Chapter 39. Benign Disorders of the Anorectum (Pelvic Floor, Fissures, Hemorrhoids, and Fistulas)

Benign diseases of the anorectum range from relatively simple disorders such as hemorrhoids and fissures to extremely complex problems associated with pelvic floor abnormalities.

The beginning of any evaluation of anorectal problems is the examination; therefore clinicians need to understand the anatomy. The normal anatomic relationships of the rectum and pelvis are important in understanding pelvic floor abnormalities and anorectal pathology. The rectum normally lies attached to its mesorectum within the curve of the sacrum with limited mobility. The junction of the rectosigmoid is most consistently found at the sacral promontory and descends only 2 or 3 cm during a Valsalva maneuver. The rectum exits the pelvis anteriorly surrounded by a sling of muscle from the pubis through a slit in the pelvic floor. The sling is created by the horseshoe-shaped puborectalis muscle that circles around behind the rectum and reinserts on the pubis anteriorly. Contraction of the muscle pulls the rectum forward, creating a more acute angle at the anal outlet. The anal canal itself measures 3–4 cm and is a funnel-shaped extension of the pelvic floor musculature. The pressure generated by this voluntary muscle prevents egress of rectal contents. The internal sphincter muscle is a continuation of the thickened circular muscle of the rectum. As such, it is an autonomic muscle and has no voluntary control.

The anorectum receives both sympathetic and parasympathetic nerves. The sympathetic nerves originate from thoracolumbar segments and unite below the inferior mesenteric artery to form the inferior mesenteric plexus. These fibers then descend to the superior hypogastric plexus located just inferior to the aortic bifurcation. These purely sympathetic fibers bifurcate and descend as the hypogastric nerves. Parasympathetic fibers from S2, S3, and S4 (the Nervi erigentes) join the hypogastric nerves anterolateral to the rectum to form the inferior hypogastric plexuses. Mixed fibers from the plexuses innervate the prostate, rectum, bladder, penis, and internal anal sphincter. These autonomic plexuses of the pelvic nerves run around the lateral aspect of the pelvic rim to enter the prostate and seminal vesicles anteriorly. The sympathetic innervation of the internal sphincter is motor, while the parasympathetic innervation is inhibitory. Injury to the pelvic autonomic nerves during pelvic surgery may result in bladder dysfunction, impotence, or both.

The innervation of the voluntary muscles of the pelvic floor is via direct fibers from S2, S3, and S4 in the pelvis from the sacrum (Fig. 39-1). The nerves of the external sphincter are derived from S2, S3, and S4 nerve roots from the sacral plexus and they arrive at the external sphincter via the pudendal nerve around the ischial spine at Alcock's canal. The uterus and vagina are closely approximated to the anterior surface of the rectum but not attached. There is no ligamentous suspension of the rectum or the uterus at the lower aspect of the pelvis. The slit-like defect in the pelvic floor through which the rectum passes also provides an outlet for the vagina and the urinary bladder.

The alimentary tract terminates at the anus, which provides continence of flatus and feces. It is useful to consider the anus and surrounding structures as a single unit, the anorectum (Fig. 39-2). The anorectum includes the perianal skin, the anal canal, the anal sphincters, and the distal rectum. The three main anatomic points of reference are the anal verge, the dentate line, and the anorectal ring. The distal external boundary of the anal canal is the anal verge, which is also the junction between the anal and perianal skin. Anal epithelium (anoderm) is devoid of the hair follicles, sebaceous glands, and apocrine glands that are present in the perianal skin, a fact worth remembering when attempting to distinguish between hidradenitis (inflammation of the apocrine glands in the perianal skin) and cryptoglandular anal disease.

The cephalad border of the anal canal is a true mucocutaneous junction, the dentate line. This union of the embryonic ectoderm with the endodermal gut resides approximately 1.0–1.5 cm above the anal verge. In a transitional zone of 6–12 mm in length, the columnar epithelium of the rectum changes to cuboidal epithelium that joins the squamous epithelium at the dentate line.

The upper border of the anal sphincteric complex is the anorectal ring. It may be palpated by digital examination about 1.0–1.5 cm above the dentate line. Anatomists consider the anal canal to begin at the dentate line and end at the anal verge. However, most surgeons consider the anal canal to start at the anorectal ring and terminate at the anal verge. This latter definition of the anal canal is used throughout this chapter.

Just above the dentate line, the rectal mucosa forms 8–14 longitudinal folds known as the rectal columns. Between each two columns at the dentate line is a small pocket termed an anal crypt. Small, rudimentary anal glands open into some, but not all, of these anal crypts. The glands may extend through the internal sphincter as far as the intersphincteric plane, but they do not extend into the external sphincter.

Below the dentate line, cutaneous sensations of heat, cold, touch, and pain are conveyed by afferent fibers in the inferior rectal nerves. Cephalad to the dentate line, poorly defined dull sensations, elicited when the mucosa is pinched or internal hemorrhoids are ligated, are probably carried by parasympathetic fibers.

The superior rectal artery, the terminal branch of the inferior mesenteric artery, descends to the upper rectum where it divides into lateral branches. Subsequent smaller divisions penetrate the rectal wall. The middle rectal arteries arise from the internal iliac arteries and supply the distal rectum and upper anal canal. The inferior rectal arteries, branches from the internal pudendal arteries, cross the ischiorectal fossae to supply the anal sphincters (Fig. 39-3).

There are two paths for venous blood return from the anorectum. Above the dentate line, venous blood flows into the portal system through the superior rectal vein and inferior mesenteric vein. Below the dentate line, the external hemorrhoidal plexus drains into the internal iliac vein via the middle rectal vein or via the pudendal vein, which receives blood from the inferior rectal vein.

Pathophysiology

Mechanical disruption is usually due to obstetric injury, trauma, or fistula disease in which the external muscle is divided or damaged (Table 39-1). Neurogenic incontinence is due to stretching of the pudendal nerves during prolonged labor, descent of the perineum and nerve stretch during straining at stool or rectal prolapse, or systemic disease such as multiple sclerosis, scleroderma, or spinal cord injury. Idiopathic incontinence is due to medical disease such as diarrhea in a patient with limited rectal capacity, irritable bowel syndrome, or sedatives that cause poor sensation in the anal canal in patients with no evidence of neurogenic or mechanical incontinence.

The normal continence mechanism has several components. Rectal capacitance and compliance are essential. The rectum normally holds between 200 and 250 mL. It distends readily with filling and has limited muscular activity intrinsically. The internal anal sphincter provides 80% of the resting anal sphincter pressure that provides the resistance to gas and mucus at the anal canal. The sampling reflex is a function of rectal distension causing internal anal sphincter relaxation via an intramural reflex to the internal sphincter. The rectal contents can then be sensed in the sensory nerve–rich transitional zone and anoderm to discriminate the true nature of the rectal contents. This sampling reflex occurs frequently throughout the day to provide continence and also serves to initiate the defecation process. The voluntary external sphincter muscle contraction in response to this sampling reflex provides the final active component of fecal continence. The subconscious voluntary contraction of the external sphincter, puborectalis, and pelvic floor muscles provide complete control of rectal contents. The pelvic floor muscles maintain continual activity, even during sleep, to provide fecal continence. This also seems to be a learned response because infants and children require 1–2 years to achieve control.

Fecal incontinence is defined as the inability to control the passage of gas, liquid, or stool until a socially acceptable time or place for evacuation. The frequency of incontinence may vary, and the loss of control may involve solid stool, liquid stool, or gas only. Frequent episodes of incontinence to gas alone may be as incapacitating as infrequent episodes of solid stool. Evaluation of fecal incontinence should include assessment of severity as well as impact of disease. The American Society of Colon and Rectal Surgeons has validated a fecal incontinence severity index and a fecal incontinence quality-of-life index to help standardize the assessment of fecal incontinence.1–3

Diagnosis and Evaluation

A problem-focused history as well as physical examination should be performed. History should include information on gastrointestinal or neurologic disorders, obstetrics, and previous anorectal surgery. On physical examination, a thin perineal body with scarring between the vagina and the anal canal and a poor squeeze on command may indicate a sphincter problem. In the setting of an anterior sphincter injury, it is essential to evaluate for the presence of a rectovaginal fistula.

Anal manometry is useful to document reduced resting and squeeze pressures as well as sphincter length in individual sphincter quadrants. Normal resting pressure is at least 40 mm Hg. Normal squeeze pressure is 80 mm Hg, which is usually double the resting pressure. Sphincter length is greater than 3 cm. Normal sensation should allow detection of a balloon inflated with 10–20 mL of air in the distal rectum. Maximal tolerable volume is at least 100 mL of air-filled balloon distention.

Electromyography

Pudendal nerve terminal motor latency (PNTML) determination measures the conduction velocity of the nerve action potential through the terminal 4 cm of the pudendal nerve between Alcock's canal and the external sphincter (Fig. 39-4). A delay in conduction reflects injury to the fast-conducting fibers of the nerve. This injury usually is the result of stretch, direct trauma, or systemic disease. The normal terminal motor latency is 2.0 ± 0.2 milliseconds. A delay in conduction velocity greater than this indicates nerve injury. Measurement of the PNTML has been shown to be clinically less useful than originally thought. The defect in the nerve must be fairly advanced to see a change in conduction and is therefore somewhat inaccurate for assessing minor defects. Single-fiber or concentric needle electromyography (EMG) is most accurate but not very useful clinically due to pain during the test.

Transrectal Ultrasound

The most sensitive method for documenting sphincter injury may be the anal ultrasound using a 360-degree rotating 10-MHz transducer covered with an anal cap and inserted into the anal canal. The focal length of the anal probe is approximately 1–2 cm and allows evaluation of the anal sphincter muscles in three dimensions as the probe is withdrawn from the rectum (Fig. 39-5). The ultrasound can detect scarring at the site of an injury, as well as rectovaginal fistula. The presence of a sphincter defect alone, however, may not correlate with fecal incontinence. Figure 39-6 shows an algorithm for the evaluation and management of fecal incontinence using these diagnostic techniques.

High-resolution magnetic resonance imaging (MRI) with an endoanal coil is a diagnostic modality that can detect sphincter defects similarly to endoanal ultrasound. Endoanal coil MRI may also show sphincter atrophy or thinning not detectable by endoanal ultrasound that may be useful for predicting success of surgical repair.4 Focused pelvic floor MRI with a surface coil and dynamic MRI are being evaluated as methods of evaluating fecal incontinence.5,6

Treatment

Therapy depends on severity of symptoms. For milder forms of fecal incontinence, an improvement in symptoms may occur with dietary changes such as increased fiber intake or antidiarrheal agents. A bowel regimen with high fiber, suppositories, and enemas every morning may be appropriate in patients with incontinence that cannot be repaired because of comorbidities or other confounding factors.

Muscle Sensory Retraining or Biofeedback

Operant conditioning using surface EMG, manometric, and balloon sensation techniques may be helpful in patients who do not respond to dietary changes.7 Biofeedback may improve symptoms in patients with a mechanical sphincter defect before repair or who have persistent or recurrent symptoms after sphincter repair. Improvement in symptoms is reported in 64–89% of patients.8 Prediction of the subset of patients who may benefit from biofeedback is difficult, but in general those with poor pudendal nerve function or complete disruption of the anal sphincter have less benefit. A trained physical therapist or anal physiotherapist experienced with anal and pelvic floor treatment is critical to the degree of success achieved.

Anal Sphincter Reconstruction

Anal sphincter repair can be performed successfully in most patients who have an isolated mechanical sphincter defect. A complete bowel preparation is highly recommended. The ends of the obstetrically injured sphincter are identified in the anterior perineum and either overlapped and sutured “pants over vest” or reefed in the midline to reconstruct the circular muscle (Fig. 39-7). Control of solid and liquid stool will be adequate in 90% of patients after this type of repair. However, complete continence is usually only achieved in 75% of patients and the long-term results may even be less satisfactory.9 Leakage of liquid, mucus, and gas may continue to affect patients after repair. Improvement in squeeze pressures has been shown to correlate best with functional outcome.10 The presence of at least one normal pudendal nerve is important for functional improvement after sphincter reconstruction. Complications of wound infection, fistula formation, and breakdown of the sphincter repair may be reduced by leaving a drain in the perineal body after the repair. A repeat procedure is equally successful in patients in whom the sphincter repair is noted to be disrupted by endoanal ultrasound.11,12

Other Treatments and New Modalities

Sacral nerve stimulation using implanted electrodes at the S2–4 foramen has been found to be of benefit for patients with fecal incontinence.13–16 Complications requiring removal of the device seem to be uncommon. Rarely, infection and pain at the site can be encountered. This technique is now approved in the United States for fecal incontinence. The mechanism of action is not fully delineated but may be due to the lift of the pelvic floor provided by levator ani continual contraction. Placement of the electrodes can be performed as an outpatient under local anesthesia.

For patients with a severely damaged sphincter, dynamic graciloplasty or implantation of a neurostimulator that provides constant activity into a muscle transferred to the anal canal may be appropriate, but it has been discontinued in the United States.17 Alternatively, an artificial sphincter of silicone with water-filled circum-anal cuff, called artificial bowel sphincter, may be implanted. Although the rate of explantation secondary to infection remains high, this technique can provide improvement in fecal continence. This technique has been removed from the market.18,19

When all other treatments fail, or if a patient desires, a stoma may be appropriate. Attention should be directed preoperatively to correct siting of the stoma to prevent pouching difficulties. Quality-of-life measures show that patients are generally satisfied. In a series from St. Mark's hospital, 83% of patients with a permanent colostomy reported improvement in lifestyle.20

Pathophysiology

The true etiology of rectal prolapse and intussusception is unknown. The mechanism is influenced by three components: (1) The rectum and rectosigmoid junction have increased mobility off the sacrum; (2) descent of the rectosigmoid junction into the pelvis allows a funnel-shaped intussusception into the rectum as the rectum attempts to expel itself; and (3) poor relaxation of the pelvic floor and external sphincter mechanism occurs during straining (Fig. 39-8). Persistent straining against this outlet obstruction may lead to descent of the perineum, expulsion of the rectum, and true rectal prolapse. This sequence of events from progression of internal intussusception (funnel formation) to full rectal prolapse is supported anecdotally. Consequences of rectal prolapse include anal canal injury from stretch of the internal sphincter during rectal prolapse and/or injury to the pudendal nerve during descent of the perineum. The classic defecographic picture of rectal prolapse and severe intussusception is a funnel that descends into the deep pelvis as the rectosigmoid junction descends. A ball valve obstruction occurs at the level of the anal canal before it is pushed through to the outside.

A distal mucosal prolapse is occasionally mistaken for full rectal prolapse. The typical appearance of a mucosal prolapse is that of mucosa separated by radial lines around the anus (Fig. 39-9A). Concentric rings of mucosa are seen in true rectal prolapse (Fig. 39-9B). Defecography is helpful to distinguish between these two entities, as they are treated differently.

Diagnosis and Evaluation

Signs and symptoms of rectal prolapse include rectal pressure and pain, incomplete evacuation, outlet obstruction, and constipation causing prolonged straining. Mucus discharge and bleeding from the fully prolapsed tissue may also be present. Examination most often reveals concentric rings of rectal tissue with a patulous anal canal, poor voluntary tone, and a very mobile rectum within the vault. Proctosigmoidoscopy reveals descent of tissue during straining and occasionally an ulcer on the anterior wall (caused by ischemia at the lead point of the intussusception). Defecography reveals extreme mobility of the rectum from its point of fixation to the sacrum, redundancy of the mesorectum, and funnel formation as the rectum prepares to descend through the anal canal opening at the pelvic floor. Defecography is most useful in cases that cannot be visualized in an office setting. Thickened barium simulates stool and cinedefecography allows visualization of the defecating process; this is particularly helpful in cases in which mucosal prolapse is suspected and the intent is to rule out full rectal prolapse. Triple-contrast cinedefecography (rectum, vagina, and small bowel and bladder as needed) also helps delineate complex pelvic floor abnormalities. This technique is gradually being replaced, or at least supplemented, by dynamic MRI and three-dimensional (3D) ultrasound of the pelvic floor.

A grading system of intussusception has been developed to assist one in planning management (Table 39-2). Mild to moderate intussusception with some mobility, some funnel formation, and descent of the rectum can usually be treated conservatively. However, grade 4 intussusception with severe outlet obstruction may require operative resection of the redundant rectum or rectopexy to secure the rectum to the sacrum.21 The most appropriate setting for operative treatment of internal intussusception is the patient who has developed moderate incontinence from the intussusception and straining or the patient who has severe bleeding from the solitary rectal ulcer at the tip of the funnel.

Anal manometry can be useful to document the preoperative function of the sphincter if there is not an obvious patulous anal canal on examination. PNTMLs provide objective evidence of pudendal nerve injury and allow some prediction of continued recovery after repair.

Management

Rectal Prolapse.

There are numerous techniques for management of rectal prolapse; over 100 procedures have been described. The four basic types of procedures include rectopexy, low anterior resection, perineal proctectomy, and anal encirclement procedures.22

Rectopexy relies on foreign material or sutures to attach the rectum to the sacrum. The rectum is mobilized down to the pelvic floor, and the rectum is stretched out of the pelvis to fit into the curve of the sacrum. For patients who report constipation preoperatively, the redundant sigmoid colon and rectum may be removed. The low anterior resection technique uses the standard technique for removal of the middle and upper portions of the rectum and redundant sigmoid colon. The left colon is reattached to the upper or middle third of the rectum by using either a double-staple or hand-sewn technique (Fig. 39-10). The rectum is mobilized to the level of the pelvic floor circumferentially, but preserving the anterolateral ligaments carrying the middle rectal arteries and splanchnic nerves. The left colon and rectum (now in continuity) are returned to the curve of the sacrum. The incidence of fecal incontinence may be higher after this procedure because the rectal capacitance is reduced. As well, postoperative evacuation difficulties may be noted if the anterolateral ligaments have been divided. Preoperative anal physiological testing may assist in the selection of patients who are candidates for low anterior resection (ie, no evidence of sphincter injury or dysfunction).

Suture rectopexy with or without sigmoid resection in patients with constipation-associated rectal prolapse have low recurrence rates in well-selected patients. Laparoscopic rectopexy is a reasonable alternative that may be associated with fewer complications and a shorter hospital stay.23,24 A technique of anterior Prolene mesh rectopexy has been described by D'Hoore, which only mobilizes the anterior rectum to the anal canal and suspends the rectum with the mesh with sutures placed along the anterior rectum at the level of the rectovaginal septum and attached to the sacral promontory. The redundant cul-de-sac is excised and the peritoneum is closed over the mesh along its length.25

The use of a perineal proctectomy with anterior and posterior reefing of the sphincter muscle has become more popular for the treatment of rectal prolapse in the elderly patient with full rectal prolapse and comorbidities. This is a revival of the Altemeier perineal resection technique. The entire prolapsing rectum and redundant sigmoid are removed through a perineal approach beginning at the top of the transitional zone columns (Fig. 39-11). The left colon or proximal sigmoid is sutured to the transitional zone 1–2 cm above the dentate line. The external anal sphincter and pelvic floor muscles can be reefed in the anterior and posterior midline to restore anal tone in patients with incontinence as described by Prasad et al.26 The incidence of recurrent prolapse is approximately 10% in patients with good sphincter function. Even though the operation is generally recommended for elderly patients, it may be appropriate for patients of all ages with severe compromise of sphincter tone and pronounced procidentia. This procedure is not technically possible in patients who have mucosal prolapse alone or patients with high rectal prolapse and an intact anal canal and normal sphincter.

Anal encirclement procedures have been mostly replaced by the perineal proctectomy. The anal encirclement procedure using synthetic material such as nylon mesh should be limited to the extremely debilitated patient or the elderly patient who cannot withstand perineal proctectomy. It can be effectively performed under local anesthesia in patients with prohibitive surgical risks and decreased life expectancy.

Internal Intussusception of the Rectum

The treatment of internal intussusception of the rectum is primarily conservative with use of a high-fiber diet. High doses of psyllium may prevent formation of the funnel and outlet obstruction with normalization of bowel function. Patients with pelvic floor outlet obstruction (nonrelaxation of the puborectalis) may benefit from biofeedback. In patients without pelvic floor outlet obstruction and with severe symptoms from the intussusception (ie. bleeding or incontinence), an operation may be considered. A low anterior resection or rectopexy is appropriate for these patients depending on whether they have constipation or incontinence, respectively. The treatment of a bleeding solitary rectal ulcer by low anterior resection sometimes requires an ultralow anterior resection and coloanal anastomosis in the setting of an extremely thickened anterior rectal wall that overwhelms even the thickest staple height. Perineal proctectomy is not recommended because the sphincter mechanism is intact and resection of redundant rectum will be extremely difficult in patients with an incomplete prolapse. Tests that are obtained prior to operation for internal intussusception include colonic transit times to document normal colonic transit, defecography that shows the level of the funnel formation within the rectum, and a balloon expulsion test to eliminate pelvic floor outlet obstruction as a cause of the intussusception.

The use of transanal stapling (STARR [(stapled transanal rectal resection)] or Transtar) procedures has become popular in Europe. Patient selection is important as those with other abnormalities such as enteroceles, larger rectoceles, or nonrelaxation of the puborectalis were found not to have good response after the STARR procedure.27 Complications include bleeding, perineal pain, recurrence, or incontinence. In a trial comparing STARR versus biofeedback, the STARR procedure was found to be more effective in improving symptoms of obstructed defecation. It may be performed in unhealthy individuals under local by a properly trained individual after failure of biofeedback.28

Pathophysiology

The presenting complaints of patients with pelvic floor outlet obstruction usually include some form of constipation and straining. Defecation is a learned process and pelvic floor outlet obstruction may be either a change in the defecating mechanism or a failure to learn the appropriate series of events to allow normal function. The muscle of the pelvic floor is completely normal, but the function and control are abnormal. There may be a psychologic influence in this syndrome because patients who have been sexually abused or have been psychologically traumatized may develop this outlet obstruction. The need to dominate and control has also been documented in these patients. The syndrome results from obstruction of the anal canal due to anterior displacement of the puborectalis muscle and contraction of the pelvic floor and external sphincter during straining to defecate. Attempts to defecate against a closed pelvic floor result in chronic funnel formation of the rectum and descent of the anterior rectal wall into the anal canal. This chronic trauma and ischemia may lead to the formation of an ulcer on the anterior wall of the rectum. The stimulus to defecate is often neglected. The end result is an uncoordinated effort at defecation with pelvic floor obstruction of the outlet, even as the rectum begins to distend and the autonomic muscles begin to relax.

It is possible that pelvic floor outlet obstruction is etiologically related to rectal prolapse and intussusception. However, no long-term studies have provided conclusive evidence. Patients may also present with megarectum from outlet obstruction, fecal incontinence due to nerve injury from chronic straining, or severe mucosal prolapse or hemorrhoids.

The solitary rectal ulcer is assumed to be due to ischemia of an isolated portion of the anterior rectal wall, approximately 10 cm above the anal verge, which prolapses partially into the anal canal and becomes ischemic during prolonged straining. The healing process may occasionally incorporate mucosal glands beneath the new mucosal surface and form a localized area of colitis cystica profunda. These entrapped glands continue to produce mucus and are occasionally mistaken for an early neoplasm of the rectum.

Diagnosis and Evaluation

Patients with pelvic floor outlet obstruction may complain of a number of problems that include constipation and straining at defecation, the need for digital maneuvers to evacuate the rectum, bleeding, mucosal prolapse, and hemorrhoids. They occasionally present with chronic pain of the anal canal and symptoms of severe spasm of the anal canal and pelvic floor. In the past this was classified as anismus, proctalgia fugax, or levator ani syndrome. Digital rectal examination may reveal paradoxical motion (tightening instead of relaxing) of the puborectalis muscle during attempts to push the finger out of the rectum. Defecography generally shows a persistent puborectalis impression on the posterior rectum as the patient attempts to evacuate the rectal contents. Defecography tends to overdiagnose the problem of nonrelaxing puborectalis. This may be due to an unnatural setting in a cold radiology suite or possible patient embarrassment. The presence of nonrelaxing puborectalis muscle must therefore be confirmed using some other technique. The method best suited to our practice has been to have the patient expel a 60-mL air-filled soft latex balloon while sitting in a private bathroom. This simple technique of expulsion of the balloon within the confines of a private bathroom seems to be adequate.29 Surface EMG is also useful in the diagnosis and treatment of nonrelaxing puborectalis muscle, as it documents decreased pelvic floor electrical activity during proper straining techniques and an increase during paradoxical contraction. Colonic transit study will demonstrate accumulation of all of the administered radiopaque markers within the rectum after an elapsed period adequate for clearance (>7 days). An algorithm used to deal with pelvic floor disorders is shown in Fig. 39-12.

Treatment and Management

The initial steps in the treatment of outlet obstruction problems include high doses of fiber and establishment of a normal bowel routine. Outpatient biofeedback using surface EMG, balloon expulsion, sensation techniques, and a simulated stool are also effective in severe cases of nonrelaxing puborectalis muscle.30 Psychological counseling and relaxation techniques may be of help in patients who have a psychological component to their problem.

Rectocele, Enterocele, and Complex Pelvic Floor Abnormalities

Outpouching or bulging of the rectum into the vagina (rectocele) can be seen on defecography in patients with pelvic floor disorders. These findings, however, can also be found in patients without any pelvic or bowel complaints. Surgical repair does not always lead to resolution of symptoms. No predictors of successful outcome of surgery are universally accepted from various studies examining characteristics on defecography and symptomatology. Surgical technique is the surgeon's preference and can be performed via a transanal, transvaginal, or perineal approach to bolster, pleat, and reconstruct the muscle in the rectovaginal septum. Fortunately, the majority of patients improve with medical management.31,32 Rectoceles occurring in patients with rectal prolapse generally resolve after repair of the prolapse as long as the rectum is mobilized all along the rectovaginal septum.

Enteroceles or bulging of small bowel into the rectogenital area can also be detected on defecography. This is a common finding in patients who are status post hysterectomy, in patients with symptoms of obstructive defecation, or in asymptomatic patients. An enterocele can be repaired transabdominally in conjunction with operative management of other pelvic floor abnormalities by reefing or excising and reclosing the redundant pelvic peritoneum to prevent herniation of small bowel into the pelvic floor.

Pelvic floor disorders may also involve bladder or gynecological complaints. A multidisciplinary team approach for evaluation and operative management of complex pelvic floor abnormalities may include a urogynecologist for bladder or vaginal suspension in addition to rectopexy/resection, and pelvic floor suspension. Dynamic MRI may be a useful modality for the diagnosis of some of these challenging pelvic floor cases.33 High-resolution 3D endovaginal and endorectal ultrasonographies are increasingly being used for evaluation of pelvic floor disorders.34,35

Current theories about the development of hemorrhoids consider the nature of anal “cushions.” Such cushions are aggregations of blood vessels (arterioles, venules, and arteriolar-venular communications), smooth muscle, and elastic connective tissue in the submucosa that normally reside in the left lateral, right posterolateral, and right anterolateral anal canal.36 Smaller discrete secondary cushions may reside between the main cushions. Hemorrhoids are likely the result of a sliding downward of these anal cushions. Hemorrhoids provide tissue to close the anal canal during rest. It appears that the disintegration of the anchoring and supporting connective tissue and the terminal fibers of the longitudinal muscle above the hemorrhoids allows these structures to slide distally.

Classification

Anal skin tags are discrete folds of skin located at the anal verge. These may be the end result of resolved thrombosed external hemorrhoids or, more rarely, may be associated with inflammatory bowel disease. Internal hemorrhoids reside above the dentate line and are covered by transitional and columnar epithelium (Fig. 39-13). First-degree internal hemorrhoids cause painless bleeding with defecation. Second-degree hemorrhoids protrude through the anal canal at the time of defecation but spontaneously reduce. Third-degree internal hemorrhoids protrude and bleed with defecation, but they must be manually reduced. Fourth-degree internal hemorrhoids are permanently fixed below the dentate line and cannot be manually reduced.

External hemorrhoids consist of the dilated vascular plexus located below the dentate line and are covered by squamous epithelium. Mixed hemorrhoids are composed of elements of both internal and external hemorrhoids.

Evaluation of Internal Hemorrhoids

Even though internal hemorrhoids are the most common source of rectal bleeding, it is imperative that other causes be excluded. Because internal hemorrhoids cannot be detected by digital examination, diagnosis can only be made by anoscopy. It is mandatory that colonoscopy be performed in high-risk patients to exclude other sources of bleeding, such as carcinoma or proctitis (eg, for patients aged >40 years and those with a personal or family history of colorectal neoplasia or a change in bowel habits).

Treatment

Regulation of diet and avoidance of prolonged straining at the time of defecation comprise the initial treatment of mild symptoms of bleeding and protrusion. Increasing the fiber content of the diet to at least 25–35 g daily with raw vegetables, fruits, whole-grain cereals, and hydrophilic bulk-forming agents can reduce and often alleviate all symptoms. If bleeding and protrusion persist, however, the hemorrhoids should be treated surgically.

Elastic ligation of the friable redundant hemorrhoidal tissue is quite satisfactory for first-, second- and third-degree hemorrhoids. The procedure is quite simple. The hemorrhoid is visualized with the aid of an anoscope and grasped with forceps. The redundant tissue is pulled into a double-sleeved cylinder on which there are two latex bands. The bands are discharged from the cylinder, and the hemorrhoidal bundle is ligated (Fig. 39-14).

Certain precautions, however, must be taken with this form of treatment. The ligatures must be placed at least 1–2 cm above the dentate line to avoid extreme discomfort. Ideally, the ligatures should be placed at the top of the hemorrhoidal cushion. About 25% of patients experience mild, dull anorectal discomfort lasting for 2–3 days following the procedure. Mild analgesics and warm baths are usually sufficient to relieve the discomfort. In about 1% of patients, brisk bleeding that may require suture ligation occurs when the necrotic tissue sloughs off at 7–10 days. About 2% of patients treated with ligation of the internal hemorrhoid develop thrombosis of an external hemorrhoid, which may cause considerable discomfort. Necrotizing pelvic or perineal sepsis is rare and almost always associated with immune compromise but must be immediately recognized in the setting of increased pain, fever, or urinary dysfunction. Treatment requires immediate examination under anesthesia for debridement of all necrotic tissue, intravenous antibiotics, and observation in the intensive care unit. Patients with poorly functioning neutrophils or reduced numbers of white blood cells for any reason should be treated with another method or at least warned of and observed for the occurrence of this potentially life-threatening complication.

Hemorrhoidal ligation is an office procedure, and no special preparation is required. Patients with a bleeding diathesis or with portal hypertension are not good candidates for ligation. Usually only one hemorrhoid is ligated on the first treatment visit. Ligations can be performed every 2–4 weeks until all symptoms of bleeding or prolapse are alleviated. The second ligation can be multiple if the first treatment is well tolerated. Other minimally invasive procedures such as infrared coagulation, diathermy coagulation, and ultrasound-guided vascular pedicle ligation achieve the same result with variable success and need for effort.

Although diet, bowel regulation, or elastic ligation will alleviate most symptoms of internal hemorrhoids, occasionally further surgical treatment may be needed. Excisional hemorrhoidectomy is indicated for large, mixed (combined internal/external) hemorrhoids that are not amenable to ligation because the ligature would have to incorporate pain-sensitive tissue at or below the dentate line.

Circular stapled hemorrhoidectomy is a newer technique indicated for the elective treatment of circumferential third- and fourth-degree hemorrhoids that are not permanently prolapsed due to scar.37 This involves placing a purse-string suture incorporating the mucosa of the anal canal with a stapled circumferential mucosectomy at a level 4–5 cm above the dentate line. This can be performed under regional anesthesia with minimal morbidity in experienced hands. Potential complications include bleeding if the staple line is incomplete, pain if the staple line is too close to the dentate line, rectovaginal fistula if the purse string captures the rectovaginal septum, complete closure of the rectum if the stapler and purse string are malpositioned, and return of symptoms if the purse string is incomplete.

Occasionally, the internal hemorrhoidal tissue may be incarcerated outside the anal canal, resulting in spasm of the anal sphincter, massive local edema, and severe pain. In such circumstances, the edematous tissue may be injected with a local anesthetic containing epinephrine. Dissipation of the edema by manual compression then can be achieved, allowing reduction in the prolapsed tissue. Observation and use of stool softeners with tub soaks usually allow the acute episode to resolve without an operation because the hemorrhoidal vessels have been naturally thrombosed. The thrombosed internal hemorrhoids will sclerose and may not require surgery. If symptoms persist or recur, a three-quadrant hemorrhoidectomy may then be necessary. If necrotic tissue is present at the time of acute thrombosis, emergent excisional hemorrhoidectomy is necessary. Care should be taken to preserve the anoderm. The patient should be kept in the hospital after the procedure until the pain is minimal and until spontaneous voiding is possible and to ensure resolution of any potential infection.

Mixed Hemorrhoids

The mucosal component of mixed hemorrhoids occasionally can be treated by elastic ligation. Large symptomatic, nonreducing mixed hemorrhoids generally are treated by excisional hemorrhoidectomy. The patient is placed in the prone flexed position under local anesthesia using a perianal field block with 0.25% bupivacaine with or without epinephrine. The apex of the vascular pedicle is ligated first with a 3-0 chromic catgut suture. An elliptical excision incorporates the external and internal hemorrhoids from the perianal skin to the anorectal ring. The hemorrhoidal tissue is sharply dissected from the underlying internal sphincter (Fig. 39-15). The entire wound is then closed by running the apex chromic catgut suture to the distal perianal skin edge. The largest hemorrhoid is excised first, with care taken not to excise excessive tissue that may result in a stricture. If there is any concern of leaving an adequate anal aperture covered by normal anoderm, it is best to modify a planned three-quadrant hemorrhoidectomy and instead perform a two-quadrant hemorrhoidectomy and band the remaining internal component.

Thrombosed External Hemorrhoids

The external venous plexus is located at the anal verge and encircles the anal canal. A segmental thrombus is confined to the anoderm and perianal skin and does not extend above the dentate line. The problem presents as a painful perianal mass. The overlying skin may be stretched to 2 cm or more. Pain usually peaks within 48 hours and generally becomes minimal after the fourth day. If untreated, the thrombus is absorbed within a few weeks. The pressure of the underlying clot will occasionally cause the adjacent skin to become necrotic, and the clot will be extruded through the area of necrosis. This is noted by the patient as rectal bleeding followed by relief of the anal pain. A partially extruded clot can be removed in the office to provide relief.

Treatment of thrombosed hemorrhoids is aimed at relief of the pain. If symptoms are minimal, mild analgesics, sitz baths, proper anal hygiene, and bulk-producing agents will suffice. However, if pain is severe, excision of the thrombosed hemorrhoid may be beneficial. Because numerous vessels usually are involved, it is necessary to excise the entire mass along with the overlying skin and subcutaneous tissue. The wound is left open without packing. Postoperative care consists of mild analgesics and warm sitz baths or showers.

An anal fissure is a split in the anoderm over the hypertrophied band of internal sphincter at the anal verge (Fig. 39-16). The fissure is almost always located close to the midline of the anal canal; in men, 95% are near the posterior midline and 5% near the anterior midline, whereas in women, about 80% will be located posteriorly and 20% anteriorly. The precise cause of an anal fissure has yet to be determined. However, fissures probably are related to tearing of the anoderm at the time of defecation. The increased anal canal pressure that accompanies an anal fissure is associated with ischemia in the area of the fissure and prevents healing, as spasm recurs with each bowel movement.38 An anal ulcer is the chronic form of an anal fissure with heaped-up edges, sentinel skin tag, and occasionally hypertrophied anal papilla.

Clinical Features and Diagnosis

Most fissures are superficial and heal rapidly with no specific treatment. Occasionally, the fissure may extend deeply through the anoderm to expose the fibers of the internal sphincter. Surprisingly, secondary infection rarely occurs.

Fissures that are aberrantly located may be caused by previous anal operations that result in scarring, stenosis, and loss of anoderm. Individuals with chronic diarrhea may develop anal stenosis associated with a fissure. Crohn's disease often is complicated by anal fissures, which may be a primary manifestation of the disease. These fissures usually are associated with the shiny anal skin tags typical of anal Crohn's disease and may lie laterally instead of close to the midline of the anus.

Patients with anal fissures usually complain of anal pain accompanying and following defecation. Bright red bleeding may accompany a bowel movement, although it is usually minimal. A slight discharge also may be present.

An anal fissure is detected by gently separating the buttocks to reveal the lower edge of the fissure at the anal verge, where a sentinel tag also may be seen. A soft touch of a cotton swab to this area will elicit the pain and help with the diagnosis. A deep gluteal cleft or tight spasm of the sphincter may sometimes obscure the fissure, and, if the patient can tolerate, examination with a small anoscope may be required.

Anal sphincter hypertonicity and an increase in ultraslow waves on anal manometry characterize typical anal fissures.

Treatment

Dietary recommendations and prescription of bulking agents to promote soft stools are beneficial, and warm tub soaks may provide comfort. The majority of acute fissures will heal with conservative management. The use of 2% nifedipine ointment applied to the anoderm outside the anal verge relaxes the sphincter and dilates local vessels to promote healing. Most of the remainder of acute fissures will heal with this added therapy.39

The injection of 20–25 units of botulinum A toxin into both edges of an anal ulcer and directly into the internal sphincter muscle at the ulcer base (total of 75–1000 units) is a simple procedure that has had some mixed success in healing anal fissures.40 It can be done with local anesthesia as an outpatient procedure, with delay of symptomatic relief by approximately 1 week. The paralysis of the internal sphincter reverses in several months, but the fissure may recur. Repeat treatments can be performed if the initial response was adequate, but it is expensive with at best modest healing rates.

Surgical treatment may be required for deep, chronic fissures associated with a sentinel skin tag, hypertrophied anal papilla, and exposed internal sphincter. Excellent results can be achieved if the internal sphincter is divided laterally rather than in the midline. Furthermore, lateral sphincterotomy is not associated with keyhole deformity. Only the thickened band of the internal sphincter is divided (ie, partial sphincterotomy), which limits the amount of internal sphincter transection and reduces the potential for fecal incontinence.

Sphincterotomy can be performed under local anesthesia, using either an open or closed technique (Fig. 39-17). The open technique consists of radial incision of the anoderm over the intersphincteric groove and limited division of the internal sphincter only up to the proximal extent of the fissure under direct vision. The closed method entails dividing the internal sphincter by a subcutaneous approach. Both techniques may be used in the outpatient setting and afford rapid pain relief. Approximately 98% of fissures heal following sphincterotomy. However, there is a small incidence of fecal incontinence following the procedure, so careful patient selection is mandatory. Elderly patients with decreased anorectal sensation are generally not ideal candidates for internal sphincterotomy because of this risk. Consideration should be given to a diamond skin advancement flap to cover the ulcer bed in women. This flap requires isolation of a postage stamp–sized island of skin based on a subcutaneous fat pedicle from the inner aspect of the buttock posteriorly or the perineum anteriorly. The ulcer is excised leaving a defect in the size of the flap. The flap is advanced to the open area in the anoderm and secured to the freshly cut mucosal edges (Figs. 39-18 and 39-19).

Diagnosis and Classification

More than 95% of all anorectal abscesses are caused by infections arising in the anal glands that communicate with the anal crypts (cryptoglandular disease). The acute phase of the infection causes an anorectal abscess, while the chronic stage is recognized as an anal fistula. The anal glands lie in the intersphincteric space between the internal and external anal sphincters. Inflammation of an anal gland leads to the formation of a local abscess in the intersphincteric plane. The clinical presentation, natural history, and proper treatment of anorectal abscess and fistula are understood easily if it is recognized that the disease originates as an intersphincteric abscess.

As the abscess enlarges, it escapes the confines of the intersphincteric plane and spreads in one of several possible directions (Fig. 39-20). The most common of all anorectal abscesses is a perianal abscess, which presents as a tender, erythematous bulge at the anal verge. An ischiorectal abscess is formed when a growing intersphincteric abscess penetrates the skeletal muscle of the external sphincter below the level of the puborectalis and expands into the fat of the ischiorectal fossa. These abscesses can become quite large, because the levator ani (the upper border of the ischiorectal fossa) slopes upward. Thus an ischiorectal abscess may be palpated as a bulge above the puborectalis, although it actually lies below the levator ani musculature. In contrast to the perianal abscess, this abscess seldom presents as a visible bulge because of the large potential space in the ischiorectal fossa. Thus the abscess preferentially expands upward rather than protruding through the skin of the buttock. Rarely, an intersphincteric abscess may expand upward between the circular internal sphincter and the external sphincter, forming a supralevator abscess.

Treatment

Perianal abscesses should be drained immediately, before wide fluctuance or cellulitis develops. Antibiotics are not indicated and should be used only in the presence of extensive cellulitis, valvular heart disease, diabetes, or compromised immunity. If the diagnosis is suspected but not readily evident, examination under regional anesthesia should be performed.

With adequate regional anesthesia, the abscess can be detected and localized by digital examination. An intersphincteric abscess is treated definitively by performing an internal sphincterotomy over the length of the abscess cavity, which serves to unroof and drain the abscess. However, if the infection has developed into a perianal or an ischiorectal abscess, adequate drainage of the abscess cavity first must be done by making a cruciate incision in the skin overlying the abscess as close to the anal canal as possible, or excising a small disc of overlying skin to permit complete evacuation of the contents of the abscess cavity. Incision and drainage alone will result in complete resolution of the infection in about half of patients. In the other half, an anal fistula occurs, which consists of a chronically infected tract with an internal opening located in a crypt at the level of the dentate line and an external opening located at the drainage site of the earlier abscess.

The appropriate treatment for an anal fistula is dependent on the anatomy and the location of the fistula tract. Goodsall's rule states that if the anus is bisected by a line in the frontal plane, an external opening anterior to the line (within 2 cm of the anal verge) will connect to an internal opening by a short, direct fistula tract (Fig. 39-21). However, if the external opening is located posterior to this imaginary line or anteriorly but outside 2 cm from the anal verge, the fistula tract follows a curved course to the crypt in the posterior midline. This rule, while useful, is not infallible.

Occasionally, an external opening located more than 2 cm from the anal verge anterior to the imaginary bisecting line connects to an internal opening in the posterior midline. Because of its shape, this fistula is usually called a horseshoe fistula. Horseshoe fistulas usually have an internal opening in the posterior midline of the anus and may extend anteriorly and laterally to both ischiorectal spaces by way of the deep space. The posterior opening is incised into the postanal space to deal with the primary cause. The anterior extensions of the horseshoe tracts then can be drained by a secondary opening, avoiding a long skin incision that would unroof the entire tract (Fig. 39-22). This is the Hanley procedure for a horseshoe abscess/fistula.

If a perianal abscess develops into a fistula and the fistula tract involves a small portion of the sphincter muscle, the condition can be treated by simple fistulotomy, which divides a portion of the internal sphincter and unroofs the tract entirely.

An anorectal fistula that persists after drainage of an ischiorectal fossa abscess usually is a transsphincteric fistula, because the tract crosses the lower portion of the external sphincter. The fistulotomy required to unroof this tract results in division of a portion of the internal sphincter as well as a portion of the lower external sphincter. If the tract lies below the posterior midline puborectalis, the external sphincter usually can be divided at the site of the fistula tract without loss of continence. However, the puborectalis must not be divided, or incontinence will invariably ensue.

The external anal sphincter is much less prominent in the anterior midline. Thus fistulotomy as treatment for an anterior midline anal fistula is associated with an increased risk of anal incontinence, particularly in women. Consequently, treatment of such fistulas often involves eradicating the internal opening of the fistula at the level of the dentate line by advancing a flap of rectal mucosa. It is important to ensure adequate drainage of the fistula through the external opening until the suture line of the advancement flap is well healed; otherwise an abscess can reform and disrupt the suture line, causing a recurrence of the fistula (Fig. 39-23). Injection of Fibrin glue and insertion of collagen plugs into the fistula tract is also an alternative with minimal morbidity and mixed success.41,42 A newer technique involving ligation of the intersphincteric fistula tract (LIFT) has also been described with minimal morbidity and mixed success.43,44 A dissection in the intersphincteric plane to the level of the fistula with double-suture ligation and partial excision of the intersphincteric portion of the tract will result in healing of approximately 50% of fistulas treated this way. Minimal damage to the sphincter mechanism and anal canal allows other treatments to be used if the technique fails.

Repair of rectovaginal fistulas after obstetric injury can also be performed in the same manner as the sliding advancement flap.45,46 It is important to perform preoperative testing to evaluate for an associated external sphincter defect that may need to be repaired at the time of the advancement flap.

Although most anorectal abscesses originate in the anal crypts, other disease entities must be considered if the pathology appears atypical. Crohn's disease should be suspected if there are numerous complex fistula tracts associated with edematous skin tags, or if there is inflammation of the rectal mucosa. Tuberculosis is now a rare cause of anal abscesses and fistulas but has recently been observed in immigrants to America. Hidradenitis suppurativa also may mimic cryptoglandular suppurative disease. Close examination, however, will reveal that the disease arises from the perianal skin and not the anal crypts. Actinomycosis should be suspected if typical sulfur-like granules are seen in the abscess cavity or fistula tract. Pilonidal disease sometimes can be confused with a posterior perianal abscess, but careful examination should reveal that there is no communication with the anus. Hair obtained from the abscess cavity when the pilonidal abscess is drained will indicate the true nature of the disease.

During recent years there has been a profound change in the prevalence and types of sexually transmitted diseases. Genital-anal, oral-anal, and other anal-based practices among homosexual or bisexual men and among women who engage in anal receptive intercourse account for the transmission of most of these diseases.

The recognition of the acquired immunodeficiency syndrome (AIDS) has led to public concern over the transmission of the causative agent, the human immunodeficiency virus (HIV). The incidence of other venereal diseases appears to be increasing. Although a detailed discussion of these infections is beyond the scope of this textbook, the surgeon will often be consulted for evaluation of complications of these diseases.47

Human Papillomavirus

Human papillomavirus (HPV) is the etiological agent causing venereal warts. These lesions are most common in homosexual men and can have a varied appearance, including (1) discrete warts: papillary or acuminate white lesions, usually occurring singly or in clusters at or below the dentate line; (2) circumferential wart ring lesions located at the dentate line and encompassing 60–100% of the anal canal; and (3) flat white epithelium: pale areas of smooth opaque epithelium that often extend cephalad to the dentate line. These latter lesions may be detected more easily by using a colposcope to magnify the anal canal. A high prevalence of histologically confirmed dysplasia in these internal lesions can be detected in asymptomatic homosexual men. Dysplasia was found in 70% of HIV-seronegative men and 85% and 90% of nonimmunosuppressed and immunosuppressed HIV-seropositive men, respectively. Biopsy of the lesions was necessary for detection, because it could not be predicted by the gross appearance of the warts.

The association of dysplasia with HPV is now well recognized. There are at least 60 different HPV types. Types 6 and 11 are associated with warts and low-grade dysplasia. Types 16 and 18 have been found in cervical cancer and high-grade cervical dysplasia, and type 16 has been found in high-grade anal dysplasia and invasive cancers. HPV types 31, 33, and 35 are thought to pose an intermediate cancer risk.

While it is clear that HPV is implicated in the pathogenesis of anal cancer in homosexual men, the rates of progression from dysplasia to cancer in the anal canal are unknown. It is likely that the progression rate is low, but further study is needed for documentation.

Anal intraepithelial neoplasia (AIN) is believed to be a precursor of anal neoplasm. Low-grade anal squamous intraepithelial lesion (LSIL) is equivalent to AIN grade I and high-grade anal squamous intraepithelial lesion (HSIL) is equivalent to AIN grade II or III. AIN III is defined as nuclear abnormalities that have penetrated through the full thickness of the epithelium. AIN III may be found in the pathology specimen after surgery for an unrelated problem such as hemorrhoids. One can apply acetic acid to the perianal area to visualize the lesions. The technique of anal mapping using biopsies at 1-cm intervals starting at the dentate line around the anus may also be used. Depending on the size and location of the lesion around the anus, the appropriate therapy for AIN is ablation of the lesions, either by excision, electrocautery, or laser. Medical options include topical 5-fluorouracil (5-FU) cream or imiquimod. Wide local excision may result in morbidity including anal stenosis or incontinence. Despite treatment of AIN, it is not known if treatment will reduce cancer risk. Thus, patients should be followed closely, especially those with immunocompromise.48

Chlamydial Infections

Chlamydial infections are now the most common sexually transmitted disease in the United States and they account for increasing numbers of cases of proctitis in patients who practice receptive anal intercourse. There are 15 recognized immunotypes of Chlamydia trachomatis, but for practical purposes it should be recognized that there are lymphogranulomatous causing lymphogranuloma venereum (LGV) and nonlymphogranulomatous (non-LGV) types. The non-LGV organisms are a common cause of urethritis, epididymitis, and pelvic inflammatory disease. At least half of the genital infections previously diagnosed as “nonspecific” or “nongonococcal” are caused by non-LGV Chlamydia. Chlamydial proctitis may coexist with other rectal infections, especially gonorrhea. Several serotypes are responsible for proctitis, and serotypes L1, L2, and L3 are responsible for lymphogranuloma venereum. The pathogen is introduced by either genital-anal or oral-anal intercourse. The non-LGV organisms are obligate intracellular parasites that can penetrate only columnar or transitional epithelium. The LGV organisms also can penetrate mononuclear cells, which may account for the prominent lymphadenopathy in patients with lymphogranuloma venereum.

Infection may be asymptomatic or may consist of nonspecific symptoms such as anal pain, pruritus, purulent discharge, and bleeding. More severe forms of infection, especially severe proctitis, usually indicate the presence of one of the LGV serotypes. Perianal fistulas and rectovaginal fistulas may develop, with untreated cases progressing to severe rectal stricture. Two weeks after the initial symptoms, inguinal lymphadenopathy becomes predominant and the inguinal nodes may fuse together in a large mass.

The organism is an obligate intracellular organism, and rectal cultures are usually inconclusive. A biopsy of the rectal mucosa is probably the most commonly used method to confirm the diagnosis. The diagnosis of chlamydial infections used to be difficult because satisfactory culture techniques were not widely available. Diagnosis usually required the detection of rising antibody titers. The organism, however, now can be identified by using tissue culture techniques or DNA probes.

Chlamydial infections should be treated as soon as the diagnosis is suspected. The recommended treatment for non-LGV chlamydial infection is doxycycline or, alternatively, erythromycin for 7–14 days. LGV chlamydial infection should be treated with tetracycline and sulfonamides for a minimum of 21 days.

As with all acute STDs, sexual abstinence until eradication is complete as well as education, testing, and treatment of sexual partners, when appropriate, is recommended.

Herpes Simplex Virus

Anorectal herpes is usually caused by the type 2 herpes simplex virus (HSV-2), although the HSV-l virus is responsible for approximately 10% of anal infections. Patients who have been previously infected have virus-specific antibodies. The first symptoms of infection are perianal pruritus or paresthesia, followed by intense anal pain. Small vesicles surrounded by red areolas may appear. These vesicles subsequently rupture, leaving small ulcers that appear on the perianal skin, in the anal canal, or even on the rectal mucosa. Fever and malaise are frequently present. The ulcerated lesions may become secondarily infected, with increased pain and discharge. The lesions usually heal in about 2 weeks. Unfortunately, a chronic relapsing course is common, although recurrent lesions are usually much less painful.

Scrapings from the base of a ruptured vesicle can be stained to show typical intranuclear inclusion bodies, but the diagnosis is most expeditiously made by viral HSV culture.

There is no known cure for herpes. Primary or initial infections are treated with oral acyclovir, famciclovir, or valacyclovir for 7–10 days.49 Acyclovir should be taken at the onset of recurrent symptoms, which may reduce the formation of new vesicles. Chronic suppressive therapy or self-initiation of antiviral treatment with recurrent episodes may be helpful in patients with more than six recurrences per year. AIDS patients with perianal herpes resistant to acyclovir may benefit from two newer compounds, foscarnet or vidarabine.50

Patients are contagious while the lesions are present and should abstain from sexual activity until all lesions are completely healed. Even after the lesions have completely healed, a condom should be used during sexual intercourse.

Gonorrhea

Anorectal infections caused by the bacterium Neisseria gonorrhoeae are common in the male homosexual population and frequently accompany other venereal diseases. Over half of homosexual men seen in screening clinics have been found to be infected, with the rectum being the only site infected in about half of cases. The majority of these infections are asymptomatic.51

Symptoms vary from none to intense anorectal pain and tenesmus accompanied by a viscid, yellow anal discharge. Anoscopy may reveal anusitis or distal proctitis. Diagnosis is confirmed by obtaining cultures from the rectal discharge or mucosa, or more recently by DNA probes.

Treatment should be initiated if the disease is suspected. Untreated rectal gonorrhea can lead to septic arthritis, endocarditis, perihepatitis, and meningitis, as well as infection of sexual partners. Several drugs (penicillin, tetracycline, ampicillin, and spectinomycin) may be used for treatment, although increasing numbers of resistant strains are being recognized. Cultures should be repeated after treatment is completed, because antibiotic therapy may fail in as many as one-third of the patients. All sexual contacts also must be treated. All patients with confirmed rectal gonorrhea should have a serologic test for syphilis 3 months after treatment is completed.

Syphilis

The classic lesion of primary syphilis is a chancre on the genitalia, but in homosexual males the chancre usually presents in the anal canal or at the anal verge.52 These ulcerated lesions may mimic an anal fissure, but an aberrant location of the lesion (eg, lateral anus instead of midline) should arouse suspicion. Classic descriptions indicate that the syphilitic chancre is a painless lesion, but anal chancres may be extremely painful. The causative organism is the spirochete, Treponema pallidum, which may occasionally cause severe proctitis without an accompanying chancre. Inguinal adenopathy is common.

Early syphilis can be diagnosed by examining scrapings from the base of the chancre with dark-field microscopy; these lesions teem with spirochetes that can be seen as corkscrew-shaped motile fluorescent yellowish-green organisms. Serology is also very helpful in establishing the diagnosis. In untreated primary syphilis, the Venereal Disease Research Laboratory assay is reactive in about 75% of cases, in early latent syphilis about 95%, and in the secondary state it is 100% reactive. The fluorescent treponemal antibody absorption test usually becomes positive about 4–6 weeks after the initial infection. Rapid plasma reagin and darkfield microscopy are the appropriate tests for suspected early syphilis.

The second stage of anal syphilis appears 6–8 weeks after the chancre has healed in untreated patients. It may present as condyloma latum, a pale-brown or flesh-colored flat verrucous lesion, or as a mucocutaneous rash. All three serologic tests for syphilis will be positive at this stage. Skin lesions are highly contagious.

Benzathine penicillin G is the treatment of choice for syphilis. Alternative treatments include doxycycline, tetracycline, or erythromycin. Patients with syphilis must abstain from sexual contact until treatment is complete. All sexual contacts within the preceding 90 days should be prophylactically treated.