Anal/Rectal Pathology

i. Hemorrhoids

ii. Anal fissure

iii. Perirectal abscess

iv. Pruritis ani

v. Fecal Incontinence

Estimates of the prevalence and significance of hemorrhoidal disease in the general population are varied. The profusion and popularity of over-the-counter medications for anorectal complaints suggests that symptomatic hemorrhoids affect a large portion of the adult population at some time in their lives. Only about 10% of all patients referred for specialist treatment require surgical intervention, however, understanding the location and grade of symptomatic hemorrhoids facilitates management for the majority of patients who can be treated conservatively.

The hemorrhoidal venous plexus encircles the anal canal and provides a cushion to the anal canal. The process that exaggerates these venous cushions and produces symptomatic hemorrhoids is not known. Because the work of Burkitt proposed a link between low fiber intake and hemorrhoids, consensus has been that constipation and straining aggravate hemorrhoidal disease.

Hemorrhoids are classified by their relationship to the dentate (or pectinate) line. The dentate line marks, albeit indistinctly, the transition between the rectal mucosa and the anal canal mucosa. Internal hemorrhoids are located above the dentate line. They occur most commonly in three positions: right posterior, right anterior, and left lateral. Internal hemorrhoids typically present with painless bleeding. Pain is a less frequent finding because the mucosa above the dentate line has no somatic innervation. Pruritis ani, seepage, and mild discomfort can be associated. Internal hemorrhoids are graded in four levels (see table) On anoscopic examination, the internal hemorrhoid appears as a pink-blue swelling of mucosa. The tissue may prolapse into the anoscope lumen with straining. Grades I through II usually can be treated successfully with dietary modifications and office procedures. Symptomatic grade IV hemorrhoids (irreducibly prolapsed) generally require surgical hemorrhoidectomy.







Prominent hemorrhoidal vessels on anoscopy

Painless bleeding

Change in diet and other habits


Hemorrhoid prolapses and returns spontaneously

Mild discomfort, bleeding

Change in diet and other habits, sclerotherapy, rubber band ligation


Hemorrhoids require manual reduction

Pain, bleeding, discharge

Sclerotherapy, rubber band ligation


Irreducible hemorrhoids

Pain, bleeding, possible strangulation


Treatment begins with education to redirect the patient's diet and behavior. Recommended dietary changes include an increased intake of nonabsorbable fiber. This can be in the form of raw fruits and vegetables, cereal, or fiber products. Most Americans currently consume well below the recommended 25 to 30 g of insoluble fiber per day. Fluid intake of caffeine-free beverages should be increased to six to eight glasses per day. Prolonged periods in the bathroom, straining during defecation, and excessive use of toilet paper should be discouraged.

These simple measures frequently lead to cessation of bleeding in grade I and grade II hemorrhoids and ameliorate symptoms for Grade III hemorrhoids. For persistent symptoms, several office procedures are available. Injection sclerotherapy is easily learned and has a low complication rate. Using a spinal needle through an anoscope, a small volume of sclerosant is instilled in the submucosa of the internal hemorrhoid. The scarring in response to the sclerosant obliterates the vessels and stops bleeding from the hemorrhoid. This method is particularly useful for grade I and mild grade II hemorrhoids in which there may be a paucity of tissue for banding. The recurrence rate of symptomatic hemorrhoids is higher with this method of treatment than with rubber-band ligation or hemorrhoidectomy, however.

Rubber-band ligation is efficacious and easy to learn and has few complications. It is especially useful for grade II and grade III hemorrhoids that bleed and prolapse. The hemorrhoid is visualized through the anoscope. The ligator is introduced through the anoscope, and the hemorrhoid is grasped with a forceps through the ligator. The tissue should be grasped at least 5 mm above the dentate line to avoid incorporating anoderm. The hemorrhoid tissue is pulled into the drum of the ligator, and the handle is compressed, releasing the rubber-band. If the patient feels pain at any point, the instruments should be repositioned. If placement of the band causes significant pain it should be removed promptly by elevating the band with a crypt hook and cutting it.

It is preferable to limit banding to one or two sites per session. Subsequent bandings can be performed at 4-week intervals. The patient who requires more than three bandings per hemorrhoid probably should be referred for surgical consideration.

A properly placed rubber-band will strangulate the hemorrhoid, and the tissue eventually will slough. Bleeding is the most common complication after ligation. Aspirin and nonsteroidal anti-inflammatory products are to be avoided for 2 weeks after the procedure. Most bleeding is of scant quantity, and patients can be reassured that it will resolve. A patient rarely will experience significant bleeding between 7 and 10 days postligation, when the hemorrhoid sloughs. Examination by a surgeon will indicate whether the patient requires injection of epinephrine, suture ligation of a bleeding vessel, or formal hemorrhoidectomy. Another complication of banding is precipitation of an acute hemorrhoid attack with external hemorrhoid thrombosis. These patients experience significant pain and swelling. They usually can be managed with conservative measures and pain medication. The most severe, life-threatening complication of ligation is, fortunately, exceedingly rare: perianal sepsis. Patients who experience fever, chills, or urinary hesitancy with pain should be referred for surgical evaluation immediately. These patients may require hospital admission, intravenous antibiotics, examination under anesthesia, removal of the rubber-band, and possible débridement of tissue.

For patients with large grade III or grade IV hemorrhoids, surgical hemorrhoidectomy is often the most efficient management. Acutely prolapsed, engorged, strangulating hemorrhoids that cannot be reduced are an indication for immediate surgical intervention.

Further evaluation of the patient with hemorrhoidal bleeding is directed by the patient's age and other risk factors. If the patient is younger than 40 years of age and there is an obvious hemorrhoidal source for bleeding, directed therapy is appropriate. For patients older than the age of 40, sigmoidoscopy should be performed at some point in the evaluation and treatment.

External hemorrhoids arise below the dentate line. They frequently are seen as bluish lumps at the anal verge. The blue color is caused by the thrombosed venous blood in the complex.

Digital rectal examination and, if possible, anoscopy should be performed to verify that the hemorrhoid is solely external. Thrombosed external hemorrhoids cannot be reduced.

Symptoms of an isolated thrombosed external hemorrhoid range from minimal discomfort to severe pain. Perianal itching and bleeding are usually less prominent features. The severity of the patient's symptoms and timing of presentation direct treatment.

For the patient with mild to moderate discomfort, symptomatic relief frequently can be achieved with a conservative regimen. Components of the regimen include increased fiber consumption, increased fluid intake, Sitz baths to relieve muscle spasm and pain, local lubricant such as a suppository, stool softener, and analgesics.

For those patients in severe pain who present within 48 to 72 hours of thrombosis, excisional thrombectomy is a good option. Incision and drainage should not be considered. The high recurrence rate with this method of treatment condemns the patient to beginning the whole painful process again as the complex rethromboses. Excisional hemorrhoidectomy can be performed in the office under local anesthesia with minimal instrumentation. After preparation with an antiseptic solution and draping of the area, local anesthesia with epinephrine is infiltrated with a small gauge needle. The anesthetic is placed at the margin of the thrombosis and dispersed through the local area. An elliptical incision is begun at the lateral verge of the thrombosis, and the organized clot is dissected free of the submucosal fibers. The ellipse of skin excised should be significantly smaller than the total volume of the hemorrhoid. A dressing is applied and the patient is started on conservative management while the wound heals.

Patients who present more than 72 hours after the initial event are further along in the course of resolution of the hemorrhoid and are likely to have less pain. These patients with mild to moderate pain should be offered conservative measures. Recurrent painful external hemorrhoids are an indication for surgical hemorrhoidectomy.


Anal fissure:
An anal fissure is a tear in the lining of the anal canal from the dentate line to the anal verge. They are located most commonly in the posterior midline, although up to 10% of fissures may occur anteriorly in women.  The precise cause of anal fissure has not been elucidated. Some theorize that it is a traumatic lesion secondary to difficult passage of a hard stool. Elevated resting internal anal sphincter pressures have been implicated as a direct cause and as a contributing factor toward anal mucosa ischemia.

The most common presentation is anal pain, often burning in nature, associated with a bowel movement. The pain begins with a bowel movement and persists for minutes to hours after the event. Patients may report small amounts of blood on the toilet tissue, itching, or drainage. Pain is the most prominent component, however, and it is frequently far out of proportion to the findings on examination.

The fissure often can be visualized by gently spreading the perianal skin and inspecting the posterior midline. If a superficial tear is seen in the anal mucosa, the diagnosis is confirmed and further examination may be deferred until the patient is more comfortable. Associated physical findings include sentinel skin tag at the anal verge, a hypertrophied anal papilla, thickened margins of mucosa at the fissure edge, and spasm of the anal sphincter. If digital rectal examination is possible, the patient often will have point tenderness to palpation of the fissure.

The goal of treatment of an acute anal fissure is relief of anal sphincter spasm to relieve pain and possibly increase blood flow. A conservative regimen of bulking agents, increased fluid intake, Sitz baths, suppositories for lubrication, and stool softener or mild laxatives is effective for most patients. Patients can expect significant relief of symptoms within a week. Healing usually is completed within 2 to 4 weeks. Another recently described treatment is nitroglycerin applied to the fissure. In a small series, 80% of fissure patients had relief of pain and healing within 1 month with this therapy.12

The factors that retard healing of an acute fissure and promote progression to a chronic fissure are not clear. On examination, the white transverse fibers of the internal sphincter muscle may be seen in the base of a chronic fissure. Once sphincter fibers are visible, it is unlikely that the fissure will heal with conservative measures. Surgical referral is indicated for evaluation for sphincterotomy. Anal dilatation previously was recommended for chronic fissure and other benign anorectal conditions. This procedure now is understood to have a low success rate and a high frequency of post-treatment incontinence. It should not be recommended. Surgical treatment with partial lateral internal sphincterotomy is now the treatment of choice. Lateral sphincterotomy produces a significant decrease in resting internal sphincter pressure.  Outcome is excellent with lateral sphincterotomy. Failure, in the form of nonhealing or recurrence, is seen in only 1% to 3% of patients.21 The risk of anal sphincter dysfunction ranges from 0% to 15% in various series, and it usually manifests as partial incontinence to flatus.

Perirectal abscess:

All perirectal abscesses originate with blockage and infection of the anal glands opening into the crypts of Morgagni at the level of the dentate line, hence the term cryptoglandular origin. The anal canal structures are composed of a tube (the internal sphincter muscles) within a tube (the external sphincter muscles). The internal sphincter is a continuation of the circular smooth muscle of the large bowel. The external sphincter muscle is a continuation of the puborectalis and the levator musculature. The anal glands lie in the space between these two tubes of sphincter muscle. All perirectal abscesses begin as intersphincteric abscesses.

An undrained abscess will drain itself. The direction in which the abscess necessitates guides the authors' clinical description of the abscess. The most common progression is downward in the intersphincter plane to the anal verge, creating a perianal abscess. An erythematous, tender lump is seen at the anal verge. An ischiorectal abscess is created when the infection burrows through the external sphincter muscle and spreads in the ischiorectal fossa. These abscesses can become large with modest external demarcation because of the large potential space in the ischiorectal fossa. On examination, the patient may have asymmetry without an obvious lump. Digital examination may allow palpation of a bulge under the levators, reflecting the expanding infection. Finally, abscesses may spread cephalad in the intersphincteric plane to present as supralevator abscess. This abscess is appreciated as a fullness along the levators.

The treatment of all abscesses is drainage. Drainage of a perianal abscess is accomplished easily in the office. After preparation with antiseptic solution, the area is infiltrated with local anesthetic with epinephrine. A small cruciate incision is made over the most medial aspect of the abscess and the collection drained. The incision is placed close to the anal verge, so that if a fistula forms it will be the shortest possible length. The corner flaps of the drainage incision then are excised to allow for continued drainage. Ischiorectal abscesses with obvious superficial perianal involvement can be drained in the same manner. The wounds are left open or stented with a small amount of gauze packing. Extensive packing impedes complete drainage of the infection. The patient can perform Sitz baths and place a simple dressing over the wound. Healing can be expected within 7 to 14 days. Antibiotics are not prescribed routinely. In the setting of marked cellulitis or in a diabetic or immunocompromised patient, antibiotics may be prudent. Immunocompromised patients or those with extensive cellulitis should be considered for inpatient hospitalization, intravenous antibiotics, and examination under anesthesia. Oral antibiotics, warm compresses, or expectant waiting for a process to come to a head are not appropriate primary management techniques of anorectal abscesses. These measures risk progression of infection, sepsis, and a more complex problem. Intersphincteric and supralevator abscesses require internal drainage into the rectum. These processes must be drained under anesthesia by a surgeon. Recurrent or atypical abscesses should prompt investigation for inflammatory bowel disease.

The most common complication of anorectal abscess is fistula formation. This occurs in about 25% of patients despite adequate drainage.  It is unclear why fistulas form despite apparently adequate drainage. It is evident, however, that fistula rates will be higher in patients who undergo more extensive exploration than simple drainage.  Fistulas are described in the same manner as the abscesses from which they are derived. An intersphincteric or perianal abscess becomes an intersphincteric fistula. An ischiorectal abscess becomes a transsphincteric fistula because it penetrates the external sphincter muscle in its course. Goodsall's rule suggests where to find the primary opening of a fistula. Most fistulas in the anterior hemicircumference of the anus will track straight to the dentate line. Most fistula openings in the posterior hemicircumference of the anus will track in a curved line to the posterior midline of the anal canal.  Probing of fistula tracks in the office setting is discouraged, however. There is a possibility of creating false tracks that may complicate management.

Suprasphincteric and supralevator fistulas are generated by abscesses extending higher in the perirectal planes. These fistulas demand complex, staged surgical management to resolve the infection and minimize impairment of continence. Fortunately, most fistulas are simple, low intersphincteric or transsphincteric fistulas that respond well to fistulotomy.  A simple fistulotomy is a laying open of the fistula track, with debridement, to allow healing by secondary intention. Nearly 95% of patients undergoing this procedure will be healed.


Pruritis ani:

Pruritis ani is a common complaint. Perianal itching may be idiopathic or related to one or more causes. The approach to the patient who complains of perianal itching is twofold: evaluation for an underlying pathologic condition and treatment directed to relief of the symptom complex.

The patient with pruritis ani typically reports an escalating course of itching and scratching of the perianal region. The patient rarely can elucidate a precipitating event or recurrent time period. In children, the most common cause of pruritis ani is pinworms. The itching is most pronounced at night as the worms migrate through the anus to lay their eggs on the perianal skin. This is rarely the case in adults. Early in the patient's course, the perianal skin shows minimal erythema. As the cycle of itching and scratching progresses, the skin begins to break down. First, punctate abrasions are seen, followed by desquamated areas of ulceration. In long-standing pruritis ani, the perianal skin can become leathery and white.

Most cases of pruritis ani are of indeterminate cause. Two groups of factors appear to play a significant role in perpetuating the unpleasant cycle, however. Excessive perianal cleansing, not lack thereof, frequently is related. Patients infer that suboptimal hygiene is the culprit and increase their efforts at cleansing the affected area, exacerbating the problem. Dietary factors also play a role. Although the mechanism is not clear, certain foods and beverages, consumed in quantity, clearly worsen the situation. The most common offending agents are coffee, tea, cola, chocolate, and beer.

Patients may experience pruritis ani in conjunction with other anorectal or colorectal pathology. Hemorrhoids, dermatoses, infection, fissures, polyps, and cancer all can cause excessive perianal moisture and itching. Any patient who does not respond to treatment within 1 month should undergo full evaluation for other pathologies.

With a working diagnosis of pruritis ani, the initial treatment measures are alteration of the diet and a gentle, drying perianal regimen. Potentially causative foods and beverages should be eliminated from the diet. The patient should be instructed in a perianal cleansing regimen that emphasizes Sitz baths, blotting of the skin rather than rubbing, drying with a hand-held dryer, and a cotton ball at the anal verge to absorb excess moisture. Most patients have treated themselves with over-the-counter creams and ointments before presentation. These should be discontinued as they may exacerbate moisture. These simple interventions will resolve the symptoms for up to 90% of patients.

For those patients who do not respond to treatment, further evaluation should consist of biopsy of the affected area and complete colonic evaluation. Examination under anesthesia and mapping biopsies may be performed as an outpatient. An array of 3-mm to 4-mm tissue samples is obtained in a radial pattern from the dentate line to the perianal skin. Grossly normal and abnormal tissue is selected. It is important to document clearly the biopsy sites so that if further excision is necessary it will be directed appropriately. The pathologist assesses for dermatoses and neoplasia. Proctosigmoidoscopy and barium enema or colonoscopy complete the survey for underlying problems.

Fecal Incontinence

Patients are distressed by the inability to control gas or stool. There are a multitude of reasons for episodes of incontinence. The most common cause is also the least worrisome: liquid stool. Diarrhea, with the large bolus of liquid stool delivered to the rectum, can overwhelm a physiologically normal sphincter and compromise control. Treatment of the underlying cause of the diarrhea, whether gastroenteritis, inflammatory bowel disease, or irritable bowel syndrome, will resolve the problem. Other causes for incontinence include neurologic disease such as paralysis or systemic or local neuropathy. Disruption of the sphincter muscle complex by obstetric injury is the most common mechanical cause of incontinence. Previous surgery, such as sphincterotomy or fistulotomy, can contribute. Severe trauma and impalement injuries are less common and do not present to the primary care provider.

Neuropathic causes are determined during specialized testing for nerve dysfunction and by the exclusion of other diagnoses. Mechanical disorders often are appreciated on physical examination alone. The directed examination of the patient who complains of fecal incontinence begins with inspection of the perineum. Obvious deformity or scarring is noted, as well as the resting tone of the anal sphincter. A patulous or gaping anus suggests a neurologic cause. The patient is asked to strain to identify excessive descent of the perineum or prolapse of the rectal mucosa. The external sphincter muscle is palpated for obvious discontinuity. Women who have suffered anal sphincter disruption as a result of childbirth typically have a U-shaped puckering of the posterior hemicircumference of the anus. The anterior hemicircumference, particularly the anterior midline, is smooth or scarred, reflecting the sphincter disruption. Digital examination is used again to palpate for obvious defects and to assess resting and squeezing tone.

Treatment is directed at the presumed cause. The patient with loose stool is treated with dietary education, bulking agents, and appropriate therapy for any underlying disease. Specialized evaluation, including manometry, pudendal nerve testing, ultrasound, and defecography, may be necessary for the patient with a possible mechanical or neurologic problem. Any female patient who reports a change in continence more than 3 months after childbirth deserves complete evaluation. Obstetric injury to the sphincter muscles is uncommon but highly correctable by surgical sphincteroplasty.

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