Acute Proctitis

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Background

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 gonorrhea and chlamydia, or less commonly lymphogranuloma venereum or herpes virus. Nonsexually transmitted causes include autoimmune disease of the colon, such as Crohn disease and ulcerative colitis, celiac disease, chemicals, rectal instrumentation, and trauma to the anorectal area. It may also occur as idiopathic proctitis.

For more information on Crohn disease and ulcerative colitis, see Medscape's Inflammatory Bowel Disease Resource Center.

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.

Etiology

Causes of proctitis may include the following:

Epidemiology

United States data

Frequencies of proctitis are associated with their individual etiologies.

Radiation therapy accounts for 5-20% of patients with acute proctitis, usually within 6 months of treatment with a total dose of greater than 50 Gy. Chronic radiation proctitis has a more delayed onset from 9-14 months after initial radiation exposure but can occur any time up to 30 years post irradiation.[1]

Proctitis occurs predominantly in adults.

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 or proctectomy.[2, 3]

Complications

Complications of proctitis may include the following:

History

General symptoms of acute proctitis include the following:

Idiopathic proctitis

Symptoms of idiopathic proctitis include the following:

Infectious proctitis

Infectious proctitis may have the following features:

Radiation-induced proctitis

Radiation-induced proctitis includes the following symptoms:

Physical Examination

Physical examination findings may include the following:

Laboratory Studies

Consider the following laboratory studies:

Procedures

Proctosigmoidoscopy reveals the following:

Perform a biopsy for histology, culture, viral studies, and Chlamydia studies.

Perform 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.

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, including the following:

In an observational study, investigators analyzed data from 26 patients with acute proctitis symptoms. Lymphogranuloma venereum (LGV) serovar L2 was confirmed in all patients, all of whom were men who have had sex with men (MSM) and 24 of whom were HIV-positive. After standard treatments with doxycycline 100 mg twice per day for 3 weeks, the cure rate was 100%.[8]

Discharge

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.

For patient education resources, see the Digestive Disorders Center, as well as Rectal Pain and Rectal Bleeding.

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, topical formaldehyde is effective in controlling bleeding with no serious complication, but further studies are needed.[6]

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.

Medication Summary

Drug therapy consists of antibiotics, antivirals, corticosteroids, and GI agents.

Metronidazole (Flagyl)

Clinical Context:  Active against various anaerobic bacteria and protozoa. Appears to be absorbed into cells. Intermediate metabolized compounds are formed and bind DNA and inhibit protein synthesis, causing cell death. Antimicrobial effect may be due to production of free radicals.

Indicated for invasive E histolytic infections.

Vancomycin (Vancocin)

Clinical Context:  Has excellent in vitro activity against C difficile. Kills organism by inhibiting cell wall synthesis. Significant luminal levels after PO vancomycin can be obtained because it is poorly absorbed from the GI tract. Major disadvantage is cost. PO vancomycin is relatively expensive, with a wholesale cost of approximately $150 for a 10-d supply. Because of the cost and the concern over the emergence of vancomycin-resistant enterococci strains, its use should be reserved for patients who cannot tolerate metronidazole, patients who do not respond to metronidazole, pregnant patients, and patients < 10 y. Also preferred for severe cases and in patients who are high risk. Unlike IV metronidazole, IV vancomycin is not excreted into the GI lumen; therefore, delivering effective doses by this route is difficult.

Ciprofloxacin (Cipro)

Clinical Context:  Fluoroquinolone that inhibits bacterial DNA synthesis and, consequently, growth, by inhibiting DNA gyrase and topoisomerases, which are required for replication, transcription, and translation of genetic material. Quinolones have broad activity against gram-positive and gram-negative aerobic organisms. Has no activity against anaerobes. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.

Usually administered on empiric basis in patients with severe colitis in addition to steroids. Also used for the treatment of pouchitis after colectomy and ileo-anal anastomosis.

Ceftriaxone (Rocephin)

Clinical Context:  Used because of an increasing prevalence of penicillinase producing N gonorrhoeae. It inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, causing bacterial growth inhibition.

Doxycycline (Doryx, Bio-Tab, Vibramycin)

Clinical Context:  Required with ceftriaxone for the treatment of gonorrheal proctitis. Inhibits protein synthesis and, thus, bacterial growth by binding with the 30S and possibly the 50S ribosomal subunits of susceptible bacteria.

Penicillin G benzathine (Bicillin L-A)

Clinical Context:  A bactericidal used in the treatment of rectal syphilis. Interferes with bacterial cell wall synthesis during active multiplication, inhibiting bacterial growth.

Tetracycline (Sumycin)

Clinical Context:  Treats susceptible bacterial infections of both gram-positive and gram-negative organisms as well as infections caused by Mycoplasma, Chlamydia, and Rickettsia species. Inhibits bacterial protein synthesis and, thus, bacterial growth by binding with 30S and possibly 50S ribosomal subunit(s) of susceptible bacteria.

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Sulfasalazine (Azulfidine)

Clinical Context:  Useful in the management of ulcerative colitis; acts locally in the colon to decrease the inflammatory response and systemically inhibits prostaglandin synthesis.

Mesalamine (Rowasa, Asacol, Canasa, Pentasa)

Clinical Context:  Used for treatment of mildly to moderately active ulcerative colitis. The usual course of therapy in adults is 3-6 wk. Some patients may need concurrent oral and rectal therapy.

Class Summary

These agents decrease inflammation associated with proctitis, perhaps by inhibiting prostaglandin synthesis.

Acyclovir (Zovirax)

Clinical Context:  Reduces duration of symptomatic lesions. Indicated for patients who present within 48 h of experiencing rash. Patients taking acyclovir experience less pain and faster resolution of cutaneous lesions.

Class Summary

These agents are used for the treatment of herpes-related proctitis. They inhibit viral replication by competing with deoxyguanosine triphosphate for viral DNA polymerase.

Dexamethasone (AK-Dex, Alba-Dex, Baldex, Decadron, Dexone)

Clinical Context:  Has many pharmacologic benefits but significant adverse effects. Stabilizes cell and lysosomal membranes, increases surfactant synthesis, increases serum vitamin A concentration, and inhibits prostaglandin and proinflammatory cytokines (eg, TNF-alpha, IL-6, IL-2, and IFN-gamma). The inhibition of chemotactic factors and factors that increase capillary permeability inhibits recruitment of inflammatory cells into affected areas. Suppresses lymphocyte proliferation through direct cytolysis and inhibits mitosis. Breaks down granulocyte aggregates, and improves pulmonary microcirculation. Adverse effects are hyperglycemia, hypertension, weight loss, GI bleeding or perforation synthesis, cerebral palsy, adrenal suppression, and death. Most of the adverse effects of corticosteroids are dose-dependent or duration-dependent.

Readily absorbed via the GI tract and metabolized in the liver. Inactive metabolites are excreted via the kidneys. Lacks salt-retaining property of hydrocortisone.

Patients can be switched from an IV regimen to a PO regimen in a 1:1 ratio.

Prednisolone (Articulose-50, Delta-Cortef, PediaPred)

Clinical Context:  Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.

Prednisone (Sterapred)

Clinical Context:  May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immunity to diverse stimuli.

Amifostine (Ethyol)

Clinical Context:  Prodrug that is dephosphorylated by alkaline phosphatase in tissues to a pharmacologically-active free thiol metabolite. The free thiol is available to bind to, and detoxify, reactive metabolites of cisplatin; and can also act as a scavenger of free radicals that may be generated (by cisplatin or radiation therapy) in tissues.

Class Summary

These agents reduce the cumulative renal toxicity associated with the repeated administration of chemotherapy agents like cisplatin.

Pentosan polysulfate sodium (Elmiron)

Clinical Context:  Response rate is 71-100%, and recurrence rate is 23%. Protects transitional epithelium by restoring the bladder glycosaminoglycan layer.

Class Summary

Agents that serve as buffers and protect the tissues from chemotherapeutic agents can be used.

What is acute proctitis?What is the pathophysiology of acute proctitis?What causes acute proctitis?What is the prevalence of acute proctitis?What is the prognosis of acute proctitis?What are the possible complications of acute proctitis?What are the signs and symptoms of acute proctitis?What are the signs and symptoms of idiopathic proctitis?What are the signs and symptoms of infectious proctitis?What are the signs and symptoms of radiation-induced proctitis?Which physical findings are characteristic of acute proctitis?What are the differential diagnoses for Acute Proctitis?What is the role of lab tests in the workup of acute proctitis?What is the role of proctosigmoidoscopy in the workup of acute proctitis?What is the role of biopsy in the workup of acute proctitis?What is the role of colonoscopy in the workup of acute proctitis?What is the role of barium studies in the workup of acute proctitis?What is included in discharge instructions for acute proctitis?How is acute proctitis treated?What is the role of maintenance therapy for idiopathic proctitis?How is the progression of radiation proctitis prevented?Which specialist consultations are beneficial to patients with acute proctitis?What is the role of medications in the treatment of acute proctitis?Which medications in the drug class Urinary analgesics are used in the treatment of Acute Proctitis?Which medications in the drug class Chemoprotective agent are used in the treatment of Acute Proctitis?Which medications in the drug class Corticosteroids are used in the treatment of Acute Proctitis?Which medications in the drug class Antivirals are used in the treatment of Acute Proctitis?Which medications in the drug class Rectal anti-inflammatory agents are used in the treatment of Acute Proctitis?Which medications in the drug class Antibiotics are used in the treatment of Acute Proctitis?

Author

Lisandro Irizarry, MD, MPH, FACEP, Chair, Department of Emergency Medicine, Wyckoff Heights Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Ibis Yarde, MD, Staff Physician, Department of Emergency Medicine, Brooklyn Hospital Center

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Barry E Brenner, MD, PhD, FACEP, Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Sanz Laniado Medical Center, Netanya, Israel

Disclosure: Nothing to disclose.

Additional Contributors

Michael S Beeson, MD, MBA, FACEP, Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Disclosure: Nothing to disclose.

Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Disclosure: Nothing to disclose.

Acknowledgements

Eugene Hardin, MD, FAAEM, FACEP Former Chair and Associate Professor, Department of Emergency Medicine, Charles Drew University of Medicine and Science; Former Chair, Department of Emergency Medicine, Martin Luther King Jr/Drew Medical Center

Disclosure: Nothing to disclose.

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