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CHAPTER 102: Vulvovaginitis 647 FIGURE 101-10. Midline vertical incision from xiphoid to symphysis pubis. Go through skin, fat, fascia, and peritoneum. Uterus Cut edge of parietal peritoneum FIGURE 101-11. Uterine midline vertical incision. Make the uterine incision large enough for 2 fingers and elevate the uterine wall off the fetus with your fingers. Then use scissors to divide the uterus between your 2 fingers. Apply steady pressure FIGURE 101-12. Delivering the fetus. lap pad and inspected for any residual membranes. Pitocin should be administered if possible. At this point the provider may decide to pack both the uterus and incision to allow closure by a surgeon in the operating room. However, if there is a need to close the uterus, more equipment is needed. Once the uterine cavity is empty, the uterus can be closed with the 0 or 1–0 delayed absorbable suture in a running fashion. The second layer of the uterine closure is usually closed in a running fashion. In some cases, a third layer may be required. The rest of the incision is closed in mass. Acknowledgments: The authors gratefully acknowledge the contribu tions of Michael J. VanRooyen, Jennifer A. Scott, and Kimberly B. Fortner, coauthors of this chapter in the previous editions, and Janet Y oung for the chapter “Maternal Emergencies After 20 Weeks of Pregnancy and in the Peripartum Period” in the previous edition. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Vulvovaginitis Ciara J. Barclay-Buchanan Melissa A. Barton INTRODUCTION Vulvovaginitis, or vulvovaginal inflammation, results from infectious and noninfectious processes that cause symptoms that include burning, irritation, itching, odor, and abnormal vaginal discharge. The factors associated with acute vaginitis are listed in Table 102-1. The clinical diagnosis may be challenging because more than one disease can be present, signs and symptoms are nonspecific to a single cause, and polymicrobial infection is common. In approximately 30% of women with vaginal complaints, no etiology is determined even after comprehensive testing. 1-3 Although infectious vaginitis rarely requires hospitalization, it can lead to serious sequelae. Both bacterial vaginosis (BV) and trichomoniasis are associated with premature rupture of membranes, preterm labor, and low infant birth weight. 4,5 Trichomonas vaginitis increases the risk of human immunodeficiency virus (HIV) acquisition and transmission CHAPTER Tintinalli_Sec11_p0607-0668.indd 647 8/2/19 4:21 PM

ae. Both bacterial vaginosis (BV) and trichomoniasis are associated with premature rupture of membranes, preterm labor, and low infant birth weight. 4,5 Trichomonas vaginitis increases the risk of human immunodeficiency virus (HIV) acquisition and transmission CHAPTER Tintinalli_Sec11_p0607-0668.indd 647 8/2/19 4:21 PM 648 SECTION 11: Obstetrics and Gynecology TABLE 102-1 Factors Associated With Acute Vulvovaginitis •  Infections •  Irritant  or allergic contact •  Local  response to a vaginal foreign body •  Lack  of estrogen in perimenopausal and postmenopausal women (atrophic vaginitis) •  Postradiation  changes TABLE 102-2 Diagnosis of Vaginitis Based on Vaginal Secretions Test Finding Diagnosis pH 4.0–4.5 Normal 4.0–4.5 Candidiasis >4.5 Bacterial vaginosis >4.5 Trichomoniasis Microscopy of specimen prepared with normal saline solution Clue cells Bacterial vaginosis Motile trichomonads Trichomoniasis Pseudohyphae and/or buds Candidiasis Whiff test of swab specimen prepared with potassium hydroxide Fishy odor Bacterial vaginosis Microscopy of specimen prepared with potassium hydroxide Pseudohyphae and/or buds Candidiasis TABLE 102-3 Vaginitis Signs and Symptoms Causative Organism Sign or Symptom Candida Thick, curdy discharge Itching Gardnerella or other bacteria Fishy odor Whitish-gray, thin discharge Trichomonas Frothy, odorous discharge Vaginal erythema or edema due to the loss of the protective effect found with normal vaginal lacto bacilli and is also associated with pelvic inflammatory disease in patients who are known to be HIV positive.6,7 PATHOPHYSIOLOGY In females of childbearing age, estrogen helps develop a thick vaginal epithelium with a large number of superficial glycogen-containing cells that serves a protective function. Normal flora, such as lactobacilli and acidogenic corynebacteria, use glycogen to form lactic and acetic acids. The resulting acidic environment favors the normal flora, discouraging growth of pathogenic bacteria. Low estrogen levels in postmenopausal women result in atrophy due to loss of the protective glycogen-containing superficial cells and the altered pH environment. Normal vaginal secretions vary in consistency from thin and watery to thick, white, and opaque. The volume may also vary from a scant to a copious amount. Secretions are odorless and produce no symptoms. Normal vaginal pH varies between 3.8 and 4.5. Alkaline secretions from the cervix before and during menstruation, as well as alkaline semen, reduce acidity and predispose to infection. Before menarche and after menopause, the vaginal pH varies between 6 and 7. Vulvovaginal inflammation is the most common gynecologic disor der in prepubertal girls and includes both infectious causes (e.g., bacte rial, fungal, pinworm) and noninfectious causes (e.g., contact/irritant, lichen sclerosis, foreign body). Factors thought to contribute to vaginitis in prepubertal females include less protective covering of the vestibule by the labia minora, low estrogen concentration resulting in a thinner epithelium, exposure to chemical irritants (e.g., bubble bath), poor hygiene, front-to-back wiping, short distance between the vagina and anus, foreign bodies, chronic medical conditions (e.g., eczema, sebor rhea), and sexual abuse. Infectious causes include respiratory and enteric bacterial organisms such as Haemophilus influenzae, Staphylococcus aureus, group A Streptococcus , S. pneumoniae, Escherichia coli, Shigella flexneri, Neisseria gonorrhoeae, and Chlamydia, as well as Candida and pinworms. Infectious causes may be more common in adolescents, especially those who are sexually active. CLINICAL FEATURES AND DIAGNOSIS The most common infectious causes of vaginitis in symptomatic premenopausal women are BV , vulvovaginal candidiasis, and Trichomonas vaginitis.

, and Chlamydia, as well as Candida and pinworms. Infectious causes may be more common in adolescents, especially those who are sexually active. CLINICAL FEATURES AND DIAGNOSIS The most common infectious causes of vaginitis in symptomatic premenopausal women are BV , vulvovaginal candidiasis, and Trichomonas vaginitis. Candidiasis, contact vaginitis, and atrophic vaginitis may occur in virgins and postmenopausal women. Obtain a detailed gynecologic history. History should include details of vaginal discharge, odor, irritation, itching, burning, bleeding, dysuria, and dyspareunia. Inquire about associated abdominal pain, new sexual partners, use of barrier protection during intercourse, relationship of symptoms to menses, recent use of antibiotics, hygiene practices, and use of over-the-counter and homeopathic treatments (e.g., douching, boric acid, intravaginal yogurt and probiotics, apple cider vinegar). Perform a pelvic examination. Note the presence of vulvar edema or erythema, vaginal discharge, cervical inflammation, abdominal tender ness, and cervical motion tenderness. External vulvar inflammation and minimal discharge suggest the possibility of mechanical, chemical, allergic, or other noninfectious causes of vulvovaginitis. During speculum examination, obtain a swab of the discharge. All sexually active women should be tested for gonorrhea and chlamydial infection. If a patient refuses pelvic examination or it is not feasible, the patient may submit a self-swab of vaginal secretions and in some cases a urine sample, as self-administered vaginal swabs are accurate screening tests for sexually transmitted infections.8-11 The Centers for Disease Control and Preven tion also recommends HIV and syphilis testing for women engaged in high-risk sexual behavior (i.e., new or multiple sexual partners, unpro tected intercourse). Finally, women of childbearing age should have a pregnancy test because pregnancy impacts treatment. Microscopic evaluation of fresh vaginal secretions using both normal saline solution and 10% potassium hydroxide (KOH) slide preparations, the KOH whiff test, and pH testing may help establish a specific diagnosis (Tables 102–2 and 102–3). Microscopic examination is time consuming and tedious. Results depend on operator skill, and although hospitals have laboratories, not all EDs have microscopes and appropriate reagents. Secretions from the mid-sidewall of the vagina are mixed with one to two drops of 0.9% normal saline in a test tube. A slide with a coverslip is prepared for microscopic evaluation. Microscopy should be performed immediately following sample collection as trichomonads lose motility quickly. Additionally, a drop of 10% KOH is added to the test tube and assessed for a fishy (amine) smell. KOH can also aid in the visualization of yeast. To test the pH, obtain a sample from the mid-portion of the vaginal sidewall to avoid false elevations in pH caused by mucus. Sampling from the posterior fornix may yield inaccurate results because cervi cal mucus, blood, semen, douche products, and vaginal medications can elevate the pH. Apply a small amount of the secretions directly onto pH paper to determine the pH. BACTERIAL VAGINOSIS BV is the most common cause of vaginitis in acutely symptomatic women. However, up to 50% of women who meet criteria for this diag nosis are asymptomatic. BV is usually a polymicrobial infection that occurs when the nor mal hydrogen peroxide–producing lactobacilli are replaced by other species, including Gardnerella vaginalis, Ureaplasma, Mycoplasma , Mobiluncus , Prevotella , and various other anaerobes. However, research exists suggesting that BV is not a true infection, but rather a bacterial imbalance.

ion that occurs when the nor mal hydrogen peroxide–producing lactobacilli are replaced by other species, including Gardnerella vaginalis, Ureaplasma, Mycoplasma , Mobiluncus , Prevotella , and various other anaerobes. However, research exists suggesting that BV is not a true infection, but rather a bacterial imbalance. 13 Risk factors include multiple sexual partners (female or male), intercourse with an uncircumcised male partner, vaginal intercourse immediately after receptive anal intercourse, lack of condom use, douching, and absence of peroxide-producing Tintinalli_Sec11_p0607-0668.indd 648 8/2/19 4:21 PM

ion that occurs when the nor mal hydrogen peroxide–producing lactobacilli are replaced by other species, including Gardnerella vaginalis, Ureaplasma, Mycoplasma , Mobiluncus , Prevotella , and various other anaerobes. However, research exists suggesting that BV is not a true infection, but rather a bacterial imbalance. 13 Risk factors include multiple sexual partners (female or male), intercourse with an uncircumcised male partner, vaginal intercourse immediately after receptive anal intercourse, lack of condom use, douching, and absence of peroxide-producing Tintinalli_Sec11_p0607-0668.indd 648 8/2/19 4:21 PM CHAPTER 102: Vulvovaginitis 649 lactobacilli in the vaginal flora. 14,15 Women who have never been sexually active are less commonly affected. BV is not caused by the transmission of a single sexually transmitted pathogen; however, it is generally agreed that sexual activity plays a role in transmission and may promote infection. BV has been associated with several adverse health outcomes, including increased risk of coinfection with sexually transmitted infections such as HIV , herpes simplex virus (HSV) type 2, Chlamydia trachomatis, and N. gonorrhoeae by decreasing local secretory leukocyte protease inhibitor levels. 17 BV is also linked to complications related to pregnancy and gynecologic surgical procedures, such as spontaneous abortion, premature rupture of membranes, amniotic fluid infection, chorioamnio nitis, preterm delivery, postpartum endometritis, pelvic inflammatory disease, postoperative wound infection, and infection after vaginal and abdominal hysterectomy.  DIAGNOSIS The most common clinical presentation is malodorous, vaginal dis charge. Classically, it is described as a thin, whitish-gray discharge associated with increased volume and a fishy smell. The absence of discharge or the presence of only a mild discharge makes the diagnosis less likely. Introital and vaginal irritation are uncommon. The diagnosis is based on history, pelvic examination, microscopic evaluation of vaginal secretions, and point-of-care testing. The presence of three of the following four criteria supports the diagnosis and correlates with a positive Gram stain (the gold standard for diagnosing BV) 19: 1. A thin, homogeneous vaginal discharge 2. More than 20% clue cells on a wet mount (Figure 102-1) 3. Positive results on test for amine release or whiff test 4. A vaginal pH level >4.5 The diagnostic criterion with the highest sensitivity is vaginal pH, whereas that with the highest specificity is a positive amine odor. If vaginal pH is >4.5 and there is an amine odor, then the diagnosis of BV can be made with confidence. 20 Commercially available DNA probe–based and vaginal fluid sialidase activity–based tests perform similar to Gram stain. 14 Diagnostic cards that detect an elevated pH and trimethylamine are available, but have a low sensitivity and specificity and thus are not recommended. Cultures are not beneficial because Gardnerella is part of the normal vaginal flora. FIGURE 102-1. Bacterial vaginosis. Saline wet mount with clue cells ( arrow). [Reproduced with permission from DeCherney AH, Nathan L, Laufer N, Roman AS (eds): Current Diagnosis & Treatment: Obstetrics & Gynecology, 11th ed. New York, NY: McGraw-Hill, Inc.; 2013. Fig. 39-9.] TABLE 102-4 Treatment Regimens for Bacterial Vaginosis Agent Dosage Recommended Regimens Metronidazole 500 milligrams PO BID for 7 d Clindamycin cream 2% One full applicator intravaginally (5 g) QHS for 7 d Metronidazole gel 0.75% One full applicator intravaginally (5 g) QHS for 5 d Alternative Regimens Clindamycin 300 milligrams PO BID for 7 d Clindamycin ovules 100 milligrams intravaginally QHS for 3 d Tinidazole 2 grams PO daily for 2 d Tinidazole 1 gram PO daily for 5 d Abbreviations: BID = twice a day; QHS = every night at bedtime.  TREATMENT Treatment is recommended for all symptomatic women and can be considered in asymptomatic women. Beyond symptom control, the benefit of treatment includes reducing the risk of acquiring C. trachomatis, N. gonorrhoeae, T. vaginalis, HIV , and HSV-2.

reviations: BID = twice a day; QHS = every night at bedtime.  TREATMENT Treatment is recommended for all symptomatic women and can be considered in asymptomatic women. Beyond symptom control, the benefit of treatment includes reducing the risk of acquiring C. trachomatis, N. gonorrhoeae, T. vaginalis, HIV , and HSV-2. Recommended treatment regimens are listed in Table 102-4. Counsel patients receiving nitroimidazoles against consuming alcoholic bever ages during the treatment period and for 24 hours (for metronidazole) and 72 hours (for tinidazole) after the last dose to avoid a disulfiramlike reaction. Advise all patients to refrain from intercourse or to use condoms during treatment. Clindamycin cream and ovules may weaken diaphragms and condoms. Advise patients to use alternative contraceptives or abstain during and for 5 days after treatment. Symptomatic pregnant women should be treated with the same medications as nonpregnant women ( Table 102-4). Asymptomatic low-risk pregnant women should not be screened for BV . Although BV is correlated with poor pregnancy outcomes, studies have not demon strated that treatment prevents adverse outcomes. 14,21-23 Overall cure rates 4 weeks after treatment do not differ significantly between a 7-day regimen of oral metronidazole, metronidazole vaginal gel, or clindamycin vaginal cream. Metronidazole vaginal gel has fewer side effects (e.g., GI disturbance and unpleasant taste), but should not be used in women who are allergic to the oral preparation. Recurrence is common, and some pathogens are developing resis tance to standard therapies. Consider suppressive therapy in women with multiple recurrences. The use of Lactobacillus intravaginal suppositories and probiotics to restore the normal vaginal flora is an alternative, especially for recurrent BV . Treatment of male sexual partners has not been shown to prevent recurrence. CANDIDA VAGINITIS Candida species are the second most common cause of infectious vaginitis.24 Candida is isolated in up to 20% of asymptomatic, healthy women of childbearing age, some of whom are celibate. Incidence decreases after menopause unless using estrogen replacement, which further emphasizes the hormonal dependence of the infection. Women can remain entirely asymptomatic despite being heavily colonized with Candida species. C. albicans strains account for 85% to 92% of Candida organisms isolated from the vagina. Candida glabrata and Candida tropicalis are the most common non-albicans strains and are often more resistant to conventional therapy. Candidal vaginitis can be classified as an uncomplicated or compli cated infection. Uncomplicated infections are sporadic with mild to moderate symptoms, are due to C. albicans, and occur in the nonpreg nant, immunocompetent host. Complicated infections are recurrent (four or more infections per year), produce severe symptoms or find ings, result from suspected or proven non- albicans Candida species, or occur in an abnormal host (e.g., women who have uncontrolled diabetes, debilitation, or immunosuppression, or are pregnant). 14,25 Candidal organisms gain access to the vaginal lumen predominantly from the adjacent perianal area. The growth of Candida is limited by Tintinalli_Sec11_p0607-0668.indd 649 8/2/19 4:21 PM

or occur in an abnormal host (e.g., women who have uncontrolled diabetes, debilitation, or immunosuppression, or are pregnant). 14,25 Candidal organisms gain access to the vaginal lumen predominantly from the adjacent perianal area. The growth of Candida is limited by Tintinalli_Sec11_p0607-0668.indd 649 8/2/19 4:21 PM 650 SECTION 11: Obstetrics and Gynecology FIGURE 102-2. Hyphae of Candida albicans, potassium hydroxide wet mount. [Repro duced with permission from Knoop et al:  The Atlas of Emergency Medicine, 3rd ed. © 2010 McGraw-Hill, Inc. Fig. 25–16. Photo contributor: H. Hunter Handsfield: Atlas of Sexually Transmitted Diseases. New York, NY: McGraw-Hill, Inc., 1992.] TABLE 102-5 Treatment Regimens for Uncomplicated Vulvovaginal Candidiasis* Agent Formulation Dosage Butoconazole† 2% cream 1 applicator intravaginally QHS × 3 d Clotrimazole 1% cream 2% cream 1 applicator intravaginally QHS × 7 d 1 applicator intravaginally QHS × 3 d Miconazole 2% cream 4% cream 1 applicator intravaginally QHS × 7 d 1 applicator intravaginally QHS × 3 d Nystatin 100,000-unit vaginal tablet 1 vaginal tablet QHS × 14 d Terconazole 0.4% cream 0.8% cream 80-milligram suppository 1 applicator intravaginally QHS × 7 d 1 applicator intravaginally QHS × 3 d 1 suppository intravaginally QHS × 3 d Tioconazole 6.5% ointment 1 applicator intravaginally QHS × 1 dose Fluconazole† 150-milligram oral tablet 1 tablet PO × 1 dose Abbreviation: QHS = every night at bedtime. *Not all possible regimens listed. †Not recommended in pregnancy. the normal vaginal flora, and symptoms of vaginitis usually occur only when the normal balance is upset. Increased Candida colonization resulting in subsequent symptomatic infection may be caused by conditions that (1) inhibit the growth of normal vaginal flora, particularly Lactobacillus species (e.g., systemic antibiotics); (2) diminish the glyco gen stores in vaginal epithelial cells (e.g., diabetes mellitus, pregnancy, oral contraceptive use, hormonal replacement therapy); or (3) increase the pH of vaginal secretions (e.g., menstrual blood or semen). Vaginal candidiasis is not considered a sexually transmitted infection, although it may be transmitted by sexual intercourse. The wearing of tight-fitting, synthetic undergarments may also contribute because of increased temperature. Although all of these factors are thought to be associated with symptomatic disease, no causation has been proven.  DIAGNOSIS Clinical symptoms include discharge, vaginal pruritus, external dysuria, and dyspareunia. Vaginal pruritus is the most common and specific symptom. The discharge varies from none to watery to homogeneously thick and “cottage cheese–like. ” Symptoms vary in severity. An exacerbation frequently presents in the week prior to menses or following coitus, perhaps because each causes the pH to become more alkaline. Odor is unusual and, if present, favors a diagnosis of BV rather than vulvovaginal candidiasis. Pelvic examination often reveals vulvar erythema and edema, vaginal erythema, and a whitish discharge that adheres to the vaginal walls. The diagnosis is confirmed with a normal vaginal pH (4.0 to 4.5) and visualization of budding yeast and pseudohyphae on slide preparation of vaginal secretions (Figure 102-2). The sensitivity of microscopic examination using a sample prepared with normal saline is only 40% to 60%. Adding two drops of 10% KOH to the vaginal secretions dissolves the epithelial cells while leaving yeast buds and pseudohyphae intact and increases the sensitivity to 80% and specificity to nearly 100%.  TREATMENT Recommended treatment regimens are listed in Table 102-5. Topi cally applied azole drugs are more effective than nystatin, with relief of symptoms in 80% to 90% of patients who complete treatment.

leaving yeast buds and pseudohyphae intact and increases the sensitivity to 80% and specificity to nearly 100%.  TREATMENT Recommended treatment regimens are listed in Table 102-5. Topi cally applied azole drugs are more effective than nystatin, with relief of symptoms in 80% to 90% of patients who complete treatment. Consider patient preference because creams, lotions, sprays, vaginal tablets, sup positories, and coated tampons are all equally efficacious.26 Pregnant women should be treated with topical azoles for 7 days. Oral fluconazole is a category C medication and thus should be avoided in pregnancy. The azole drugs are all available over the counter in treatment regi mens of 1, 3, or 7 days. Uncomplicated disease responds to all azoles, including single-dose therapy. 27 Other than initial burning and irrita tion, side effects of topical agents are unusual. Single-dose treatment with oral fluconazole is as effective as topical therapy in the treat ment of uncomplicated disease. Patient preference should be consid ered, because oral therapy is often more convenient. Oral treatment occasionally causes GI symptoms, headache, and rash. 28 Oral azoles interact with a variety of other medications. Sexual partners should not be treated unless they are also symptomatic. Self-medication is occasionally advised in women with recurrence of previously diagnosed disease, although accuracy of self-diagnosis is poor. 4,29 Women who fail to respond to over-the-counter therapy or have recurrence within 2 months should be evaluated by a physician. Complicated Vulvovaginal Candidiasis Vaginal and microscopic examinations should be performed if symptoms persist or recur within 2 months, and precipitating factors, such as high blood glucose levels, should be controlled. However, most women with recurrences do not have obvious precipitating causes. Vaginal cultures should be obtained to confirm a clinical diagnosis and identify any unusual species, such as C. glabrata, as azoles are ineffective in treating vaginitis caused by C. glabrata. The treatment of severe or recurrent vulvovaginal candidiasis requires a longer duration of therapy. Consider treating with a topical azole for 7 to 14 days. More resistant cases may require fluconazole, 150 milligrams orally on days 1, 4, and 7 for a total of three doses. 14,28,29 Very severe cases may require long-term suppression and gynecologic referral. TRICHOMONAS VAGINITIS Trichomoniasis, a parasitic infection with the single-celled protozoan T. vaginalis, a flagellated organism, is a sexually transmitted infection. Both men and women can be infected. Infection can produce local inflammation when the organism attaches to the vaginal mucosa. Clinically symptomatic women present with vaginal discharge, pruritus, and irritation. Classically, the discharge is frothy, greenish in color, and malodorous. On speculum examination, the cervix may be inflamed and small punctate hemorrhages may be seen (“strawberry cervix”). Symptoms generally develop within 5 to 28 days of exposure; however, untreated infections can last for months to years and produce symptoms at any time. 30 Many infections are asymptomatic. Tintinalli_Sec11_p0607-0668.indd 650 8/2/19 4:21 PM

be inflamed and small punctate hemorrhages may be seen (“strawberry cervix”). Symptoms generally develop within 5 to 28 days of exposure; however, untreated infections can last for months to years and produce symptoms at any time. 30 Many infections are asymptomatic. Tintinalli_Sec11_p0607-0668.indd 650 8/2/19 4:21 PM CHAPTER 102: Vulvovaginitis 651  DIAGNOSIS Clinical diagnosis of Trichomonas vaginitis traditionally relies on microscopic examination of the vaginal secretions and visualization of motile trichomonads (Figure 102-3). Culture of vaginal secretions is 95% sensitive and has long been considered the gold standard in diagnosis. However, results may not be available for 2 to 5 days. Several newer testing options, such as nucleic acid amplification tests, have been approved by the Food and Drug Administration for the detection of T. vaginalis in endocervical, vaginal, and urine specimens. These newer tests provide rapid results and are highly sensitive and specific. 14,31,32  TREATMENT Treatment regimens for acute Trichomonas vaginitis are listed in Table 102-6. The nitroimidazoles, metronidazole, and tinidazole are the only medications effective in treating trichomoniasis. Metronidazole gel is not recommended. Single-dose treatment is preferable because of lower cost, fewer side effects, and greater patient adherence to the regi men. Sexual partners should be treated simultaneously. Counsel patients to abstain from sexual intercourse until (1) therapy has been completed; (2) both the patient and partner(s) have been treated; and (3) all are asymptomatic. Patients receiving nitroimidazoles should be advised to avoid consuming alcoholic beverages during the treatment period and for 24 hours (metronidazole) and 72 hours (tinidazole) after the last dose to avoid a disulfiram-like reaction.  TRICHOMONIASIS COMPLICATIONS The spread of T. vaginalis infection is common because many of those infected are asymptomatic. Reinfection is common and can be difficult to differentiate from treatment failure. If treatment failure is suspected, consider treating those who have failed the single-dose 2-gram metro nidazole regimen with a 7-day course because resistance is quantitative, not qualitative. The Centers for Disease Control and Prevention has a hotline to provide assistance for suspected cases of nitroimidazole resistance (telephone 414-718-4141). T. vaginalis infection is associated with several adverse health outcomes, including preterm birth, delivery of low-birth-weight infants, pelvic inflammatory disease, and increased transmission of several other FIGURE 102-3. Trichomonad. [Reprinted with permission of Piotr Rotkiewicz.] TABLE 102-6 Treatment Regimens for Trichomoniasis Agent Dosage Recommended regimens Metronidazole 2 grams PO in a single dose Tinidazole 2 grams PO in a single dose Alternative regimen for treatment failures Metronidazole 500 milligrams PO twice a day for 7 d infections, including HIV , HSV-2, and human papillomavirus infection. Not only does Trichomonas infection increase the likelihood of HIV acquisition, but it also promotes transmission and viral shedding. 33,34  SPECIAL POPULATIONS HIV-positive individuals are more likely to become infected with T. vaginalis and have higher complication rates. HIV-positive patients should be treated with the 7-day metronidazole regimen. Due to the potential adverse pregnancy outcomes, pregnant women should receive treatment with oral metronidazole . Women can be safely treated with single-dose metronidazole therapy at any stage of pregnancy. Breastfeeding mothers should consider withholding nursing during treatment with metronidazole and for 12 to 24 hours after the last dose. Tinidazole safety in pregnancy is not well studied and should be avoided.

etronidazole . Women can be safely treated with single-dose metronidazole therapy at any stage of pregnancy. Breastfeeding mothers should consider withholding nursing during treatment with metronidazole and for 12 to 24 hours after the last dose. Tinidazole safety in pregnancy is not well studied and should be avoided. If treated with tinidazole, patients should withhold breastfeeding for 3 days after the last dose. HERPES SIMPLEX VIRUS INFECTION Genital herpes is a lifelong viral infection caused by HSV-1 or HSV-2. HSV-2 more commonly causes genital lesions and is associated with higher recurrence rates. The majority of infected individuals are asymptomatic and unknowingly expose their sexual partners. Prevalence increases with age, and women are more commonly infected. 35 Genital herpes may present as either a primary or recurrent infection. Classically, the lesions are found on the perineum, labia, urethral meatus, and introitus and are characterized by groups of painful, erythematous vesicles that quickly ulcerate (Figure 102-4). Primary infections are more severe and often associated with systemic symptoms (e.g., headache, fever, malaise, reginal lymphadenopathy, myalgias). Dysuria is common, and HSV can mimic symptoms of a urinary tract infection. Recurrent HSV infections result from reactivation of the dormant virus from the dorsal root gan glion following a stressor (e.g., acute illness, immunosuppression, psy chological stress). Recurrent infections tend to be less severe but are often preceded by a prodromal period of itching, burning, or tingling before the lesions appear. Over time, recurrences tend to become less frequent. HSV-2–seropositive individuals are at increased risk of acquiring HIV infection. Extragenital complications include meningoencepha litis, pneumonitis, hepatitis, and disseminated disease. Neonatal HSV infection can result from spread of the infection from an HSV-positive pregnant mother to her child during delivery and is associated with significant morbidity and mortality.  DIAGNOSIS AND TREATMENT When active lesions are present, polymerase chain reaction swabs are both sensitive and specific; viral culture is less sensitive. Type-specific serologic testing is available as both laboratory and point-of-care tests. A positive HSV-2 test implies an anogenital infection, whereas a posi tive HSV-1 test is difficult to interpret. Routine screening in the general population is not recommended. Although oral antiviral therapy does not eradicate the virus, it can help provide symptom relief and shorten the outbreak. Topical anti virals are not effective. Patients should be counseled regarding the possibility of future outbreaks, safe sex practices to reduce the risk of sexual transmission, and consequences of perinatal transmission. Treatment regimens for primary HSV infections, recurrent HSV infections, and daily suppressive therapy are shown in Table 102-7. If the patient remains symptomatic after 10 days of therapy, then treatment should be extended. Daily suppressive therapy may reduce viral shedding and decrease, but not eliminate, the likelihood of transmission to sexual partners. Patients with severe disease or complications may require admission and treatment with intravenous acyclovir. Sexual partners should be advised to seek evaluation, and if asymp tomatic, they may benefit from type-specific testing. If a sexual partner’s HSV status is unknown or discordant, sexual contact should be avoided during outbreaks with strict condom use between outbreaks. Immunocompromised patients, such as those with HIV infection, may have more severe symptoms or prolonged outbreaks. Additionally, HSV shedding is increased in HIV-positive patients. Patients with HIV Tintinalli_Sec11_p0607-0668.indd 651 8/2/19 4:21 PM

e avoided during outbreaks with strict condom use between outbreaks. Immunocompromised patients, such as those with HIV infection, may have more severe symptoms or prolonged outbreaks. Additionally, HSV shedding is increased in HIV-positive patients. Patients with HIV Tintinalli_Sec11_p0607-0668.indd 651 8/2/19 4:21 PM 652 SECTION 11: Obstetrics and Gynecology FIGURE 102-4. Herpes lesions. [Used with permission from Dr. William Griffith.] TABLE 102-7 Treatment Regimens for Genital HSV Infections Antiviral Agent Choices Dose Primary Outbreak Acyclovir 400 milligrams PO three times a day × 7–10 d 200 milligrams PO five times daily × 7–10 d Valacyclovir 1 gram PO two times daily × 7–10 d Famciclovir 250 milligrams PO three times daily × 7–10 d Episodic Therapy for Recurrent Outbreaks Antiviral Agent Choices Dose Acyclovir 400 milligrams PO three times a day × 5 d 800 milligrams PO three times a day × 2 d Valacyclovir 500 milligrams PO two times a day × 3 d 1 gram PO once a day for 5 days Famciclovir 1 gram PO two times a day × 1 d Suppressive Therapy for Recurrent Outbreaks Antiviral Agent Choices Dose Acyclovir 400 milligrams PO twice a day Valacyclovir 500 milligrams PO once a day (may be as effective as 1000) Famciclovir 250 milligrams PO twice a day Abbreviations: BID = twice a day; QD = once a day; TID = three times a day. often require higher doses and longer durations of therapy in order to achieve symptomatic relief. CONTACT VULVOVAGINITIS Contact dermatitis results from the exposure of the vulvar epithelium and vaginal mucosa to a primary chemical irritant or allergen. Irritant dermatitis is more common than allergic dermatitis. 36 Common irritants or allergens include chemically scented douches, soaps, bubble baths, and deodorants; perfumes, dyes, and scents in toilet paper, tampons, pads, and feminine hygiene products; topical vaginal antibiotics; laundry detergents, dryer sheets, and fabric softeners; and tight slacks, pantyhose, and synthetic underwear. Benzocaine, used by women to control vulvar discomfort, can also cause a particularly severe contact dermatitis. Diagnosis may be difficult due to variation in symptom severity and preexisting conditions. Clinically, patients report localized swell ing, itching, or a burning sensation. Physical findings range from local erythema and edema to excoriation, ulceration, and secondary infec tion. Local vesiculation and ulceration are more common with primary irritants used in strong concentrations, but herpes infection must also be considered. Vaginal pH changes may promote colonization and infection with C. albicans that can obscure the primary cause. Diagnosis of contact vulvovaginitis is made by ruling out an infectious cause and identifying the offending agent. Most cases of mild vul vovaginal contact dermatitis resolve spontaneously when the causative agent is withdrawn. Cool sitz baths and application of wet compresses of dilute boric acid or Burow’s solution may afford relief for patients with severe painful reactions. A few days of therapy with topical corticosteroids, such as hydrocortisone acetate (0.5% to 2.5%), fluocinolone acetonide (0.01% to 0.2%), or triamcinolone acetonide (0.025%), applied two or three times daily, provide symptomatic relief and promote heal ing. If a true allergic reaction is present, then oral antihistamines may be helpful. Superinfection with C. albicans should be treated as previously described in the section on Candida vaginitis. ATROPHIC VAGINITIS Vaginal atrophy, present in 60% of women 4 years after menopause, can result in atrophic vaginitis. 37 Decreased ovarian steroid production in menopausal women leads to profound changes in the vulva, vagina, cervix, urethra, and bladder.

ed as previously described in the section on Candida vaginitis. ATROPHIC VAGINITIS Vaginal atrophy, present in 60% of women 4 years after menopause, can result in atrophic vaginitis. 37 Decreased ovarian steroid production in menopausal women leads to profound changes in the vulva, vagina, cervix, urethra, and bladder. The vagina loses its normal rugae with the mucosa becoming attenuated, pale, and almost transparent as a result of decreased vascularity. The cellular glycogen content decreases, resulting in atrophy of the epithelium and loss of elasticity. The vaginal pH ranges from 5.5 to 7.0. The upper one third of the vagina constricts, shortening the length of the vagina. The mucosa is only three or four cells thick and is less resistant to minor trauma and infection. The cervix atrophies and retracts and may become flush with the apex of the vault. Symptoms include vaginal dryness, soreness, itching, dyspareunia, and occasional spotting or discharge. Discharge is thin, scant, and yellowish or pink. The vaginal epithelium appears thin, inflamed, and even ulcerated. A clinical vaginal infection with copious purulent discharge may develop due to increased vaginal pH, which permits growth of non acidophilic coliform organisms and the disappearance of Lactobacillus species. Candida and Trichomonas infections are rare in the postmeno pausal woman unless estrogenic replacement therapy is used. Wet preparations demonstrate erythrocytes, increased polymor phonuclear neutrophils, and small, round epithelial cells, which are Tintinalli_Sec11_p0607-0668.indd 652 8/2/19 4:21 PM

obacillus species. Candida and Trichomonas infections are rare in the postmeno pausal woman unless estrogenic replacement therapy is used. Wet preparations demonstrate erythrocytes, increased polymor phonuclear neutrophils, and small, round epithelial cells, which are Tintinalli_Sec11_p0607-0668.indd 652 8/2/19 4:21 PM CHAPTER 102: Vulvovaginitis 653 immature squamous cells that have not been exposed to sufficient estrogen. Treatment of atrophic vaginitis consists primarily of topical vaginal estrogen. Creams, pessaries, tablets, and the estradiol vaginal ring are all effective in treating the symptoms. 37 Side effects of treatment may include uterine bleeding, breast pain, perineal pain, and endometrial hyperstimulation. Estrogen should not be prescribed to patients with a history of cancer of any of the reproductive organs. Atrophic vaginitis is uncommon in patients taking systemic estrogen replacement therapy. Women should be referred to their primary care provider for treat ment and follow-up to monitor therapy, because all formulations of estrogen, even at low dosages, show systemic absorption and have potentially harmful side effects. 38 In addition, any patient with post menopausal bleeding, either by history or physical examination, should be referred to a gynecologist to rule out carcinoma. BARTHOLIN GLAND CYST AND ABSCESS Bartholin glands are located in the labia minora. The ducts of the glands drain into the posterior vestibule at the 4 o’ clock and 8 o’ clock positions. Normally the glands are pea sized. The glands begin to function at puberty to provide moisture to the vestibule and involute as women age. Obstruction of the duct may result in a cyst or abscess. A cyst does not need to be present before an abscess can develop. Abscesses may become quite large and cause extreme pain. E. coli is the most common bacterial isolate, but many abscesses are polymicrobial. 39 Less common organisms include N. gonorrhoeae and C. trachomatis.  DIAGNOSIS AND TREATMENT Bartholin gland abscess is characterized as a mass in the posterior introitus near the 4 o’ clock or 8 o’ clock positions that has developed over several days. If preceded by a cyst, the abscess may develop over a lon ger period of time. Pain, induration, and fluctuance are usually present. Systemic symptoms (e.g., fever and chills) are rarely present. Incision and drainage is usually necessary but should not be per formed until the abscess is a well-defined, walled-off structure. An ultrasound of the area can confirm the presence of a discrete fluid col lection. If the abscess is not clearly defined, prescribe broad-spectrum antibiotics and analgesics and advise warm sitz baths and short-term follow-up. Most patients present with an exquisitely tender, hyperemic, fluctuant mass that needs drainage by the emergency physician. Care should be taken to distinguish a Bartholin’s abscess from an abscess of the labia majora, which requires gynecologic consultation. Consider providing parenteral analgesia and even conscious seda tion or low-dose ketamine in order to facilitate incision and drainage. To drain the abscess, first provide analgesia with a local injection of 2 to 4 mL of 1% lidocaine. Make a stab incision with a #11 scalpel on the mucosal surface of the vestibule, just lateral to the hymenal ring in the region of the Bartholin gland, where the abscess cavity is closest to the mucosal surface and has the greatest fluctuance. Extend the stab inci sion only for a few millimeters; an incision that is too large will result in displacement of the Word catheter. A Word catheter ( Figure 102-5) is the size of a #10 Foley catheter with a 1-in. (2.5-cm) stem and an inflat able balloon.

closest to the mucosal surface and has the greatest fluctuance. Extend the stab inci sion only for a few millimeters; an incision that is too large will result in displacement of the Word catheter. A Word catheter ( Figure 102-5) is the size of a #10 Foley catheter with a 1-in. (2.5-cm) stem and an inflat able balloon. Once fully drained, insert a Word catheter into the incision site and inflate the balloon with 2 to 4 mL of water. Tuck the end of the catheter into the vagina. The catheter should remain in place for 4 to 6 weeks to avoid recurrence. 40 Case reports describe using plastic tub ing (Figure 102-6) when a Word catheter is not available. 41 There are many different treatment techniques, none of which have been found to be superior. 42 Prescribe analgesics and broad-spectrum antibiotics and give instructions for follow-up care. If N. gonorrhoeae and C. trachomatis infection are possible, direct antibiotic coverage accordingly (Table 102-2). Patients with recurrent abscess may require definitive surgical care and should be provided with specialty referral. FIGURE 102-5. Word catheter. [Reproduced with permission from Reichman EF: Emergency Medicine Procedures, 2nd ed. New York, NY: McGraw-Hill, Inc., 2013. Figure 138-2, p. 932.] BC D FIGURE 102-6. A. Obtain 7 cm of narrow tubing, and insert silk suture through tubing. B. After drainage, make a second stab incision into the abscess cavity and insert the threaded tubing. C. Use a hemostat to grasp the threaded tubing through both stab sites. D. Suture the threads so they are secure. [Reproduced with permission from Reichman EF: Emergency Medicine Procedures, 2nd ed. New York, NY: McGraw-Hill, Inc., 2013. Figure 138–5, Parts A, E, F, G, p. 934.] Tintinalli_Sec11_p0607-0668.indd 653 8/2/19 4:21 PM