Proctitis

Proctitis is defined as an inflammation of the rectal mucosa, which is the tissue identified between the anal canal and the colon. Many infections involve the anus as well and are therefore considered “anorectal” infections. Although STD-related rectal infections are frequently associated with anal intercourse among homosexual men, they may also occur in women. Such infections in women are less well defined and, with gonorrhea, are often asymptomatic and associated with endocervical gonorrhea. The microbiological etiologic agents of anorectal infection among sexually active adolescents include N. gonorrhoeae, C. trachomatis (lymphogranuloma venereum, LGV, strains), HSV, T. pallidum, and food-borne enteric organisms. Sexually transmitted enteric organisms, such as Giardia, Entamoeba, Campylobacter, Shigella, and hepatitis A, can be associated with anal intercourse. HIV-infected individuals may also have severe herpes proctitis or be infected with organisms generally not sexually transmitted, including CMV, Mycobacterium avium-intracellulare, and others.

Whereas the anus is highly innervated, resulting in pain with inflammation, the rectum lacks such innervation; thus, proctitis that does not involve the anus is usually painless. Symptoms of anorectal disease include mucus or blood in the stools, loose stool, cramping, anal itching, pain with defecation leading to constipation, and tenesmus. On examination, the anus may appear inflamed and tender. Mucopurulent discharge with or without blood may be present. Anoscopy may reveal the presence of mucopurulent discharge and erythema of the mucosa with friability and ulceration. Diagnostic evaluation includes a careful sexual history to determine risk for anal intercourse; STDs; testing for STD-related urethritis in men (

Fig. 3-6) and endocervicitis in women (Fig. 3-7); rectal cultures for N. gonorrhoeae, C. trachomatis, and HSV; appropriate stool and rectal specimens for enteric bacteria and parasites; and syphilis serology (

Table 3-16).

Treatment is outlined in

Table 3-16 and depends on the etiologic agent responsible.

References


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Revision date: July 8, 2011
Last revised: by Andrew G. Epstein, M.D.