V

Vaginal, cervical, and vulvar infections

Definition

Infection and inflammation of the vagina, cervix, and vulva commonly occur when the natural defenses of the acid vaginal secretions (maintained by sufficient estrogen level) and the presence of Lactobacillus are disrupted. A woman’s resistance may also be decreased as a result of aging, poor nutrition, and the use of drugs (e.g., antibiotics, hormones) that alter the bacterial flora or mucosa.

Pathophysiology

Organisms gain entrance to these areas through contaminated hands, clothing, and douche tips and during intercourse, surgery, and childbirth. Table 83 presents the etiology, clinical manifestations, diagnostic methods, and collaborative care of common infections of the lower genital tract.

■ Most lower genital tract infections are related to sexual intercourse. Vulvar infections, such as herpes and genital warts, can be sexually transmitted when no lesions are present (see Herpes, Genital, p. 309, and Warts, Genital, p. 672).

■ Oral contraceptives, antibiotics, and corticosteroids may produce changes in the vaginal pH and trigger an overgrowth of the organisms present. For example, Candida albicans may be present in small numbers in the vagina. An overgrowth of this organism causes vulvovaginitis.

Table 83

Infections of the Lower Genital Tract

Infection and Etiology	Manifestations and Diagnostic Methods	Drug Therapy
Vulvovaginal Candidiasis (VVC) (Monilial Vaginitis)
Candida albicans (fungus)	Commonly found in mouth, GI tract, and vagina. Pruritus, thick white curdlike discharge. KOH microscopic examination: pseudohyphae, pH 4.0-4.7.	Antifungal agents (e.g., miconazole [Monistat], clotrimazole [Gyne-Lotrimin, Mycelex] [available over the counter, in cream or suppository]) Fluconazole (Diflucan).
Trichomonas Vaginitis
Trichomonas vaginalis (protozoa)	Sexually transmitted. Pruritus, frothy greenish or gray discharge. Hemorrhagic spots on cervix or vaginal walls. Saline microscopic examination: swimming trichomonads, pH >4.5.	Metronidazole (Flagyl) for patient and partner.
Bacterial Vaginosis
Gardnerella vaginalis Corynebacterium vaginale	Mode of transmission unclear. Watery discharge with fishy odor. May or may not have other symptoms. Saline microscopic examination: epithelial cells, pH >4.5.	Oral or vaginal metronidazole (Flagyl) or clindamycin (Clindesse). Examine and treat partner. Lactobacillus acidophilus taken orally by diet (e.g., yogurt, fermented soy products) or supplements can decrease unwanted vaginal bacteria.
Cervicitis
Chlamydia trachomatis	Sexually transmitted; mucopurulent discharge with postcoital spotting from cervical inflammation. Culture for Chlamydia and Neisseria gonorrhoeae.	Azithromycin (Zithromax). Treat patient and partner.
Severe Recurrent Vaginitis
C. albicans (most often)	May be indication of HIV infection. All women who are unresponsive to first-line treatment should be offered HIV testing.	Drug appropriate to opportunistic organism.

KOH, Potassium hydroxide.

Clinical manifestations

■ Abnormal vaginal discharge and reddened vulvar lesions are common.

■ In addition to a thick, white, curdy discharge, women with vulvovaginal candidiasis (VVC) often experience intense itching and dysuria.

■ The hallmark of bacterial vaginosis is the fishy odor of the discharge.

■ Women with cervicitis may notice spotting after intercourse.

Postmenopausal older women may develop gynecologic problems, such as lichen sclerosis, a chronic inflammatory condition associated with intense itching in the genital skin area. The lesions are white with a “tissue paper” appearance initially, although scratching produces changes in the appearance.

Diagnostic studies

■ History, physical examination, and sexual history.

■ Culture ulcerative lesions for herpes.

■ Vulvar dystrophies are examined by colposcope with biopsy specimens taken.

■ Microscopy and culture of vaginal discharge are done.

■ Bacterial vaginosis, VVC, and trichomoniasis are diagnosed by a wet mount.

■ For cervicitis, endocervical cultures are obtained for chlamydia and gonorrhea. If purulent discharge is observed coming from the cervix, endocervical cells may be taken to do a Gram stain.

Collaborative care

Antibiotics taken as directed will cure bacterial infections. Antifungal preparations (in oral or cream preparations) are indicated for VVC. Women with vaginal conditions or cervical infection should abstain from intercourse for at least 1 week. Douching should be avoided as it has been adversely linked to pelvic inflammatory disease, sexually transmitted infections, and ectopic pregnancy. Sexual partners must be evaluated and treated if the patient is diagnosed with trichomoniasis, chlamydia, gonorrhea, syphilis, or HIV.

Treatment of vulvar dystrophies is symptomatic and involves controlling the itching and hence the scratching. Interrupting the “itch-scratch cycle” prevents further secondary damage to the skin.

Nursing management

Teach women about common genital conditions and how to reduce their risks. Recognize symptoms that indicate a problem and help women seek care in a timely manner.

When a woman is diagnosed with a genital condition, ensure that she fully understands the directions for treatment. Taking the full course of medication is especially important to decrease the chance of relapse. Because genitals are such a private area, use of graphs and models is especially helpful for patient teaching.

When a woman is using a vaginal medication such as an antifungal cream for the first time, show her the applicator and how to fill it. Also teach where and how the applicator should be inserted by using visual aids or models. Vaginal creams should be inserted before going to bed so that the medication will remain in the vagina for a long period of time. Women using vaginal creams or suppositories may wish to use panty liners during the day when the residual medication may drain out.

Valvular heart disease

Description

Valvular heart disease is defined according to the affected valve or valves (mitral, aortic, tricuspid, pulmonary) and the type of functional alteration: stenosis or regurgitation.

■ The pressure on either side of an open valve is normally equal. However, in stenosis the valve opening is smaller, impeding the forward flow of blood and creating a pressure difference on the two sides of the open valve. The degree of stenosis (constriction or narrowing) is reflected in the pressure differences (i.e., the higher the gradient, the greater the stenosis).

■ In regurgitation (also called incompetence or insufficiency), incomplete closure of valve leaflets results in a backward flow of blood.

Valve disorders occur in children and adolescents mainly from congenital conditions. Aortic stenosis and mitral regurgitation are the common valve disorders in older adults. Other causes of valve disease in adults include disorders related to acquired immunodeficiency syndrome (AIDS) and the use of some antiparkinsonian drugs (e.g., pergolide [Permax]).

Clinical manifestations of valvular heart disease are presented in Table 84.

Table 84

Manifestations of Valvular Heart Disease

Type	Manifestations
Mitral valve stenosis	Dyspnea on exertion, hemoptysis; fatigue. Atrial fibrillation on ECG, palpitations, stroke. Loud, accentuated S₁. Low-pitched, diastolic murmur.
Mitral valve regurgitation	Acute: Generally poorly tolerated. New systolic murmur with pulmonary edema and cardiogenic shock developing rapidly. Chronic: Weakness, fatigue, exertional dyspnea, palpitations. An S₃ gallop, holosystolic murmur.
Mitral valve prolapse	Palpitations, dyspnea, chest pain, activity intolerance, syncope. Holosystolic murmur.
Aortic valve stenosis	Angina, syncope, dyspnea on exertion, heart failure. Normal or soft S₁, diminished or absent S₂, systolic murmur, prominent S₄
Aortic valve regurgitation	Acute: Abrupt onset of profound dyspnea, chest pain, left ventricular failure and cardiogenic shock. Chronic: Fatigue, exertional dyspnea, orthopnea, PND. Water-hammer pulse. Heaving precordial impulse. Diminished or absent S₁, S₃, or S₄. Soft high-pitched diastolic murmur, Austin-Flint murmur.
Tricuspid and pulmonic stenosis	Tricuspid: Peripheral edema, ascites, hepatomegaly. Diastolic low-pitched murmur with increased intensity during inspiration. Pulmonic: Fatigue, loud midsystolic murmur.

PND, Paroxysmal nocturnal dyspnea.

Mitral valve stenosis

Pathophysiology

Most cases of adult mitral valve stenosis result from rheumatic heart disease. Less common causes include congenital mitral stenosis, rheumatoid arthritis, and systemic lupus erythematosus (SLE).

■ Rheumatic endocarditis causes scarring of valve leaflets and chordae tendineae. Contractures and adhesions develop between the commissures (the junctional areas).

■ The stenotic mitral valve takes on a “fish mouth” shape because of the thickening and shortening of mitral valve structures. Flow obstruction increases left atrial pressure and volume, resulting in higher pulmonary vasculature pressure and eventually involving the right ventricle.

Clinical manifestations

The primary symptom is exertional dyspnea due to reduced lung compliance. Fatigue and palpitations from atrial fibrillation may also occur. Heart sounds include a loud first heart sound and a low-pitched, rumbling diastolic murmur (best heard at the apex with the stethoscope bell). Other clinical manifestations are identified in Table 84.

Mitral valve regurgitation

Pathophysiology

Mitral valve function depends on the integrity of mitral leaflets, chordae tendineae, papillary muscles, left atrium (LA), and left ventricle (LV). A defect in any of these structures can result in regurgitation. Myocardial infarction with left ventricular failure increases the risk for rupture of the chordae tendineae and acute mitral regurgitation (MR).

■ Most cases of MR are caused by myocardial infarction, chronic rheumatic heart disease, mitral valve prolapse, ischemic papillary muscle dysfunction, and infective endocarditis.

■ MR allows blood to flow backward from the LV to the LA because of incomplete valve closure during systole. Both chambers of the left side of the heart must work harder to preserve an adequate cardiac output (CO).

■ In acute MR, abrupt dilation of the LA or LV does not occur. The sudden increase in pressure and volume is transmitted to the pulmonary bed, resulting in pulmonary edema and cardiogenic shock.

■ In chronic MR, the additional volume load results in left atrial enlargement and left ventricular dilation and hypertrophy, and finally a decrease in CO.

Clinical manifestations

Patients with acute MR have thready peripheral pulses and cool, clammy extremities. A low CO may mask a new systolic murmur. Rapid assessment (e.g., cardiac catheterization) and intervention (e.g., valve repair or replacement) are critical for a positive outcome.

Patients with chronic MR may remain asymptomatic for many years until the development of some degree of left ventricular failure. Manifestations are identified in Table 84.