Vaginal Discharge Dr.A Danesh

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Presentation transcript:

Vaginal Discharge Dr.A Danesh

Differential Diagnosis of the Abnormal Vaginal Discharge Normal (physiologic) vaginal secretions Vaginal infections Trichomoniasis Vulvovaginal candidiasis Bacterial vaginosis Desquamative inflammatory vaginitis Cervicitis Infections Noninfectious Estrogen deficiency

Trichomoniasis Etiology and Pathogenesis Protozoan Trichomonas vaginalis Exogenous sexually transmitted infection Transmission almost always occurs through sexual contact. After an incubation period of a few days, patients develop a purulent discharge associated with varying degrees of vulvar irritation, dysuria, and dyspareunia. An abnormal odor is often present, usually signifying concomitant BV.

Treatment Metronidazole and tinidazole A single 2g oral dose of metronidazole is the treatment of choice. 500 mg can be given twice daily for 7 days treatment all recent sexual partners

If this treatment fails treatment of all current sexual partners should be assured Initial retreatment should be with oral metronidazole, 500 mg twice daily for 7 days. If this regiment is not successful oral metronidazole in a single dose of 2 g can be prescried for 3 to 5 days. If the latter metronidazole regimen fails, the patient can be assumed to have clinically significant metronidazole resistance

Alternative regimens High doses of metronidazole are usually oral (2 Alternative regimens High doses of metronidazole are usually oral (2.5 g daily) vaginal (0.5 g daily) metronidazole up to 3 weeks (Antiemetics) Intravenous regimens next choice is usually tinidazole nonoxynol-9 Furazolidone Zinc sulfate douches given in combination with oral metronidazole discontinuation of estrogen replacement treatment in a postmenopausal woman was associated with resolution of vaginal trichomoniasis

Trichomoniasis in pregnancy premature rupture of the menbranes low birth weight (theoretical mutagenicity oncogenicity) Pregnant women who have symptomatic trichomoniasis should be treated with 2g of metronidazole.

Vulvovaginal Candidiasis Etiology and pathogenesis Candida albicans 80% to 90% candida tropicalis 1% to 5% higher rate of recurrence Candida glabrata less intense itching and dyspareunia Non-alibecans infections are assoiated with recurrent disease with HIV infection

Risk factors antimicrobial treatment Antimicrobial treatment high estrogen levels. Users of oral contraceptives Poorly controlled diabetes mellitus tight, insulating clothing impairment of phagocytic cells or of cell mediated immunity (transplantation, chemotherapy) HIV infection especially if they have low CD4 T-cell counts. Onset of sexual activity

The severity of symptoms in vulvovaginal candidiasis is not directly related to the number of yeast cells present . An immunologic reaction has been suggested as the mechanism for symptomatic

Classification of patients with vulvovaginal candidiasis uncomplicated infection Sporadic No underlying disease caused by candida albicans patient is not pregnant Mild to moderate severity Complicated infection Underlying illness Human immunodefiency virus disease Diabetes mellitus Recurrent infection (four or more episodes per year) Caused by non-albicans species of candida Severe infection

Treatment Uncomplicated vulvovaginal candidiasis short courses of vaginal nystatin, miconazole, clotrimazole, butoconazole, terconazole, and tioconazole , 1,3,7, or 14 days Oral antifungals fluconazole in a single 150 mg dose effetive as Ketoconazole and itraconazole, are effective but have not been approved by the FDA for the treatment of uncomplicated vulvovaginal candidiasis

Pregnant women Should be treated with topical agents for at least 7 days. Oral azole antifungal agents should not be used during pregnancy.

Comlicated treatment should begin with a vaginal culture treatment for 7 to 14 days or longer is usually required chronic suppressive treatment with an oral antifungal agent may e useful in preventing recurrences once the current infection has use of 100 mg of ketoconazole daily or flucomazole 100 to 200 mg of per week for at least 6 months

not respond to the available topical and oral agents, intravaginal boric acid. powder (600mg)is placed into size 0 gelatin capsules and administered vaginally for 14 days. Treatment of sexual partners Unpasteurzed yogurt product that contains live lactobacilli is prophylactic agent for recurrent vulvovaginal candidiasis

Diagnosis B V Gray and homogenous discharge Fishy vaginal odor During menstruation After intercourse Minimal itching or irritation Vulvovaginal irritation is not prominent symptom-hence, “vaginosis’’ rather than “vaginitis”.

Women who have BV Increased risk for the development of infection with herpes simplex virus type 2 N. gonorrhoeae C.trachomatis BV is more prevalent and more persistent among HIV infected women. (Low CD4 T-cell)

Treatment Oral metronidazole. 500 mg twice a day for 7 days Treatment Oral metronidazole. 500 mg twice a day for 7 days. Oral clindamycin A single 2g dose of metronidazole, is less effective. Vaginal preparations containing 0.75% metronidazole gel or 2% clindamycin cream, ovules containing 100 mg of clindamycin lyophilized hydrogen peroxide-producing Lactobacillus acidophilus organisms. Intravaginal boric acid,600 mg at bedtime. Once the symptoms have been controlled, the dosing interval can be increased. Some patients remain symptom free using boric acid capsules once or twice a week.

Postoperative infections occur more often in women undergoing gynecologic surgery. Vaginal cuff infections. Treatment of BV before induced abortion reduces the risk of subsequent pelvic inflammatory disease.

BV during pregnancy Premature membrane rupture BV during pregnancy Premature membrane rupture. Preterm birth postpartum endometritis. Oral metronidazole or oral clindamycin. Topical agents do not appear to be as effective as oral agents. clindamycin cream has been associated with adverse events such as prematurity and neonatal infections. Treatment of sexual partners is not recommended.

DESQUAMATIVE INFLAMMATORY VAGINITIS Etiology and pathogenesis Unknown, cause it mimics estrogen deficiency vaginitis and trichomoniasis but usually occurs in women of reproductive age who have normal hormonal function and no evidence of any sexually transmitted conditions

Occurs in perimenopausal women or After pregnancy role for changes in the level of estrogen background to have the A26 and B35 histocompatibility antigens gram positive cocci and group sreptococci can be recovered from some patients especially those who are perimenopausal local manifestation of a systemic illness such as systemic lupus erythematosus may also have erosive lichen planus involving oral or genital mucous membranes always part of the lichen planus complex

Diagnosis Purulent vaginal discharge varying degrees of vulvar irritation dysuria and dyspareunia there is of ten a history of multiple unsuccessful treatments with a variety of topical and oral antimicrobial agents Confused with trichomoniasis

Treatment Topical corticosteroids and topical boric acid 2% clindamycin vaginal creams 5 g of the cream (containing 100 mg of clindamycin) vagina at bedtime for 14 days. A few patients require a second 14 day course of treatment to induce a remission

Relapses occur months to years later retreatment with topical clindamycin very frequent relapses require continual biweekly intravaginal clindamycin or corticosteroids to remain in remission perimenopausal patients who are estrogen deficient may require estrogen replacement as well as topical clindamycin to sustain a remission

Cervicitis Acute Chronic Infectious cervicitis is endocervicitis. N Cervicitis Acute Chronic Infectious cervicitis is endocervicitis. N.gonorrhoeae, C.trachomatis, Noninfectious cervicitis is usually ectocervicitis . Primary herpes simplex ectocervicitis.

Examination vulva and of the vaginal mucosa are usually normal infections endocervicitis the purulent secretions can be seen to flow from the endocervical canal noninfectious ectecervicitis the purulent secretions can be seen to emanate from the ectropion noninfectious endocervicitis the abnormal secretions are solely endocervical presumably reflecting the noninfectious endocervicitis

Treatment if the volume of secretions arising from an ectropion is bothersome destruction of the ectopic endocervical mucosa of the ectropion with cryotherapy allows the ectocervix to become reepithelialized with squamous epithelium

ESTROGEN DEFICIENCY VAGINITIS Etiology and Pathogenesis postmenopausal Younger women who have become estrogen deficient because of disease or because of treatment with pharmaceuticals that interfere with the production or the activity of estrogen breast – feeding Thinning of the mucosa may result in vulvar discomfort and introital dyspareunia. The thin vaginal mucosa may become infected, presumably enteric organisms and others that are able to colonize the vagina in the absence of lactobacilli. Frequent urinary tract infections may occur . Estrogen deficiency vaginitis overlaps with DIV.

Diagnosis The vestibular and vaginal mucosae are pale, often with patches of erythema . Vainal secretions, if present,may be purulent. Vaginal PH is elevated . No odor when the secretions are mixed with 10% KOH. Microscopic examination of the parabasal vaginal cells without leukocytes.

Treatment Estrogen replacement or cessation of antiestrogenic drugs or breast-feeding Topical antibacterial agents containing sulfonamides or clindamycin may improve symptomatic vaginitis, lubricating agents may relieve vaginal dryness and dyspareunia . Without estrogen replacement, symptoms may recur after cessation of treatment