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PREMENSTRUAL SYNDROME AND DYSMENORRHEA 13
18. What causes the pain of primary dysmenorrhea?
Primary dysmenorrhea is likely associated with myometrial ischemia secondary to frequent and
prolonged uterine contraction. The principal cause seems to be increased production of prostaglandin
F
2α
that stimulates uterine contraction. Prostaglandin F
2α
can also contribute to systemic symptoms
(e.g., nausea, diarrhea, and headaches).
19. How is dysmenorrhea treated?
Both primary and secondary dysmenorrhea can be treated with NSAIDs or OCPs, or both. NSAIDs
decrease prostaglandin production and can provide symptom relief in 70% to 90% of patients. In
primary amenorrhea, OCPs are considered a first-line agent in sexually active female patients. These
drugs cause atrophy of the endometrium, which is the principal site of prostaglandin production. They
can also reduce the amount and duration of bleeding.
In secondary dysmenorrhea, treatment may be directed at the underlying pathologic process,
once it has been identified. In the case of uterine myomas or endometriosis, surgical management
may be considered. However, medical therapy is usually attempted before resorting to surgical
intervention.
20. What nonmedical options exist for treatment of dysmenorrhea?
A vegetarian diet, vitamin E, exercise, and the direct application of a heating pad to the lower abdo-
men may be helpful for some women. Evidence is insufficient to recommend dietary changes for all
women with dysmenorrhea, but two clinical trials have shown improvement of symptoms with use of
a heated abdominal patch or wrap for 8 to 12 hours compared with placebo.
21. What should be done when the response to medical therapy is inadequate?
Women with secondary dysmenorrhea should be offered treatment of the underlying pathologic
process; this often involves surgical intervention. Women with primary dysmenorrhea should
be offered a more extensive workup to see whether their symptoms have a previously unrec-
ognized cause. This investigation can involve pelvic ultrasound examination, hysteroscopy, or
laparoscopy.
BiBliography
1. Andersch B, Milsom I. An epidemiologic study of young women with dysmenorrhea. Am J Obstet Gynecol.
1982;144:655–660.
2. Brandenburg S, Tuynman-Qua H, Verheij R, Pepplinkhuizen L. Treatment of premenstrual syndrome with fluoxetine: an
open study. Int Clin Psychopharmacol. 1993;8:315–317.
3. Casper RF, Hearn MT. The effect of hysterectomy and bilateral oophorectomy in women with severe premenstrual
syndrome. Am J Obstet Gynecol. 1990;162:105–109.
4. Chan AF, Mortola JF, Wood SH, et al. Persistence of premenstrual syndrome during low-dose administration of the
progesterone antagonist RU 486. Obstet Gynecol. 1994;84:1001–1005.
5. Ford O, Lethaby A, Roberts H, et al. Progesterone for pre-menstrual syndrome. Cochrane Database Syst Rev.
2009;2:CD003415.
6. Frank RT. The hormonal causes of premenstrual tension. Arch Neurol Psychiatry. 1931;26:1052.
7. Freeman E, Rickels K, Sondheimer S, Polanski M. Ineffectiveness of progesterone suppository treatment for premen-
strual syndrome. JAMA. 1990;264:349–353.
8. Freeman E, Rickels K, Sondheimer S, Polansky M. A double-blind trial of oral progesterone, alprazolam, and placebo in
treatment of severe PMS. JAMA. 1995;274:51–57.
9. Fritz MA, Speroff L. Menstrual disorders. In: Clinical Gynecologic Endocrinology and Infertility. 8th ed. Philadelphia:
Lippincott Williams & Wilkins; 2011:567–589.
10. Ginsburg KA. Some practical approaches to treating PMS. Contemp Obstet Gynecol. 1995;40:24.
11. Green R, Dalton K. The premenstrual syndrome. Br Med J. 1953;1:1007.
12. Mark AS, Hricak H, Heinrichs LW, et al. Adenomyosis and leiomyoma: differential diagnosis with MR imaging.
Radiology. 1987;163:527–529.
13. Morrison BW, Daniels SE, Kotey P, et al. Rofecoxib, a specific cyclooxygenase-2 inhibitor, in primary dysmenorrhea: a
randomized controlled trial. Obstet Gynecol. 1999;94:504–508.
14. Pearlstein TB, Bachmann GA, Zacur HA, et al. Treatment of premenstrual dysphoric disorder with a new drospirenone-
containing oral contraceptive formulation. Contraception. 2005;72:414–421.
15. Rapkin AJ, Akopians AL. Pathophysiology of premenstrual syndrome and premenstrual dysphoric disorder. Menopause
Int. 2012;18:52–59.
16. Rapkin AJ, Winer SA. The pharmacologic management of pre-menstrual dysphoric disorder. Expert Opin Pharmacother.
2008;9:429–445.
17. Smith S, Rinehart JS, Ruddock VE, Schiff I. Treatment of premenstrual syndrome with alprazolam: results of a double-
blind, placebo-controlled, randomized crossover clinical trial. Obstet Gynecol. 1987;70:37–42.
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14 GENERAL GYNECOLOGY
18. Sundell G, Milsom I, Andersch B. Factors influencing the prevalence and severity of dysmenorrhea in young women.
Br J Obstet Gynecol. 1990;97:588–594.
19. Thys-Jacobs S, Starkey P, Bernstein D, et al. Calcium carbonate and the premenstrual syndrome: effects on premen-
strual and menstrual symptoms. Premenstrual Syndrome Study Group. Am J Obstet Gynecol. 1998;179:444–452.
20. Yonkers KA, Brown C, Pearlstein TB, et al. Efficacy of a new low-dose oral contraceptive with drospirenone in premen-
strual dysphoric disorder. Obstet Gynecol. 2005;106:492–501.
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15
1. What is a normal menstrual cycle and a normal amount of uterine bleeding?
A normal menstrual cycle averages 28 days but can range from 21 to 35 days, and menses last for an
average of 4 days. Normal blood loss is approximately 35 mL.
2. What is abnormal uterine bleeding (AUB)?
AUB is bleeding from the uterine corpus that is abnormal in regularity, volume, frequency, or duration
in the absence of pregnancy. It is usually subjective (i.e., a patient’s bleeding pattern or amount
changes from what she considers normal).
3. Is AUB common?
Yes. Thirty-three percent of gynecologist office visits and up to 70% of gynecology consultations for
perimenopausal and postmenopausal women are for AUB.
4. How is AUB categorized?
Categorization is necessary to define the underlying cause and help direct treatment. Historically,
terms such as menorrhagia (>80 mL of blood loss per menses) and metrorrhagia (bleeding between
periods) were used. However, these terms have been replaced by heavy menstrual bleeding (HMB)
and intermenstrual bleeding (IMB), which can be further classified using the PALM-COIEN mnemonic
system (Table 3-1). Oligomenorrhea and polymenorrhea have also been discarded in favor of more
descriptive terms (e.g., AUB-HMB/IMB with bleeding every 2 weeks, AUB with no bleeding for 6
months followed by 29 days of bleeding).
Structural causes (mnemonic PALM):
Polyp: Overgrowth of endometrium into the uterine cavity. Usually benign, but up to 5% of polyps in
postmenopausal women can contain malignant cells. Can be seen and potentially removed using
hysteroscopy.
Adenomyosis: Growth of endometrial glands into the muscular layer of the uterus (myometrium).
Can cause painful periods and make the uterus globular and enlarged.
Leiomyoma: Benign smooth muscle tumors, present in up to 70% of women. Also referred to as
fibroids. Mainly seen in reproductive years and thought to be hormonally driven, although their
exact cause is unknown. Range in size from 0.5 cm to massive (filling entire abdomen); symp-
toms generally depend on location.
• Submucosal: Partially inside endometrial cavity, can cause heavy bleeding. Can be seen and
potentially removed using hysteroscopy.
• Other: Subserosal, intramural or pedunculated; less likely to cause bleeding but can cause pain
and pressure symptoms.
CHAPTER 3
ABNORMAL UTERINE BLEEDING
Hannah Newmark, MD
Table 3-1. Categorization of Abnormal Uterine Bleeding and the PALM-COIEN
Mnemonic System
TYPE OF BLEEDING
STRUCTURAL
CAUSES (PALM)
NONSTRUCTURAL
CAUSES (COEIN)
Abnormal uterine bleeding (AUB) Polyp Coagulopathy
Heavy menstrual bleeding (HMB) Adenomyosis Ovulatory dysfunction
Intermenstrual bleeding (IMB) Leiomyoma Endometrial
Postmenopausal bleeding (PMB) Malignancy/hyperplasia Iatrogenic
Not yet classified
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16 GENERAL GYNECOLOGY
For more information on leiomyoma classification, see Chapter 5, Figure 5-1.
Malignancy and hyperplasia: Usually manifest in perimenopausal or postmenopausal women, most
often as painless postmenopausal bleeding. Can manifest as AUB in premenopausal women.
Nonstructural causes (mnemonic COEIN):
Coagulopathy: Most commonly resulting from von Willebrand disease (note: although up to 1% of
women have von Willebrand disease, only 1 in 10,000 women has symptoms)
Ovulatory dysfunction: Many causes (e.g., perimenopause, polycystic ovarian syndrome, pregnancy,
lactation, anorexia, pituitary dysfunction, and premature ovarian failure)
Endometrial: Primary endometrial dysfunction; a diagnosis of exclusion
Iatrogenic: Many causes (e.g., instrumentation, anticoagulation, other therapies)
Not yet classified: Used to indicate that a workup has not been completed or the cause is uncertain
5. What elements of a history and physical examination can help elucidate
the cause of AUB?
History:
• What is a normal bleeding pattern for the patient, and when did it change?
• Age of menarche? Menopause?
• Associated symptoms? (Pain can indicate infection; bruising or bleeding can indicate coagulopa-
thy; lightheadedness can be a symptom of anemia or thyroid disease; hot flashes can indicate
perimenopause or menopause.)
• Medical conditions or medications (e.g., anticoagulation, high-dose nonsteroidal anti-inflammatory
drugs [NSAIDs], oral contraceptives).
• Medical and surgical history.
• Family history or symptoms concerning for bleeding disorder.
Physical examination:
• Look for signs of anemia or a bleeding disorder (bleeding or bruising, pallor), hypothyroidism
or hyperthyroidism (fine tremor, goiter, delayed deep tendon reflexes), and hyperandrogenism
(acanthosis nigricans, hirsutism, central obesity).
• Speculum examination: Assess for a cervical mass or polyps or a prolapsing leiomyoma.
• Bimanual examination: Assess the size of the uterus and the presence or absence of pain.
6. Do the common causes of AUB vary with age?
Yes. The differential diagnosis is affected by the patient’s stage of her reproductive lifespan.
• Ages 13 to 18 years: Many adolescents do not have a fully mature hypothalamic pituitary axis and
can experience anovulatory cycles for up to 2 years after menarche. Have a strong suspicion of an
underlying bleeding disorder if hospitalization or transfusion is required. Other common causes are
imperfect hormonal contraceptive use, pregnancy, or infection.
• Ages 19 to 39 years: Common causes include pregnancy, structural lesions such as polyps or
fibroids, anovulatory cycles (most commonly from polycystic ovarian syndrome), or endometrial
hyperplasia or malignant disease.
• Age 40 years to menopause: Anovulatory cycles can occur during perimenopause. Other common
causes are structural lesions, endometrial hyperplasia, and malignant disease.
7. What laboratory tests should be ordered in a patient with AUB?
• All women with abnormal bleeding should be tested for pregnancy.
• A complete blood count (CBC) can rule out anemia and thrombocytopenia.
• A thyroid-stimulating hormone (TSH) level can assess thyroid function.
• If a bleeding disorder is suspected, prothrombin time (PT), partial thromboplastin time (PTT), von
Willebrand factor, ristocetin cofactor activity, and factor VIII levels should be ordered. Bleeding time
is neither sensitive nor specific and should not be obtained.
• Other laboratory tests to consider are prolactin (if concern exists for a prolactinoma), hemoglobin A1c
(if signs of insulin resistance or polycystic ovarian syndrome are present), and follicle-stimulating
hormone (FSH) (if patient is perimenopausal or concern for primary ovarian insufficiency exists).
8. What types of imaging can be used to evaluate AUB?
Transvaginal ultrasound is the most commonly used technique and can detect larger structural abnor-
malities. An intracavitary lesion (endometrial polyp or submucosal leiomyoma) can be identified with a
saline-infused sonogram, in which saline is injected into the uterus at the time of an ultrasound exami-
nation. Hysteroscopy can also be performed. Magnetic resonance imaging (MRI) is not considered a
first-line study but can be used when knowledge of the precise location and size of fibroids is important.
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ABNORMAL UTERINE BLEEDING 17
9. When and how can AUB be treated empirically?
If a patient is not at risk for hyperplasia or malignant disease, a trial of medical management may be
appropriate. If it is not successful, further evaluation is required. Treatment options include NSAIDs,
progestin analogues, oral contraceptives, the levonorgestrel intrauterine device, and depot
medroxyprogesterone acetate.
10. How can AUB caused by structural lesions be treated?
If a structural abnormality is found, surgical treatment may be required. For intramural, subserosal,
and pedunculated leiomyomas, surgical options include myomectomy (laparoscopic or abdominal)
and hysterectomy. Another option is treatment with a gonadotropin-releasing hormone agonist, which
induces a menopause-like state. Amenorrhea results, and the leiomyomas decrease in size. Because
of side effects, this treatment is best used as a temporary bridge to surgical management.
For intracavitary lesions, operative hysteroscopy can be performed. This minimally invasive option
can allow many patients to avoid hysterectomy, and small lesions can even be removed in a clinic
without general anesthesia. Larger lesions (up to 5 cm) are generally removed in the operating room.
11. What is endometrial ablation, and when it performed?
Endometrial ablation is a procedure designed to destroy the outer layer of the endometrium. It can
be done in either the clinic or the operating room, and it is an option for women who have completed
childbearing and are not at risk for hyperplasia. Many different techniques are available: freezing,
instillation of hot water, thermal balloon use, electrocautery, microwaves, or radio waves. Success
rates are similar, and up to 85% of patients will achieve long-term resolution of their AUB.
12. Which patients with AUB should be screened for endometrial cancer?
Endometrial biopsy to rule out hyperplasia and malignant disease should be performed in women who
are more than 45 years old, or at any age if risk factors (obesity, chronic anovulation, or poor response
to medical management) are present.
BiBliography
1. American College of Obstetricians and Gynecologists. Diagnosis of abnormal uterine bleeding in reproductive-aged
women. ACOG practice bulletin no. 128. Obstet Gynecol. 2012;120:197–206.
2. American College of Obstetricians and Gynecologists. Management of abnormal uterine bleeding associated with
ovulatory dysfunction. ACOG practice bulletin no. 136. Obstet Gynecol. 2013;122:176–185.
KEY POINTS: ABNORMAL UTERINE BLEEDING
1. A normal menstrual cycle averages 28 days; normal menses last 4 days, and blood loss is approxi-
mately 35 mL.
2. AUB is categorized by cause.
3. For women with AUB, endometrial biopsy should be performed to rule out hyperplasia and malignant
disease in those who are more than 45 years old or who have risk factors.
4. If a patient is not at risk for hyperplasia or malignant disease, a trial of medical management may
be appropriate.
5. Surgical treatments for abnormal uterine bleeding include endometrial ablation, operative hysteros-
copy, myomectomy, and hysterectomy.
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18
1. What is endometriosis?
Endometriosis is a chronic, inflammatory condition in which hormonally responsive endometrial
glands and stroma are present outside the uterine cavity.
2. How common is endometriosis?
The true prevalence is unknown. It is thought to occur in 6% to 10% of women of reproductive age. It
is more frequent among women with chronic pelvic pain (50% to 87%) and infertility (20% to 50%).
Having a first-degree relative with endometriosis is considered a risk factor.
3. How does endometriosis develop?
Several theories have been proposed, although the true pathogenesis is uncertain and is likely multifactorial.
1. Retrograde menstruation (Sampson’s theory): Endometriosis is the result of retrograde menstrua-
tion; endometrial tissue is carried through the fallopian tubes into the peritoneal cavity, where
it implants and proliferates. Support for this theory includes the common finding of endometrial
lesions in dependent areas of the peritoneal cavity, direct visualization of menstrual fluid extrava-
sating from the fallopian tubes at time of laparoscopy, and increased incidence of endometriosis in
women with uterine outlet obstruction.
2. Coelomic metaplasia (Meyer’s theory): Endometriosis is caused by transformation of pluripotent
peritoneal cells into endometrial cells.
3. Lymphatic or hematologic spread (Halban’s theory): Endometrial tissue metastasizes to extrauterine
sites through the lymphatic or vascular system. Support for this theory includes the presence of
endometriosis outside the peritoneal cavity, including lymph nodes.
4. Induction theory: Certain hormonal, immunologic, or inflammatory factors stimulate
differentiation into endometrial tissue and/or allow ectopic endometrial cells to implant and
proliferate. Support for this theory includes the finding of increased numbers of activated
macrophages and proinflammatory cytokines (interleukin-6 [IL-6], IL-8, and tumor necrosis
factor-α [TNF-α]) in the peritoneum, local production of prostaglandins in endometrial lesions,
and local production of estrogen in endometrial lesions stimulated by increased aromatase
activity.
4. What are the symptoms of endometriosis?
The classic symptoms are cyclic pelvic pain beginning just before the menses, infertility,
and dyspareunia. Patients may also present with noncyclic chronic pelvic pain, dysuria, pain
with defecation (dyschezia), or an endometrioma (a type of adnexal mass in patients with
endometriosis).
5. What are the physical examination findings associated with endometriosis?
Patients may have diffuse pelvic pain, uterosacral nodularity or tenderness, an adnexal mass, or a
fixed, retroverted uterus. Other patients may have no distinct examination findings.
6. How is endometriosis diagnosed?
In symptomatic patients, the diagnosis can be made clinically based on history and physical
exam and empiric medical therapy can be initiated. Endometriomas can be identified on
transvaginal pelvic ultrasound by their classic “ground glass” appearance. Visual recognition of
characteristic lesions (black, blue, red, white, or clear vesicular lesions and associated findings
of scarring or fibrosis) at the time of laparoscopy is possible. Definitive diagnosis is made by
laparoscopy with peritoneal biopsy and histopathologic confirmation of endometrial glands and
stroma or hemosiderin-laden macrophages. Endometriomas can also be identified at the time of
surgical intervention by visualization of their hallmark brown cyst fluid (“chocolate cysts”).
CHAPTER 4
ENDOMETRIOSIS
AND ADENOMYOSIS
Julia Switzer, MD
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ENDOMETRIOSIS AND ADENOMYOSIS 19
7. What are the most common anatomic sites of endometriosis?
Endometrial lesions are commonly found on the ovary, uterosacral ligaments, fallopian tubes,
rectosigmoid colon, pelvic peritoneum, and posterior cul-de-sac. Endometriosis has also been
reported at distant anatomic sites including the lung and incisional sites.
8. How is endometriosis staged?
Although no clear correlation exists between the extent of disease and symptoms, the American
Society of Reproductive Medicine staging system describes the location and type of disease and
ranges from 1 to 4 (minimal to severe). This system is used to record operative findings and compare
results of different therapies.
9. What medical treatments are available?
Treatment of pain associated with endometriosis is aimed at downregulating estradiol production by
inhibiting ovulation, which induces endometrial atrophy and counteracts the chronic inflammatory
state.
• Combinedoralcontraceptivepills(OCPs)inducedecidualizationandatrophyofendometrialtissue
by suppressing ovarian estradiol production. They are effective for many (60% to 85%) patients;
continuous use (skipping placebo pills) can be helpful if women experience symptoms during
menses.
• Gonadotropin-releasinghormone(GnRH)agonistssuppresspituitaryfunctionbydownregulat-
ingpituitary(GnRH)receptors,thusleadingtoanovulationandendometrialatrophy.Treatmentis
generally limited to 6-month intervals to avoid long-term consequences of hypoestrogenism on bone
metabolism and cardiovascular health. Side effects (hot flashes, vaginal dryness, headache, insomnia,
libido changes, fatigue, bone loss) can be ameliorated with “add-back therapy” using a progestogen
or combined OCP.
• Progestinsinducedecidualizationandatrophyofendometrialtissuebysuppressingluteinizing
hormone (LH), which inhibits ovulation. More than 80% of women will have some pain relief. The
levonorgestrel-releasing intrauterine device (IUD) has been shown to improve pelvic pain and
dyspareunia in patients with endometriosis.
• Aromataseinhibitorsdecreasecirculatingestrogenlevelsby50%andappeartoregulatelocal
estrogen production within endometriotic lesions.
• Danazol,aderivativeof17α-ethinyltestosterone, suppresses LH and follicle-stimulating hormone
(FSH), thereby causing anovulation and hyperandrogenism. Although it has been shown to be
effective in relieving pain, it is rarely used because of its androgenic side effects (acne, deepening
of voice, weight gain, hair growth, decreased breast size).
• Nonsteroidalantiinammatorydrugs(NSAIDs)mayinhibitprostaglandinproductioninectopic
endometrial tissue and effectively treat dysmenorrhea.
10. What surgical treatments are available?
• Conservative:laparoscopicexcisionorablationofendometrialimplantsorlaparoscopicremovalof
an endometrioma. This is the treatment of choice for women in whom medical therapy has failed
but who desire future fertility. Although pain relief after 1 year ranges between 50% and 95%,
many patients eventually develop recurrent symptoms. Ablation is performed with unipolar cautery,
bipolar cautery, laser, or ultrasonic coagulation. Excision requires removal of tissue. No evidence
indicates that one surgical technique is superior to another. Laparoscopic uterosacral nerve abla-
tion and presacral neurectomy may decrease midline dysmenorrhea, but these procedures are less
commonly performed.
• Denitive:hysterectomywithorwithoutbilateralsalpingo-oophorectomy.Iftheovariesare
removed, surgical menopause occurs and leads to atrophy of ectopic endometrial tissue.
11. How does endometriosis lead to infertility?
The inflammatory nature of endometriosis is thought to contribute to infertility by altering folliculo-
genesis leading to poor quality oocytes, decreasing endometrial receptivity, damaging tubal motility or
patency, and impairing sperm function.
12. What is the relationship between endometriosis and malignant disease?
The rate of clear cell and endometrioid-type epithelial ovarian carcinoma is higher in women with
endometriosis compared with the general population. However, ovarian carcinoma associated with
endometriosis is usually diagnosed at an earlier stage and lower grade, and it is associated with a
better overall survival rate.
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20 GENERALGYNECOLOGY
13. What is adenomyosis?
Adenomyosis is a chronic condition characterized by invasion of endometrial glands and stroma into
the myometrium which induces hypertrophy and hyperplasia.
14. What are the symptoms of adenomyosis?
Classic symptoms of adenomyosis are dysmenorrhea and heavy, prolonged menstrual bleeding.
15. What physical findings are associated with adenomyosis?
Patients with adenomyosis often have an enlarged, globular uterus.
16. How is adenomyosis diagnosed?
Definitive diagnosis is made on histologic examination of a hysterectomy specimen. On magnetic
resonance imaging (MRI), a thickened junctional zone is suggestive of adenomyosis.
17. What treatments are available for adenomyosis?
Denitivetherapyistotalhysterectomy.Thelevonorgestrel-releasingIUD,GnRHagonists,NSAIDs,and
OCPs are options for medical management.
BiBliography
1. AmericanCollegeofObstetriciansandGynecologists.ManagementofEndometriosis.ACOGpracticebulletinno.114.
Washington,DC:AmericanCollegeofObstetriciansandGynecologists;2010.
2. American Society for Reproductive Medicine. Revised American Society for Reproductive Medicine classification of
endometriosis. 1996. Fertil Steril. 1997;67:817–821.
3. BenagianoG, Habiba M. Brosens, I. The pathophysiology of adenomyosis: an update. Fertil Steril. 2012;98:572–579.
4. Fritz M, Speroff L. Clinical Gynecologic Endocrinology and Infertility. 8th ed. Philadelphia: Lippincott Williams &
Wilkins; 2011.
5. Hoffman B, Schorge J, Schaffer J, et al., eds. Williams Gynecology.2nded.NewYork:McGraw-Hill;2012.
6. Levgur M. Diagnosis of adenomyosis: a review. J Reprod Med. 2007;52:177–193.
7. Practice Committee of the American Society for Reproductive Medicine. Treatment of pelvic pain associated with
endometriosis. Fertil Steril. 2008;90:S260–S269.
8. Practice Committee of the American Society for Reproductive Medicine. Endometriosis and infertility: a committee
opinion. Fertil Steril. 2012;98:591–598.
9. Vlahos NF, Kalampokas T, Fotiou S. Endometriosis and ovarian cancer: a review. Gynecol Endocrinol. 2010;26:213–219.
10. Wong AY, Tang LC, Chin RK. Levonorgestrel-releasing intrauterine system (Mirena) and depot medroxyprogesterone
acetate (Depo-Provera) as long-term maintenance therapy for patients with moderate to severe endometriosis: a
randomized controlled trial. Aust N Z J Obstet Gynaecol. 2010;50:273–279.
KEY POINTS: ADENOMYOSIS
1. Adenomyosis, endometrial tissue in the myometrium, causes abnormal uterine bleeding and dys-
menorrhea.
2. It is often suggested by MRI (thickened junctional zone), but definitive diagnosis is made only by
microscopic uterine inspection after hysterectomy.
3. Adenomyosis can be treated initially with NSAIDs and OCPs or cyclic progesterone, but it may
require hysterectomy for persistent symptoms.
KEY POINTS: ENDOMETRIOSIS
1. Endometriosis, endometrial tissue outside the uterus, causes pelvic pain, dyspareunia, and infertility.
2. Theories about the etiology of endometriosis include metastasis and metaplasia.
3. Endometriosis is typically diagnosed by laparoscopy, but the visible extent may not correlate with
the degree of symptoms.
4. CommontherapiesareNSAIDsandOCPsformilderdiseaseandGnRHagonistsorsurgicalinterven-
tion for more severe disease.
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21
1. What is a leiomyoma?
Leiomyomas are benign, monoclonal tumors of the smooth muscle cells of the myometrium. They are
composed of large amounts of extracellular matrix containing collagen, fibronectin, and proteogly-
can. Collagen type I and type III are abundant, but the fibrils are formed abnormally and in disarray.
Leiomyomas are also called fibroids, fibromyomas, or myomas.
2. How common are leiomyomas?
Leiomyomas are the most common tumors in women of reproductive age. Rarely observed before
puberty, these tumors are most prevalent during the reproductive years and regress after menopause.
In white women, the incidence of leiomyomas is thought to be as high as 43% by age 35 years and
almost 59% by age 50 years. The incidence is even higher among African-American women, at 59%
by age 35 years and more than 75% by age 50 years.
3. What causes leiomyomas?
Leiomyomas are thought to arise from a somatic mutation of a monoclonal myometrial cell line.
Possible factors responsible for initiating genetic changes include intrinsic abnormalities of the
myometrium, congenitally increased estrogen receptors in the myometrium, hormonal changes, and
ischemic injury at the time of menses.
4. How does estrogen affect leiomyomas?
Leiomyomas contain both progesterone and estrogen receptors and are sensitive to estrogen levels.
Factors that increase overall lifetime exposure to estrogen, such as obesity and early menarche,
increase the incidence of these tumors.
5. How common is malignancy in a leiomyoma?
Very rare. Genetic differences between leiomyomas and leiomyosarcomas indicate that these tumors most
likely have distinct origins and that leiomyosarcomas do not result from malignant degeneration of leio-
myomas. Malignancy should always be considered when leiomyomas increase in size after menopause.
6. How are leiomyomas classified?
Leiomyomas are classified by their location (Fig. 5-1).
• Submucosal: beneath the endometrium; distort the uterine cavity; can also become pedunculated
and prolapse through the cervix
• Intramural: within the myometrium
• Subserosal: beneath the peritoneal surface of the uterus; can become pedunculated or even
detach and obtain blood supply from another organ (“parasitic leiomyoma”)
• Cervical: within the cervix
7. What symptoms are associated with leiomyomas?
Although leiomyomas are asymptomatic in approximately 50% of affected women, they can also
cause significant morbidity and affect a woman’s quality of life. The peak incidence of symptoms
occurs among women in their 30s and 40s, and it is often related to the location and size of the
leiomyomas. The most common symptoms overall are dysmenorrhea, abnormal uterine bleeding, and
pressure. Submucosal leiomyomas are often associated with heavy menstrual bleeding. Intramural
leiomyomas may be associated with dysmenorrhea or abnormal bleeding. Although leiomyomas in
any location can cause pain through dysmenorrhea or degeneration, large leiomyomas can cause
symptoms in adjacent organ systems (e.g., urinary frequency or constipation).
8. How do leiomyomas cause abnormal uterine bleeding?
Several mechanisms are possible:
• Increased surface area of the endometrium
• Increased vascularity of the uterus
• Ulceration of the overlying endometrium
CHAPTER 5
LEIOMYOMATOUS UTERUS
Elena Martinez, MD
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22 GENERAL GYNECOLOGY
• Distortion of the uterine wall that prevents contraction and subsequent closure of spiral arteries
during menses
• Development of abnormal microvasculature, with stasis and changes in venous drainage
9. Do leiomyomas affect fertility?
In general, leiomyomas are not thought to be a major cause of infertility. Although the American
Society of Reproductive Medicine reports that these tumors may be associated in up to 5% to 10%
of cases, this number falls to only 2% to 3% when all other causes of infertility are excluded. If
leiomyomas do have an impact, it is thought to be through distortion of the uterine cavity that leads
to recurrent miscarriage. Data from assisted reproduction technology (ART) suggest that submucosal
and intramural leiomyomas that distort the uterine cavity should be removed.
10. What effect do leiomyomas have on an ongoing pregnancy, and how does
pregnancy affect these tumors?
Some studies have shown leiomyomas to be associated with an increased risk of preterm delivery,
placenta previa, postpartum hemorrhage, and cesarean section.
Degeneration manifesting with acute pain is the classically recognized complication during
pregnancy. Its incidence is believed to be approximately 5%. Pregnancy also appears to have a vari-
able and unpredictable effect on leiomyoma growth; the size of the tumors may increase, decrease, or
remain the same.
Interstitial
(intramural)
Pedunculated,
subserous
Subserous,
displacing tube
Pedunculated,
submucous
Pedunculated, submucous,
protruding through external os
Histology of fibroid
Subserous
Intraligamentary
Cervical
Submucous
Figure 5-1. Uterine leiomyomata. (From Smith RP: Netter’s Obstetrics and Gynecology. 2nd ed. Philadelphia: Elsevier;
2015. Copyright 2015 Elsevier Inc. All rights reserved. www.netterimages.com.)
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