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Desquamative Inflammatory Vaginitis by Dr Tori Hudson, ND

Desquamative Inflammatory Vaginitis by Dr Tori Hudson, ND

The term inflammatory vaginitis (IV) distinguishes a mild to moderate pattern from the florid inflammatory pattern of DIV. Many symptomatic women who have an obvious abnormal wet prep with an inflammatory response do not meet the criteria for desquamative inflammatory vaginitis (DIV). These women typically have a copious discharge with a subtle odor and vulvovaginal irritation that is mildly annoying rather than distressing, as with DIV.

Desquamative inflammatory vaginitis (DIV) is one of those uncommon forms of chronic purulent vaginal discharge that you won’t see frequently in a women’s health practice, but you need to know of its characteristics, and you must consider it when the most common causes of abnormal discharge in pre- and postmenopausal women, such as bacterial vaginosis, vulvovaginal candidiasis, and trichomonas vaginitis, have been excluded. DIV is considered a noninfectious cause of inflammatory vaginitis with the highest incidence in perimenopausal Caucasian women (1). One of the challenges with DIV is that the symptoms and signs are nonspecific, but the main symptoms are purulent discharge, vestibule-vaginal irritation, and dyspareunia. A vaginal wall exam appears inflammatory with increased erythema and petechiae. Vaginal pH is > 4.5. Under the microscope, a wet mount of the vaginal secretions shows up as an increase in inflammatory cells and immature squamous cells, called parabasal cells. Microscopic viewing also reveals numerous leukocytes and few to no lactobacilli. The background has clumps of bacteria, and squamous cells are speckled with bacteria.

The etiology and pathogenesis remain unknown, but because it responds to anti-inflammatory agents, this suggests that it is immune-mediated. A conventional approach includes either local vaginal clindamycin and/or vaginal corticosteroids. A conventional approach also admits that it is considered a chronic condition with common relapses and thus ongoing or intermittent treatment is needed.

DIV, while considered a noninfectious etiology can have secondary bacterial microbiota disruption, and some investigators and clinicians believe the condition is due to altered vaginal flora, namely Escherichia coli, and refer to it as aerobic vaginitis with a low or near absence of lactic acid-producing lactobacilli (2). Others propose that the underlying mechanisms include estrogen deficiency, a toxic reaction to Staphylococcus aureus, or some immune abnormality (3,4).

Key clinical history points:

  • More common in perimenopausal women but can occur in premenopausal or postmenopausal.
  • Women with DIV present with pain and copious vaginal discharge.
  • The pain can be described as dyspareunia, vaginal/introital pain, burning, or a combination.
  • The discharge can be white, gray, green, or yellowish.
  • A diffuse exudative vaginal wall inflammation may be visible.
  • Women with DIV have often had symptoms for more than one year and have been treated multiple times for other causes of vaginitis without relief.

What to look for on exam:

  • External genitalia – Normal vulvovaginal architecture. The vestibule may be thinned, sensitive, erythematous, and edematous (this may be a result of irritation from the discharge or, more likely, due to inflammation of the vestibule similar to what we see on the vaginal wall).
  • Vagina – a spotty ecchymotic rash or diffuse or focal erythema or linear erosions.
  • Cervix – Erosive lesions, similar to those seen with trichomoniasis infection; Ectropion may be visible.

Laboratory tests/Diagnostic evaluation:

  • Vaginal pH > 4.5 (remember: inflammatory vaginitis (not desquamative), atrophic vaginitis, and trichomonas may also have this elevated pH, although atrophic vaginitis tends to be > 5).
  • Wet mount microscopy: increased number of parabasal and inflammatory cells, and the leukocyte to epithelial cell ratio is greater than 1:1.
  • Microscopically: On low power – there are numerous leukocytes but with no clustering or sheets. On high power – there is a mixture of leukocytes but mainly agranulocytes (particularly lymphocytes) and few to no lactobacilli. The background has clumps of bacteria, and squamous cells are speckled with bacteria.
  • Laboratory tests for gonorrhea, chlamydia, bacterial vaginosis, candidiasis, and trichomoniasis are performed to exclude these causes and any women with vesicular lesions should be tested for herpes simplex virus. Peri- and postmenopausal women with a pH > 4.5 with reports of vaginal and/or vulvar dryness and/or itching, and dyspareunia, likely have atrophic vaginitis due to low estrogen. Severe atrophic vulvovaginitis can mimic DIV. A trial of low-dose vaginal estrogen and a result in relief of symptoms clarifies the diagnosis as atrophic vaginitis, now called genitourinary syndrome of menopause (GSM).
  • Erosive or dermatologic disorders include erosive lichen planus, pemphigus vulgaris, and cicatricial pemphigoid. It is important to know that DIV typically occurs in perimenopausal women, while erosive lichen planus and cicatricial pemphigoid typically occur in menopausal women. Biopsies are needed to confirm these diagnoses.

The diagnosis of DIV requires ALL of the following criteria:

  • At least one of the following symptoms: vaginal discharge, dyspareunia, pruritus, burning, irritation
  • Vaginal inflammation (spotted ecchymotic rash, erythema, focal, or linear erosion)
  • Vaginal pH > 4.5 (some report > 6)
  • Wet mount microscopy showing increased numbers of parabasal and inflammatory cells (leukocyte to epithelial cell ratio greater than 1:1


The two most common conventional treatments are intravaginal clindamycin and glucocorticoids. Options for initial therapy include either of the following:

  • 2% clindamycin cream; 5 grams (dosed by vaginal applicator) intravaginally once daily for 1-3 weeks, with some reports of up to 4-6 weeks. Consider maintenance of once or twice a week for 2-6 months


  • 10% hydrocortisone cream 300 to 500 mg (dosed by vaginal applicator) intravaginally once daily for 3 weeks and up to 6-8 weeks. Consider maintenance once or twice a week for 2-6 months. It may be used longer if one lowers the strength to 0.5% or uses less of the 10%. Ten percent hydrocortisone cream is not commercially available but can be compounded by a pharmacist. For mild disease, twice daily vaginal insertion of hydrocortisone cream 0.5% could be considered.  Duration is individual, but the goal is resolution symptomatically, visually with exam, and microscopically.

Also use:

  • Low-dose vaginal estrogen if also atrophic vaginitis (one example Rx: 0.01% estradiol vaginal cream; 2 gm once daily for 1-2 weeks followed by 1 gm 1-3 times weekly maintenance and on-going into the distant future).

A more integrative approach:

I have found that using the vaginal antibiotic along with vaginal estrogen is important for this condition in those women who also have atrophic changes, which is typically the perimenopausal and even more so, menopausal women. While I do frequently incorporate the hydrocortisone cream to reduce inflammation, there are specialty creams compounded from a compounding pharmacy that you can inquire about; consider a compounded formulation from the compounding pharmacy of: Glutamine 10 mg/g; cromolyn sodium 20 mg/g; aloe 20 mg/g. If inadequate as a replacement for hydrocortisone, it may be a good follow-up strategy to prevent relapse.

My clinical experience, understanding of the underlying vaginal flora imbalance and knowing of the low rates of cure and high rates of relapse with conventional treatment has caused me to improve vaginal ecology with vaginal-specific lactobacillus – these vaginal suppositories need to include Lactobacillus rhamnosus, L. reuteri, L. acidophilus, L. plantarum, L. salivarius, and possibly L. crispatus. I would insert one capsule daily for 2 weeks then 1-2 times weekly for 12 weeks.

Measures of success

Complete symptom relief, clinical exam normal, and a normal microscopic exam are necessary to achieve complete success. If all of these are achieved, the clindamycin and hydrocortisone can be stopped. Keep in mind that during the use of clindamycin, colonization of lactobacilli is reduced, especially during use of hydrocortisone cream. This is why I advocate for using the vaginal-specific lactobacilli during and following the main phase of treatment.

Recurrence and Relapse

For those women who do not relapse within 3-6 months, they are likely cured.  Unfortunately, with the conventional treatment only, recurrence is common after discontinuation of therapy and about 30% relapse within 6 weeks after discontinuing treatment, and 25% of women remained disease-free at one year after a single course of treatment.

The maintenance plan and tapering plan are quite variable from patient to patient. If one tried clindamycin first and there was relapse, then the second attempt could be switched to the hydrocortisone, and vice versa. The practitioner can continue to taper slowly as long as the patient remains symptom free and there is no increase in leukocytes and parabasal cells on microscopy. I typically see these patients every 4-6 weeks for the first 6 months and then less often, but again stressing the importance of achieving good vaginal colonization with lactobacilli and a return to a normal pH of 3.5-4.5.

Some women may require use of suppressive therapy for months or years before it is possible to discontinue therapy without relapse. For women who do not respond to either the clindamycin or the hydrocortisone, there are careful regimens using tacrolimus 0.03% or clobetasol 0.05%. If you are not familiar with these medicines, then you should seek the advice of a specialist.

Be aware that when such robust use of clindamycin or hydrocortisone is used, a vaginal candida infection may occur. This is one more reason to incorporate the lactobacillus suppositories, but boric acid suppositories or oral antifungals such as fluconazole may be necessary.

Treating women with DIV requires being well informed, patience, creative and flexible thinking, empathy, and availability to the women struggling with this condition. They’ve likely been to several doctors with an inaccurate diagnosis and thus an unsatisfactory outcome. We can’t make promises, but with a deeper understanding of the condition, treatment options, and the fundamental principle of restoring a normal vaginal ecosystem, more women will be helped more of the time.


  1. Nyirjesy P, Peyton C, Weitz MV, et al. Causes of chronic vaginitis: analysis of a prospective database of affected women. Obstet Gynecol 2006; 108:1185.
  2. Sobel JD, Reichman O, Misra D, Yoo W. Prognosis and treatment of desquamative inflammatory vaginitis. Obstet Gynecol 2011; 117:850.
  3. Reichman O, Sobel J. Desquamative inflammatory vaginitis. Best Pract Res Clin Obstet Gynaecol 2014; 28:1042.
  4. Jacobson M, Krumholz B, Franks A Jr. Desquamative inflammatory vaginitis. A case report. J Reprod Med 1989; 34:647.

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