Updated: Apr 27, 2009
Proctitis is inflammation of the lining of the rectum, called the rectal mucosa. Proctitis can be short term (acute) or long term (chronic). Proctitis has many causes. It may be a side effect of medical treatments like radiation therapy or antibiotics. 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 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, chemicals, rectal instrumentation, and trauma to the anorectal area. It may also occur as idiopathic proctitis. Other causes include radiation therapy or celiac disease.
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 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.
Frequencies of proctitis are associated with their individual etiologies. With radiation therapy, 5-20% of patients display proctitis, usually within 3-24 months after completion of therapy with a total dose greater than 50 Gy.
Incidence is higher in Jewish persons.
Males are affected more often than females.
Proctitis occurs predominantly in adults.
| 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 |
Traumatic proctitis
Infections (eg, shigellosis, amebiasis)
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.
500-750 mg PO tid for 10 d
35-50 mg/kg PO divided tid for 10 d
May increase toxicity of anticoagulants, cyclosporine, lithium, phenytoin, tacrolimus, and carbamazepine; cimetidine may increase toxicity of metronidazole; disulfiram reaction may occur with orally ingested ethanol; coadministration increases amiodarone toxicity (QT prolongation); increases disulfiram toxicity (psychotic symptoms) with concurrent use; phenobarbital and rifampin may increase metabolism of metronidazole
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution with liver impairment, blood dyscrasias, CNS disease; reduce dosage with severe hepatic disease; monitor for seizures and development of peripheral neuropathy
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.
125 mg PO qid for 10-14 d
40 mg/kg/d PO divided tid/qid for 7-10 d; not to exceed 2 g/d
Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal failure, neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few min) but rarely happens when dose given IV over 2 h administration or as PO or IP administration; red man syndrome is not an allergic reaction
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.
500 mg PO bid
400 mg IV bid
<18 years: Not recommended
>18 years: Administer as in adults
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Dosage adjustments (adult adjustments)
CrCl (mL/min) <10: 50% of PO or IV dose q12h
HD: 0.25-0.5 g PO or 0.2-0.4 g IV q12h
During peritoneal dialysis: 0.25-0.5 g PO or 0.2-0.4 g IV q8h
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Not drug of first choice in pediatrics because of increased incidence of adverse events compared with controls, including arthropathy; no data exist for dose for pediatric patients with renal impairment (ie, CrCl <50 mL/min)
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.
250 mg IM once
Neonates >7 days: 25-50 mg/kg IM once; not to exceed 125 mg
Infant or child: 125 mg IM once plus doxycycline
Aminoglycosides increase nephrotoxic potential; probenecid increases effects by decreasing clearance
Documented hypersensitivity
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in renal impairment
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.
Acute infections: 200 mg PO immediately, then 100 mg PO hs on d 1, followed by 100 mg PO bid for 3 d; or 300 mg PO stat followed by 300 mg PO in 1 h; alternatively, use 100 mg PO bid for 7 d
<8 years: Not recommended
>8 years: 2-5 mg/kg/d PO qd or divided bid; not to exceed 200 mg/d
Antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate can decrease bioavailability
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Avoid prolonged exposure to sunlight or tanning equipment to prevent a photosensitivity reaction; use of tetracyclines during tooth development (last half of pregnancy through age 8 y) can cause permanent discoloration of teeth
A bactericidal used in the treatment of rectal syphilis. Interferes with bacterial cell wall synthesis during active multiplication, inhibiting bacterial growth.
2.4 million U IM once in 2 injection sites
50,000 U/kg IM once; not to exceed 2.4 million U
Probenecid can increase the effects by decreasing clearance; conversely, coadministration of tetracyclines can decrease effects
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in impaired renal function
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.
250-500 mg PO q6h
25-50 mg/kg/d PO divided q6h
Antacids containing aluminum, calcium, magnesium, iron, or bismuth subsalicylate can decrease bioavailability; can increase hypoprothrombinemic effects of anticoagulants; coadministration can decrease the pharmacologic effects of oral contraceptives, causing breakthrough bleeding and an increased risk of pregnancy
Documented hypersensitivity; severe hepatic dysfunction
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Prolonged exposure to sunlight or tanning equipment can cause a photosensitivity reaction; use lower-than-usual doses in patients with renal impairment; use of tetracyclines during tooth development (last half of pregnancy through age 8 y) can cause a permanent discoloration of teeth; never administer outdated tetracyclines, the degradation products are highly nephrotoxic and can cause a Fanconilike syndrome
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.
Initial dose: 1 g PO tid/qid
Maintenance dose: 2 g/d PO divided tid/qid
<2 years: Not established
>2 years: 40-60 mg/kg/d PO in 3-6 divided doses
Maintenance dose: 20-30 mg/kg/d PO divided qid
Decreases the effect of iron, digoxin, and folic acid; conversely, increases effect of oral anticoagulants, oral hypoglycemic agents, and methotrexate
Documented hypersensitivity; GI or GU obstruction
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Renal or hepatic impairment; blood dyscrasias; urinary obstruction
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.
Oral: 1 g cap PO qid or 800 mg tab PO tid
Rectal: One 500-mg supp PR bid or one 4-g susp enema PR qd (retained for 8 h)
Not established
Decreases effects of iron, digoxin, and folic acid; conversely, it increases the effect of oral anticoagulants, methotrexate, and oral hypoglycemic agents
Documented hypersensitivity to mesalamine or to suppository vehicle (saturated vegetable fatty acid esters)
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Elderly persons may have difficulty administering and retaining rectal suppositories; use caution in patients with renal or hepatic impairment; susp contains potassium metabisulfite, so care must be taken in individuals with documented sulfite allergy
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.
Initial episode: 200 mg PO q4h (while awake) 5 times/d for 10 d
Recurrence: 200 mg PO q4h (while awake) 5 times/d for 10 d
Not established
Suggested dose: 10-20 mg/kg/dose PO (up to 800 mg) qid for 5 d; start treatments within 24 h of rash onset
Concomitant use of probenecid or zidovudine prolongs half-life and thus increases CNS toxicity
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Renal failure; coadministration of other nephrotoxic drugs
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.
0.75-9 mg/d PO in divided doses q6-12h
0.08-0.3 mg/kg/d or 2.5-10 mg/m2/d divided PO q6-12h
Effects decrease with coadministration of barbiturates, phenytoin, and rifampin; dexamethasone decreases effect of salicylates and vaccines used for immunization
Documented hypersensitivity; active bacterial or fungal infection
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Increases risk of multiple complications, including severe infections; monitor adrenal insufficiency when tapering drug; abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections are possible complications of glucocorticoid use
Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability.
5-60 mg/d PO/IV/IM
Not established
Decreases effects of salicylates and toxoids (for immunizations); phenytoin, carbamazepine, barbiturates, and rifampin decrease effects of corticosteroids
Documented hypersensitivity; fungal, tubercular skin, connective tissue, or viral infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hyperthyroidism, osteoporosis, cirrhosis, nonspecific ulcerative colitis, peptic ulcer, diabetes, and myasthenia gravis
May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.
5-60 mg/d PO qd or divided bid/qid; taper over 2 wk, as symptoms resolve
4-5 mg/m2/d PO; alternatively, 0.05-2 mg/kg PO divided bid/qid; taper over 2 wk, as symptoms resolve
Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics
Documented hypersensitivity; fungal, tubercular skin, connective tissue, or viral infections; peptic ulcer disease; hepatic dysfunction; GI bleeding or ulceration
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Abrupt discontinuation of glucocorticoids may cause adrenal crisis; hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use
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.
Prevention of radiation proctitis in rectal cancer (unlabeled use): 340 mg/m2 IV qd prior to radiation therapy
Not established
May potentiate hypotensive effects of antihypertensive medications (withhold antihypertensive medications for 24 h prior to amifostine administration; if antihypertensive therapy can not be withheld, do not administer amifostine)
Documented hypersensitivity to aminothiol compounds or any component of the formulation
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Serious cutaneous reactions, including erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis, toxoderma, and exfoliative dermatitis reported (discontinue treatment for severe/serious cutaneous reaction, or with fever; withhold treatment and obtain dermatologic consultation for rash involving lips or mucosa (of unknown etiology outside of radiation port) and for bullous, edematous or erythematous lesions on hands, feet, or trunk; reinitiate only after careful evaluation)
Rare hypersensitivity reactions, including anaphylaxis and allergic reaction, reported; discontinue if allergic reaction occurs; do not rechallenge; medications for treatment of hypersensitivity reactions should be available
Monitor serum calcium levels in patients at risk of hypocalcemia, such as those with nephrotic syndrome, or patients receiving multiple amifostine doses (may require calcium supplementation)
Hypotension may occur during or shortly after infusion (hypotensive or dehydrated should not receive amifostine)
Adequately hydrate prior to treatment and keep in supine position during infusion (monitor blood pressure every 5 min during infusion; if hypotension requiring interruption of therapy occurs, patients should be placed in Trendelenburg position and given infusion of normal saline using a separate IV line; subsequent infusions may require a dose reduction)
Infusions >15 min are associated with higher incidence of adverse effects
Incidence of nausea and vomiting is higher in patients receiving amifostine compared to chemotherapy alone
Antiemetic medications, including dexamethasone 20 mg IV and serotonin 5-HT3 receptor antagonist, should be administered prior to and in conjunction with amifostine
Use with caution in patients whom adverse effects of nausea/vomiting may have serious adverse events
Caution in patients with cardiovascular disease or whom adverse effects of hypotension may have serious adverse events
Use with caution in patients with cerebrovascular disease; not for use (in patients receiving chemotherapy for malignancies other than ovarian cancer) where chemotherapy is expected to provide significant survival benefit or in patients receiving definitive radiotherapy, unless within the context of a clinical trial
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inflammation of the rectum, rectal mucosa, proctosigmoiditis, rectal tissue ischemia, rectal pain, rectal bleeding, proctitis, mucosal cell loss, acute inflammation of the lamina propria, eosinophilic crypt abscess, endothelial edema of the arterioles, mucosal friability, ulcers, strictures, fistula formation, colitis, Crohn disease, Crohn's disease, ulcerative colitis
Lisandro Irizarry, MD, MPH, FAAEM, Chair, Department of Emergency Medicine, Brooklyn Hospital Center; Assistant Professor, Department of Emergency Medicine, Weill Cornell School of Medicine
Lisandro Irizarry, MD, MPH, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Ibis Yarde, MD, Staff Physician, Department of Emergency Medicine, Brooklyn Hospital Center
Disclosure: Nothing to disclose.
Michael S Beeson, MD, MBA, FACEP, Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine; Program Director, Emergency Medicine Residency, Summa Health System
Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.
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.
John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Robert E O'Connor, MD, MPH, Professor and Chair, Department of Emergency Medicine, University of Virginia Health System
Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physician Executives, American Heart Association, American Medical Association, Medical Society of Delaware, National Association of EMS Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society
Disclosure: Nothing to disclose.
Clinical guidelines
Proctitis, proctocolitis, and enteritis. Sexually transmitted diseases treatment guidelines 2006. Centers for Disease Control and Prevention, Workowski KA, Berman SM. Proctitis, proctocolitis, and enteritis. Sexually transmitted diseases treatment guidelines 2006. MMWR Morb Mortal Wkly Rep 2006 Aug 4;55(RR-11):78.
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