Vulvovaginitis in Emergency Medicine 

  • Author: Mark J Leber, MD, MPH; Chief Editor: Pamela L Dyne, MD   more...
 
Updated: Apr 16, 2012
 

Background

Vulvovaginitis is common, affecting women of all ages. Vulvovaginitis is an inflammation of the vagina and vulva, most often caused by a bacterial, fungal, or parasitic infection. Vulvovaginitis, one of the most common reasons why women visit their gynecologist, causes vaginal discharge, irritation, and itching. Normally, a woman may have a vaginal discharge, the amount and consistency of which varies during the course of the menstrual cycle; however, vulvovaginitis causes a symptomatic increased vaginal discharge. Other symptoms associated with this condition are dyspareunia, dysuria, and odor.

Women with vulvovaginitis tend to be embarrassed or are worried about sexually transmitted diseases (STD). Self-treatment is usually the norm and close to 50% ineffective.[1] In this country alone, millions of dollars are wasted on over-the-counter antifungals because of self-treatment for candidiasis.[2] Providers may also be uncomfortable or do not have adequate time to diagnose the true etiology and may treat the wrong condition. Thus, vulvovaginitis is probably underdiagnosed.

Etiologies and the approach of management for a patient with vulvovaginitis are age dependent. Vulvovaginitis can be divided into 3 age categories: premenarchal, childbearing, and postmenopausal.

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Pathophysiology

The normal vaginal epithelium cornifies (develops into a thickened layer of epithelial cells) under the influence of estrogen, protecting women against infection. A normal vaginal discharge consists of 1-4 mL of fluid that is white or transparent, thick, and odorless. This physiologic discharge is formed by sloughing epithelial cells, normal bacteria, and vaginal transudate. The discharge may be noticeable during pregnancy, oral contraceptive pill use, or at mid menstrual cycle, close to the time of ovulation.

The normal pH of vaginal secretions is 4.0-4.5.[3] The pH is maintained by lactobacillus, which produces hydrogen peroxide and lactic acid; diphtheroids; and Staphylococcus epidermidis.[2] Lactobacillus is found in 62-88% of women.[3] Vaginal pH may increase with age, phase of menstrual cycle, sexual activity, contraception choice, pregnancy, presence of necrotic tissue or foreign bodies, and use of hygienic products or antibiotics.[3]

Bacterial vaginosis is secondary to bacterial overgrowth and not due to tissue inflammation. The organisms associated with bacterial vaginosis are Gardnerella vaginalis, Mycoplasma hominis, and Mobiluncus, a facultative anaerobe.[4, 5] Summarizing, practically any condition changing the vaginal milieu may result in vulvovaginitis.

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Epidemiology

Frequency

United States

Premenarchal

Vulvovaginitis is the most common gynecologic problem affecting prepubertal girls and is responsible for the largest number of visits to the gynecologist.

Childbearing age

Bacterial vaginosis is the most important cause of vulvovaginitis. Estimating the number of patients presenting with bacterial vaginosis is difficult because G vaginalis can be recovered from the vagina in 30-50% of asymptomatic women.[6]

Trichomonas vaginalis affects 2-3 million women annually in the United States. The organism also is detected in 30-40% of men who are exposed to women with T vaginalis.[3] The prevalence of T vaginalis infection at clinics treating sexually transmitted diseases (STDs) varies from 8-31%. In men, T vaginalis may account for as many as 17% of cases of nongonococcal, nonchlamydial urethritis. T vaginalis infection appears to be more common in the southern United States.

Candidal vulvovaginitis is considered slightly less common than bacterial vaginosis, yet, 3 out of every 4 women in the United States will have at least 1 bout of vulvovaginal candidiasis (VVC) during their lifetime.[4, 6] Patients with recurrent or severe vulvovaginal candidiasis warrant a screening test for diabetes mellitus.

Postmenopausal

After menopause, most women experience some vaginal atrophy as estrogen levels fall. Incidence of atrophic vaginitis depends on how it is defined. Vulvovaginitis related to infection is much less common after menopause. Desquamative inflammatory vaginitis, an exception, has an unknown etiology, but a Gram stain of culture often reveals streptococci. This is treated with intravaginal clindamycin cream or a topical or intravaginal steroid.[7] Postirritation vulvovaginitis may occur in women undergoing pelvic irradiation for cancer.

International

Bacterial vaginosis is the most common cause of vaginitis in women of childbearing age, with prevalence of 50-60% across the globe.

Trichomoniasis affects 180 million women worldwide.

Mortality/Morbidity

No mortality has been documented primarily from vulvovaginitis.

  • Premenarchal: Persistent vulvovaginitis in children is sometimes mistaken for an infection rather than for a foreign body. Labial adhesion, possibly to the point of occlusion of the vaginal orifice, may occur as an isolated finding, be secondary to urinary tract infections (UTIs), or be secondary to vulvovaginitis. These adhesions usually do not cause long-term problems. The presence of chlamydia or gonorrhea from vaginal secretions indicates child abuse.
  • Childbearing age
    • A variety of complications has been associated with bacterial vaginosis, including the following:
      • Pelvic inflammatory disease
      • Increased incidence of abdominal pain, uterine bleeding, and uterine and adnexal tenderness
      • Increased complications of pregnancy, especially premature delivery, chorioamnionitis, postpartum endometritis, and ectopic pregnancy
    • Candidal vulvovaginitis may develop into chronic or recurrent candidal infection related to the following:[8, 3, 9]
      • Diabetes mellitus[7]
      • Oral contraceptive (OCP) use
      • Antibiotic use
      • Immunodeficiency
      • Tight-fitting undergarments
    • Some authors have suggested that T vaginalis, considered a sexually transmitted organism, may act as a vector for other types of infections. The organism can be identified in 30-40% of male sexual partners of infected women, although carriage in men is self-limited and transient.
  • Postmenarchal: Vaginal bleeding may occur from the thin mucosa. Dyspareunia may also occur as a complication.

Race

  • Premenarchal: Significance of race is not clearly defined.
  • Childbearing age: In the National Health and Nutrition Examination Survey (NHANES) IV, the overall incidence in women of Trichomonas vaginalis was 3.9%. Incidence varied across different ethnic groups: white non-Hispanic 1.1%, Mexican American 1.8%, and African American 13.3%.[8, 10] These differences remained after controlling for sociodemographic, sexual, and behavioral variables. Overall, 1 in 7 women attending an STD clinic over a year period became infected with Trichomonas. Bacterial vaginosis does not seem to have any significant racial variation.[11]

Sex

Vulvovaginitis does not occur in males. Males may be carriers of G vaginalis and T vaginalis.

Age

  • Premenarchal: Vulvovaginitis predominately affects school-aged children.
  • Childbearing age
    • Trichomonas species can occur in any age group, yet it is most common in older women peaking at the age of 30-34 years.[12]
    • Bacterial vaginosis has a fairly equal distribution across all age groups up until menopause. Prevalence does not vary significantly with age.
    • Candida species infections are most common during childbearing years.
  • Postmenarchal: Atrophic vaginitis may develop several years after menopause. Most women with vaginal atrophy do not develop symptomatic atrophic vaginitis.
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Contributor Information and Disclosures
Author

Mark J Leber, MD, MPH  Assistant Professor of Emergency Medicine in Clinical Medicine, Weill Cornell Medical College; Attending Physician, Lincoln Medical and Mental Health Center

Mark J Leber, MD, MPH is a member of the following medical societies: American College of Emergency Physicians and American College of Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Anuritha Tirumani, MD  Research Coordinator, Department of Emergency Medicine, Brooklyn Hospital Center

Disclosure: Nothing to disclose.

Specialty Editor Board

David S Howes, MD  Professor of Medicine and Pediatrics, Emergency Medicine Residency Program Director Emeritus, Head, Phemister Society, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine

David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mark Zwanger, MD, MBA  Assistant Professor, Department of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University

Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Pamela L Dyne, MD  Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center

Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Reza Keshavarz, MD, to the development and writing of this article.

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The photomicrograph reveals bacteria adhering to vaginal epithelial cells known as clue cells. The presence of clue cells is a sign that the patient has bacterial vaginosis. Source CDC Phil/ M.Rein.
Candida albicans photomicrograph. Source CDC.
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