Gynecology_Novak

Gynecology_Novak. Skene duct cyst 4. Infections 2. Solid tumors Abscess—Bartholin, Skene, periclitoral, other Cherry angioma 5. Ectopic Figure 14.33 Skene’s gland cyst. rapidly enlarging, painful, inﬂammatory mass (a Bartholin abscess). An inﬂatable bulb-tipped catheter was described by Word and is quite easy to use (239). The small catheter is inserted through a small stab wound into the abscess after infiltration of the skin with local anesthesia; the balloon of the catheter is inﬂated with 2 to 3 mL of saline and the catheter remains in place for 4 to 6 weeks, allowing epithelialization of a tract and the creation of a permanent gland opening. Skene’s Duct Cysts These are cystic dilations of the Skene glands, typically located adjacent to the urethral meatus within the vulvar vestibule. Although most are small and often asymptomatic, they may enlarge and cause urinary obstruction, requiring excision (Fig 14.33).


Gynecology_Novak

Gynecology_Novak. Painful Intercourse Painful intercourse (dyspareunia) may be caused by many different vulvovaginal conditions, including common vaginal infections and vaginismus (see Chapters 11 and 18). A careful sexual history is essential, as is a careful examination of the vulvar area and vagina. Vulvodynia is the term used to describe unexplained vulvar pain, sexual dysfunction, and the resultant psychological disability (240,241). The term vulvar vestibulitis was previously used to describe a situation in which there is pain during intercourse or when attempting to insert an object into the vagina; pain on pressure to the vestibule on examination and vestibular erythema (known as Friedrich’s triad); this entity is now described as localized provoked vulvodynia in the International Society for the Study of Vulvovaginal Disease (ISSVD) (240–243) (see Chapter 16). A number of recent studies failed to demonstrate a consistent relationship with any genital infectious organism, including C.


Gynecology_Novak

Gynecology_Novak. for the Study of Vulvovaginal Disease (ISSVD) (240–243) (see Chapter 16). A number of recent studies failed to demonstrate a consistent relationship with any genital infectious organism, including C. trachomatis, gonorrhea, Trichomonas, mycoplasma, Ureaplasma, Gardnerella, candida, or HPV, and the condition has been characterized as multifactorial, with both inﬂammatory, neuropathic, and functional components. Although the symptoms of dyspareunia with insertion can be disabling, no curative therapies were found. Both medical and behavioral therapies are of some benefit, and some authors encourage surgery, but the role of this treatment and newer therapies such as the injection of botulinum toxin A is not well established (241).


Gynecology_Novak

Gynecology_Novak. Vulvar Ulcers A number of STDs can cause vulvar ulcers, including herpes simplex virus, syphilis, lymphogranuloma venereum, and granuloma inguinale (see Chapter 18). Crohn’s disease can include vulvar involvement with abscesses, fistulae, sinus tracts, fenestrations, and other scarring. Although medical treatment, with systemic steroids and other systemic agents, is the standard therapy, surgical therapy for both intestinal and vulvar disease may be required. Behcet’s Disease This systemic condition is characterized by genital and oral ulcerations with ocular inﬂammation and many other manifestations (244). The cause and the most effective therapy are not well established, although anti-inﬂammatory and immunosuppressive therapies may be effective (245).


Gynecology_Novak

Gynecology_Novak. Lichen Planus This condition causes oral and genital ulcerations. Typically, there is desquamative vaginitis with erosion of the vestibule. Treatment is based on the use of both topical and systemic steroids. Plasma cell mucositis appears as erosions in the vulvar area, particularly the vestibule. Biopsy is essential in establishing the diagnosis.


Gynecology_Novak

Gynecology_Novak. Vaginal discharge is one of the most common vaginal symptoms. Conditions ranging from vaginal candidiasis to chlamydia cervicitis to bacterial vaginosis to cervical carcinoma may cause vaginal discharge. Infectious vaginal conditions are addressed more completely in Chapter 18. Vaginal lesions may occasionally be palpable to a woman. More commonly, vaginal lesions are discovered on examination by a clinician. They may contribute to symptoms (such as bleeding or discharge) or they may be entirely asymptomatic. Vaginitis, cervicitis, and vaginal or cervical lesions (including malignancies) can be causes of vaginal discharge. Other noninfectious causes of discharge are as follows: 1. Retained foreign body—tampon, pessary 2. Ulcerations—tampon-induced, lichen planus, herpes simplex infection 3. Malignancy—cervical, vaginal


Gynecology_Novak

Gynecology_Novak. Some vaginal lesions are asymptomatic and are noted incidentally on examination. Fibroepithelial polyps consist of polypoid folds of connective tissue, capillaries, and stroma covered by vaginal epithelium. Although they can be excised easily in the office, their vascularity can be troublesome, and excision is not necessary unless the diagnosis is in question. Cysts of embryonic origin can arise from mesonephric, paramesonephric, and urogenital sinus epithelium. Gartner’s duct cysts are of mesonephric origin and are usually present on the lateral vaginal wall. They rarely cause symptoms and, therefore, do not require treatment. Other embryonic cysts can arise anterior to the vagina and beneath the bladder. Cysts that arise from the urogenital sinus epithelium are located in the area of the vulvar vestibule. Vaginal adenosis, the presence of epithelial-lined glands within the vagina, is associated with in utero exposure to diethylstilbestrol. No therapy is necessary other than close


Gynecology_Novak

Gynecology_Novak. the vulvar vestibule. Vaginal adenosis, the presence of epithelial-lined glands within the vagina, is associated with in utero exposure to diethylstilbestrol. No therapy is necessary other than close observation and periodic palpation to detect nodules that may need to be evaluated by biopsy to rule out vaginal clear cell adenocarcinoma (see Chapter 36).


Gynecology_Novak

Gynecology_Novak. Women will sometimes describe a bulging lesion of the vagina and vulvar area, variably associated with symptoms of pressure or discomfort. The most common cause of such a lesion is one of the disorders of vaginal support. Management of these conditions is discussed in Chapter 27. Other genital lesions, such as urethral diverticula or embryonic cysts, may cause similar symptoms. Differential Diagnosis The causes of postmenopausal bleeding and the percentage of patients who seek treatment for different conditions are presented in Table 14.16.


Gynecology_Novak

Gynecology_Novak. Differential Diagnosis The causes of postmenopausal bleeding and the percentage of patients who seek treatment for different conditions are presented in Table 14.16. Hormone therapy may be used to manage troublesome menopausal symptoms; it is recommended to treat with the lowest effective dose with the risks versus benefits regularly reviewed by a woman and her doctor (246). Women who are taking hormone therapy during menopause may be using a variety of hormonal regimens that can result in bleeding (see Chapter 34). Because unopposed estrogen therapy can result in endometrial hyperplasia, various regimens of progestins are typically added to the estrogen regimen; they are given in a continuous fashion, although they may be given in a sequential fashion for women within 1 year of menopause (246). Table 14.16 Etiology of Postmenopausal Bleeding From Hacker NF, Moore JG. Essentials of obstetrics and gynecology, 3rd ed. Philadelphia: WB Saunders, 1998:635, with permission.


Gynecology_Novak

Gynecology_Novak. Table 14.16 Etiology of Postmenopausal Bleeding From Hacker NF, Moore JG. Essentials of obstetrics and gynecology, 3rd ed. Philadelphia: WB Saunders, 1998:635, with permission. Endometrial sampling is indicated for any unexpected bleeding that occurs with hormonal therapy. A significant change in withdrawal bleeding or breakthrough bleeding (e.g., absence of withdrawal bleeding for several months followed by resumption of bleeding or a marked increase in the amount of bleeding) should prompt endometrial sampling. Patient adherence to hormonal regimens is a significant issue with hormone therapy, with the challenges of oral therapy mitigated by nonoral routes of administration (247). Missed doses of oral medication and failure to take the medication in the prescribed fashion can lead to irregular bleeding or spotting that is benign in origin but that can result in patient dissatisfaction (248).


Gynecology_Novak

Gynecology_Novak. The problems that women most often report with hormone therapy include vaginal bleeding and weight gain. The use of a continuous low-dose combined regimen has the advantage that for many women, bleeding will ultimately cease after several months, during which irregular and unpredictable bleeding may occur (248,249). Some women are unable to tolerate these initial months of irregular bleeding. The risk of endometrial hyperplasia or neoplasia with this regimen is low.


Gynecology_Novak

Gynecology_Novak. Other benign causes of bleeding include atrophic vaginitis and endometrial and cervical polyps, which may become apparent as postcoital bleeding or spotting. Women who experience bleeding after menopause may attempt to minimize the extent of the problem; they may describe it as “spotting” or “pink or brownish discharge.” However, any indication of bleeding or spotting should be evaluated. In the absence of hormone therapy, any bleeding after menopause (classically defined as absence of menses for 1 year) should prompt evaluation with endometrial sampling. Studies of transvaginal ultrasonography revealing an endometrial thickness 4 mm or less correlate with a low risk of endometrial malignancy, and thus endometrial sampling is not required (250). Endometrial polyps and other abnormalities can be seen in women who are taking tamoxifen. These polyps are more likely to involve cystic dilation of glands, stromal condensation around the glands, and squamous metaplasia of the overlying


Gynecology_Novak

Gynecology_Novak. can be seen in women who are taking tamoxifen. These polyps are more likely to involve cystic dilation of glands, stromal condensation around the glands, and squamous metaplasia of the overlying epithelium (251). These polyps can be benign, although they must be distinguished from endometrial malignancies, which may occur when taking tamoxifen. The incidence of endometrial polyps not associated with tamoxifen increases with age during the reproductive years; it is not clear whether the incidence subsequently peaks or decreases during the postmenopausal years (162). Endometrial polyps are more likely to be malignant in postmenopausal women, and hypertension is associated with an increased risk of malignancy (252).


Gynecology_Novak

Gynecology_Novak. Endometrial, cervical, and ovarian malignancies must be ruled out in the presence of post-menopausal bleeding. One series found a malignancy (endometrial or cervical) in approximately 10% of women with postmenopausal bleeding (253). A Pap test is essential when postmenopausal bleeding is noted, although the Pap test is an insensitive diagnostic test for detecting endometrial cancer. The Pap test results are negative in some cases of invasive cervical carcinoma because of tumor necrosis. Cervical malignancy is diagnosed by cervical biopsy of grossly visible lesions and colposcopically directed biopsy for women with abnormal Pap test results (see Chapter 19). Functional ovarian tumors may produce estrogen and lead to endometrial hyperplasia or carcinoma, which may cause bleeding. Diagnosis of Postmenopausal Abnormal Bleeding


Gynecology_Novak

Gynecology_Novak. Diagnosis of Postmenopausal Abnormal Bleeding Pelvic examination to detect local lesions and a Pap test to assess cytology are essential first steps in finding the cause of postmenopausal bleeding. Pelvic ultrasonographic examination and, in particular, transvaginal ultrasonography or sonohysterography can suggest the cause of bleeding (250,254). Endometrial sampling, through office biopsy, hysteroscopy, or D&C, is usually considered essential. An endometrial thickness of less than 5 mm measured by transvaginal ultrasonography is unlikely to indicate endometrial cancer, although some authors suggest that the diagnostic accuracy is overestimated and recommend a cutoff of 3 mm (250,255). Management of Postmenopausal Abnormal Bleeding


Gynecology_Novak

Gynecology_Novak. Management of Postmenopausal Abnormal Bleeding Benign Disorders The management of bleeding caused by atrophic vaginitis includes topical (vaginal) or systemic use of estrogens after other causes of abnormal bleeding are excluded. Such therapy can provide significant benefits in terms of quality of life, but must be weighed with each individual, considering contraindications and patient preferences (256,257). Serum levels appear to be lower with vaginal administration using creams, tablets, or rings (258). Cervical polyps can easily be removed in the office.


Gynecology_Novak

Gynecology_Novak. Endometrial Hyperplasia The terminology used to describe endometrial hyperplasia is confusing, and the clinician must consult with the pathologist to ensure an understanding of the diagnosis. The World Health Organization (WHO) system classifies endometrial hyperplasia as simple hyperplasia, complex hyperplasia, simple atypical hyperplasia, and complex atypical hyperplasia (259). Approximately 40% to 50% of women with atypical hyperplasia have concurrent carcinoma. The management of endometrial hyperplasia is based on an understanding of the natural history of the lesion involved. The risk of progression of hyperplasia without atypia is low but is approximately 30% among those with atypical hyperplasia (259). Hysterectomy is recommended for treatment of atypical endometrial hyperplasia in postmenopausal women. Management of endometrial cancer with surgical staging and multidisciplinary review of pathology and treatment planning is addressed in Chapter 35.


Gynecology_Novak

Gynecology_Novak. Progestin therapy (oral, parenteral, or intrauterine device delivery) may be used in women with atypical endometrial hyperplasia who are poor operative candidates. These women should have an endometrial biopsy every 3 months to check for recurrence, with recurrence risks approaching 50% (185). A suggested scheme of management is outlined in Figure 14.34. This treatment is discussed in more detail in Chapter 35.


Gynecology_Novak

Gynecology_Novak. Differential Diagnosis Ovarian Masses During the postmenopausal years, the ovaries become smaller. Ovarian volume is related to age, menopausal status, weight, height, and use of exogenous hormones (260). A large body habitus and uterine size make it more difficult to palpate and assess ovarian size, particularly among postmenopausal women, and transvaginal ultrasonography is significantly more accurate than clinical examination. Transvaginal ultrasonography is suggested in addition to annual pelvic examination among overweight postmenopausal women (261). Although ovarian cancer is notoriously difficult to diagnose at any early stage, the concept that it is frequently asymptomatic is challenged. Symptoms may include back pain, fatigue, bloating, constipation, abdominal pain, and urinary symptoms; these symptoms are of greater severity and more recent onset in women with ovarian malignancy (262). Thus it is argued that among primary clinicians, the possibility of an ovarian mass


Gynecology_Novak

Gynecology_Novak. symptoms; these symptoms are of greater severity and more recent onset in women with ovarian malignancy (262). Thus it is argued that among primary clinicians, the possibility of an ovarian mass (either benign or malignant) in women with these symptoms warrants further diagnostic investigation. However, the positive predictive value of these symptoms is not high for the prediction of early-stage disease, and the use of symptoms to trigger an evaluation for ovarian cancer is noted to result in diagnosis of the disease in only 1 in 100 women in the general population with such symptoms (263). Ovarian cancer is predominantly a disease of postmenopausal women; the incidence increases with age, and the average patient age is about 56 to 60 years (see Chapter 37).


Gynecology_Novak

Gynecology_Novak. With increased use of pelvic ultrasonographic evaluation, a new problem arose in post-menopausal women: the discovery of a small ovarian cyst. This is particularly troublesome in CHAPTER 14 Benign Diseases of the Female Reproductive Tract Perform D&C to rule out endometrial carcinoma in symptomatic patients Desire to retain uterus Persistent atypical hyperplasia Normal or atrophic endometrium  Continue Provera 5 mg/day 10 days/month for 12 months  Consider annual endometrial biopsy  Ovulation induction if childbearing desired Provera 10–20 mg/day for 11 to 14 days per month Repeat endometrial biopsy in 3 to 6 months Trial of high dose progestins (e.g., Provera 40–100 mg/day for 3 months) No desire to retain uterus Hysterectomy


Gynecology_Novak

Gynecology_Novak. Figure 14.34 Management of endometrial hyperplasia. (Reproduced with permission from Berek & Hacker’s Gynecologic Oncology, 5th edition, Lippincott Williams & Wilkins, 2010, p 410.) a woman who is entirely asymptomatic and whose ultrasonographic examination was performed for indications unrelated to pelvic pathology. It is suggested that when the cyst is asymptomatic, small (<5–10 cm in diameter), unilocular, and thin walled, with a normal CA125 level, the risk of malignancy is extremely low and these masses can be followed conservatively, without surgery (220,264,265). Surgery may be indicated in some women with a strong family history of ovarian, breast, endometrial, or colon cancer, or with a mass that appears to be enlarging (see Chapter 37). The addition of color ﬂow Doppler examination and other ultrasonographic characteristics may be helpful in distinguishing benign from malignant masses, although the role of Doppler ultrasonography remains somewhat controversial (Tables 14.4


Gynecology_Novak

Gynecology_Novak. and other ultrasonographic characteristics may be helpful in distinguishing benign from malignant masses, although the role of Doppler ultrasonography remains somewhat controversial (Tables 14.4 and 14.13) (220).


Gynecology_Novak

Gynecology_Novak. Uterine and Other Masses Many postmenopausal women have not had regular gynecologic care, and the discovery of a pelvic mass may reﬂect the persistence of a uterine leiomyoma that previously was not discovered. The possibility of transient ovarian cysts is noted above, and it may be difficult to distinguish an ovarian from a uterine mass. Some women may not remember having been told they had a pelvic mass. Thus, a review of medical records may be helpful in determining the preexistence of a benign pelvic mass. Uterine leiomyomas are hormonally responsive and typically decrease in size or resolve after menopause (see Chapter 15).


Gynecology_Novak

Gynecology_Novak. Diagnosis A personal and family medical history is helpful in detecting individuals at increased risk for the development of ovarian cancer. Several hereditary family cancer syndromes involve ovarian neoplasms (see Chapter 37). However, patients with hereditary forms of epithelial ovarian cancer account for only a small percentage of all cases; 90% to 95% of cases of ovarian cancer are sporadic and without identifiable heritable risk.


Gynecology_Novak

Gynecology_Novak. In postmenopausal women with a pelvic mass, a CA125 measurement may be helpful in predicting a higher likelihood of a malignancy, which may guide decisions regarding management, consultation, or referral. A high index of suspicion by both women and their clinicians represents the best way to detect early ovarian cancer. Persistent symptoms such as an increase in abdominal size, bloating, fatigue, abdominal pain, indigestion, inability to eat normally, urinary frequency, pelvic pain, constipation, back pain, new onset of urinary incontinence, or unexplained weight loss require evaluation and consideration of the possibility of ovarian cancer. A physical examination, transvaginal ultrasonography, and CA125 measurement are appropriate. A normal CA125 level does not rule out ovarian cancer; up to 50% of early-stage ovarian malignancies and 20% to 25% of advanced cancers have normal values of CA125 (266).


Gynecology_Novak

Gynecology_Novak. A normal CA125 level does not rule out ovarian cancer; up to 50% of early-stage ovarian malignancies and 20% to 25% of advanced cancers have normal values of CA125 (266). Management The use of improved imaging techniques may allow the nonoperative management of ovarian masses that are probably benign (Table 14.13). A suspicious or persistent complex mass requires surgical evaluation. A physician trained to appropriately stage and debulk ovarian cancer, such as a gynecologic oncologist, should perform the surgery in a hospital with the necessary support and consultative services to optimize the patient’s outcome (266). When a malignant ovarian mass is discovered and the appropriate surgical staging and debulking procedure cannot be performed by the generalist obstetrician-gynecologist, a gynecologic oncologist should be consulted. Comprehensive surgical staging facilitates appropriate therapy and optimizes prognosis.


Gynecology_Novak

Gynecology_Novak. Anatomic changes that occur in postmenopausal women include atrophy of the labia majora and increasing prominence of the labia minora. The epithelium of the hymen and vestibule become thin; there is a shift in vaginal cellular maturation in response to estrogen deprivation, with resultant thinning. Although these changes lead to minimal symptoms in most women, external dysuria, pruritus, tenderness, dyspareunia, and bleeding can result from fissuring and excoriations. Because of the risk of VIN and malignancy, suspicious lesions require vulvar biopsy. Vulvar Dermatoses Several vulvar conditions occur most commonly in postmenopausal women. Symptoms are primarily itching and vulvar soreness, in addition to dyspareunia.


Gynecology_Novak

Gynecology_Novak. In the past, numerous terms were used to describe disorders of vulvar epithelial growth that produce a number of nonspecific gross changes. These terms included leukoplakia, lichen sclerosus and atrophicus, atrophic and hyperplastic vulvitis, and kraurosis vulvae. The ISSVD in 2006 recommended a classification of vulvar dermatoses based on histologic patterns, listed with the likely clinical diagnoses, rather than on the basis of clinical morphology as in the previous categorization (see Chapter 19) (267). This classification system excludes neoplastic and infectious conditions. Vulvar conditions that are described in this classification system include atopic, allergic, and irritant contact dermatitis, psoriasis, lichen simplex chronicus, lichen sclerosus, lichen planus, pemphigoid, aphthous ulcers, Behcet’s disease, and Crohn’s disease.


Gynecology_Novak

Gynecology_Novak. Lichen sclerosus is the most common white lesion of the vulva. Lichen sclerosus can occur at any age, although it is most common among postmenopausal women and prepubertal girls (Fig. 14.4). The symptoms are pruritus, dyspareunia, and burning. Lichen sclerosus characteristically is associated with decreased subcutaneous fat to the extent that the vulva is atrophic, with small or absent labia minora, obliteration of the anatomic landmarks, thin labia majora, and sometimes phimosis of the prepuce. The surface is pale with a shiny, crinkled pattern (described as having characteristics like “cigarette paper”), often with fissures and excoriation. The lesion tends to be symmetric and often extends to the perineal and perianal areas. The diagnosis is confirmed by biopsy. Invasive cancer is associated with lichen sclerosus, although the significance of this association is unclear in terms of causation (289).


Gynecology_Novak

Gynecology_Novak. Treatment is with an ultrapotent topical steroid such as 0.05% clobetasol. Approximately 93% of patients respond satisfactorily (269). Maintenance therapy is frequently required, and a graduated reduction from ultrapotent to medium-and low-potency topical steroids can help to maintain remission of symptoms (269–271). The topical calcineurin inhibitors pimecrolimus and tacrolimus were effective in individuals not responding to topical steroids, although the FDA approved a warning suggesting possible risk of cancer from this class of drugs and caution is thus advised with long-term use avoided (272).


Gynecology_Novak

Gynecology_Novak. Squamous vulvar intraepithelial neoplasia is seen most often in postmenopausal women but may occur during the reproductive years. Pruritus is the most common symptom, although “lumps” may be described and are sometimes confused with condyloma (268). Current terminology describes two types of VINs: VIN, usual type, that is typically HPV-related and encompassing former VIN-2 and -3 with warty, basaloid, and mixed types; and VIN, differentiated type (273). The lesion appears thickened and hyperkeratotic, and there may be excoriation. Lesions may be discrete but may be symmetric and multiple. About one-third of women will have a history of HPV related cervical disease or condyloma (268). Most women with VIN are smokers. Biopsy is necessary to confirm the diagnosis and to exclude malignancy. See Chapter 19 for management of VIN.


Gynecology_Novak

Gynecology_Novak. The urethra and vagina have a common embryonic origin and are steroid-dependent tissues. Urethral caruncles and prolapse of the urethral mucosa are examples of vulvar lesions that may be seen in other age groups but that occur more commonly among older women. Both conditions can be treated with topical or systemic estrogen preparations. Various vulvar skin lesions, including seborrheic keratoses and cherry hemangiomas (senile hemangiomas), occur more commonly on aging skin.


Gynecology_Novak

Gynecology_Novak. Up to 50% of postmenopausal women have symptoms of atrophic vaginitis (257). Symptoms include an external dysuria, pruritus, tenderness, dyspareunia, and bleeding from fissuring or ulcerations. In addition to the clinical findings of a shiny, ﬂat, thin-appearing vaginal mucosa without rugae, microscopic examination of vaginal secretions reveals an increased number of white blood cells. Treatment with local or systemic estrogens effectively manages the symptoms and restores normal pH levels with ongoing therapy (274,275). Systemic absorption does occur with topical estrogen therapy, and rates of absorption differ depending on the degree of atrophy. Topical emollients may be helpful if estrogens are not desired or are contraindicated. Vaginal lubricants are universally useful in minimizing symptoms of dyspareunia for postmenopausal women (275). 1.


Gynecology_Novak

Gynecology_Novak. 1. Biro FM, Lucky AW, Simbartl LA, et al. Pubertal maturation in girls and the relationship to anthropometric changes: pathways through puberty. J Pediatr 2003;142:643–646. 2. Herman-Giddens ME, Slora EJ, Wasserman RC, et al. Secondary sexual characteristics and menses in young girls seen in office practice: a study from the Pediatric Research in Office Settings network. Pediatrics 1997;99:505–512. 3. Euling SY, Herman-Giddens ME, Lee PA, et al. Examination of US puberty-timing data from 1940 to 1994 for secular trends: panel findings. Pediatrics. 2008;121(Suppl 3):S172–S191. 4. Apter D, Hermanson E. Update on female pubertal development. Curr Opin Obstet Gynecol 2002;14:475–481. 5. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child 1969;44:291–303. 6. Harlan WR, Harlan EA, Grillo GP. Secondary sex characteristics of girls 12 to 17 years of age: the U.S. Health Examination Survey. J Pediatr 1980;96:1074–1078. 7.


Gynecology_Novak

Gynecology_Novak. 6. Harlan WR, Harlan EA, Grillo GP. Secondary sex characteristics of girls 12 to 17 years of age: the U.S. Health Examination Survey. J Pediatr 1980;96:1074–1078. 7. Anveden-Hertzberg L, Gauderer MW, Elder JS. Urethral prolapse: an often misdiagnosed cause of urogenital bleeding in girls. Pediatr Emerg Care 1995;11:212–214. 8. Allen AL, Siegfried EC. The natural history of condyloma in children. J Am Acad Dermatol 1998;39:951–955. 9. Siegfried E, Rasnick-Conley J, Cook S, et al. Human papillomavirus screening in pediatric victims of sexual abuse. Pediatrics 1998;101(Pt 1):43–47. 10. Powell J, Wojnarowska F. Childhood vulval lichen sclerosus and sexual abuse are not mutually exclusive diagnoses. BMJ 2000; 320:311. 11. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus: an increasingly common problem. J Am Acad Dermatol 2001;44:803– 806. 12.


Gynecology_Novak

Gynecology_Novak. 11. Powell J, Wojnarowska F. Childhood vulvar lichen sclerosus: an increasingly common problem. J Am Acad Dermatol 2001;44:803– 806. 12. Smith YR, Berman DR, Quint EH. Premenarchal vaginal discharge: findings of procedures to rule out foreign bodies. J Pediatr Adolesc Gynecol 2002;15:227–230. 13. Kaplowitz PB, Oberfield SE. Reexamination of the age limit for defining when puberty is precocious in girls in the United States: implications for evaluation and treatment. Drug and Therapeutics and Executive Committees of the Lawson Wilkins Pediatric Endocrine Society. Pediatrics 1999;104(Pt 1):936–941. 14. Flinn S. Child sexual abuse I: an overview. Advocates for Youth 1995 available at http://www.advocatesforyouth.org/index.php?option= com content&task=view&id=410&Itemid=336. 15. Anonymous. American Medical Association Diagnostic and Treatment Guidelines on Child Sexual Abuse. Arch Fam Med 1993;2:19–27. 16.


Gynecology_Novak

Gynecology_Novak. 15. Anonymous. American Medical Association Diagnostic and Treatment Guidelines on Child Sexual Abuse. Arch Fam Med 1993;2:19–27. 16. Iqbal CW, Jrebi NY, Zielinski MD et al. Patterns of accidental genital trauma in young girls and indications for operative management. J Pediatr Surg 2010;45:930–933. 17. Adams JA. Evolution of a classification scale: medical evaluation of suspected child sexual abuse. Child Maltreat 2001;6:31–36. 18. Sapp MV, Vandeven AM. Update on childhood sexual abuse. Curr Opin Pediatr 2005;17:258–264. 19. Holm K, Laursen EM, Brocks V, et al. Pubertal maturation of the internal genitalia: an ultrasound evaluation of 166 healthy girls. Ultrasound Obstet Gynecol 1995;6:175–181. 20. Oltmann SC, Garcia N, Barber R, et al. Can we preoperatively risk stratify ovarian masses for malignancy? J Pediatr Surg 2010;45:130– 134. 21. Servaes S, Victoria T, Lovrenski J, et al. Contemporary pediatric gynecologic imaging. Semin Ultrasound CT MR 2010;31:116–140. 22.


Gynecology_Novak

Gynecology_Novak. 21. Servaes S, Victoria T, Lovrenski J, et al. Contemporary pediatric gynecologic imaging. Semin Ultrasound CT MR 2010;31:116–140. 22. Stepanian M, Cohn DE. Gynecologic malignancies in adolescents. Adolesc Med Clin 2004;15:549–568. 23. Breen JL, Maxson WS. Ovarian tumors in children and adolescents. Clin Obstet Gynecol 1977;20:607–623. 24. Diamond MP, Baxter JW, Peerman CG Jr, et al. Occurrence of ovarian malignancy in childhood and adolescence: a community-wide evaluation. Obstet Gynecol 1988;71(Pt 1):858–860. 25. van Winter JT, Simmons PS, Podratz KC. Surgically treated adnexal masses in infancy, childhood, and adolescence. Am J Obstet Gynecol 1994;170:1780–1789. 26. Helmrath MA, Shin CE, Warner BW. Ovarian cysts in the pediatric population. Semin Pediatr Surg 1998;7:19–28. 27. Warner BW, Kuhn JC, Barr LL. Conservative management of large ovarian cysts in children: the value of serial pelvic ultrasonography. Surgery 1992;112:749–755. 28.


Gynecology_Novak

Gynecology_Novak. 27. Warner BW, Kuhn JC, Barr LL. Conservative management of large ovarian cysts in children: the value of serial pelvic ultrasonography. Surgery 1992;112:749–755. 28. Hernon M, McKenna J, Busby G, et al. The histology and management of ovarian cysts found in children and adolescents presenting to a children’s hospital from 1991 to 2007: a call for more paediatric gynaecologists. BJOG 2010;117:181–184. 29. Lee PA, Houk CP, Ahmed SF, et al. Consensus statement on management of intersex disorders. International Consensus Conference on Intersex. Pediatrics 2006;118:e488–e500. 30. Consortium on the Management of Disorders of Sex Development. Clinical guidelines for the management of disorders of sex development in childhood. Intersex Society of North America. Avail able at http://dsdguidelines.org/files/clinical.pdf. 31. Muram D, Buxton BH. The importance of the gynecologic examination in the newborn. J Tenn Med Assoc 1983;76:239. 32.


Gynecology_Novak

Gynecology_Novak. 31. Muram D, Buxton BH. The importance of the gynecologic examination in the newborn. J Tenn Med Assoc 1983;76:239. 32. Posner JC, Spandorfer PR. Early detection of imperforate hymen prevents morbidity from delays in diagnosis. Pediatrics 2005;115: 1008–1012. 33. Berenson AB. A longitudinal study of hymenal morphology in the first 3 years of life. Pediatrics 1995;95:490–496. 34. Hillard PJ. Imperforate hymen. eMedicine 2010. Available online at: http://emedicine.medscape.com/article/269050-overview 35. Garmendia G, Miranda N, Borroso S, et al. Regression of infancy hemangiomas with recombinant IFN-alpha 2b. J Interferon Cytokine Res 2001;21:31–38. 36. Bouchard S, Yazbeck S, Lallier M. Perineal hemangioma, anorectal malformation, and genital anomaly: a new association? J Pediatr Surg 1999;34:1133–1135. 37. Stricker T, Navratil F, Sennhauser FH. Vulvovaginitis in prepubertal girls. Arch Dis Child 2003;88:324–326. 38.


Gynecology_Novak

Gynecology_Novak. 37. Stricker T, Navratil F, Sennhauser FH. Vulvovaginitis in prepubertal girls. Arch Dis Child 2003;88:324–326. 38. Pokorny SF. The genital examination of the infant through adolescence. Curr Opin Obstet Gynecol 1993;5:753–757. 39. Emans SJ. Office Evaluation of the Child and Adolescent in Emans, SJ, Laufer MR, Goldstein DP, eds. Pediatric and adolescent gynecology. 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2005: 1–50 40. Van Eyk N, Allen L, Giesbrecht E, et al. Pediatric vulvovaginal disorders: a diagnostic approach and review of the literature. J Obstet Gynaecol Can 2009;31:850–862. 41. Garzon MC, Paller AS. Ultrapotent topical corticosteroid treatment of childhood genital lichen sclerosus. Arch Dermatol 1999;135:525– 528. 42. Muram D. Treatment of prepubertal girls with labial adhesions. J Pediatr Adolesc Gynecol 1999;12:67–70. 43.


Gynecology_Novak

Gynecology_Novak. 42. Muram D. Treatment of prepubertal girls with labial adhesions. J Pediatr Adolesc Gynecol 1999;12:67–70. 43. Shapiro RA, Makoroff KL. Sexually transmitted diseases in sexually abused girls and adolescents. Curr Opin Obstet Gynecol 2006;18:492–497. 44. Adams JA. Medical evaluation of suspected child sexual abuse. J Pediatr Adolesc Gynecol 2004;17:191–197. 45. Sinal SH, Woods CR. Human papillomavirus infections of the genital and respiratory tracts in young children. Semin Pediatr Infect Dis 2005;16:306–316. 46. Huppert JS, Gerber MA, Deitch HR, et al. Vulvar ulcers in young females: a manifestation of aphthosis. J Pediatr Adolesc Gynecol 2006;19:195–204. 47. Herman-Giddens ME. Vaginal foreign bodies and child sexual abuse. Arch Pediatr Adolesc Med 1994;148:195–200. 48.


Gynecology_Novak

Gynecology_Novak. 47. Herman-Giddens ME. Vaginal foreign bodies and child sexual abuse. Arch Pediatr Adolesc Med 1994;148:195–200. 48. Siegel RM, Schubert CJ, Myers PA, et al. The prevalence of sexually transmitted diseases in children and adolescents evaluated for sexual abuse in Cincinnati: rationale for limited STD testing in prepubertal girls. Pediatrics 1995;96:1090–1094. 49. Herbst R. Perineal streptococcal dermatitis/disease: recognition and management. Am J Clin Dermatol 2003;4:555–560. 50. Pokorny SF, Stormer J. Atraumatic removal of secretions from the prepubertal vagina. Am J Obstet Gynecol 1987;156:581–582. 51. Treloar AE, Boynton RE, Behn BG, et al. Variation of the human menstrual cycle through reproductive life. Int J Fertil 1967;12(Pt 2): 77–126. 52. Hillard PJ. Menstruation in young girls: a clinical perspective. Obstet Gynecol 2002;99:655–662. 53. Flug D, Largo RH, Prader A. Menstrual patterns in adolescent Swiss girls: a longitudinal study. Ann Hum Biol 1984;11:495–508.


Gynecology_Novak

Gynecology_Novak. 53. Flug D, Largo RH, Prader A. Menstrual patterns in adolescent Swiss girls: a longitudinal study. Ann Hum Biol 1984;11:495–508. 54. World Health Organization Task Force on Adolescent Reproductive Health. Longitudinal study of menstrual patterns in the early postmenarcheal period. Duration of bleeding episodes and menstrual cycles. J Adolesc Health Care 1986;7:236–244. 55. Fraser IS, Critchley HO, Munro MG, et al. A process designed to lead to international agreement on terminologies and definitions used to describe abnormalities of menstrual bleeding. Fertil Steril 2007;87:466–476. 56. Fraser IS, McCarron G, Markham R, et al. Blood and total ﬂuid content of menstrual discharge. Obstet Gynecol 1985;65: 194–198. 57. Warner PE, Critchley, HO, Lumsden, MA, et al. Menorrhagia II: is the 80-mL blood loss criterion useful in management of complaint of menorrhagia? Am J Obstet Gynecol 2004;190:1224–1229. 58.


Gynecology_Novak

Gynecology_Novak. 57. Warner PE, Critchley, HO, Lumsden, MA, et al. Menorrhagia II: is the 80-mL blood loss criterion useful in management of complaint of menorrhagia? Am J Obstet Gynecol 2004;190:1224–1229. 58. Warner PE, Critchley HO, Lumsden MA, et al. Menorrhagia I: measured blood loss, clinical features, and outcome in women with heavy periods: a survey with follow-up data. Am J Obstet Gynecol 2004;190:1216–1223. 59. Fraser IS, McCarron G, Markham R. A preliminary study of factors inﬂuencing perception of menstrual blood loss volume. Am J Obstet Gynecol 1984;149:788–793. 60. Venturoli S, Porcu E, Fabbri R, et al. Menstrual irregularities in adolescents: hormonal pattern and ovarian morphology. Horm Res 1986;24:269–279. 61. ACOG Committee Opinion No. 349. Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Obstet Gynecol 2006;108:1323–1328. 62.


Gynecology_Novak

Gynecology_Novak. 61. ACOG Committee Opinion No. 349. Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Obstet Gynecol 2006;108:1323–1328. 62. Apter D, Vihko R. Early menarche, a risk factor for breast cancer, indicates early onset of ovulatory cycles. J Clin Endocrinol Metab 1983;57:82–86. 63. Gavin L, MacKay AP, Brown K, et al. Sexual and reproductive health of persons aged 10–24 years—United States, 2002–2007. MMWR Surveill Summ 2009;58:1–58. 64. Fraser IS, Hickey M, Song JY. A comparison of mechanisms underlying disturbances of bleeding caused by spontaneous dysfunctional uterine bleeding or hormonal contraception. Hum Reprod 1996;11(Suppl 2):165–178. 65. Rosenberg MJ, Burnhill MS, Waugh MS, et al. Compliance and oral contraceptives: a review. Contraception 1995;52:137–141. 66. Rosenberg MJ, Long SC. Oral contraceptives and cycle control: a critical review of the literature. Adv Contracept 1992;8(Suppl 1): 35–45. 67.


Gynecology_Novak

Gynecology_Novak. 66. Rosenberg MJ, Long SC. Oral contraceptives and cycle control: a critical review of the literature. Adv Contracept 1992;8(Suppl 1): 35–45. 67. Oakley D, Sereika S, Bogue EL. Oral contraceptive pill use after an initial visit to a family planning clinic. Fam Plann Perspect 1991;23:150–154. 68. Balassone ML. Risk of contraceptive discontinuation among adolescents. J Adolesc Health Care 1989;10:527–533. 69. Woods JL, Shew ML, Tu W, et al. Patterns of oral contraceptive pill-taking and condom use among adolescent contraceptive pill users. J Adolesc Health 2006;39:381–387. 70. Mishell DR Jr, Guillebaud J, Westhoff C, et al. Combined hormonal contraceptive trials: variable data collection and bleeding assessment methodologies inﬂuence study outcomes and physician perception. Contraception 2007;75:4–10. 71. Fraser IS. Bleeding arising from the use of exogenous steroids. Baillieres Best Pract Res Clin Obstet Gynaecol 1999;13:203–222. 72.


Gynecology_Novak

Gynecology_Novak. 71. Fraser IS. Bleeding arising from the use of exogenous steroids. Baillieres Best Pract Res Clin Obstet Gynaecol 1999;13:203–222. 72. Abdel-Aleem H, d’Arcangues C, Vogelsong KM, et al. Treatment of vaginal bleeding irregularities induced by progestin only contraceptives. Cochrane Database Syst Rev 2007;4:CD003449. 73. Kaunitz AM. Long-acting injectable contraception with depot medroxyprogesterone acetate. Am J Obstet Gynecol 1994;170(Pt 2): 1543–1549. 74. Kaunitz AM. Current concepts regarding use of DMPA. J Reprod Med 2002;47(Suppl):785–789. 75. Lockwood CJ, Schatz F, Krikun G. Angiogenic factors and the endometrium following long term progestin only contraception. Histol Histopathol 2004;19:167–172. 76. Krettek JE, Arkin SI, Chaisilwattana P, et al. Chlamydia trachomatis in patients who used oral contraceptives and had intermenstrual spotting. Obstet Gynecol 1993;81(Pt 1):728–731. 77. Ferenczy A. Pathophysiology of endometrial bleeding. Maturitas 2003;45:1–14. 78.


Gynecology_Novak

Gynecology_Novak. 77. Ferenczy A. Pathophysiology of endometrial bleeding. Maturitas 2003;45:1–14. 78. Claessens EA, Cowell CA. Acute adolescent menorrhagia. Am J Obstet Gynecol 1981;139:277–280. 79. Philipp CS, Faiz A, Dowling N, et al. Age and the prevalence of bleeding disorders in women with menorrhagia. Obstet Gynecol 2005;105:61–66. 80. James AH. Bleeding disorders in adolescents. Obstet Gynecol Clin North Am 2009;36:153–162. 81. James AH, Kouides PA, Abdul-Kadir R, et al. Von Willebrand disease and other bleeding disorders in women: consensus on diagnosis and management from an international expert panel. Am J Obstet Gynecol 2009;201:12e1–e8. 82. Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2006. MMWR Recomm Rep 2006;55(RR11):1–94. 83. Gray-Swain MR, Peipert JF. Pelvic inﬂammatory disease in adolescents. Curr Opin Obstet Gynecol 2006;18:503–510. 84.


Gynecology_Novak

Gynecology_Novak. 83. Gray-Swain MR, Peipert JF. Pelvic inﬂammatory disease in adolescents. Curr Opin Obstet Gynecol 2006;18:503–510. 84. Carmina E, Oberfield SE, Lobo RA. The diagnosis of polycystic ovary syndrome in adolescents. Am J Obstet Gynecol 2010;203:201e1–e5. 85. Rosenfield RL, Lucky AW. Acne, hirsutism, and alopecia in adolescent girls. Clinical expressions of androgen excess. Endocrinol Metab Clin North Am 1993;22:507–532. 86. Legro RS. Detection of insulin resistance and its treatment in adolescents with polycystic ovary syndrome. J Pediatr Endocrinol Metab 2002;15(Suppl 5):1367–1378. 87. ACOG Practice Bulletin No. 109. Cervical cytology screening. Obstet Gynecol 2009;114:1409–1420. 88. Church DG, Vancil JM, Vasanawala SS. Magnetic resonance imaging for uterine and vaginal anomalies. Curr Opin Obstet Gynecol 2009;21:379–389. 89.


Gynecology_Novak

Gynecology_Novak. 88. Church DG, Vancil JM, Vasanawala SS. Magnetic resonance imaging for uterine and vaginal anomalies. Curr Opin Obstet Gynecol 2009;21:379–389. 89. Economy KE, Barnewolt C, Laufer MR. A comparison of MRI and laparoscopy in detecting pelvic structures in cases of vaginal agenesis. J Pediatr Adolesc Gynecol 2002;15:101–104. 90. Warren-Ulanch J, Arslanian S. Treatment of PCOS in adolescence. Best Pract Res Clin Endocrinol Metab 2006;20:311–330. 91. Demers C, Derzko C, David M, et al. Gynaecological and obstetric management of women with inherited bleeding disorders. Int J Gynaecol Obstet 2006;95:75–87. 92. Parker MA, Sneddon AE, Arbon P. The menstrual disorder of teenagers (MDOT) study: determining typical menstrual patterns and menstrual disturbance in a large population-based study of Australian teenagers. BJOG 2010;117:185–192. 93.


Gynecology_Novak

Gynecology_Novak. 93. Lethaby A, Augood C, Duckitt K, et al. Nonsteroidal anti-inﬂammatory drugs for heavy menstrual bleeding. Cochrane Database Syst Rev 2007;4:CD000400. 93a. U.S. Food and Drug Adminstration. FDA approves lysteda to treat heavy menstrual bleeding. http://www.fda.gov/About FDA/Stay Informed/RSSFeeds/ucm144575.htm 94. Finer LB, Henshaw SK. Disparities in rates of unintended pregnancy in the United States, 1994 and 2001. Perspect Sex Reprod Health 2006;38:90–96. 95. Anonymous. Facts on American teens’ sexual and reproductive health. New York: Guttmacher Institute, 2010. 96. Anonymous. How is the 3 in 10 statistic calculated? Fact Sheet, The National Campaign to Prevent Teen Pregnancy. Pregnancy. Wash ington, DC: 2008. Available at http://www.thenationalcampaign.org/ resources/pdf/FastFacts 3in10.pdf 97. Lethaby A, Irvine G, Cameron I. Cyclical progestogens for heavy menstrual bleeding. Cochrane Database Syst Rev 2008;1: CD001016. 98.


Gynecology_Novak

Gynecology_Novak. Lethaby A, Irvine G, Cameron I. Cyclical progestogens for heavy menstrual bleeding. Cochrane Database Syst Rev 2008;1: CD001016. 98. Speroff L, Fritz MA. Dysfunctional uterine bleeding. In Clinical gynecologic endocrinology and infertility. New York: Lippincott Williams & Wilkins, 2005:558–559. 99. Fraser IS, Porte RJ, Kouides PA, et al. A benefit-risk review of systemic haemostatic agents: part 2: in excessive or heavy menstrual bleeding. Drug Saf 2008;31:275–282. 100. Lethaby AE, Cooke I, Rees M. Progesterone or progestogenreleasing intrauterine systems for heavy menstrual bleeding. Cochrane Database Syst Rev 2005;4:CD002126. 101. Yen S, Saah T, Hillard PJ. IUDs and adolescents—an under-utilized opportunity for pregnancy prevention. J Pediatr Adolesc Gynecol 2010;23:123–128. 102. Nelson AL. Levonorgestrel intrauterine system: a first-line medical treatment for heavy menstrual bleeding. Womens Health (Lond) 2010;6:347–356. 103.


Gynecology_Novak

Gynecology_Novak. 102. Nelson AL. Levonorgestrel intrauterine system: a first-line medical treatment for heavy menstrual bleeding. Womens Health (Lond) 2010;6:347–356. 103. ACOG Committee Opinion No. 448. Menstrual manipulation for adolescents with disabilities. Obstet Gynecol 2009;114:1428–1431. 104. Kucuk T, Ertan K. Continuous oral or intramuscular medroxyprogesterone acetate versus the levonorgestrel releasing intrauterine system in the treatment of perimenopausal menorrhagia: a randomized, prospective, controlled clinical trial in female smokers. Clin Exp Obstet Gynecol 2008;35:57–60. 105. Martin-Johnston MK, Okoji OY, Armstrong A. Therapeutic amenorrhea in patients at risk for thrombocytopenia. Obstet Gynecol Surv 2008;63:395–402; quiz 405. 106. Legro RS, Pauli LG, Kunselman AR, et al. Effects of continuous versus cyclical oral contraception: a randomized controlled trial. J Clin Endocrinol Metab 2008;93:420–429. 107.


Gynecology_Novak

Gynecology_Novak. 106. Legro RS, Pauli LG, Kunselman AR, et al. Effects of continuous versus cyclical oral contraception: a randomized controlled trial. J Clin Endocrinol Metab 2008;93:420–429. 107. Pillai M, O’Brien K, Hill E. The levonorgestrel intrauterine system (Mirena) for the treatment of menstrual problems in adolescents with medical disorders, or physical or learning disabilities. BJOG 2010;117:216–221. 108. Miller L, Hughes JP. Continuous combination oral contraceptive pills to eliminate withdrawal bleeding: a randomized trial. Obstet Gynecol 2003;101:653–661. 109. Baldaszti E, Wimmer-Puchinger B, Loschke K. Acceptability of the long-term contraceptive levonorgestrel-releasing intrauterine system (Mirena): a 3-year follow-up study. Contraception 2003;67:87– 91. 110. Diaz S, Croxatto HB, Pavez M, et al. Clinical assessment of treatments for prolonged bleeding in users of Norplant implants. Contraception 1990;42:97–109. 111.


Gynecology_Novak

Gynecology_Novak. 110. Diaz S, Croxatto HB, Pavez M, et al. Clinical assessment of treatments for prolonged bleeding in users of Norplant implants. Contraception 1990;42:97–109. 111. Bulas DI, Ahlstrom PA, Sivit CJ, et al. Pelvic inﬂammatory disease in the adolescent: comparison of transabdominal and transvaginal sonographic evaluation. Radiology 1992;183:435–439. 112. Kozlowski KJ. Ovarian masses. Adolesc Med 1999;10:337–350, vii. 113. Looijenga LH, Hersmus R, de Leeuw BH, et al. Gonadal tumours and DSD. Best Pract Res Clin Endocrinol Metab 2010;24: 291–310. 114. Schellhas HF. Malignant potential of the dysgenetic gonad. Part 1. Obstet Gynecol 1974;44:298–309. 115. Cools M, Looijenga LH, Wolfenbuttel KP, et al. Disorders of sex development: update on the genetic background, terminology and risk for the development of germ cell tumors. World J Pediatr 2009;5:93–102. 116.


Gynecology_Novak

Gynecology_Novak. 116. Linam LE, Darolia R, Nafaa LN, et al. US findings of adnexal torsion in children and adolescents: size really does matter. Pediatr Radiol 2007;37:1013–1019. 117. Servaes S, Zurakowski D, Laufer MR, et al. Sonographic findings of ovarian torsion in children. Pediatr Radiol 2007;37:446–451. 118. Breech LL, Hillard PJ. Adnexal torsion in pediatric and adolescent girls. Curr Opin Obstet Gynecol 2005;17:483–489. 119. Laufer MR, Goltein L, Bush M, et al. Prevalence of endometriosis in adolescent girls with chronic pelvic pain not responding to conventional therapy. J Pediatr Adolesc Gynecol 1997;10:199–202. 120. Laufer MR, Sanfilippo J, Rose G. Adolescent endometriosis: diagnosis and treatment approaches. J Pediatr Adolesc Gynecol 2003;16(Suppl):S3–S11. 121. Capito C, Echaleb A, Lortat-Jacob S, et al. Pitfalls in the diagnosis and management of obstructive uterovaginal duplication: a series of 32 cases. Pediatrics 2008;122:e891–e897. 122.


Gynecology_Novak

Gynecology_Novak. 121. Capito C, Echaleb A, Lortat-Jacob S, et al. Pitfalls in the diagnosis and management of obstructive uterovaginal duplication: a series of 32 cases. Pediatrics 2008;122:e891–e897. 122. Martinez F, Lopez-Arregui E. Infection risk and intrauterine devices. Acta Obstet Gynecol Scand 2009;88:246–250. 123. Baeten JM, Nyange PM, Richardson BA, et al. Hormonal contraception and risk of sexually transmitted disease acquisition: results from a prospective study. Am J Obstet Gynecol 2001;185:380–385. 124. Eaton DK, Kann L, Kinchen S, et al. Youth risk behavior surveillance—United States, 2009. MMWR Surveill Summ 2010;59: 1–142. 125. Mol BW, Ankum WM, Bossuyt PM, et al. Contraception and the risk of ectopic pregnancy: a meta-analysis. Contraception 1995;52: 337–341. 126. Molander P, Cacciatore B, Sjoberg J, et al. Laparoscopic management of suspected acute pelvic inﬂammatory disease. J Am Assoc Gynecol Laparosc 2000;7:107–110. 127.


Gynecology_Novak

Gynecology_Novak. 126. Molander P, Cacciatore B, Sjoberg J, et al. Laparoscopic management of suspected acute pelvic inﬂammatory disease. J Am Assoc Gynecol Laparosc 2000;7:107–110. 127. Aboulghar MA, Mansour RT, Serour GI. Ultrasonographically guided transvaginal aspiration of tuboovarian abscesses and pyosalpinges: an optional treatment for acute pelvic inﬂammatory disease. Am J Obstet Gynecol 1995;172:1501–1503. 128. Buchweitz O, Malik E, Kressin P, et al. Laparoscopic management of tubo-ovarian abscesses: retrospective analysis of 60 cases. Surg Endosc 2000;14:948–950. 129. Muram D, Gold SS. Vulvar ulcerations in girls with myelocytic leukemia. South Med J 1993;86:293–294. 130. Reddy J, Laufer MR. Hypertrophic labia minora. J Pediatr Adolesc Gynecol 2010;23:3–6. 131. Ferris DG, Nyirjesy P, Sobel JD, et al. Over-the-counter antifungal drug misuse associated with patient-diagnosed vulvovaginal candidiasis. Obstet Gynecol 2002;99:419–425. 132.


Gynecology_Novak

Gynecology_Novak. 131. Ferris DG, Nyirjesy P, Sobel JD, et al. Over-the-counter antifungal drug misuse associated with patient-diagnosed vulvovaginal candidiasis. Obstet Gynecol 2002;99:419–425. 132. Workowski KA, Berman S. Sexually transmitted diseases Treatment guidelines 2010. MMWR Recomm Rep 2010;59(RR12):1–110. 133. Majewski S, et al. The impact of a quadrivalent human papillomavirus (types 6, 11, 16, 18) virus-like particle vaccine in European women aged 16 to 24. J Eur Acad Dermatol Venereol 2009;23:1147– 1155. 134. Huppert JS, Biro FM, Mehrabi J, et al. Urinary tract infection and chlamydia infection in adolescent females. J Pediatr Adolesc Gynecol 2003;16:133–137. 135. Cook RL, Hutchison SL, Ostergaard L, et al. Systematic review: noninvasive testing for Chlamydia trachomatis and Neisseria gonorrhoeae. Ann Intern Med 2005;142:914–925. 136. Schuchat A, Broome CV. Toxic shock syndrome and tampons. Epidemiol Rev 1991;13:99–112. 137.


Gynecology_Novak

Gynecology_Novak. 136. Schuchat A, Broome CV. Toxic shock syndrome and tampons. Epidemiol Rev 1991;13:99–112. 137. Hajjeh RA, Reingold A, Weil A, et al. Toxic shock syndrome in the United States: surveillance update, 1979–1996. Emerg Infect Dis 1999;5:807–810. 138. Hochwalt A, Parsonnet J, Modern P. Vaginal S. aureus and TSST-1 antibody prevalence among teens. Poster presentation at North American Society for Pediatric and Adolescent Gynecology, 2005. New Orleans, LA. 139. Reichman O, Sobel JD. MRSA infection of buttocks, vulva, and genital tract in women. Curr Infect Dis Rep 2009;11:465–470. 140. Brook I. Microbiology and management of polymicrobial female genital tract infections in adolescents. J Pediatr Adolesc Gynecol 2002;15:217–226. 141. Fraser IS, Critchley HO, Munro MG. Abnormal uterine bleeding: getting our terminology straight. Curr Opin Obstet Gynecol 2007;19:591–595. 142.


Gynecology_Novak

Gynecology_Novak. 141. Fraser IS, Critchley HO, Munro MG. Abnormal uterine bleeding: getting our terminology straight. Curr Opin Obstet Gynecol 2007;19:591–595. 142. Fraser IS, Warner P, Marantos PA. Estimating menstrual blood loss in women with normal and excessive menstrual ﬂuid volume. Obstet Gynecol 2001;98(Pt 1):806–814. 143. ACOG Practice Bulletin. Management of anovulatory bleeding. Int J Gynaecol Obstet 2001;72:263–271. 144. Mosher WD, Jones J. Use of contraception in the United States: 1982–2008. Vital Health Stat 2010;23:1–44. 145. Henshaw SK. Unintended pregnancy in the United States. Fam Plann Perspect 1998;30:24–29, 46. 146. Moodliar S, Bagratee JS, Moodley J. Medical vs. surgical evacuation of first-trimester spontaneous abortion. Int J Gynaecol Obstet 2005;91:21–26. 147. Ballagh SA, Harris HA, Demasio K. Is curettage needed for uncomplicated incomplete spontaneous abortion? Am J Obstet Gynecol 1998;179:1279–1282. 148.


Gynecology_Novak

Gynecology_Novak. 147. Ballagh SA, Harris HA, Demasio K. Is curettage needed for uncomplicated incomplete spontaneous abortion? Am J Obstet Gynecol 1998;179:1279–1282. 148. Fontanarosa M, Galiberti S, Fontanarosa N. Fertility after nonsurgical management of the symptomatic first-trimester spontaneous abortion. Minerva Ginecol 2007;59:591–594. 149. Sotiriadis A, Makrydimas G, Papatheodorou S, et al. Expectant, medical, or surgical management of first-trimester miscarriage: a meta-analysis. Obstet Gynecol 2005;105(Pt 1):1104–1113. 150. Stubblefield PG. Menstrual impact of contraception. Am J Obstet Gynecol 1994;170(Pt 2):1513–1522. 151. Rosenberg MJ, Waugh MS, Burnhill MS. Compliance, counseling and satisfaction with oral contraceptives: a prospective evaluation. Fam Plann Perspect 1998;30:89–92, 104. 152. Rosenberg MJ, Waugh MS, Meehan TE. Use and misuse of oral contraceptives: risk indicators for poor pill taking and discontinuation. Contraception 1995;51:283–288. 153.


Gynecology_Novak

Gynecology_Novak. 152. Rosenberg MJ, Waugh MS, Meehan TE. Use and misuse of oral contraceptives: risk indicators for poor pill taking and discontinuation. Contraception 1995;51:283–288. 153. Bachmann G, Korner P. Bleeding patterns associated with non-oral hormonal contraceptives: a review of the literature. Contraception 2009;79:247–258. 154. ACOG Committee Opinion No. 450. Increasing use of contraceptive implants and intrauterine devices to reduce unintended pregnancy. Obstet Gynecol 2009;114:1434–1438. 155. Krassas GE. Thyroid disease and female reproduction. Fertil Steril 2000;74:1063–1070. 156. Rebar RW. Premature ovarian failure. Obstet Gynecol 2009;113: 1355–1363. 157. Nelson LM. Clinical practice. Primary ovarian insufficiency. N Engl J Med 2009;360:606–614. 158. Azziz R, Woods KS, Reyna R, et al. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab 2004;89:2745–1749. 159.


Gynecology_Novak

Gynecology_Novak. 158. Azziz R, Woods KS, Reyna R, et al. The prevalence and features of the polycystic ovary syndrome in an unselected population. J Clin Endocrinol Metab 2004;89:2745–1749. 159. Guzick DS. Polycystic ovary syndrome. Obstet Gynecol 2004;103: 181–193. 160. Palomba S, Falbo A, Russo T, et al. Systemic and local effects of metformin administration in patients with polycystic ovary syndrome (PCOS): relationship to the ovulatory response. Hum Reprod 2010;25:1005–1013. 161. Cibula D, Fanta M, Vrbikova J, et al. The effect of combination therapy with metformin and combined oral contraceptives (COC) versus COC alone on insulin sensitivity, hyperandrogenaemia, SHBG and lipids in PCOS patients. Hum Reprod 2005;20:180–184. 162. Ryan GL, Syrop CH, Van Voorhis BJ. Role, epidemiology, and natural history of benign uterine mass lesions. Clin Obstet Gynecol 2005;48:312–324. 163.


Gynecology_Novak

Gynecology_Novak. 162. Ryan GL, Syrop CH, Van Voorhis BJ. Role, epidemiology, and natural history of benign uterine mass lesions. Clin Obstet Gynecol 2005;48:312–324. 163. Okolo S. Incidence, aetiology and epidemiology of uterine fibroids. Best Pract Res Clin Obstet Gynaecol 2008;22:571–588. 164. Day Baird D, Dunson DB, Hill MC, et al. High cumulative incidence of uterine leiomyoma in black and white women: ultrasound evidence. Am J Obstet Gynecol 2003;188:100–107. 165. Tamura-Sadamori R, Emoto M, Naganuma Y, et al. The sonohysterographic difference in submucosal uterine fibroids and endometrial polyps treated by hysteroscopic surgery. J Ultrasound Med 2007;26:941–948. 166. Lieng M, Qvigstad E, Dahl GF, et al. Flow differences between endometrial polyps and cancer: a prospective study using intravenous contrast-enhanced transvaginal color ﬂow Doppler and three-dimensional power Doppler ultrasound. Ultrasound Obstet Gynecol 2008;32:935–940. 167.


Gynecology_Novak

Gynecology_Novak. 167. Dreisler E, Stampe Sorenson S, Ibsen PH, et al. Prevalence of endometrial polyps and abnormal uterine bleeding in a Danish population aged 20–74 years. Ultrasound Obstet Gynecol 2009;33:102– 108. 168. Lieng M, Istre O, Sandvik L, et al. Prevalence, 1-year regression rate, and clinical significance of asymptomatic endometrial polyps: cross-sectional study. J Minim Invasive Gynecol 2009;16:465–471. 169. DeWaay DJ, Syrop CH, Nygaard IE, et al. Natural history of uterine polyps and leiomyomata. Obstet Gynecol 2002;100:3–7. 170. Lieng M, Istre O, Qvigstad E. Treatment of endometrial polyps: a systematic review. Acta Obstet Gynecol Scand 2010;89:992–1002. 171. James AH, Manco-Johnson MJ, Yawn BP, et al. Von Willebrand disease: key points from the 2008 National Heart, Lung, and Blood Institute guidelines. Obstet Gynecol 2009;114:674–678. 172. Dubinsky TJ. Value of sonography in the diagnosis of abnormal vaginal bleeding. J Clin Ultrasound 2004;32:348–353. 173.


Gynecology_Novak

Gynecology_Novak. 172. Dubinsky TJ. Value of sonography in the diagnosis of abnormal vaginal bleeding. J Clin Ultrasound 2004;32:348–353. 173. Bignardi T, Van den Bosch T, Condous G. Abnormal uterine and post-menopausal bleeding in the acute gynaecology unit. Best Pract Res Clin Obstet Gynaecol 2009;23:595–607. 174. Breitkopf DM, Frederickson RA, Snyder RR. Detection of benign endometrial masses by endometrial stripe measurement in premenopausal women. Obstet Gynecol 2004;104:120–125. 175. Lane BF, Wong-You-Cheong JJ. Imaging of endometrial pathology. Clin Obstet Gynecol 2009;52:57–72. 176. Stock RJ, Kanbour A. Prehysterectomy curettage. Obstet Gynecol 1975;45:537–541. 177. Grimes DA. Diagnostic dilation and curettage: a reappraisal. Am J Obstet Gynecol 1982;142:1–6. 178. van Dongen H, de Kroon CD, Jacobi CE, et al. Diagnostic hysteroscopy in abnormal uterine bleeding: a systematic review and meta-analysis. BJOG 2007;114:664–675. 179.


Gynecology_Novak

Gynecology_Novak. 178. van Dongen H, de Kroon CD, Jacobi CE, et al. Diagnostic hysteroscopy in abnormal uterine bleeding: a systematic review and meta-analysis. BJOG 2007;114:664–675. 179. Clark TJ, Mann CH, Shah N, et al. Accuracy of outpatient endometrial biopsy in the diagnosis of endometrial cancer: a systematic quantitative review. BJOG 2002;109:313–321. 180. Clark TJ, Mann CH, Shah N, et al. Accuracy of outpatient endometrial biopsy in the diagnosis of endometrial hyperplasia. Acta Obstet Gynecol Scand 2001;80:784–793. 181. Heliovaara-Peippo S, Halmesmaki K, Hurskainen R, et al. The effect of hysterectomy or levonorgestrel-releasing intrauterine system on lower abdominal pain and back pain among women treated for menorrhagia: a five-year randomized controlled trial. Acta Obstet Gynecol Scand 2009;88:1389–1396. 182.


Gynecology_Novak

Gynecology_Novak. 182. Dueholm M. Levonorgestrel-IUD should be offered before hysterectomy for abnormal uterine bleeding without uterine structural abnormalities: there are no more excuses! Acta Obstet Gynecol Scand 2009;88:1302–1304. 183. ACOG Practice Bulletin. Alternatives to hysterectomy in the management of leiomyomas. Obstet Gynecol 2008;112(Pt 1):387–400. 184. Farquhar C, Brown J. Oral contraceptive pill for heavy menstrual bleeding. Cochrane Database Syst Rev 2009;4:CD000154. 185. ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists, management of endometrial cancer. Obstet Gynecol 2005106: 413–425. 186. Cetin NN, Karabacak O, Korucuoglu U, et al. Gonadotropinreleasing hormone analog combined with a low-dose oral contraceptive to treat heavy menstrual bleeding. Int J Gynaecol Obstet 2009;104:236–239. 187. Haynes PJ, Hodgson H, Anderson AB, et al. Measurement of menstrual blood loss in patients complaining of menorrhagia. BJOG 1977;84:763–788. 188.


Gynecology_Novak

Gynecology_Novak. 187. Haynes PJ, Hodgson H, Anderson AB, et al. Measurement of menstrual blood loss in patients complaining of menorrhagia. BJOG 1977;84:763–788. 188. Nickelsen C. Diagnostic and curative value of uterine curettage. Acta Obstet Gynecol Scand 1986;65:693–697. 189. Banu NS, Manyonda IT. Alternative medical and surgical options to hysterectomy. Best Pract Res Clin Obstet Gynaecol 2005;19:431– 449. 190. Lethaby A, Shepperd S, Cooke I, et al. Endometrial resection / ablation techniques for heavy menstrual bleeding. Cochrane Database Syst Rev 2009;4:CD001501. 191. Kuppermann M, Learman LA, Schembri M, et al. Predictors of hysterectomy use and satisfaction. Obstet Gynecol 2010;115:543– 551. 192. Persson P, Brynhildsen J, Kjolhede P. Short-term recovery after subtotal and total abdominal hysterectomy—a randomised clinical trial. BJOG 2010;117:469–478. 193.


Gynecology_Novak

Gynecology_Novak. 192. Persson P, Brynhildsen J, Kjolhede P. Short-term recovery after subtotal and total abdominal hysterectomy—a randomised clinical trial. BJOG 2010;117:469–478. 193. Yen JY, Chen YH, Long CY, et al. Risk factors for major depressive disorder and the psychological impact of hysterectomy: a prospective investigation. Psychosomatics 2008;49:137–142. 194. Hernandez E, Miyazawa K. The pelvic mass. Patients’ ages and pathologic findings. J Reprod Med 1988;33:361–364. 195. Wallach EE, Vlahos NF. Uterine myomas: an overview of development, clinical features, and management. Obstet Gynecol 2004; 104:393–406. 196. Cannistra SA. Cancer of the ovary. N Engl J Med 2004;351:2519– 2529. 197. Koonings PP, Campbell K, Mishell DR Jr, et al. Relative frequency of primary ovarian neoplasms: a 10-year review. Obstet Gynecol 1989;74:921–926. 198.


Gynecology_Novak

Gynecology_Novak. 197. Koonings PP, Campbell K, Mishell DR Jr, et al. Relative frequency of primary ovarian neoplasms: a 10-year review. Obstet Gynecol 1989;74:921–926. 198. Holt VL, Cushing-Haugen KL, Daling JR. Risk of functional ovarian cyst: effects of smoking and marijuana use according to body mass index. Am J Epidemiol 2005;161:520–525. 199. Christensen JT, Boldsen JL, Westergaard JG. Functional ovarian cysts in premenopausal and gynecologically healthy women. Contraception 2002;66:153–157. 200. Cochrane Update. Oral contraceptives for functional ovarian cysts. Obstet Gynecol 2009;114:679–680. 201. Grimes DA, Hughes JM. Use of multiphasic oral contraceptives and hospitalizations of women with functional ovarian cysts in the United States. Obstet Gynecol 1989;73: 1037–1039. 202. Hallatt JG, Steele CH Jr, Snyder M. Ruptured corpus luteum with hemoperitoneum: a study of 173 surgical cases. Am J Obstet Gynecol 1984;149:5–9. 203.


Gynecology_Novak

Gynecology_Novak. 202. Hallatt JG, Steele CH Jr, Snyder M. Ruptured corpus luteum with hemoperitoneum: a study of 173 surgical cases. Am J Obstet Gynecol 1984;149:5–9. 203. Joshi R, Dunaif A. Ovarian disorders of pregnancy. Endocrinol Metab Clin North Am 1995;24:153–169. 204. Vessey M, Metcalfe A, Wells C, et al. Ovarian neoplasms, functional ovarian cysts, and oral contraceptives. Br Med J (Clin Res Ed) 1987;294:1518–1520. 205. Holt VL, Daling JR, McKnight B, et al. Functional ovarian cysts in relation to the use of monophasic and triphasic oral contraceptives. Obstet Gynecol 1992;79:529–533. 206. Lanes SF, Birmann B, Walker AM, et al. Oral contraceptive type and functional ovarian cysts. Am J Obstet Gynecol 1992;166:956– 961. 207. Grimes DA, Godwin AJ, Rubin A, et al. Ovulation and follicular development associated with three low-dose oral contraceptives: a randomized controlled trial. Obstet Gynecol 1994;83:29–34. 208.


Gynecology_Novak

Gynecology_Novak. Grimes DA, Godwin AJ, Rubin A, et al. Ovulation and follicular development associated with three low-dose oral contraceptives: a randomized controlled trial. Obstet Gynecol 1994;83:29–34. 208. Hart RJ, Hickey M, Maouris P, et al. Excisional surgery versus ablative surgery for ovarian endometriomata. Cochrane Database Syst Rev 2008;2:CD004992. 209. Anonymous. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004;81:19–25. 210. Jonard S, Robert Y, Dewailly D. Revisiting the ovarian volume as a diagnostic criterion for polycystic ovaries. Hum Reprod 2005;20:2893–2898. 211. Polson DW, Adams J, Wadsworth J, et al. Polycystic ovaries—a common finding in normal women. Lancet 1988;1:870–872. 212.


Gynecology_Novak

Gynecology_Novak. 211. Polson DW, Adams J, Wadsworth J, et al. Polycystic ovaries—a common finding in normal women. Lancet 1988;1:870–872. 212. Karimzadeh MA, Javedani M. An assessment of lifestyle modification versus medical treatment with clomiphene citrate, metformin, and clomiphene citrate-metformin in patients with polycystic ovary syndrome. Fertil Steril 2010;94:216–220. 213. Kurman R, ed. Blaustein’s pathology of the female genital track. Vol. 5. New York: Springer, 2005. 214. Templeman CL, Fallat ME, Lam AM, et al. Managing mature cystic teratomas of the ovary. Obstet Gynecol Surv 2000;55: 738–745. 215. Milingos S, Protopapas A, Drakakis P, et al. Laparoscopic treatment of ovarian dermoid cysts: eleven years’ experience. J Am Assoc Gynecol Laparosc 2004;11:478–485. 216. Laberge PY, Levesque S. Short-term morbidity and long-term recurrence rate of ovarian dermoid cysts treated by laparoscopy versus laparotomy. J Obstet Gynaecol Can 2006;28:789–793. 217.


Gynecology_Novak

Gynecology_Novak. 216. Laberge PY, Levesque S. Short-term morbidity and long-term recurrence rate of ovarian dermoid cysts treated by laparoscopy versus laparotomy. J Obstet Gynaecol Can 2006;28:789–793. 217. Kondo W, Bourdel N, Cotte B, et al. Does prevention of intraperitoneal spillage when removing a dermoid cyst prevent granulomatous peritonitis? BJOG 2010;117:1027–1030. 218. Stein AL, Koonings PP, Schlaerth JB, et al. Relative frequency of malignant parovarian tumors: should parovarian tumors be aspirated? Obstet Gynecol 1990;75:1029–1031. 219. Van Calster B, Timmerman D, Bourne T, et al. Discrimination between benign and malignant adnexal masses by specialist ultrasound examination versus serum CA-125. J Natl Cancer Inst 2007;99:1706–1714. 220. ACOG Practice Bulletin. Management of adnexal masses. Obstet Gynecol 2007;110:201–214. 221.


Gynecology_Novak

Gynecology_Novak. 220. ACOG Practice Bulletin. Management of adnexal masses. Obstet Gynecol 2007;110:201–214. 221. Liu J, Xu Y, Wang J. Ultrasonography, computed tomography and magnetic resonance imaging for diagnosis of ovarian carcinoma. Eur J Radiol 2007;62:328–334. 222. Medeiros LR, Rosa DD, da Rosa MI, et al. Accuracy of ultrasonography with color Doppler in ovarian tumor: a systematic quantitative review. Int J Gynecol Cancer 2009;19:1214–1220. 223. Huchon C, Staraci S, Fauconnier A. Adnexal torsion: a predictive score for pre-operative diagnosis. Hum Reprod 2010;25:2276– 2280. 224. Huchon C, Fauconnier A. Adnexal torsion: a literature review. Eur J Obstet Gynecol Reprod Biol 2010;150:8–12. 225. Bottomley C, Bourne T. Diagnosis and management of ovarian cyst accidents. Best Pract Res Clin Obstet Gynaecol 2009;23:711–724. 226.


Gynecology_Novak

Gynecology_Novak. 225. Bottomley C, Bourne T. Diagnosis and management of ovarian cyst accidents. Best Pract Res Clin Obstet Gynaecol 2009;23:711–724. 226. Vaisbuch E, Dgani R, Ben-Arie A, et al. The role of laparoscopy in ovarian tumors of low malignant potential and early-stage ovarian cancer. Obstet Gynecol Surv 2005;60:326–330. 227. Cho JE, Liu C, Gossner G, et al. Laparoscopy and gynecologic oncology. Clin Obstet Gynecol 2009;52:313–326. 228. Mettler L, Meinhold-Heerlein I. The value of laparoscopic surgery to stage gynecological cancers: present and future. Minerva Ginecol 2009;61:319–337. 229. Minelli L, Ceccaroni M, Ruffo G, et al. Laparoscopic conservative surgery for stage IV symptomatic endometriosis: short-term surgical complications. Fertil Steril 2010;94:1218–1222. 230. Medeiros LR, Rosa DD, Bozzetti MC, et al. Laparoscopy versus laparotomy for benign ovarian tumour. Cochrane Database Syst Rev 2009;2:CD004751. 231.


Gynecology_Novak

Gynecology_Novak. 230. Medeiros LR, Rosa DD, Bozzetti MC, et al. Laparoscopy versus laparotomy for benign ovarian tumour. Cochrane Database Syst Rev 2009;2:CD004751. 231. Ragnarsson-Olding BK, Kanter-Lewensohn LR, Lagerlof B, et al. Malignant melanoma of the vulva in a nationwide, 25-year study of 219 Swedish females: clinical observations and histopathologic features. Cancer 1999;86:1273–1284. 232. Ribe A. Melanocytic lesions of the genital area with attention given to atypical genital nevi. J Cutan Pathol 2008;35(Suppl 2):24–27. 233. Hood AF, Lumadue J. Benign vulvar tumors. Dermatol Clin 1992; 10:371–385. 234. Trager JD. Pubic hair removal—pearls and pitfalls. J Pediatr Adolesc Gynecol 2006;19:117–123. 235. Alikhan A, Lynch PJ, Eisen DB. Hidradenitis suppurativa: a comprehensive review. J Am Acad Dermatol 2009;60:539–563. 236. Hermanns-Le T, Scheen A, Pierard GE. Acanthosis nigricans associated with insulin resistance: pathophysiology and management. Am J Clin Dermatol 2004;5:199–203.


Gynecology_Novak

Gynecology_Novak. 236. Hermanns-Le T, Scheen A, Pierard GE. Acanthosis nigricans associated with insulin resistance: pathophysiology and management. Am J Clin Dermatol 2004;5:199–203. 237. Higgins SP, Freemark M, Prose NS. Acanthosis nigricans: a practical approach to evaluation and management. Dermatol Online J 2008;14:2. 238. Kaufman R, Faro S, Brown D, eds. Cystic tumors in Benign diseases of the vulva and vagina. 5 ed. Philadelphia: Elsevier Mosby, 2005:449. 239. Word B. Office treatment of cysts and abscess of Bartholin’s gland duct. South Med J 1968;61(5): 514-8. 240. Farage MA, Galask RP. Vulvar vestibulitis syndrome: a review. Eur J Obstet Gynecol Reprod Biol 2005;123:9–16. 241. Petersen CD, Lundvall L, Kristensen E, et al. Vulvodynia. Definition, diagnosis and treatment. Acta Obstet Gynecol Scand 2008; 87:893–901. 242. Moyal-Barracco M, Lynch PJ. 2003 ISSVD terminology and classification of vulvodynia: a historical perspective. J Reprod Med 2004;49:772–777. 243.


Gynecology_Novak

Gynecology_Novak. 242. Moyal-Barracco M, Lynch PJ. 2003 ISSVD terminology and classification of vulvodynia: a historical perspective. J Reprod Med 2004;49:772–777. 243. Friedrich EG Jr. Vulvar vestibulitis syndrome. J Reprod Med 1987;32:110–114. 244. Sakane T, Takeno M, Suzuki N, et al. Behcet’s disease. N Engl J Med 1999;341:1284–1291. 245. Gul A. Standard and novel therapeutic approaches to Behcet’s disease. Drugs 2007;67:2013–2022. 246. Furness S, Roberts H, Marjoribanks J, et al. Hormone therapy in postmenopausal women and risk of endometrial hyperplasia. Cochrane Database Syst Rev 2009;2:CD000402. 247. Sitruk-Ware R. New hormonal therapies and regimens in the post-menopause: routes of administration and timing of initiation. Climacteric 2007;10:358–370. 248. Kenemans P, van Unnik GA, Mijatovic V, et al. Perspectives in hormone replacement therapy. Maturitas 2001;38(Suppl 1):S41– S48. 249.


Gynecology_Novak

Gynecology_Novak. 248. Kenemans P, van Unnik GA, Mijatovic V, et al. Perspectives in hormone replacement therapy. Maturitas 2001;38(Suppl 1):S41– S48. 249. Shoupe D. HRT dosing regimens: continuous versus cyclic-pros and cons. Int J Fertil Womens Med 2001;46:7–15. 250. ACOG Committee Opinion No. 426. The role of transvaginal ultrasonography in the evaluation of postmenopausal bleeding. Obstet Gynecol 2009;113(Pt 1):462–464. 251. Hann LE, Kim CM, Gonen M, et al. Sonohysterography compared with endometrial biopsy for evaluation of the endometrium in tamoxifen-treated women. J Ultrasound Med 2003;22:1173– 1179. 252. Savelli L, De Iaco P, Santini D, et al. Histopathologic features and risk factors for benignity, hyperplasia, and cancer in endometrial polyps. Am J Obstet Gynecol 2003;188:927–931. 253. Karlsson B, Granberg S, Wikland M, et al. Transvaginal ultrasonography of the endometrium in women with postmenopausal bleeding—a Nordic multicenter study. Am J Obstet Gynecol 1995; 172:1488–1494.


Gynecology_Novak

Gynecology_Novak. Karlsson B, Granberg S, Wikland M, et al. Transvaginal ultrasonography of the endometrium in women with postmenopausal bleeding—a Nordic multicenter study. Am J Obstet Gynecol 1995; 172:1488–1494. 254. Epstein E, Valentin L. Managing women with post-menopausal bleeding. Best Pract Res Clin Obstet Gynaecol 2004;18:125–143. 255. Timmermans A, Opmeer BC, Khan KS, et al. Endometrial thickness measurement for detecting endometrial cancer in women with postmenopausal bleeding: a systematic review and meta-analysis. Obstet Gynecol 2010;116:160–167. 256. Castelo-Branco C, Cancelo MJ, Villero J, et al. Management of post-menopausal vaginal atrophy and atrophic vaginitis. Maturitas 2005;52(Suppl 1):S46–S52. 257. Santoro N, Komi J. Prevalence and impact of vaginal symptoms among postmenopausal women. JSexMed 2009;6:2133–2142. 258.


Gynecology_Novak

Gynecology_Novak. 257. Santoro N, Komi J. Prevalence and impact of vaginal symptoms among postmenopausal women. JSexMed 2009;6:2133–2142. 258. Dorr MB, Nelson AL, Mayer PR, et al. Plasma estrogen concentrations after oral and vaginal estrogen administration in women with atrophic vaginitis. Fertil Steril 2010;94:2365–2368. 259. Lacey JV Jr, Chia VM. Endometrial hyperplasia and the risk of progression to carcinoma. Maturitas 2009;63:39–44. 260. Pavlik EJ, DePriest PD, Gallion HH, et al. Ovarian volume related to age. Gynecol Oncol 2000;77:410–412. 261. Ueland FR, DePriest PD, Desimone CP, et al. The accuracy of examination under anesthesia and transvaginal sonography in evaluating ovarian size. Gynecol Oncol 2005;99:400–403. 262. Goff BA, Mandel LS, Melancon CH, et al. Frequency of symptoms of ovarian cancer in women presenting to primary care clinics. JAMA 2004;291:2705–2712. 263.


Gynecology_Novak

Gynecology_Novak. 262. Goff BA, Mandel LS, Melancon CH, et al. Frequency of symptoms of ovarian cancer in women presenting to primary care clinics. JAMA 2004;291:2705–2712. 263. Rossing MA, Wicklund KG, Cushing-Haugen KL, et al. Predictive value of symptoms for early detection of ovarian cancer. J Natl Cancer Inst 2010;102:222–229. 264. Greenlee RT, Kessel B, Williams CR, et al. Prevalence, incidence, and natural history of simple ovarian cysts among women >55 years old in a large cancer screening trial. Am J Obstet Gynecol 2010;202:373e1–e9. 265. Modesitt SC, Pavlik EJ, Ueland FR, et al. Risk of malignancy in unilocular ovarian cystic tumors less than 10 centimeters in diameter. Obstet Gynecol 2003;102:594–599. 266. ACOG Committee Opinion No. 280. The role of the generalist obstetrician-gynecologist in the early detection of ovarian cancer. Obstet Gynecol 2002;100:1413–1416. 267.


Gynecology_Novak

Gynecology_Novak. 266. ACOG Committee Opinion No. 280. The role of the generalist obstetrician-gynecologist in the early detection of ovarian cancer. Obstet Gynecol 2002;100:1413–1416. 267. Lynch PJ, Moyal-Barracco M, Bogliatto F, et al. 2006 ISSVD classification of vulvar dermatoses: pathologic subsets and their clinical correlates. J Reprod Med 2007;52:3–9. 268. Maclean AB, Jones RW, Scurry J, et al. Vulvar cancer and the need for awareness of precursor lesions. J Low Genit Tract Dis 2009;13:115–117. 269. Ayhan A, Guven ES, Guven S, et al. Testosterone versus clobetasol for maintenance of vulvar lichen sclerosus associated with variable degrees of squamous cell hyperplasia. Acta Obstet Gynecol Scand 2007;86:715–719. 270. Sinha P, Sorinola O, Luesley DM. Lichen sclerosus of the vulva. Long-term steroid maintenance therapy. J Reprod Med 1999;44:621– 624. 271. Bradford J, Fischer G. Long-term management of vulval lichen sclerosus in adult women. Aust N Z J Obstet Gynaecol 2010;50:148– 152.


Gynecology_Novak

Gynecology_Novak. 271. Bradford J, Fischer G. Long-term management of vulval lichen sclerosus in adult women. Aust N Z J Obstet Gynaecol 2010;50:148– 152. 272. Yesudian PD. The role of calcineurin inhibitors in the management of lichen sclerosus. Am J Clin Dermatol 2009;10:313–318. 273. Sideri M, Jones RW, Wilkinson EJ, et al. Squamous vulvar intraepithelial neoplasia: 2004 modified terminology, ISSVD Vulvar Oncology Subcommittee. J Reprod Med 2005;50:807–810. 274. Ballagh SA. Vaginal hormone therapy for urogenital and menopausal symptoms. Semin Reprod Med 2005;23:126–140. 275. Palacios S. Managing urogenital atrophy. Maturitas 2009;63:315– 318. William H. Parker Fibroids are very common and most are asymptomatic and can be managed expectantly. There is no definite relationship between oral contraceptives and the presence of fibroids. First-degree relatives of women with fibroids have a 2.5 times increased risk of developing fibroids.


Gynecology_Novak

Gynecology_Novak. There is no definite relationship between oral contraceptives and the presence of fibroids. First-degree relatives of women with fibroids have a 2.5 times increased risk of developing fibroids. The risk of having fibroids is 2.9 times greater in African American women than in white women. Women with fibroids are only slightly more likely to experience pelvic pain than women without fibroids. Rapid uterine growth is not well defined, and almost never indicates sarcoma in premenopausal women; sarcomas are rare and more likely occur in postmenopausal women with symptoms of pain and bleeding. Sonography is the most readily available and least costly imaging technique to differentiate fibroids from other pelvic pathology; however, MRI permits more precise evaluation of the number, size and position of fibroids and can better evaluate the proximity to the endometrial cavity.


Gynecology_Novak

Gynecology_Novak. The presence of submucosal fibroids decreases fertility and removing them can increase fertility; subserosal fibroids do not affect fertility and removing them does not increase fertility; and intramural fibroids may slightly decrease fertility, but removal does not increase fertility. Most fibroids do not increase in size during pregnancy. For women who are mildly or moderately symptomatic with fibroids, watchful waiting may allow treatment to be deferred, perhaps indefinitely. As women approach menopause watchful waiting may be considered because there is limited time to develop new symptoms, and after menopause bleeding stops and fibroids decrease in size. Surgical treatment options include abdominal myomectomy, laparoscopic myomectomy, hysteroscopic myomectomy, endometrial ablation, and abdominal, vaginal, or laparoscopic hysterectomy. An inability to evaluate the ovaries on pelvic examination is not an indication for surgery.


Gynecology_Novak

Gynecology_Novak. An inability to evaluate the ovaries on pelvic examination is not an indication for surgery. Myomectomy should be considered as a safe alternative to hysterectomy, even for those women who have large uterine fibroids and wish to retain their uterus. Submucous fibroids, sometimes associated with increased menstrual bleeding or infertility, often can be removed hysteroscopically. Routine ultrasound follow-up is sensitive, but may detect many clinically insignificant fibroids. Uterine artery embolization (UAE) is an effective treatment for selected women with uterine fibroids. The effects of UAE on early ovarian failure, fertility, and pregnancy are unclear.


Gynecology_Novak

Gynecology_Novak. Uterine artery embolization (UAE) is an effective treatment for selected women with uterine fibroids. The effects of UAE on early ovarian failure, fertility, and pregnancy are unclear. Fibroids (leiomyomas, myomas) are an important health care concern because they are the most frequent indication for the performance of hysterectomy, accounting for nearly 240,000 such procedures in the United States (1). In comparison, approximately 30,000 myomectomies were performed that year. Inpatient surgery for fibroids costs $2.1 billion per year in the United States, and the cost of outpatient surgeries, medical and nonmedical costs, and time away from work or family add significantly to these expenditures (2). Origins of Uterine Fibroids Fibroids are benign, monoclonal tumors of the smooth muscle cells of the myometrium and contain large aggregations of extracellular matrix composed of collagen, elastin, fibronectin, and proteoglycan (3).


Gynecology_Novak

Gynecology_Novak. Incidence Fibroids are remarkably common. Fine serial sectioning of uteri from 100 consecutive women subjected to hysterectomy discovered fibroids in 77%, some as small as 2 mm (4). A random sampling of women ages 35 to 49, screened by self-report, medical record review, and sonography, found that among African American women by age 35 the incidence of fibroids was 60%, and it was over 80% by age 50 (Fig. 15.1). White women have an incidence of 40% at age 35 and almost 70% by age 50 (5). Rate 0.004 0.0035 0.003 0.0025 0.002 0.0015 0.001 0.0005 0 White Black Hispanic White Black Hispanic Hysterectomy rate 0.018 0.016 0.014 0.012 0.01 0.008 0.006 0.004 0.002 0 Figure 15.1 A: Age-and race-specific incidence of myomectomy, 1997, based on NIS and


Gynecology_Novak

Gynecology_Novak. White Black Hispanic Hysterectomy rate 0.018 0.016 0.014 0.012 0.01 0.008 0.006 0.004 0.002 0 Figure 15.1 A: Age-and race-specific incidence of myomectomy, 1997, based on NIS and U.S. Census Bureau estimates. B: Age-and race-specific incidence of hysterectomy for fibroids, 1997, based on NIS and U.S. Census Bureau estimates. (From Health Services/ Technology Assessment Tests (HSTAT). Available at http://www.ncbi.nlm.nih.gov/books/ bv.fcgi?rid=hstat1.section.48317.)


Gynecology_Novak

Gynecology_Novak. Serum levels of estrogen and progesterone are similar in women with and without clinically detectable fibroids. However, as a result of increased levels of aromatase within fibroids, de novo production of estradiol is higher than in normal myometrium (12). Progesterone is important in the pathogenesis of fibroids, which have increased concentrations of progesterone receptors A and B compared with normal myometrium (13,14). The highest mitotic counts are found in fibroids at the peak of progesterone production (15). Gonadotropin-releasing hormone (GnRH) agonists decrease the size of fibroids, but progestin given concurrently with GnRH prevents a decrease in size (14).


Gynecology_Novak

Gynecology_Novak. Human fibroid tissue, grafted to immunodeficient mice, increased in size in response to estradiol plus progesterone, but the growth was blocked by the antiprogestin RU486 (16). The volume of grafted fibroid tissue decreased after progesterone withdrawal. Treatment with estradiol alone did not increase the graft size, but did induce expression of progesterone receptors and supported the action of progesterone on the grafts (16).


Gynecology_Novak

Gynecology_Novak. For the majority of postmenopausal women with fibroids, hormone therapy will not stimulate fibroid growth. If fibroids do grow, progesterone is likely to be the cause (32). One study evaluated postmenopausal women with fibroids who were given 2 mg of oral estradiol daily and randomized to 2.5 or 5 mg of medroxyprogesterone acetate (MPA) per day (32). One year after starting treatment, 77% of women taking 2.5 mg MPA had either no change or a decrease in fibroids diameters and 23% had a slight increase. However, 50% of women taking 5 mg MPA had an increase in fibroid size (mean diameter increase of 3.2 cm).


Gynecology_Novak

Gynecology_Novak. Postmenopausal women with fibroids treated with 0.625 of conjugated equine estrogen (CEE) and 5 mg MPA were compared over 3 years to a similar group of women not taking hormone therapy (33). By the end of the third year, only 3 of 34 (8%) treated and 1 of 34 (3%) untreated women had any increase in fibroid volume over baseline (32). Postmenopausal women with known fibroids, followed with sonography, were noted to have an average 0.5 cm increase in the diameter of fibroid after using transdermal estrogen patches plus oral progesterone for 12 months (33). Women taking oral estrogen and progesterone had no increase in fibroid size (34).


Gynecology_Novak

Gynecology_Novak. Tissue Injury Cellular injury or inﬂammation resulting from an environmental agent, infection, or hypoxia was proposed as a mechanism for initiation of fibroid formation (43). Repetitive tissue injury to the endometrium and endothelium might promote the development of monoclonal smooth muscle proliferations in the muscular wall. Frequent mucosal injury with stromal repair (menstruation) may release growth factors that promote the high frequency of uterine fibroids (43). No increased incidence was found in women with prior sexually transmitted infections, prior intrauterine device (IUD) use or prior talc exposure (35). Herpes simplex virus (HSV) I or II, cytomegalovirus (CMV), Epstein-Barr virus (EBV), and chlamydia were not found in fibroids.


Gynecology_Novak

Gynecology_Novak. Fibroids are almost never associated with mortality, but they may cause morbidity and significantly affect quality of life (44). Women who have hysterectomies because of fibroid-related symptoms have significantly worse scores on SF-36 quality-of-life questionnaires than women diagnosed with hypertension, heart disease, chronic lung disease, or arthritis (44). Of 116 women with fibroids larger than 5 cm on sonographic examination and uterine size greater than 12 cm on pelvic examination, 42% were satisfied with their initial level of symptoms, including stress, bleeding, and pain (45). Most of the 48 women who chose to have treatment within 1 year were more likely to have higher scores on bleeding and pain scales and be more concerned about their symptoms. Most women chose myomectomy (n = 20), hysterectomy (n = 15), or hysteroscopic myomectomy (n = 4), and symptoms scores improved markedly during the 7.5 months (mean) of follow-up.


Gynecology_Novak

Gynecology_Novak. Abnormal Bleeding The association of fibroids with menorrhagia is not clearly established. Therefore, other possible etiologies, including coagulopathies such as von Willebrand’s disease, should be considered in a woman with heavy menstrual bleeding (46). A random sample of women aged 35 to 49 was evaluated by self-reported bleeding patterns and by abdominal and transvaginal sonography to determine the presence, size, and location of fibroids (47). Of the 878 women screened, 564 (64%) had fibroids and 314 (36%) did not. Forty-six percent of women with fibroids reported, “gushing blood” during menstrual periods, compared with 28% without fibroids. Gushing blood and length of periods were related to the size of fibroids but not to the presence of submucous fibroids or multiple fibroids.


Gynecology_Novak

Gynecology_Novak. Another study found that women with fibroids used 7.5 pads or tampons on the heaviest day of bleeding compared with 6.1 pads or tampons used by women without fibroids (48). Women with fibroids larger than 5 cm had slightly more gushing and used about three more pads or tampons on the heaviest day of bleeding than women with smaller fibroids.


Gynecology_Novak

Gynecology_Novak. Pain Women with fibroids are only slightly more likely to experience pelvic pain than women without fibroids. Transvaginal sonography was performed on a population-based cohort of 635 non-care-seeking women with an intact uterus to determine the presence of uterine fibroids (49). Dyspareunia, dysmenorrhea, or noncyclic pelvic pain was measured by visual analog scales. The 96 women found to have fibroids were only slightly more likely to report moderate or severe dyspareunia or noncyclic pelvic pain and had no higher incidence of moderate or severe dysmenorrhea than women without fibroids. Neither the number nor the total volume of fibroids was related to pain. However, women who present for clinical evaluation for fibroid-associated pain may be different from those in the general population (49).


Gynecology_Novak

Gynecology_Novak. Fibroid degeneration may cause pelvic pain. As fibroids enlarge, they may outgrow their blood supply, with resulting cell death (50). Types of degeneration determined both grossly and microscopically include hyaline degeneration, calcification, cystic degeneration, and hemorrhagic degeneration. The type of degeneration appears to be unrelated to the clinical symptoms (50). Pain from fibroid degeneration is often successfully treated with analgesics and observation. Torsion of a pedunculated subserosal fibroid may produce acute pelvic pain that requires surgical intervention (51).


Gynecology_Novak

Gynecology_Novak. Urinary Symptoms Fibroids may cause urinary symptoms, although few studies examined this association. Following uterine artery embolization with a 35% reduction in mean uterine volume, frequency and urgency were greatly or moderately improved in 68% of women, slightly improved in 18%, and unchanged or worse in only 14% (52). This finding suggests that increased uterine volume associated with fibroids is related to urinary symptoms. Fourteen women with large fibroids and urinary symptoms were given six monthly injections of GnRH agonist (GnRH-a) with a resulting 55% decrease in uterine volume (53). Following therapy, urinary frequency, nocturia, and urgency decreased. There were no changes in urge or stress incontinence as measured by symptoms or urodynamic studies. It is not clear whether these findings are related to a decrease in uterine volume or to other effects of GnRH treatment. Natural History of Fibroids


Gynecology_Novak

Gynecology_Novak. Natural History of Fibroids Most fibroids grow slowly. A prospective, longitudinal study of 72 premenopausal women (38 black, 34 white) using computer analysis of serial MRI found that the median growth rate was 9% over 12 months (17). However, multiple fibroids in the same individual were found to have highly variable growth rates, suggesting that growth results from factors other than hormone levels. After age 35, growth rates declined with age for white women but not for black women, which likely explains the increased fibroid-related symptoms noted in black women. Seven percent of fibroids regressed over the study period. Continued follow-up of these women is planned and should provide a better understanding of this important issue.


Gynecology_Novak

Gynecology_Novak. Rapid Fibroid Growth In premenopausal women, “rapid uterine growth” almost never indicates presence of uterine sarcoma. One study found only 1 sarcoma among 371 (0.26%) women operated on for rapid growth of presumed fibroids (54). No sarcomas were found in the 198 women who had a 6-week increase in uterine size over 1 year, which is the definition of rapid growth that was used in the past.


Gynecology_Novak

Gynecology_Novak. Uterine Sarcoma Women found to have uterine sarcoma are often clinically suspected of having a pelvic malignancy (54,55). Women with pain and bleeding and who are closer to menopause or postmenopausal may have a rare sarcoma. Of nine women found to have uterine sarcomas, all were postmenopausal and eight were admitted with abdominal pain and vaginal bleeding (55). All eight had presumed gynecologic malignancies: uterine sarcoma in four, endometrial carcinoma in three, and ovarian cancer in one. One additional woman had surgery for prolapse and a sarcoma was found incidentally (55). Between 1989 and 1999, the Surveillance, Epidemiology, and End Results (SEER) database reported 2,098 women with uterine sarcomas with an average age of 63 years, whereas a literature review found a mean age of 36 years in women subjected to myomectomy (54,56).


Gynecology_Novak

Gynecology_Novak. Pelvic Examination Clinically significant subserosal and intramural fibroids can usually be diagnosed by pelvic examination based on findings of an enlarged, irregularly shaped, firm and non-tender uterus (57). Uterine size assessed by bimanual examination, even for most women with BMI greater than 30, correlates well with uterine size and weight at pathological examination (58). Routine sonographic examination is not necessary when the diagnosis is almost certain. However, a definite diagnosis of submucous fibroids often requires saline-infusion sonography, hysteroscopy, or magnetic resonance imaging (MRI) (59). Fibroid Location The FIGO fibroid classification system categorizes submucous, intramural, subserosal, and transmural fibroids. Type 0 -intracavitary (e.g., a pedunculated submucosal fibroid entirely within the Type 1 -less than 50% of the fibroid diameter within the myometrium Type 2 -50% or more of the fibroid diameter within the myometrium


Gynecology_Novak

Gynecology_Novak. Type 1 -less than 50% of the fibroid diameter within the myometrium Type 2 -50% or more of the fibroid diameter within the myometrium Type 3 -abut the endometrium without any intracavitary component Type 4 -intramural and entirely within the myometrium, without extension to either the endometrial surface or to the serosa Type 7 -subserosal attached to the serosa by a stalk Type 8 -no involvement of the myometrium; includes cervical lesions, those in the round or broad ligaments without direct attachment to the uterus, and Transmural fibroids are categorized by their relationship to both the endometrial and the serosal surfaces, with the endometrial relationship noted first, e.g., type 2–3 (Table 15.1; Fig 15.2) (60).


Gynecology_Novak

Gynecology_Novak. Imaging For symptomatic women, consideration of medical therapy, noninvasive procedures, or surgery often depends on an accurate assessment of the size, number, and position of fibroids. Transvaginal sonography (TVS), saline-infusion sonography (SIS), hysteroscopy, and MRI were all performed on 106 women scheduled for hysterectomy and the findings were compared to pathologic examination (59). Submucous fibroids were best identified with MRI (100% sensitivity, 91% specificity). Identification was about equal with transvaginal sonography (sensitivity 83%, specificity 90%), saline-infusion sonography (sensitivity 90%, specificity 89%), and hysteroscopy (sensitivity 82%, specificity 87%). MRI is not technique dependent and has low interobserver variability for diagnosis of submucous fibroids, intramural fibroids, and adenomyosis when compared with TVS, SIS, and hysteroscopy (61,62). Table 15.1 FIGO Leiomyoma Classification System


Gynecology_Novak

Gynecology_Novak. Table 15.1 FIGO Leiomyoma Classification System The presence of adenomyosis is associated with junctional zone thickness of more than 15 mm (or 12 mm in a nonuniform junctional zone). Focal, not well-demarcated, and high or low intensity areas in the myometrium correlate with adenomyosis (63). MRI allows evaluation of the number, size, and position of submucous, intramural, and subserosal fibroids and can evaluate their proximity to the bladder, rectum, and endometrial cavity. MRI helps define what can be expected at surgery and might help the surgeon avoid missing fibroids during surgery (64). For women who wish to preserve fertility, MRI to document location and position relative to the endomyometrium may be helpful prior to hysteroscopic, laparoscopic, or abdominal myomectomy. Figure 15.2 FIGO Leiomyoma Classification System. Imaging of Uterine Sarcomas


Gynecology_Novak

Gynecology_Novak. Figure 15.2 FIGO Leiomyoma Classification System. Imaging of Uterine Sarcomas Sonography is the most readily available and least costly imaging technique to differentiate fibroids from other pelvic pathology and is reasonably reliable for evaluation of uterine volume less than 375 cc and containing four or fewer fibroids (61). Sonographic appearance of fibroids can be variable, but often they appear as symmetrical, well-defined, hypoechoic and heterogenous masses. Areas of calcification or hemorrhage may appear hyperechoic, while cystic degeneration may appear anechoic. SIS utilizes saline inserted into the uterine cavity to provide contrast and better defines submucous fibroids (61).


Gynecology_Novak

Gynecology_Novak. The preoperative diagnosis of leiomyosarcoma may be possible. Diagnosis with total serum lactate dehydrogenase (LDH) and LDH isoenzyme 3 measurements along with gadolinium-enhanced diethylenetriamine penta-acetic acid (Gd-DTPA) dynamic MRI was reported to be highly accurate (65). MRI images are taken during the arterial phase, between 40 and 60 seconds after infusion of gadolinium. Sarcomas have increased vascularity and show increased enhancement with gadolinium, while degenerating fibroids have decreased perfusion and exhibit decreased enhancement. Using LDH measurements and Gd-DTPA, a study of 87 women with uterine fibroids, 10 women with leiomyosarcomas, and 130 women with degenerating fibroids reported 100% specificity, 100% positive predictive value, 100% negative predictive value, and 100% diagnostic accuracy for leiomyosarcoma (Fig. 15.3).