results have been reported, with 89% of patients reporting improvement and 36% reporting full

continence.38 SNS may be offered to patients both with and without evidence of sphincter defects. Tibial

nerve stimulation has also been shown to lead to improvement in anal continence, however this therapy

is currently not approved for use in the United States.39

In patients with severe incontinence for whom alternative methods have failed, creation of a sigmoid

colostomy may improve quality of life and allow them to resume normal daily activities.

Sexually Transmitted Diseases of the Anorectum

The annual incidence of sexually transmitted diseases is approximately 15 million cases in the United

States. As anal erotic practices have increased, the incidence of sexually transmitted diseases of the anus

and rectum has also increased. These are typically the result of anal receptive intercourse, but in some

instances represent contiguous spread from genital infections.

Gonorrhea

Gonorrhea is caused by the gram-negative intracellular diplococcus Neisseria gonorrhoeae, with an

incubation period that ranges from 3 days to 2 weeks. Symptomatic anorectal gonococcal infection

results in pruritus or tenesmus, accompanied by a mucoid and sometimes bloody rectal discharge. Left

untreated, a more advanced systemic infection can occur resulting in such conditions as endocarditis,

pericarditis, and a unilateral migratory gonococcal arthritis of large joints.

Anorectal gonorrhea results in a thick yellow mucopurulent discharge from the anus. This purulent

material is often able to be expressed from the anal crypts and can be visualized directly by applying

gentle external pressure while viewing the distal anorectum through an anoscope. Sigmoidoscopy may

reveal a proctitis extending to no more than about 10 cm from the anal verge. Although these findings

may be mistaken for an ulcerative or nonspecific proctitis, abscesses, fistulae, and ulcers are not typical.

Diagnosis is confirmed by culture on a Thayer–Martin medium plate incubated in a carbon dioxide

environment.

Due to the increasing prevalence of penicillinase-producing N. gonorrhoeae, penicillin G is no longer

recommended. First-line treatment is a single intramuscular injection of 250 mg of ceftriaxone.

Alternative treatments that have been proposed include single oral dose of 500 mg of cefixime or a

single oral dose of a fluoroquinolone. Because of the high rate of concomitant infection with Chlamydia,

patients should be given appropriate treatment for Chlamydia as well. Sexual partners from the past 60

days should also be treated.

Chlamydia/Lymphogranuloma Venereum

Chlamydia trachomatis is the most common sexually transmitted bacterial infection worldwide. In the

United States, male homosexuals account for the majority of rectal Chlamydial infections. With 15

known serotypes, anorectal Chlamydia infection can cause proctitis (serotypes D-K) or

lymphogranuloma venereum (LGV) (serotypes L1–L3). Transmission of disease is through anoreceptive

intercourse, with an incubation period ranging from 5 days to 2 weeks; secondary involvement can also

occur as a late manifestation of genital infection.

Symptoms of non-LGV anorectal infection include rectal pain, tenesmus, and fever, although a

substantial number of infected patients will be asymptomatic. Examination reveals enlarged matted

inguinal lymph nodes and proctosigmoidoscopy shows an erythematous rectal mucosa without frank

ulcerations. Patients with LGV also complain of pain, fever, and tenesmus but often have a slight

mucopurulent discharge and hematochezia. The inguinal lymph nodes in LGV are often more enlarged

as they fuse into a large indurated mass with overlying erythema. Evaluation of the rectal mucosa

reveals a more severe granular proctitis with mucosal friability and frank ulceration. Left untreated, the

disease may progress to fistulae, abscesses, and late rectal strictures. In this setting, LGV may be

confused for perianal Crohn’s disease, however the marked inguinal lymphadenopathy may help

distinguish LGV from Crohn’s.

Treatment of Chlamydia infection is with a single oral dose of azithromycin (1 g) or doxycycline (100

mg) twice a day for 7 days. Alternative therapy includes erythromycin or a fluoroquinolone. Treatment

of LGV is a 21-day course of either erythromycin or doxycycline. Sexual partners also require treatment

to prevent reinfection.

Herpes Simplex Virus

Herpes is the most prevalent sexually transmitted disease in the United States where it is estimated that

20% of the general population are affected. The majority of anorectal herpes infections are caused by

1877

HSV-2 with only about 10% being caused by HSV-1. Transmission is through autoinoculation or direct

contact with an infected individual who is shedding the virus, and the clinical infection may begin 4 to

21 days following anoreceptive intercourse. Patients present with small red vesicles which may be

clustered or scattered in the perianal skin, anal canal or perineum, are extremely painful to touch.

Proctoscopy reveals friable mucosa, ulceration, and the mucopurulent discharge. These findings will be

limited to the distal 10 cm on proctoscopy. Tender inguinal adenopathy occurs in up to 50% of patients

with HSV proctitis. Recurrent attacks are generally milder and shorter in duration.

Diagnosis is made on clinical examination, finding multinucleated giant cells with intranuclear

inclusion bodies on Pap smear, a positive Tzank preparation or a positive culture. As the acute infection

is self-limited, treatment includes warm sitz baths and oral analgesics. The use of antiviral medications

has been shown to shorten the length of symptoms, but does not affect recurrence rates. Acyclovir (400

mg five times/day for 10 days) is most commonly used for initial infection. Recurrent attacks may be

treated with acyclovir (200 mg five times/day) or valacyclovir (500 mg twice/day). Suppressive

antiviral therapy may be considered in patients who have more than five attacks per year.

Condyloma Acuminata

7 Anal condylomata acuminate or “warts” are caused by the human papilloma virus (HPV). HPV is a

papovirus, and more than 80 subtypes of HPV have been identified. Serotypes 6 and 11 are most

commonly associated with the benign, exophytic condylomata of the anogenital region. Serotypes 16

and 18 have been associated with more aggressive lesions that can progress to invasive squamous cell

cancers.

The primary mode of transmission of anogenital HPV is sexual intercourse. Inoculation of the anal

epithelium allows entry of the HPV into the basal cell layers. As these cells proliferate viral replication

occurs in the nucleus. The basal cells then migrate toward the surface and infective particles are

released in the form of visible warts. Mature infectious particles are found in the surface layers of these

lesions.

Condyloma acuminata are easily recognized as epithelialized cauliflower-like projections. They may

be flat, raised, sessile or pedunculated, and range in size from millimeters to a large fungating lesions

known as giant condyloma acuminatum (Buschke–Lowenstein). They may be in clusters or grow to

cover the perineum and anal canal in a “carpet-like” fashion. The warts may be asymptomatic or may

cause pruritus, bleeding, or discharge. Anoscopy is important in evaluating for lesions within the anal

canal.

The goal of treatment is removal of all gross disease while minimizing morbidity, although this does

not ensure eradication of infection. Tangential excision, cryotherapy, or fulguration of small lesions

with local anesthesia can be performed as an office procedure with little discomfort to the patient.

Larger lesions are treated by excision in the operating room, while electrodessication is performed of

any remaining smaller condyloma.

Topical agents such as podofilox and imiquimod can be applied by the patient, but neither is approved

for use in the anal canal. Imiquimod is an immune response modifier that increases local production of

interferon. Complete response can be expected in 50% of patients treated with imiquimod, with 11% of

patients experiencing a recurrence. It can be used as initial treatment with electrodessication reserved

for those who have incomplete response, or following destructive treatment and epithelial healing to

treat remaining or recurrent disease.40

Anal Intraepithelial Neoplasia

The role of HPV in the development of cervical cancer in females has been clearly established, however

its significance in the development of anal cancer is not as well defined. Serotypes 16 and 18 have a

higher propensity to initiate the development of carcinoma, and have a predilection for the less stable

epithelium of the upper anal canal transition zone rather than the modified skin of the lower anal canal

anoderm. They may, however, be identified in the anal skin margin as well.

The incidence of anal cancer in HIV-positive homosexual males is estimated to be 38 times that of the

general population and twice the risk in HIV-negative homosexual males.41 HPV infection has been

reported in 93% of HIV-positive homosexual males compared with 60% of HIV-negative homosexual

males.42 Anal intraepithelial neoplasia (AIN), a precursor to the development of anal cancer, also has a

markedly increased incidence in HIV-positive individuals. It is felt that as HIV disease has become a

chronic, manageable condition, patients are living long enough to progress from AIN to anal cancer.

Some have therefore recommended screening and surveillance programs similar to those for cervical

cancer.

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Evaluation

A thorough history is important, as it will frequently lead the physician to the potential underlying

causes of the incontinence. Obstetrical and surgical history should be noted, as well as any change in

bowel consistency. It is helpful to quantify the frequency and degree of fecal incontinence with the use

of a validated incontinence scoring system.31 Symptoms of other pelvic floor conditions including

urinary incontinence, and rectal prolapse should also be elicited. Physical examination should include

inspection of the perianal skin for scars from previous surgery or obstetrical injury, excoriation from

chronic soiling, or large prolapsing hemorrhoids. Digital examination can provide a gross assessment of

both resting tone and squeeze effort.

In addition to the history and physical examination, several tests of anorectal anatomy and physiology

can be done to investigate the cause of incontinence. Endoanal ultrasonography can provide a

circumferential anatomic image of the anal canal, including visualization of the internal and external

sphincters and any defects in these. Anorectal manometry may help to establish a baseline of resting and

squeeze pressures, and may help to identify decreased rectal compliance. Electromyography of the

pelvic floor with evaluation of pudendal nerve terminal motor latency may help to identify a neurologic

cause of incontinence. Defecography may aid in operative planning by identifying previously

unrecognized disorders such as rectocele or intussusception. The evaluation of a patient with fecal

incontinence must also include an assessment of the impact of the symptoms on the patient’s quality of

life. This is important because the need for intervention is often based on the patient’s desires rather

than a threat to his or her health.

Figure 70-25. Transabdominal rectopexy. After full mobilization of the rectum (A,B), the endorectal fascia and peritoneum on

each side is sutured to presacral fascia, below the promontory of the sacrum (C).

1874

Management

Patients with chronic diarrhea, neurologic conditions, or systemic illnesses are best treated medically.

This treatment is generally directed at regulation of bowel habits, with the goal of decreasing the

frequency of bowel movements. The addition of a fiber supplement adds bulk to the stool and absorbs

fluid, creating a more solid stool that is easier to sense and to control. Constipating agents such as

loperamide, diphenoxylate atropine, codeine, and bile acid binders may help to make stool harder and

less frequent, thereby making it easier for the patient to control. In an effort to decrease leakage, some

patients may benefit from the use of regular enemas to maintain an empty rectum.

Biofeedback is a pelvic floor retraining physical therapy program that can be very helpful in the

treatment of patients with disorders of the pelvic floor. This “retraining” aims to provide increased

strength to the sphincters, sensation of the anorectum, and coordination of the pelvic floor. Biofeedback

typically employs the use of a pressure-sensitive probe placed into the anal canal to monitor the

strength and coordination of the anal sphincter and pelvic floor musculature. The data from the probe

are then transmitted to a monitor, where the patient is able to watch the manometric tracings. Through

a series of coached exercises and visual feedback, improvements can be made in pelvic muscle control,

threshold of sensation within the rectum, and overall control of defecation. Several studies have

demonstrated the effectiveness of biofeedback in improving continence, with success rates ranging from

50% to 90%,32 however, results are often dependent on the quality of the therapist and the motivation

of the patient.

Other options for patients with less severe fecal incontinence include radiofrequency treatment and

the injection of biocompatible bulking agents into the anal canal. The SeccaTM procedure involves the

use of radiofrequency delivered to the anal sphincter, which results in tissue remodeling.33,34 Several

case series have demonstrated the efficacy of this procedure, with more than half of patients treated

reporting improvement in their symptoms.35 Injection of a bulking agent (silicone or carbon-coated

microbeads) into the anal submucosal or intersphincteric space may help to increase resting pressures by

augmenting the anal cushions or restoring anal symmetry.

Operative management of anal incontinence is reserved for patients with frequent symptoms that

have significant impact on a patient’s quality of life. For patients with incontinence resulting from

obstetrical injury or previous anorectal surgery and evidence of an external anal sphincter defect on

imaging, overlapping sphincteroplasty is an option. With the patient in the prone position, a curved

incision parallel to the anus is made over the perineal body. The two ends of the sphincter muscle are

identified and are mobilized laterally. In order to recreate the complete circle of the anal sphincter, the

ends of the muscle are sutured in an overlapping fashion (Fig. 70-26). Short-term outcomes following

sphincteroplasty are quite good, with up to 85% of patients reporting improvement, however, many

patients report deterioration of function over time.36

The artificial bowel sphincter (ABS) involves the placement of a cuff around the anal canal that

generates external pressure to maintain tonic closure. This inflatable cuff is attached to a pressureregulating reservoir placed in the retropubic space, and a control pump which is implanted into the

labium majoris or scrotum (Fig. 70-27). When the patient feels the urge to defecate, the cuff is deflated

for several minutes, thereby opening the anal canal to allow passage of stool. The complication rate of

this procedure is quite high, with reports of explantation or revision of the device in almost half of all

patients due to infection or malfunction, however the majority of patients with a functioning device

report marked improvement in continence.37 Although the ABS is no longer commercially available, the

magnetic anal sphincter, now in trials in the USA, may allow for the significant benefits of the ABS

without the very high rates of infection, extrusion, and explantation.

1875

Figure 70-26. Overlapping sphincteroplasty. A. An anterior curvilinear incision is made over the perineal body, the scar is divided,

and the edges of the external sphincter are grasped with Allis clamps. B. The external sphincter is dissected until the edges can be

overlapped for several centimeters. C and D. An overlapping repair is performed with four mattress sutures.

Figure 70-27. Implanted silicone neosphincter. A: Female. B: Male.

Sacral nerve stimulation (SNS) involves the percutaneous placement of an electrode into the foramen

of the sacral vertebrae, most commonly S3. SNS was initially used to treat urinary incontinence,

however it was noted that patients with combined incontinence had improvement in fecal continence as

well; the exact mechanism of action is unknown. Following lead placement under fluoroscopy, the

patient undergoes a 2-week test period to assess the effect of stimulation. If continence is significantly

improved, a permanent stimulator is implanted subcutaneously at a second operation. Durable 5-year

1876

 

Figure 70-23.Perineal rectosigmoidectomy. The patient is placed in the prone jack knife position with both legs in gynecologic

stirrups. A and B: A circular incision is made on the prolapsed rectum 2 cm proximal to the dentate line. C: The peritoneal

attachment is dissected from the anterior rectal wall, thus opening into the peritoneal cavity. D: The mesorectum or mesosigmoid

is clamped and divided laterally and posteriorly. E: This is followed by approximation of the puborectalis. F: The anterior wall of

the protruding rectum is cut 1 cm distal to the anal verge. G: Stay sutures of 2-0 synthetic absorbable material are placed in four

quadrants. H: Anastomosis with interrupted stitches; I: Colonic J pouch.

Transabdominal rectopexy involves a thorough mobilization of the rectum to the level of the pelvic

floor musculature, followed by fixation of the mesorectum to the presacral fascia below the sacral

promontory (Fig. 70-25). Fixation may be performed through a laparotomy or Pfannenstiel incision, or

with a minimally invasive approach (laparoscopic or robotic assisted). Fixation of the rectum can be

accomplished with suture, tacks, or the placement of a mesh (posterior to the rectum or as a supportive

sling around the rectum). In patients with a history of chronic constipation and evidence of slow transit

on colonic transit studies, rectopexy may be combined with resection of the sigmoid colon. In these

cases, the anastomosis should be performed above the level of the rectopexy to reduce the risk of

anastomotic complications. Recurrence rates following rectopexy are generally lower than 10%, and

many patients will have improvement in fecal continence. While division of the “lateral stalks” during

resection rectopexy seems to reduce recurrence rates, it may exacerbate constipation.

One multicenter cohort study of 643 patients who underwent an abdominal repair of rectal prolapse

demonstrated pooled 5- and 10-year recurrence rates of 7% and 29%, respectively.29 No difference was

identified based on the degree of mobilization or resection. In addition, similar recurrence rates were

seen in patients who underwent suture rectopexy and mesh rectopexy, and in patients who underwent

open or laparoscopic repairs. Another abdominal approach, ventral rectopexy, has also been recently

popularized for the treatment of rectal intussusception and prolapse. This procedure involves

mobilization of the anterior rectum, with no or minimal posterior dissection, followed by anterior mesh

placement and sacral fixation. This technique was devised in an effort to spare patients from the risk of

autonomic complications associated with complete rectal mobilization. Published recurrence rates are

similar to those for other abdominal approaches. The abdominal operations can be performed as open,

1872

laparoscopic, or robotic procedures.

Fecal Incontinence

Fecal incontinence is an embarrassing and socially devastating condition that affects up to 18% of the

population and up to 50% of nursing home residents.30 Incontinence may be as severe as the

involuntary passage of solid stool, but also includes patients who are unable to control the passage of

flatus and those who suffer from chronic leakage that requires the use of pads. It is important to

understand that fecal incontinence is not a diagnosis, but a symptom of which there are multiple

potential causes.

Figure 70-24. Modified Delorme procedure. Patient is placed in the prone position. A and B: With a Pratt speculum used for

exposure, a circumferential incision is made 1 cm proximal to the dentate line. The submucosa is dissected from the underlying

internal sphincter. At the level of the anorectal ring, the Pratt speculum is replaced by Lonestar (r) retractors placed at a right angle

to the dentate line. C and D: Proximal to the anorectal ring, the dissection continues in the mucosal plane until the mucosa resists

being pulled down. The mucosal tube is then cut. E and F: With 2-0 synthetic absorbable sutures, the mucosa at the upper cut end

is brought down to the mucosa at the lower cut end, taking along the denuded anorectal wall. Eight such sutures are placed all

around. G: At completion of the anastomosis, the anorectum is plicated.

Anal continence requires a complex integration of function between the anal sphincters and pelvic

floor (see Physiology), but is also dependent on the volume and consistency of the stool, the compliance

of the rectum, and normal neurologic function. It is for this reason that a large volume of diarrheal stool

entering the rectum may overcome anal continence, even in a healthy patient. Other disease states such

as inflammatory bowel disease and radiation proctitis, as well as central nervous system pathologies

such as spinal cord injury may also produce incontinence. Incontinence is far more common in female

patients, although obstetrical tears of the anal sphincter may not present as incontinence for two or

more decades following the injury. Injury to the pelvic floor muscles and pudendal nerves may also

result following childbirth. Damage to the sphincter complex can result from surgical intervention

(fistulotomy or internal sphincterotomy), trauma, or chronic stretching as seen in rectal prolapse.

1873

 

Figure 70-21. Endorectal advancement of anorectal flap. A: Exposure is gained by an anal speculum, and the fistula is identified.

Outline of endorectal flap, extending proximally to 7 cm from the anal verge. B: The full-thickness flap is created to include the

internal sphincter muscle. C: Lateral mobilization is made on each side in the submucosal plane. D: Anorectal wall on each side is

approximated. E and F: The endorectal flap is pulled down to cover the wound and sutured. The fistula is excised. The aperture in

the vagina is not sutured but is left open for drainage.

As excision often leads to a large defect, numerous flap closures have been described for pilonidal

disease. These include a rhomboid rotational flap, gluteus maximus rotational flap, z-plasty, and an

advancement flap of skin and gluteal fat (Karydakis flap).25 Excellent results have been reported from

specialty centers using these approaches.

The Bascom procedure is based on the premise of removing the pilonidal disease while avoiding

excision of large areas of normal tissue. This involves making a vertical incision at least 1 cm off the

midline overlying the chronic cavity, without excising the walls of the cavity. The sinus tracts leading to

the midline pits are probed and curetted to remove any granulation tissue. The midline pits are then

excised and closed, while the lateral incision is left to close by secondary intention. Excellent results

have been reported with this procedure,26 however, no trials comparing this to other techniques have

been published.

Rectal Prolapse

4 Rectal prolapse (procidentia) is a relatively uncommon condition in which there is a full-thickness

protrusion of the rectum through the anal canal. A related condition is rectal intussusception, which is

where the rectum telescopes into itself but not through the anus. Rectal prolapse is significantly more

common in females than in males, and many patients have a long standing history of straining and

constipation. Association with other pelvic floor conditions such as urinary incontinence, voiding

disorders, and cystoceles is common. Prolapse is also more commonly found in patients with dementia,

mental retardation, and schizophrenia.

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Pathophysiology

The exact cause of rectal prolapse is not known, however it likely represents chronic progression of

intussusception. As the rectum or rectosigmoid infolds onto itself, it progressively pulls the rectal wall

away from its attachments to the sacrum and pelvic sidewall. With persistent straining, the bowel

continues to intussuscept, eventually leading the entire wall of the rectum to evert through the anal

opening. Studies of anorectal function in patients with rectal prolapse demonstrate that these patients

often have impaired resting and voluntary squeeze pressures in the anal sphincter, decreased rectal

capacity, impaired continence, and inadequate puborectalis relaxation during defecation. Incontinence is

likely secondary to chronic mechanical stretching of the sphincters from the prolapse, stretch injury to

the pudendal nerves, and loss of normal sensation of the anal canal. Several anatomic abnormalities are

typically seen in patients with chronic rectal prolapse ( Table 70-5), however, it is unclear whether

these are factors that lead to prolapse or whether they are caused by the condition.

ETIOLOGY

Table 70-5 Anatomic Abnormalities in Rectal Prolapse

Solitary rectal ulcer syndrome (SRUS) is a rare condition that is also likely related to intussusception

of the rectum. The straining from constipation can lead to an ulcer in the anterior rectal wall from

repeated mucosal trauma. In severe cases, SRUS may lead to gastrointestinal hemorrhage and chronic

pain. Biopsies of these ulcers often demonstrate mucosal glands displaced within the submucosa, which

may lead to the misdiagnosis of carcinoma.

Evaluation

The diagnosis of rectal prolapse is clinically made on the basis of the history and physical examination.

Patients typically present complaining of a mass with defecation that may or may not spontaneously

reduce. Prolapse is often associated with fecal or mucous soilage and pelvic discomfort; pain is not

typically present. Digital rectal examination often demonstrates a patulous anus with decreased

sphincter tone. Full-thickness rectal prolapse will appear as concentric rectal rings protruding through

the anus (Fig. 70-22). It is important to differentiate full-thickness prolapse from prolapsed hemorrhoids

or mucosal prolapse, which will appear as radial folds. If the prolapse is not obvious, it is best

demonstrated by asking the patient to strain while seated on a commode. Anoscopy or proctoscopy will

often show mildly inflamed mucosa or ulceration. Patients should be evaluated with a colonoscopy to

evaluate for bleeding and to rule out a mass, which can rarely serve as the lead point of intussusception.

For those patients with chronic constipation, a colonic transit study may help to determine whether

colonic resection may be necessary. Anal manometry is not typically useful other than to document

baseline function. When intussusception is suspected but cannot be visualized, defecography may be

helpful and may demonstrate other related conditions such as enterocele or puborectalis dyssynergy.

Patients with other pelvic floor complaints require further evaluation by urogynecology.

Management

Surgical intervention is the gold standard for treating full-thickness rectal prolapse, however

nonoperative management with treatment of the constipation and pelvic floor strengthening exercises

has been described in patients who are poor surgical candidates. While the objective is to resolve the

prolapse, repair may also help to improve or restore fecal continence and correct functional

constipation. Several different operations have been described for rectal prolapse, either from an

abdominal or perineal approach. The benefit of a perineal approach is that it can be performed under

regional anesthesia and generally is less painful that an abdominal approach. The perineal procedures

may be ideal for older patients or those individuals who may not tolerate general anesthesia or major

abdominal surgery. The trade-off is that the recurrence rates of a perineal approach are generally higher

(up to 38%) than an abdominal approach (less than 12%).27 Perineal repair of rectal prolapse includes

the Altemeier perineal rectosigmoidectomy and Delorme plication. Abdominal approaches include

rectopexy, with or without concomitant sigmoid colon resection.

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Figure 70-22. Full-thickness rectal prolapse will appear as concentric rectal rings protruding through the anus.

Perineal rectosigmoidectomy (Altemeier procedure) is a transanal surgery in which the prolapsed

rectum and redundant sigmoid colon are excised through the rectum. The procedure is typically

performed in the prone jack-knife position and can be performed under general or spinal anesthesia

(Fig. 70-23). The rectum and sigmoid colon are resected and a low anastomosis is performed just

proximal to the dentate line. Ideally a levator muscle imbrication and a colonic j-pouch are performed

prior to a stapled or hand-sewn anastomosis. The former maneuver may help improve continence while

the latter adjunct may help decrease bowel frequency. Without these steps, loss of the compliant rectum

combined with low resting anal sphincter pressures often results in incontinence, soiling, and urgency.

Major long-term complications include recurrence, fecal urgency, tenesmus, and anastomotic stricture.

Overall results vary, but there is some data to suggest that among the perineal approaches, the

Altemeier procedure has the lowest recurrence rates and best functional outcomes.28

The Delorme procedure is also typically performed in the prone position, and is useful in patients

whose rectum does not prolapse more than 5 cm. This procedure involves stripping the mucosa of the

prolapsed rectum from the muscularis propria, followed by plication of the muscularis propria and

reanastomosis of the mucosal ring (Fig. 70-24). This procedure may also be combined with

levatoroplasty or sphincter repair in an effort to improve functional outcomes. This technique has a high

recurrence rate but has very low associated morbidity, and may therefore be useful in frail, older

patients.

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Clinical Manifestations

The clinical presentation of a rectovaginal fistula depends on the size and location of the fistula. In

patients with small or low fistulas, the most common symptom is the passage of flatus from the vagina.

Patients with large fistulas may complain of vaginal discharge with fecal odor, passage of flatus or stool

from the vagina, recurrent urinary tract infections, or painful vaginitis.

Diagnosis is typically made on physical examination. Digital rectal examination or bimanual

examination of rectum and vaginal may demonstrate the defect. Anoscopy may be helpful in visualizing

the opening in low fistulas, while proctoscopy or flexible sigmoidoscopy may be required in mid or high

fistulas. If a rectovaginal fistula is suspected clinically but no defect can be visualized, a methylene blue

rectal enema may be administered following vaginal tampon insertion. Staining on the tampon is

suggestive of a fistula. A contrast rectal enema under fluoroscopy may be needed in more complex cases

to identify the fistula.

CLASSIFICATION

Table 70-4 Classification System Based on the Location, Size, and Cause of

Rectovaginal Fistula

Management

Spontaneous healing of rectovaginal fistulas may occur in some small fistulas that are secondary to

obstetrical trauma. In these patients, it is important to wait 3 to 6 months before considering surgical

repair, as this will allow resolution of any inflammation. Nonoperative healing is much less likely to

occur in patients with fistulas secondary to inflammatory bowel disease or radiation. In patients with

small fistulas and minimal symptoms, medical treatment with bulk agents such as fiber may be

sufficient in controlling symptoms.

Treatment of low rectovaginal or anovaginal fistulas may be accomplished by endorectal

advancement flap, vaginal advancement flap, or perineal procedures. Advancement flap is typically the

initial procedure in patients without symptoms of incontinence. Most colorectal surgeons prefer to

perform an advancement flap transanally rather than vaginally as the repair is to the high-pressure side.

After the fistula site in the rectum is excised and closed, a rectal flap consisting of mucosa, submucosa,

and a portion of the internal sphincter muscle is advanced to cover the opening in the rectal wall (Fig.

70-21). The opening in the vagina may be left open to drain. Success rates of endorectal advancement

flaps for simple low rectovaginal fistulas are as high as 83%.23

If a low rectovaginal fistula is associated with incontinence secondary to a defect in the anal

sphincter, repair with an overlapping sphincter repair has been shown to have good results. Using this

technique, an incision is made over the perineal body, and the plane between the rectum and vagina is

developed. The cut ends of the anal sphincter are identified and mobilized. The fistula tract is excised

and closed, and the ends of the sphincter muscle are reapproximated in an overlapping fashion. Patients

with no evidence of sphincter defect who have failed endorectal advancement flap may be candidates

for closure with an interposition graft. This involves closure of the fistula and placement of wellvascularized tissue between the rectum and vagina. The bulbocavernosus muscle (Martius flap) and

gracilis muscle are the most commonly used muscle flaps. These latter procedures are usually performed

1867

after a stoma has been created. The stoma is closed after healing has been documented by both rectal

and vaginal contrast studies and examination under anesthesia.

Rectovaginal fistulas located higher in rectum often require a transabdominal repair. Simple fistulas

with healthy surrounding tissue may sometimes be repaired by mobilization of the rectovaginal septum,

division of the fistula, and layered closure of the rectal defect. Most cases, particularly larger fistulas

and/or fistulas associated with Crohn’s disease or radiation, will require resection of the rectum to

below the site of the fistula as a low anterior resection with coloanal anastomosis. It may be useful in

these cases to also place healthy tissue such as omentum or muscle between the rectum and vagina to

prevent recurrent fistula. While patients with simple rectovaginal fistulas do not typically require fecal

diversion, those with complex fistulas will often require creation of a colostomy in conjunction with

surgical repair. Elderly patients or patients with severe Crohn disease may be better served by a

permanent colostomy.

Pilonidal Disease

Pilonidal disease refers to a subcutaneous infection occurring in the midline of the sacrococcygeal area,

the gluteal cleft. Pilonidal disease typically presents in young patients, occurs more frequently in men

than women, and is more prevalent in hirsute individuals. The exact etiology of pilonidal disease is

unknown, however it is believed to be related to hair. Pilonidal abscess or sinuses develop either from

an infection within hair follicles in the area, or from a foreign-body reaction to hairs that become

embedded in the skin.

Diagnosis

The presenting symptoms in many patients with pilonidal abscess are pain, swelling, and erythema near

the top of the gluteal cleft. A pilonidal sinus occurs following spontaneous or surgical drainage of a

pilonidal abscess, and present as a nonhealing wound or chronic drainage from the area. Early in the

development, patients may complain of pain while sitting, and may have only mild cellulitis. A painful

fluctuant mass can often easily be seen in patients with acute abscess. Chronic pilonidal sinuses can be

visualized in the intergluteal fold. The majority of these tracts run cephalad, however occasionally a

tract may run toward the anus; in these patients, it is important to differentiate pilonidal disease from

hidradenitis suppurativa and anal fistula. Careful examination can demonstrate an opening or openings

in the midline referred to as “pits,” and likely represent either ruptured hair follicles or the site at which

a hair shaft penetrates the skin.

Treatment

Incision and drainage is the treatment of choice for an acute pilonidal abscess. This can typically be

done in the office with the use of local anesthesia, although rarely may require drainage in the

operating room. A longitudinal or elliptical incision is made over the abscess, and any hair within the

cavity is removed. Patients are instructed to clean the wound regularly and to cover the wound. Packing

is not necessary. Antibiotics are not indicated, unless there is significant associated cellulitis.

Chronic pilonidal sinuses have been treated in numerous ways, however no one specific treatment has

proved completely satisfactory. Nonoperative treatments that have been suggested include shaving or

laser hair removal of the area surrounding the sinus until healing has occurred, although the efficacy of

this strategy is unknown. The most common surgical treatments include wide local excision, excision

with flap closure, or specialized procedures such as the Bascom procedure.

Wide local excision incorporates removal of the pilonidal sinus, any associated pits, as well as some

normal surrounding tissue. The wound may be left open to heal by secondary intention, or may be

primarily closed. Patients whose wounds are left open often require intensive wound care with wet-todry dressings and gentle debridement of devitalized tissue and exudates, and complete healing may take

several months. In an effort to reduce wound healing times, the edges of the wound may be

“marsupialized” by suturing the wound edges to the base. As the pilonidal sinus may be chronically

infected, postoperative infection is a concern in patients with primary closure. In a randomized trial,

patients who underwent primary closure had significantly higher rates of postoperative infection and

recurrence when compared with those patients whose wounds were left open.24

1868

 

Figure 70-19. Goodsall’s rule for anal fistula.

Management

Options in the surgical treatment of an anal fistula include fistulotomy, cutting seton, fibrin glue,

collagen plug, ligation of the intersphincteric fistula tract (LIFT), and advancement flaps. Specific

treatment is dictated by the path of the fistula and the amount of sphincter complex that is involved in

the tract. Any division of the sphincter muscle during treatment of a fistula carries with it a risk of

impaired continence. Patients at higher risk of incontinence include those with pre-existing impaired

continence (elderly patients and women with a history of episiotomy) and patients with chronically

loose stools (colitis and Crohn’s disease). The location of the fistula is also important; the sphincter

complex is shorter anteriorly in women, and division of muscle here is particularly risky.

Simple submucosal, intersphincteric, and low transsphincteric fistulas may be managed with

fistulotomy with very low risk of postoperative incontinence. Under regional or general anesthesia, the

patient is placed in the prone jack-knife position. A fistula probe is inserted from the external opening to

identify the internal opening at the dentate line. If there is no significant muscle overlying the probe,

the tissue is incised and any granulation tissue is curetted. The wound is left open to heal by secondary

intention, or the wound may be marsupialized by suturing the wound edges to the tract.

Fistulas that involve a significant portion of the sphincter muscle (high transsphincteric and

suprasphincteric fistulas) are better managed in a staged fashion with the use of a seton. A seton is a

suture or vessel loop that is passed through the fistula tract and is tied to itself to form a ring between

the internal and external openings. The purpose of this is to facilitate drainage of the fistula and

promote wound contracture. Setons may be used as a bridge to a more definitive procedure, or may be

used in a “cutting” fashion. A cutting seton is tightened at regular intervals, gradually cutting through

the sphincter muscle. In theory, this leads to fibrosis of the sphincter muscle rather than a retracted

defect. This may be continued until the fistula has completely resolved, or a staged fistulotomy may be

performed to divide the remaining sphincter muscle.

In an effort to minimize postoperative incontinence, fibrin glue and collagen plugs have been used in

the treatment of anal fistulas. The mere existence of this plethora of therapeutic alternatives attests to

the lack of satisfactory efficacy with all of them. Fibrin glue is made of a combination of fibrinogen,

thrombin, and calcium. Injection of this into the fistula tract is thought to induce clot formation and

promote the growth of collagen to close the fistula. Short-term success rates have been reported as high

as 70%, however late recurrences despite initial healing are common.16 Fistula plugs made of porcine

submucosal collagen inserted into the fistula tract are intended to provide a scaffold for the growth of

fibroblasts to heal the fistula. Long-term healing with fistula plugs has also been disappointing, with

success rates of only 30%,17 however, success rates may be higher in long fistula tracts.

LIFT is a surgical technique that avoids division of the sphincter complex. With the patient in the

prone jack-knife position, a probe is passed through the fistula tract. An incision is then made in the

intersphincteric groove directly overlying the probe, and plane between the two muscles is dissected.

The fistula tract is then divided and ligated between the internal and external sphincter muscles. Success

with this procedure has been reported as high as 88%.18 If the LIFT procedure fails, the fistula often

recurs in the intersphincteric plane, thereby allowing treatment with a fistulotomy.

The use of endorectal advancement flaps has been advocated for high transsphincteric and

suprasphincteric fistulas, fistulas associated with inflammatory bowel disease, fistulas in patients who

have failed other treatments, and anterior fistulas in female patients. In this procedure, the fistula tract

is either cored out or curetted, and the internal opening is identified and excised. A full-thickness flap of

rectal mucosa and submucosa is raised and advanced, typically 1 cm below the level of the internal

1865

opening. It is important to maintain adequate blood supply by creating a flap, the base of which is twice

the width of the apex. Successful healing following an endorectal advancement flap has been reported in

as high as 90% of patients, although much lower in patients with Crohn’s disease and/or receiving

steroids.19

Anal Fistula Associated with Crohn’s Disease

Treatment of anal fistulas in patients with Crohn’s disease can be particularly challenging. Surgical

treatment of these fistulas is associated with poor wound healing and the risk of sphincter injury.

Medical treatment of the underlying Crohn’s disease is therefore extremely important in improving the

chance of fistula healing. Antibiotics such as ciprofloxacin and metronidazole have been shown useful; 8

weeks of oral metronidazole has reportedly eliminated drainage, erythema, and induration in up to 80%

of patients.20 Treatment with azathioprine and methotrexate have been shown to have little impact on

fistula healing. Infliximab, a monoclonal antibody against tumor necrosis factor-α, has been shown to be

effective in Crohn’s anal fistulas. Treatment with infliximab alone has been shown to reduce the number

of draining fistulas by half in 62% of Patients with Crohn’s disease (compared with only 26% of patients

treated with placebo).21 When combined with surgical intervention, fistulas in patients treated with

infliximab may heal faster than those treated with surgery alone.22

Surgical intervention in patients with Crohn’s anal fistulas should be conservative and limited initially

to adequate drainage with liberal use of draining setons. Although fistulotomy for subcutaneous fistulas

may be considered, active Crohn’s disease within the rectum is associated with poor outcomes. Due to

the high likelihood of recurrence or the development of additional fistulas, any division of the sphincter

muscle should be avoided. Once any infection has been drained and the underlying Crohn’s disease has

been optimally controlled with medication, repair with either an endorectal advancement flap or LIFT

may be an option. In rare cases of Crohn’s anal fistulas, fecal diversion with a stoma or proctectomy

may be warranted.

Rectovaginal Fistula

A rectovaginal fistula is a communication between the anterior wall of the anal canal or rectum and the

posterior wall of the vagina. Obstetrical injury is the most frequent cause of acquired rectovaginal

fistulas, however trauma, infection, and radiation may also result in their development (Table 70-3).

Rectovaginal fistulas can be classified according to their location (Fig. 70-20). In low fistulas, the rectal

opening is at or below the dentate line; in high fistulas, the vaginal opening is at or near the cervix. A

second classification system is based on the location, size, and cause of the fistula (Table 70-4).

Figure 70-20. Rectovaginal fistula classified by location. Fistulas are low when located at or just cephalad to the dentate line, high

when near the cervix, and mid when located in between.

ETIOLOGY

Table 70-3 Causes of Rectovaginal Fistula

1866

 

has been reported to be as high as 47%.13

In patients who are at high risk of experiencing postoperative incontinence, an alternative approach

may be the use of an advancement flap. This procedure involves excision of the fissure, surrounding scar

tissue, and any skin tags. A variety of flap configurations including V-Y, Y-V, house, and others have

been employed to help close the defect. Healing rates following fissurectomy and advancement flap are

comparable to those following sphincterotomy.

Anorectal Abscess

The vast majority of anorectal abscesses result from infection of the glands that empty into the anal

crypts within the anal canal at the level of the dentate line. Other causes of anorectal abscess include

inflammatory bowel disease, trauma including iatrogenic (usually gynecologic or surgical) trauma,

infections such as tuberculosis and actinomycosis, and malignancy. Since these glands lie within the

intersphincteric space, blockage of a duct results first in an intersphincteric abscess which can then

spread to the surrounding spaces (Fig. 70-16). The most commonly encountered anorectal abscess occurs

in the perianal area, followed in frequency by ischioanal, intersphincteric, and supralevator (Fig. 70-17).

Figure 70-16. Pathways of infection start in the intersphincteric space (A) and then spread to perianal spaces, forming perianal

abscesses (B).

Figure 70-17. Classification of anorectal abscess.

Clinical Manifestations

Most patients with anal abscess present with pain. In patients with perianal or ischioanal abscesses, pain

may be accompanied by swelling and erythema. Conversely, patients with supralevator abscess are less

likely to present with swelling and may have accompanying fever. Patients with severe rectal pain may

also develop urinary retention.

Management

Treatment of anorectal abscesses requires incision and drainage; antibiotics alone are ineffective and

may allow the suppurative process to progress to a more complicated abscess. The use of antibiotics in

conjunction with drainage may be considered in the patient with concomitant cellulitis or in

immunocompromised patients.

Most patients with perianal abscesses can be treated in an outpatient setting under local anesthesia.

An elliptical or cruciate incision is made over the most tender area or area of fluctuance, and the skin

edges are trimmed to prevent early closure of the wound, and all loculations are drained. Routine

culture of the drainage is not recommended. Packing is also not necessary; rather, patients are

instructed to soak the area in warm water and simply keep the wound covered with gauze.

Patients with superficial ischioanal abscesses may be treated in a similar fashion, however patients

1862

with deeper or more complex abscesses typically require an examination under anesthesia with drainage

in the operating room. Less commonly, patients may present with bilateral ischioanal abscess, a

condition referred to as a horseshoe abscess. These infections typically begin in the deep postanal space,

which spread to both ischioanal areas. Treatment requires that the deep postanal space be drained,

which is accomplished by making a longitudinal incision in the skin between the tip of the coccyx and

the anus and exposing the anococcygeal ligament. The ligament is then divided and the deep postanal

space drained; counter incisions are then made overlying the ischioanal areas as well.

Patients with intersphincteric abscess often present with severe anorectal pain, however no indurated

or fluctuant area is evident. These patients also typically require an examination under anesthesia. In

the operating room, an intersphincteric abscess can be diagnosed by palpation of a protrusion into the

anal canal or aspiration of purulent fluid from the intersphincteric space. Drainage is performed by

dividing a portion of the internal sphincter muscle along the length of the abscess cavity.

Supralevator abscesses are less common and can often be difficult to diagnose. Because the location of

the abscess is adjacent to the abdominal cavity, patients may present with abdominal or pelvic pain.

Digital examination may demonstrate induration or a tender mass located in the distal rectum above the

level of the anorectal ring. The etiology of a supralevator abscess dictates its management. These

abscesses may result as an extension of an intersphincteric abscess, extension of an ischioanal abscess, or

may result from an intra-abdominal abscess from perforated diverticulitis, appendicitis, or Crohn’s

disease. Supralevator abscess secondary to extension from an ischioanal abscess should be drained

through the ischioanal area. Supralevator abscess secondary to extension from an intersphincteric

abscess should be drained into the rectum, as drainage through the ischioanal area may result in a

complex suprasphincteric fistula. Percutaneous drainage may be an option in patients with supralevator

abscess secondary to an intra-abdominal source.

Rarely, anorectal abscess can result in necrotizing infection and death, a condition referred to as

Fournier gangrene. This situation may result from a delay in diagnosis and management of an anorectal

abscess, infection with a highly virulent organism, or may be due to patient factors such as diabetes or

compromised immune function. The infection superficially spreads around the perineum, causing

necrosis of the skin and underlying muscle and fascia. Treatment includes empiric broad-spectrum

intravenous antibiotics and prompt surgical debridement of the necrotic tissue until healthy tissue is

encountered.

Anal Fistula

6 A fistula is generally defined as an abnormal communication between two epithelialized surfaces. Anal

fistula (or fistula-in-ano) represents a communication between the anorectal canal and the perianal skin

as the result from spontaneous or surgical drainage of an anorectal abscess. The incidence of fistulas

following abscess drainage ranges from 5% to 83% in the medical literature, but is generally thought to

occur in one-quarter to one-third of patients.14 Anal fistulas may also occur in up to 30% of patients

with Crohn’s disease.

Classification

Treatment of anal fistulas is in part dictated by the type of fistula. Fistulas are classified by their

relation to the anal sphincter complex (Fig. 70-18).15 The most common type is the intersphincteric

fistula, followed by transsphincteric, suprasphincteric, and extrasphincteric (Box 70-1).

Clinical Manifestations

The majority of patients with anal fistula have a history of previous anorectal abscess which either

spontaneously drained or were surgically incised. Recurrence of anorectal abscess in the same location

often indicates the presence of an underlying fistula. Patients complain of drainage, intermittent

swelling, pain with defecation, and occasional bleeding. Physical examination often demonstrates an

external opening on the perianal skin with granulation tissue. Drainage of fecal, purulent, or

serosanguinous drainage may be evident or can be elicited with digital rectal examination or

compression of the fistula tract.

1863

Figure 70-18. The four main anatomic types of fistula.

Box 70-1 Classification of Anal Fistulas

Intersphincteric Fistula. The tract of the fistula lies within the intersphincteric space and the external

opening lies close to the anal verge. These fistulas are the most common, and typically result following

a perianal abscess.

Transsphincteric Fistula. The fistula tract begins in the intersphincteric space and then traverses

through a portion of the external sphincter muscle. The external opening typically lies over the

ischioanal fossa.

Suprasphincteric Fistula. The fistula tract begins in the intersphincteric space and then passes upward

above the external sphincter and then perforates the levator ani muscles to drain through the ischioanal

fossa.

Extrasphincteric Fistula. The fistula tract begins in the distal rectum rather than the anal canal and

perforates the levator ani muscles to drain through the ischioanal fossa. These fistulas are rare and

develop typically from Crohn’s disease or rectal trauma.

Hidradenitis suppurativa may present in a similar fashion to anal fistula, with multiple openings on

the perianal skin with surrounding induration. Unlike anal fistulas, however, any tracks associated with

hidradenitis are superficial and do not communicate with the anal canal. A pilonidal sinus with perianal

extension may also mimic an anal fistula, but in this situation the tract moves superiorly, away from the

anal canal. Much less commonly actinomycosis can mimic a complex fistula.

Examination under anesthesia is recommended in order to treat any undrained abscess and to identify

the internal opening. Flexible sigmoidoscopy may also be performed to evaluate for concomitant

inflammatory bowel disease or malignancy. Under anoscopic guidance, a fistula probe can be inserted

into the external opening through the fistula tract to determine the location of the internal opening.

Goodsall rule states that if an imaginary line is drawn transversely across the anus, an external fistula

opening seen posterior to this line will originate from an internal opening in the posterior midline,

whereas an opening anterior to this line will originate from the closest anal crypt (Fig. 70-19).

Locating the internal opening is not always possible with a fistula probe, and in this situation other

diagnostic maneuvers may be necessary. Injection of the external opening with hydrogen peroxide

either with or without the use of endoanal ultrasound may help identify smaller fistulas. For patients

with multiple or complex fistulas, fistulography with a water soluble contrast and fluoroscopy has been

described, although the use of magnetic resonance imaging has largely replaced this.

1864

 

severe constipation. Patients typically present with a painful, tender mass in the perianal area.

Frequently, the thrombosis will lead to necrosis of the overlying skin and patients will complain of

bleeding that is independent of bowel movements.

The management of thrombosed external hemorrhoids depends on when in the course of the disease

the patient presents. The pain associated with this condition typically peaks within 48 hours and

normally begins to subside after 4 days. If left untreated, the clot in the thrombosed vessels will

dissolve within several weeks. Following resolution, large thrombosed hemorrhoids may remain as skin

tags.

Because this condition is self-limiting, management is typically conservative and includes pain control

with a mild analgesic, warm sitz baths, and a bulk-producing agent (usually psyllium fiber). If the

patient presents within the first 48 hours, the procedure of choice is excision of the entire thrombosed

hemorrhoid (Fig. 70-14). This procedure may be performed in the office or emergency room with the

use of a local anesthetic. Using scissors, the thrombosed hemorrhoid is excised with the underlying vein;

it is important to excise the entire thrombus in order to prevent recurrence. The skin edges are then

reapproximated with the use of an absorbable suture or may be left open.

Incarcerated Hemorrhoids. Rarely, patients will present with prolapsed fourth-degree hemorrhoids

which have become incarcerated. While internal hemorrhoids do not typically cause pain, patients with

incarcerated hemorrhoids often have severe pain and may develop urinary retention. Edematous

prolapsed hemorrhoids are seen, often in combination with large external components as well.

Traditionally this condition has been treated with an urgent or emergent hemorrhoidectomy, however

there is concern that leaving inadequate anoderm between the excision sites may lead to postoperative

stenosis. Instead, patients may be treated with oral or intravenous pain medications and stool softeners,

allowing the edema to resolve and the prolapse to reduce. These patients should then be offered an

elective hemorrhoidectomy to prevent recurrence.

Anal Fissure

5 Anal fissure is an ulcer-like tear in the mucosal lining of the anal canal distal to the dentate line.

Although more commonly found in younger patients, fissures can occur at any age and equally afflict

male and females. Fissures can be classified as acute or chronic, and as primary or secondary. Primary

anal fissures are almost always located in the posterior or anterior midline, and are not associated with

any underlying disease. Secondary fissures may occur in a lateral position, and should alert the clinician

to the possibility of Crohn’s disease, HIV infection, tuberculosis, syphilis, or a hematologic malignancy.

Anal fissures that have been present for longer than 6 weeks duration are arbitrarily classified as

chronic.

The exact etiology is not known, however several mechanisms are thought to lead to the development

of anal fissure. Trauma to the anal canal appears to be the initiating factor, most commonly as the result

of passage of hard stool, as a low fiber diet seems to be associated with the development of anal

fissure.8 Fissure may also occur following prolonged bouts of diarrhea, or following childbirth, most

likely the result of forces from the fetus on the anal canal.

Hypertonicity of the IAS with resultant ischemia has also been implicated in development of chronic

anal fissure. Ninety percent of fissures are found in the posterior midline of the anal canal, where

Doppler flow studies and cadaver vascular injections have demonstrated relatively low perfusion.

Studies have shown that when compared with normal subjects, patients with chronic anal fissure have

higher resting pressure of the IAS. If the pressure within the anal sphincter approaches or exceeds the

intra-arterial pressure of the inferior rectal artery, this may lead to relative ischemia and the

development of an ischemic ulcer. This theory is strengthened by the fact that reduction of anal pressure

following sphincterotomy improves blood flow to the anal canal, thereby promoting healing of the

fissure.9

Clinical Manifestations

Anal fissure typically presents with pain during defecation and rectal bleeding. Patients often describe

the pain as knifelike or as a tearing sensation, which may persist for several hours or longer after bowel

movements. Rectal bleeding is typically bright red, and is separate from the stool and often seen only

after wiping. Constipation is a common complaint of patients with anal fissure, and is frequently both a

precipitating event and a result of patients’ fear of a painful bowel movement.

The diagnosis of anal fissure can be made on physical examination by gently spreading the buttocks

1860

apart to visualize the anal verge. Fissures will appear as a longitudinal or oval-shaped tear and may be

associated with a sentinel pile, a protruding skin tag at the distal end of the fissure. Fibers of the IAS

may be visible in chronic anal fissures. Once a diagnosis of fissure has been made, digital examination

or anoscopy adds little other than increased pain for the patient, and should therefore be avoided.

Management

Medical Management. Symptomatic relief of anal pain from fissures may be obtained by warm sitz

baths two to three times per day. Topical anesthetics or anti-inflammatory ointments may also be of

benefit. The majority of patients with acute anal fissure will respond to conservative measures including

sitz baths and the addition of a bulking agent such as psyllium fiber. Acute anal fissures often heal

within 6 weeks, although the recurrence rate approaches 20%.10

As anal fissure is associated with hypertonicity of the anal sphincter, medical therapy is directed as

decreasing resting anal pressures. Nitric oxide is a potent neurotransmitter that induces relaxation of the

IAS. Application of 0.2% nitroglycerin ointment twice daily has been shown to induce healing in as

many as 85% of patients,11 however, patient compliance is often low due to nitrate-induced headache.

Calcium-channel blockers have also been shown to reduce anal pressures. Topical diltiazem or nifedipine

has been shown to have healing rates equivalent or superior to nitroglycerin12 without the associated

side effects. Unfortunately, recurrence rates with all of these therapies approach 50% in many series.

Botulinum toxin is an endopeptidase that blocks acetylcholine release at the neuromuscular junction,

resulting in temporary paralysis of skeletal muscle. Although its exact mechanism of action in smooth

muscle is not understood, injection of the toxin also results in relaxation of the IAS. The technique, dose,

and success rates have widely varied in the literature, however some authors have reported success in

60% to 80% of patients. The most common side effect is temporary anal incontinence, typically only to

flatus. The use of botulinum toxin may be an option in patients who have failed topical treatment, but

who may be at a high risk of complications from surgery.

Figure 70-15. Lateral internal sphincterotomy (open method). A: The fissure in the midline is left alone. B: With a speculum used

to expose the left lateral quadrant, an incision is made through the subcutaneous tissue to expose both the subcutaneous external

sphincter and the internal sphincter. C: The internal sphincter is incised to its full thickness; care is taken not to cut the external

sphincter. D: The wound is closed.

Surgical Management. In patients with chronic or recurrent fissures that fail to heal with medical

management, surgical intervention is warranted. The most commonly performed procedure is the lateral

internal sphincterotomy, which is an outpatient procedure that may be performed under local, spinal, or

general anesthesia. When performed in an open fashion, an incision is made overlying the anal sphincter

complex in the lateral position away from the fissure (Fig. 70-15). The internal sphincter is identified,

and a portion of the muscle is cut typically extending cephalad to the level of the apex of the fissure.

The wound is then closed with an absorbable suture. The procedure can also be performed in a closed

fashion, where the scalpel is inserted into the intersphincteric groove, turned horizontally, and used to

cut the internal sphincter as the anal canal is stretched open with a speculum. Healing rates following

sphincterotomy range from 90% to 100%, however, impairment of continence following the procedure

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Depending on the severity of the symptoms and the grade of the hemorrhoids, patients may be treated

through nonoperative measures, office-based procedures, or operative therapy.

Nonoperative Management

As constipation and excessive straining during defecation are often the underlying causes of

hemorrhoids, symptoms can be reduced or eliminated in many patients by altering their dietary intake

and lifestyle. This goal is often achieved in patients with grade 1 or 2 hemorrhoids by increasing fluid

and fiber in the diet, increasing physical exercise, and adding supplemental fiber. Fiber helps to add

moisture to the stool to decrease constipation, and the addition of fiber has been shown in a doubleblind, placebo controlled trial to be effective in reducing hemorrhoidal bleeding.3 Warm sitz baths,

suppositories, and topical creams or ointments may also help to alleviate symptoms, however they often

do not provide a long-term solution.

2 In patients with first-, second-, or third-degree internal hemorrhoids with no symptomatic external

disease who fail conservative therapy, office-based therapies such as rubber band ligation,

sclerotherapy, or photocoagulation may be an option. Rubber band ligation can be performed through

an anoscope in the office without the use of anesthesia. The band is placed around the hemorrhoid

above the dentate line, causing localized ischemia of the intervening tissue (Fig. 70-11). More than one

hemorrhoid may be banded at one time, however multiple synchronous bands may lead to increased

pain. A portion of the hemorrhoid and the rubber band are passed during defecation 48 to 72 hours

following application. Fibrosis that occurs at the site of the banding causes fixation of the remaining

hemorrhoidal tissue, which helps to prevent further prolapse and bleeding. Relief of symptoms may be

achieved in up to 80% of patients who undergo banding, however recurrence rates as high as 30% have

been reported.4 Complications of hemorrhoidal banding include severe pain requiring removal of the

band, increased bleeding, and thrombosis of the hemorrhoids. Severe perianal sepsis is a rare

complication, and should be suspected in any patient who develops worsening pain, fever, or the

inability to void.

Figure 70-11. Rubber band ligation of an internal hemorrhoid.

Sclerotherapy involves the injection of a sclerosing agent into the submucosa that leads to fibrosis of

the surrounding tissue. Many different injection agents have been described, however phenol is most

commonly used. Injection is performed through an anoscope, and may be an option for symptomatic

hemorrhoids that are too small to band. It is important not to inject the sclerosant directly into the

hemorrhoids or thrombosis may ensue. Infrared photocoagulation causes thrombosis and tissue

destruction within the anal canal. The probe is applied just proximal to the internal hemorrhoids

through an anoscope. Results with both sclerotherapy and photocoagulation are varied and tend to be

temporary only.

Operative Treatment

3 Excisional hemorrhoidectomy should be considered in patients who fail conservative or office-based

procedures, who have combined internal and external hemorrhoids, who have hemorrhoids that require

manual reduction (grade 3), or who have associated pathology such as ulceration, fissures, or fistulas.

1856

Hemorrhoidectomy is typically an outpatient procedure, and in most cases local or regional (spinal)

anesthesia may be used, however general anesthesia may also be employed. The patient is placed in the

prone jack-knife position with the buttocks taped apart. An elliptical incision is made, beginning on the

anoderm to remove any external component of the hemorrhoid, and is continued to the base of the

hemorrhoid above the dentate line (Fig. 70-12). It is critical to preserve the underlying IAS muscle, as

damage to the IAS may lead to postoperative incontinence. One, two, or three hemorrhoidal bundles

may be excised at once, however it is also critical to ensure that normal anoderm is left between the

excision sites; failure to preserve this anoderm may lead to postoperative anal stenosis. The dissection

may be undertaken with the use of a scalpel, scissors, electrocautery, or controlled electrical energy

such as ultrasonic shears or a bipolar vessel sealing device. The wound may be left open or, more

commonly, may be closed with absorbable suture.

Excisional hemorrhoidectomy is superior to office-based therapies in achieving complete remission of

hemorrhoidal symptoms, however complications including stenosis and hemorrhage are more common.5

Patients who undergo hemorrhoidectomy are also less likely to require multiple treatments. Surgical

treatment of hemorrhoids can unfortunately also result in significant postoperative pain, and patients

often require narcotic pain medication and may require up to 2 to 4 weeks to recover.

Stapled hemorrhoidopexy, while initially described as a treatment of mucosal prolapse, is also an

option for prolapsing and bleeding hemorrhoids. Also known as the Procedure for Prolapse and

Hemorrhoids (or PPH), this technique involves the removal of a circumferential sleeve of mucosa and

submucosa of the distal rectum and anus. A circular stapler creates an anastomosis which elevates the

anal canal and fixes the anal cushions into their normal anatomic positions. Because the resection is

performed above the level of the dentate line, this technique is advantageous as it may result in less

postoperative pain. It has no effect on external hemorrhoids, and therefore its use is somewhat limited.

Stapled hemorrhoidopexy is begun by placing a purse string suture in the mucosa and submucosa

approximately 4 cm above the dentate line, incorporating all the redundant tissue circumferentially

(Fig. 70-13). Correct placement of this suture is critical to prevent placement of the stapler too close to

the dentate line, which can result in chronic pain. The anvil of a specialized circular stapler is then

passed above the purse string, and the suture is used to pull the mucosa and submucosa into the stapler

head. The stapler is then fired, which excises the sleeve of tissue and creates the anastomosis.

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Figure 70-12. Technique of internal closed hemorrhoidectomy. A: Exposure of hemorrhoid with elliptic excision starting at

perianal skin and extending to anorectal ring. B: Submucosal hemorrhoidal plexus dissected from the internal sphincter, anoderm,

and mucosa. C: Wound closed with a running suture.

A meta-analysis of prospective randomized studies demonstrated that when compared with excisional

hemorrhoidectomy, stapled hemorrhoidopexy offers some short-term benefits including less

postoperative pain and earlier return to normal activity.6 In long-term follow-up, however, stapled

hemorrhoidopexy has been associated with a higher rate of recurrent symptoms. Although PPH has been

associated with several unique complications (rectovaginal fistula, staple line bleeding, and chronic

pain), the overall rates of postoperative complications did not differ between the procedures.

Doppler-guided transanal hemorrhoid devascularization involves suture ligation of each hemorrhoidal

column with resection of the hemorrhoid. A specific anoscope that includes a Doppler probe is used to

identify the signal of the vessel feeding each hemorrhoidal column, typically above or just at the top of

the column. Once the vessel is identified, it is then ligated with a suture and the Doppler probe is again

used to confirm the disappearance of the signal. Typically the hemorrhoidal column is then also

oversewn with this suture. The purported benefit of this procedure is that because the ligation occurs

above the dentate line, postoperative pain should be significantly lower than with an excisional

hemorrhoidectomy. Long-term results with this procedure are limited, however some authors have

reported effectiveness in 90%.7

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Figure 70-13. Stapled circular hemorrhoidectomy or procedure for prolapsing hemorrhoids. A: A purse-string suture is placed in

the rectal mucosa proximal to hemorrhoids. B: The stapler anvil is placed proximal to the purse string, and the purse string is tied

down to draw hemorrhoidal tissue into the staple line. C: The stapler is fired and removed, excising a sleeve of distal rectal tissue

and creating a stapled anastomosis.

Figure 70-14. A, B: Excision of the entire thrombosed hemorrhoid.

Special Hemorrhoid Situations

Thrombosed External Hemorrhoids. Thrombosed external hemorrhoids are a relatively common

complication of hemorrhoidal disease. The exact etiology is unknown, however their presence is often

associated with physical exertion or straining (heavy exercise, moving or lifting furniture) or a bout of

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Figure 70-8. Lymphatic drainage of the anal canal.

Defecation involves both voluntary and involuntary mechanisms. If the call to defecate is answered,

either the sitting or squatting position is assumed, thereby helping to straighten the anorectal angle.

Straining by increasing the intra-abdominal pressure leads to a reflex relaxation of the puborectal

muscle which further opens the anorectal angle and shortens the anal canal. Both the internal and

external anal sphincters relax, the pelvic floor descends, and a funneling occurs, allowing the rectal

contents to be expelled. After completion of rectal evacuation, a “closing reflex” occurs, where transient

contraction of the external anal sphincter and puborectalis help to restore tonic contracture of the IAS

(Fig. 70-10).

Diagnostic Evaluation of the Anus

Accurate diagnosis of anorectal disorders requires a detailed history and physical examination, and may

include both anatomical and functional testing. Underlying illness or mediation use may present with

symptoms in the anal area, and it is important to know about travel history and sexual activity. The

most common presenting symptoms of anorectal disease are pain, bleeding, discharge, and change in

bowel habits.

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Figure 70-9. Sympathetic and parasympathetic nerve supply of the rectum.

Bleeding may be seen as the result of an anal condition, or may represent bleeding from a more

proximal source in the gastrointestinal system. Obtaining a history of the type and frequency of

bleeding may help in making the diagnosis. Bleeding that is bright red and is not mixed with the stool

may indicate an anal source, while blood in the form of clots or melena is more indicative of a colonic

source. Even in patients with rectal bleeding in whom an anal disorder is found, it is important to

consider colonoscopic evaluation of the colon to exclude other sources, particularly in patients who are

at increased risk for cancer.

Anal pain associated with swelling that may or may not be related to defecation may be indicative of

a thrombosed external hemorrhoid or an abscess. Pain that occurs during or immediately after

defecation is often secondary to an anal fissure. Episodic pain (unrelated to bowel movements) that lasts

for a short duration may be due to a condition known as proctalgia fugax or levator ani syndrome.

Physical examination of the anus should include a visual inspection of the perianal area as well as a

digital examination (Table 70-1). Patients can be examined in either the left lateral decubitus or prone

jack-knife position. Simple explanation and reassurance about the planned examination helps to ensure

cooperation of the patient and minimize discomfort. Inspection of the anus may demonstrate skin tags

or external hemorrhoids, fissures, scars, or excoriation of the skin. Straining during inspection may help

to demonstrate rectal prolapse or perineal descent. Digital examination with a well-lubricated gloved

index finger will give information including the tone of the anal sphincters as well identification of any

rectal masses.

More detailed evaluation of the anus includes anoscopy, rigid or flexible proctosigmoidoscopy, and

ultrasonography, as well as physiologic tests such as anal manometry, electromyography, pudendal

nerve assessment, and defecography. Use of these tests for specific conditions will be discussed later in

the chapter.

BENIGN ANORECTAL DISEASE

Hemorrhoids

Hemorrhoids are cushions of vascular tissue found in the anal canal found from birth. Histologically,

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this tissue contains vascular structures whose walls do not contain muscle, and are therefore considered

sinusoids instead of veins. The number and location of hemorrhoids may vary, however most commonly

there are three pillars located in the left lateral, right anterior, and right posterior quadrants.

The term “hemorrhoids” typically refers to clinical situations where these vascular cushions are

abnormal and cause symptoms. External hemorrhoids are defined by their location distal to the dentate

line and are covered with squamous epithelium. Although these may swell and make anal hygiene

difficult, they may also cause pain secondary to formation of clot within the sinusoid (thrombosed

external hemorrhoids). Internal hemorrhoids are located proximal to the dentate line and are covered

by transitional epithelium. As there are no somatic nerve endings here, internal hemorrhoids do not

cause pain, but may present with bleeding or downward displacement of the cushion during defecation

(referred to as prolapse). Hemorrhoids are classified according to the degree of prolapse (Table 70-2).

Figure 70-10. Mechanics of defecation.

Clinical Manifestations

1 Although patients may present with complaints of “hemorrhoids,” many of the symptoms of pain,

itching, burning, and swelling may not be related to hemorrhoidal disease, instead being due to anal

fissure, prolapsed anal papilla, or pruritus ani. The most common symptoms of internal hemorrhoids are

bleeding with bowel movements and prolapse of tissue with defecation. Patients will often describe

blood dripping into the bowl and staining the toilet water bright red. After passing a firm stool or a

forceful straining, bleeding may continue with bowel movements for several days and then resolve for a

variable length of time. It is rare that hemorrhoidal bleeding is severe enough to result in anemia.

Patients may also complain of a sensation of incomplete evacuation of the rectum, and in chronic cases

of prolapse may complain of mucous drainage or incontinence.

Physical examination should include inspection both at rest and during straining, digital rectal

examination, and anoscopy. Evaluation may be performed in either the left lateral or prone jack-knife

position. Inspection will help to exclude other pathology, including anal fissure, external opening of an

anal fistula, and perianal excoriation, as well as to evaluate for the presence of skin tags, external

hemorrhoids, and prolapse. Internal hemorrhoids are soft and cannot be reliable diagnosed with the

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examining finger, however digital rectal examination may help to rule out a low rectal or anal

neoplasm. If prolapse is present, it is possible to reduce the hemorrhoidal tissue during the examination.

Anoscopy provides definitive examination of the anal canal, however this should be avoided in patients

with anal pain due to fissure or abscess. While anoscopy may provide the diagnosis of hemorrhoids or

other intra-anal pathology, patients presenting with rectal bleeding should also undergo assessment of

the large intestine. In young patients, a flexible sigmoidoscopy may be sufficient, however in patients

over the age of 50, those with significant risk factors for polyps or malignancy, or patients with

inflammatory bowel disease, a colonoscopy should be performed.

Table 70-1 The Complete Digital Rectal Examination

CLASSIFICATION

Table 70-2 Hemorrhoids Classification

Treatment

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The Anal Canal and Sphincters

The anal canal is the terminal portion of the intestinal tract, and extends from the rectum for

approximately 4 cm through the pelvic floor musculature to the hair-bearing skin of the anal margin.

The circular smooth muscle layer of the rectum continues distally and thickens to form the internal anal

sphincter (IAS), which extends to approximately 1.5 cm below the dentate line. The internal sphincter is

surrounded by a continuous sheet of striated muscle of the pelvic floor, which is comprised of three

distinct muscles – the puborectalis muscle, the levator ani muscle, and the external anal sphincter (Fig.

70-2). These muscles are critical both in the maintenance of continence and in defecation. The levator

ani muscle is a broad, thin, funnel-shaped muscle that forms the floor of the pelvic cavity (Figs. 70-3

and 70-4). The puborectalis muscle originates on the posterior aspect of the pubic bones and forms a ushaped sling around the anal canal that helps to maintain an acute angle between the rectum and anus.

The external sphincter is an elliptical-shaped muscle that extends from the coccyx (anococcygeal

ligament) around the internal sphincter. The external sphincter extends slightly caudad to the IAS,

thereby forming the intersphincteric groove at the anal verge. The superficial fibers of the external anal

sphincter insert into the skin of the anal verge as the corrugator cutis ani. The perineal body lies at the

central portion of the perineum where the external sphincter, bulbospongiosus, and transverse perineal

muscles meet and separates the anus from the vagina.

The lining of the anal canal contains different types of epithelium at different levels. At the anal

verge, the skin becomes anoderm, a squamous lining without hair. Approximately 2 cm from the anal

verge, the dentate line appears as a comb-like line due to folds in the mucosa. These folds are named

the columns of Morgagni, and typically contain a small pocket or crypt at the inferior end. The mucosa

at this level is a mixture of squamous, transitional, and columnar epithelium; this is referred to as the

anal transition zone. The mucosa of the upper anal canal is lined by columnar epithelium. The internal

hemorrhoidal plexus lies deep to the mucosa within the anal canal.

Figure 70-1. Fascial attachments of the rectum.

Understanding the various types of epithelium within the anal canal is important for the diagnosis of

both benign and malignant conditions of the anus. The histology of tumors of the anal canal is critical to

understanding the typical behavior and management of the disease. Squamous cell lesions that arise at

the anal margin are often treated as skin cancers (wide excision), whereas those arising within the anal

canal are treated with chemoradiation. Adenocarcinomas of the anal canal typically arise from the upper

anus and are treated similar to adenocarcinomas of the distal rectum. Fistulas of the anal canal typically

originate from the crypts at the dentate line, however fistulas associated with Crohn’s disease will often

arise from the columnar epithelium of the upper anal canal, and those associated with hidradenitis will

originate from the mucosa or skin below the dentate line.

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Figure 70-2. Arrangement of the external sphincter muscles.

The rectum and anus receive abundant blood supply from the superior, middle, and inferior rectal

arteries (Fig. 70-5). The superior rectal (hemorrhoidal) artery starts as the terminal branch of the

inferior mesenteric artery, descending posterior to the rectum where it bifurcates to supply the rectum

and upper anal canal. The middle rectal arteries arise from the internal pudendal or inferior gluteal

arteries (branches of the internal iliac artery). The inferior rectal arteries also arise from the internal

pudendal arteries (in Alcock canal) and traverse the ischioanal fossa to supply the anal sphincters and

anal canal. There are multiple communications among these three vessels.

The venous drainage of the anus is via both the portal and system venous systems (Fig. 70-6). The

superior rectal vein drains the rectum and upper anal canal into the portal venous system through the

inferior mesenteric vein. The middle and inferior rectal veins drain into the systemic venous system via

the internal iliac veins. Because of the rich communication between these veins, patients with portal

hypertension may develop porto-systemic shunts resulting in bleeding rectal varices.

Figure 70-3. Anatomy of the anal canal.

Lymphatic drainage of the rectum and anus mirrors the arterial supply (Figs. 70-7 and 70-8). Drainage

from the upper and middle rectum flows to the inferior mesenteric lymph nodes. The lower rectum and

upper anal canal may drain to the inferior mesenteric nodes, or may drain laterally to the internal iliac

nodes. Lymph from the anus below the level of the dentate line typically drains to the inguinal lymph

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nodes, however drainage may also occur to the inferior mesenteric and internal iliac nodes. Clinically

this drainage pattern is important in patients with squamous cell cancers of the anus, as palpation of

enlarged inguinal lymph nodes may signify metastatic disease.

The rectum and urogenital organs are supplied by a vast network of both sympathetic and

parasympathetic nerves (Fig. 70-9). The sympathetic nerves branch from the sympathetic trunk from

the first three segments of the lumbar spinal cord and synapse at the preaortic plexus. Some

postsynaptic nerves innervate the upper rectum, while others travel distally to form the hypogastric

plexus, which extends laterally along the rectum to form the pelvis plexus. The parasympathetic nerves

(nervi erigentes) originate from the second, third, and fourth sacral nerve roots. These nerves then join

the sympathetic nerves in the pelvic plexus to supply both the lower rectum and urogenital organs. This

plexus lies within the lateral attachments of the rectum and along Denonvillers fascia.

Figure 70-4. Muscles of the pelvic floor.

Preservation of both the hypogastric and pelvic plexuses during proctectomy is essential in

maintaining normal sexual function.2 In men, parasympathetic innervation is responsible for erection,

while a complex interaction between sympathetic, parasympathetic, and somatic pathways produces

ejaculation. Injury to the nervi erigentes may result in impotence, while injury to the hypogastric

sympathetic trunks may cause retrograde ejaculation. Injury to the pelvic nerves may also lead to

bladder dysfunction. In women, dysfunction following nerve injury is less well understood, however

some patients do report dyspareunia and decreased lubrication during intercourse following pelvic

surgery.

The IAS receives both sympathetic and parasympathetic nerves, and maintains tonic contraction at

rest. The external anal sphincter is innervated by the inferior rectal branch of the pudendal nerve and

perineal branch of the fourth sacral nerve. The inferior rectal nerve also carries sensory information

from the anal canal. The majority of sensory nerve endings within the anal canal are located distal to

the dentate line, however patients may sense painful stimuli up to 1.5 cm proximal to this area.

Clinically this anatomy is relevant, as external hemorrhoids (below the dentate line) are sensitive to

touch, while internal hemorrhoids (above the dentate line) may often be manipulated (banding, etc.)

without the need for anesthesia. In addition, sensory receptors within the anal canal allow the

discrimination between solid or liquid stool and flatus.

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Figure 70-5. Arterial supply of the rectum and anal canal.

Figure 70-6. Venous drainage of the rectum and anal canal.

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Figure 70-7. Lymphatic drainage of the rectum.

Physiology

The principal function of the anus is the maintenance of continence and regulation of defecation. The

physiology of the defecation and maintenance of continence are complex, and involve both voluntary

and involuntary muscular activities. Continence is also affected by the compliance and tone of the

rectum, the consistency and volume of the stool, the sensation of the anorectum, and the muscular

activity of the pelvic floor muscles. The hemorrhoidal plexus may also contribute to continence by

acting as a “cushion” to keep the anus closed. Alterations of any of these mechanisms of continence may

result in impaired continence.

The primary function of the rectum is to act as a reservoir for stool until it is a socially acceptable

time and place for evacuation. When stool enters the rectum from the colon and the rectum becomes

distended, receptors within the puborectal muscle initiate the rectoanal inhibitory reflex. This distension

leads to simultaneous relaxation of the IAS and contraction of the external anal sphincter, allowing the

stool to descend toward the anal canal. This sphincter response allows for “sampling,” or determination

by the sensory epithelium of the anal canal as to whether the distension is from gas or stool. If

defecation is deferred, the musculature of the rectum relaxes, thereby decreasing the pressure within

the rectum; this is referred to as accommodation.

Continence is maintained by the fact that the pressure within the anal canal is higher than the

pressure within the rectum. This high-pressure zone (between 40 and 70 mm Hg) within the anal canal

is primarily accounted for by the IAS, however the external sphincter and puborectal muscle contribute

as well. Autonomic innervation keeps the internal sphincter under tonic contraction and cannot be

altered by voluntary control. Contraction of the external anal sphincter will often more than double the

intra-anal pressure, however this muscle can typically be contracted voluntarily for only 40- to 60-

second periods. The angle between the anus and rectum also may aid in the maintenance of continence

by creating a flap valve and preventing stool from entering the anus. This anteroposterior angle is

maintained by the contraction of the sling-shaped pubrectalis muscle.

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49. Graham SM, Ballantyne GH. Cecal diverticulitis. A review of the American experience. Dis Colon

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73. Makela J, Vuolio S, Kiviniemi H, et al. Natural history of diverticular disease: when to operate? Dis

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74. Parks TG. Natural history of diverticular disease of the colon. A review of 521 cases. Br Med J

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75. Makela J, Kiviniemi H, Laitinen S. Prevalence of perforated sigmoid diverticulitis is increasing. Dis

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76. Zaidi E, Daly B. CT and clinical features of acute diverticulitis in an urban U.S. population: rising

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78. Nelson RS, Velasco A, Mukesh BN. Management of diverticulitis in younger patients. Dis Colon

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82. Anaya DA, Flum DR. Risk of emergency colectomy and colostomy in patients with diverticular

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1155.

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Chapter 70

Anorectal Disorders

David J. Maron and Steven D. Wexner

Key Points

1 The most common manifestation of internal hemorrhoids is painless, bright red rectal bleeding

associated with bowel movements. A high-fiber diet supplemented with bulk-forming agents may

reduce symptoms of hemorrhoids and is ideal for first- and second-degree hemorrhoids.

2 Rubber band ligation is suitable for symptomatic first- and second- and some third-degree internal

hemorrhoids that do not respond to bulk-forming agents.

3 Hemorrhoidectomy is required in only a few patients with symptomatic hemorrhoids. It should be

considered when conservative therapy has failed, or when hemorrhoids are complicated by

associated pathology such as ulceration, fissures, fistulas, large hypertrophied anal papillae, or

extensive skin tags.

4 Anal fissure is an ischemic ulcer in the lower portion of the anal canal; its treatment, both medical

and surgical, involves relaxing the internal anal sphincter.

5 Anal fistula is a chronic form of perianal abscess, spontaneously or surgically drained, in which the

tract persists, with an internal opening at the dentate line and an external opening on the perianal

skin.

6 Rectal prolapse results from intussusception that extends beyond the anal verge. Fit patients are best

treated with transabdominal rectopexy. Patients with significant medical comorbidities are best

treated using a perineal approach.

7 Anal condylomata acuminata are caused by human papillomavirus, as are anal intraepithelial

neoplasia and anal cancers.

8 Palpable lesions of the anal canal are not hemorrhoids and may be cancers; examination under

anesthesia and biopsy allow for correct diagnosis.

ANATOMY AND PHYSIOLOGY

A detailed understanding of the anatomy and physiology of the rectum and anus is critical to accurate

diagnosis and management of anorectal disorders.

The Rectum

The rectum begins at the level of the sacral promontory and measures approximately 15 cm in length. It

descends along the curvature of the sacrum and passes through the levator ani muscles, where it

becomes the anal canal. Although the rectum develops from the hindgut in conjunction with the sigmoid

and left colon, it differs from the colon in that the outer muscular layer is continuous, characterized by

the merging of the three taenia bands. The rectum has three lateral curves whose infoldings form

submucosal folds in the lumen, known as the valves of Houston. Because of these curves, the rectum

may gain 5 cm in length when straightened during resection.

The posterior aspect of the rectum lacks peritoneum and is directly adherent to the mesorectum.

Anteriorly, the upper two-thirds of the rectum are covered by peritoneum; the lower third has no

peritoneal covering. The level of the anterior peritoneal reflection (also referred to as the pouch of

Douglas) is variable, but is usually 7 to 9 cm from the anal verge in men and 5 to 7 cm in women. The

mesorectum is covered with a thin layer of investing fascia (fascia propria), which is distinct from the

fascia overlying the sacrum. It is in this plane between these two fascial layers that a “total mesorectal

excision” for rectal cancer is performed. The endopelvic fascia that covers the sacrum posterior to the

rectum is also referred to as Waldeyer fascia; anteriorly, Denonvilliers fascia lies between the rectum

and the vagina in females and the seminal vesicles in males (Fig. 70-1).1

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