Proctitis and Anusitis 

Updated: Mar 27, 2020
Author: David E Stein, MD, MHCM; Chief Editor: John Geibel, MD, MSc, DSc, AGAF 



Inflammation of the mucosal lining of the rectum is defined as proctitis, whereas anusitis is simply inflammation of the anal canal. Inflammation in these areas can cause symptoms, such as itching, burning, rectal bleeding, pelvic pressure, and foul-smelling discharge. The distinction between proctitis and anusitis is not overly pertinent, in that the etiology and the treatment of anusitis and proctitis are similar. For the purposes of this article, the term proctitis will be understood to include anusitis.

Several different etiologies exist, including inflammatory bowel disease (IBD), infectious organisms (eg, Neisseria gonorrhoeae, Salmonella, Shigella), noninfectious causes (eg, radiation, ischemic, diversion), and idiopathic causes. For convenience, these etiologies may be divided into three broad categories: IBD, infectious proctitis, and noninfectious proctitis.

Proctitis can occur in both the acute setting and the chronic setting and can cause significant anorectal complaints. Treatment is generally nonsurgical; however, in certain cases, surgery is indicated.


It is important to recognize that most inflammatory processes of the rectum also involve the adjacent colon and the anus. Controversy remains regarding the anatomy of the rectum and the anus. Some authorities say that the rectum starts at the level of the third sacral vertebra, whereas others consider the start of the rectum to be at the sacral promontory.

Where the rectum ends also is debated. Some say that it ends when it passes through the levator ani muscles, but most agree that the rectum transitions to the anus where the epithelial cells change from columnar cells to squamous cells.

The World Health Organization (WHO) and the American Joint Cancer Committee define the anal canal as the distal portion of the gastrointestinal (GI) tract that corresponds to the internal anal sphincter.

In proctitis and anusitis, the anatomy does not change therapy, because a significant overlap between anorectal inflammation and rectosigmoid inflammation exists.


The pathophysiology of proctits is dependent on the various etiologies and is not completely understood. In addition, some patients seem more susceptible to this inflammatory condition, with factors such as young age, previous abdominal surgery, hypertension, vasculopathy, and diabetes cited as possible contributing factors. The pathophysiology of proctitis in IBD is believed to be caused by an autoimmune process, though the specific antigen has not been elicited.

Infectious etiologies may be related to the organism itself or to a toxin produced by the organism.

Radiation proctitis may be due to cellular injury secondary to ischemia from radiation. Diversion proctitis is thought to be caused by a deficiency of short-chain fatty acids. Ischemic proctitis may be due to mesenteric venous occlusion, aortoiliac surgery, radiotherapy, vascular intervention, atherosclerotic disease, or drug use (eg, cocaine).

Regardless, all three categories of proctitis (ie, IBD, infectious, and noninfectious) result in an unrestrained inflammatory response, with the inflammatory cells being products that mediate cellular-tissue injury.


This article divides the etiologies of proctitis into the following three categories:

  • Proctitis due to inflammatory bowel colitides (eg, ulcerative colitis, Crohn disease)
  • Proctitis from infectious causes (eg, Clostridium difficile and Salmonella species); in most cases, the rectal inflammation caused by an infection most likely causes inflammation in the colon as well
  • Proctitis due to noninfectious conditions (eg, diversion, ischemia, and radiation)


No epidemiologic studies have been performed to determine the prevalence of proctitis in the general population. However, one can ascertain the incidence of proctitis when analyzing specific disease states. For example, patients with ulcerative colitis displayed a 31-50% frequency of proctitis upon diagnosis, depending on age at diagnosis. A study in the pediatric ulcerative colitis population demonstrated a significant increase in the occurrence of proctitis in female children as compared with males.[1] The reported frequency of chronic radiation-induced proctitis is in the range of 2-20% and is influenced by total radiation dose, mode of delivery, and dose fractionation.[2]


In the acute setting, most bouts of proctitis have a good outcome and prognosis. More specifically, once appropriately treated, infectious proctitis tends not to recur.

For the more chronic diseases, such as IBD, outcomes and prognoses vary. Clearly, in medically treated ulcerative colitis and proctitis, approximately 40-70% of cases do not require operation. If proctocolectomy is performed, the patient is cured of the disease. Crohn disease is another story. Because it can occur in all portions of the GI tract, even after a proctectomy, recurrence of Crohn disease ranges from 45-90%.

Diversion proctitis generally has a good outcome and prognosis once the diversion is reversed.

The outcome and prognosis of radiation proctitis vary with the severity of proctitis. Outcomes range from requiring a few medical treatments in the form of enemas to surgery. Complication rates for surgical treatment have been reported to be as high as 75%.



History and Physical Examination

A patient with proctitis may present with some of the following symptoms and/or signs:

  • Rectal bleeding tends to be bright red in color and persistent but is rarely severe; it may last for several weeks or longer
  • Changes in bowel habits tend to occur, usually with a decrease in volume and an increase in mucoid contents; patients will complain of a mild diarrhea with a lot of mucus; the mild diarrhea is the most common complaint
  • Patients may report tenesmus or fecal urgency
  • Severe diarrhea generally is uncommon
  • Constipation may occur if the inflammation is severe
  • Patients may also complain of abdominal cramping; this is caused by the inflammation in the pelvis

In taking the patient's history, pertinent questions should include a personal history of inflammatory bowel disease (IBD), pelvic irradiation, travel history, and sexual history (including questions regarding anal intercourse).[3] The patient's HIV status is important to note as well. Obtaining a list of medications used (eg, nonsteroidal anti-inflammatory drugs [NSAIDs] or antibiotics) is clearly important. A family history of IBD or other gastrointestinal (GI) diseases is extremely important.

A review of systems is needed to review any systemic symptoms that can be related to the proctitis, such as IBD and collagen vascular disorders. In addition, identifying patients who are immunocompromised is important, because some infections that may cause proctitis (eg, cytomegalovirus, cryptosporidiosis) affect only this subset of patients.

The physical examination findings may be unremarkable. Abdominal tenderness may be seen in IBD, infectious colitides, and ischemic proctitis. As a consequence of tenderness, it may not be possible to perform a digital rectal examination. If this is the case, an evaluation under anesthesia is required.



Laboratory Studies

In general, for all patients diagnosed with proctitis, a routine workup should be performed to rule out infectious etiologies. The laboratory workup includes stool cultures, ova and parasite analysis, and fecal smears.

In patients at risk, obtain and send an anorectal swab for gonococcal, chlamydial, and herpes simplex viral proctitis. Darkfield microscopy and Venereal Disease Research Laboratory (VDRL)/rapid plasma reagin (RPR) tests should be performed for suspected syphilitic proctitis. Additional tests (eg, polymerase chain reaction [PCR], serologic studies, and nucleic acid amplification tests [NAATs]) may be performed, depending on the suspected etiology.

If the patient is immunocompromised, perform fungal and viral cultures. (Note that fungal and viral anorectal infections are rare in the immunocompetent population.)

Regarding pseudomembranous proctitis or colitis due to C difficile, send the stool for C difficile toxin titers for any patient with a history of current or recent use of antibiotic usage. This must be sent three times to ensure an accurate result; many of the tests have a sensitivity of only 60%. Sending the collection and cultures in accordance with the laboratory specifications is important because the specifications may vary from hospital to hospital.

Entamoeba histolytica is diagnosed by finding the amoeba in the stool; one must send three stool samples for the analysis to be valid. In addition, serologic tests exist, including indirect hemagglutination, indirect electrophoresis, and an enzyme-linked immunosorbent assay (ELISA).

Imaging Studies

Generally, no imaging studies are needed if the inflammation is known to be limited to the rectum and the anus. However, if the possibility of inflammatory bowel disease (IBD; that is, either Crohn disease or ulcerative colitis) or ischemia exists, then further imaging studies may be necessary.

If Crohn disease is a possibility, a contrast upper gastrointestinal (GI) radiograph with a small bowel follow-through may reveal terminal ileal disease and jejunal ileal strictures. A baseline computed tomography (CT) scan of the abdomen and pelvis may also show enteroenteric fistulas and bowel wall thickening consistent with Crohn disease.

In infectious colitides, if the patient has been admitted to the hospital, a CT scan may be obtained, which may show colonic and rectal wall inflammation. This may help in determining the diagnosis.

In ischemic proctitis, a CT scan of the abdomen and pelvis with oral and intravenous contrast is obtained. The most common finding is mural thickening confined to the rectum and the sigmoid colon, which is associated with perirectal fat stranding.


The diagnostic procedure of choice for patients with proctitis and anusitis is endoscopy, including anoscopy, sigmoidoscopy (rigid or flexible), and colonoscopy. (See the image below.) These tests allow the provider to view the mucosa of the anus and rectum as well as the area above the rectum into the sigmoid. In addition, tissue biopsies may be taken with these procedures. A full colonoscopy is recommended for patients with proctitis; biopsy specimens obtained from the right side of the colon may show hallmarks of IBD, such as cell metaplasia.

Proctitis seen on flexible endoscopy. Proctitis seen on flexible endoscopy.

Histologic Findings

Histologic findings are usually consistent with inflammation. However, detailed histology leading to the etiology is often not possible. Severe inflammation destroys the specific histopathologic findings of other diseases, such as IBD or C difficile infection.

Regarding infectious etiologies, diversion colitis, or radiation proctitis, the inflammatory histology is not pathognomonic. The one exception is cytomegalovirus colitis in patients who are immunocompromised, in which inclusion bodies may be seen.



Approach Considerations

The indications for therapy vary according to the etiology of the proctitis. For example, in patients with inflammatory bowel disease (IBD), a colonoscopy should be performed to find out the extent of the inflammation. Many patients with IBD who present with proctitis may progress to left-side colitis and possibly pancolitis. The first-line management of these patients is medical therapy (see below). Surgical treatment is indicated for failed medical therapy, any dysplasia seen on biopsy specimens, and cancer.

Surgery is rarely indicated for proctitis secondary to an infectious etiology. The goal of therapy is to treat the infection causing the inflammation. Rarely, profound sepsis may necessitate surgical resection as a life-saving maneuver.

Finally, the indication for treatment of chronic radiation proctitis is also based on the symptomatology and grade of proctitis. Persistent rectal bleeding and diarrhea initiate a workup, including a rigid proctoscopy and/or colonoscopy. The presence of intractable bleeding despite multiple medical/endoscopic modalities, perforation, strictures, or fistulas is an indication for surgical intervention.

In the course of any proctitis, antispasmodic agents may prove helpful in alleviating the abdominal complaints. In addition, the use of a low-residue diet and stool softeners is beneficial because of the friability of the rectal mucosa and its vulnerability to damage from the fecal contents.

Medical Therapy

Medical treatment of proctitis depends on the etiology (see below).

Idiopathic proctitis and inflammatory bowel disease

If proctitis is idiopathic or related to IBD, steroids, sulfasalazine, mesalamine, 5-aminosalicylic acid (5-ASA) products, and even immunosuppressive medications may be used. Many of these products are available as oral medications as well as enemas and suppositories.[4] Combination therapy using both oral agents and topical agents, such as 5-ASA, has been shown to be more effective than therapy with either modality alone. In cases of refractory ulcerative proctitis, infliximab has been found to be effective in inducing a clinical response.[5, 6]

Infectious proctitis

If the cause of proctitis is infectious, the treatment is targeted toward the pathogen responsible.

Infectious proctitis due to Salmonella species is usually self-limited, and antibiotics are not required. Maintaining adequate fluid and electrolyte balances and providing supportive care are all that is required.

Shigella proctitis is usually self-limited, but the duration may be shortened by the addition of antibiotics. Antibiotics for 1 week may include ampicillin, tetracycline, ciprofloxacin, and trimethoprim-sulfamethoxazole (preferred).

Yersinia proctitis is also self-limited and should not be treated with antibiotics unless systemic septicemia occurs; in which case, antibiotics (eg, trimethoprim-sulfamethoxazole, aminoglycosides, tetracycline, third-generation cephalosporin) should be used.

Campylobacter proctitis is usually self-limited as well.

E histolytica generally is treated with metronidazole and iodoquinol.

Sexually transmitted proctitis requires treatment similar to the corresponding treatment for a genital infection. Chlamydia trachomatis infection is treated with doxycycline; gonorrheal proctitis is treated with ceftriaxone or cefixime. Syphilitic proctitis responds to intramuscular (IM) penicillin G benzathine, and herpes simplex virus type 2 infection is treated with acyclovir.

C difficile infection generally is treated with intravenous (IV) or oral metronidazole or oral vancomycin.[7] A more aggressive C difficile mutation has been seen and may have a rapidly progressive course toward septicemia and toxic colitis. In patients who do not appear to be responding to metronidazole and who have leukocytosis (leukocyte count >20,000/┬ÁL), therapy should be switched to oral vancomycin. Vancomycin enemas may also be used in individuals in whom oral antibiotics may not reach a part of the colon (eg Hartman pouch, ileostomy, colonic diversion). Discontinuation of any other antibiotics should be ordered if the clinical situation allows.

Patients colonized with C difficile have a likelihood of recurrence; consequently, whenever they are placed on antibiotics, they should be aware of the possibility of diarrhea. In patients with recurrent C difficile infections, physicians may consider fecal microbiota transplantation, which has been reported to achieve cure rates of 90% and higher in multiple studies.

Noninfectious proctitis

Acute radiation proctitis is usually a self-limited condition, but supportive medical management (eg, hydration, antidiarrheals, and steroid or 5-ASA enemas) may be of benefit.[8]

Chronic radiation proctitis involves more extensive medical treatment, including both oral and rectal therapies. Oral medications include 5-ASA, sulfasalazine, steroids, and metronidazole. Another therapeutic approach is the use of WF10, an IV therapy initially developed as an adjunctive AIDS treatment. Initial studies demonstrate control of bleeding within two doses of therapy and maintenance of results with once- to twice-yearly repeat therapy.[9]

Rectal therapy for chronic radiation proctitis with sucralfate or pentosan polysulfate has been shown to result in better symptomatic relief than oral anti-inflammatory therapy. Studies demonstrate sucralfate enemas to be the most effective medical therapy for radiation proctitis when administered twice daily for 3 months. Such rectal therapies are believed to work via stimulation of epithelial healing and formation of a protective barrier.

Steroid and short-chain fatty acid enemas have also been used with moderate success.[10] In terms of steroid enemas, hydrocortisone seems to be more effective in relieving symptoms and rectal bleeding compared with other steroids, such as betamethasone. Whereas short-chain fatty acid enemas, such as butyrate, have some proven benefit in other types of proctitis, no studies have conclusively demonstrated that they have any beneficial effect on proctitis secondary to radiation.

Research has shown hyperbaric oxygen treatment to have some efficacy in the treatment of radiation-induced proctitis.[11, 12] A large single-center study reported a 63% response rate in patients with gastrointestinal radionecrosis, supporting the findings of several previous smaller series.[13] Hyperbaric oxygen therapy has emerged as a potential therapy for radiation proctitis because of its ability to increase the number of blood vessels in irradiated tissues by acting as a stimulant for angiogenesis; however, further studies must be performed to establish the efficacy of this treatment modality.[14]

Other medical therapies aimed at the treatment of radiation proctitis, such as antioxidant therapy with vitamins A, C, and E, have showed efficacy in small single-institution studies,[15] but at present, the evidence is insufficient to justify recommendation. Additionally, ozone therapy via rectal insufflation and topical ozonized oil has shown some possible efficacy, but large randomized clinical trials are lacking.

More invasive management of radiation proctitis with rectal/topical formalin is believed to work via sclerosis of neovasculature in a form of chemical cauterization. Multiple studies have demonstrated the efficacy of formalin in the resolution of hemorrhagic proctitis, with success rates in the range of 70-80%.[16, 17, 18] Of note, significant complications from treatment include stricture and skin damage to the perianal skin.

Symptomatic diversion proctitis generally improves after the ostomy is taken down and bowel continuity is restored. However, in patients who need to be out of circuit indefinitely, short-chain fatty acid enemas may be beneficial.

Surgical Therapy

Many factors come into play in deciding when to operate and which operation to perform. For most cases of proctitis, medical treatment should suffice. However, for certain disease processes, surgical treatment is more likely.

Choice of procedure

For patients with ulcerative colitis requiring surgical therapy, a total proctocolectomy should be performed because of the risk of cancer in the remaining rectal stump.[19] Ileostomy or reconstruction with an ileal pouch may be offered after total proctocolectomy. In patients with severe Crohn colitis or proctitis, options range from fecal diversion to proctectomy to total proctocolectomy, depending on the extent of the disease process.

In the infectious causes of proctitis, surgical treatment is rarely required. In cases of severe C difficile colitis, a subtotal colectomy may be warranted.

For patients with radiation proctitis complicated by refractory bleeding, endoscopic therapy seems to be more effective than medical therapy; it also results in less morbidity than surgical therapy. Specifically, argon plasma coagulation (APC)[16, 20, 21] has proved to be superior to formalin and endoscopic laser treatments. Other endoscopic therapies include endoscopic thermal methods, such as heater probes and lasers, which destroy telangiectasias to stop bleeding.

If, despite medical and endoscopic measures, significant hemorrhage still occurs, a laparoscopic fecal diversion (ileostomy or colostomy) should be performed. Although fecal diversion alleviates patients' symptoms, it rarely eliminates them entirely; it should be reserved for truly refractory cases. Fewer than 10% of patients do not respond to some form of medical management and require surgical intervention.

Rarely, radiation proctitis can be so severe that it ulcerates, potentially leading to the formation of a rectourethral fistula. In these cases, temporary fecal and urinary diversion should be performed until the inflammation subsides. Definitive therapy may then be provided. The procedure of choice is a perineal approach with repair of the defect with muscle and mucosal flaps.

Preparation for surgery

As always, general surgical preparation includes optimizing medical status and providing deep vein thrombosis (DVT) prophylaxis, bowel preparation, and preoperative antibiotic prophylaxis. A Foley catheter will be placed after induction of anesthesia.

Preoperative nutritional status may be the most significant predictor of outcomes. Every effort should be given to assess the patient's nutritional status and improve it if necessary. The author's current practice is to obtain a prealbumin level on all patients scheduled to undergo laparotomy. If it is low, the author will delay the surgery and place them on nutritional supplementation.

If the patient is going to have a stoma, preoperative counseling with a trained enterostomal nurse is essential. The nurse will educate the patient about life with a stoma and also mark the patient preoperatively to ensure optimal stoma placement.

For patients requiring a subtotal colectomy, an assessment of their sphincter complex is helpful in determining postoperative fecal continence. This is also true for patients undergoing a total proctocolectomy with an ileal pouch.

In addition, for patients undergoing a proctectomy, it is important to discuss their sexual and urinary function before performing the procedure; there is a small but real possibility of diminished sexual function and bladder continence after pelvic surgery.

Operative details

Good surgical technique is imperative. In the performance of a pelvic dissection, knowing the anatomic planes and adjacent structures is important for avoiding injury.

The presacral nerves are on the anterior aspect of the sacrum. These nerves usually can be identified at the sacral promontory, approximately 1 cm lateral to the midline.

Be aware of the parasympathetic innervation to the urinary and genital organs and the rectum at the lateral edges of the rectum, near the lateral stalks. The parasympathetic nerve supply in this area is from the nervi erigentes. Dissection that is too lateral will likely affect this nerve supply.

Maintain the correct plane of dissection along the posterior rectum. Along the same principles of total mesorectal excision, the plane outside the mesorectum but above the presacral fascia is the correct plane to dissect. Dissection that is too anterior results in entry into the mesorectum. Dissection that is too deep through the presacral fascia risks presacral bleeding.

Maintain the correct plane of dissection along the anterior rectum. Clearly, important structures exist in both females (vagina) and males (prostate, seminal vesicles).

Remain cognizant of the course of the ureters along the lateral rectum when dissection enters into the pelvis.

Postoperative Care

As with any major surgical procedure, close monitoring of fluid status, cardiac status, pulmonary status, and return of gastrointestinal (GI) function is important. For patients who require a hospital stay, DVT prophylaxis is essential. Many centers have different protocols for removing a Foley catheter. The author tends to remove the Foley catheter on the third postoperative day.

One of the more important concerns includes those patients with a perineal wound. Often, tension on the wound may be significant, depending on whether the sphincter mechanism is resected or not. Because patients often are in the supine position, overlooking examination of the perineal wound is easy. Close observation of this area is important; problems with wound healing in this area are significant. The risk of wound complications increases in those patients who have undergone irradiation of the pelvis.


Wound infection may develop with a proctectomy. It is not uncommon for the perineal wound to separate slightly during the immediate postoperative period. If any discharge or erythema is noted around the wound, especially if there was some tension upon closure, opening the wound earlier rather than later is prudent. Addressing the open wound with wet-to-dry dressing changes routinely allows the wound to close without incident.

Sexual dysfunction can occur when the pelvic nerves are injured. The best way to deal with this complication is to be cognizant of the possibility prior to surgery and avoid it. Once it occurs, very little can be done to help the nerves. The role of medications such as sildenafil remains unclear, though sildenafil has been reported to help.

As with sexual dysfunction, every effort should be made to avoid urinary dysfunction in the operating room.

Avoiding ureteral injury by remaining cognizant of the ureteral anatomy is a paramount consideration. Once the injury occurs, recognizing this at the time of operation clearly is best. The repair is dictated by where the injury occurs in the ureter. Consultation with a urologist is prudent.

In a few cases, presacral bleeding has been reported to progress to death. Clearly, avoidance is the best way to deal with this complication. If it does occur in the midst of the procedure, cautery or pressure generally does not stop true presacral bleeding from the pelvic veins. The usual method of stopping the bleeding is to use a thumbtack. A muscle pledget is also a clever way to cauterize the bleeding. Take a piece of rectus muscle, apply it to the bleeding site, and cauterize the muscle on a high coagulation setting.

Long-Term Monitoring

Follow-up care with regard to the surgical wounds (both perineal and abdominal) and the colostomy is important. In addition, postoperative sexual and urinary function should be discussed and a further workup initiated if required.



Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.


Class Summary

These agents are the treatments of choice for an acute inflammatory bowel disease (IBD) attack; administer IV in severe disease. Administer increased or stress doses to patients already on steroids. Do not use steroids for maintaining remission because of their lack of efficacy and potential complications, including avascular necrosis, osteoporosis, cataracts, emotional lability, hypertension, diabetes mellitus, cushingoid features, acne, and facial hair. Cortenema, Cortifoam, and Anusol-HC suppositories are useful in treating distal disease (proctitis and proctosigmoiditis).

Budesonide (Entocort EC, Uceris)

Budesonide alters the level of inflammation in tissues by inhibiting multiple types of inflammatory cells and decreasing the production of cytokines and other mediators involved in inflammatory reactions.

Hydrocortisone (Cortenema, Anusol-HC, Proctocort, Proctocream HC, Proctosol HC)

Adrenocortical steroids act as potent inhibitors of inflammation. It may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative adrenocortical steroids may be used in equivalent dosage.

Methylprednisolone (Depo-Medrol, Medrol, Solu-Medrol)

Adrenocortical steroids act as potent inhibitors of inflammation. They may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative adrenocortical steroids may be used in equivalent dosage.

Dexamethasone (Dexamethasone Intensol)

Dexamethasone has many pharmacologic benefits, but also significant adverse effects. It stabilizes cell and lysosomal membranes, increases surfactant synthesis, and inhibits prostaglandin and proinflammatory cytokines.

Prednisone (Deltasone, Prednisone Intensol, Rayos)

Prednisone acts as a potent inhibitor of inflammation. It may cause profound and varied metabolic effects, particularly in relation to salt, water, and glucose tolerance, in addition to their modification of the immune response of the body. Alternative corticosteroids may be used in equivalent dosage.

5-Aminosalicylic Acid Derivatives

Class Summary

These agents are effective in reducing inflammatory reactions. All of the aminosalicylates are useful for treating flares of IBD and for maintaining remission.

Sulfasalazine (Azulfidine, Azulfidine EN)

This agent is considered best for colonic disease, although it is also considered first-line therapy for Crohn disease. It is used for acute disease and for maintenance of remission.

Mesalamine (Apriso, Asacol HD, Delzicol, Pentasa, Rowasa)

Mesalamine is a 5-ASA and acts systemically. It also has activity as a topical anti-inflammatory.

Balsalazide (Colazal, Giazo)

Balsalazide is a prodrug 5-ASA connected to a 4-aminobenzoyl-(beta)-alanine carrier by an azo bond; colonic bacteria break the azo bond, releasing the active 5-ASA. Metabolites of the drug may decrease inflammation by blocking the production of arachidonic acid metabolites in colonic mucosa.

Olsalazine (Dipentum)

This aminosalicylate is useful for active disease and maintenance of remission in ulcerative colitis. Olsalazine is 5-ASA connected to a 5-ASA by an azo bond; colonic bacteria break the azo bond, releasing the active 5-ASA.


Class Summary

Agents in this class neutralize cytokine TNF-alpha and inhibit its binding to the TNF-alpha receptor.

Infliximab (Remicade)

Infliximab, given intravenously, consists of monoclonal antibodies to TNF-alpha. Approved by the FDA for use in IBD, in both Crohn disease and ulcerative colitis. Infliximab is somewhat more effective against CD than UC. The drug appears to promote mucosal healing. Furthermore, it heals perianal and enterocutaneous fistulae and has been shown to reduce signs and symptoms, achieve clinical remission, and eliminate corticosteroid use. Indicated for patients who have experienced inadequate response to conventional therapy.


Class Summary

Antimicrobial therapy must cover all likely pathogens in the context of the clinical setting. Antibiotics are used sparingly in persons with ulcerative colitis, because ulcerative colitis increases the risk of developing antibiotic-associated pseudomembranous colitis.


Ampicillin, a broad-spectrum penicillin, interferes with bacterial cell-wall synthesis during active replication, causing bactericidal activity against susceptible organisms.

Ciprofloxacin (Cipro, Cipro XR)

Inhibits DNA gyrase and topoisomerase IV for bactericidal activity. Use as an alternative for MRSA infection.


Tetracycline inhibits bacterial protein synthesis by binding with 30S and possibly 50S ribosomal subunit(s). This agent treats gram-positive and gram-negative organisms and mycoplasmal, chlamydial, and rickettsial infections.

Doxycycline (Acticlate, Adoxa, Avidoxy, DoryxMonodox, Vibramycin)

Doxycycline inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS)

This combination agent inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid. Trimethoprim is a dihydrofolate reductase inhibitor that prevents tetrahydrofolic acid production in bacteria. It is active in vitro against a broad range of gram-positive and gram-negative bacteria, including uropathogens (eg, Enterobacteriaceae and Staphylococcus saprophyticus). Resistance is usually mediated by decreased cell permeability or alterations in amount or structure of dihydrofolate reductase. It demonstrates synergy with sulfonamides, potentiating inhibition of bacterial tetrahydrofolate production

Metronidazole (Flagyl, Flagyl ER, Metro)

Metronidazole is a widely available, inexpensive antibiotic and antiprotozoal agent. Inhibits protein synthesis and causes cell death in susceptible organisms by diffusing into the organism and causing a loss of helical DNA structure and strand breakage.

Rifaximin (Xifaxan)

Rifaximin is a nonabsorbed (<0.4%), broad-spectrum antibiotic specific for enteric pathogens of the gastrointestinal tract (ie, gram-positive, gram-negative, aerobic, anaerobic). It is a rifampin structural analog and it binds to the beta-subunit of bacterial DNA-dependent RNA polymerase, thereby inhibiting RNA synthesis.

Penicillin G benzathine (Bicillin LA)

Interferes with synthesis of cell wall mucopeptides during active multiplication, which results in bactericidal activity. Used to treat syphilis and for prophylaxis of recurrent streptococcal infections.

Vancomycin (Vancocin)

Potent antibiotic directed against gram-positive organisms and active against Enterococcus species. Useful in the treatment of septicemia and skin structure infections. Indicated for patients unable to receive or have failed to respond to penicillins and cephalosporins or have infections with resistant staphylococci. For abdominal penetrating injuries, is combined with an agent active against enteric flora and/or anaerobes.

Ceftriaxone (Rocephin)

Third-generation cephalosporin with broad-spectrum gram-negative activity; lower efficacy against gram-positive organisms; higher efficacy against resistant organisms. Arrests bacterial growth by binding to one or more penicillin binding proteins.


Aminoglycoside antibiotic for gram-negative coverage. Used in combination with an agent against gram-positive organisms and one that covers anaerobes.

Cefixime (Suprax)

Potent long-acting oral cephalosporin with increased gram-negative coverage.

Ampicillin/sulbactam (Unasyn)

Drug combination of beta-lactamase inhibitor with ampicillin. Covers skin, enteric flora, and anaerobes. Not ideal for nosocomial pathogens.


Class Summary

Parasite biochemical pathways are sufficiently different from the human host to allow selective interference by chemotherapeutic agents in relatively small doses.

Iodoquinol (Aloquin)

Amebicidal against E histolytica. Considered effective against trophozoite and cyst forms.Halogenated hydroxyquinoline. Luminal amebicide; acts primarily in bowel lumen because it is poorly absorbed. Best tolerated when given with meals. Because it is active only against intraluminal form of amebiasis, it is used to eradicate cysts of E histolytica after treatment of invasive disease.

Antivirals, HSV

Class Summary

The goals of using antivirals are to shorten the clinical course, prevent complications, prevent development of latency and subsequent recurrences, decrease transmission, and eliminate established latency.

Acyclovir (Zovirax)

Acyclovir is the drug of choice for HSE. It has demonstrated inhibitory activity against both herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2) and is taken up selectively by infected cells. Mortality from HSE before use of acyclovir was 60-70%; since acyclovir, it is approximately 30%.

Gastrointestinal Agents, Other

Class Summary

Agents in this class protect the gastric lining against peptic acid.

Sucralfate (Carafate)

Sucralfate binds to positively charged proteins in exudates to form a complex, which is a viscous paste-like, adhesive substance. It forms a protective coating that acts locally to protect the gastric lining against peptic acid, pepsin, and bile salts.


Questions & Answers


What are proctitis and anusitis?

Which anatomy is relevant to proctitis and anusitis?

What is the pathophysiology of proctitis and anusitis?

What causes proctitis and anusitis?

What is the prevalence of proctitis and anusitis?

What is the prognosis of proctitis and anusitis?


What are the signs and symptoms of proctitis?

What is the focus of the clinical history for suspected proctitis and anusitis?


What is the role of lab studies in the diagnosis of proctitis and anusitis?

What is the role of imaging studies in the diagnosis of proctitis and anusitis?

What is the role of endoscopy in the diagnosis of proctitis and anusitis?

Which histologic findings are characteristic of proctitis and anusitis?


How are proctitis and anusitis treated?

How is medical therapy for proctitis and anusitis selected?

How are idiopathic proctitis and inflammatory bowel disease-related proctitis treated?

How is infectious proctitis treated?

How is noninfectious proctitis treated?

When is surgery indicated in the treatment of proctitis and anusitis?

What is included in the preoperative evaluation of proctitis and anusitis?

How is surgery for proctitis and anusitis performed?

What postoperative care is provided following proctitis and anusitis surgery?

What are the possible complications of proctitis and anusitis surgery?

What is included in the long-term monitoring following proctitis and anusitis surgery?


What are the goals of drug treatment for proctitis and anusitis?

Which medications in the drug class Gastrointestinal Agents, Other are used in the treatment of Proctitis and Anusitis?

Which medications in the drug class Antivirals, HSV are used in the treatment of Proctitis and Anusitis?

Which medications in the drug class Amebicides are used in the treatment of Proctitis and Anusitis?

Which medications in the drug class Antibiotics are used in the treatment of Proctitis and Anusitis?

Which medications in the drug class Immunosuppressants are used in the treatment of Proctitis and Anusitis?

Which medications in the drug class 5-Aminosalicylic Acid Derivatives are used in the treatment of Proctitis and Anusitis?

Which medications in the drug class Corticosteroids are used in the treatment of Proctitis and Anusitis?