Menstrual Problems

Jennifer C. Edman and Mary-Ann Shafer

The attainment of ovulatory menstrual cycles is one feature of maturation and synchronization of the hypothalamic-pituitary-gonadal axis. Despite frequent anovulatory cycles, the majority of menstrual cycles during adolescence range from 21 to 42 days with duration of menstrual flow lasting 2 to 8 days. Young women frequently complain of menstrual abnormality when their cycle falls within the expected range of normal. Charting cycles on a calendar is a useful tool to evaluate cycle irregularity.¹ The most common menstrual disorders in adolescents, including amenorrhea, dysfunctional uterine bleeding, and dysmenorrhea, are discussed in this section.

AMENORRHEA

Amenorrhea is traditionally divided into 2 categories: primary and secondary. Primary amenorrhea is defined as either (1) the failure to menstruate by age 16 (age of expected menarche) in the presence of breast development and normal growth or (2) delayed menarche by 14 years of age in the absence of secondary sexual characteristics. Despite evidence that puberty may be occurring earlier, no revision to the definition of delayed puberty and primary amenorrhea is uniformly endorsed. When significant delay in secondary sexual development and accompanying amenorrhea is detected, prompt evaluation rather than waiting for an adolescent to meet strict criteria should occur.^2,3

Secondary amenorrhea is defined as either (1) cessation of menses for more than 3 cycle intervals or 6 consecutive months in females with previous regular menses or (2) cessation of menses for more than 12 months in females with previous irregular menses.^1,2 The categorization of primary and secondary amenorrhea is retained; however, the clinical approach to primary and secondary amenorrhea in the female adolescent and young adult is similar. All causes of secondary amenorrhea may also present as primary amenorrhea. Oligomenorrhea, or infrequent menses, is considered as amenorrhea in this discussion. Amenorrhea is further discussed with delayed puberty in Chapter 541.

DIFFERENTIAL DIAGNOSIS

Pregnancy is the most common cause of secondary amenorrhea and must not be overlooked as a potential cause of primary amenorrhea. The diagnosis of pregnancy is reviewed in Chapter 77. Beyond pregnancy, the etiology of primary and secondary amenorrhea falls into 3 categories depending on the function of the pituitary gland in relation to the ovary: hypogonadotropic gonadism, hypergonadotropic hypogonadism, and eugonadotropic eugonadism.^2,3

Hypogonadotropic Hypogonadism

Hypogonadotropic hypogonadism indicates inadequate hypothalamic-pituitary stimulation of the ovary and is characterized by low levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estrogen.² Hypothalamic amenorrhea results from partial or complete inhibition of gonadotropin-releasing hormone (GnRH) release. It may be associated with constitutional delay of puberty; nutritional deficiencies secondary to chronic diseases such as regional enteritis, cystic fibrosis, and poorly controlled diabetes; anorexia nervosa; excessive exercise and accompanying alterations in body fat and weight as found in the female athlete triad (disordered eating, amenorrhea, osteoporosis); stress; isolated GnRH deficiency; endocrinopathies such as hypothyroidism, congenital adrenal hyperplasia, and Cushing disease; and specific drugs. Local lesions in the hypothalamus, such as infiltrative processes, calcifications, gliomas, germinomas, and central nervous system radiation, are rare causes of GnRH deficiency. Isolated GnRH deficiency has been associated with the absence (anosmia) or impairment (hyposmia) of the ability to smell (Kallman syndrome). In addition, certain medications and illicit drugs, such as phenothiazine derivatives, methadone, and heroin, result in amenorrhea.

Pituitary deficiencies or the inability to synthesize adequate amounts of gonadotropins may result from tumors such as craniopharyngiomas, infiltrative processes (tuberculosis, sarcoidosis, or histiocytosis), or infarction (eg, Sheehan syndrome). Isolated gonadotropin deficiency is rare. More commonly, hypogonadotropism is a component of panhypopituitarism. Gonadotropin deficiency may be detected before the development of changes in thyroid and adrenal function.

The most common pituitary tumor causing amenorrhea in reproductive-aged females is the prolactin-secreting adenoma. Unlike space-occupying lesions, these tumors cause inhibition of the hypothalamic-pituitary-gonadal axis by secreting abnormally high levels of prolactin. Galactorrhea is found in only 50% to 60% of females with adenomas; therefore, the absence of this sign does not eliminate suspicion for the tumor. Rarely, adenomas increase in size, causing symptoms associated with space-occupying lesions. Other causes of hyperprolactinemia include psychoactive drugs (eg, haloperidol, phenothiazines, amitriptyline, benzodiazepine, and cocaine), breast-feeding, and renal failure. Both hypercortisolism and hypothyroidism have been associated with hyperprolactinemia and amenorrhea.

Hypergonadotropic Hypogonadism

Amenorrhea secondary to hypergonadotropic hypogonadism is characterized by high levels of luteinizing hormone and follicle-stimulating hormone. Ovarian failure resulting in inadequate estrogen and progesterone production despite adequate gonadotropin stimulation manifests clinically with menstrual irregularities. Such disorders include gonadal dysgenesis (abnormal ovarian development) and premature ovarian failure (etiologies include idiopathic, infection, hemorrhage or compromised blood supply, trauma, autoimmune oophoritis, radiation or chemotherapy in survivors of childhood cancer). One common cause of primary amenorrhea is gonadal dysgenesis (see Chapter 541), including Turner syndrome (45, XO) or mosaic Turner variant and women with normal karyotype (46, XX) gonadal dysgenesis. Secondary amenorrhea can also be associated with mosaic Turner syndrome.

Other rare causes of hypergonadotrophic hypogonadal amenorrhea include pseudo-ovarian failure secondary to gonadotropin-resistant ovary syndrome (an abnormality of ovarian follicle-stimulating hormonereceptors) and defects in estrogen biosynthesis, including 17-hydroxylase deficiency and 17-ketosteroid reductase deficiency. Congenital defects in steroid synthesis, such as 21-hydroxylase deficiency (late onset congenital adrenal hyperplasia), may first present with secondary amenorrhea and are associated with signs of virilization (clitoromegaly and hirsutism). Androgen insensitivity (46, XY) or testicular feminization is characterized by insensitivity of peripheral tissues to circulating androgens, external female phenotype, and amenorrhea.^2,3 For further discussion, see Chapter 459.

Eugonadotropic Eugonadism

Normal follicle-stimulating hormone, luteinizing hormone, and estrogen levels characterize the eugonadotropic state. Primary amenorrhea in patients with normal pubertal development is usually anatomic in origin (uterine, cervical, vaginal). Defects in the development of the müllerian duct system are associated with primary amenorrhea resulting in imperforate hymen, vaginal atresia, or absence or malformations of the cervix and the uterus. Except in cases of absence of uterine cavity or endometrium, developmental genital tract obstructions usually present with painful swelling of the reproductive tract above the area of the blockage: hematocolpos (vaginal), hematometra (uterus), and hematoperitoneum (leakage of menstrual blood into peritoneal cavity). The pain is cyclic and coincides with a menstrual cycle. Rokitansky-Kuster-Hauser syndrome is müllerian agenesis with primary amenorrhea secondary to absence or hypoplasia of the vagina, cervix, and/or uterus.

Secondary amenorrhea associated with normal follicle-stimulating hormone, luteinizing hormone, and estrogen levels has a wide differential diagnosis, including uterine scarring, hyperandrogenic states including polycystic ovarian syndrome (PCOS), and substance abuse. Uterine synechiae (Asherman syndrome) occurring after endometrial manipulation and/or infection (eg, pregnancy, dilation and curettage, pelvic inflammatory disease) can lead to secondary amenorrhea with partial or total obliteration of the endometrial cavity. Causes of amenorrhea, hirsutism, and virilization (abnormal circulating androgenic hormones) include PCOS, virilizing ovarian tumors, adrenal adenomas, carcinomas, and specific drugs, both licit (eg, phenytoin and oral contraceptives) and illicit (eg, cocaine, anabolic steroids).

Polycystic ovarian syndrome (PCOS) This is the most common endocrine disorder in reproductive-aged women and a common cause of eugonadotropic secondary amenorrhea (less common cause of primary amenorrhea) in adolescents. Differing definitions and diagnostic criteria are currently in use. The 1990 National Institutes of Health criteria define PCOS as a disorder characterized by evidence of hyper-androgenism and chronic anovulation when other causes of androgen excess have been excluded.⁴ The Rotterdam criteria (2003) state that 2 of the 3 following findings are required for diagnosis: menstrual irregularity due to anovulation or oligo-ovulation, evidence of clinical (hirsutism, acne, male pattern hair loss) or biochemical (high serum androgens) hyperandrogenism, or polycystic ovaries (by ultrasound).¹

The hallmarks of PCOS include menstrual dysfunction, hyperandrogenism secondary to ovarian thecal cell proliferation and excess testosterone production, and metabolic defects including insulin resistance. Enlarged ovaries have multiple developing follicles and thickened stroma, which produce increased amounts of androgens. Peripheral insulin resistance and an increase in luteinizing hormone (LH) relative to follicle-stimulating hormone (FSH) are hypothesized to contribute to thecal proliferation and further stimulation of androgen production.^2,4,5 One laboratory indicator of PCOS is an LH-FSH ratio greater than 2.5:1, although this is only present in approximately 50% of patients.¹ Clinical manifestations in addition to menstrual dysfunction may be variable and include hirsutism, acne, obesity, insulin resistance, glucose intolerance, diabetes, unfavorable high-density lipoprotein to low-density lipoprotein ratios, metabolic syndrome, and acanthosis nigricans. Management of PCOS is discussed below.

EVALUATION AND MANAGEMENT OF AMENORRHEA

History The evaluation of amenorrhea is accomplished through history and physical assessment. Sexual history is essential. The possibility of pregnancy must be excluded by a urine β-hCG pregnancy test before an extensive workup of amennorhea is performed. Information regarding the onset of puberty and sexual maturity rating (SMR) as indicators of the stage of development of the hypothalamic-pituitary-gonadal axis is critical. Factors associated with common hypogonadal causes of amenorrhea should be queried, including body image, weight loss, nutritional intake, excessive exercise, and stress.

Physical examination The exam should include height, weight, blood pressure, pulse, and SMR rating. Pubic, axillary, and facial hair distribution is noted as a sign of androgen effect. Breast and vulvar vaginal mucosal maturation is examined as a sign of estrogenic effect. Physical signs of genetic syndromes associated with amenorrhea, such as Turner syndrome, are noted (see Chapter 541). The thyroid is examined. The areola and nipple are gently compressed to elicit galactorrhea. Neurologic examination is required to assess for increased intracranial pressure or expanding mass (bilateral temporal hemianopsia is common to pituitary tumors). Signs of androgen excess include hirsutism, acne, deepening of the voice, and clitoromegaly. The abdomen is palpated to assess the size of the uterus (hematocolpos, pregnancy, tumor) and presence of tenderness. The vulva, introitus, and vaginal mucosa are evaluated for clitoromegaly, hymenal patency, and estrogen effect. A pelvic examination is also helpful to determine vaginal patency and presence or absence of the reproductive organs. If a complete pelvic examination is not possible for anatomic, cultural, or psychosocial reasons, a rectal abdominal examination can be done. Patency and depth of the vagina can be determined by passing a lubricated cotton swab through the vaginal opening. If a pelvic examination cannot be completed, or anatomic abnormalities are noted, a pelvic ultrasound or computed tomography scan should be performed.

Screening laboratory tests Tests should include serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH), prolactin concentration to determine the presence of a pituitary microadenoma, and thyroid function tests. If excess androgen is suspected on physical examination, serum testosterone (free and total) and dehydroepiandrosterone (DHEAS) levels are indicated. Further workup for adrenal dysfunction is discussed in Chapter 532. Estrogen effects may be evaluated from vaginal cytology (presence of mature superficial epithelial cells) and by examination of cervical mucus for the presence of typical ferning pattern. High levels of LH and FSH warrant a chromosomal evaluation.²

Provocative testing If FSH and LH are normal or low, a progesterone challenge will indirectly evaluate the presence of endogenous estrogen as well as the competence of the reproductive outflow tract from uterus to vaginal opening.² Administer 10 mg of oral medroxyprogesterone acetate per day for 7 days. Within 2 to 7 days of completion of the course of progesterone, uterine withdrawal bleeding should occur, which confirms minimal competence of the hypothalamic-pituitary-gonadal axis and patency of the outflow tract. If no bleeding occurs after progesterone challenge, either the reproductive outflow tract is abnormal or endogenous estrogen is inadequate or absent. In that case, the second step of the hormonal challenge test is to prime the endometrium with exogenous estrogen followed by progesterone to induce bleeding: 2.5 mg oral conjugated estrogen (Premarin) is administered for 25 days with 10 mg oral medroxyprogesterone acetate added from day 16 to day 25. It may be necessary to repeat this combination challenge a second time if no bleeding is elicited. If bleeding occurs, minimal competence of the uterus, endometrium, and cervicovaginal outflow tracts is confirmed. If no bleeding occurs, pelvic sonography and appropriate hormonal assays, including a serum estradiol level, should be obtained.⁶

Treatment approaches If an outflow obstruction of the reproductive tract is diagnosed, treatment depends on the type and location of the problem. Obstructions leading to painful menstrual flow blockage require urgent surgical intervention after appropriate pelvic ultrasound or other radiologic studies define the existing anatomy. Surgical correction of vaginal agenesis is appropriate before sexual debut.

The complete evaluation and treatment of hypothalamic-pituitary failure is reviewed in Chapters 523 and 541. If an asymptomatic pituitary microadenoma is suspected in the presence of elevated prolactin levels, bromocriptine (a dopamine agonist) therapy should be considered. Ovarian failure is treated with hormone replacement therapy, 0.3 to 0.625 mg of conjugated estrogen (lowest amount to achieve desired estrogen effect) on days 1 through 25. Medroxyprogesterone acetate 10 mg is added on days 16 through 25 to avoid the effect of unopposed estrogen on the endometrium, which has been linked to endometrial cancer in women. Counseling regarding bone health and calcium requirements is imperative. Anatomic abnormalities should be referred for reconstructive surgery, as indicated. When irreversible infertility of any cause is determined, counseling is indicated.

Treatment of polycystic ovarian syndrome PCOS treatment includes cycling with estrogen and progesterone to prevent endometrial hyperplasia. Ovulation and regular menstrual cycles may also be attained through diet, exercise, and weight loss. PCOS-associated hirsutism and acne may be treated with oral contraceptives and spironolactone.⁷ Topical eflornithine is prescribed for the treatment of facial hirsutism, but electrolysis is often needed.⁵ Infertility may be treated with clomiphene citrate, among other gynecologic interventions. Metformin therapy, while not FDA approved for the treatment of PCOS, improves insulin sensitivity and may decrease circulating androgen levels in women with PCOS, both decreasing hirsutism and improving ovulation and menstrual cyclicity. Metformin may be used simultaneously with combination oral contraceptives.⁵ All patients with PCOS should be screened for dyslipidemia and glucose intolerance/type 2 diabetes regardless of body mass index or weight.

DYSFUNCTIONAL UTERINE BLEEDING

Dysfunctional uterine bleeding is vaginal bleeding that occurs in cycles less than 21 days or longer than 42 days, lasts longer than 8 days, results in blood loss greater than 80 mL, and/or is associated with anemia. There are 2 general types: anovulatory and ovulatory dysfunctional uterine bleeding. These are further categorized by etiology: hormonal, local pathology (vagina, cervix, uterus), bleeding diathesis (platelet disorder, coagulopathy), or pregnancy related.^2,8

DIFFERENTIAL DIAGNOSIS

Hormonal Causes

The most common cause of dysfunctional uterine bleeding in adolescents is anovulation with exposure of the endometrium to unopposed estrogen, resulting from the immaturity or dysfunction of the hypothalamic-pituitary-gonadal axis. Rhythmic fluctuations of estrogen levels are initiated early in puberty and increase in amplitude as puberty progresses. Eventually, peak estrogen levels sufficient to stimulate endometrial proliferation, menstruation, and ovulation are attained. Anovulatory cycles are common during the first 2 to 3 years after menarche (may persist up to 5 years) and are characterized by oscillations in estrogen levels and lack of progesterone production (see Chapters 64 and 540). Prolonged absence of progesterone results in an abnormally thick and fragile endometrial lining that may slough in a disorderly and irregular fashion, leading to irregular and excessive menstrual bleeding. Bleeding secondary to anovulation is a diagnosis of exclusion and should be made only after a careful evaluation to eliminate other more serious causes. Although characteristically associated with amenorrhea or oligomenorrhea, problems including polycystic ovary disease, hyperthyroidism, hypothyroidism, Addison disease, elevated serum prolactin and congenital adrenal hyperplasia may also present with dysfunctional uterine bleeding. Common medications such as hormonal contraceptives (Depo-Provera, oral contraceptive pills, Implanon) result in abnormal bleeding.

Local Pathology

Underlying diseases and abnormalities of the reproductive organs, including vagina, cervix, uterus, and ovary, are a common cause of dysfunctional uterine bleeding. Vaginal causes of abnormal bleeding include foreign bodies (eg, forgotten tampons or condoms), intrauterine devices, lacerations from either sexual abuse or intravaginal insertion of objects, hymenal tears, and tumors (sarcomas). Cervical factors associated with bleeding include cervicitis, dysplasia, malignancy, hemangiomas, cervical polyps, and large fragile condylomas. Cervical and vaginal abnormalities are usually associated with light spotting or postcoital bleeding rather than frank vaginal bleeding. Uterine causes of unusual bleeding include endometritis with or without salpingitis. Endometritis most commonly results from ascending infections with sexually transmitted organisms such as Chlamydia trachomatis and Neisseria gonorrhoeae. Submucosal myomas, endometriosis, arteriovenous malformations, and uterine cancers are associated with irregular bleeding. Ovarian cysts and malignant and benign tumors may also be related to abnormal bleeding.

Bleeding Diatheses

The most common cause of excessive menstrual bleeding requiring hospitalization is a bleeding disorder. Abnormal vaginal bleeding at the time of menarche may be the initial manifestation. Soaking through double protection or leaking onto the sheets at night indicates the need for further evaluation. The most common cause is von Willebrand disease, which has a prevalence of 1%.¹ Factor VIII or IX deficiency, hereditary or acquired thrombocytopenia (including chemotherapy induced), platelet disorders, consumptive coagulopathies, thalassemia major, Fanconi anemia, aplastic anemia, and leukemia should also be considered. The depletion of vitamin K–dependent clotting factors, fibrinogen, and plasminogen secondary to liver or mucosal bowel disease may also contribute to excessive bleeding. Patients receiving hemodialysis or chemotherapy may have uterine bleeding problems leading to excessive blood loss. Other chronic disease states that present with clotting abnormalities associated with dysfunctional uterine bleeding include renal failure, iatrogenic bone marrow suppression, and anticoagulant therapy (heparin, Coumadin).^2,8-11

Pregnancy-Related Causes

Complications of pregnancy are common causes of abnormal bleeding and include spontaneous abortion, incomplete abortion, threatened abortion, ectopic pregnancy, molar pregnancy, and complications from legal or illegal therapeutic abortions. Endometritis can also occur after gynecologic procedures such as therapeutic abortions and delivery (postpartum infections).

EVALUATION AND MANAGEMENT

The evaluation of a patient with abnormal vaginal bleeding should be performed systematically. Causes requiring immediate intervention must be excluded first. The primary goals of clinical assessment are to determine the acuity, duration, and volume of blood loss as well as assess the need for medication, hospitalization, surgical intervention, or transfusion. Physical examination includes orthostatic blood pressures and pulse, neurologic examination, and pelvic examination. Laboratory evaluation includes a complete blood and platelet count, appropriate sexually transmitted disease cultures, and a urine pregnancy test. Patients with vaginal bleeding with an acute abdominal complaint and/or positive pregnancy test should have immediate gynecologic consultation for possible ectopic pregnancy. Patients with significant blood loss resulting in anemia should be evaluated for both bleeding disorders and thyroid disorders. Because both polycystic ovarian syndrome and prolactinomas can occasionally present with irregular bleeding, measurement of luteinizing hormone, follicle-stimulating hormone, and prolactin levels should be considered.

A complete description of the management of all of the causes of vaginal bleeding is beyond the scope of this section. Patients with significant orthostatic blood pressure or heart rate changes or who present with an acute abdomen should have appropriate fluid, electrolyte, and hemostatic stabilization. Abdominal and pelvic evaluation (pelvic examination, ultrasonography, and other radiographic techniques) and gynecologic and surgical consultation should be pursued as indicated. Brisk uterine bleeding can be stopped with administration of Premarin, 25 mg intravenously every 6 hours for a total of 6 doses. Combination oral contraceptives should be started simultaneously with the intravenous Premarin in order to stabilize the endometrium. If the patient is hemodynamically stable and only mildly anemic, the bleeding can be stopped by initiating a fixed-dose estrogen-progesterone combination oral contraceptive, 1 pill every 6 hours until bleeding stops. The dose is tapered over the following 3 to 4 weeks, at which time a withdrawal bleed of 3 to 5 days is permitted, and cyclic combination oral contraceptive therapy is initiated. Antiemetics may be necessary with high-dose estrogen therapy. After 4 to 6 months, an attempt to discontinue medication can be evaluated under close medical supervision. Other regimens include cyclic progesterone therapy. This regimen appears to be less efficacious in patients with primary dysfunctional uterine bleeding. Iron replacement may be necessary for anemic patients (Hb < 12 g/dL). For patients with mild breakthrough bleeding secondary to hormone use (eg, progesterone-only contraception), a trial of nonsteroidal anti-inflammatory drugs is recommended to decrease blood flow to the endometrium.^2,8 Dilation and curettage (D&C) is rarely indicated in treatment of adolescents with dysfunctional uterine bleeding and is contraindicated in patients with bleeding disorders.⁹

If an underlying disorder of hemostasis is suspected, it is important to obtain laboratory testing before the initiation of hormonal therapy or blood product administration because clotting studies may be impacted. Laboratory evaluation for von Willebrand disease should include von Willebrand factor antigen, factor VIII activity, or ristocetin cofactor.¹ Other important studies include a prothrombin time and partial thromboplastin time. Management strategies include decreasing the frequency of menstrual flow and/or inducing an atrophic endometrium. Options include continuous daily combined oral contraceptive use with a controlled withdrawal bleed every 3 to 4 months or induction of endometrial atrophy with either daily oral progesterone, intramuscular Depo-Provera every 3 months, or GnRH analogs such as leuprolide acetate. In addition to hormonal therapy, intranasal 1-desamino-8-d-arginine vasopressin (DDAVP) is an alternative therapy for individuals with von Willebrand disease or platelet dysfunction.^2,8,12 Other therapies include antifibrinolytics (eg, tranexamic acid). Nonsteroidal anti-inflammatory drugs are contraindicated in individuals with inherited bleeding disorders.¹²

DYSMENORRHEA

Dysmenorrhea, the experience of painful menstrual cramping and other menstruation-associated symptoms, remains one of the most common reproductive system complaints of menstruating female adolescents and is a leading cause of school and work absenteeism.

Epidemiology and clinical presentation The prevalence of dymenorrhea approaches 60% in middle to late adolescence after the establishment of ovulatory menstrual cycles. Primary dysmenorrhea is secondary to painful prostaglandin- and leukotriene-stimulated uterine vasoconstriction and myometrial contractions. There are 2 distinct pathways involved: the cyclooxygenase-dependent synthesis of prostaglandins (PGE₂, PGD₂, and PGF_2α) and the lipoxygenase-dependent synthesis of leukotrienes.⁸ A major increase of prostaglandins is seen within the endometrium during the first 36 to 48 hours of menses, which parallels the usual time of greatest discomfort. The 30% to 40% of females who do not respond to cyclooxygenase inhibitors (eg, ibuprofen, naproxen sodium) are thought to have dysmenorrhea mediated primarily through the lipooxygenase-dependent pathway. Primary dysmenorrhea may not become problematic until 1 year or more after menarche because it is linked to ovulatory cycles.

Secondary dysmenorrhea is associated with specific physiological and pathologic conditions, including pelvic infections (eg, endometritis, pelvic inflammatory disease), ectopic pregnancy, miscarriage, endometriosis, adhesions, intrauterine contraceptive device, uterine leiomyomas (rare in adolescence), ovarian cyst, cervical stenosis, and other anatomic abnormalities causing obstruction of the outflow tract.

Evaluation A confidential history should include the assessment of the last menstrual period, age at menarche, previous pregnancies and outcomes, use of contraceptives including condoms, sexually transmitted disease history and current symptomatology, date of onset of pain, relationship of onset and duration of pain to menses, and impact of previous pain medications by type. Associated symptoms may include nausea, vomiting, diarrhea, fatigue, headache, low back pain, thigh pain, dizziness, and syncope. Assessment includes a complete physical examination and pelvic examination with screening for sexually transmitted diseases.

Treatment Therapy for primary dysmenorrhea focuses on inhibiting the synthesis or action of prostaglandins. Standard therapy includes ibuprofen, naproxen sodium, or mefenamic acid begun 1 to 2 days before the expected onset of menses. Combination oral contraceptive pills improve symptoms in 90% of young women with primary dysmenorrhea but may take 3 cycles to achieve maximum therapeutic benefit.² In addition, patients should be counseled to avoid smoking and also to increase dietary omega-3 polyunsaturated fatty acids.⁸ Patients diagnosed with primary dysmenorrhea who do not improve with adequate therapy should be evaluated for causes of secondary dysmenorrhea.

REFERENCES

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