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Vulvovaginitis
By James Holencik, DO
Introduction
• Vulvovaginitis is inflammation of the vulva
and vaginal tissues.
• Characterized by vaginal discharge and/or
vulvar itching and irritation as well as
possible vaginal odor.
• Accounts for 10 million visits yearly in the
US and is the most common gynecologic
complaint in prepubertal girls.
Introduction cont.
• Most common causes of acute vulvovaginitis:
infections, irritant or allergic contact, local
response to a vaginal FB, atrophic vaginitis.
• The 3 most common infectious causes are:
bacterial vaginosis, candidiasis, and
trichomoniasis.
• Vulvovaginal candidiasis, contact vaginitis, and
atrophic vaginitis may occur in virgins and after
menopause, while other forms of infectious
vulvovaginitis are seen in sexually active women.
General Approach to
Vulvovaginitis
• A detailed gyn history as well as a pelvic
exam should be completed.
• Microscopic evaluation of fresh vaginal
secretions using both NSS (clue cells for
BV and motility for trich) and 10% KOH
slide (yeast or pseudohyphae for candida)
and the whiff test (fishy odor for BV) will
provide the diagnosis is most cases.
General Approach to
Vulvovaginitis Cont.
• Another diagnostic tool is the use of Nitrazine
paper for testing the Ph.
• Normal Ph of 4-4.5.
• Candida Ph of 4-4.5.
• BV and Trich Ph >4.5.
• Signs of vulval inflammation and minimal D/C in
the absence of vaginal pathogens suggest possible
mechanical, chemical, allergic or other
noninfectious causes.
Normal Vulvovaginal
Environment
• In females of childbearing age, estrogen causes the
development of a thick vaginal epithelium with a
large number of superficial cells serving a
protective function and containing large store of
glycogen.
• Lactobacilli and acidogenic corynebacteria use the
glycogen to produce lactic and acetic acids.
• This results in an acidic environment protecting
from the growth of pathogenic bacteria.
Normal Vulvovaginal
Environment Cont.
• Normal vaginal secretions vary from thin, watery
material to one that is thick, white and opague.
• Alkaline secretions from the cervix before and
during menstruation and semen reduce acidity, and
predispose for infections.
• Before menarche and after menopause, the vaginal
secretions vary between a pH of 6-7.
Bacterial Vaginosis
• BV is a clinical syndrome that occurs when the
normal H2O2-producing lactobacillus species in
the vagina are replaced by high concentrations of
anaerobic bacteria, G. vaginalis and Mycoplasma
hominis.
• BV is the most common cause of a malodorous
D/C, but more than half of the women who meet
criteria for diag. are asymptomatic.
Bacterial Vaginosis Cont.
•
•
1.
2.
3.
4.
BV is associated with having multiple sexual
partners.
3 of the 4 signs or symptoms per the CDC must
be met for the diag.
Homogeneous, white, noninflammatory
discharge that smoothly coats the vaginal walls.
Presence of clue cells on microscopic exam.
pH >4.5
A fishy odor to the discharge after addition of
KOH.
Bacterial Vaginosis Cont.
• Gram staining that demonstrates a concentration
of bacterial morphotypes characteristic of BV may
also be used for diag.
• BV has a high association with adverse outcomes
in pregnancy such as preterm labor and PROM.
• BV is also associated with PID, endometritis, and
vaginal cuff cellulitis after surgical procedures.
Bacterial Vaginosis Cont.
• All symptomatic patients should be treated with
metronidazole regardless of pregnancy status.
• Treatment can be metronidazole 500mg po bid for
7 days or 2 gm po single dose. Also clindamycin
or metronidazole cream may be used. Patients can
be treated as well with clindamycin 300mg tablets
bid x 7 days.
• Overall cure rates after 4 weeks with either po or
intravaginal creams do not differ significantly.
Candida Vaginitis
• It is estimated that 75% of women in childbearing
years will experience at least one yeast infection.
• The organism can be isolated from up to 20% of
asymptomatic women of childbearing years, some
of whom are celibate.
• Candida vaginitis infection is not considered to be
a STD but can be spread sexually.
Candida Vaginitis Cont.
• Factors that favor increased rates of asymptomatic
vaginal colonization are pregnancy, oral
contraceptives, uncontrolled DM, and frequent
STD clinic visits.
• C. albicans strains account for 85-92% of those
strain isolated from the vagina.
• C. glabrata and C. tropicalis are the commonest
non-albicans strains and are more resistant to
conventional therapies.
Candida Vaginitis Cont.
• Candida organisms gain access to the vaginal
lumen and secretions predominately from the
adjacent perianal area.
• Risk factors for yeast infections are: loss of
normal vaginal flora (po antibiotics), diminished
glycogen stores (DM, pregnancy, BCP, and
hormone replacement), increase of vaginal pH
(menstrual blood or semen) or tight-fitting
undergarments causing increase temp, moisture,
and local irritation.
Candida Vaginitis Cont.
• Clinical symptoms include leukorrhea, severe
vaginal pruritus, external dysuria, and
dyspareunia. Odor is unusual.
• Gyn exam may reveal vulvar erythema and edema,
vaginal erythema, and thick cottage-cheese D/C.
• The diagnosis is made by have a normal pH4-4.5
and positive results on microscopic exam (yeast
buds and pseudohyphae).
• Culture is only use with symptomatic patients with
negative findings on microscopic exam.
Candida Vaginitis Cont.
• Most treatment are effective; topical azoles are
more effective than nystatin.
• For uncomplicated infections any topical agent as
well as oral diflucan will treat candida.
• Complicated infections can be treated with
lotrinmin 500mg vag. supp 1 weekly or Diflucan
150mg po day 1 and 3.
• For pregnant patients must receive topical azole
therapy applied for 7 days, can not use oral
diflucan.
Trichomonas Vaginalis
• Trich is a flagellated protozoan.
• It is estimated that 2-3 million American women
contract the disease annually.
• Trich is almost always a STD, and it prevalance
correlates with the overall level of sexual activity.
• Trich infection is associated with adverse
pregnancy outcomes (PROM and preterm labor).
Trichomonas Vaginalis Cont.
• 70% of men having intercourse with infected
women demonstrate the disease in 48 hours while
if the reverse occurs 85% of women with contract
the infection.
• There is a high prevalence of gonorrhea in women
with trich.
• BCP, spermicidal agents, and barrier
contraceptives all are thought to reduce the
transmission.
Trichomonas Vaginalis Cont.
• Infections range from asymptomatic to severe.
• Vaginal D/C is reported in 50-75% of patients.
• The D/C may vary from the classic yellowishgreen frothy type to a grayish or even no D/C at
all.
• Other symptoms include: vulvovaginal
soreness/irritation, pruritis, dysuria, malodorous
D/C, dyspareunia.
Trichomonas Vaginalis Cont.
• Gyn exam reveals the classic strawberry cervix in
only 2% of patients with diffuse erythema seen in
10-33%.
• The diag. Is made with the NSS microscopic scale
revealing flagellated trichomonads.
• Cultures are approx. 95% sensitive and should be
considered in symptomatic patients with elevated
pH >4.5 and excess PMNs absent of motile
tichomonads and clue cells.
Trichomonas Vaginalis Cont.
• Trich can survive up to 24h in tap water, hot
tubes, urine, toilet seats, and swimming
pools.
• Due to 25% of women and 90% of men
harboring the organism and being
asymptomatic, it is difficult to control the
spread of the disease.
Trichomonas Vaginalis Cont.
• Metronidazole is still the cornerstone of
treatment.
• There is a 90% cure rate with either the
single dose or 7 day course.
• Treatment: Metronidazole 2gm po single
dose or 500mg po bid for 7 days.
Genital Herpes
• Approx. 25 million Americans are infected.
• Transmission can occur during an asymptomatic
time.
• Two types HSV 1 and 2.
• HSV-1 used to be thought to cause oral and HSV-2
genital lesions; now with recent studies HSV-2
causes 85-90% and the rest is caused by HSV-1.
• Currently there is no cure for the virus.
Genital Herpes Cont.
• Initial presentation occurs 1-45 days after
exposure and is usually more severe and last
longer than recurrences.
• The lesions begin as painful, fluid filled
vesicles or papules, progressing to wellcircumscribed shallow based ulcers.
• These usually last 4-15 days with total
healing in 21days.
Genital Herpes Cont.
• Symptoms can include inguinal lymphadenopathy,
severe pelvic pain, urethritis, dysuria, urethral
spasm, and urinary retention.
• The initial disease involves the cervix 80% of the
time.
• Pharyngitis and secondary spread of lesions to
other areas of the body, usually below the waist
occur in up to 2/3 of the patients.
Genital Herpes Cont.
• Systemic symptoms include: fever, malaise,
HA, and myalgias.
• Also hepatitis, aseptic meningitis, and
autonomic nervous system dysfunction can
occur.
• The recurrent infections are milder and
usually do not have systemic infections.
Genital Herpes Cont.
• The recurrent lesions are typically fewer,
smaller and more unilateral with recurrence
in the same location.
• Intervals between attacks vary.
• The average number of attacks yearly are 58.
Genital Herpes Cont.
• Diagnosis is suspected by clinical presentation and
confirmed by either culture (preferred by CDC) or
PCR.
• The virus can be isolated from the vesicular fluid
for the above mentioned.
• Also scrapings may be taken for a PAP smear or
Tzanck preparation stained with Wright or Giemsa
(multinucleated giant cells).
Genital Herpes Cont.
• Treatment is not curative.
• Systemic antiviral only provide partial
control of the signs and symptoms as well
as accelerating healing.
• Typical therapy is ineffective.
• In recurrent episodes treatment should be
started either during the prodrome or within
1 day for benefit.
Genital Herpes Cont.
• Daily suppressive therapy reduces the
recurrence by at least 75% but should only
be used in patients with 6 or more outbreaks
yearly.
• Patients asymptomatic or on suppressive
therapy can still transmit the disease to
partners.
Genital Herpes Cont.
• All antiviral agents are categorized as class
B drugs in pregnancy.
• Women treated with acyclovir during
pregnancy should be reported to the GlaxoWellcome registry (1-800-722-9292).
Contact Vulvovaginitis
• Contact dermatitis results from the exposure of
vulvar epithelium and vaginal mucosa to a
primary chemical irritant or an allergen.
• Common irritants and/or allergens include:
perfumes, dyes, soaps, bubble baths, deodorants,
tampons, pads, feminine hygiene products, topical
antibiotics, tight slack/pantyhose, synthetic
underwear or sented toilet paper.
Contact Vulvovaginitis Cont.
• Clinically there may be local swelling,
itching or burning sensation, ulcerations or
even secondary infections.
• Candida colonization may occur depending
on the pH making the diagnosis difficult.
• Diagnosis is made by ruling out infectious
causes and identifying the offending agent.
Contact Vulvovaginitis
• Mild cases resolve spontaneously.
• Treatment for more severe cases include:
cool sitz baths, wet compresses of dilute
boric acid or Burow’s solution, topical
corticosteroids, and oral antihistamines.
Vulvovaginitis in the HIV-1Positive Women
• Presence of vulvovaginitis may predispose
women to infection by HIV.
• Women with HIV have an increased
incidence of vulvovaginitis and may be
more likely to infect others.
• Rate of Candida colonization is equal in
immune competent HIV women as those
without the virus.
Vulvovaginitis in the HIV-1Positive Women Cont.
• When T-cell counts are <200 the rates of
colonization increase.
• Treatment for HIV positive women is
undefined, therefore these patient should be
treated as a HIV negative women.
Vaginal Foreign Bodies
• Any foreign body left in place for >48 hours can
cause severe localized infections due to E. coli
anaerobes, or overgrowth of normal vaginal flora.
• Patients present with a foul-smelling and/or
bloody D/C.
• The only treatment is removal of the FB.
• Most cases the vaginal D/C and odor with go
away in several days.
Pinworms
• Pinworms (Enterobius Vermicularis) may migrate
from the anus to the vagina in children causing
intense pruritis (most intense at night).
• Cellophane tape can be used to obtain material for
a slide analysis (large and double-walled ova).
• Child and all family members need treatment with
antiparasitic agent (mebendazole, albendazole, or
pyrantel pamoate).
• Repeat treatment must be done in 2 weeks.
Atrophic Vaginitis
• During menarche, pregnancy, lactation and after
menopause the vaginal epithelium lack estrogen
stimulation.
• The maturation of the vagina and urethra mucosa
depends on the presence of estrogen.
• Menopause results in a vaginal mucosa that is
attenuated, pale, and almost transparent as a result
of decreased vascularity.
Atrophic Vaginitis
• Thus the vagina loses it rugae, the
squamous epithelium atropies, glycogen
content decreases, and the pH increases
(5.5-7.0), thus possibly causing atrophic
vaginitis.
• When symptomatic vaginitis occurs the
vaginal epithelium is thin, inflamed, and
ulcerated.
Atrophic Vaginitis
• Symptoms include vaginal soreness,
dyspareunia, and occasional spotting or
D/C.
• A PAP smear of the cervix and vagina is
mandatory in the face of bleeding.
• Treatment consists of topical vaginal
estrogen or nightly vaginal tablets.
Pelvic Inflammatory Disease
PID
• Is a common and serious disease initiated by
ascending infection from the cervix and vagina.
• PID includes salpingitis, endometritis, and tuboovarian abscess and may extend to produce pelvic
peritonitis or perihepatitis.
• The annual rate in industrialized countries is 10-20
per 1000 with as many as 1.5 million cases in the
US yearly.
PID
• Long term sequelae include tubal factor
infertility, ectopic pregnancy, chronic pain
and dyspareunia.
• The annual direct costs of the acute disease
and its sequelae are estimated at 1.88 billion
dollars.
Etiology
• Neiseria gonorrhoeae and Chlamydia
trachomatis can be isolated in many cases.
• However since the newer more sensitive
and specific culture techniques arise it is
found that many are polymicrobial
(anaerobic and aerobic vaginal flora).
• Per laproscopic culture 30-40% are mixed
infections.
Etiology Cont.
• Pathogenic organisms include anaerobes,
Gardnerella vaginalis, enteric gram-neg
rods, H. influenzae, strep agalatiae,
Mycoplasma hominis, and Ureaplasma
urealyticum.
• HIV-1 infection is associated with an
increased incidence of C. trach infection
and increased risk of PID progression.
Pathology and Risk Factors
• Most cases of PID are presumed to originate with
sexually transmitted diseases of the lower genital
tract, followed by ascending infection of the upper
genital tract.
• 10-20% of untreated gonococcal or chlamydial
infections may progress to PID.
• The mechanisms by which infection and
inflammation in the upper genital tract are initiated
and propagated remain under investigation.
Pathology and Risk Factors Cont.
• Uterine infection usually is limited to the
endometrium but may be more invasive in a
gravid or postpartum uterus.
• Tubal infection initially affects only the mucosa,
but acute, complement-mediated transmural
inflammation may develop rapidly.
• Inflammation may extend to uninfected
parametrial structures, including the bowel.
Pathology and Risk Factors Cont.
• If purulent material spills into the abdomen,
pelvic peritonitis can occur.
• Also, infection may extend by direct or
lymphatic spread to involve the hepatic
capsule with acute perihepatitis and focal
peritonitis (FitzHugh-Curtis syndrome).
Pathology and Risk Factors Cont.
• Risk factors for PID within a sexually active
population include multiple sexual partners, H/O
other STD’s, H/O sexual abuse, frequent vaginal
douching, and younger age.
• Consistent barrier contraception is associated with
lower risk of PID.
• Recent data suggests that OCP’s may have no
effect on PID incidence.
Pathology and Risk Factors Cont.
• IUD use has been associated with a 2-9 fold
increase risk for PID, but new data indicate
that the risk with current IUDs may be
much less.
• In addition to host factors, genetic
polymorphisms of PID pathogens may
affect the likelihood that a lower tract
infection with progress to PID.
Pathology and Risk Factors Cont.
• P9-Opa(b) protein expression in N.
gonorrhoeae and CHSP60 antigen
expression in C. trachomatis are recent
examples of specific bacterial genes
implicated in PID pathogenesis.
Clinical Findings
• Lower abdominal pain is the most frequent
presenting complaint in PID.
• Other symptoms include: abnormal vaginal
D/C, vaginal bleeding, postcoital bleeding,
dyspareunia, irritative voiding symptoms,
fever, malaise, nausea, and vomiting.
• PID may be minimally symptomatic or
asymptomatic.
Clinical Findings Cont.
• The differential diagnosis includes: cervicitis,
ectopic pregnancy, endometriosis, ovarian cyst,
ovarian torsion, spontaneous abortion, septic
abortion, cholecystitis, gastroenteritis,
appendicitis, diverticulitis, pyelonephritis, and
renal colic.
• The PE is usually notable for lower abd. pain,
cervical motion tenderness, and uterine and/or
adnexal tenderness.
Clinical Findings Cont.
• One large multicenter trial found adnexal
tenderness to be the most sensitive finding
on PE.
• Mucopurulent cervicitis is common and has
a significant negative predictive value when
absent.
Laboratory Evaluation
• Laboratory evaluation in the ED always should
include a pregnancy test.
• Saline and KOH-treated wet preps of vaginal
secretions for leukorrhea, trich, and clue cells.
• Endocervical swabs for cultures.
• Elevated WBC’s, ESR, and CRP support the
diagnosis.
• The RPR for syphilis.
• Blood cultures don’t aid in the diagnosis of PID.
Procedures
• Transvaginal pelvic ultrasounds may demonstrate
thickened fluid-filled fallopian tubes or free pelvic
fluid, but these finding alone are not specific
enough to make the diagnosis.
• Endometrial biopsy can be used for the
histopathologic diagnosis of endometritis.
• Endometritis is uniformly associated with
salpingitis.
• Endometrial biopsy is approx. 90% specific and
sensitive.
Procedures Cont.
• Culdocentesis can be performed rapidly in
the ED, but the findings of leukocytes and
bacteria are nonspecific.
• Laparoscopy is the gold standard for the
diagnosis of PID.
Diagnostic Guidelines
• Current guidelines for PID stratify
diagnostic criteria into 3 groups.
• 1. Minimum criteria
-Uterine or adnexal tenderness
-Cervical motion tenderness
-Empirical treatment indicated if no other
etiology to explain findings above.
Diagnostic Guidelines Cont.
• 2. Additional criteria improving diagnostic
specificity.
-Oral temp. >101/38.3
-Abnormal cervical or vag. Mucopurulent
secretions
-Elevated ESR or CRP.
-Laboratory evidence of cervical infection
with gonorrheae or Chlamydia.
Diagnostic Guidelines Cont.
• 3. Specific criteria for PID based on
procedures that may be appropriate for
some patients
- Laparoscopic confirmation.
- Transvag ultrasound (or MRI) showing
thickened, fluid-filled tubes w/ or w/o free
pelvic fluid or tubo-ovarian complex.
- Endometrial biopsy showing endometritis
Therapy
• Treatment of PID is aimed at relieving acute
symptoms, eradicating current infection,
and minimizing the risk for long-term
sequelae.
• NO clear rule for anti-inflammatory drugs.
• All regimens should be effective against
anaerobes, gram neg, and strep as well as
gonorrheae and Chlamydia.
Therapy Cont.
• Current parenteral treatment regimens.
1. Cefotetan 2g IV or cefoxitin 2g IV and
doxycycline 100mg PO or IV
2. Clindamycin 900mg IV and gentamicin
2mg/kg loading dose.
3. Ofloxacin 400mg IV or levaquin 500mg
IV w/ or w/o metronidazole 500mg IV or
Unasyn 3g IV and doxy 100mg IV or PO
Therapy Cont.
• Current oral/outpatient regimens
• 1. Ofloxacin 400mg bid for 14 days or
levaquin 500mg daily for 14 days w/ or w/o
metronidazole 500mg bid for 14 days.
• 2. Ceftriaxone 250mg IM once or cefoxitin
2g IM once and probenecid 1g po once and
doxy 100mg bid for 14 days w/ or w/o
metronidazole 500 bid for 14 days.
Therapy Cont.
• If an IUD is present, it should be removed.
• All patients should be reevaluated in 72
hours for evidence of substantial clinical
improvement.
Surgical Interventions
• Patients who don’t improve within 72 hours
should be reevaluated for possible
laparoscopic or surgical interventions.
• The majority of tubo-ovarian abscesses )6080%) will respond with antibiotics.
Disposition
• Admission Considerations
1. Surgical emergency can’t be excluded
2. Pregnancy
3. Failure to respond to outpatient treatment
4. Inability to tolerate or comply w/ outpt.
Treatment
5. Severe toxicity, nausea, vomiting
6. Tubo-ovarian abscess
Questions
• What is the most frequent presenting
symptom in PID.
a. vaginal bleeding
b. abnormal vaginal D/C
c. lower abdominal pain.
d. voiding symptoms
T or F Bacterial vaginosis is associated with
clue cells on microscopic evaluation.
Questions Cont.
• Which one is not a risk factor for PID.
a. multiple sexual partners
b. vaginal douching
c. young age
d. barrier contraception
T or F. Trichomonas is associated with
premature rupture of membranes in
pregnancy.
Questions
• Which is not a long term complication of
PID.
a. Tubal factor infertility
b. chronic vaginal D/C
c. ectopic pregnancy
d. chronic pain
Answers: C, T, D, T, B.