Differential Diagnosis of the Abnormal Vaginal Discharge
Download
Report
Transcript Differential Diagnosis of the Abnormal Vaginal Discharge
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 (2.5 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.
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.
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.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