Pelvic Inflammatory Disease and Vaginitis

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[edit] Pelvic Inflammatory Disease and Vaginitis

J. Chris Carey

[edit] PELVIC INFLAMMATORY DISEASE

[edit] Epidemiology

Pelvic inflammatory disease (PID) is estimated to be responsible for 2.5 million outpatient visits each year, as well as 275,000 hospitalizations. The disease is more common in younger reproductive-age women, single women, women with multiple sexual partners or a new partner in the last 6 months, and nonwhite women. Women who use barrier contraceptives are at lower risk. Use of an intrauterine device has been associated with an increased risk of PID, mainly related to the risk of insertion and to acquisition of a sexually transmitted disease (STD).

[edit] Pathophysiology

PID results from an ascending infection by organisms that have colonized the endocervix. The syndrome includes nonpuerperal endometritis, salpingitis, oophoritis, and adnexitis. Neisseria gonorrhoeae and Chlamydia trachomatis are the most common etiologic agents, but secondary infection with a variety of anaerobic and aerobic agents also occurs. A polymicrobial infection with aerobic and anaerobic bacteria is found in up to 40% of women who have laparoscopically proven acute salpingitis. Many of these organisms found in the upper tract are the same organisms found in increased numbers in the vagina of women with bacterial vaginosis, which is more common in women with PID. It is not known, however, whether bacterial vaginosis is a risk factor for development of PID, or develops concurrently with PID, or develops as a result of PID.

Retrograde menstruation is thought to play a role in the development of PID. Sexually transmitted organisms that inhabit the endocervix may be spread to the fallopian tubes by retrograde menstruation. Secondary infection of the fallopian tubes by aerobic and anaerobic organisms may lead to abscess formation or overt sepsis. Tuboovarian abscesses usually contain anaerobic bacteria.

Infertility is an important sequela of PID. The risk of tubal factor infertility roughly doubles after each episode of PID. After one, two, and three episodes of PID the risk of infertility is 8%, 19.5%, and 40%, respectively. The risk of ectopic pregnancy is increased fourfold after documented salpingitis.

[edit] Patient Evaluation

[edit] History.

PID may present with a wide variety of symptoms and signs. The classic history is of acute lower abdominal pain, usually after menstruation, with fever and a foul or purulent vaginal discharge (Table 46-1). Many women with PID, however, have subtle or mild symptoms. Pelvic and lower abdominal pain is the most common symptom, is usually bilateral, and may not be severe. Endocervicitis may lead to a complaint of vaginal discharge. Persistent spotting while taking oral contraceptives (OCs) or after pregnancy termination may be a symptom of PID. Nausea and vomiting may result from peritonitis with or without fever. Inflammation of the liver by peritoneal spread can lead to acute hepatitis (Fitz-Hugh–Curtis syndrome).

Table 46-1 Essential Elements of History in Suspected Pelvic Inflammatory Disease (PID)

[edit] Physical Examination.

The triad of lower abdominal tenderness, adnexal tenderness, and cervical motion tenderness is considered sufficient to make the diagnosis of PID if no other cause for the illness can be found. Other physical findings consistent with the diagnosis of PID include mucopurulent cervicitis, which can be diagnosed by a marked increase of inflammatory cells on a saline preparation of the endocervical mucus. A palpable adnexal mass suggests a tuboovarian abscess. An elevated temperature is further evidence of PID.

[edit] Diagnosis

Acute PID is difficult to diagnose because of the wide variation in symptoms and signs. Many cases of PID go unrecognized. On the other hand, many women who have other conditions are treated for PID. No single historic, physical, or laboratory finding is both sensitive and specific for the diagnosis of PID. Combinations of diagnostic findings that improve either sensitivity or specificity do so at the expense of the other. Therefore the diagnosis of PID is usually based on clinical findings. The clinical diagnosis of acute PID is also imprecise. A clinical diagnosis of symptomatic PID has a positive predictive value (PPV) for salpingitis of 65% to 90% compared with laparoscopy. The PPV of a clinical diagnosis of acute PID differs depending on epidemiologic characteristics and the clinical setting, with higher PPVs among sexually active young (especially teenage) women and among patients attending STD clinics or from settings where rates of gonorrhea or chlamydial infection are high.

Because of the difficulty in diagnosis and the potential for infertility after even mild PID, primary care physicians should maintain a high suspicion for PID and a low threshold for its diagnosis (Box 46-1). Empiric therapy for PID can be instituted based on minimum criteria in patients with initial episodes. Initiation of antibiotic therapy for PID is unlikely to interfere with the diagnosis and management of other causes of lower abdominal pain. Women with repeated episodes, failed initial therapy, or questionable diagnosis of PID should have additional diagnostic studies.

[edit] Diagnostic Procedures

[edit] Cultures.

Cultures or other screening methods for N. gonorrhoeae and C. trachomatis should be obtained from every woman with suspected PID. A positive culture not only supports the diagnosis of PID but emphasizes the need to treat sex partners. Screening tests for other STDs, such as human immunodeficiency virus (HIV) and syphilis, are also recommended.

[edit] Ultrasound.

Ultrasound is indicated if an adnexal mass is suspected, if the diagnosis is in question, or if a patient does not respond to initial therapy. Ultrasound is both sensitive and specific for the presence of a tuboovarian abscess. The presence of tubal edema and fluid is highly suggestive of PID, but a nondiagnostic ultrasound does not exclude PID.

[edit] Laparoscopy.

Although it can be used to obtain a more accurate diagnosis of PID and a more complete specimen for culture, laparoscopy is not always available for immediate diagnosis. The expense and risk of laparoscopy are difficult to justify for routine diagnosis of PID. Laparoscopy may not detect endometritis or subtle salpingitis. Laparoscopy should be considered in women with an uncertain diagnosis, particularly if an ectopic pregnancy is suspected, and women with a history of multiple outpatient treatments for PID to exclude other causes of pain (e.g., endometriosis). Laparoscopy may also be useful in preserving fertility by lysis of adhesions.

[edit] Endometrial Biopsy.

Acute or chronic inflammation on an endometrial biopsy offers an alternative, objective method of diagnosing upper tract inflammation. Endometrial biopsy is useful in patients with subtle signs, including abnormal bleeding.

[edit] Differential Diagnosis.

Ectopic pregnancy should be considered in every woman with signs suggestive of PID. A negative serum pregnancy test should exclude ectopic pregnancy. In any woman who is thought to be pregnant and have PID, it is imperative to exclude an ectopic pregnancy. Ultrasound to localize the pregnancy should be the first step. If ectopic pregnancy cannot be excluded by ultrasound, laparoscopy should be considered.

Appendicitis can be difficult to distinguish from PID. Appendicitis more often presents with unilateral pain, nausea, vomiting, and peritoneal signs. Physical examination and ultrasound can sometimes distinguish appendicitis and PID. If appendicitis is suspected, a laparoscopy may be indicated. Endometriosis typically presents with cyclic pain and dysmenorrhea and can be difficult to distinguish from PID. The definitive diagnosis of endometriosis can be made only by laparoscopy. Ovarian cysts may present with acute symptoms similar to PID. Midcycle onset of pain, unilateral pain, palpation of a cyst, and absence of mucopurulent cervicitis suggest an ovarian cyst. Ultrasound is useful in this diagnosis.

[edit] Management

[edit] Nonpharmacologic Therapy.

Prevention of STDs is the mainstay of nonpharmacologic management of PID. Counseling of patients about safe sexual practices and the risks of acquiring STDs should be part of contraceptive counseling. Women at risk for acquisition of an STD who use OCs should be counseled to use condoms as well. Screening for asymptomatic N. gonorrhoeae and C. trachomatis is indicated for at-risk populations (e.g., women under age 25 with new partner in last year, populations with high incidence of STDs). Women with clinically apparent mucopurulent cervicitis should also be screened for these organisms.

[edit] Pharmacologic Therapy.

Antibiotic therapy for PID must provide empiric, broad-spectrum coverage of likely pathogens. Antimicrobial coverage should include N. gonorrhoeae, C. trachomatis, anaerobes, gram-negative facultative bacteria, and streptococci. Several antimicrobial regimens have been effective in achieving clinical and microbiologic cure in randomized clinical trials with short-term follow-up (Box 46-2). However, few investigations have assessed and compared these regimens with regard to elimination of infection in the endometrium and fallopian tubes or have determined the incidence of long-term complications, such as infertility or ectopic pregnancy. Oral ofloxacin is effective against both N. gonorrhoeae and C. trachomatis and as a single agent. The addition of metronidazole provides ofloxacin's lack of anaerobic coverage. Amoxicillin/clavulanate plus doxycycline has obtained short-term clinical response, but gastrointestinal symptoms might limit the overall success of this regimen.

[edit] Consultation and Hospitalization.

Some authorities recommend intravenous therapy for all PID patients or for women with PID who have not completed childbearing (Box 46-3). The physician should decide whether hospitalization is necessary (Box 46-4). No currently available data compare the efficacy of parenteral with oral therapy or inpatient with outpatient treatment settings. Until the results from ongoing trials comparing parenteral inpatient therapy with oral outpatient therapy for women with mild PID are available, such decisions must be based on observational data and consensus opinion.

Patients receiving oral or parenteral therapy should show substantial clinical improvement in 3 days. Defervescence usually precedes subsidence of pain. Patients who do not show improvement in 3 days usually require additional therapy or surgery. Women treated as outpatients should be reexamined in 3 days and evaluated for improvement. Some authorities recommend repeat screening in 4 to 6 weeks for patients who had positive tests for N. gonorrhoeae or C. trachomatis. If a polymerase or ligase chain reaction (PCR, LCR) was used as a screening test, at least 4 weeks should elapse to prevent false-positive repeat screens.

[edit] Special Issues

[edit] Sexual Partners.

Sexual partners of women with PID should be screened for N. gonorrhoeae and C. trachomatis if they have had intercourse within the last 60 days. Negative cervical cultures or other screens do not exclude carriage of these organisms by sexual partners. Screening and treatment of sexual partners are important to prevent reacquisition of STDs and recurrent PID.

[edit] Pregnancy.

Because of the high risk for maternal morbidity, fetal wastage, and preterm delivery, pregnant women with suspected PID should be hospitalized and treated with parenteral antibiotics. Ectopic pregnancy must be excluded in every pregnant woman who may have PID. Disseminated gonococcal infection is more common in pregnant women than nonpregnant women, and women with suspected infection should be treated with parenteral therapy. Doxycycline and ofloxacin are contraindicated in pregnancy, as is erythromycin estolate. Pregnant patients with PID must receive a sufficiently long course of an agent against C. trachomatis. Erythromycin base, 500 mg four times a day for 7 days, is recommended. The safety and efficacy of azithromycin has not been established in pregnant or lactating women.

[edit] HIV Infection.

It is not clear whether PID has different clinical manifestations in HIV-infected women and HIV-negative women. Early observational studies found that HIV-infected women with PID were more likely to require surgical intervention. In a subsequent and more comprehensive observational study, HIV-infected women with PID had more severe symptoms than HIV-negative women but responded equally well to standard parenteral antibiotic regimens. Immunosuppressed HIV-infected women with PID should be managed aggressively using parenteral antimicrobial regimens.

[edit] VAGINITIS

[edit] Epidemiology

Vaginitis is one of the most common reasons for physician visits by women, accounting for approximately 10 million office visits per year. No reliable figures define the incidence of vaginitis in the United States. Its prevalence is difficult to estimate because (1) many women with abnormal flora may have minimal symptoms and may not complain of vaginitis, and (2) many women self-medicate with over-the-counter medications. The largest studies of prevalence of vaginitis were performed in pregnant women. The Vaginal Infections and Prematurity study screened 13,914 pregnant women for vaginal and cervical pathogens. Candida albicans was isolated from 8.2%, Trichomonas vaginalis was isolated by culture from 12.5%, and bacterial vaginosis was diagnosed by Gram's stain in 16.2%. Data from Great Britain indicate that the incidence of symptomatic vulvovaginal candidiasis increased from 118 to 200 per 100,000 from 1980 to 1990. Sales of antifungal medications in the United States have also increased, indicating a greater incidence of vaginitis.

The prevalence and type of vaginitis vary greatly by age and race. Bacterial vaginosis and T. vaginalis are more common in reproductive-age women and in black women, whereas candidiasis is more common in white women. Atrophic vaginitis is more common in postmenopausal women.

[edit] Pathophysiology

Lactobacilli are the predominant organisms in the normal vagina. Because lactobacilli produce lactic acid and hydrogen peroxide, the vagina normally has a pH of 3.8 to 4.4 and has a high oxidative potential. The combination of these two factors helps prevent growth of other organisms, such as anaerobic bacteria. Each gram of vaginal discharge usually has about 10⁴ organisms. Five to 15 different organisms can usually be cultured from the vagina of a normal woman (Box 46-5). The normal vaginal discharge consists primarily of desquamated epithelial cells and is white to gray, flocculent, and not malodorous.

Infectious vaginitis results from an alteration of normal vaginal flora and has several common causes (Box 46-6). Becauseto other organisms almost never cause vaginitis, their treatment is rarely if ever indicated.

In bacterial vaginosis the lactobacilli decrease in number with an overgrowth of other organisms, such as Gardnerella vaginalis, anaerobic bacteria, and mycoplasmas. The total number of bacteria increase from 10⁴ to 10¹¹ per gram of vaginal discharge. Symbiotic metabolism produces aromatic amines such as putrescine, cadaverine, and trimethylamine, which cause the characteristic “dead fish” or “dead mouse” malodorous discharge. Bacterial vaginosis is a noninflammatory condition; patients rarely have significant pain or burning but may have some itching. Approximately half of patients with bacterial vaginosis are asymptomatic.

[edit] Patient Evaluation

[edit] History.

Symptoms of vaginitis include vaginal discharge, itching, burning, and dyspareunia. Symptoms help delineate different forms of vaginitis. Women with C. albicans typically have a white, clumpy discharge that may have a yeastlike odor. Itching and to a lesser degree burning are the primary complaints. Women with a noncandidal fungal infection often have less discharge and have more burning than itching. Women with bacterial vaginosis have an increased or different discharge that is gray and malodorous. Because bacterial vaginosis is noninflammatory, patients usually do not have the degree of itching seen with candidal infections. T. vaginalis causes an intense inflammatory response with pain, edema, and purulent discharge. Symptoms overlap greatly, however, and the diagnosis of vaginitis cannot be made from symptoms alone.

Other important elements of the history include duration of symptoms, prior episodes, including prior therapies and results; associated conditions and other illnesses or infections; antibiotic use or other medications; and any conditions or medications that could cause immunosuppression. Prior therapies should include prescription, over-the-counter (OTC), alternative, and home remedies. Many patients will have used OTC or alternative therapies. Patients with vaginitis may have developed a secondary inhibited sexual desire from dyspareunia. Although this complication is uncommon with acute vaginitis, it is common in women with chronic vaginitis. Patients with chronic or recurrent vaginitis should be asked about inhibited sexual desire.

[edit] Physical Examination.

The general examination should document any dermatitis or signs of other infections. Pelvic examination should document any skin changes of the external genitalia and the amount and character of any vaginal discharge. The cervix should be examined for discharge. The remainder of the pelvic examination is completed as usual.

[edit] Diagnosis

[edit] Diagnostic Procedures.

Microscopy is the cornerstone of diagnosis. A wet mount can be prepared by taking a swab from the junction of the upper third and lower two thirds of the vaginal side wall and placing the swab in a small test tube containing three drops of normal saline. The swab is then rotated to obtain a uniform suspension. A wet mount and a 10% potassium hydroxide (KOH) preparation can then be made at microscopy. The vaginal pH can be measured by using narrow-range pH paper from the swab. The wet mount and KOH prep should be examined under both low and high power. The saline mount should be examined for motile trichomonads and for clue cells, epithelial cells coated with coccobacilli. The KOH prep is examined for hyphae and buds. Gram's stain of the vaginal smear is easily prepared in the office, with the types of bacteria quantified to make the diagnosis of bacterial vaginosis.

Vaginal cultures are rarely indicated. Cultures are used only if the appropriate transport media are available, if the laboratory can isolate the organisms of interest, and if qualitative culture results are available. Fungal cultures may be indicated for recurrent or persistent infections.

Vulvar biopsy should be performed if the vulvar skin has visible lesions. Postmenopausal women who are diagnosed with atrophic vaginitis but do not respond to estrogen should have a vulvar biopsy if another cause cannot be determined.

[edit] Differential Diagnosis.

The diagnosis of bacterial vaginosis can be made by meeting three of the following four criteria: (1) thin, gray, malodorous discharge that adheres to vaginal wall, (2) elevated vaginal pH (over 4.5), (3) clue cells and decreased lactobacilli, and (4) positive “whiff” test (release of amine odor with addition of KOH).

Fungal vaginitis presents with itching and burning and a thick, white, “cottage cheese” discharge. Microscopy shows the presence of hyphae or buds. The pH is usually normal (3.8 to 4.4).

Trichomoniasis presents with a copious, purulent discharge that may have an amine or foul odor. The patient usually has erythema and edema of the vagina and vulva. The pH is usually elevated (over 4.5). Microscopy reveals the presence of motile trichomonads.

Atrophic vaginitis may present with a reddened, inflamed vagina or with a pale, thin mucosa. Patients may have pain or itching. The pH is usually elevated. Microscopy reveals intermediate and parabasal epithelial cells that have a round shape and large nuclei.

Vulvar dystrophies may present with itching or burning. Symptoms are usually limited to the vulva, and the vulvar skin appears abnormal. Vaginal discharge is normal.

Vulvar vestibulitis is a rare condition characterized by inflammation of the minor vestibular glands. Physical findings are erythema of the vestibule and extreme tenderness to light touch of the vestibule.

Vulvodynia is a symptom and means “painful vulva.” Conditions that cause vulvodynia include chronic fungal infections, vestibulitis, and neuropathic (essential) vulvodynia.

[edit] Management

The key step in management of vaginitis is establishing a correct diagnosis (Table 46-2). Management of uncomplicated vaginitis is usually straightforward.

Table 46-2 Recommended Treatment for Various Types of Vaginitis

[edit] Bacterial Vaginosis.

Bacterial vaginosis is treated with either oral or vaginal metronidazole or clindamycin. Women who do not respond to these therapies may be treated with other oral antibiotics active against anaerobes or with intravaginal sulfas. Treatment of sexual partners has not been shown to increase the success of therapy or decrease the risk of recurrence of bacterial vaginosis. Gardnerella vaginalis can be isolated from the prostatic secretions of sexual contacts of women with bacterial vaginosis, however, and some advocate treatment of sexual partners in cases of recurrent bacterial vaginosis.

[edit] Fungal Vaginitis.

Initial therapy of fungal vaginitis is vaginal imidazoles or triazoles. One-day, 3-day, or 7-day therapies appear to be equally effective, and symptom resolution occurs at approximately the same rate, 3 to 5 days after beginning therapy. Oral fluconazole, 150 mg as a single dose, seems as effective as vaginal preparations.

The treatment of women who do not respond to initial therapy or who have recurrent cyclic candidal vaginitis has not been established. Some of these patients may respond to intravaginal boric acid (600 mg for 10 nights). The boric acid can be compounded into a water-based suppository or placed in a number-three gelatin capsule. Noncandidal strains are often resistant to imidazoles and may respond to boric acid, high-dose triazoles (e.g., itraconazole, 200 to 400 mg/day for 14 days), intravaginal gentian violet, oral terbinafine (Lamisil), oral ketaconozole (200 mg/day for 14 days), or rarely, intravaginal 5% amphotericin B cream. These latter therapies are not approved by the U.S. Food and Drug Administration (FDA) and should be used only after consultation.

[edit] Trichomoniasis.

Metronidazole is the only FDAapproved drug that is active against T. vaginalis. Various regimens have been recommended, and all appear to have 90% to 95% efficacy. It is important to treat all sexual partners to prevent reacquisition of the organism.

[edit] Atrophic Vaginitis.

The primary treatment of atrophic vaginitis is oral or vaginal estrogen. Women who develop atrophic vaginitis progress from a normal, pink vaginal epithelium to a red, inflamed epithelium and then a pale, thin vaginal mucosa. With treatment the process reverses; women with a pale, thin epithelium develop a red epithelium that may itch because of increased blood supply to the vagina. Because patients may interpret this process as an allergy or irritation and stop the medication, they should be told to continue the treatment and that the process will continue to a normal, pink vagina.

[edit] Consultation and Hospitalization.

Hospitalization is rarely indicated for vaginitis. Consultation should be considered for women who (1) fail initial therapy, (2) do not have a clear diagnosis, (3) have repeated recurrences, (4) have vulvar dystrophies or vulvar vestibulitis, and (5) have associated sexual dysfunctions.

[edit] Special Issues

[edit] Pregnancy.

A variety of vaginal and cervical infections have been associated with preterm birth or low birth weight. Studies have shown an association between bacterial vaginosis and preterm birth, but randomized clinical trials have failed to show that treatment prevents preterm birth. T. vaginalis has also been associated with preterm birth, but no data show a reduced risk of preterm birth after treating trichomoniasis. Programs to screen and treat women for vaginal infections should not be undertaken until data from randomized clinical trials show a benefit of treatment.

[edit] HIV Infection.

Recurrent fungal vaginitis can be the first symptom of HIV infection. Women with HIV infection are more likely to have fungal vaginitis and to be infected with noncandidal strains and are less likely to respond to standard antifungal agents. Fungal vaginitis does not appear to increase the risk of mother-to-infant transmission of HIV or of heterosexual transmission of HIV.

Bacterial vaginosis is also associated with HIV infection in both pregnant and nonpregnant women. It is not clear whether HIV leads to increased risk for bacterial vaginosis, or vice versa, or if both are associated with other STDs.

[edit] ADDITIONAL READINGS

• American College of Obstetricians and Gynecologists: Vaginitis, Technical bulletin 226 Washington, DC: The College; 1996:
• American College of Obstetricians and Gynecologists: Antibiotics and gynecologic infections, Educational bulletin 237 Washington, DC: The College; 1997:
• Centers for Disease Control and Prevention: 1998 Guidelines for treatment of sexually transmitted diseases. MMWR 1998; 47 (RR-1):