Atrophic vaginitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Dima Nimri, M.D. [2]

Synonyms and keywords: Atrophic vulvovaginitis; vaginal atrophy; urogenital atrophy; genitourinary syndrome of menopause

Overview

Historical Perspective

Classification

Pathophysiology

Pathogenesis

The pathogenesis of atrophic vaginitis is due to decreased estrogen levels. Estrogen is a vasoactive hormone, which increases blood flow and maintain vaginal lubrication through fluid transudation from blood vessels.[1] The following are the manifestations of decreased estrogen levels:[1][2][3]

  • A hypoestrogenic state, such as that seen in menopause, causes the vaginal epithelium to lose its rugae, as well as become thin and pale or erythematous with fine petechial hemorrhages.
  • Decreased glycogen content within the epithelium due to decreased thickness leads to less glycogen content available for the lactobacilli to utilize and turn it into lactic acid. As a result, the vaginal pH rises with a resultant overgrowth of other bacteria, such as group B streptococci, Staphylococci and diptheroids. As a result, vaginal infections, UTI and inflammation become more common in the setting of atrophic vaginitis.

Genetics

There are no genetic factors associated with atrophic vaginitis.

Gross Pathology

Gross pathology findings in atrophic vaginitis include:[4]

  • Vaginal dryness
  • Loss of vaginal rugae
  • Changes in vaginal mucosa: pallor and friability or redness and petechiae of the mucosa

Microscopic Pathology

Cytology of the vaginal cells show an increase in the parabasal cells and decreased superficial cells.

Associated Conditions

Causes

Atrophic vaginitis is caused by any condition that may lead to decreased circulating estrogen levels. A hypoestrogenic state may be due to ovarian failure or other causes:[1]

Ovarian Failure Other causes
Menopause Elevated Prolactin
Premature Ovarian Failure

Bilateral oophorectomy

Pituitary Adenoma
Chemotherapy and Radiation Medication with anti-estrogenic effect

Epidemiology and Demographics

  • Atrophic vaginitis is often an underdiagnosed condition, because many women are embarrassed to discuss their symptoms. Some others think of the symptoms associated with atrophic vaginitis as a process of natural aging.[1]
  • Based on self-reported symptoms of vaginal dryness, the prevalence of atrophic vaginitis ranged from 4% to 47%, depending on the stage of menopause (early or late menopause).[2]

Risk Factors

The risk factors associated with vaginal atrophy are related to decreased estrogen levels, which can be due to menopause (most common cause) or other causes that may lead to hypoestrogenism or vaginal atrophy. These include:[1][5]

Screening

There are no screening recommendations for atrophic vaginitis.[6]

Differentiating atrophic vaginitis from other diseases

Atrophic vaginitis must be differentiated from other disease processes that may present with similar symptoms. These can be divided into 4 categories:[2] [1]

The following is a list of differential diagnosis for Atrophic Vaginits: [7][8][5][9][10]

Disease Findings
Atrophic vaginitis
  • Progressive symptoms
  • Presents with yellow and malodorous vaginal discharge, vaginal dryness, postcoital bleeding, and dyspareunia with the signs of vaginal inflammation and elevated vaginal pH (>5)
  • Diagnosis is critical and laboratory tests help to confirm hypoestrogenic state
Trichomoniasis
  • Presents with purulent, malodorous, thin discharge associated with burning, pruritus, and dysuria, with the signs of vaginal inflammation and elevated vaginal pH (>4.5)
  • Motile trichomonads on wet mount are demonstrated
  • Positive culture (Gold standard)
  • Positive nucleic acid amplification test (NAAT)
Bacterial Vaginosis
  • Presents with dysuria, vaginal discharge
  • Fishy odor (positive whiff test)
  • Normal vaginal PH (<4.5)
  • On speculum examination signs of vaginal inflammation are demonstrated
Candida Vulvovaginitis
  • Presents with vulvar pruritus and cottage cheese-like vaginal discharge with no or minimal odor with normal vaginal pH (4-4.5)
  • presence of Candida on wet mount (adding 10% KOH destroys the cellular elements and facilitates recognition of budding yeast, pseudohyphae, and hyphae)
Lichen Sclerosus
  • Affects pre-pubertal and post-menopausal women, reflecting its nature of occurrence in low estrogen states[11]
  • Pruritus is the predominant symptom, burning with urination and dyspareunia can also be seen
  • On examination characteristically the lesions follow a figure of eight pattern affecting the areas around the vagina and anus
  • Signs of active disease include white atrophic plaques with cigarette-paper wrinkling, petechiae, fissures and erosions can be demonstrated
  • Examination findings of chronic disease include clitoral hood phimosis and labia minora resorption
  • Diagnosis confirmed with skin punch biopsy
Lichen Planus
  • Affects pre-menopausal and post menopausal women[12]
  • T-cell mediated inflammatory disease affecting mucosal membranes.
  • In erosive form patients present with vulvar pain, dyspareunia and dysuria.
  • Non-erosive form presents with pruritus
  • On examination appears lesions appear as red plaques or erosions, with overlying white violaceous or reticular plaques( Wickham Striae)
  • Diagnosis confirmed by shave or punch biopsy
Lichen simplex chronicus
  • On examination leasion appear as thick, erythematous lichenified skin (epidermal thickening and accentuation of skin markings)
  • Due to long-term rubbing or scratching secondary to conditions such as recurrent yeast infections, contact dermatitis, psychiatric illness[13]
Contact dermatitis
  • It could be allergic or irritant contact dermatitis
  • Presents with redness, swelling, and pruritus[14]
  • Ocassionally blistering and painful bright red swelling can be seen
Vulvar intraepithelial neoplasm
  • Bimodal peak is observed - between 40-44years and above 55years[15]
  • Red, white, or dark raised or eroded multifocal lesions [16][17]
Vulvar Cancer
  • Presents as a solitary ulcer with raised or indurated edge
  • Histologically it can be a melanoma, squamous cell carcinoma, basal cell carcinoma or neuroendocrine cancer[18]
Extramammary Paget disease
  • Seen in postmenopausal women
  • On examination it appears as a erythematous plaque with typical white scaling known as “cake-icing scaling”[19]
  • Biopsy is characterized by the presence of intraepithelial mucin-producing neoplastic cells known as Paget cells[20]

Natural History, Complications and Prognosis

Natural History

Complications

Complications of atrophic vaginitis include:[1][21]

Prognosis

Diagnosis

History and Symptoms

Symptoms of atrophic vaginitis can be divided into three categories:[1][2][3]

  • External genital symptoms:
    • Vaginal dryness
    • Vaginal irritation
    • Vaginal itching
    • Vaginal discharge
  • Sexual symptoms:
    • Painful sexual intercourse (dyspareunia)
    • Postcoital bleeding
    • Loss of bleeding
    • Loss of arousal
    • Pelvic pain
  • Urological symptoms:

Physical Examination

Physical examination in women with atrophic vaginitis includes a general inspection of the external genitalia, as well as a speculum examination of the internal genitalia.[3][5]

  • Physical examination in women with atrophic vaginitis begins with inspection of the external genitalia. Findings include decreased elasticity of the skin, sparsity of pubic hair, dryness of the labia and/or fusion of the labia minora.
  • Gynecologic examination is carried using a small speculum to avoid damage to the atrophic vaginal or vulvar tissue. Vaginal epithelium may be atrophic and appear pale, smooth and shiny, or it may be inflamed, with patchy erythema, petechiae and increased friability.
  • Other findings may include: pelvic organ prolapse, such as cystocele and/or rectocele, urethral polyps or eversion of the urethral mucosa.

Laboratory Findings

CT

MRI

Ultrasound

An ultrasound of the uterus may demonstrate thinning of the endometrium lining to 4-5mm.[5]

Other Diagnostic Studies

Treatment

Medical Therapy

Atrophic vaginitis is a chronic condition which mandates continuous treatment. The choice of therapy is based on the severity of the symptoms and associated factors such as history of harmone dependent cancer.

  • In patients with mild symptoms lubricants are helpful to relieve symptoms.
  • In patients with moderate to severe symptoms topical estrogen or oral estrogen therapy is encouraged.
  • In patients with history of hormone dependent cancer, topical estrogen or other treatment modalities can be used, however endometrial surveillance is advised.

The following table is the description of available options for the treatment of Atrophic vaginitis[22]:

Treatment Modality Improvement in symptoms Advantages Limitations
Topical Estrogen[23][2][24]

(Creams and Estradiol releasing vaginal rings)

  • Restores vaginal epithelium and associated vaginal vasculature[25]
  • Improves vaginal secretions
  • Lowers vaginal pH and restores healthy vaginal flora
  • Relieves urinary symptoms
  • Effective resolution of dyspareunia, vaginal itching, and dryness[26]
  • No systemic absorption
  • 80 to 90% patients have symptomatic improvement[27]
  • Creams can be messy to use
  • Rings are expelled in patients with cystocele and rectocele
  • Side effects include vaginal secretion, vaginal spotting, and genital pruritus
Oral Estrogen Therapy

In addition to the changes with topical estrogen other actions include:

  • Relief from hot flashes and protection from osteoporosis
Treats menopausal symptoms like hot flashes
  • Adverse effects include :breast tenderness and/or enlargement, vaginal bleeding or spotting, nausea, and weight gain
  • Contraindications include: known or suspected cases of breast cancer, estrogen-dependent cancers, undiagnosed vaginal bleeding, history of thromboembolism, endometrial hyperplasia or cancer, hypertension, hyperlipidemia, liver disease,history of stroke, venothrombotic events, coronary heart disease, pregnancy, smoking in those age >35 years, migraines with neurologic symptoms, and acute cholecystitis/cholangitis.
Selective estrogen receptor modulator

Ospemifene[28]

  • Safe in treating vulvovaginal atrophy
  • Treats dyspareunia by improving vaginal structure and pH
Less than 1% risk of developing endometrial hyperplasia after treatment for 52weeks[29] Increased risk of venous thromboembolism
Laser Therapy
  • Fractional microablative carbon-dioxide lazer improves vascularity, glycogen storage, extracellular matrix production cellular proliferation[30]
  • Impreovement of vaginal epithelial thickness and viability[31]
  • Improvement of symptoms sustained at 12 weeks after therapy
  • Improved sexual activity[32]
Lack of longterm evidence on efficacy and safety[33]
  • Common adverse effect is hot flashes
  • Contraindicated in patients with DVT
Tibolone

Synthetic steriod

  • Improves VMI, sexual desire with the androgenic activity[34]
  • Improvement in urinary symptoms
  • Improvement of urinary symptoms
  • No endometrial hyperplasia [35]
Lack of longterm evidence on efficacy

Increases recurrence risk of breast cancer in patients with history of breast cancer

Vaginal spotting and bleeding[36]

Oxytocin Oxytocin gel improves vaginal secretions and epithelial thickness and pH[37][38] No endometrial hyperplasia No longterm evidence[39]
Intravaginal dehydroepiandrosterone Improves vaginal epithelium thickness and secretions[40][41] None Lacks longterm studies
Moisturizers and lubricants[42] Polymers adhere to the epithelial and mucin improving vaginal lubrication Temporary relief for patients with mild symptoms Doesnt reverse atrophic changes

Assessment of Response to treatment

  • Atrophic vaginitis being a chronic disease continuous therapy is recommended. Response to treatment is assessed by the following:
    • Vaginal Maturation Index(VMI)
    • Vaginal pH assessment

Primary Prevention

Secondary Prevention

References

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