1
 A complete history should include the following:  Age at menarche Menstrual frequency, length of period, estimated menstrual flow, and presence or absence of intermenstrual bleeding  Associated symptoms Onset, duration, type, and severity of pain, as well as its relation to the menstrual cycle External factors affecting the pain Impact of dysmenorrhea on physical and social activity rogression of symptom severity !exual and obstetric history "linical features of primary dysmenorrhea include the following: Onset shortly after menarche #$% months& 'sual duration of ()*+ hours #often starting several hours before or -ust after the menstrual flow& "ramping or laborli.e pain /ac.ground of constant lower abdominal pain, rad iating to the bac. or thigh Often unremar.able pelvic examination findings #including rectal& 0he following may indicate secondary d ysmenorrhea 12, 3 : 4ysmenorrhea beginning in the 5s or 65s, after previous relatively painless cycles 7eavy menstrual flow or irregular bleeding 4ysmenorrhea occurring during the first or second cycles after menarche elvic abnormality with physical examination oor response to nonsteroidal anti*inflammatory drugs #8!AI4s& or oral contraceptives #O"s& Infertility 4yspareunia 9aginal discharge  A complete physical examination should be performed A pelvic examination is crucial for excluding uterine irregularities, cul*de*sac tenderness, or suggestive nodularities and includes the following: Inspection of the external genitalia Inspection of the vaginal vault Inspection of the cervix /imanual examination !ee resentation for more detail Diagnosis 8o tests are specific to the diagnosis of primary dysmenorrhea 0he following laboratory studies ma y be performed to identify or exclude organic causes of secondary dysmenorrhea: "omplete blood count with differential ;onococcal and chlamydial c ultures, en<yme immunoassay, and 48A probe testing =uantitative human chorionic gonadotropin level Erythrocyte sedimentation rate 'rinalysis !tool guaiac "ancer antigen 2> assay If pelvic pathology is suspected, the following imaging studies may be considered:  Abdominal or transvaginal ultrasonography 7ysterosalpingography Intravenous pyelography "omputed tomography Magnetic resonance imaging Other more invasive studies that may be considered are as follows: ?aparoscopy 7ysteroscopy

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 A complete history should include the following:

•  Age at menarche

• Menstrual frequency, length of period, estimated menstrual flow, and presence or absence of

intermenstrual bleeding

•  Associated symptoms

•Onset, duration, type, and severity of pain, as well as its relation to the menstrual cycle

• External factors affecting the pain

• Impact of dysmenorrhea on physical and social activity

• rogression of symptom severity

• !exual and obstetric history

"linical features of primary dysmenorrhea include the following:

• Onset shortly after menarche #$% months&

• 'sual duration of ()*+ hours #often starting several hours before or -ust after the menstrual flow&

• "ramping or laborli.e pain

• /ac.ground of constant lower abdominal pain, radiating to the bac. or thigh

• Often unremar.able pelvic examination findings #including rectal&

0he following may indicate secondary dysmenorrhea12, 3 :

• 4ysmenorrhea beginning in the 5s or 65s, after previous relatively painless cycles

• 7eavy menstrual flow or irregular bleeding

• 4ysmenorrhea occurring during the first or second cycles after menarche

• elvic abnormality with physical examination

• oor response to nonsteroidal anti*inflammatory drugs #8!AI4s& or oral contraceptives #O"s&

• Infertility

• 4yspareunia

• 9aginal discharge

 A complete physical examination should be performed A pelvic examination is crucial for excluding uterineirregularities, cul*de*sac tenderness, or suggestive nodularities and includes the following:

Inspection of the external genitalia• Inspection of the vaginal vault

• Inspection of the cervix

• /imanual examination

!ee resentation for more detail

Diagnosis

8o tests are specific to the diagnosis of primary dysmenorrhea 0he following laboratory studies may beperformed to identify or exclude organic causes of secondary dysmenorrhea:

• "omplete blood count with differential

• ;onococcal and chlamydial cultures, en<yme immunoassay, and 48A probe testing

• =uantitative human chorionic gonadotropin level

• Erythrocyte sedimentation rate

• 'rinalysis

• !tool guaiac

• "ancer antigen 2> assay

If pelvic pathology is suspected, the following imaging studies may be considered:

•  Abdominal or transvaginal ultrasonography

• 7ysterosalpingography

• Intravenous pyelography

• "omputed tomography

• Magnetic resonance imaging

Other more invasive studies that may be considered are as follows:

• ?aparoscopy

• 7ysteroscopy

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• 4ilatation and curettage

!ee @or.up for more detail

Management

harmacotherapy is the most reliable and effective treatment for relieving dysmenorrhea 0reatment ofsecondary dysmenorrhea involves correction of the underlying organic cause

8!AI4s specifically approved by the 4A for treatment of dysmenorrhea are as follows:

• 4iclofenac

• Ibuprofen

• Betoprofen

• Meclofenamate

• Mefenamic acid

• 8aproxen

Other 8!AI4s and analgesics that have been used include the following:

•  Aspirin

•  Acetaminophen

• "OC* inhibitors

• 8arcotics

• Montelu.ast

 Although not approved by the 4A for treating dysmenorrhea, the following O"s are also used:

• "ombination O"s #eg, ethinyl estradiol with progestin or drospirenone&

• ?evonorgestrel intrauterine device

• 4epot medroxyprogesterone acetate

reventive measures for outpatient management of dysmenorrhea include the following:

• ?ifestyle modification

• !mo.ing cessation

Exercise

Epidemiologi

4ysmenorrhea may affect more than >5D of menstruating women, and its reported prevalence has been

highly variable #eg, (>*>D12(3 & A survey of 226 patients in a family practice setting showed a prevalence of

*((D,1663 but figures as high as 5D in women aged 2)*(> years have been reported 163 0he use of oral

contraceptives #O"s& and nonsteroidal anti*inflammatory drugs #8!AI4s&, both of which are effective in

ameliorating symptoms of primary dysmenorrhea, may hinder accurate assessment of prevalence

rimary dysmenorrhea pea.s in late adolescence and the early 5s 16(3 0he incidence falls with increasing

age and with increasing parity In many studies, 1, 6>, 6%3 though not all,163 the reported prevalence and severityof dysmenorrhea in parous women are substantially lower An epidemiologic study found no significant

differences in prevalence and severity of dysmenorrhea between nulligravid women and those in whom

pregnancy had been terminated by either spontaneous or induced abortion 13

In an epidemiologic study of an adolescent population #age range, 2*2+ years&, Blein and ?itt reported that

dysmenorrhea had a prevalence of >+D 16+3 Of patients reporting pain, 2D described it as severe, 6+D as

moderate, and (D as mild 4ysmenorrhea caused 2(D of patients to miss school frequently Although

blac. adolescents reported no increased incidence of dysmenorrhea, they were absent from school more

frequently #6%D& than whites were #26D&, even after socioeconomic status was ad-usted for

International statistics

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0he prevalence of dysmenorrhea worldwide is similar to that in the 'nited !tates Feported prevalences

have ranged from 2>)D to )>D, with higher rates reported in adolescent populations 16), 6, (5, , (2, 6>, (, (63

 A study of (5) young Italian women found that the prevalence of dysmenorrhea was )(2D when only

menstrual pain was considered, >>D when menstrual pain was associated with a need for medication,

62D when menstrual pain was associated with absenteeism, and >6D when menstrual pain was

associated with both a need for medication and absenteeism 1((3

In a longitudinal population study of ,5%+ Australian women, researchers found that those who began

smo.ing by age 26 had the greatest ris. of developing chronic dysmenorrhea Overall, approximately %5D

of the women reported experiencing dysmenorrhea symptoms at some time during the study period 1(>, (%3

0he prevalence of period pain was higher among current smo.ers #D& than nonsmo.ers #6D&

"ompared with never*smo.ers, ex*smo.ers had a 66D increased ris. of chronic symptoms #odds ratio,

266G >D confidence interval, 25> * 2%)&, while current smo.ers had a (2D increased ris. #odds ratio,

2(2G >D "I, 22+ * 2+5& After ad-ustment for socioeconomic status, lifestyle, and reproductive factors,

women who began smo.ing before or by age 26 had a >D increased ris. #odds ratio, 2>G >D "I, 22)

 H 2>&, those who began at ages 2(*2> had a >5D increased ris. #2>5G >D "I 22) to 25&, and thosewho began at age 2% or older had a %D increased ris. #2%G >D "I 256 to 2>>& 1(>, (%3

In a cross*sectional study of 622 female Iranian undergraduate students #aged 2)*+ y&, the prevalence of

primary dysmenorrhea was )2D1(+3 actors that were significantly associated with higher dysmenorrhea

pain intensity included younger age as well as familial factors #eg, low maternal formal education, family

history of dysmenorrhea&, social factors #living at home&, and menstruation factors #eg, higher menstrual

bleeding severity and shorter menstrual intervals&1(+3

 Age* and race*related demographics

0he most common causes of dysmenorrhea differ by age 0he prevalence of this condition is estimated tobe >D among adult women and as high as 5D among adolescents

8o data suggest that race affects the incidence of dysmenorrhea

atofisiologiGGGGG

7istorical attitudes toward menstrual pain were often dismissive ain was often attributed to womensemotional or psychological states or to misconceptions about sex and sexual behaviors Although theetiology and pathophysiology of dysmenorrhea have not been fully elucidated, research has led to datasupporting concrete physiologic explanations for dysmenorrhea, which discredit these prior dismissivetheories12, 26, 2(3

Primary dysmenorrhea

"urrent evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin J#;J&, a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium 12>3 0he responseto prostaglandin inhibitors in patients with dysmenorrhea supports the assertion that dysmenorrhea isprostaglandin*mediated !ubstantial evidence attributes dysmenorrhea to prolonged uterine contractionsand decreased blood flow to the myometrium

Elevated prostaglandin levels were found in the endometrial fluid of women with dysmenorrhea andcorrelated well with the degree of pain 12%3 A 6*fold increase in endometrial prostaglandins occurs from thefollicular phase to the luteal phase, with a further increase occurring during menstruation 12+3 0he increase inprostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increasedmyometrial tone and excessive uterine contraction 1+3

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?eu.otrienes have been postulated to heighten the sensitivity of pain fibers in the uterus !ubstantialamounts of leu.otrienes have been demonstrated in the endometria of women with primary dysmenorrheathat does not respond to treatment with prostaglandin antagonists 125, 2), 2, 5, 23

0he posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduceduterine blood flow, and pain in primary dysmenorrhea 1, 6, 2, (3 9asopressins role in the endometrium maybe related to prostaglandin synthesis and release

In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea0ype " pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium@omen with dysmenorrhea appear to have enhanced pain sensitivity compared to women withoutdysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain12(3 0his enhanced pain sensitivity may increase the ris. of affected women to other chronic conditions #eg,fibromyalgia& as well as negatively impact their quality of life 12(3

rimary dysmenorrhea has also been attributed to behavioral and psychological factors Although thesefactors have not been convincingly demonstrated to be causative, they should be considered if medicaltreatment fails

In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basalbody temperature, sleep patterns, and the central nervous system #"8!&, the extent of which is not

completely understood123

Secondary dysmenorrhea

Elevated prostaglandins may also play a role in secondary dysmenorrhea, but by definition, concomitantpelvic pathology must be present A number of factors may be involved in the pathogenesis of secondarydysmenorrhea, including the following:

• Endometriosis

• elvic inflammatory disease #I4&

• Ovarian cysts and tumors

• "ervical stenosis or occlusion

•  Adenomyosis

• ibroids• 'terine polyps

• Intrauterine adhesions

• "ongenital malformations #eg, bicornuate uterus or subseptate uterus&

• Intrauterine contraceptive device #I'"4&, or intrauterine device #I'4&

• 0ransverse vaginal septum

• elvic congestion syndrome

•  Allen*Masters syndrome

 Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain

Etiologi

Fis. factors for primary dysmenorrhea include the following:

• Early age at menarche #K 2 years&

• 8ulliparity

• 7eavy or prolonged menstrual flow

• !mo.ing

• ositive family history

• Obesity

Fis. factors for secondary dysmenorrhea include the following :

• ?eiomyomata #fibroids&

• I4

• 0ubo*ovarian abscess

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• Ovarian torsion

• Endometriosis

In the following sections, the more common causes of secondary dysmenorrhea are briefly summari<ed

Uterine leiomyoma

'terine leiomyomata are benign tumors of the uterine musculature that are a common cause ofdysmenorrhea because they enlarge when stimulated by estrogen 0hey are up to times more common inblac. women than in white women1>3

In addition to pain with menses, patients may present with menorrhagia, abdominal distention, or pressureelvic examination may reveal a uterine mass or irregularity 'ltrasonography is often used for determiningsi<e and location of fibroids, though computed tomography #"0& is used if ultrasonographic information islimited1%, +3 'nless patients are symptomatic from profound anemia, these patients can be safelydischarged with appropriate gynecologic follow*up otential complications are anemia and infertility1)3

Pelvic inflammatory disease

I4 is an infection of the uterus and fallopian tubes, with or without ovarian or parametrial involvement It isan ascending infection that develops during or immediately after mensesG if chronic, it can lead todysmenorrhea 0he most common causative pathogens are Chlamydia trachomatis and Neisseriagonorrhoeae, though I4 also can be caused by other organisms, such asGardnerella vaginalis,anaerobes, and gram*negative rods1%3

reviously, the diagnosis of I4, though primarily clinical, was based on the presence of 6 ma-or criteria#abdominal pain, adnexal pain, and cervical motion tenderness&, and 2 minor criterion #fever, vaginaldischarge, leu.ocytosis, positive cervical cultures, gram*negative stain, intracellular diplococci, or whiteblood cells 1@/"s3 on vaginal smear&1%3

4ata from the EA"7 #elvic inflammatory disease Evaluation And "linical 7ealth& trial shows that thepresence of adnexal tenderness has a sensitivity of >>D for histologic endometritis 0he findings of thistrial support empiric treatment of all women at ris. for I4 with adnexal tenderness and no other obviouscause

On the basis of data from the EA"7 trial, the "enters for 4isease and "ontrol and revention #"4"&recommends that all women who are at ris. for I4 and who exhibit adnexal, uterine, or pelvic tendernesson bimanual examination in the absence of any other explanation for these findings be treated empiricallyfor I413

In addition to appropriate analgesia, patients require appropriate antibiotic coverage 0he most commonlyused regimen consists of ceftriaxone >5 mg IM and doxycycline 255 mg daily for 2( days 1%3 atientsshould be hospitali<ed if outpatient therapy fails, if they have intractable nausea or vomiting, if they have acomplicating tubo*ovarian abscess, or if they are immunocompromised 1%3"omplications include tubo*ovarian abscess and it<*7ugh "urtis syndrome#perihepatitis& if pus from the fallopian tubes lea.s into theperitoneum

Tubo-ovarian abscess

0ubo*ovarian abscess is a loculated infection within the fallopian tubes or ovaries, usually occurring as asequela of I4 It is often polymicrobial

Most commonly, patients present with fever and gradually worsening pelvic pain and tendernessG nausea,vomiting, and vaginal bleeding or discharge may be present as well Examination may elicit tenderness oncervical motion and in the adnexal area A pelvic mass may be present, though it is often difficult to palpate1%3 0ubo*ovarian abscesses can be detected on pelvic ultrasonography or abdominal "0 as a complex cysticstructure in the pelvis, with or without loculations 1+3

atients are often admitted for intravenous #I9& antibiotic therapy coveringNeisseria gonorrhoeae,Chlamydia, anaerobes, and gram*negative organisms If medical therapy fails or if peritoneal signs arefound on examination, surgical drainage is indicated1%3 Infertility is almost always a complication of tubo*ovarian abscess1%3 0he most feared complication, however, is rupture, which can lead toseptic shoc. anddeathG this is a true surgical emergency1)3

Ovarian torsion

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Ovarian torsion involves twisting of the adnexal structures, which leads to ischemia and ultimately necrosisif the process is not reversed in time In a nonpregnant woman, it is almost always caused by anabnormality in the ovary, such as a cyst or a tumor 0orsion can occur in pregnancy without a requisiteadnexal abnormality, and in one large series, 5D of the patients found to have torsion were pregnant 1653

atients often present with severe, intermittent, colic.y, unilateral pelvic or lower abdominal pain, frequentlyassociated with nausea and vomiting 0he diagnosis is often delayed because the presentation of ovariantorsion can resemble those of other disease entities, such as appendicitis or renal colic 1%, )3

/ecause of these resemblances and the consequent potential for diagnostic uncertainty, "0 is oftenperformed before any other imaging modality It is important to be familiar with the typical "0 findings fortorsion: ovarian enlargement exceeding > cm with a cor.screw appearance of the ipsilateral fallopian tube1+3 A sonogram will usually show a large ovarian mass or cyst, but ultrasonographic evidence of torsion isdifficult to obtain, because the appearance changes depending on the length of time elapsed 1)3

If there is a high level of suspicion for ovarian torsion, a gynecologic consultation should be obtained early?aparoscopy is not only diagnostic but also therapeutic and potentially fertility*saving 1)3 0hese patients areall admitted

Ovarian cyst rupture or hemorrhage

 A hemorrhagic ovarian cyst comes from an ovarian follicle in the absence of ovulationG consequently, thesecysts are exclusively found in menstruating females

atients often present with the acute onset of pelvic or abdominal pain, along with nausea and vomitingExamination may reveal an adnexal mass, but almost all patients with ruptured ovarian cysts have somelevel of adnexal tenderness !igns of peritoneal irritation may be apparent as well Although "0 andultrasonography can be used to visuali<e hemoperitoneum and the cyst, 1+3 laparoscopy is required for thedefinitive diagnosis1%3

Endometriosis

Endometriosis is the presence of endometriumli.e tissue found outside of the uterus, most commonly in theovaries @omen often present with dyspareunia and pelvic and bac. pain Although endometriosis is adiagnosis of exclusion, patients may give a history of dysmenorrhea that was cyclic with menses 1%3 It is

important to note, however, that endometriosis can exist concomitantly with other disease processescausing dysmenorrheaG this ma.es the diagnosis even more difficult 1623

0he history may also include chronic pelvic pain unresponsive to antibiotics or analgesics In addition, agood obstetric history may elicit frequent miscarriages or difficulty conceiving 1%, 623 0he classic examinationfinding is a fixed uterus with Lash spots #purple*blue discolorations& on the cervix, though this finding is notalways present1%3

In the future, "0 may hold some promise as a diagnostic tool,1+3 but at present, endometriosis can bedefinitively diagnosed only via laparoscopy or laparotomy !ome argue that definitive diagnosis may noteven be necessary1623 Often, endometriosis, if found, is assumed to be the cause of discomfort when it maynot be Even if endometriosis is the cause of dysmenorrhea, surgery may not be necessary if pain iscontrolled with hormonal therapy or analgesia 1623 0he main complication of endometriosis is rupture of anendometrioma

denomyosis

 Adenomyosis is defined as an invasion of myometrium by uterine adrenal glands It is a rare disease andcan resemble uterine leiomyomas and endometrial carcinoma in its presentationG accordingly, diagnosis isdifficult

4efinitive diagnosis is typically accomplished by means of transvaginal ultrasonography or magneticresonance imaging #MFI& @hen the latter is used, the .ey finding is a thic.ened -unctional <one #N line&Pthat is, the border between myometrium and endometrium One paper showed that adenomyosis should bein the differential diagnosis when a patient is treated for presumptive endometriosis and has chronicpersistent pain163

!ntrauterine contraceptive device

I'"4s #I'4s& may cause bladder or uterine perforation 0he sooner a patient has a uterine perforationafter I'"4 placement, the more li.ely it is that she will present with peritoneal signs 1%3 atients with bladder 

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perforation may have recurrent cystitis that is unresponsive to antibiotics 0he I'"4 must be removedimmediately to prevent further damage to the uterine or bladder walls Abdominal radiographs may revealthe location of an I'"4 if the string is not seen in the vaginal vault A gynecologist should be consultedearly1%3

Premenstrual dysphoric disorder 

/esides dysmenorrhea, patients with premenstrual dysphoric disorder  #formerly premenstrual syndrome&may have bloating, body aches, migraine headaches, breast tenderness, and emotional complaints 0heeffects of these symptoms are occasionally debilitating Aside from possible vaginal brownish discharge orbleeding, pelvic examination findings are normal It is the emergency physicians responsibility to ensureadequate analgesia and appropriate follow*up with a gynecologist