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.
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.
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
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.
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 of proctitis may include the following:
Chronic ulcerative colitis
Fistula formation
Abscess
Treatment failure
Perforation
General symptoms of acute proctitis include the following:
Feeling of rectal fullness
Anal and rectal pain
Diarrhea, usually frequent, small amounts
Frequent or continuous urge to have a bowel movement
Pain in the lower left abdomen
Passing mucus through the rectum
Rectal bleeding
Symptoms of idiopathic proctitis include the following:
Passage of blood and mucus per rectum
Tenesmus
Occasionally, passage of loose stool, with or without lower abdominal pain or rectal cramping
Infectious proctitis may have the following features:
Pruritus
Rectal and anal pain (may become severe)
Avoidance of defecation due to pain
Most common causes - Neisseria gonorrhoeae, Chlamydia trachomatis, herpes simplex virus (HSV) types 1 and 2
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 includes the following symptoms:
Early symptoms include tenesmus and diarrhea that resolve shortly after the radiation treatment period.
Later symptoms of proctitis (occurring months to years after the completion of radiation therapy) include tenesmus, bleeding, low-volume diarrhea, and rectal pain.
Symptoms of radiation-induced proctitis are associated with low-grade obstruction or fistulous tracts into adjacent organs.
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[4]
Clostridium difficile colitis/proctitis
Infections (eg, shigellosis, amebiasis)
Traumatic proctitis
Vulvovaginitis
Consider the following 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.
C-reactive protein level is elevated in patients with extensive pancolitis but is frequently 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.
Proctosigmoidoscopy reveals the following:
Pallor or erythema
Loss of usual vascularity of mucosa
Prominent telangiectasia
Friability
Bleeding
Ulcerations
Edema
Scattered areas of scarring
Vesicles/pustules
Strictures
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.
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:
Sitz baths, antispasmodic medications, stool softeners, low residue diet (may provide relief)
Steroid enemas or suppositories for ulcerative proctitis canasa 1 g enema or suppository daily for a month
Ceftriaxone and doxycycline for gonorrheal proctitis
Acyclovir for herpetic proctitis
Tetracycline or doxycycline for chlamydial proctitis
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).
Yersinia proctitis is usually self-limiting, but, if systemic bacteremia occurs, treat with intravenous antibiotics such as tetracycline or ceftriaxone.
Campylobacter proctitis is a self-limiting disease; treatment is aimed at symptomatic relief.
Metronidazole (Flagyl) or iodoquinol for amebiasis proctitis
Metronidazole (Flagyl) or oral vancomycin for C difficile proctitis
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.[5, 6, 7]
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 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]
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.
Drug therapy consists of antibiotics, antivirals, corticosteroids, and GI agents.
Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.
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.
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.
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.
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.
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.
A bactericidal used in the treatment of rectal syphilis. Interferes with bacterial cell wall synthesis during active multiplication, inhibiting bacterial growth.
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.
These agents decrease inflammation associated with proctitis, perhaps by inhibiting prostaglandin synthesis.
Useful in the management of ulcerative colitis; acts locally in the colon to decrease the inflammatory response and systemically inhibits prostaglandin synthesis.
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.
These agents are used for the treatment of herpes-related proctitis. They inhibit viral replication by competing with deoxyguanosine triphosphate for viral DNA polymerase.
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.
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immunity to diverse stimuli.
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.
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
These agents reduce the cumulative renal toxicity associated with the repeated administration of chemotherapy agents like cisplatin.
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.
Agents that serve as buffers and protect the tissues from chemotherapeutic agents can be used.
Response rate is 71-100%, and recurrence rate is 23%. Protects transitional epithelium by restoring the bladder glycosaminoglycan layer.
Overview
What is the pathophysiology of acute proctitis?
What is the prevalence of acute proctitis?
What is the prognosis of acute proctitis?
What are the possible complications of acute proctitis?
Presentation
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?
DDX
What are the differential diagnoses for Acute Proctitis?
Workup
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?
Treatment
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?
Medications
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 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 Antibiotics are used in the treatment of Acute Proctitis?