Many women suffer with undiagnosed symptoms of vulvar disease. Patients presenting with chronic vulvar symptoms should be carefully interviewed, examined, and a vulvar biopsy obtained whenever the diagnosis is in question, the patient is not responding to treatment, or premalignant or malignant disease is suspected. Vulvar conditions such as contact dermatitis, atrophic vulvovaginitis, lichen sclerosis, lichen planus, lichen chronicus simplex, Paget’s disease, Bowen’s disease, and invasive vulvar cancer are not uncommon. Systemic diseases like psoriasis, eczema, Crohn’s disease, Behçet’s disease, vitiligo, and seborrheic dermatitis may also involve the vulvar skin.
Vulvar Contact Dermatitis
This dermatitis is a common cause of acute or chronic vulvar pruritus and can be irritant or allergic.4 Irritant dermatitis usually results from overzealous hygiene habits, such as the use of harsh soaps and frequent douching. It is also common in patients with urinary or fecal incontinence, especially the elderly and the disabled. Allergic vulvar dermatitis is caused by a variety of allergens, such as fragrances and topical antibiotics. The mainstay of treatment is to identify and discontinue the offending agent or practice or providing a skin barrier in the case of incontinence.
There are three types of leukoplakia, a flat white abnormality. Lichen sclerosis is the most common cause of leukoplakia.4 It affects women 30 to 40 years of age. Classically, it results in a figure-of-eight pattern of white epithelium around the anus and vulva resulting in variable scaring and itching and, less commonly, pain. Diagnosis is confirmed with biopsy, and treatment consists of topical steroids. Lichen planus is a cause of leukoplakia with an onset in the fifth and sixth decades of life. Lichen planus, in contrast to lichen sclerosis, which is limited to the vulva and perianal skin, can involve the vagina and oral mucosa, and erosions occur in the majority of patients, leading to a variable degree of scaring. Patients usually have a history and dysuria and dyspareunia and complain of a burning vulvar pain. Histology is not specific, and biopsy is recommended. Treatment is with steroid ointments. Systemic steroids are indicated for severe and/or unresponsive cases. Lichen simplex chronicus is the third cause of leukoplakia but is distinguished from the other lichen diseases by epidermal thickening, absence of scaring, and a severe intolerable itch.4 Intense scratching is not uncommon and contributes to the severity of the symptoms and predisposes the cracked skin to infections. Treatment consists of cessation of the scratching, which sometimes requires sedation; elimination of any allergen or irritant; suppression of inflammation with potent steroid ointments; and treatment of any coexisting infections.
Bartholin’s Cyst or Abscess
Bartholin’s glands, great vestibular glands, are located at the vaginal orifice at the four and eight o’clock positions; they are rarely palpable in normal patients. They are lined with cuboidal epithelium and secrete mucoid material to keep the vulva moist. Their ducts are lined with transitional epithelium, and their obstruction secondary to inflammation may lead to the development of a Bartholin’s cyst or abscess. Bartholin’s cysts range in size from 1 to 3 cm and are detected on exam or are recognized by the patient. They occasionally result in discomfort and dyspareunia and require treatment. Cysts and ducts can become infected and form abscesses. Infections are often polymicrobial; however, sexually transmitted N. gonorrhoeae and C. trachomatis are sometimes implicated. Treatment consists of incision and drainage and placement of a Word catheter, a small catheter with a balloon tip, for 2 to 3 weeks to allow for formation and epithelialization of a new duct. Appropriate antibiotic therapy should be instituted. Recurrent cysts or abscesses are usually marsupialized, but on occasion necessitate excision of the whole gland. Marsupialization is done by incising the cyst or abscess wall and securing its lining to the skin edges with interrupted sutures.5 Cysts or abscesses that fail to resolve after drainage and those occurring in patients over age 40 should be biopsied to exclude malignancy.
Molluscum contagiosum presents with dome-shaped papules and is caused by the poxvirus. The papules are usually 2 to 5 mm in diameter and classically have a central umbilication. They are spread by direct skin contact and present on the vulva, as well as abdomen, trunk, arms, and thighs. Lesions typically clear in several months but can be treated with cryotherapy, curettage, or cantharidin, a topical blistering agent.
The frequency of the infectious etiologies of genital ulcers varies by geographic location. The most common causes of sexually transmitted genital ulcers in young adults in the United States are, in descending order of prevalence, herpes simplex virus (HSV), syphilis, and chancroid.6 Others infectious causes of genital ulcers include lymphogranuloma venereum and granuloma inguinale. Noninfectious etiologies include Behçet’s disease, neoplasms, and trauma. Table 41-3 outlines a rational approach to their evaluation and diagnosis.
Table 41-3Clinical features of genital ulcers syndromes ||Download (.pdf) Table 41-3 Clinical features of genital ulcers syndromes
| ||HERPES ||SYPHILIS ||CHANCROID ||LYMPHOGRANULOMA VENEREUM ||GRANULOMA INGUINALE (DONOVANOSIS) |
|Pathogen ||Herpes simplex virus (HSV) type II and less commonly HSV type I ||Treponema palladium ||Haemophilus ducreyi ||Chlamydia trachomatis L1-L3 ||Calymmatobacterium granulomatis |
|Incubation period ||2–7 days ||2–4 weeks (1–12 weeks) ||1–14 days ||3 days–6 weeks ||1–4 weeks (up to 6 months) |
|Primary lesion ||Vesicle ||Papule ||Papule or pustule ||Papule, pustule, or vesicle ||Papule |
|Number of lesions ||Multiple, may coalesce ||Usually one ||Usually multiple, may coalesce ||Usually one ||Variable |
|Diameter (mm) ||1–2 ||5–15 ||2–20 ||2–10 ||Variable |
|Edges ||Erythematous ||Sharply demarcated, elevated, round, or oval ||Undermined, ragged, irregular ||Elevated, round, or oval ||Elevated, irregular |
|Depth ||Superficial ||Superficial or deep ||Excavated ||Superficial or deep ||Elevated |
|Base ||Serous, erythematous ||Smooth, nonpurulent ||Purulent ||Variable ||Red and rough (“beefy”) |
|Induration ||None ||Firm ||Soft ||Occasionally firm ||Firm |
|Pain ||Common ||Unusual ||Usually very tender ||Variable ||Uncommon |
|Lymphadenopathy ||Firm, tender, often bilateral ||Firm, nontender, bilateral ||Tender, may suppurate, usually unilateral ||Tender, may suppurate, loculated, usually unilateral ||Pseudo-adenopathy |
|Treatment ||Acyclovir (ACV) 400 mg PO tid for 7–10 days for primary infection and 400 mg PO tid for 5 days for episodic management || |
Primary, secondary, and early latent (<1 year): penicillin G (PCN-G) benzathine 2.4 million U IM × 1
Late latent (>1 year) and latent of unknown duration: PCN-G benzathine 2.4 million U IM every week × 3
Azithromycin 1 g PO or ceftriaxone 250 mg IM × 1 or ciprofloxacin 500 mg PO bid for 3 days
Erythromycin base 500 mg PO tid for 7 days
|Doxycycline 100 mg PO bid for 21 days or erythromycin base 500 mg PO qid for 21 days ||Doxycycline 100 mg PO bid for 3 weeks until all lesions have healed |
|Suppression ||ACV 400 mg PO bid for those with frequent outbreaks || || || || |
Condylomata acuminata (anogenital warts) are viral infections caused by HPV.7 Genital infection with HPV is the most common sexually transmitted infection in the United States today. HPV types 6 and 11 are the most common low-risk types and are implicated in 90% of cases of genital warts.8 High-risk types can be found in association with invasive cancers. Genital warts are skin-colored or pink and range from smooth flattened papules to verrucous papilliform lesions. Lesions may be single or multiple and extensive. Diagnosis should be confirmed with biopsy because verrucous vulvar cancers can be mistaken for condylomata.9 Treatment modalities range from patient-applied ointments to physician-applied agents and office procedures. If small, self-administered topical imiquimod 5% cream or trichloroacetic acid for in-office applications may be tried. Extensive lesions may require surgical modalities that include cryotherapy, laser ablation, cauterization, and surgical excision.
Paget’s Disease of the Vulva
Paget’s disease of the vulva is an intraepithelial disease of unknown etiology that affects mostly white postmenopausal women in their sixth decade of life. It causes chronic vulvar itching and is sometimes associated with an underlying invasive vulvar adenocarcinoma or invasive cancers of the breast, cervix, or gastrointestinal tract. Grossly, the lesion is variable but usually confluent, raised, erythematous to violet, and waxy in appearance. Biopsy is required for diagnosis; the disease is intraepithelial and characterized by Paget’s cells with large pale cytoplasm. Treatment is assessment for other potential concurrent adenocarcinomas, and then surgical removal by wide local resection of the involved area with a 2-cm margin. Free margins are difficult to obtain because the disease usually extends beyond the clinically visible area.10,11 Intraoperative frozen section of the margins can be done; however, Paget’s vulvar lesions have a high likelihood of recurrence even after securing negative resection margins.
Vulvar Intraepithelial Neoplasia (VIN)
VIN is similar to its cervical intraepithelial neoplasia (CIN) counterpart and is graded on the degree of epithelial involvement as mild (VIN I), moderate (VIN II), severe (VIN III), or vulvar carcinoma in situ (Bowen’s disease).12 Risk factors include HPV infection, prior VIN, HIV infection, immunosuppression, smoking, vulvar dermatoses such as lichen sclerosis, CIN, and cervical cancer. VIN can be unifocal or multifocal. Unifocal lesions commonly affect postmenopausal women and lack a clear association with HPV, while multifocal disease mostly affects younger reproductive-age females and has a strong association with HPV infection. Fifty percent of patients are asymptomatic, with vulvar pruritus being the most common complaint in those with symptoms. Lesions may be vague or raised and velvety with sharply demarcated borders. Diagnosis is made with a vulvar skin biopsy, and multiple biopsies are sometimes necessary. Colposcopy with application of 5% acetic acid and identification of the acetowhite lesions of VIN is a valuable diagnostic tool for subtle lesions and will help guide the biopsy. Evaluation of the perianal and anal area is important as the disease may involve these areas, particularly in immunocompromised and/or nicotine-addicted women. Once invasive disease is ruled out, treatment usually involves wide surgical excision; however, the initial treatment approach may include 5% imiquimod cream, CO2 laser ablation, or cavitational ultrasonic surgical aspiration, and depends on the number of lesions and their severity. When laser ablation is used, a 1-mm depth in hair-free areas is usually sufficient, whereas hairy lesions require ablation to a 3-mm depth because the hair follicles’ roots can reach a depth of 2.5 mm. Unfortunately, VIN tends to recur in up to 30% of cases, and high-grade lesions (VIN III, carcinoma in situ) progress to invasive disease in approximately 10% of patients if left untreated.13
Vulvovaginal symptoms are extremely common, accounting for over 10 million office visits per year in the United States. The causes of vaginal complaints are commonly infectious in origin, but they include a number of noninfectious causes, such as chemicals or irritants, hormone deficiency, foreign bodies, systemic diseases, and malignancy. Symptoms are commonly nonspecific and include abnormal vaginal discharge, pruritus, irritation, burning, odor, dyspareunia, bleeding, and ulcers. A purulent discharge from the cervix should always raise suspicion of these infections even in the absence of pelvic pain or other signs.
Normal vaginal discharge is white or transparent, thick, and mostly odorless. It increases during pregnancy, with use of estrogen-progestin contraceptives, or at mid-cycle around the time of ovulation. Complaints of foul odor and abnormal vaginal discharge should be investigated. Candidiasis, bacterial vaginosis, and trichomoniasis account for 90% of vaginitis cases. The initial workup includes pelvic examination, vaginal pH testing, microscopy, vaginal cultures if microscopy is normal, and gonorrhea/chlamydia NAAT (see earlier section, Common Screening and Testing).14 The pH of normal vaginal secretions is 3.8 to 4.4, which is hostile to growth of pathogens. A pH greater than or equal to 4.9 is indicative of a bacterial or protozoal infection. Treatment of vaginal infection before anticipated surgery is appropriate, particularly for bacterial vaginosis, which may be associated with a higher risk for vaginal cuff infections (Fig. 41-8).
Treatment algorithm for vulvovaginitis.
BV accounts for 50% of vaginal infections. It results from reduction in concentration of the normally dominant lactobacilli and increase in concentration of anaerobic organisms like Gardnerella vaginalis, Mycoplasma hominis, Bacteroides species, and others.15 Diagnosis is made by microscopic demonstration of clue cells. The discharge typically produces a fishy odor upon addition of KOH (amine or Whiff test). Initial treatment is usually a 7-day course of metronidazole.
Vulvovaginal Candidiasis (VVC)
VVC is the most common cause of vulvar pruritus. It is generally caused by Candida albicans and occasionally by other Candida species. It is common in pregnant women, diabetics, patients taking antibiotics, and immunocompromised hosts. Initial treatment is usually with topical antifungals, although single-dose oral antifungal treatments are also common.
Trichomoniasis is a sexually transmitted infection of a flagellated protozoan and can present with malodorous, purulent discharge. It is typically diagnosed with visualization of the trichomonads during saline wet mount microscopy. Initial treatment is usually a 7-day course of metronidazole.
A Gartner’s duct cyst is a remnant of the Wolffian tract; it is typically found on the lateral vaginal walls. Patients can be asymptomatic or present with complaints of dyspareunia or difficulty inserting a tampon. If symptomatic, these cysts may be surgically excised or marsupialized. If surgery is planned, a preoperative magnetic resonance imaging (MRI) scan should be obtained to determine the extent of the cyst.
The etiology and treatment of vaginal condyloma is similar to vulvar condyloma (see earlier section, Vulvar Condyloma).
Vaginal Intraepithelial Neoplasia
Vaginal intraepithelial neoplasia, or VaIN, is similar to VIN and is classified based on the degree of epithelial involvement as mild (I), moderate (II), severe (III), or carcinoma in situ.12 Sixty-five percent to 80% of VaIN or vaginal cancers are associated with HPV infection. The majority of lesions are located in the upper one third of the vagina. Lesions are usually asymptomatic and found incidentally on cytologic screening. Diagnosis is made via guided biopsy of acetowhite lesions at the time of colposcopy. Lesions may appear flat or raised and white with sharply demarcated borders and may show vascular changes. The presence of aberrant vessels with marked branching is suggestive of invasive disease. VaIN is treated with laser ablation, surgical excision, or topical 5-fluorouracil therapy.
Benign lesions of the cervix include endocervical polyps, Nabothian cysts (clear, fluid-filled cysts with smooth surfaces), trauma (such as delivery-related cervical tear or prior cervical surgery), malformation of the cervix, and cervical condyloma. For endocervical polyps, exploration of the base of the polyp with a cotton swab tip to identify that it is cervical and not uterine and to identify the stalk characteristics can help identify the appropriate surgical approach. Small polyps with identifiable base can be removed by grasping the polyp with ring forceps and slowly rotating it until separated from its base. Use of loop electro-excisional procedure (LEEP) is appropriate for larger lesions. Laser or other ablative procedures are appropriate for condyloma proven by biopsy.
Cervical Intraepithelial Neoplasia (CIN)
High-grade cervical dysplasia (CIN II or III) has a high chance of persistent HPV infection with risk of transformation to malignancy; thus an excisional procedure is usually indicated. This serves a therapeutic purpose by removal of dysplastic cells and a diagnostic purpose for histologic review to rule out concomitant early-stage cervical cancer. Either a LEEP or cold knife conization (CKC) may be used for surgical excision of the squamocolumnar junction (SCJ) and outer endocervical canal. Risks of both procedures include bleeding, postprocedure infection, cervical stenosis, and risk of preterm delivery with subsequent pregnancies. A looped wire attachment for a standard monopolar electrosurgical unit is used to perform a LEEP excision. Loops range in a variety of shapes and sizes to accommodate different sizes of cervix. Optimally, one pass of the loop should excise the entire SCJ. Hemostasis of the remaining cervix is achieved with the ball electrode and ferrous sulfate paste (Monsel’s solution).
Different from a LEEP, a cervical CKC does not use energy to excise the specimen. The advantage of this procedure is that the margin status is not obscured by cauterized artifact. This is important in cases of adenocarcinoma in situ and microinvasive squamous cell carcinoma, where margin status dictates the type of and indication for future therapy. During a CKC, a #11 blade is used to circumferentially excise the conical biopsy. Hemostasis is achieved with the ball electrode, Monsel’s solution, or suture.
Two HPV vaccines have been developed and approved by the U.S. Food and Drug Administration (FDA).16 Gardasil is a quadrivalent vaccine that targets HPV genotypes 16 and 18, which cause approximately 70% of cervical cancers and about 50% of precancerous lesions (CIN II/III) worldwide, and HPV genotypes 6 and 11, which cause 90% of genital warts. Cervarix is a bivalent vaccine that targets HPV genotypes 16 and 18. In contrast to natural infection, the vaccine is highly immunogenic, activating both humoral and cellular immune responses. Vaccination generates high concentrations of neutralizing antibodies to HPV L1 protein, the antigen in both vaccines. It is thought that vaccination may provide protection against HPV infection through neutralization of virus by serum immunoglobulin that diffuses from capillaries to the genital mucosal epithelium.17
Several randomized clinical trials18,19,20 involving approximately 35,000 young women have shown that both Gardasil and Cervarix prevent nearly 100% of the HPV subtype-specific precancerous cervical cell changes for up to 4 years after vaccination among women who were not infected at the time of vaccination; vaccination occurred before sexual debut. These major clinical trials have used prevention of CIN II/III and carcinoma in situ as the efficacy endpoints. Vaccination has not yet been shown to protect women who are already infected with HPV-16 or HPV-18 at the time of vaccination.
Current FDA approval applies to use in women who are between 9 and 26 years of age for the prevention of the following: cervical, vulvar, and vaginal cancer caused by HPV-16 or -18, genital warts caused by HPV-6 or -11, and lesions caused by HPV-6, -11, -16, or -18 (CIN I, II, and III; cervical carcinoma in situ; VIN; or VaIN II/III). The Advisory Committee on Immunization Practices (ACIP) recommends routine vaccination for females 11 to 12 years of age, maybe starting at age 9; catch-up vaccination is recommended for females 13 to 26 years of age who did not get all three doses when they were younger. Studies to evaluate the efficacy of the vaccine in healthy women 26 years of age and older with no prior exposure to HPV is ongoing, and additional information on the length of protection is forthcoming. In 2009, the FDA approved the quadrivalent vaccine for use to prevent genital warts in men and boys, and in 2011, the ACIP recommended that all males 11 to 12 years of age be vaccinated, stating that this may reduce some of the HPV-related burden suffered by women.
Immunocompromised women may receive the quadrivalent vaccine. Although the safety and immunogenicity of HPV vaccination in this population are not well established, the vaccine could be beneficial in these women since they are at increased risk for HPV-related cancers. Vaccination is not recommended for pregnant women, although neither vaccine has been shown to be causally associated with adverse outcomes in pregnant women or their fetuses. If pregnant women are vaccinated inadvertently, completion of the series should be delayed until after the pregnancy.
Cervical cancer screening continues to play an important role in detection and treatment of CIN II/III and prevention of cervical cancer in these high-risk patients. Cervical cancer screening continues to be of great importance since HPV immunization will not prevent approximately 25% to 30% of cervical cancers in HPV-naïve women and does not protect against the development of cancer in women already infected with carcinogenic HPV types.
The average age of menarche, or first menstrual period, in the United States is 12 years and 5 months. Duration of normal menstruation is between 2 and 7 days, with a flow of less than 80 mL, cycling every 21 to 35 days.21 Nonpregnant patients, who present with heavy bleeding and are 35 years of age and older or have risk factors for endometrial cancer, must be ruled out for malignancy as the first step in their management (see earlier section, Endometrial Biopsy).
Abnormal Uterine Bleeding (AUB)
Abnormal uterine bleeding is described based on the bleeding pattern. Menorrhagia is prolonged (>7 days) or excessive (>80 mL daily) menstrual cycles occurring at regular intervals, and metrorrhagia is bleeding between menstrual periods. Menometrorrhagia is the occurrence of both. Intermenstrual bleeding, also known as spotting, is bleeding of variable amounts occurring between regular menstrual cycles. Poly-, oligo-, and amenorrhea are menstrual cycles of less than 21 days, longer than 35 days, or the absence of uterine bleeding for 6 months or a period equivalent to three missed cycles, respectively. Because there are many causes of AUB, they are divided into two categories: structural causes and nonstructural causes.22 Structural causes include polyps, adenomyosis, leiomyomata, and malignancy. Nonstructural causes can include coagulopathy, ovulatory dysfunction, endometrial effects, and iatrogenic causes.
Endometrial polyps are localized hyperplastic growth of endometrial glands and stroma around a vascular core forming sessile or pedunculated projections from the surface of the endometrium.23 Endometrial polyps are rarely neoplastic (<1%) and may be single or multiple. Many are asymptomatic; however, they are responsible for about 25% of cases of abnormal uterine bleeding, usually metrorrhagia. Polyps are common in patients on tamoxifen therapy and in peri- and postmenopausal women. Up to 2.5% of patients with a polyp may harbor foci of endometrial carcinoma.24 Diagnosis can be made with saline-infused hysterosonography, hysterosalpingogram, or direct visualization at the time of hysteroscopy. Definitive treatment, in the absence of malignancy, involves resection with an operative hysteroscope or by sharp curettage.
Adenomyosis refers to ectopic endometrial glands and stroma situated within the myometrium. When diffuse, it results in globular uterine enlargement secondary to hyperplasia and hypertrophy of the surrounding myometrium. Adenomyosis is very common, tends to occur in parous women, and is frequently an incidental finding at the time of surgery. Diagnosis is suspected in a parous woman with menorrhagia, dysmenorrhea, and diffuse globular uterine enlargement. MRI may reveal islands within the myometrium with increased signal intensity.25 Hysterectomy is the only treatment, providing material for definitive pathologic diagnosis.
Leiomyomas, also known colloquially as fibroids, are the most common female pelvic tumor and occur in response to growth of the uterine smooth muscle cells (myometrium). They are common in the reproductive years, and by age 50, at least 60% of white and up to 80% of black women are or have been affected. Leiomyomas are described according to their anatomic location (Fig. 41-9) as intramural, subserosal, submucosal, pedunculated, cervical, and rarely ectopic.21 Most are asymptomatic; however, abnormal uterine bleeding caused by leiomyomas is the most common indication for hysterectomy in the United States. Other manifestations include pain, pregnancy complications, and infertility. Pain generally results from degenerating myomas that outgrew their blood supply or from compression of other pelvic organs such as the bowel, bladder, and ureters. High levels of pregnancy hormones frequently cause significant enlargement of pre-existing myomas, which may lead to significant distortion of the uterine cavity resulting in recurrent miscarriages, fetal malpresentations, intrauterine growth restriction, obstruction of the birth canal and the subsequent need for cesarean delivery, abruption, preterm labor, and pain from degeneration.
Bleeding is usually heavy and irregular (menometrorrhagia) and can be severe at times, requiring hospitalization. Examination reveals an enlarged irregular uterus and, in severe cases, a large solid pelvic mass extending to the upper abdomen. Diagnosis is usually made by transvaginal ultrasonography. Other diagnostic modalities, including MRI, computed tomography (CT), and hysterosalpingogram or saline-infused hysterosalpingography, are especially useful in the cases of submucosal and intrauterine myomas. Most are benign; malignant degeneration occurs in less than 1% of cases and is usually encountered in the menopausal years. Management options of leiomyomas are tailored to the individual patient depending on her age and desire for fertility and the size, location, and symptoms of the myomas. Conservative management options include oral contraceptive pills, medroxyprogesterone acetate, gonadotropin-releasing hormone (GnRH) agonists, uterine artery embolization, and myomectomy.26,27,28 Uterine artery embolization is contraindicated in patients planning future pregnancy and frequently results in acute degeneration of myomas requiring hospitalization for pain control. Myomectomy is indicated in patients with infertility and those who wish to preserve their reproductive capacity. Hysterectomy is the only curative therapy. Treatment with GnRH agonists for 3 months prior to surgery is recommended in anemic patients and may allow them time to normalize their hematocrit, avoiding transfusions; GnRH also decreases blood loss at hysterectomy and shrinks the myomas by an average of 30%. The latter may make the preferred vaginal surgical approach more feasible.
Endometrial hyperplasia is caused by chronic unopposed hyperestrogenic state (relative absence of progesterone) and is characterized by proliferation of endometrial glands resulting in increased gland-to-stroma ratio. It can be asymptomatic or, more commonly, result in abnormal vaginal bleeding. Hyperplasia can be either simple or complex, based on the architecture of the glands. Of greater importance is the presence or absence of nuclear atypia, described by the World Health Organization (WHO) classification.29 Untreated endometrial hyperplasia progresses to malignancy in 1%, 3%, 8%, and 29% of cases of simple, complex, simple with atypia, and complex hyperplasia with atypia, respectively.30 Simple and complex hyperplasias can be treated with progestins, and women should have repeat endometrial sampling in 3 to 6 months. Atypical hyperplasia is considered a premalignant condition and is treated ideally with simple hysterectomy. When a patient has a preoperative diagnosis of complex atypical hyperplasia, the likelihood of a concomitant endometrial cancer at hysterectomy is 38% to 60%.31 If preservation of fertility is desired or surgery contraindicated, treatment with high-dose progestins such as megestrol acetate 40 to 160 mg/d usually reverses these lesions. Close follow-up and repeated sampling are necessary.
Procedures Performed for Structural Causes of Abnormal Uterine Bleeding
The patient is placed on the operating table in a lithotomy position, and the vagina and cervix are prepared as for any vaginal operation. The cervix is grasped on the anterior lip with a tenaculum. Some traction on the cervix is necessary to straighten the cervical canal and the uterine cavity. A uterine sound is inserted into the uterine cavity, and the depth of the uterus is noted. The cervical canal is then systematically dilated beginning with a small cervical dilator. Most operations can be performed after the cervix is dilated to accommodate a number 8 or 9 Hegar dilator or its equivalent. Dilatation is accomplished by firm, constant pressure with a dilator directed in the axis of the uterus (Fig. 41-10). After the cervix is dilated to admit the curette, the endocervical canal should be curetted and the sample submitted separately from the endometrial curettings. The endometrial cavity is then systemically scraped with a uterine curette. Uterine perforation is the major complication of dilatation and curettage, diagnosed when the operator finds no resistance to a dilator or curette. Laparoscopy to identify any damage to vessels or bowel may be required. Curettage of the postabortal uterus must be approached carefully because the uterus is extremely soft and perforation can occur with very little warning. Using the largest curette available or suction curettage is a safer choice than a small curette, which tends to cause perforation with less pressure.
A through C. Dilatation and curettage of the uterus.
Hysteroscopy, like laparoscopy, has gained widespread support for use both for diagnosis and treatment of intrauterine pathology and for ablation of the endometrium as an alternative to hysterectomy for the treatment of abnormal uterine bleeding. Scopes can have an objective lens that is offset from the long axis from 0° to 30°. The diagnostic hysteroscope usually has an external diameter of 5 mm. Some diagnostic sheaths allow passage of flexible instruments for biopsy and cutting. An operative hysteroscope is wider and usually has an integral unipolar or bipolar resecting loop identical to a urologic resectoscope. The loop can be replaced with a roller ball for endometrial ablation.
Several types of distention media exist and vary by electrolyte composition and osmolarity. High-viscosity (e.g., dextran 70), low-viscosity/electrolyte-poor (e.g., glycine and sorbitol), and low-viscosity/electrolyte-containing (e.g., normal saline and lactated Ringer’s solution) medias are commonly used for distension of the uterus during hysteroscopy.32 The use and safety profiles of these medias vary, however. Dextran 70 allows excellent visibility, but the manufacturer recommends that no more than 250 mL be absorbed because of the concern for pulmonary edema. Anaphylactic reactions and coagulopathy are rare complications that have been described.33 Glycine and sorbitol allow the use of monopolar cautery during operative hysteroscopy. Large volume deficits have been associated with secondary hyponatremic hypervolemia due to their metabolism to free water after intravasation.33 When fluid deficits reach 1000 to 1500 mL, the procedure should be terminated, and the patient’s serum electrolytes assessed. Patients who have excessive intravasation experience headache, nausea, vomiting, and agitation.34 This manifestation can progress to pulmonary and cerebral edema. These patients require close monitoring and diuretic administration.
Unlike glycine and sorbitol, normal saline and lactated Ringer’s solution have physiologic osmolarity and contain sodium. Although excessive intravasation does not lead to hyponatremia, it can lead to volume overload. Media deficits of greater than 2500 mL should prompt conclusion of the procedure and assessment of electrolytes.35 Fluid-management systems are available to monitor the amount of distension media lost during hysteroscopy. Media intravasation can be lessened by using the minimum intrauterine pressure needed to perform the hysteroscopy and by minimizing operating time. The physician must be aware that certain procedures such as endometrial ablation and resection of myomas open vascular channels and place the patient at increased risk for fluid overload.33
Following dilation of the cervix, a diagnostic hysteroscope is placed and the uterine cavity distended with the media of choice. Inspection of the cavity includes identifying the uterine fundus, cornua, and any other anomalies to include polyps, leiomyomas, or uterine septum.
Hysteroscopic Polypectomy or Myomectomy
If an intrauterine polyp is discovered, the base of the polyp is incised with hysteroscopic scissors, and the polyp is grasped with grasping forceps. The hysteroscope, sleeve, and polyp are removed simultaneously, because most polyps will not fit through the operating channel. Extremely large polyps may have to be removed piecemeal. Any residual base of the polyp may be removed with biopsy forceps. Pedunculated or submucosal leiomyoma can be removed safely hysteroscopically. Because myoma tissue is relatively dense, a power cutting instrument is required. The most common method is use of electrosurgery. A monopolar device may be used with an electrolyte-poor distention medium. Only bipolar devices may be used with normal saline or lactated Ringer’s solution. Both pedunculated and submucosal fibroids are shaved into small pieces with the hysteroresectoscope. Stalk resection should only be done to release a pedunculated fibroid if it is 10 mm or less in size; larger fibroids are difficult to remove in one piece without excessive cervical dilatation. Morcellation is much easier when the stalk is still attached for stability. Hysteroscopes with a morcellation attachment have been recently developed.36
A common treatment for abnormal uterine bleeding in the absence of endometrial hyperplasia is ablation of the endometrium. Historically, this was performed with an operative hysteroscope using an electrosurgical “roller ball,” where the endometrium was destroyed down to the myometrium in a systematic fashion. Currently, hysteroscopic endometrial ablation has been widely supplanted by various devices, including heated free fluid, cryotherapy, thermal balloon, microwave, and radiofrequency electricity. Most ablation techniques result in amenorrhea in approximately half the patients and decreased menstruation in another third of the patients over the first year of therapy.37
Myomectomy (Fig. 41-11) is the removal of fibroids, and it can be treatment for abnormal uterine bleeding, bulk symptoms, or infertility. Hemostasis during myomectomy can be aided medically by direct injection of dilute vasopressin at the site of the intended uterine incision (10 U in 50 mL). It can be aided further through the placement of a Penrose drain around the base of the uterus, pulled through small perforations in the broad ligament lateral to the uterine blood supply on either side and clamped to form a tourniquet for uterine blood flow. An incision is then made through the uterine serosa into the myoma. The pseudocapsule surrounding the tumor is identified and the tumor is bluntly dissected out with scissors, or bluntly if open. Vessels to the myoma are dessicated with the electrosurgical unit. Several myomas may be removed through a single incision, depending on size. The uterine wounds are closed with absorbable sutures to obliterate the dead space and provide hemostasis. The uterine serosa is closed with a 3-0 absorbable suture, placed subserosally if possible. Because myomectomies are associated with considerable postoperative adhesion formation, barrier techniques are used to decrease adhesion formation.
Myomectomy. A. Hemostatic “tourniquet’” in place before myomectomy. B. Uterine incision for myomectomy. C. Removal of myoma. D. Several myomas may be removed through a single incision. E. The uterine wound is closed with an absorbable suture. F. The uterine wound covered with mesh to retard adhesions.
During a laparoscopic myomectomy, hemostasis is assisted by intrauterine injection of dilute vasopressin (10 U in 50 mL) at the site of incision, similar to an open procedure. This is usually performed percutaneously with a spinal needle. Pedunculated leiomyomas can be excised at the base using scissors or a power instrument. Intramural leiomyomas require deep dissection into the uterine tissue, which must be closed subsequently with laparoscopic suturing techniques. Removing the specimen often requires morcellation, and power morcellators have been developed that significantly expedite this technique. Adhesion barriers are placed laparoscopically.
Total Abdominal Hysterectomy
Hysterectomy. A. The uterus grasped at the cornua. B. The round ligament is cut. C. The ovarian ligament and fallopian tube are isolated. D. The bladder is mobilized. E. The uterine vessels are clamped. F. The cardinal ligaments are clamped. G. The vagina is entered. H. The cardinal ligaments are sutured to the vagina. I. The vagina is “closed open.”
After the abdomen is entered, the upper abdomen is examined for evidence of extrapelvic disease, and a suitable retractor is placed in the abdominal incision. The uterus is grasped at either cornu with clamps and pulled up into the incision. The round ligament is identified and divided. The peritoneal incision is extended from the round ligament to just past the ovarian hilum, lateral to the infundibulopelvic ligament, if the ovaries are to be removed. The retroperitoneal space is bluntly opened, the ureter identified on the medial leaf of the broad ligament, and the infundibulopelvic ligament isolated, clamped, cut, and suture-ligated; a similar procedure is carried out on the opposite side. If the ovaries are to be left in situ, the ureter is identified and an opening below the utero-ovarian ligament and fallopian tube created. The fallopian tube and utero-ovarian ligament are clamped, cut, and ligated. The bladder is mobilized by sharply dissecting it free of the anterior surface of the uterus and cervix. Clamps are placed on the uterine vessels at the cervicouterine junction, and they are cut and suture-ligated. The cardinal ligaments are then serially clamped, cut, and ligated. Following division of the remaining cardinal ligaments, the uterus is elevated and the vagina clamped. The cervix is amputated from the vagina with scissors or a knife. Sutures are placed at each lateral angle of the vagina, and the remainder of the vagina is closed with a running absorbable suture. Pelvic reperitonealization is not necessary.
Vaginal hysterectomy. A. Traction is placed on the uterus. B. The posterior cul-de-sac is entered. C. The vaginal mucosa is circumcised. D. The anterior cul-de-sac is entered. E. The uterosacral ligaments are clamped. F. The uterosacral ligaments are tied. G. The fallopian tube, round ligament, and ovarian ligament are ligated. H. The peritoneum is closed. I. The vaginal mucosa is closed.
Vaginal hysterectomy is the preferred approach in patients in whom the uterus descends and the pubic arch allows enough space for a vaginal operation. A bladder catheter can be placed before the procedure, and the patient is placed in a lithotomy position. A weighted vaginal speculum is placed in the vagina, and the cervix is grasped with a tenaculum and pulled in the axis of the vagina. Injection of the cervix and paracervical tissue with analgesic with epinephrine may be helpful in defining planes and decreasing obscuring bleeding. A circumferential incision may be made with a scalpel or scissors. The posterior cul-de-sac is identified and entered with scissors. A long weighted speculum is then placed through this opening into the peritoneal cavity. Metzenbaum scissors are used to dissect anteriorly on the cervix down to the pubocervical-vesical fascia, reflecting the bladder off the lower uterine segment. When the peritoneum of the anterior cul-de-sac is identified, it is entered with the scissors, and a retractor is placed in the defect. The uterosacral ligaments are identified, doubly clamped, cut, and ligated. Serial clamps are placed on the parametrial structures above the uterosacral ligament; these pedicles are cut and ligated. At the cornu of the uterus, the tube, round ligament, and utero-ovarian ligament of the ovary are doubly clamped and cut. The procedure is carried out usually concurrently on the opposite side, and the uterus is removed. The pelvis is inspected for hemostasis; all bleeding must be meticulously controlled at this point.
The pelvic peritoneum is closed with a running purse-string suture incorporating the uterosacral and ovarian pedicles, those that were held. This exteriorizes those areas that might tend to bleed. The sutures attached to the ovarian pedicles are cut. The vagina may be closed with interrupted mattress stitches, incorporating the uterosacral ligaments into the corner of the vagina with each lateral stitch. On occasion, the uterus, which is initially too large to remove vaginally, may be reduced in size by morcellation (Fig. 41-14). After the uterine vessels have been clamped and ligated, serial wedges are taken from the central portion of the uterus in order to reduce the uterine mass. This procedure will allow the vaginal delivery of even very large uterine leiomyomas.
Uterine morcellation through the vagina.
Laparoscopy has been used to augment vaginal hysterectomy to avoid laparotomy in patients with known pelvic adhesions, with endometriosis, or in whom the uterus is enlarged by leiomyoma. Although multiple variations in technique exist, there are three basic laparoscopic approaches for hysterectomy: laparoscopic-assisted vaginal hysterectomy (LAVH), total laparoscopic hysterectomy (TLH), and laparoscopic supracervical hysterectomy (LSH). The technically simplest is the LAVH. A multiple-port approach is used to survey the peritoneal cavity, and any pelvic adhesions are lysed. The round ligaments are then occluded and divided, and the uterovesical peritoneum and peritoneum lateral to the ovarian ligament are incised. The course of the ureter and any adhesions or implants, such as endometriosis that might place the ureter in the way of the surgical dissection, are carefully dissected. Next, the proximal uterine blood supply is dissected for identification and then occluded with a laparoscopic energy device. When the ovaries are removed, the infundibulopelvic ligaments containing the ovarian vessels are divided. If the ovaries are conserved, the utero-ovarian ligament and blood vessels are divided and occluded. In many cases, the posterior cul-de-sac is also incised laparoscopically and the uterosacral ligaments separated with an energy device. The amount of dissection that is done prior to the vaginal portion depends on individual patient characteristics and may include as little as ovarian and adhesion management to full dissection including bladder dissection, with only the last vaginal incision done by the vaginal approach. During a TLH, the vaginal incision is performed laparoscopically, and the vaginal incision may be closed with laparoscopic suturing. This procedure is used for the indications listed earlier and also when lack of uterine descent makes the vaginal approach impossible.
During an LSH, the uterine vessels are divided after the bladder is dissected from the anterior uterus. The ascending branches of the uterine arteries are occluded, and the entire uterine fundus is amputated from the cervix. The endocervix is either cauterized or cored out. The fundus is then morcellated and removed through a 12-mm abdominal port or through a special transcervical morcellator. The end result is an intact cervix, with no surgical dissection performed below the uterine artery. This approach avoids both a large abdominal incision and a vaginal incision. According to its advocates, this approach minimizes operating time, recovery time, and risk of both infection and ureteral injury. LSH has yet to be widely applied, in part out of concern for the subsequent risk of developing cancer in the residual cervical stump. In addition, women may develop bleeding from the remaining lower uterine segment that can be bothersome, even if preventive measures had been taken.
Benign Ovarian and Fallopian Tube Lesions
The most common ovarian benign findings include functional follicular cysts, endometriomas (due to ovarian endometriosis), and serous cystadenomas or cystadenofibromas. These can present with varying degrees or pelvic pain, or sometimes be completely asymptomatic. Ultrasound is the best initial imaging modality for evaluating ovarian abnormalities.
When a cystic lesion persists or causes pelvic pain, surgical intervention is usually justified. Performing a cystectomy with ovarian preservation is recommended in women who desire future fertility. Whether the cystectomy is performed laparoscopically or by laparotomy, the procedure is initiated with inspection of the peritoneal cavity, peritoneum, diaphragm, liver, and pelvis. In the absence of signs of malignancy, pelvic washings are obtained and the ovarian capsule is incised superficially sharply or with the electrosurgical unit. The cyst is shelled out carefully through the incision. During laparoscopy, it is placed in a bag, intact if possible, and the bag opening is brought through a 10-mm port. If a cyst should rupture before removal, contents are aspirated thoroughly, and the cyst wall is removed and sent for pathologic evaluation. The peritoneal cavity is copiously rinsed with Ringer’s lactate solution. This is especially important when a dermoid cyst is ruptured, because the sebaceous material can cause a chemical peritonitis unless all the visible oily substance is carefully removed. A cyst may need to be drained to facilitate removal, but only after bag edges are firmly out of the abdomen assuring no leakage within the abdomen. Hemostasis of the ovary is achieved with bipolar electrocoagulation, but the ovary is usually not closed. If there are solid growths within the cyst, it should be sent for frozen section to verify the absence of the malignancy. If malignancy is detected, immediate definitive surgery is recommended.
Indications for removal of adnexa include persistent ovarian cyst, pelvic pain, concern for malignancy, and risk reduction surgery in women with genetic predisposition for ovarian or endometrial cancers (BRCA1/2 mutation carrier, Lynch syndrome). In general, the peritoneum lateral to the infundibulopelvic (IP) ligament is incised in a parallel fashion to allow retroperitoneal dissection and identification of the ureter. Once this has been accomplished, the IP ligament is ligated with suture or an energy source (ultrasonic or bipolar). The remaining posterior leaf of the broad ligament is incised toward the uterus in a direction parallel to the utero-ovarian ligament, to avoid ureteral injury. The fallopian tube and utero-ovarian ligaments are then ligated with either suture or an energy source. If performed laparoscopically, the specimen or specimens are removed in a bag as described earlier.
As in diagnostic laparoscopy, a one- or two-port technique can be used. Fallopian tubes are occluded in the mid-isthmic section, approximately 3 cm from the cornua, using clips, elastic bands, or bipolar electrosurgery. With electrosurgery, approximately 2 cm of tube should be desiccated. Pregnancy rates after any of these techniques have been reported in the range of 3 per 1000 women.
Chronic pelvic pain is defined as pain below the umbilicus that has lasted at least 6 months or causes functional disability, requiring treatment. While there can be gastrointestinal and urologic causes of chronic pelvic pain, gynecologic causes are frequently identified. Often, a surgical evaluation is needed for diagnosis and/or intervention. The most common gynecologic causes of chronic pelvic pain include endometriosis, adenomyosis, uterine leiomyomas, and adhesive disease.
Endometriosis is the finding of ectopic endometrial glands and stroma outside the uterus. It affects 10% of the general population and is an incidental finding at the time of laparoscopy in more than 20% of asymptomatic women. It is especially prevalent in patients suffering from chronic pelvic pain (80%) and infertility (20%–50%).21 The pathophysiology of endometriosis is poorly understood; etiologic theories explaining dissemination of endometrial glands include retrograde menstruation, lymphatic and vascular spread of endometrial glands, and coelomic metaplasia. Endometriosis commonly involves the ovaries, pelvic peritoneal surfaces, and uterosacral ligaments. Other possible sites include the rectovaginal septum, sigmoid colon, intraperitoneal organs, retroperitoneal space, ureters, incisional scars, umbilicus, and even the thoracic cavity. Involvement of the fallopian tubes may lead to scarring, blockage, and subsequent infertility. Ovarian involvement varies from superficial implants to large complex ovarian masses called endometriomas or “chocolate cysts.” Endometriomas are found in approximately one third of women with endometriosis and are often bilateral.
While endometriosis can be totally asymptomatic, more commonly, women are symptomatic, and complaints vary from mild dyspareunia and cyclic dysmenorrhea to debilitating chronic pelvic pain with acute exacerbations at the time of menses. Less common manifestations include painful defecation, hematochezia, and hematuria if there is bowel and/or bladder involvement. Pelvic examination in symptomatic patients typically demonstrates generalized pelvic tenderness and nodularity of the uterosacral ligaments, and at times, a pelvic mass may be appreciated if an endometrioma is present. The severity of symptoms does not correlate with the degree of clinical disease present. Endometriosis can also cause increases in serum cancer antigen 125 (CA-125). Definitive diagnosis usually requires laparoscopy and visualization of the pathognomonic endometriotic implants. These appear as blue, brown, black, white, or yellow lesions that can be raised and at times puckered, giving them a “gunpowder” appearance. Biopsy is not routinely done but should be obtained if the diagnosis is in doubt.
Treatment is guided by severity of the symptoms and whether preservation of fertility is desired and varies from expectant, to medical, to surgical.38,39 Expectant management is appropriate in asymptomatic patients. Those with mild symptoms can be managed with oral contraceptive pills and/or nonsteroidal anti-inflammatory analgesia; moderate symptoms are treated with medroxyprogesterone acetate. Severe symptoms are treated with GnRH agonists to induce medical pseudo-menopause.
Surgical management for endometriosis varies depending on the age and fertility desires of the patient. A diagnostic laparoscopy with biopsies may be indicated to confirm the diagnosis of endometriosis. If endometriosis is suspected, an operative laparoscopy with ablation of endometriotic implants usually decreases the severity of pelvic pain. Ablation of endometriotic implants can be performed with CO2 laser or electrocautery and/or resection of deep endometriotic implants.38 Endometriomas can cause pain and, if found, should be treated by ovarian cystectomy. Complete resection of the cyst wall is required because recurrence of the endometrioma is common after partial removal. Conservative surgical therapy in endometriosis patients with patent fallopian tubes results in pregnancy in about 50% of cases. Unfortunately, endometriosis is a chronic disease and conservative therapy, medical or surgical, provides only temporary relief, with the majority of patients relapsing with 1 to 2 years. Patients with severe debilitating symptoms who do not desire future fertility and have not responded to conservative management can undergo extirpative surgery to remove the uterus, ovaries, and fallopian tubes; this intervention is curative and should be considered.
Pelvic adhesions usually are related to previous surgery, endometriosis, or infection, the latter of which can be either genital (i.e., pelvic inflammatory disease) or extra-genital (e.g., ruptured appendix) in origin. Adhesions can be lysed mechanically with scissors if not vascular, harmonic scissors, or any of the power techniques as discussed elsewhere in this text. Postoperatively, adhesion barrier methods have been shown to decrease adhesion formation in both animal and human studies but have not been demonstrated to improve outcome in terms of either subsequent pregnancies or pain relief.
Pelvic Inflammatory Disease
Pelvic inflammatory disease (PID) is an infection of the upper female genital tract involving the uterus, fallopian tubes, and ovaries resulting in endometritis, salpingitis, and oophoritis. It often involves contiguous pelvic organs, resulting in peritonitis, tubo-ovarian abscesses, and occasionally perihepatitis (Fitz-Hugh-Curtis syndrome). Long-term sequelae can include infertility, chronic pelvic pain, and increased risk of ectopic pregnancy.40,41 PID is mostly a sexually transmitted ascending infection caused by N. gonorrhoeae and/or C. trachomatis, but numerous other organisms have been implicated, including normal vaginal flora. Screening for concomitant HIV infection is strongly recommended. Less commonly, PID may result from extension of other pelvic and abdominal infections, such as appendicitis and diverticulitis, or may be precipitated by a medical procedure, such as hysterosalpingography, endometrial biopsy, or dilation and curettage.
Differential diagnosis includes appendicitis, cholecystitis, inflammatory bowel disease, pyelonephritis, nephrolithiasis, ectopic pregnancy, and ovarian torsion.40,41 The Centers for Disease Control and Prevention recommend treatment of suspected PID in patients with pelvic or lower abdominal pain who also exhibit cervical motion tenderness, uterine tenderness, or adnexal tenderness (Table 41-4). Transvaginal ultrasound may reveal thickened fluid-filled tubes with or without free pelvic fluid. Laparoscopic findings include swollen erythematous tubes with exudates. Criteria for hospitalization and intravenous antibiotic treatment include the following42: surgical emergencies (e.g., appendicitis), infection during pregnancy, failure to respond to or inability to follow or tolerate outpatient oral medication regimens, severe illness with nausea and vomiting or high fever, and tubo-ovarian abscess.
Table 41-4CDC recommended treatment of PID (2010)42 ||Download (.pdf) Table 41-4 CDC recommended treatment of PID (2010)42
|ORAL REGIMENS |
|Ceftriaxone 250 mg IM in a single dose plus doxycycline 100 mg PO bid for 14 days |
|with or without metronidazole 500 mg PO bid for 14 days |
|Cefoxitin 2 g IM in a single dose and probenecid 1 g PO administered concurrently in a single dose plus doxycycline 100 mg PO bid for 14 days with or without metronidazole 500 mg PO bid for 14 days |
|Other parenteral third-generation cephalosporin (e.g., ceftizoxime or cefotaxime) plus doxycycline 100 mg PO bid for 14 days with or without metronidazole 500 mg PO bid for 14 days |
|parenteral regimens |
|Recommended Regimen A |
|Cefotetan 2 g IV every 12 hours or cefoxitin 2 g IV every 6 hours plus doxycycline 100 mg PO or IV every 12 hours |
|Recommended Regimen B |
|Clindamycin 900 mg IV every 8 hours plus gentamicin loading dose IV or IM (2 mg/kg of body weight), followed by a maintenance dose (1.5 mg/kg) every 8 hours; single daily dosing may be substituted |
|Alternative Parenteral Regimen |
|Ampicillin/sulbactam 3 g IV every 6 hours plus doxycycline 100 mg PO or IV every 12 hours |
First-line treatment for tubo-ovarian abscess includes broad-spectrum antibiotics and, sometimes, percutaneous drainage. Surgical intervention becomes necessary if medical therapy fails or if the abscess ruptures. Rupture is a surgical emergency with a high mortality rate if not recognized and managed promptly. In addition to management of the septic shock state, hysterectomy and bilateral salpingo-oophorectomy is the procedure of choice; however, conservative surgery must be considered in young patients desiring future fertility. The abdomen should be explored for metastatic abscesses, and special attention must be paid to bowel, bladder, and ureteral safety due to the friability of the infected tissue and the adhesions commonly encountered at the time of surgery. Placement of an intraperitoneal drain and mass closure of the peritoneum, muscle, and fascia with delayed-absorbable or permanent sutures is advised. Closure of the skin and subcutaneous layer should be avoided in patients with frank pus, and delayed primary closure or closure by secondary intention is recommended because of the high rate of wound infections. Conservative surgery, when feasible, may be attempted by laparoscopy and may involve unilateral salpingo-oophorectomy or drainage of the abscess and liberal irrigation of the abdomen and pelvis.