Normal menstrual cycles during adolescence occur every 21 to 45 days, with duration of bleeding up to 7 days and blood loss of 20 to 60 mL (see Chapter 533). For those whose cycles are abnormal, the most common menstrual disorders in adolescents include amenorrhea, abnormal uterine bleeding, and dysmenorrhea, which are discussed in this chapter.
Amenorrhea, the absence of menses, can be either temporary or permanent. Traditionally, there are two categories: primary amenorrhea and secondary amenorrhea. Primary amenorrhea is defined as failure to menstruate either (1) by age 15 in the presence of breast development and normal growth, (2) within 3 years of thelarche, or (3) by age 13 with the absence of secondary sexual characteristics. Also, when delay in secondary sexual development and amenorrhea exists or cyclic pelvic pain accompanies primary amenorrhea, prompt evaluation should occur.
Secondary amenorrhea is cessation of menses for greater than 3 months or 90 days. While the etiologies of primary amenorrhea are typically genetic or anatomic, all causes of secondary amenorrhea may also present as primary amenorrhea. The evaluation of infrequent menses with cycle length longer than 6 weeks is the same as amenorrhea in this discussion. See Chapter 534 for further discussion on amenorrhea in the setting of delayed puberty.
Do not overlook pregnancy, the most common cause of secondary amenorrhea, as a cause of primary amenorrhea. (See Chapter 80 for more information on the diagnosis of pregnancy.) Beyond pregnancy, the etiologies of primary and secondary amenorrhea include anatomic abnormalities or fall into three categories depending on the function of the pituitary gland in relation to the ovary: hypogonadotropic hypogonadism, hypergonadotropic hypogonadism, and eugonadotropic eugonadism. Another common classification system divides causes based on location of dysfunction within the hypothalamic–pituitary–adrenal (HPA) axis: hypothalamic, pituitary, ovarian, or other.
Hypogonadotropic hypogonadism indicates inadequate hypothalamic–pituitary stimulation of the ovary, and low levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and estrogen characterize this state. Hypothalamic amenorrhea results from partial or complete inhibition of gonadotropin-releasing hormone (GnRH) release from the hypothalamus. See Table 79-1 for causes of amenorrhea characterized by hypogonadotropic hypogonadism. Excessive exercise and weight loss leading to amenorrhea may represent an eating disorder (see Chapter 76). Local lesions in the hypothalamus (eg, infiltrative processes, calcifications, gliomas, and germinomas), traumatic brain injury (TBI), and central nervous system radiation are all rare causes of GnRH deficiency. Isolated GnRH deficiency is associated with the absence (anosmia) or impairment (hyposmia) of the ability to smell (Kallman syndrome). Medications and illicit drugs may also result in amenorrhea.
TABLE 79-1DIFFERENTIAL DIAGNOSES FOR PRIMARY AND SECONDARY AMENORRHEA, NEGATIVE PREGNANCY TEST ||Download (.pdf) TABLE 79-1DIFFERENTIAL DIAGNOSES FOR PRIMARY AND SECONDARY AMENORRHEA, NEGATIVE PREGNANCY TEST
| ||Hypogonadotropic Hypogonadism ||Hypergonadotropic Hypogonadism ||Eugonadotropic Eugonadism |
|Gonadotropin Levels ||Low FSH, normal/low LH, low estradiol ||High FSH, normal/high LH ||Normal FSH, LH, and estradiol |
|Differential Diagnosis || |
Constitutional delay of puberty
Anorexia nervosa/female athlete triad
Isolated GnRH deficiency (Kallaman Syndrome)
Primary ovarian insufficiency
Compromised blood supply
Turner syndrome (45,XO)
Androgen insensitivity (46,XY)
Abnormalities of ovarian FSH receptors
Defects in estrogen biosynthesis
Pituitary dysfunction and deficiencies or the inability to synthesize adequate amounts of gonadotropins may result from pituitary lesions, but panhypopituitarism and prolactinomas are more common. In panhypopituitarism, gonadotropin deficiency occurs before the development of changes in thyroid or adrenal function; isolated gonadotropin deficiency is rare.
The most common pituitary tumor causing amenorrhea is the prolactinoma. This type of tumor causes inhibition of the hypothalamic–pituitary–gonadal axis by secreting abnormally high levels of prolactin. Only 50% to 60% of females with adenomas have galactorrhea. The absence of galactorrhea does not eliminate suspicion for the tumor. Rarely, adenomas increase in size, causing symptoms such as vision change and headache associated with space-occupying lesions. Other causes of hyperprolactinemia include psychoactive drugs (eg, haloperidol, phenothiazines, amitriptyline, benzodiazepine, and cocaine), breastfeeding, and renal failure. Both hypercortisolism and hypothyroidism are associated with hyperprolactinemia and amenorrhea.
High levels of LH and FSH characterize hypergonadotropic hypogonadism. This ovarian dysfunction manifests clinically with menstrual irregularities. Such disorders include gonadal dysgenesis (abnormal ovarian development) and primary ovarian insufficiency (POI). There are multiple etiologies for POI (Table 79-1). Gonadal dysgenesis is seen in Turner syndrome (45,XO) (see Chapter 534) and fragile X, and in women with normal karyotype (46,XX) gonadal dysgenesis. Secondary amenorrhea is also associated with mosaic Turner syndrome.
Rarer causes of hypergonadotropic hypogonadal amenorrhea include pseudo-ovarian failure secondary to gonadotropin-resistant ovary syndrome (an abnormality of ovarian follicle-stimulating hormone receptors) and defects in estrogen biosynthesis, including 17-hydroxylase deficiency and 17-ketosteroid reductase deficiency. Late-onset congenital adrenal hyperplasia (CAH, 21-hydroxylase deficiency) may first present with secondary amenorrhea and signs of virilization (eg, clitoromegaly and hirsutism). Androgen insensitivity (46,XY) is the insensitivity of peripheral tissues to circulating androgens, external female phenotype, and amenorrhea.
Normal FSH, LH, and estrogen levels characterize the eugonadotropic state. If primary amenorrhea occurs in this context, it is anatomic in origin. Defects in the development of the müllerian duct system are associated with primary amenorrhea resulting in imperforate hymen, vaginal atresia or absence, or other malformations of the cervix and the uterus. Except in cases of absence of the uterine cavity or endometrium, developmental genital tract obstructions present with painful swelling of the reproductive tract above the area of the blockage. These include hematocolpos (vaginal), hematometra (uterus), and hematoperitoneum (leakage of menstrual blood into the peritoneal cavity). The pain is cyclic in nature, coinciding with the timing of a menstrual cycle. Mayer-Rokitansky-Küster-Hauser syndrome is müllerian agenesis with primary amenorrhea resulting from absence or hypoplasia of the vagina, cervix, and/or uterus.
Secondary amenorrhea associated with normal FSH, LH, and estrogen levels has a wide differential diagnosis (Table 79-1), including uterine scarring and hyperandrogenic states. Uterine synechiae (Asherman syndrome) occurring after endometrial manipulation (eg, pregnancy, dilation and curettage) or infection (eg, pelvic inflammatory disease, tuberculous endometritis) can lead to secondary amenorrhea. Causes of amenorrhea and hyperandrogenism (eg, hirsutism and/or virilization) include polycystic ovarian syndrome (PCOS), virilizing ovarian or adrenal tumors, and drugs, including phenytoin, oral contraceptives, cocaine, and anabolic steroids.
Polycystic Ovarian Syndrome
PCOS is the most common endocrine disorder in reproductive-aged women and a common cause of eugonadotropic secondary amenorrhea in adolescents. PCOS can also cause primary amenorrhea. Differing definitions and diagnostic criteria describe this clinically heterogeneous syndrome. The hallmarks of PCOS include ovulatory dysfunction and hyperandrogenism. Ovulatory dysfunction is clinical evidence of menstrual cycle irregularity or polycystic ovaries on ultrasound or other imaging. Hyperandrogenism is either (1) the clinical presence of hirsutism, inflammatory acne, or androgenic alopecia, or (2) biochemical elevations in serum testosterone and/or dehydroepiandrosterone sulfate (DHEAS). The hyperandrogenism is secondary to ovarian thecal cell proliferation and the resultant excess androgen production. The current hypothesis is that peripheral insulin resistance, which may or may not manifest as increased serum insulin levels, and an increase in serum LH relative to FSH contribute to thecal cell proliferation and further stimulation of androgen production. Although LH elevations and insulin resistance are common in women with PCOS, they are not required for diagnosis. Other clinical comorbidities include obesity, insulin resistance, glucose intolerance, and type II diabetes; mixed dyslipidemia (eg, low high-density lipoprotein, elevated triglycerides); metabolic syndrome; infertility; and endometrial cancer.
There are four accepted sets of diagnostic criteria. The National Institutes of Health criteria (1990) define PCOS by evidence of hyperandrogenism and chronic anovulation with exclusion of other causes of androgen excess. The Rotterdam criteria (2003) state that 2 of the following 3 findings are required for diagnosis: menstrual irregularity due to anovulation or oligo-ovulation, clinical and /or biochemical signs of hyperandrogenism, or polycystic ovaries (by ultrasound). The Androgen Excess and PCOS Society criteria (2006) specify that both androgen excess and ovulatory dysfunction must be present. Recent Pediatric Endocrine Society criteria for adolescent PCOS include the otherwise unexplained combination of abnormal uterine bleeding that persists for 1 to 2 years post-menarche and evidence of hyperandrogenism.
Since increased androgen levels may occur during normal pubertal development, confirmatory testing of hyperandrogenism is advisable. While PCOS accounts for up to 85% of adolescent hyperandrogenism, it is important to exclude other potential causes including CAH and other disorders of adrenal steroid metabolism, virilizing tumors, acromegaly, drugs such as valproic acid, and others. Routine ultrasound examination of the ovaries for diagnosing PCOS during adolescence is controversial since polycystic appearing ovaries may be a normal finding.
See Table 79-2 for a guide to history, physical examination, and evaluation.
TABLE 79-2HISTORY, PHYSICAL EXAMINATION, AND LABORATORY EVALUATION OF ADOLESCENT MENSTRUAL PROBLEMS ||Download (.pdf) TABLE 79-2HISTORY, PHYSICAL EXAMINATION, AND LABORATORY EVALUATION OF ADOLESCENT MENSTRUAL PROBLEMS
|History || |
Pubertal development: age at pubarche and thelarche
Menstrual pattern: age at menarche, cycle length, number of days bleeding, number of pads or tampons/day (PBAC), pain with menses
Sexual activity: age at coitarche, partners (male and/or female), practices (vaginal, oral, anal, paraphernalia), past STI, pregnancy, protection (condoms, birth control)
Past medical and surgical: premature birth, chronic illnesses (liver, kidney, bleeding disorders), known endocrinopathy, uterine procedures
Family: pubertal delay, bleeding disorders, thyroidal illness, menstrual problems
Review of systems: Weight changes, dieting and exercise habits, easy bruising and bleeding (epistaxis, frequent gum bleeding), galactorrhea, headaches, visual field defects, vaginal discharge, cyclic pelvic pain, dyspareunia, mental health (stress, anxiety, depression)
Medications and illicit drugs: contraceptives, antiepileptics, SSRIs, haloperidol, phenothiazine, benzodiazepines, heroin, cocaine
|Physical Examination || |
Vital signs: height, weight, body mass index, blood pressure, pulse, temperature
Thyroid: assess for thyromegaly
Skin: hirsutism (Ferriman-Gallwey score), inflammatory acne, bruising, acanthosis nigricans
Breast: SMR, galactorrhea
Abdomen: hepatomegaly, enlarged uterus
Pelvic: SMR, clitoromegaly, vulva, introitus (hymen, color of vaginal mucosa, vaginal patency), vaginal discharge, cervical abnormalities such as polyps, hematocolpos, hematometra
Other: Turner stigmata (webbed neck, shield chest, and wide-spaced nipples), anosmia
|Laboratory Studies || |
Amenorrhea and AUB: FSH, prolactin, TSH
Androgen excess: testosterone (free and total), SHBG, DHEAS, 17-OHP
AUB/HMB: PT/PTT, CBC, von Willebrand comprehensive panel
As indicated: cortisol, estradiol, karyotype, expanded coagulopathy evaluation
|Diagnostic Imaging ||Pelvic ultrasound |
The evaluation of amenorrhea requires a careful history and physical assessment. Taking a developmentally appropriate sexual history is essential. Exclude pregnancy via urine or serum pregnancy test before performing further workup. Constitutional delay is more common in boys and should be a diagnosis of exclusion. Inquire about family history of pubertal delay, stature in relation to family members, and presence of neonatal health problems including prematurity. Elucidate information suggesting additional causes of secondary amenorrhea, including symptoms of estrogen deficiency (eg, hot flashes, vaginal dryness) or risk factors for uterine scarring.
Neurologic examination is required to assess for increased intracranial pressure (papilledema) or expanding mass (bitemporal hemianopsia is one hallmark of pituitary tumors). If a complete pelvic examination is not possible for anatomic, cultural, or psychosocial reasons, an alternative is recto-abdominal examination. 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 MRI should be performed.
Screening Laboratory Tests
After ruling out pregnancy, initial tests should include serum FSH levels, prolactin, and thyroid function tests (TSH) (Fig. 79-1). If physical examination reveals hyperandrogenism, obtain serum testosterone (free and total) and DHEAS levels. Very high DHEAS levels are concerning for adrenal dysfunction. Prolactin levels of 20 to 60 µg/L may be difficult to interpret and need repeating while levels > 200 µg/L suggest macroadenoma. Some clinicians will also order a serum estradiol level. High FSH levels warrant a chromosomal evaluation.
Evaluation of primary and secondary amenorrhea. CNS, central nervous system; DHEAS, dehydroepiandrosterone sulfate; FSH, follicle-stimulating hormone; TSH, thyroid-stimulating hormone; UA, urinalysis.
Confirm any abnormal laboratory results. A progesterone challenge indirectly evaluates the presence of endogenous estrogen and the competence of the reproductive outflow tract from uterus to vaginal opening. Prescribe medroxyprogesterone acetate 10 mg by mouth daily for 7 days; within 2 to 7 days of completion, uterine withdrawal bleeding should occur. Bleeding confirms competence of the hypothalamic–pituitary–gonadal axis and patency of the outflow tract. If no bleeding occurs after progesterone challenge, the reproductive outflow tract is abnormal or endogenous estrogen is inadequate. In such situations, the second step of the hormonal challenge test is to prime the endometrium: 2.5 mg of oral conjugated estrogen for 25 days with 10 mg of oral medroxyprogesterone acetate added from day 16 to day 25. It may be necessary to repeat this a second time if no bleeding is elicited. If no bleeding occurs after the second round, obtain pelvic sonography and further hormonal assays, including a serum estradiol level.
Suspected outflow obstruction of the reproductive tract necessitates appropriate imaging studies, further defining existing anatomy. Treatment of anatomic abnormalities is reconstructive surgery. Surgical correction of vaginal agenesis is appropriate prior to adulthood and before sexual debut.
Chapters 516 and 534 review the complete evaluation and treatment of hypothalamic-pituitary failure. Elevated prolactin levels in an asymptomatic patient suggest pituitary microadenoma; consider bromocriptine (a dopamine agonist) therapy. Treat ovarian failure with hormone replacement therapy, 0.3 to 0.625 mg of conjugated estrogen (the lowest amount to achieve the desired estrogen effect) on days 1 through 25 along with medroxyprogesterone acetate 10 mg on days 16 through 25 to avoid the effect of unopposed estrogen on the endometrium, which is linked to endometrial cancer. Counseling regarding bone health and calcium requirements is imperative. Provide appropriate counseling resources for those diagnosed with irreversible infertility of any cause.
PCOS treatment begins with lifestyle modification, emphasizing dietary adjustment and exercise. A 5% reduction in weight may regulate ovulation and improve cycle regularity. Combined oral contraceptives (or the combination patch or vaginal ring) is the first-line pharmacologic intervention since each provides cycle regulation and endometrial protection along with anti-androgenic effects mediated by increases in sex hormone-binding globulin. For women in whom estrogen is contraindicated, progesterone-only therapies (eg, the pill, monthly injection, subdermal implant, or IUD) will also provide endometrial protection but are limited in anti-androgenic effects. Anti-androgens such as spironolactone are effective against acne and hirsutism. Treatments for facial hirsutism include topical eflornithine and electrolysis. Metformin therapy improves insulin sensitivity and may decrease circulating androgen levels in women with PCOS, both decreasing hirsutism and improving ovulation and cycle regularity. Simultaneous use of metformin and combination oral contraceptives is beneficial. All patients with PCOS should be screened for dyslipidemia (fasting lipid profile) and glucose intolerance/type 2 diabetes (2-hour oral glucose tolerance test or hemoglobin A1C) regardless of body mass index or weight.
ABNORMAL UTERINE BLEEDING
Abnormal uterine bleeding (AUB) is vaginal bleeding that occurs in cycles shorter than 21 days or longer than 45 days, lasts longer than 8 days, results in blood loss greater than 80 mL, and/or is associated with anemia. There are two general types: anovulatory and ovulatory dysfunctional uterine bleeding, with further classification by etiology: hormonal, local pathology (ie, vagina, cervix, and uterus), coagulopathy, and pregnancy related.
The International Federation of Gynecology and Obstetrics (FIGO) recommends using the PALM-COEIN classification system to identify the etiology of AUB and heavy menstrual bleeding (HMB). PALM- COEIN stands for polyp, adenomyosis, leiomyoma, malignancy and hyperplasia, coagulopathy, ovulatory dysfunction, endometrial, iatrogenic, and not yet classified. Under this system, etiologies are written as AUB followed by the corresponding letter, eg, AUB- P (AUB caused by polyps). Multiple etiologies may exist in one patient; some conditions are uncommon in the adolescent population. The most common adolescent causes are AUB-C, AUB-O, and AUB-I.
Polyp, Adenomyosis, Leiomyoma, Malignancy, and Endometrial
In general, polyps (AUB-P), adenomyosis (AUB-A), leiomyoma (AUB-L), and malignancies of the vagina and uterus (AUB-M) do not occur frequently in adolescents but should be included in the differential diagnosis when evaluating an adolescent with AUB and HMB. 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. Endometritis (AUB-E) most commonly results from subclinical infections with sexually transmitted organisms such as Chlamydia trachomatis. Submucosal myomas, endometriosis, arteriovenous malformations, and uterine cancers are associated with irregular bleeding.
Ovulatory dysfunction (AUB-O) is the most common cause of AUB in adolescents, resulting from the immaturity or dysfunction of the hypothalamic–pituitary–gonadal axis. Anovulatory cycles are common during the first 1 to 2 years after menarche (75% are normal by year 1, 95% by year 5) and are characterized by oscillations in estrogen levels and lack of, or inadequate, progesterone production (see Chapters 66 and 533). This results in an abnormally thick and fragile endometrial lining that may slough in a disorderly and irregular fashion, leading to irregular menstrual bleeding and HMB. Bleeding secondary to anovulation is a diagnosis of exclusion and made only after a careful evaluation to eliminate other more serious causes. Potential hormonal causes of AUB include those previously described for secondary amenorrhea (Table 79-1).
Iatrogenic (AUB-I) causes include common medications such as hormonal contraceptives (injectable, implants, oral contraceptive pills, IUD), antiepileptics, anticoagulants, chemotherapy, etc. Drug interactions with hormonal contraceptives and noncompliance can cause AUB.
Coagulopathies (AUB-C) are the most common cause of HMB requiring hospitalization. AUB at the time of menarche may be the initial manifestation. Soiling clothes, 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%; one should consider other primary and acquired coagulopathies and thrombocytopenias as well. 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 with renal disease or hemodialysis might have AUB leading to HMB.
Vaginal causes of AUB (AUB-N) include foreign bodies (eg, forgotten tampons or condoms), lacerations from either sexual abuse or intravaginal insertion of objects, and hymen tears. Ovarian cysts and malignant and benign tumors may also cause abnormal bleeding.
Complications of pregnancy may present as AUB (Chapter 80). Medical emergencies include ectopic pregnancy and threatened abortions.
EVALUATION AND MANAGEMENT
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. First, exclude causes requiring immediate intervention. Table 79-2 outlines the pertinent history, physical examination, and laboratory evaluation. Women with vaginal bleeding, an acute abdominal complaint, and/or positive pregnancy test need immediate gynecologic consultation as this may indicate an ectopic pregnancy. Patients with significant blood loss resulting in anemia should be evaluated for both coagulopathies and thyroid disorders.
Stabilize patients with hemodynamic changes or an acute abdomen using appropriate fluid, electrolyte, and hemostatic stabilization. Stop acute HMB by administering conjugated estrogen, 25 mg intravenously every 6 hours for a total of 6 doses, with simultaneous use of combination oral contraceptives to stabilize the endometrium. If the patient is hemodynamically stable and only mildly anemic, prescribe a fixed-dose estrogen-progesterone combination oral contraceptive, one pill every 6 hours until bleeding stops. Taper the dose over the following 3 to 4 weeks, at which time a withdrawal bleed of 3 to 5 days is permitted, followed by cyclic combination oral contraceptive therapy. An antiemetic may be necessary with high-dose estrogen therapy. After 4 to 6 months, attempt to discontinue medication under close medical supervision. Other regimens include cyclic progesterone therapy; this regimen appears to be less efficacious in patients with primary AUB. Iron and folate replacement may be necessary for anemic patients (Hgb < 12 g/dL). For patients with mild breakthrough bleeding secondary to hormone use (eg, progesterone-only contraception), a trial of nonsteroidal anti-inflammatory drugs (NSAIDs) is recommended to decrease blood flow to the endometrium. Treatment of adolescents with AUB rarely requires dilation and curettage; it is contraindicated in patients with bleeding disorders.
Management strategies for AUB-O 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-deamino-8-D-arginine vasopressin (DDAVP) is an alternative therapy for individuals with von Willebrand disease or platelet dysfunction. Other therapies include antifibrinolytics (eg, tranexamic acid). An inherited bleeding disorder is a contraindication for the use of NSAIDs.
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 and decreased quality of life. The prevalence of dysmenorrhea approaches 50% to 93% during adolescence, peaking 1 to 2 years after menarche. This coincides with the establishment of ovulatory cycles. Most experience mild-to-moderate pain, but incapacitation occurs in 10% to 20% for 1 to 3 days each month; even more miss school and social activities.
PATHOPHYSIOLOGY AND CLINICAL PRESENTATION
Alterations in four chemicals cause primary dysmenorrhea: prostaglandins, leukotrienes, prostacyclin, and vasopressin. Increased levels of prostaglandin (PGF2α) and leukotriene C4 and D4 stimulate uterine vasoconstriction, pain sensitization, and myometrium contractions. Prostacyclin is a vasodilator and muscle relaxant, but decreased levels occur in women with dysmenorrhea. Lastly, overproduction of vasopressin further increases uterine contractions. These four alterations lead to intense uterine contractions, vasoconstriction, and ischemic pain. During the first 36 to 48 hours of menses, prostaglandins increase within the endometrium, corresponding with the time of greatest discomfort. Beyond pain, systemic effects of the altered chemical milieu include nausea, vomiting, diarrhea, fatigue, headache, low back pain, thigh pain, dizziness, and syncope.
Secondary dysmenorrhea is associated with specific physiological and pathologic conditions, including pelvic infections (eg, endometritis, pelvic inflammatory disease), ectopic pregnancy, miscarriage, endometriosis, adhesions, IUD placement, uterine leiomyomas (rare in adolescence), ovarian cyst, cervical stenosis, and other anatomic abnormalities causing obstruction of the outflow tract. Nongynecologic causes include inflammatory bowel disease, irritable bowel syndrome, urinary tract problems, musculoskeletal conditions, and psychogenic (abuse).
A thorough history should detail age at menarche, date of onset of pain, relationship of onset and duration of pain to menses, date of last menstrual period, and impact of previous pain medications by type. A confidential interview should include the assessment of sexual activity and practices, history of abuse, use of contraceptives including condoms, sexually transmitted disease history, and previous pregnancies and outcomes. A review of systems will identify associated systemic symptoms. Evaluation includes a complete physical examination and pelvic examination with screening for secondary causes as described earlier in this chapter. If there is a secondary cause or there is minimal improvement after 6 months of treatment, proceed with additional laboratory studies, diagnostic imaging, and surgical procedures as necessary.
Therapy for primary dysmenorrhea focuses on inhibiting the synthesis or action of prostaglandins. Standard therapy includes appropriately dosed NSAIDs such as ibuprofen, naproxen sodium, or mefenamic acid begun 1 to 2 days before the expected onset of menses and continued through day 2 to 3 of bleeding. The 30% to 40% of females who do not respond to cyclooxygenase inhibitors (NSAIDs) potentially have dysmenorrhea mediated primarily through the lipoxygenase-dependent leukotriene pathway. Combination oral contraceptive pills (OCPs) improve symptoms in 90% of young women with primary dysmenorrhea, but it may take 3 cycles to achieve maximum therapeutic benefit. NSAIDs and OCPs used together can improve symptom relief. In addition, patients should be counseled to avoid smoking and caffeine. Alternative treatments noted to be effective include omega-3 polyunsaturated fatty acids, vitamin E, vitamin B1, and minerals such as magnesium. Patients diagnosed with primary dysmenorrhea who do not improve with 6 months of adequate therapy should be evaluated for causes of secondary dysmenorrhea.
PJ. Menstruation in adolescents: what do we know? And what do we do with the information? J Pediatr Adolesc Gynecol
American College of Obstetricians and Gynecologists. ACOG Committee Opinion No. 651: Menstruation in girls and adolescents: using the menstrual cycle as a vital sign. Obstet Gynecol
NA. The medical management of abnormal uterine bleeding in reproductive-aged women. Am J Obstet Gynecol
G. Evaluation and management of adolescent amenorrhea. Ann N Y Acad Sci
Z. Dysmenorrhea in adolescents and young adults: an update on pharmacological treatments and management strategies. Expert Opin Pharmacother
G. The prevalence and risk factors of dysmenorrhea. Epidemiol Rev
et al. Diagnosis and treatment of polycystic ovary syndrome: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab
IS; FIGO Working Group on Menstrual Disorders. FIGO classification system (PALM-COEIN) for causes of abnormal uterine bleeding in nongravid women of reproductive age. Int J Gynaecol Obstet
RL. The diagnosis of polycystic ovary syndrome in adolescents. Pediatrics
F. Adolescent dysmenorrhea. In: Sultan
C, ed. Pediatric and Adolescent Gynecology: Evidence–Based Clinical Practice. 2nd ed. Basel, Switzerland: Karger; 2012:171–180.