistulas, more subtle complaints of a foul vaginal discharge, recurrent vaginitis, or dyspareunia may be more common while the feculent drainage from larger fistulas may be confused with fecal incontinence. If the etiology of the fistula is due to inflammatory bowel disease then rectal complaints such as tenesmus or bloody diarrhea may predominate.

On digital rectal examination, the fistula can often be identified as a dimpling or pit in the anterior rectal mucosa, which can be easily be confirmed by anoscopy. Inspection of the vagina will reveal staining of the mucosa with stool and the hyperemic mucosa of the fistula opening contrasting with the normal pink background of the vaginal mucosa. Occasionally, the identification of the fistula can be more challenging despite very suggestive symptoms. In these instances, a thorough examination under anesthesia may be indicated. With a saline-filled vagina, air can be instilled per rectum via a proctoscope. Air bubbles may help identify fistulas that are not readily apparent. Alternatively, diluted methylene blue can be instilled per rectum with a tampon in place in the vagina. Staining of the tampon with methylene blue will confirm the presence of a fistula.

B. Laboratory Studies and Imaging

Adjunct studies are sometimes necessary to identify the fistula location and to determine the quality of the surrounding tissue. Retrograde contrast enemas and CT scans with rectal contrast may identify contrast extravasation into the vagina. CT scans have the added benefit of identifying any associated inflammatory changes. MRI and endorectal ultrasound have also been used with varying results. Endoscopy is a valuable diagnostic tool to assess any underlying inflammatory conditions such as Crohn disease and to exclude underlying malignancy. Biopsies should be performed on any abnormal mucosa in the rectum or around the fistula orifice.

Differential Diagnosis

The most common cause of rectovaginal fistulas is obstetrical trauma accounting for 70%-80% of cases. These fistulas may present immediately but more frequently they manifest weeks after delivery, typically after third- and fourth-degree lacerations. In the Western hemisphere, the incidence has been estimated at up to 0.1% of all vaginal deliveries. Other etiologies include—inflammatory bowel disease—primarily Crohn disease, postoperative trauma, radiation, malignancy, and infection.

Treatment

The management of rectovaginal fistulas primarily depends on its complexity, as determined by the location, etiology, and the quality of the surrounding tissue. Simple fistulas are typically small in diameter, low on the rectovaginal septum, and are secondary to either traumatic injury or infection. On the other hand, complex fistulas are larger in diameter, higher on the rectovaginal septum, and are associated with underlying inflammatory bowel disease, radiation, neoplasm, or previous failed repairs. There are several well-described operative approaches that can generally be divided into transanal, transvaginal, transperineal, and transabdominal repairs.

Common transanal repairs include fistula excision with layered closure, endorectal advancement flap, and rectal sleeve advancement. The mucosal advancement flap is appropriate for simple, low fistulas. During this procedure, a flap composed of mucosa, submucosa, and a portion of internal sphincter muscle is mobilized proximally and used to cover the fistula defect. The base of the flap should be wider than the apex in order to ensure adequate perfusion of the flap. The muscle is then reapproximated in the midline—closing the fistula. The flap is then advanced into the anal canal and secured with absorbable sutures. Success rate are varied in literature, ranging from 50% to 100%.

Rectal sleeve advancement is a reasonable approach for rectovaginal fistulas with extensive stenosis and anal ulcerations due to Crohn disease. Starting at the dentate line, a circumferential incision is made and extended cephalad. The dissection becomes full thickness above the anorectal ring and is extended until the distal rectum is adequately mobilized. The rectum is then pulled down through the anal canal and the diseased rectum is transected. The fistula opening in the vaginal is closed and the rectum is sutured to the dentate line. This repair is often done with a protective diverting ostomy.

Perineoproctectomy is a perineal technique that essentially converts a RVF into a fourth-degree laceration. The vaginal mucosa, sphincter muscles, and the rectum are divided between the fistula openings and reapproximated in layers, ultimately obliterating the fistula tract.

Tissue interpositions are also typically performed through the perineal approach and include the gracilis muscle flap and the Martius (bulbocavernosus muscle) flap. The fundamental concept in these procedures is that normal, healthy tissue is placed between the fistula openings after dissecting the plane between the rectum and the vagina. Successful closure with these procedures has been reported as high as 80% and is an ideal repair for RVF that have failed previous repairs or with abnormal surrounding tissues.

Rectovaginal fistulas that are higher in the rectovaginal septum are usually approached through an abdominal approach. There are several potential procedures, ranging from simple fistula division and closure with interposition of pedicled omentum, to proctectomy with colorectal or coloanal anastomosis. The choice of procedure depends on the quality of surrounding tissues, location, and the etiology of the fistula.

Finally, the last decade has seen increasing use of bioprosthetic plugs and sheets in the management of RVFs. Small series have shown promising results but there is still a paucity of long-term data.

Prognosis

The prognosis for rectovaginal fistulas relates to its overall complexity. Simple, low fistulas can be approached with relatively straightforward transanal or perineal techniques with good results. Fistulas that are higher or associated with inflammatory bowel disease, radiation, or neoplasm are understandably more challenging, often requiring multiple repairs.

General Considerations

Neoplasms of the anus and surrounding skin are uncommon—accounting for only about 3% of all colorectal malignancies. Approximately 5200 cases are diagnosed annually in the United States, resulting in more than 700 deaths. The overall management of these lesions depends primarily on the histology, the size, and location of the lesion. While the definitions can be confusing, the anal canal is commonly defined, by surgeons, as the region extending from the anal verge to the anorectal ring at the top of the sphincter complex. The lymphatic drainage in this area is variable but clinically important. Proximal to the dentate line, the lymphatic system drains to the internal iliac and inferior mesenteric nodes while distal to the dentate line, drainage is typically to the inguinal nodes. It is important to realize that lesions in this area may not be completely visualized on routine inspection of the perineum. The anal margin is generally defined as the perianal skin extending circumferentially within 5 cm of the anal verge. Lesions in this area are easily visible on examination.

Tumors of the Anal Margin

A. Squamous Cell Carcinoma

The majority of malignant neoplasms of the anal margin are squamous cell cancers (SCC). They have similar presentation to SCCs that occur elsewhere on the skin and are subsequently staged similarly based on size, which has been shown to correlate with lymph node positivity. The American Joint Committee on Cancer (AJCC) staging system is summarized in Table 31–6. The overall incidence of anal margin cancers is low and the prognosis is often more favorable than squamous cell carcinoma of the anal canal. These lesions are typically well differentiated, indolent, and are rarely associated with distant metastasis.

Lesions in this location may present with pain, bleeding, pruritus, tenesmus, or incontinence if locally advanced. On examination, there are rolled, everted edges often with central ulceration. Palpable lymph nodes may be identified in the inguinal region.

The management of anal margin SCC consists of wide local excision for T1 and early T2 lesions that can be easily resected with a 1-cm margin without compromising sphincter function. Poorly differentiated tumors, T3, or T4 cancers should be treated with chemoradiation, including the inguinal and pelvic nodes in the field of treatment. Abdominoperineal resection (APR) should be reserved for recurrent disease, residual disease after radiation, or bulky tumors that are invading the sphincter complex.

B. Basal Cell Carcinoma

Basal cell cancers (BCC) of the anal margin are exceedingly rare, accounting for 0.2% of anorectal cancers. They typically present in older men and approximately one-third of patients will have a history of BCC or a synchronous lesion elsewhere. The appearance of these lesions is similar to that of other areas of the body with irregular, raised, pearly edges with superficial plaques or ulcers. Local I invasion and metastatic potential are both typically low.

Wide local excision with an adequate margin is the treatment of choice for small lesions. Local recurrence is fairly uncommon and can usually be re-excised. Larger, bulky lesions can be treated with abdominoperineal resection or radiation.

C. Bowen Disease

Historically, the term Bowen disease referred to squamous cell carcinoma in situ. This term as well as anal intraepithelial neoplasia (AIN) II and III have largely been replaced by the classification of high-grade squamous intraepithelial lesion (HSIL), which has similar histologic features. Human papilloma virus infection is common. Patients may complain of itching or pain and examination reveals scaly, erythematous, and sometimes pigmented lesions.

Traditionally, these lesions have been treated wide local excision, often with complex reconstructions for larger lesions. This approach has been plagued by high recurrence rates and generally very morbid. More recent data suggest that HSIL can be adequately treated with targeted biopsy with high-resolution anoscopy, ablation, and close surveillance every 3-6 months. The application of topical Imiquimod (Aldara) or topical 5-FU have been proposed to minimize recurrence, but are generally limited by local skin irritation.

D. Verrucous Carcinoma

Perianal verrucous carcinoma is often referred to as a Buschke-Lowenstein tumor or Giant Condyloma, given its exophytic, cauliflower-like appearance. These lesions can vary in size but are generally slow growing and locally invasive. Histologically, they are considered benign but larger lesions may certainly encompass underlying malignancy—usually invasive squamous cell carcinoma. Patients frequently present with complaints of an anal mass but may also describe pain, fistulas, or abscesses. Wide local excision is recommended for the majority of these lesions and, if large, the resulting defects may require more complex closure with plastic surgeons. More advanced cases with invasion into the sphincter complex may require APR.

E. Paget Disease

Paget disease is a rare condition characterized by an intraepithelial adenocarcinoma of the perianal skin. The most common presenting complaint is intolerable pruritus and examination typically reveals a well-demarcated, erythematous, eczematous rash. Diagnosis is made after a full-thickness biopsy, which shows the pathognomonic Paget cell with a pale vacuolated cytoplasm and peripheral nucleus. These lesions often are associated with synchronous gastrointestinal malignancies, so a complete evaluation of the intestinal tract should be performed.

In the absence of invasive disease, wide local excision is the treatment of choice. It is important to obtain intraoperative frozen sections to ensure negative margins. Large defects can be covered with skin grafts or adjacent tissue transfers. Patients with invasive disease have a poor prognosis and should be considered for radical resection with abdominoperineal resection. Inguinal lymphadenectomy should be added for clinically positive nodal involvement. The role of chemoradiation is not well defined but has been used as an adjunct in invasive and recurrent disease.

1. Epidermoid Carcinoma

Clinical Findings

Tumors of the anal canal are rare, accounting for about 2% of all colorectal malignancies. Of these, epidermoid carcinomas are the most common. The term epidermoid carcinoma encompasses several histological subtypes including squamous cell, basaloid, mucoepidermoid, and transitional cancers.

The clinical manifestation of anal canal tumors can be quite variable and many patients are initially diagnosed with benign anorectal conditions. They are typically slow growing and the resulting mass commonly causes pain and bleeding. Digital rectal examination and anoscopy are important tools for an accurate diagnosis, during which the size, location, consistency, and degree of fixation should be noted. Additionally, the presence of any palpable inguinal adenopathy should be documented. A biopsy of the lesion confirms the diagnosis and provides the specific subtype. The staging of anal tumors is summarized in Table 31–6. Endoanal ultrasound, MRI, and PET/CT are important adjuncts that aid in defining that degree of distant spread, local invasion, and surrounding adenopathy.

Treatment

Since its introduction in 1974, radiation and chemotherapy with 5FU and mitomycin C (Nigro Protocol) have largely replaced surgery in the treatment of anal cancer. There is ample data that demonstrates equivalent local control, survival rates with preservation of sphincter function. Approximately 30% of patients have persistent or recurrent disease after chemoradiation for anal SCC. Salvage abdominoperineal resection is reserved for recurrent or residual pelvic disease after chemoradiation.

The management of inguinal node disease is variable. Due to the high morbidity rate, prophylactic groin dissection is not recommended. Clinically significant inguinal adenopathy can be included in the field of radiation.

The overall response to chemoradiation should be assessed clinically at about 8 weeks after the completion of treatment. At this point, up to 85% of patients will have complete clinical response. Those with good partial response may be observed closely to ensure that complete response does occur. Any lesions suspicious for residual disease or progression of disease should be biopsied at that time. For those patients with complete clinical response, surveillance entails DRE and examination of inguinal nodes every 3-6 months for the first 2 years and annually thereafter up to 5 years. There is no consensus on the routine use of imaging in surveillance, but it is often practiced.

Prognosis

Complete response rates approach 90% for smaller tumors with 5-year survival that ranges between 70% and 90%. Residual or recurrent disease confers a poorer prognosis with 5-year survival rates between 24% and 58% after salvage APR.

2. Melanoma of the Anal Canal

The anorectum is the third most common site overall for melanoma, but it is the most common site of primary melanoma of the gastrointestinal tract—making it an exceedingly rare condition. It accounts for up to 2% of all melanomas and 2%-4% of all anorectal tumors.

Clinical Findings

Pain, bleeding, and a palpable mass are the most consistent clinical findings with melanoma of the anal canal. Patients may also present with tenesmus, change in the caliber of stools, and weight loss. Like its cutaneous counterpart, anal melanoma are raised and pigmented; however, it is important to note that these lesions may be amelanotic, which may mimic more benign disease.

Treatment

For localized disease, surgery offers the only chance for cure, as there has been no proven benefit for chemotherapy or radiation. Both radical resection with APR and wide local excision have been advocated. Abdominoperineal resection does not confer a survival advantage and is associated with high morbidity rates, subsequently, wide local excision is recommended as the initial surgical approach for localized disease. Large, bulky tumors that involve the sphincter complex will require radical resection.

Prognosis

The prognosis for anorectal melanoma is universally poor because many patients present with advanced disease. Survival rates generally range from 6% to 28% in the literature. The overall 5-year survival for large, deeply invading, or metastatic disease is less than 10% with a median survival of 12-18 months.

Anorectal physiology is very complex. It requires coordination between the pelvic nerves, pelvic floor muscles, the rectum, and the sphincter complex that results in normal, controlled evacuation of intestinal waste.

Like the colon, the rectum is comprised of two layers of smooth muscle—an inner circular layer and an outer longitudinal layer. It varies in length between 12 and 18 cm and is predominantly confined within the bony pelvis. The peritoneum covers the upper two-thirds of the rectum anteriorly, the upper third laterally, and the lower third of the rectum is extraperitoneal. The rectum is very distensible and, as such, has the capacity to hold large volumes, which is ideal since it primarily functions as a reservoir for stool prior to defecation. Alterations in rectal sensation or compliance by infection, inflammation, or fibrosis will result in urgency.

The anal canal begins at the anal verge, extending cephalad to the anorectal ring, and is surrounded by the levator ani muscles as well as the internal and external sphincter complex. The internal anal sphincter (IAS) muscle, which accounts for approximately 85% of the resting anal pressure, is an involuntary muscle that is the downward continuation of the circular, smooth muscle of the rectum. The IAS is approximately 3 cm in length and supplied by both sympathetic and parasympathetic nerves (S2-4). It is a constant state of contraction due to intrinsic slow-wave impulses. The IAS muscle is surrounded by the striated muscles of the external anal sphincter (EAS), which is a voluntary muscle but also contributes in small part to the overall resting tone. The EAS is supplied by the pudendal nerves.

The pelvic floor (levator ani muscles) is composed of symmetrical sheets of striated muscles with a central ligamentous attachment—the pubococcygeus, the iliococcygeus, and the puborectalis. These muscles surround and support the rectum, vagina, and urethra as they pass through to the perineum. The puborectalis, which wraps around the anorectal junction posteriorly and inserts on the pubic ramus anteriorly, is particularly important to overall continence by increasing the acute angle between the rectum and anal canal, known as the anorectal angle.

Normal defecation is an intricate sequence of events that relies on proper relaxation of these muscles and a few key anorectal reflexes. The stimulus for initiating defecation is distention of the rectum, which stimulates pressure receptors in the pelvic floor muscles, also known as accommodation. This in turn triggers two key reflexes: (1) relaxation of the internal sphincter, the rectoanal inhibitory reflex (RAIR) and (2) contraction of the external sphincter, the rectoanal excitatory reflex. This process allows sampling of the rectal contents that come into contact with the upper anal canal. This allows us to discriminate between gas, liquid, or solid stools. Once the decision has been made to evacuate the rectum, the puborectalis muscle relaxes, allowing straightening of the anorectal angle. Intra-abdominal pressure increases and the EAS relaxes allowing passage of contents through the anus.

In conjunction with a careful history, there are several useful modalities that are employed to investigate evacuation dysfunction. Anal manometry, defecography, endorectal ultrasound, and pudendal nerve terminal motor latency testing can be integral in the diagnosis of fecal incontinence, pelvic dyssynergia, constipation, rectocele, and intussusception, to name a few. A thorough understanding of the anatomy and the available testing modalities is imperative for diagnosis and treatment.

General Considerations

Complete anal continence results from the complex interactions between stool consistency, rectal capacity and compliance, the sphincter complex, and underlying neurological function. Impairment in one or all of these components results in varying degrees of fecal incontinence, which is generally defined as the recurrent, involuntary loss feces or gas through the anus.

The true incidence of fecal incontinence is difficult to determine due to lack of standard definitions and underreporting; however, rates up to 20% have been reported in literature, depending on the study population. Female patients predominate in most series of major incontinence but men and women are affected equally with minor incontinence. Higher rates have been reported in the elderly and patients with certain neurologic disorders.

There are numerous causes of fecal incontinence; however, the most common is related to obstetric injury. The incidence of obstetric tears with vaginal deliveries has been reported in up to 10% of cases. Additionally, occult injuries have identified by ultrasound in up to 35% of cases; therefore presentation with symptoms of incontinence or leakage may be delayed. Other causes include—congenital anomalies, neurologic disorder (eg, spinal cord injury), pelvic floor denervation (stretch-induced injury of the pudendal nerves), conditions causing poor rectal compliance (eg, Crohn disease, ulcerative colitis, radiation proctitis), functional bowel disorders (diarrhea or fecal impaction with overflow incontinence), and iatrogenic injuries (eg, anorectal surgeries).

Clinical Findings

A. Symptoms and Signs

A detailed history of the presenting symptoms is required to differentiate the patient’s ability to control gas, liquid and solid stools. Frank incontinence must be differentiated from fecal urgency or soiling which may be associated with other treatable anorectal disorders. Information on diet, activity, medications, obstetric and anorectal surgical history should also be gathered to provide more complete picture. This is understandably and potentially devastating disorder, so attempts should also be made to ascertain the overall level of impact of these symptoms on the patient’s daily activities. To aid in this characterization, there are several validated scoring systems, including the Fecal Incontinence Severity Index score, the Cleveland Clinic Florida Incontinence score, and the Fecal Incontinence Quality of Life score, which can provide an objective baseline of these symptoms and can be used to track progress throughout treatment.

Physical evaluation should begin with inspection of the anus and perineum, to document any scars from previous obstetric or anorectal procedures. Benign anorectal conditions, such as fistulas, prolapse, and hemorrhoids may also be readily excluded. Perineal descent during straining is another important finding which indicates an abnormal laxity of the pelvic floor muscles. Finally, digital rectal examination provides useful initial information on the resting sphincter tone and maximum squeeze pressure.

B. Imaging Studies

Further testing for fecal incontinence often require an integrated approach. Anal manometry, endoanal ultrasound, MRI, defecography, and pudendal nerve latency studies have all been employed in the evaluation of the patient with fecal incontinence.

Anal manometry provides an objective assessment of resting sphincter pressure, maximum squeeze pressure, inherent anorectal reflexes, as well as anorectal sensation and compliance. Resting pressure is in large part a reflection of internal sphincter muscle function while maximum squeeze pressure reflects external sphincter function.

While it may be limited by the operator, endoanal ultrasound is an extremely useful tool in the evaluation of these patients. It is an inexpensive office-based procedure that allows visualization of the length and width of the sphincter complex as well as any defects that may be present.

Defecography has a more limited role in the evaluation of incontinence. The study allows visualization of the process of defecation, including the anorectal angle, pelvic floor descent, and internal intussusception.

Pudendal nerve motor latency testing provides information about potential nerve damage to the pelvic floor. It measures the time from nerve stimulation to the onset of response of the pelvic floor muscles. Prolonged times are indicative neuropathy. The degree of denervation does not influence the severity of incontinence but does seem to provide some prognostic information about the outcomes of surgical repairs.

Treatment

The initial management of patients with fecal incontinence should include nonoperative measures. These include diet modification, fiber supplementation, and biofeedback training. If these measures fail, then consideration should be given to surgical repair. Options include sphincteroplasty, sacral nerve stimulation, injectable bulking agents, artificial bowel sphincter, and fecal diversion.

Anterior sphincteroplasty involves direct repair, either in an overlapping or end-to-end fashion, of the external sphincter muscle if a segmental defect is identified on preoperative evaluation. This technique has good short-term with up to 80% of patients experiencing improvement in function; however, at 5-10 years of follow up, function does tend to deteriorate. In literature, diminished success rates have been associated with age, duration of symptoms, and pudendal neuropathy.

Sacral nerve stimulation has recently been approved for the treatment of fecal incontinence and has been shown to be safe and effective. It provides the unique advantage of a temporary evaluation phase before permanent implantation. A temporary electrode is placed with the aid of fluoroscopy into the sacral foramen (usually the third) and the patient is subsequently stimulated for 2-3 weeks. If there is at least a 50% reduction in symptoms then a permanent stimulator is implanted. The precise mechanism of action of SNS is still unknown, but the short-term results have been promising. In many series more than 75% of study participants report greater than 50% improvement in continence episodes and 41%-75% of patients reported complete continence to liquid and solid stool. A recent randomized trial demonstrated that SNS was significantly better than best supportive measures including pelvic floor exercises, bulking agent, and dietary manipulation. Data with long-term follow up is still evolving.

The artificial bowel sphincter is another modality that is approved for treatment of incontinence but is not widely used. The device, which is surgically placed around the sphincter complex, is connected to a tunneled reservoir and pump that inflates and deflates the cuff to allow controlled defecation. This procedure has been limited by infectious complications and device erosion; therefore, is typically reserved for end-stage incontinence in patients without other alternatives except colostomy.

Passive fecal incontinence caused by internal sphincter dysfunction has been shown to respond favorably to injection of bulking agents. Small series have reported the injection of silicone biomaterial into the intersphincteric plane or submucosa with short-term improvement in continence.

If conservative and other surgical options have failed then a diverting colostomy becomes a reasonable solution that can restore a patient’s quality of life.

Prognosis

Fecal incontinence is a treatable condition; however, appropriate management requires careful evaluation and proper patient selection. Surgical intervention should be preceded by an initial trial of conservative measures if indicated. Sphincteroplasty has good short-term results with initial success rates of approximately 75%; however, success diminishes over time. Sacral nerve stimulation has been an exciting new surgical development for fecal incontinence with greater than 80% of patients maintaining more than 50% reduction of symptoms after 1-2 years of permanent implantation. Complications requiring explantation of the device are uncommon.

General Considerations

Pelvic floor dysfunction is a global term that can encapsulate several presentations including dysfunctional urinary and bowel evacuation symptoms, sexual dysfunction, as well as pain syndromes. Alternative terms, such as pelvic dyssynergia, obstructed defecation, and paradoxic puborectalis, have also been used further confounding the understanding of the topic. Functional disorders of the pelvic floor are marked by symptoms of obstructed defecation without an anatomic abnormality in the surrounding muscles. As outlined earlier, the process of defecation is intricate. It requires coordination of the pelvic nerves, the rectum, and the surrounding muscles, including the puborectalis and the remaining levator muscles. During normal defecation these muscles relax, allowing the rectum to empty; however, patients with pelvic floor dysfunction have uncoordinated activity that impairs evacuation of intestinal waste.

Understandably, this is can be a debilitating problem affecting a large number of patients, which are predominantly women. In the United States, approximately 24% of women report at least one pelvic floor disorder, which seems to increase with age, parity, and obesity.

Clinical Findings

A. Symptoms and Signs

Symptoms of pelvic floor dysfunction tend to develop slowly and insidiously; therefore, a careful history is paramount to establishing a working diagnosis and developing a strategy for diagnostic testing. Patients commonly describe constipation, straining with bowel movements, or the sense of incomplete evacuation. The residual soft stool in the rectal vault may cause soiling of the anoderm triggering the feeling of incontinence. Attention should be paid to diet as well as obstetric, urologic, and surgical histories. While these symptoms do not impose risk to the patient’s health, they do interfere with the overall quality of life. At the time of presentation patients have often tried a plethora of medications and laxatives.

A focused physical examination should start with inspection of the anus and perineum. Profound perineal descent with straining is an indication of laxity of the pelvic floor, which is common with increasing age and multiparity. Digital rectal examination is important and should be performed to rule out rectal masses, to assess pain with palpation of the puborectalis, assess sphincter tone, and contraction/relaxation of the levator muscles. Specifically, paradoxic contraction of the puborectalis with simulated straining should be assessed.

B. Laboratory and Imaging Studies

A colonoscopy and colon transit study should generally be performed to exclude an underlying malignancy and slow-transit constipation, respectively. Additional adjuncts include anal manometry with balloon expulsion and defecography. Anal manometry should assess resting and maximum squeeze pressure as well as the presence of the RAIR. Patients with pelvic floor dysfunction will typically be unable to expel a balloon, which is inserted into the rectum.

Defecography offers a more dynamic view of the rectum, pelvic floor muscles, and anal sphincters. During this examination, the rectum is filled with contrast and the patient is asked to simulate defecation. Vaginal and oral contrast materials are also usually given to provide additional information about the neighboring structures. Defecography is useful in identifying rectoceles, internal and external rectal prolapse, enteroceles, as well as a nonrelaxing pelvic floor.

Differential Diagnosis

Symptoms of constipation and defecation problems are quite common and may be due to a myriad of causes. Anatomic disorders, such as anal or rectal cancers, rectoceles, rectal prolapse, internal intussusception, and enteroceles, should be distinguished from functional disorders like a non-relaxing puborectalis.

Treatment

A. Medical Treatment

Patients with pelvic floor dysfunction due to a nonrelaxing puborectalis should be referred for pelvic floor retraining, also known as biofeedback, which has become an integral part of treatment. During these sessions with the physical therapist, patients are instructed on how to properly relax the pelvic muscles with the aid of visual feedback. This neuromuscular training program is typically instrument-based employing manometry-, or electromyography-based biofeedback.

B. Surgical Treatment

Patients with obstructed defecation due to anatomic causes are candidates for surgery if they have failed initial conservative therapy with fiber supplementation and laxatives.

Rectocele repair is indicated for large rectoceles that have demonstrated failure to empty on defecography. Several approaches have been employed with varying success, including transvaginal, transrectal, and transperineal. A newer technique that has shown some initial short-term success is the stapled Trans-Anal Rectal Resection (STARR) procedure, which uses two circular staplers to produce a circumferential transanal full-thickness resection of the lower rectum. Its widespread use is limited by the lack of data on long-term outcomes and the potential for devastating complications such as pelvic sepsis and fistulas.

Internal rectal prolapse (intussusception) can be present in up to 50% of asymptomatic individuals; therefore, the surgical treatment of internal prolapse associated with obstructed defecation symptoms remains controversial. Rectopexy without concomitant resection has been advocated by some and the STARR procedure has been used by others. Results have been varied in the literature.

Prognosis

Biofeedback has been the mainstay of treatment for nonrelaxing pelvic floor dysfunction. It is minimally invasive and repeatable with good results for those that complete the program. Improvement in symptoms has varied between 40% and 90% in several trials.

General Considerations

Abnormal rectal fixation is a general term for a group of diseases in which the attachment of the rectum to its surrounding structures has developed more laxity, allowing the rectum to, completely or incompletely, protrude through the anal canal. The exact pathophysiology is unknown but, in large part, this is related to chronic straining with defecation. Common anatomic variations may include a patulous anus, redundant sigmoid colon, diastasis of the levator ani muscles, and a deep cul-de-sac.

Rectal prolapse is characterized by an intussusception of the rectum. There are three general categories that ultimately influence symptoms and overall management: (1) internal prolapse (intussusception), which does not extend beyond the anal canal, (2) mucosal prolapse, and (3) complete prolapse, which involves full-thickness protrusion of the rectum through the anus.

In adults, older women are six times more likely to develop rectal prolapse, accounting for 80% to 90% of the patient populations. The peak incidence is after the fifth decade.

Clinical Findings

A. Symptoms and Signs

Symptoms can vary with the degree of rectal prolapse, but typical complaints include a perianal mass that protrudes with straining, mucoid or bloody discharge, incomplete evacuation, incontinence, pain if the rectum becomes incarcerated.

On examination, a patulous anus or exaggerated perineal descent may be initial clues to the diagnosis if prolapsing rectal tissue is not evident. Digital rectal may reveal diminished or absent tone with complete prolapse but may suggest a mass with straining for internal intussusception. The diagnosis is most easily made with the patient straining in the seated position, which should reproduce the rectal prolapse, identified by the concentric folds of mucosa.

B. Laboratory and Imaging Studies

If the diagnosis remains elusive, defecography should be able to clearly demonstrate either internal or complete prolapse as well as other associated abnormalities such as cystoceles, enteroceles, and rectoceles. In patients who also present with complaints of longstanding constipation, anorectal manometry, and colon transit studies are also crucial. Prior to any surgical intervention, these patients should also undergo colonoscopy.

Differential Diagnosis

Complete rectal prolapse is often confused with prolapsing internal hemorrhoids; however, the two can easily be separated by close examination of the mucosa. Prolapsing internal hemorrhoids produce radials folds in the visible rectal mucosa, which contrasts with the concentric folds seen with rectal prolapse.

Complications

The most dreaded complication for rectal prolapse is incarceration, which may lead to tissue ischemia and necrosis. Chronic reducible rectal prolapse may also impair fecal continence due to the repeated stretching of the sphincter muscles.

Treatment

A. Medical Treatment

A trial of fiber supplementation and diet modification may prove to be beneficial for mild cases of internal intussusception. Biofeedback, rectopexy, and the STARR procedure have been reported in refractory cases but their use remains controversial.

B. Surgical Treatment

Surgical treatment is indicated in patients with full-thickness rectal prolapse. Surgical treatment is broadly divided into abdominal and perineal approaches, which are dictated by the patient’s age and comorbidities as well as surgeon preference and experience. Perineal approaches generally results in reduced length of hospital stay and less perioperative morbidity and pain; however, they are plagued by higher recurrence rates.

Rectopexy, resection rectopexy, and mesh rectopexy are the three abdominal procedures that are most widely practiced. The principle component of each of these procedures is the posterior mobilization of the rectum down to the level of the levator muscles. The rectum is elevated from the deep pelvis and sutured to the presacral fascia at the level of the sacral promontory. The lateral ligaments are preserved, as this has been shown to decrease postoperative constipation. Sigmoid resection with tension-free anastomosis to the rectum is performed if excessive redundancy is encountered or if there has been a longstanding history of constipation. Mesh has also been used to fix the rectum to the presacral fascia and should be performed without a concomitant resection. Complications include bowel obstruction, erosion of the mesh, and fistulas. All of these abdominal procedures have been approached laparoscopically with similar results, while maintaining the benefits of a minimally invasive technique.

Perineal proctosigmoidectomy, also known as the Altemeier procedure, combines a perineal proctosigmoidectomy with an anterior levatoroplasty. A full-thickness, circumferential incision is made 1 cm proximal to the dentate line. The mesentery of the rectum and sigmoid colon is sequentially divided until no redundant bowel remains. The colon is transected at this level and an anastomosis is created between the colon and the anal canal with either sutures or a circular stapler. An anterior levatoroplasty is usually added to correct the laxity in the levator muscles commonly associated with this condition.

The Delorme procedure is ideal for short segment mucosal prolapse since it entails a mucosal sleeve resection starting at the dentate line. The excess mucosa is transected and the proximal and distal edges of the mucosa are approximated while the muscle is plicated with interrupted sutures placed circumferentially.

Prognosis

The described abdominal approaches have been shown to be safe and efficacious with approximately a 10% recurrence rate. Perineal approaches are also well tolerated but are associated with higher recurrence rates of 20%-30%.