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Vulvovaginitis By James Holencik, DO. Introduction Vulvovaginitis is inflammation of the vulva and vaginal tissues. Characterized by vaginal discharge.

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Presentation on theme: "Vulvovaginitis By James Holencik, DO. Introduction Vulvovaginitis is inflammation of the vulva and vaginal tissues. Characterized by vaginal discharge."— Presentation transcript:

1 Vulvovaginitis By James Holencik, DO

2 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.

3 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.

4 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.

5 General Approach to Vulvovaginitis Cont. Another diagnostic tool is the use of Nitrazine paper for testing the Ph. Normal Ph of Candida Ph of 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.

6 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.

7 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.

8 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.

9 Bacterial Vaginosis Cont. BV is associated with having multiple sexual partners. 3 of the 4 signs or symptoms per the CDC must be met for the diag. 1.Homogeneous, white, noninflammatory discharge that smoothly coats the vaginal walls. 2.Presence of clue cells on microscopic exam. 3.pH >4.5 4.A fishy odor to the discharge after addition of KOH.

10 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.

11 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.

12 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.

13 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.

14 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.

15 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.

16 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.

17 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).

18 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.

19 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 yellowish- green frothy type to a grayish or even no D/C at all. Other symptoms include: vulvovaginal soreness/irritation, pruritis, dysuria, malodorous D/C, dyspareunia.

20 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.

21 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.

22 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.

23 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.

24 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 well- circumscribed shallow based ulcers. These usually last 4-15 days with total healing in 21days.

25 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.

26 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.

27 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 5- 8.

28 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).

29 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.

30 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.

31 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 Glaxo- Wellcome registry ( ).

32 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.

33 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.

34 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.

35 Vulvovaginitis in the HIV-1- Positive 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.

36 Vulvovaginitis in the HIV-1- Positive 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.

37 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.

38 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.

39 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.

40 Atrophic Vaginitis Thus the vagina loses it rugae, the squamous epithelium atropies, glycogen content decreases, and the pH increases ( ), thus possibly causing atrophic vaginitis. When symptomatic vaginitis occurs the vaginal epithelium is thin, inflamed, and ulcerated.

41 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.

42 Pelvic Inflammatory Disease

43 PID Is a common and serious disease initiated by ascending infection from the cervix and vagina. PID includes salpingitis, endometritis, and tubo- ovarian abscess and may extend to produce pelvic peritonitis or perihepatitis. The annual rate in industrialized countries is per 1000 with as many as 1.5 million cases in the US yearly.

44 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.

45 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.

46 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.

47 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 % 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.

48 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.

49 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).

50 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.

51 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.

52 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.

53 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.

54 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.

55 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.

56 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.

57 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.

58 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.

59 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.

60 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.

61 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

62 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.

63 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

64 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.

65 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.

66 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 )60- 80%) will respond with antibiotics.

67 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

68 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.

69 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.

70 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.


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