Topic : ANORECTAL DISEASES

Anorectal disease pertains to those illnesses located in the anal and rectal portions of the large intestine. The most common diseases are:

a.) Hemorrhoids b.) Anal fistulasc.) Anal Fissuresd.) Anorectal abscesses e.) Anal cancerf.) proctitis

Anatomy of Anorectal :-

The anorectum is the terminal portion of the gastrointestinal tract. It is embedded in the osseous pelvis and surrounded by urogenital organs as well as muscular, ligamentous, and connective tissue structures. It is the functional unit that maintains fecal continence by providing both a stopper-equipped reservoir and a controlled expulsion mechanism for feces. The rectum is the last and partially extraperitoneal segment of the large intestine. It starts at the rectosigmoid junction and continues through the pelvic floor into the anal canal. The nonmobilized rectum is characterized by three distinct endoluminal curves. The resulting folds that are seen on endoscopy arereferred to as the valves of Houston.

Rectum :-

Length : about 12 cm Diameter : upper part, same as sigmoid (4cm) but lower is dilated (rectal ampulla) Beginning: rectosigmoid junction (sacral promontory). End: 2.5 cm below and in front of the tip of coccyx.

Male Female

Anterior BladderSeminal vesiclesUreters ProstateUrethra

Pouch of douglas UterusCervixPosterior vaginal wall

Lateral Lateral lig Middle rectal A.Obturator internus MSide wall of pelvisLevator ani M

Lateral lig Middle rectal A.Obturator internus MSide wall of pelvisLevator ani M

Posterior Sacrum and coccyxLoose areolar tissueFacial condensationSuperior rectal A

Sacrum and coccyxLoose areolar tissueFacial condensationSuperior rectal A

Lymphatics Lymphatics

Arterial Supply

Superior rectal artery (chief artery)

Middle rectal artery

Median Sacral artery

Venous Drainage

Internal rectal venous plexus

External rectal venous plexus

Lymphatic:

Upper ½

Lower ½

Anal canal :-

The anal canal is the terminal part of the large intestine.

It is situated between the rectum and anus, below the level of the pelvic diaphragm. It lies in the anal triangle of perineum in between the right and left ischiorectal fossae.

The anal canal is divided into three parts. The zona columnaris is the upper half of the canal and is lined by simple columnar epithelium. The lower half of the anal canal, below the pectinate line, is divided into two zones separated by Hilton's white line. The two parts are the zona hemorrhagica and zona cutanea, lined by stratified squamous non-keratinized and stratified squamous keratinized, respectively.

In humans it is approximately 2.5 to 4 cm long, extending from the anorectal junction to the anus. It is directed downwards and backwards. It is surrounded by inner involuntary and outer voluntary sphincters which keep the lumen closed in the form of an anteroposterior slit.

It is differentiated from the rectum by the transition of the internal surface from endodermal to skin like ectodermal tissue.

The anal canal is divided into two halves, upper and lower.

The upper half has longitudinal folds or elevations of tunica mucosa. Its mucosa is lined by simple columnar epithelium. Its lower ends are joined together by folds of mucus membrane called anal valves. The upper half of the anal canal is supplied by the superior rectal artery which is a branch of the inferior mesenteric artery.

The lower half of the anal canal is lined by stratified squamous epithelium that blends with the skin. The lower half of the anal canal is supplied by the inferior rectal artery which is a branch of the internal pudendal artery.

A whitish line called Hilton's white line indicates the junction between keratinized stratified squamous epithelium and unkeratinized stratified squamous epithelium.

HEMORRHOIDS

Background

Hemorrhoids are one of the most common causes of anal pathology. Subsequently, hemorrhoids are blamed for virtually any anorectal complaint by patients and medical professionals alike. Confusion

often arises because the term "hemorrhoid" has been used to refer to both normal anatomical structures and pathological structures. In the context of this article, "hemorrhoids" refers to the pathological presentation of hemorrhoidal venous cushions.

Hemorrhoidal venous cushions are normal structures of the anorectum and are universally present unless a prior intervention has taken place. Because of their rich vascular supply, highly sensitive location, and tendency to engorge and prolapse, they are common causes of anal pathology.Symptoms can range from mildly bothersome, such as pruritus, to quite concerning, such as rectal bleeding, and while it is a common condition diagnosed in clinical practice, many patients are too embarrassed to ever seek treatment. Consequently, the true prevalence of pathologic hemorrhoids is not known.

Even though hemorrhoids are responsible for a large portion of anorectal complaints, it is important to rule out more serious conditions, such as other causes of GI bleeding, before reflexively attributing symptoms to haemorrhoids.

Pathophysiology

Hemorrhoidal venous cushions are a normal part of the human anorectum and arise from subepithelial connective tissue within the anal canal.

Present in utero, these cushions surround and support distal anastomoses between the superior rectal arteries and the superior, middle, and inferior rectal veins. They also contain a subepithelial smooth muscle layer, contributing to the bulk of the cushions. Normal hemorrhoidal tissue accounts for approximately 15-20% of resting anal pressure and provides important sensory information, enabling the differentiation between solid, liquid, and gas.

Most people contain 3 of these cushions. Although classically described as lying in the right posterior (most common), right anterior, and left lateral positions, this combination is found in only 19% of patients. Hemorrhoids can be found at any position within the rectum.

Hemorrhoids are classified by their anatomic origin within the anal canal and by their position relative to the dentate line.

Internal hemorrhoids develop above the dentate line from embryonic endoderm. They are covered by the simple columnar epithelium of anal mucosa and lack somatic sensory innervation and are therefore painless.

External hemorrhoids develop from ectoderm and arise distal to the dentate line. They are covered by stratified squamous epithelium and receive somatic sensory innervation from the inferior rectal nerve rendering them painful when irritated.

Mixed hemorrhoids are confluent internal and external hemorrhoids.

Venous drainage of hemorrhoidal tissue mirrors embryologic origin:

Internal hemorrhoids drain through the superior rectal vein into the portal system. External hemorrhoids drain through the inferior rectal vein into the inferior vena cava. Rich anastomoses exist between these 2 and the middle rectal vein, connecting the portal

and systemic circulations.

Most symptoms arise from enlarged internal hemorrhoids. Abnormal swelling of the anal cushions causes dilatation and engorgement of the arteriovenous plexuses. This leads to stretching of the suspensory muscles and eventual prolapse of rectal tissue through the anal canal. The engorged anal mucosa is easily traumatized, leading to rectal bleeding that is typically bright red due to high blood oxygen content within the arteriovenous anastomoses. Prolapse leads to soiling and mucus discharge (triggering pruritus) and predisposes to incarceration and strangulation.

Most clinicians use the grading system proposed by Banov et al in 1985, which classifies internal hemorrhoids by their degree of prolapse into the anal canal. This system both correlates with symptoms and guides therapeutic approaches.

Grade I hemorrhoids project into the anal canal and often bleed but do not prolapse. Grade II hemorrhoids may protrude beyond the anal verge with straining or defecating but

reduce spontaneously when straining ceases. Grade III hemorrhoids protrude spontaneously or with straining and require manual reduction. Grade IV hemorrhoids chronically prolapse and cannot be reduced. They usually contain both

internal and external components and may present with acute thrombosis or strangulation.

CLINICAL MANIFESTATION :-

History

The most common presentation of hemorrhoids is rectal bleeding, pain, pruritus, or prolapse. However, these symptoms are extremely nonspecific and may be seen in a number of anorectal diseases. The physician must therefore rely on a thorough history to help narrow the differential and must perform an adequate physical examination (including anoscopy when indicated) to confirm the diagnosis.

An adequate history should include the onset and duration of symptoms. In addition to characterizing any pain, bleeding, protrusion, or change in bowel habits, special attention should be placed on the patient's coagulation history and immune status.

Bleeding is the most common presenting symptom. Blood is usually bright red and may drip, squirt into the toilet bowl, or appear as streaks on the toilet paper. The physician should inquire about the quantity, color, and timing of any rectal bleeding. Darker blood or blood mixed with stool should raise suspicion of a more proximal cause of bleeding.

A patient with a thrombosed external hemorrhoid may present with complaints of an acutely painful mass at the rectum .Pain truly caused by hemorrhoids usually arises only with acute thrombus formation. This pain peaks at 48-72 hours and begins to decline by the fourth day as the thrombus organizes. New-onset anal pain in the absence of a thrombosed hemorrhoid should prompt investigation for an alternate cause, such as an intersphincteric abscess or anal fissure. As many as 20% of patients with hemorrhoids will have concomitant anal fissures.

Thrombosed hemorrhoid. This hemorrhoid was treated by incision and removal of clot.

The presence, timing, and reducibility of prolapse, when present, will help classify the grade of internal hemorrhoids and guide the therapeutic approach.

o Grade I internal hemorrhoids are usually asymptomatic but, at times, may cause

minimal bleeding.o Grades II, III, or IV internal hemorrhoids usually present with painless bleeding but

also may present with complaints of a dull aching pain, pruritus, or other symptoms due to prolapse.

Familial predisposition, diet, history of constipation or diarrhea, and history of prolonged sitting or heavy lifting are also relevant, as are weight loss, abdominal pain, or any change in appetite or bowel habits. Presence of pruritus or any discharge should also be noted.

Physical

In addition to the general physical examination, physicians should also perform visual inspection of the rectum, digital rectal examination, and anoscopy or proctosigmoidoscopy when appropriate.

The preferred position for the digital rectal examination is the left lateral decubitus with the patient's knees flexed toward the chest. Topical anesthetics (eg, 20% benzocaine or 5% lidocaine ointment) may help to reduce any discomfort caused by examination.

External findings important to note include any of the following:o Redundant tissueo Skin tags from old thrombosed external hemorrhoidso Fissureso Fistulaso Signs of infection or abscess formationo Rectal or hemorrhoidal prolapse, appearing as a bluish, tender perianal mass

During the digital rectal examination, assess for any masses, tenderness, mucoid discharge or blood, and rectal tone. Internal hemorrhoids are usually not palpable unless thrombosed.

Current guidelines from most gastrointestinal and surgical societies advocate anoscopy and/or flexible sigmoidoscopy to evaluate any bright-red rectal bleeding. Colonoscopy should be considered in the evaluation of any rectal bleeding that is not typical of hemorrhoids such as in the presence of strong risk factors for colonic malignancy or in the setting of rectal bleeding with a negative anorectal examination.

Causes

Although many patients and clinicians believe that hemorrhoids are caused by chronic constipation, prolonged sitting, and vigorous straining, little evidence to support a causative link exists.

Other risk factors historically associated with the development of hemorrhoids include the following:

o Pregnancyo Lack of erect postureo Familial tendencyo Higher socioeconomic statuso Chronic diarrheao Colon malignancyo Hepatic diseaseo Obesityo Elevated anal resting pressureo Spinal cord injuryo Loss of rectal muscle toneo Rectal surgeryo Episiotomyo Anal intercourse

Varicosities caused from portal hypertension are a distinct entity from hemorrhoids.

DIFFERENTIAL DIAGNOSIS :-

Condyloma AcuminataInflammatory Bowel DiseaseProctitisRectal Prolapse

Other Problems to Be Considered

Anal cancerAnal fissureAnal fistulaPedunculated polypPerianal abscessPruritus aniColorectal tumors

METHOD OF INVESTIGATIONS :-

Laboratory Studies

A CBC may be useful as a marker for infection. Anemia due to hemorrhoidal bleeding is possible3 , albeit rare (0.5 cases per 100,000 patients), and its presence should raise suspicion of an alternate diagnosis.

Imaging Studies

Proctogram may be indicated in rectal prolapse.

Procedures

Proctoscopy may be performed to supplement anoscopy. Full evaluation of the large bowel with colonoscopy is recommended for patients with

significant abdominal symptoms, weight loss, change in bowel habits, age older than 50 years, or other risk factors for colonic malignancy.

TREATMENTS :-

Emergency Department Care

Medical management is the initial treatment of choice for grade I internal and nonthrombosed external hemorrhoids. It consists of sitz baths (bid/tid); a high-fiber diet; adequate fluid intake; stool softeners; topical and systemic analgesics; proper anal hygiene; and in some cases, a short course of topical steroid cream. Good evidence exists that high fiber diets in particular help reduce severity and duration of symptoms. The prolonged use of topical steroids should be avoided.

o Acutely thrombosed external hemorrhoids may be safely excised in the emergency

department in patients who present within 48-72 hours of symptom onset. o Infiltration of a local anesthetic containing epinephrine is followed by elliptical incision

and excision of the thrombosed hemorrhoid and overlying skin. Simple incision and clot evacuation is inadequate therapy and should not be performed.

o The incision should not extend beyond the anal verge or deeper than the cutaneous

layer. A pressure dressing is applied for several hours, after which time the wound is left to heal by secondary intention.

o In patients presenting after 72 hours from the start of symptoms, conservative

medical therapy is preferable. Internal hemorrhoids are treated according to their classification. Treatment may be surgical

or nonsurgical. Most nonsurgical procedures currently available are performed in the clinic or ambulatory setting.

o Grade I hemorrhoids are treated with conservative medical therapy and avoidance of

nonsteroidal anti-inflammatory drugs (NSAIDs) and spicy or fatty foods.o Grade II or III hemorrhoids are initially treated with nonsurgical procedures.o Very symptomatic grade III and grade IV hemorrhoids are best treated with surgical

hemorrhoidectomy. Nonsurgical techniques function by ablation, sclerosis, or necrosis of mucosal tissues.

Despite several meta-analyses and considerable personal preference, there is no clear advantage of one technique over the others.

o Rubber band ligation is the most-used remedy for grade II and grade III hemorrhoids

and is the standard to which other methods are compared. A band ligature is passed through an anoscope and placed on the rectal mucosa proximal to the dentate line. The tissue necroses and sloughs off in 1-2 weeks, leaving an ulcer that later fibroses. No anesthesia is required; complications are uncommon and usually benign.

o Jutabha et al compared endoscopic rubber band ligation with bipolar

electrocoagulation for chronically bleeding grade II or III internal hemorrhoids that were unresponsive to medical therapy.4Their randomized prospective study in 45 patients found that ligation controlled rectal bleeding and other symptoms with significantly fewer treatments (2.3+/-0.2 vs 3.8+/-0.4 for electrocoagulation, P<0.05) and had a significantly higher success rate (92% vs 62% for electrocoagulation, P<0.05). Severe pain during treatment occurred more often with ligation than with electrocoagulation (8% vs 0%, P<0.05), but treatment failure and crossovers were significantly less frequent (8% vs 38%). 

o Necrotizing pelvic sepsis is a rare, but serious, complication of rubber band ligation.

The diagnosis is suggested by the triad of severe pain, fever, and urinary retention. It occurs 1-2 weeks after ligation, frequently in immune compromised patients, and requires prompt surgical debridement.

o Infrared coagulation serves best for grade I, grade II, and some grade III

hemorrhoids. It may be as effective as banding with fewer and less severe complications.

o Bipolar electrocautery is best for lower-grade hemorrhoids; it quickly coagulates the

hemorrhoid tissue but has no effect on prolapse.o Low-voltage direct current works best for higher grade hemorrhoids. Low-voltage

direct current requires grounding time and provides excellent control of pain.o Sclerotherapy and cryotherapy are infrequently used today and generally reserved for

type I or II hemorrhoids. Although minimally invasive, they have a higher rate of post-procedure pain. Impotence, urinary retention, and abscess formation have also been reported. Recurrence rates are as high as 30%.

o Laser therapy is more costly and provides no advantage over other methods.

Operators must control the laser to avoid bleeding.o Radiowave ablation followed by suture ligation could prove to be a safe, cost-

effective, and convenient way to treat prolapsing hemorrhoids. Contraindications to the nonsurgical treatments listed above include the following:

o AIDSo Immunodeficiency disorderso Coagulopathyo Irritable bowel diseaseo Pregnancyo Immediate postpartum periodo Rectal wall prolapseo Large anorectal fissure or infectiono Tumor

Surgical hemorrhoidectomy is the most effective treatment for all hemorrhoids and in particular is indicated in the following situations:

o Nonsurgical treatment fails (persistent bleeding or chronic symptoms)o Grade III and IV hemorrhoids with severe symptomso Presence of concomitant anorectal conditions (eg, anal fissure or fistula) requiring

surgeryo Patient preference

About 5-10% of people with hemorrhoids eventually require surgical hemorrhoidectomy. Postoperative pain remains the major complication, with most patients requiring 2-4 weeks before returning to normal activities. Other possible complications include urinary retention, anal stenosis, and incontinence.

Medication

Stool softeners

Docusate sodium

Topical anesthetics

Lidocaine ointment 5% 

Analgesics

Acetaminophen

Further Outpatient Care

After excision of a thrombosed external hemorrhoid, the patient may be discharged home for several hours of bedrest followed by sitz baths tid, stool softeners, and topical or systemic analgesia. The patient should return in 48-72 hours for a wound check.

All other patients should be referred to a surgical or rectal clinic for more definitive treatment and sent home with conservative medical therapy.

Deterrence/Prevention

Avoid constipation Weight loss Avoid prolonged sitting on the toilet Avoid prolonged sitting at work Improved anorectal hygiene

Complications

Thrombosis Secondary infection Ulceration Abscess Incontinence

Prognosis

Most hemorrhoids resolve spontaneously or with conservative medical therapy alone.

ANAL FISTULAS AND FISSURES

An anal fissure is a superficial linear tear in the anoderm most commonly caused by passage of a large, hard stool. This tear is distal to the dentate line. Anal fissures are among the most common anorectal disorders in the pediatric population; however, adults also are affected.

An anal fistula is an inflammatory tract between the anal canal and skin, The 4 categories of fistulas, based on the relationship of fistula to sphincter muscles, are intersphincteric, transsphincteric, suprasphincteric, and extrasphincteric. Fissures are defined as acute if present for less than 6 weeks, and they are defined as chronic if present for more than 6 weeks.

Pathophysiology

In anal fissures, anus distal to dentate line is involved. About 90% of anal fissures occur in the posterior midline where skeletal muscle fibers that circle the anus are weakest. The remaining 10% are found in the anterior midline.

Most anal fistulas originate in anal crypts, which become infected with abscess formation. When the abscess is opened or ruptures, a fistula is formed.

Sex

Anal fissures affect both sexes equally; however, an anterior fissure is more likely to develop in women (25%) than in men (8%).

Anal fistulas are a complication of anorectal abscesses, which are more common in men than in women (male-to-female ratio of 2:1 to 3:1).

Only 8% of anal fissures are anterior in men; 75-90% of fissures in women are posteriorly located.

For reasons of intrinsic anatomy, rectovaginal fistulas are found only in women.

Age

Although anal fissures are the most common cause of rectal bleeding in infants, they are primarily seen in young adults.

Eighty-seven percent of people with a chronic anal fissure are between the ages of 20 and 60 years old.

Anal fissures in children may indicate sexual abuse.

CLINICAL MANIFESTATION :-

History

Rectal pain, usually described as burning, cutting, or tearing Pain with bowel movements; spasm of the anus is very suspicious for an anal fissure. Bloody stools

o Typically, bright-red blood appears on the surface of stools. Blood usually is not

mixed into stool.o Occasionally, blood is found on toilet paper after wiping.o Patient may report no bleeding.

Mucoid discharge Pruritus A patient with an anal fistula may complain of recurrent malodorous perianal drainage,

pruritus, recurrent abscesses, fever, or perianal pain due to an occluded tract.o Pain occasionally resolves spontaneously with reopening of a tract or formation of a

new outflow tract.o Pain occurs with sitting, moving, defecating, and even coughing.o Pain usually is throbbing in quality and is constant throughout the day.

Physical

Start by optimizing patient placement; place the patient in the left lateral decubitus position with knees drawn up toward the chest.2

Examine the patient carefully to avoid infliction of further pain or sphincter spasm. Examination may be facilitated by application of a topical anesthetic, such as Lidocaine jelly, prior to digital rectal examination.

Most fissures are visible externally when the patient bears down as if having a bowel movement.

Note the depth of the fissure and its orientation to the midline, often described using clock orientation of the hour hand.

Most tears are found in the posterior midline. Rectal examination is generally difficult to tolerate because of sphincter spasm and pain. Acute fissures are erythematous and bleed easily. With chronic fissures, classic fissure triad may be seen.

o Deep ulcero Sentinel pile, which forms when the base of the fissure becomes edematous and

hypertrophic (a resolving sentinel pile can result in a permanent skin tag or may become associated with a fistulous tract)

o Enlarged anal papillae

Bidigital rectal examination in a patient with a fistula-in-ano may reveal an indurated tract or cord.

o Fistula can be identified by small circles of granulation tissue, which exude pus when

compressed if tissue is patent.o A fistulous tract that opens internally can be visualized with aid of an anoscope.o Inguinal lymph nodes may be enlarged and painful.

In an acute fistulous abscess, cardinal signs of inflammation, rubor, dolor, calor, and tumor (eg, erythema, pain, increased temperature, edema) may be found.

Examination of the anus reveals a linear tear in fissure-in-ano.

Causes

Passage of hard stool Chronic diarrhea Childbirth (accounts for 10% of chronic anal fissures) Habitual use of cathartics Anal trauma (can occur with anal intercourse or a rectal examination using a speculum or

digit) Causes of anal fistula include opened perianal or ischiorectal abscesses, which drain

spontaneously through these fistulous tracts.

Anal fissures can be observed in patients with syphilis and other sexually transmitted diseases,tuberculosis, leukemia, inflammatory bowel disease such as Crohn disease, previous anal surgery, HIV, and other conditions or diseases.

o Incidence of anal fissures in patients with leukemia is approximately 24%.o Fistulas are also found in patients with inflammatory bowel disease, particularly

Crohn disease. The incidence of fissures in Crohn disease is 30-50%. Perianal activity often parallels abdominal disease activity, but it may occasionally be the primary site of active disease.

Anal fistulas also are associated with diverticulitis, foreign body reactions, actinomycosis,chlamydia, lymphogranuloma venereum (LGV), syphilis, tuberculosis, radiation exposure, and HIV.

Approximately 30% of patients with HIV develop anorectal abscesses and fistulas.

DIFFERENTIAL DIAGNOSIS :-

Diverticular Disease Pediatrics, Gastrointestinal Bleeding

Foreign Bodies, Rectum Pilonidal Cyst and Sinus

Herpes Simplex Proctitis

Hidradenitis Suppurativa Syphilis

HIV Infection and AIDS

Inflammatory Bowel Disease

Pediatrics, Child Sexual Abuse

Other Problems to Be Considered

Anal abrasionAnal pruritusRectal or anal carcinoma

METHODS OF INVESTIGATION :-

Laboratory Studies

Diagnosis of an anal fissure primarily is based on history and physical examination. Evaluation of an anal fistula involves at least a complete blood count (CBC) and a blood

culture.o Look at number of white blood cells (WBCs) in anyone with a significant infection.o Depending on the condition of the patient, the possibility of bacteremia or sepsis must

be considered. Blood cultures better identify the offending organism, making it possible to treat infection more effectively.

If syphilis or chlamydial infection is in the differential diagnosis, wound cultures may be necessary.

Because of the increased prevalence of methicillin-resistant Staphylococcus aureus (MRSA) bacteria encountered in the general community, wound cultures for this organism should be performed. If MRSA is present, antibiotic therapy needs to be tailored to this specific organism; otherwise, prolonged infection and complications such as bacteremia are more likely to occur.

Imaging Studies

If the extent of the underlying abscess is not known, a CT scan may be necessary to delineate its boundaries.

TREATMENTS :-

Emergency Department Care

Use the WASH regimen in treatment of anal fissures.o Warm water; shower or sitz bath after bowel movemento Analgesicso Stool softenero High-fiber diet

Most uncomplicated fissures resolve in 2-4 weeks with supportive care. Chronic anal fissures frequently require surgical treatment.

All surgical procedures involve stretching or cutting the internal sphincter. The most common surgical procedure is lateral internal sphincterotomy. Botulinum toxin has also been used with great success for treatment of anal fissures.

The use of topical glyceryl trinitrate has also been shown to be effective in the treatment of anal fissures. In one study, 75% of patients had improvement by the second week and 54% were healed after 6 weeks. The most common side effect was severe headache. Another study showed a success rate of about 69% at 2-month follow-up for those who used topical glyceryl trinitrate twice daily for 2 weeks.

Treatment of anal fistulae depends on (1) presentation of the patient, (2) evidence of sepsis or a large abscess, or (3) no worrisome findings on physical examination.

o Administer intravenous antibiotics, antipyretic, and analgesic as needed.o If the patient is septic with hypotension, intravenous fluids or a pressor may be

necessary.

Consultations

Consultation usually is not necessary for anal fissures. An emergent surgical consultation may be necessary for fistulous abscess. Consult a gastroenterologist if inflammatory bowel disease is suspected.

MEDICATION

Laxative/bulking agent

Psyllium

Muscle relaxant

Diazepam

Antibiotics

Vancomycin Metronidazole Ampicillin and sulbactam Ticarcillin and cluvulanate potassium

Clindamycin

Further Inpatient Care

In the case of anal fissures, if the patient is having a great deal of pain, a topical anesthetic may be applied.

Depending on the presence of systemic symptoms and the condition of the patient, the patient with an anal fistula may require continued intravenous antibiotics, fluids, pressors, and, possibly, surgery.

Open lateral internal sphincterotomy is considered the treatment of choice for chronic anal fissure. It reduces the hypertonia of the internal anal sphincter, decreases pain, and allows the fissure to heal.

Further Outpatient Care

For anal fissures, the WASH regimen is indicated. For anal fistulas, outpatient follow-up with a surgeon is indicated if consultation did not take

place at the time of presentation. Botulinum toxin injection has been shown to be an effective alternative to surgery for the

treatment of uncomplicated idiopathic anal fissure. Topical application of clove oil cream has demonstrated significant benefit in patients with

chronic anal fissure. The application of topical 0.5% nifedipine ointment has been used as a chemical

sphincterotomy agent. It has been shown to offer a significant healing rate for acute anal fissure and may prevent it from becoming a chronic fissure.

Inpatient & Outpatient Medications

Psyllium may be prescribed for patients with anal fissures. For patients with anal fistulas, the following medications may be useful (if the patient is stable

enough for discharge with outpatient follow-up):o Analgesicso Antipyreticso Antibiotics

Deterrence/Prevention

Stress the importance of diet modification to soften stools. Patients should increase fruits, vegetables, and soluble and insoluble fibers in their diets and

increase fluid intake.

Complications

Constipation or fecal impaction may occur. The pain from an anal fissure can be so overwhelming that it discourages people from

defecating. Acute fissures can become chronic.

Sentinel pile can result. Permanent skin tag can result. Fistulas may form. The following surgical complications may occur:

o Urinary retentiono Bleedingo Abscess formationo Flatus and liquid incontinenceo Recurrence of fissures

Without treatment, chronically infected fistulas may cause systemic illness. Carcinoma has been reported in chronic untreated anorectal fistulas.

Prognosis

Most uncomplicated fissures resolve in 2-4 weeks with supportive care. Fissures that heal with conservative treatment have a reoccurrence rate of up to 27%. Chronic anal fissures frequently require surgical treatment. Surgical treatment of anal fissures is associated with some degree of incontinence in 30% of

patients. Prognosis for fistulas is excellent after surgery.

Patient Education

Diet modification is indicated in the case of anal fissures.

ANORECTAL ABSCESS

A perianal abscess represents an infection of the soft tissues surrounding the anal canal, with formation of a discrete abscess cavity. The severity and depth of the abscess are quite variable, and the abscess cavity is often associated with formation of a fistulous tract. An anorectal abscess originates from an infection arising in the cryptoglandular epithelium lining the anal canal. The internal anal sphincter is believed to serve normally as a barrier to infection passing from the gut lumen to the deep perirectal tissues. This barrier can be breached through the crypts of Morgagni, which can penetrate through the internal sphincter into the intersphincteric space. Once infection gains access to the intersphincteric space, it has easy access to the adjacent perirectal spaces. Extension of the infection can involve the intersphincteric space, ischiorectal space, or even the supralevator space. In some instances, the abscess remains contained within the intersphincteric space.

Etiology

Perirectal abscesses and fistulas represent anorectal disorders arising predominately from the obstruction of anal crypts. Infection of the now static glandular secretions results in suppuration and abscess formation within the anal gland. Typically, the abscess forms initially in the intersphincteric space and then spreads along adjacent potential spaces.

Classification of anorectal abscess

Abscesses are classified based on their anatomic location. The most commonly described locations are perianal, ischiorectal, intersphincteric, and supralevator. The image below illustrates the different anatomic locations of anorectal abscesses.

Illustration of the major types of anorectal abscesses (submucosal not pictured).

Perianal abscesses represent the most common type of anorectal abscesses, accounting for approximately 60% of reported cases. These superficial collections of purulent material are located beneath the skin of the anal canal and do not transverse the external sphincter.

The next most common types of abscesses, in descending order of frequency, are ischiorectal, intersphincteric, and supralevator. An ischiorectal abscess forms when suppuration transverses the external sphincter into the ischiorectal space. Intersphincteric abscesses result from suppuration contained between the internal and external anal sphincters. A supralevator abscess results either from primary disease in the pelvis (eg, appendicitis, diverticular disease, gynecologic sepsis) or from suppuration extending cranially from an origin in the intersphincteric space, through the longitudinal muscle of the rectum and reaching above the levators.

Horseshoe abscesses, while rare, result from circumferential infiltration of pus within the intersphincteric planes.

The Goodsall rule for perianal fistulas

The Goodsall rule states that the external opening of a fistulous tract located anterior to a transverse line drawn across the anal verge is associated with a straight radial tract of the fistula into the anal canal/rectum. Conversely, an external opening posterior to the transverse line follows a curved, fistulous tract to the posterior midline of the rectal lumen. This rule is important for planning surgical treatment of the fistula and is illustrated in the images below.

Diagram illustrating the Goodsall rule for anorectal fistulas. Fistulas that exit in the

posterior half of the rectum generally follow a curved course toward the posterior

midline, while those that exit in the anterior half of the rectum usually follow a radial

course to the dentate line.

Illustration of the Goodsall rule for anorectal fistulas. Note the curved nature of the

posterior fistulas and the radial (straight) orientation of the anterior fistulas.

Pathophysiology

As mentioned above, perirectal abscesses and fistulas represent anorectal disorders that arise predominately from the obstruction of anal crypts. Normal anatomy demonstrates anywhere from 4-10 anal glands drained by respective crypts at the level of the dentate line. Anal glands normally function to lubricate the anal canal. Obstruction of anal crypts results in stasis of glandular secretions and, when subsequently infected, suppuration and abscess formation within the anal gland results. The abscess typically forms in the intersphincteric space and can spread along various potential spaces.

Common organisms implicated in abscess formation include Escherichia coli, Enterococcus species, andBacteroides species; however, no specific bacterium has been identified as a unique cause of abscesses.

Less common causes of anorectal abscess that must be considered in the differential diagnosis include tuberculosis, squamous cell carcinoma, adenocarcinoma, actinomycosis, lymphogranuloma venereum, Crohn's disease, trauma, leukemia, and lymphoma. These may result in the development of atypical fistula-in-ano or complicated fistulas that fail to respond to conventional surgical treatment.

Presentation

The classic locations of anorectal abscesses listed in order of decreasing frequency are as follows: perianal 60%, ischiorectal 20%, intersphincteric 5%, supralevator 4%, and submucosal 1%. These major types are illustrated in the image below. Clinical presentation correlates with the anatomic location of the abscess.

Illustration of the major types of anorectal abscesses (submucosal not pictured).

Patients with a perianal abscess typically complain of dull perianal discomfort and pruritus. Their perianal pain often is exacerbated by movement and increased perineal pressure from sitting or defecation. Physical examination demonstrates a small, erythematous, well-defined, fluctuant, subcutaneous mass near the anal orifice.

Patients with an ischiorectal abscess often present with systemic fevers, chills, and severe perirectal pain and fullness consistent with the more advanced nature of this process. External signs are minimal and may include erythema, induration, or fluctuancy. On digital rectal examination (DRE), a fluctuant, indurated mass may be encountered. Optimal physical assessment of an ischiorectal abscess may require anesthesia to alleviate patient discomfort that would otherwise limit the extent of the examination.

Patients with an intersphincteric abscess present with rectal pain and exhibit localized tenderness on DRE. Physical examination may fail to identify an intersphincteric abscess. Although rare, supralevator abscesses present a similar diagnostic challenge. As a result, clinical suspicion of an intersphincteric or supralevator abscess may require confirmation through computed tomography (CT) scanning, magnetic resonance imaging (MRI), or anal ultrasonography. Use of the last modality is limited to confirming the presence of an intersphincteric abscess.

METHODS OF INVESTIGATION

Laboratory Studies

No specific laboratory studies are indicated in the evaluation of a patient with a perianal or anorectal abscess.

Certain patients, such as individuals with diabetes and patients who are immunocompromised, are at high risk for developing bacteremia and possibly sepsis, as a

result of an anorectal abscess. In such cases, complete laboratory evaluation is important. Laboratory evaluation of the septic patient is not the focus of this article.

Imaging Studies

Imaging studies rarely are necessary in the evaluation of patients with an anorectal abscess; however, clinical suspicion of an intersphincteric or supralevator abscess may require confirmation by CT scanning, MRI, or anal ultrasonography.2,3 Use of the last modality is limited to confirming the presence of an intersphincteric abscess. The ultrasound can also be used intraoperatively to help identify a difficult abscess/fistula.

Diagnostic Procedures

Digital examination under anesthesia can be helpful in certain cases, because patient discomfort can significantly limit physical assessment. For example, optimal evaluation for an ischiorectal abscess is performed in this manner. A fistula tract can be injected with peroxide solution at the time of examination under anesthesia in order to facilitate the visualization of the internal opening of the fistula.

Evidence suggests that the use of endoscopic visualization (transrectal and transanal) is an excellent way to evaluate complex cases of perianal abscess and fistula. With the endoscopic technique, the extent and configuration of the abscess and fistulas can be clearly visualized. The endoscopic visualization has been reported to be as effective as fistulography. In experienced hands, endoscopic evaluation is the preferred diagnostic procedure in patients with perirectal pathology because of the low risk of bacterial dissemination and the low incidence of patient discomfort. Utilizing endoscopic evaluation after nonsurgical treatment is also effective for the documentation of the patient's response to therapy.

Medical Therapy

In most patients with anorectal abscess, adjuvant medical therapy with antibiotics generally is not necessary. However, the presence of a systemic inflammatory response, diabetes, or immunosuppression justifies the concomitant use of antibiotics.

Surgical Therapy

Treatment of anorectal abscesses involves early surgical drainage of the purulent collection. Primary antibiotic therapy alone is ineffective in resolving the underlying infection and simply postpones surgical intervention. Any delay in surgical drainage of anorectal abscesses prolongs infection, augments tissue damage, and may impair sphincter continence function, as well as promote stricture and/or fistula formation. The ability to drain an anorectal abscess depends on patient comfort and on the location and accessibility of the abscess.

Drainage of perianal or superficial abscesses usually can be accomplished in the office or emergency department, using local anesthetics. A small incision is made over the area of fluctuancy in close proximity to the anal verge. Pus is collected and sent for culture. Hemostasis is achieved with manual pressure, and the wound is packed with iodophor gauze. The gauze is removed after 24 hours, and the patient is instructed to take sitz baths 3 times a day and after bowel movements. Postoperative analgesics and stool softeners are prescribed to relieve pain and prevent constipation. The patient typically will follow up with his/her physician in 2-3 weeks for wound evaluation and inspection for possible fistula-in-ano. (A short fistula-in-ano coursing through a minimal amount of external sphincter is best treated with a fistulotomy.)

A potential complication of anorectal abscess drainage is the formation of fistulous tracts. Management of fistulas will be addressed later in this review. The type of organism cultured from an anorectal abscess is an important predictor of fistula formation following surgical incision and drainage. Underlying anal fistulas are present in 40% of abscess cultures that are positive for intestinal bacteria; however, cultures growing Staphylococcus species are associated with perianal skin infections and typically indicate that there is no subsequent risk that anal fistulas will develop.

Treatment of ischiorectal, intersphincteric, and supralevator abscesses is performed best under general or regional anesthesia. In the case of ischiorectal abscess, a cruciate incision is made at the site of maximal swelling. Pus is drained and cultured. The ischiorectal fossa is probed with a finger or hemostat to disrupt loculations and facilitate drainage. Placement of a drain only is indicated for the management of complex or bilateral abscesses.

To drain an ischiosphincteric abscess, a transverse incision is made in the anal canal below the dentate line posteriorly. The intersphincteric space is identified, and the plane between the internal and external sphincters is exposed. The abscess is opened to allow drainage, and a small mushroom catheter is sutured in situ to assist drainage and prevent premature wound closure.

Location and etiology determine the drainage technique to be used for supralevator abscesses. Failure to manage supralevator abscesses with consideration of the primary etiology may result in iatrogenic fistula formation. Evaluation with MRI or CT scanning can exclude intra-abdominal or pelvic pathology as possible sources.

If the supralevator abscess evolved from the extension of an ischiorectal abscess, external drainage through the ischiorectal fossa would be indicated. If the abscess resulted from an upward extension of an intersphincteric abscess, appropriate drainage would be created through the rectal mucosa. In cases of posterior supralevator abscess collections, a transverse incision is made in the posterior anal canal below the dentate line. The dissection extends from the intersphincteric plane through the puborectalis sling and into the posterior anal space. A mushroom catheter then is sutured in place to ensure adequate drainage.

Anterior supralevator abscesses are superficial and are more common in women than in men. Surgical drainage may be approached using an anteriorly directed transanal incision or by a transvaginal approach entering the posterior cul-de-sac. A mushroom catheter is placed to ensure adequate drainage of the abscess collection. Patients with systemic signs of toxicity are admitted to the hospital and treated with intravenous antibiotics. If the patient does not improve clinically over the next 24-48 hours, reevaluation of the supralevator abscess by CT scan or reoperation may be indicated. In the face of recurrent, severe supralevator abscesses, some patients may require a diverting colostomy for optimal management.9 

The anal fistula is a common surgical ailment that has been reported since the time of Hippocrates, but little systematic evidence exists on its management. Different treatment modalities have been evaluated in 443 reported trials. Examples of various research studies include the following:

Treatment with fistulotomy versus the use of fistulectomy Seton treatment10

Marsupialization Glue therapy Anal flaps Radiosurgical approaches Fistulotomy/fistulectomy at time of abscess incision Intraoperative anal retractors

Two reported meta-analyses evaluated the use of incision and drainage alone vs the employment of incision + fistulotomy. Evidence suggests that following fistulotomy, marsupialization reduces bleeding and permits faster healing. Results from small trials indicate that healing rates after flap repair may be no worse than those following fistulotomy, although this has not yet been proven. Failure rates may increase in cases in which flap repair has been combined with fibrin glue treatment of fistulas. Radiofrequency fistulotomy results in less pain on the patient's first postoperative day and may permit faster healing. However, a great deal is not yet understood about the surgical treatment of anal fistulas.Preoperative Details

Because of the acute nature of anorectal abscesses, preoperative bowel preparation is not possible and typically is unnecessary.

Intraoperative Details

Decisive management of anal fistulas relies on therapeutic interventions. Healing rarely is spontaneous, and failure to achieve adequate treatment often results in recurrent abscess, persistent drainage, and even malignancy. The main paradigms to follow in the management of anorectal fistulas include the following:

Determine the anatomy of the fistula Provide adequate drainage Eradicate the fistula tract Prevent recurrence Preserve sphincter function - Preservation of sphincter function relies on maintaining the

integrity of the anorectal ring.

Once the external opening of the anorectal fistula has been identified and the surrounding tissue has been palpated, probing of the fistula tract is warranted. Aggressive probing of the fistula is discouraged to prevent formation of false channels. Using a blunt probe (eg, a small lachrymal probe), the internal origin of a primary fistula can be identified in the majority of cases.

When searching for a fistula tract's opening in the anal canal, the Goodsall rule is an excellent guideline. This rule states that an external opening anterior to a transverse line drawn across the anal verge is associated with a straight radial tract into the canal. An external opening posterior to the transverse line follows a curved fistulous tract to the posterior midline rectal lumen. Horseshoe fistulas occasionally are associated with anterior and posterior openings in the anal canal.

Treatment options for the management of fistulas are aimed at providing definitive therapy while minimizing the morbidity of the procedure. For example, 2 widely accepted treatment interventions include fistulectomy and fistulotomy. Studies have demonstrated that removal of the entire fistula tract along with the surrounding scar tissue (ie, fistulectomy) unnecessarily results in a larger wound, prolonged healing time, and higher risks of incontinence. As a result, the more conservative approach of unroofing the tract without excising all surrounding tissue (fistulotomy) usually is preferred and decreases the risk of incontinence and fistula recurrence; fistulotomy also shortens wound healing time.

A fistulotomy is performed as a primary procedure for superficial fistulas that require minimal dissection of the fistula from the surrounding sphincter musculature. In contrast, simple fistulotomy for repair of high-level fistulas is contraindicated as the primary treatment.

The use of loose setons is warranted in high-level fistulas (ie, transsphincteric and suprasphincteric) to reduce the risk of incontinence or in cases in which poor wound healing is anticipated. Setons may

also be used as temporary initial intervention in the management of a fistula. A seton is a nonabsorbable nylon or silk suture that is guided through the fistula tract and tied exteriorly, in this way compressing and maintaining suture placement in the tract. Other material frequently used for seton placement include soft vessel loop. The seton suture must be left in place for a prolonged period of time (weeks to months).

The ischemic compression by the seton and the local inflammatory reaction of adjacent tissues initiates fibrosis. Once fibrosis of the surrounding tissue develops, it helps to maintain the integrity of the sphincter musculature during subsequent fistulotomy. Setons often are used in patients with fistulas secondary to inflammatory bowel disease (IBD). In addition, the seton allows epithelialization of the fistulous tract, thereby preventing secondary closure and facilitating the drainage of abscesses.

Another commonly used type of seton is the cutting seton, which can be used to gradually transect the anal sphincter musculature underlying the fistula by externally tightening the suture to induce pressure necrosis. Typically, retightening the seton over a period of several days is necessary (this can be performed in the outpatient setting). The cutting seton may eliminate the need for subsequent fistulotomy. While the cutting seton is used as an effective therapeutic option for high-level fistulas, it is contraindicated in patients with IBD.

Other treatment modalities include resection with coverage using advancement tissue flaps (used for more complex cases) and bioprosthetic fistula plug (made of surgisis porcine submucosa). The plug technique is indicated in selected cases with long fistulous tracts. The success rate is variable (50-70%).

Patients with anal fissures can be treated with nifedipine gel (calcium channel blocker - topical use) and Botox injections. Occasionally, sphincterotomy (lateral internal anal sphincter muscle) may be necessary.

Postoperative Details

Postoperatively, administer analgesics for pain, stool bulking agents, and stool softeners to prevent constipation. Follow-up evaluation of an incised anorectal abscess is important not only for determining whether healing is adequate, but also for assessing the potential development of anorectal fistulas. The patient typically will follow up with his/her physician in 2-3 weeks for wound evaluation and inspection for possible fistula-in-ano.

Antibiotics are used as adjuncts to surgical therapy for patients with a comorbidity, such as diabetes, valvular heart disease, or immunodeficiency.

Follow-up

The patient typically will follow up with his/her physician in 2-3 weeks for wound evaluation and inspection for possible fistula-in-ano.

ANAL CANCER

Anal cancer is a type of cancer which arises from the anus, the distal orifice of the gastrointestinal tract. It is a distinct entity from the more common colorectal cancer. The etiology, risk factors, clinical progression, staging, and treatment are all different. Anal cancer is typically asquamous cell carcinoma that arises near the squamocolumnar junction.

Pathophysiology

The mucosa in the large intestine regenerates approximately every 6 days. Crypt cells migrate from the base of the crypt to the surface, where they undergo differentiation and maturation, and ultimately lose the ability to replicate.

The significant portions of colorectal carcinomas are adenocarcinomas. The adenoma-carcinoma sequence is well described in the medical literature. Colonic adenomas precede adenocarcinomas. Approximately 10% of adenomas will eventually develop into adenocarcinomas. This process may take up to 10 years.

Three pathways to colon and rectal carcinoma have been described: 

the adenomatous polyposis coli (APC) gene adenoma-carcinoma pathway the hereditary nonpolyposis colorectal cancer (HNPCC) pathway ulcerative colitis dysplasia.

The APC adenoma carcinoma pathway involves several genetic mutations, starting with inactivation of the APCgene, which allows unchecked cellular replication at the crypt surface. With the increase in cell division, further mutations occur, resulting in activation of the K-ras oncogene in the early stages and p53 mutations in later stages. These cumulative losses in tumor suppressor gene function prevent apoptosis and prolong the cell's lifespan indefinitely. If the APC mutation is inherited, it will result in familial adenomatous polyposis syndrome.Histologically, adenomas are classified in three groups: tubular, tubulovillous, and villous adenomas. K-rasmutations and microsatellite instability have been identified in hyperplastic polyps. Therefore, hyperplastic polyps may also have malignant potential in varying degrees.5 

The other common carcinogenic pathway involves mutation in DNA mismatch repair genes. Many of these mismatched repair genes have been identified, including hMLH1, hMSH2, hPMS1, hPMS2, and hMSH6. Mutation in mismatched repair genes negatively affects the DNA repair. This replication error is found in approximately 90% of HNPCC and 15% of sporadic colon and rectal cancers.1,6 A separate carcinogenic pathway is also described in inflammatory bowel disease (IBD). Chronic inflammation such as in ulcerative colitis can result in genetic alterations which then lead into dysplasia and carcinoma formation.

CLINICAL MANIFESTATION :-

symptoms

Symptoms of anal cancer include bloating and change in bowel habits, a lump near the anus, rectal bleeding, itching or discharge.  Women may experience lower back pain due to pressure the tumor exerts on the vagina, and vaginal dryness.

History

All patients should undergo a complete history (including a family history) and assessment of risk factors for the development of rectal cancer. Many rectal cancers produce no symptoms and are discovered during digital or proctoscopic screening examinations. Bleeding is the most common symptom of rectal cancer, occurring in 60% of patients. Bleeding often is attributed to other causes (eg, hemorrhoids), especially if the patient has a history of other rectal

problems. Profuse bleeding and anemia are rare. Bleeding may be accompanied by the passage of mucus, which warrants further investigation.

Change in bowel habits is present in 43% of patients; change is not evident in some cases because the capacity of a rectal reservoir can mask the presence of small lesions. When change does occur it is often in the form of diarrhea, particularly if the tumor has a large villous component. These patients may have hypokalemia, as shown in laboratory studies. Some patients experience a change in the caliber of the stool.  Large tumors can cause obstructive symptoms. Tumors located low in the rectum can cause a feeling of incomplete evacuation and tenesmus.

Occult bleeding is detected via a fecal occult blood test (FOBT) in 26% of all cases. Abdominal pain is present in 20% of the cases. Partial large-bowel obstruction may cause colicky abdominal pain and bloating. Back pain is usually a late sign caused by a tumor invading or compressing nerve trunks. Urinary symptoms may also occur if the tumor is invading or compressing the bladder or prostate.

Malaise is a nonspecific symptom and present in 9% of rectal cancer cases. Bowel obstruction due to a high-grade rectal lesion is rare, occurring in 9% of all cases. Pelvic pain is a late symptom, usually indicating nerve trunk involvement, and is present in 5% of all cases. Other manifestations include emergencies such as peritonitis from perforation (3%) or jaundice, which may occur with liver metastases (<1%).

Physical

Physical examination is performed with specific attention to size and location of rectal cancer in addition to possible metastatic lesions, including enlarged lymph nodes or hepatomegaly. The remainder of the colon is also evaluated. Digital rectal examination (DRE) provides an opportunity to readily detect abnormal lesions. The average finger can reach approximately 8 cm above the dentate line. Rectal tumors can be assessed for size, ulceration, and presence of any pararectal lymph nodes. Fixation of the tumor to surrounding structures (eg, sphincters, prostate, vagina, coccyx and sacrum) also can be assessed. DRE also permits a cursory evaluation of the patient's sphincter function. This information is necessary when determining whether a patient is a candidate for a sphincter-sparing procedure. Rigid proctoscopy is also performed to identify the exact location of the tumor in relation to the sphincter mechanism.

Causes

The etiology of colorectal cancer is unknown, but colorectal cancer appears to be multifactorial in origin and includes environmental factors and a genetic component. Diet may have an etiologic role, especially diet with high fat content.

Approximately 75% of colorectal cancers are sporadic and develop in people with no specific risk factors. The remaining 25% of cases occur in people with significant risk factors--most commonly, a family history or personal history of colorectal cancer or polyps, which are present in 15-20% of all cases. Other significant risk factors are certain genetic predispositions, such as hereditary nonpolyposis colorectal cancer (HNPCC; 4-7% of all cases) and familial adenomatous polyposis (FAP, 1%); and inflammatory bowel disease (IBD; 1% of all cases).

Environmental factors

Diet A high-fat, low-fiber diet is implicated in the development of colorectal cancer. Specifically, people who ingest a diet high in unsaturated animal fats and highly saturated vegetable oils (eg, corn,

safflower) have a higher incidence of colorectal cancer. The mechanism by which these substances are related to the development of colorectal cancer is unknown. Saturated fats from dairy products do not have the same carcinogenic effect, nor do oils containing oleic acid (eg, olive, coconut, fish oils). Omega-3 monounsaturated fatty acids and omega-6 monounsaturated fatty acids also appear to be less carcinogenic than unsaturated or polyunsaturated fats. In fact, recent epidemiologic data suggest that high fish consumption may provide a protective effect against development of colorectal cancer. Long-term diets high in red meat or processed meats appear to increase the risk of distal colon and rectal cancers.4,7   The ingestion of a high-fiber diet may be protective against colorectal cancer. Fiber causes the formation of a soft, bulky stool that dilutes carcinogens; it also decreases colonic transit time, allowing less time for harmful substances to contact the mucosa. The decreased incidence of colorectal cancer in Africans is attributed to their high-fiber, low–animal-fat diet. This favorable statistic is reversed when African people adopt a western diet. Meta-analysis of case-controlled studies found that reduction in colorectal cancer risk occurs with increasing intake of dietary fiber.4  

Increased dietary intake of calcium appears to have a protective effect on colorectal mucosa by binding with bile acids and fatty acids. The resulting calcium salts may have antiproliferative effects, decreasing crypt cell production in the mucosa. A double-blind placebo-controlled study showed a statistically significant reduction in the incidence of metachronous colorectal adenomas.8 Other dietary components, such as selenium, carotenoids, and vitamins A, C, and E, may have protective effects by scavenging free-oxygen radicals in the colon.

AlcoholAlcohol intake of more than 30 g daily has been associated with increased risk of developing colorectal carcinoma, with risk of rectal cancer greater than that of colon cancer. Risk appears greater with beer than with wine.9Specifically, Kabat et al found that daily beer consumption of 32 ounces or more increases the risk of rectal cancer in men (odds ratio 3.5).10 

TobaccoSmoking, particularly when started at a young age, increases the risk of colorectal cancer.11 Possible mechanisms for tumor development include the production of toxic polycyclic aromatic amines and the induction of angiogenic mechanisms due to tobacco smoke.

Cholecystectomy 

Following cholecystectomy, bile acids flow freely, increasing exposure to the degrading action of intestinal bacteria. This constant exposure increases the proportion of carcinogenic bile acid byproducts.  A meta-analysis by Giovannucci et al revealed an increased risk of proximal colon carcinoma following cholecystectomy. Although a large number of studies suggest the increased risk of proximal colon cancer in patients following cholecystectomy, the data are not compelling enough to warrant enhanced screening in this patient population.1  

Hereditary factors 

The relative risk of developing colorectal cancer is increased in the first-degree relatives of affected patients. For offspring, the relative risk is 2.42 (95% CI: 2.20-2.65); when more than one family member is affected, the relative risk increases to 4.25 (95% CI; 3.01-6.08). If the first-degree family member is younger than 45 years at the time of diagnosis, the risk increase is even higher.12 

 

Regarding the personal history of colorectal cancer or polyps: Of patients with colorectal cancer, 30% have synchronous lesions, usually adenomatous polyps. Approximately 40-50% of patients have polyps on a follow-up colonoscopy. Of all patients who have adenomatous polyps discovered via a colonoscopy, 29% of them have additional polyps discovered on a repeat colonoscopy one year later. Malignancy develops in 2-5% of patients. The risk of cancer in people who have had polyps removed is 2.7-7.7 times that of the general population.13 

Genetic disorders 

Familial adenomatous polyposis (FAP)FAP is an autosomal dominant inherited syndrome that results in the development of more than 100 adenomatous polyps and a variety of extra-intestinal manifestations. The defect is in the APC gene, which is located on chromosome 5 at locus q21. The disease process causes the formation of hundreds of intestinal polyps, osteomas of bone, desmoid tumors, and, occasionally, brain tumors. Individually, these polyps are no more likely to undergo malignant transformation than are polyps in the general population. The increased number of polyps, however, predisposes patients to a greater risk of cancer. If left untreated, colorectal cancer develops in nearly 100% of these patients by age 40. Whenever the hereditary link is documented, approximately 20% of FAP cases are found to be caused by spontaneous mutation.

Hereditary nonpolyposis colorectal cancer HNPCC is an autosomal dominant inherited syndrome that occurs because of defective mismatch repair genes located on chromosomes 2, 3, and 7. Patients have the same number of polyps as the general population, but their polyps are more likely to become malignant. These patients also have a higher incidence of endometrial, gastric, thyroid, and brain cancers.The revised Amsterdam criteria are used to select at-risk patients (all criteria must apply):

three or more relatives who are diagnosed with an HNPCC-associated cancer (colorectal, endometrium, small bowel, ureter, or renal pelvis)

one affected person is a first-degree relative of the other two one or more cases of cancer are diagnosed before age 50 at least two generations are affected FAP has been excluded tumors have undergone a pathology review.

Inflammatory bowel disease 

The malignant pathway in these patients does not involve any adenoma-carcinoma sequence. Cancer risk increases with duration of disease. After 10 years, the incidence of colorectal cancer in ulcerative colitis (UC) is approximately 1% per year. Patients should be evaluated for dysplastic changes via an annual colonoscopy. Dysplasia is a precursor of cancer and when present, the risk of cancer is 30%.

The incidence of colorectal cancer in patients with Crohn's disease is 4-20 times greater than that of the general population. Cancer occurs in patients with disease of at least 10 years' duration. The average age at cancer diagnosis, 46-55 years, is younger than that of the general population. Cancers often develop in areas of strictures and in de-functionalized segments of intestine. In patients with perianal Crohn's disease, malignancy is often present in fistulous tracts.

METHODS OF INVESTIGATION :-

Laboratory Studies

Routine laboratory studies should include a complete blood count; serum chemistries, including liver and renal function tests; and a carcinoembryonic antigen (CEA) test. A cancer antigen (CA) 19-9 assay, if available, may also be useful to monitor the disease. Screening CBC may demonstrate a hypochromic, microcytic anemia, suggesting iron deficiency. The combined presence of vitamin B-12 or folate deficiency may result in a normocytic or macrocytic anemia. All men and postmenopausal women with iron deficiency anemia require a GI evaluation. Liver function tests are usually part of the preoperative workup. The results are often normal, even in patients with metastases to the liver.

Perform a CEA test in all patients with rectal cancer. A baseline level is obtained before surgery and a follow-up level is obtained after surgery. If a previously normalized CEA begins to rise in the postoperative period, this suggests possible recurrence. A CEA level higher than 100 ng/mL usually indicates metastatic disease and warrants a thorough investigation. This is the step workout :-

Other Tests

Screening for Colon and Rectal Cancer  The process of malignant transformation from adenoma to carcinoma takes several years. The purpose of screening is to eradicate potential cancers while they are still in the benign stage of the adenoma-carcinoma sequence. Screening also increases the likelihood of discovering existing cancers while they are still in the early stage.

 TREATMENTS :-

Localised diseaseLocalised disease (carcinoma-in-situ) and the precursor condition, anal intraepithelial neoplasia (anal dysplasia or AIN) can be ablated with minimally invasive methods such as Infrared Photocoagulation. (Goldstone, SE, Kawalek, AZ, Huyett, JW "Infrared Photocoagulator: A useful tool for treating anal squamous intraepithelial lesions". 2005. Diseases of the Colon & Rectum 58(5), 1042-1053.

Anal cancer is most effectively treated with surgery, and in early stage disease (i.e., localised cancer of the anus without metastasis to the inguinal lymph nodes), surgery is often curative. The difficulty with surgery has been the necessity of removing the anal sphincter, with concomitant fecal incontinence. For this reason, many patients with anal cancer have required permanent colostomies.

In more recent years, physicians have employed a combination strategy including chemotherapy and radiation treatments to reduce the necessity of debilitating surgery. This "combined modality" approach has led to the increased preservation of an intact anal sphincter, and therefore improved quality of life after definitive treatment. Survival and cure rates are excellent, and many patients are left with a functional sphincter. Some patients have fecal incontinence after combined chemotherapy and radiation. Biopsies to document disease regression after chemotherapy and radiation were commonly advised, but are not as frequent any longer. Current chemotherapy active in anal cancer includes cisplatin and 5-FU. Mitomycin has also been used, but is associated with increased toxicity

.

Metastatic or recurrent diseaseUp to 10% of patients treated for anal cancer will develop distant metastatic disease. Metastatic or recurrent anal cancer is difficult to treat, and usually requires chemotherapy. Radiation is also employed to palliate specific locations of disease that may be causing symptoms. Chemotherapy commonly used is similar to other squamous cell epithelial neoplasms, such asplatinum analogues, anthracyclines such as doxorubicin, and antimetabolites such as 5-FU and capecitabine. J.D. Hainsworth developed a protocol that includes Taxol and Carboplatinum along with 5-FU.

Prognosis

Overall 5-year survival rates for rectal cancer are as follows:o Stage I, 90%o Stage II, 60% to 85%o Stage III, 27% to 60%o Stage IV, 5% to 7%

Fifty percent of patients develop recurrence, which may be local, distant, or both. Local recurrence is more common in rectal cancer than in colon cancer.

o Disease recurs in 5-30% of patients, usually in the first year after surgery.o Factors that influence the development of recurrence include surgeon variability,

grade and stage of the primary tumor, location of the primary tumor, and ability to obtain negative margins.

o Surgical therapy may be attempted for recurrence and includes pelvic exenteration or

APR in patients who had a sphincter-sparing procedure.o Radiation therapy generally is used as palliative treatment in patients who have

locally unresectable disease.

PROCTITIS

Proctitis is inflammation of the lining of the rectum, called the rectal mucosa. Proctitis can be short term (acute) or long term (chronic). Proctitis involves an inflammatory change of the rectum (within 15 cm of the dentate line). Proctitis is similar to proctosigmoiditis but is not necessarily associated with proximal extension of disease into the colon and usually does not evolve into ulcerative colitis. If proximal extension does occur, it usually does so within the first 2 years of initial diagnosis.

Proctitis has many causes. It may be a side effect of medical treatments like radiation therapy or antibiotics. Proctitis caused by sexually transmitted diseases (STDs) is transmitted through receptive anal intercourse and is most commonly due to gonorrheaand chlamydia, or less commonly lymphogranuloma venereum or herpes virus. Nonsexually transmitted causes include autoimmune disease of the colon, such as Crohn diseaseand ulcerative colitis, celiac disease, chemicals, rectal instrumentation, and trauma to the anorectal area. It may also occur as idiopathic proctitis.

Pathophysiology

Proctitis involves mucosal cell loss, acute inflammation of the lamina propria, eosinophilic crypt abscess, and endothelial edema of the arterioles. These may improve or in turn progress with subsequent fibrosis of connective tissue and endarteritis of the arterioles, resulting in rectal tissue ischemia and leading to mucosal friability, bleeding, ulcers, strictures, and fistula formation.

CLINICAL MANIFESTATION

History

General symptomso Feeling of rectal fullnesso Anal and rectal paino Diarrhea, usually frequent, small amountso Frequent or continuous urge to have a bowel movemento Pain in the lower left abdomeno Passing mucus through the rectumo Rectal bleeding

Idiopathic proctitiso Passage of blood and mucus per rectumo Tenesmuso Occasionally, passage of loose stool, with or without lower abdominal pain or rectal

cramping Infectious proctitis

o Prurituso Rectal and anal pain (may become severe)o Avoidance of defecation due to paino Most common causes - Neisseria gonorrhoeae, Chlamydia trachomatis, herpes

simplex virus (HSV) types 1 and 2o Indolent and extensive HSV types 1 and 2 infections: Symptoms may include the

following: tenesmus, rectal pain, discharge, and hematochezia. The disease may run its natural course of exacerbations and remissions but is usually more prolonged and severe in patients with immunodeficiency disorders. Presentations may resemble dermatitis or decubitus ulcers in debilitated, bedridden patients. A secondary bacterial infection may be present.

Radiation-induced proctitis

o Early symptoms include tenesmus and diarrhea that resolve shortly after the radiation

treatment period.o Later symptoms of proctitis (occurring months to years after the completion of

radiation therapy) include tenesmus, bleeding, low-volume diarrhea, and rectal pain.o Symptoms of radiation-induced proctitis are associated with low-grade obstruction or

fistulous tracts into adjacent organs.

Physical

Physical examination findings may include the following:

Mucosal erythema Mucosal friability Groups of vesicles eroding into circular superficial ulcers enlarged Tender inguinal lymph nodes (HSV) Painless chancres Hemoccult positive stools Telangiectasias Elevated fecal calprotectin and fecal lactoferrin

Causes

Causes of proctitis may include the following:

N gonorrhoeae C trachomatis HSV 1 (10%) and HSV 2 (90%) Radiation therapy Immunodeficiency disorders Crohn disease Syphilis (usually secondary) Papillomavirus Amebiasis Lymphogranuloma venereum Ischemia Toxins (eg, hydrogen peroxide enemas) Vasculitis Cytomegalovirus (CMV) Clostridium difficile Campylobacter species

DIFFERENTIAL DIAGNOSIS:-

Anal Fistulas and Fissures Herpes Simplex

Chancroid HIV Infection and AIDS

Clostridium difficile colitis/proctitis Inflammatory Bowel Disease

Diverticular Disease Lymphogranuloma Venereum

Foreign Bodies, Rectum Syphilis

Gonorrhea Vulvovaginitis

Other Problems to Be Considered

Traumatic proctitisInfections (eg, shigellosis, amebiasis)

METHOD OF INVESTIGATION :-

Laboratory Studies

A complete blood count (CBC) is performed to evaluate for leukocytosis, if an infectious etiology, or severity of anemia due to blood loss.

A sequential multiple analysis of 7 serum tests (SMA 7) is performed to evaluate for severe electrolyte/fluid losses or to look for evidence of renal insufficiency prior to initiation of medical therapy.

C-reactive protein level is elevated in patients with extensive pancolitis but is always normal in patients with only distal disease.

Cultures of rectal swabs help diagnose gonorrhea or chlamydia. Cultures of vesicular fluid or cytologic scrapings aid in the diagnosis of HSV. Serum Venereal Disease Research Laboratory (VDRL) test and dark field examination of

scrapings from the base of the chancre reveals spirochetes and confirms the diagnosis of syphilis.

Stool specimen for C difficile toxin.

Procedures

Proctosigmoidoscopy reveals the following:o Pallor or erythemao Loss of usual vascularity of mucosao Prominent telangiectasiao Friabilityo Bleedingo Ulcerationso Edemao Scattered areas of scarringo Vesicles/pustuleso Strictures

Biopsy for histology, culture, viral studies, and Chlamydia studies Colonoscopy to exclude more proximal involvement Barium studies are helpful in patients who have obstructive symptoms and are preferred in

those patients suspected of having fistulas.

TREATMENT

Emergency Department Care

After life-threatening conditions have been excluded or controlled, aim for providing patient comfort during the examination.

Treatment depends upon the etiology. 

o Sitz baths, antispasmodic medications, stool softeners, low residue diet (may provide

relief)o Steroid enemas or suppositories for ulcerative proctitiso Ceftriaxone and doxycycline for gonorrheal proctitiso Acyclovir for herpetic proctitiso Tetracycline or doxycycline for chlamydial proctitiso Shigella proctitis is usually self-limiting but may require, under certain circumstances,

prolonged (2-4 wk) antibiotic treatment with ampicillin, tetracycline, ciprofloxacin, or trimethoprim and sulfamethoxazole (TMP-SMZ).

o Yersinia proctitis is usually self-limiting, but, if systemic bacteremia occurs, treat with

intravenous antibiotics such as tetracycline or ceftriaxone.o Campylobacter proctitis is a self-limiting disease; treatment is aimed at symptomatic

relief.o Metronidazole (Flagyl) or iodoquinol for amebiasis proctitiso Metronidazole (Flagyl) or oral vancomycin for C difficile proctitiso Radiation proctitis treatment may include the following: sucralfate alone or with rectal

prednisolone enemas, short-chain fatty acid enemas, or pentosan polysulfate. In addition, hyperbaric oxygen theoretically inhibits bacterial growth, preserves marginally perfused tissue, and inhibits toxin production. Formaldehyde, argon plasma coagulation via endoscopy and bipolar electrocoagulation (BiCap) may be used to control refractory bleeding in hemorrhagic proctitis.

Consultations

Consult a colorectal surgeon or a gastroenterologist for further evaluation of the lower gastrointestinal (GI) tract by sigmoidoscopy, if indicated (to rule out more proximal disease), after anoscopy.

A colorectal surgical consultation may also be considered for management/evaluation of deep tissue infection that is not amenable to incision and drainage in the ED.

Medication

Antibiotics Metronidazole Vancomycin Ciprofloxacin Ceftriaxone Doxycycline Tetracycline Sulfasalazine

Rectal anti-inflammatory agents Sulfasalazine Mesalamine

Anti viral Acylclovir

Corticosteroid Dexamethasone Prednisolone

Chemoprotective agent Amifostine

Further Outpatient Care

Discharge if no life-threatening condition exists and the patient is able to comply with the therapeutic regimen.

Discharge should include follow-up with a colorectal surgeon or gastroenterologist who will monitor the patient's progress clinically and endoscopically, in addition to following results of cultures, labs, and biopsies.

Inpatient & Outpatient Medications

Maintenance medical therapy is not used routinely in idiopathic proctitis unless the patient's condition is slow to respond, difficult to control, or has frequent flare-ups.

In radiation proctitis, there is no evidence that indicates that corticosteroids and/or various aminosalicylic acid derivations given as an enema or orally are beneficial in preventing the progression of the disease.

In hemorrhagic proctitis, formaldehyde is effective in controlling bleeding with no serious complication, but further studies are needed

Complications

Complications of proctitis may include the following:

Chronic ulcerative colitis Fistula formation Abscess Treatment failure Perforation

Prognosis

Failure rates as high as 35% have been reported following treatment of rectal gonorrhea; symptoms frequently recur.

Most surgeons favor a diverting colostomy for medically intractable proctitis.