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
Progression of symptom severity
Sexual and obstetric history
Clinical features of primary dysmenorrhea include the following:

Onset shortly after menarche (6 months)

Usual duration of 48-72 hours (often starting several hours before or just after the menstrual flow)
Cramping or laborlike pain
Background of constant lower abdominal pain, radiating to the back or thigh
Often unremarkable pelvic examination findings (including rectal)
The following may indicate secondary dysmenorrhea[1, 2] :

Dysmenorrhea beginning in the 20s or 30s, after previous relatively painless cycles
Heavy menstrual flow or irregular bleeding
Dysmenorrhea occurring during the first or second cycles after menarche
Pelvic abnormality with physical examination
Poor response to nonsteroidal anti-inflammatory drugs (NSAIDs) or oral contraceptives (OCs)
Infertility
Dyspareunia
Vaginal 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
Bimanual examination
See Presentation for more detail.

Diagnosis
No tests are specific to the diagnosis of primary dysmenorrhea. The following laboratory studies may be
performed to identify or exclude organic causes of secondary dysmenorrhea:

Complete blood count with differential

Gonococcal and chlamydial cultures, enzyme immunoassay, and DNA probe testing
Quantitative human chorionic gonadotropin level
Erythrocyte sedimentation rate
Urinalysis
Stool guaiac
Cancer antigen 125 assay
If pelvic pathology is suspected, the following imaging studies may be considered:

Abdominal or transvaginal ultrasonography

Hysterosalpingography
Intravenous pyelography
Computed tomography
Magnetic resonance imaging
Other more invasive studies that may be considered are as follows:

Laparoscopy
Hysteroscopy

Dilatation and curettage

See Workup for more detail.

Management
Pharmacotherapy is the most reliable and effective treatment for relieving dysmenorrhea. Treatment of
secondary dysmenorrhea involves correction of the underlying organic cause.
NSAIDs specifically approved by the FDA for treatment of dysmenorrhea are as follows:

Diclofenac
Ibuprofen
Ketoprofen
Meclofenamate
Mefenamic acid
Naproxen
Other NSAIDs and analgesics that have been used include the following:

Aspirin
Acetaminophen
COX-2 inhibitors
Narcotics
Montelukast
Although not approved by the FDA for treating dysmenorrhea, the following OCs are also used:

Combination OCs (eg, ethinyl estradiol with progestin or drospirenone)

Levonorgestrel intrauterine device
Depot medroxyprogesterone acetate
Preventive measures for outpatient management of dysmenorrhea include the following:

Lifestyle modification
Smoking cessation
Exercise

Epidemiologi
Dysmenorrhea may affect more than 50% of menstruating women, and its reported prevalence has been
highly variable (eg, 45-95%[14] ). A survey of 113 patients in a family practice setting showed a prevalence of
29-44%,[33] but figures as high as 90% in women aged 18-45 years have been reported. [3] The use of oral
contraceptives (OCs) and nonsteroidal anti-inflammatory drugs (NSAIDs), both of which are effective in
ameliorating symptoms of primary dysmenorrhea, may hinder accurate assessment of prevalence.
Primary dysmenorrhea peaks in late adolescence and the early 20s. [34] The incidence falls with increasing
age and with increasing parity. In many studies, [9, 35, 36] though not all,[3] the reported prevalence and severity
of 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. [9]
In an epidemiologic study of an adolescent population (age range, 12-17 years), Klein and Litt reported that
dysmenorrhea had a prevalence of 59.7%.[37] Of patients reporting pain, 12% described it as severe, 37% as
moderate, and 49% as mild. Dysmenorrhea caused 14% of patients to miss school frequently. Although
black adolescents reported no increased incidence of dysmenorrhea, they were absent from school more
frequently (23.6%) than whites were (12.3%), even after socioeconomic status was adjusted for.

International statistics

The prevalence of dysmenorrhea worldwide is similar to that in the United States. Reported prevalences
have ranged from 15.8% to 89.5%, with higher rates reported in adolescent populations. [38, 39, 40, 9, 41, 35, 42, 43]
A study of 408 young Italian women found that the prevalence of dysmenorrhea was 84.1% when only
menstrual pain was considered, 55.2% when menstrual pain was associated with a need for medication,
31.9% when menstrual pain was associated with absenteeism, and 25.3% when menstrual pain was
associated with both a need for medication and absenteeism. [44]
In a longitudinal population study of 9,067 Australian women, researchers found that those who began
smoking by age 13 had the greatest risk of developing chronic dysmenorrhea. Overall, approximately 60%
of the women reported experiencing dysmenorrhea symptoms at some time during the study period. [45, 46]
The prevalence of period pain was higher among current smokers (29%) than nonsmokers (23%).
Compared with never-smokers, ex-smokers had a 33% increased risk of chronic symptoms (odds ratio,
1.33; 95% confidence interval, 1.05 - 1.68), while current smokers had a 41% increased risk (odds ratio,
1.41; 95% CI, 1.17 - 1.70). After adjustment for socioeconomic status, lifestyle, and reproductive factors,
women who began smoking before or by age 13 had a 59% increased risk (odds ratio, 1.59; 95% CI, 1.18
2.15), those who began at ages 14-15 had a 50% increased risk (1.50; 95% CI 1.18 to 1.90), and those
who began at age 16 or older had a 26% increased risk (1.26; 95% CI 1.03 to 1.55). [45, 46]
In a cross-sectional study of 311 female Iranian undergraduate students (aged 18-27 y), the prevalence of
primary dysmenorrhea was 89.1%.[47] Factors 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).[47]

Age- and race-related demographics

The most common causes of dysmenorrhea differ by age. The prevalence of this condition is estimated to
be 25% among adult women and as high as 90% among adolescents.
No data suggest that race affects the incidence of dysmenorrhea
Patofisiologi;;;;;
Historical attitudes toward menstrual pain were often dismissive. Pain was often attributed to womens
emotional or psychological states or to misconceptions about sex and sexual behaviors. Although the
etiology and pathophysiology of dysmenorrhea have not been fully elucidated, research has led to data
supporting concrete physiologic explanations for dysmenorrhea, which discredit these prior dismissive
theories.[12, 13, 14]

Primary dysmenorrhea
Current evidence suggests that the pathogenesis of primary dysmenorrhea is due to prostaglandin F2
(PGF2), a potent myometrial stimulant and vasoconstrictor, in the secretory endometrium. [15] The response
to prostaglandin inhibitors in patients with dysmenorrhea supports the assertion that dysmenorrhea is
prostaglandin-mediated. Substantial evidence attributes dysmenorrhea to prolonged uterine contractions
and decreased blood flow to the myometrium.
Elevated prostaglandin levels were found in the endometrial fluid of women with dysmenorrhea and
correlated well with the degree of pain.[16] A 3-fold increase in endometrial prostaglandins occurs from the
follicular phase to the luteal phase, with a further increase occurring during menstruation. [17] The increase in
prostaglandins in the endometrium after the fall in progesterone in the late luteal phase results in increased
myometrial tone and excessive uterine contraction. [7]

Leukotrienes have been postulated to heighten the sensitivity of pain fibers in the uterus. Substantial
amounts of leukotrienes have been demonstrated in the endometria of women with primary dysmenorrhea
that does not respond to treatment with prostaglandin antagonists. [10, 18, 19, 20, 21]
The posterior pituitary hormone vasopressin may be involved in myometrial hypersensitivity, reduced
uterine blood flow, and pain in primary dysmenorrhea. [22, 23, 12, 24] Vasopressins role in the endometrium may
be related to prostaglandin synthesis and release.
In addition, a neuronal hypothesis has been advocated for the pathogenesis of primary dysmenorrhea.
Type C pain neurons are stimulated by the anaerobic metabolites generated by an ischemic endometrium.
Women with dysmenorrhea appear to have enhanced pain sensitivity compared to women without
dysmenorrhea, even during phases of the menstrual cycle when they are not experiencing menstrual pain.
[14]
This enhanced pain sensitivity may increase the risk of affected women to other chronic conditions (eg,
fibromyalgia) as well as negatively impact their quality of life.[14]
Primary dysmenorrhea has also been attributed to behavioral and psychological factors. Although these
factors have not been convincingly demonstrated to be causative, they should be considered if medical
treatment fails.
In primary dysmenorrhea, there is a highly complex interplay between hormones and mediators, basal
body temperature, sleep patterns, and the central nervous system (CNS), the extent of which is not
completely understood.[12]

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

Endometriosis
Pelvic inflammatory disease (PID)
Ovarian cysts and tumors
Cervical stenosis or occlusion
Adenomyosis
Fibroids
Uterine polyps
Intrauterine adhesions
Congenital malformations (eg, bicornuate uterus or subseptate uterus)
Intrauterine contraceptive device (IUCD), or intrauterine device (IUD)
Transverse vaginal septum
Pelvic congestion syndrome
Allen-Masters syndrome
Almost any process that can affect the pelvic viscera can produce cyclic pelvic pain.

Etiologi
Risk factors for primary dysmenorrhea include the following:

Early age at menarche (< 12 years)

Nulliparity
Heavy or prolonged menstrual flow
Smoking
Positive family history
Obesity
Risk factors for secondary dysmenorrhea include the following :
Leiomyomata (fibroids)
PID
Tubo-ovarian abscess

Ovarian torsion
Endometriosis
In the following sections, the more common causes of secondary dysmenorrhea are briefly summarized.

Uterine leiomyoma
Uterine leiomyomata are benign tumors of the uterine musculature that are a common cause of
dysmenorrhea because they enlarge when stimulated by estrogen. They are up to 9 times more common in
black women than in white women.[25]
In addition to pain with menses, patients may present with menorrhagia, abdominal distention, or pressure.
Pelvic examination may reveal a uterine mass or irregularity. Ultrasonography is often used for determining
size and location of fibroids, though computed tomography (CT) is used if ultrasonographic information is
limited.[26, 27] Unless patients are symptomatic from profound anemia, these patients can be safely
discharged with appropriate gynecologic follow-up. Potential complications are anemia and infertility.[28]

Pelvic inflammatory disease

PID is an infection of the uterus and fallopian tubes, with or without ovarian or parametrial involvement. It is
an ascending infection that develops during or immediately after menses; if chronic, it can lead to
dysmenorrhea. The most common causative pathogens are Chlamydia trachomatis and Neisseria
gonorrhoeae, though PID also can be caused by other organisms, such asGardnerella vaginalis,
anaerobes, and gram-negative rods.[26]
Previously, the diagnosis of PID, though primarily clinical, was based on the presence of 3 major criteria
(abdominal pain, adnexal pain, and cervical motion tenderness), and 1 minor criterion (fever, vaginal
discharge, leukocytosis, positive cervical cultures, gram-negative stain, intracellular diplococci, or white
blood cells [WBCs] on vaginal smear).[26]
Data from the PEACH (Pelvic inflammatory disease Evaluation And Clinical Health) trial shows that the
presence of adnexal tenderness has a sensitivity of 95.5% for histologic endometritis. The findings of this
trial support empiric treatment of all women at risk for PID with adnexal tenderness and no other obvious
cause.
On the basis of data from the PEACH trial, the Centers for Disease and Control and Prevention (CDC)
recommends that all women who are at risk for PID and who exhibit adnexal, uterine, or pelvic tenderness
on bimanual examination in the absence of any other explanation for these findings be treated empirically
for PID.[29]
In addition to appropriate analgesia, patients require appropriate antibiotic coverage. The most commonly
used regimen consists of ceftriaxone 250 mg IM and doxycycline 100 mg daily for 14 days. [26] Patients
should be hospitalized if outpatient therapy fails, if they have intractable nausea or vomiting, if they have a
complicating tubo-ovarian abscess, or if they are immunocompromised. [26]Complications include tuboovarian abscess and Fitz-Hugh Curtis syndrome(perihepatitis) if pus from the fallopian tubes leaks into the
peritoneum.

Tubo-ovarian abscess
Tubo-ovarian abscess is a loculated infection within the fallopian tubes or ovaries, usually occurring as a
sequela of PID. It is often polymicrobial.
Most commonly, patients present with fever and gradually worsening pelvic pain and tenderness; nausea,
vomiting, and vaginal bleeding or discharge may be present as well. Examination may elicit tenderness on
cervical motion and in the adnexal area. A pelvic mass may be present, though it is often difficult to palpate.
[26]
Tubo-ovarian abscesses can be detected on pelvic ultrasonography or abdominal CT as a complex cystic
structure in the pelvis, with or without loculations. [27]
Patients are often admitted for intravenous (IV) antibiotic therapy coveringNeisseria gonorrhoeae,
Chlamydia, anaerobes, and gram-negative organisms. If medical therapy fails or if peritoneal signs are
found on examination, surgical drainage is indicated.[26] Infertility is almost always a complication of tuboovarian abscess.[26] The most feared complication, however, is rupture, which can lead toseptic shock and
death; this is a true surgical emergency.[28]

Ovarian torsion

Ovarian torsion involves twisting of the adnexal structures, which leads to ischemia and ultimately necrosis
if the process is not reversed in time. In a nonpregnant woman, it is almost always caused by an
abnormality in the ovary, such as a cyst or a tumor. Torsion can occur in pregnancy without a requisite
adnexal abnormality, and in one large series, 20% of the patients found to have torsion were pregnant. [30]
Patients often present with severe, intermittent, colicky, unilateral pelvic or lower abdominal pain, frequently
associated with nausea and vomiting. The diagnosis is often delayed because the presentation of ovarian
torsion can resemble those of other disease entities, such as appendicitis or renal colic. [26, 28]
Because of these resemblances and the consequent potential for diagnostic uncertainty, CT is often
performed before any other imaging modality. It is important to be familiar with the typical CT findings for
torsion: ovarian enlargement exceeding 5 cm with a corkscrew appearance of the ipsilateral fallopian tube.
[27]
A sonogram will usually show a large ovarian mass or cyst, but ultrasonographic evidence of torsion is
difficult to obtain, because the appearance changes depending on the length of time elapsed. [28]
If there is a high level of suspicion for ovarian torsion, a gynecologic consultation should be obtained early.
Laparoscopy is not only diagnostic but also therapeutic and potentially fertility-saving. [28] These patients are
all admitted.

Ovarian cyst rupture or hemorrhage

A hemorrhagic ovarian cyst comes from an ovarian follicle in the absence of ovulation; consequently, these
cysts are exclusively found in menstruating females.
Patients often present with the acute onset of pelvic or abdominal pain, along with nausea and vomiting.
Examination may reveal an adnexal mass, but almost all patients with ruptured ovarian cysts have some
level of adnexal tenderness. Signs of peritoneal irritation may be apparent as well. Although CT and
ultrasonography can be used to visualize hemoperitoneum and the cyst, [27] laparoscopy is required for the
definitive diagnosis.[26]

Endometriosis
Endometriosis is the presence of endometriumlike tissue found outside of the uterus, most commonly in the
ovaries. Women often present with dyspareunia and pelvic and back pain. Although endometriosis is a
diagnosis of exclusion, patients may give a history of dysmenorrhea that was cyclic with menses. [26] It is
important to note, however, that endometriosis can exist concomitantly with other disease processes
causing dysmenorrhea; this makes the diagnosis even more difficult. [31]
The history may also include chronic pelvic pain unresponsive to antibiotics or analgesics. In addition, a
good obstetric history may elicit frequent miscarriages or difficulty conceiving. [26, 31] The classic examination
finding is a fixed uterus with ash spots (purple-blue discolorations) on the cervix, though this finding is not
always present.[26]
In the future, CT may hold some promise as a diagnostic tool,[27] but at present, endometriosis can be
definitively diagnosed only via laparoscopy or laparotomy. Some argue that definitive diagnosis may not
even be necessary.[31] Often, endometriosis, if found, is assumed to be the cause of discomfort when it may
not be. Even if endometriosis is the cause of dysmenorrhea, surgery may not be necessary if pain is
controlled with hormonal therapy or analgesia. [31] The main complication of endometriosis is rupture of an
endometrioma.

Adenomyosis
Adenomyosis is defined as an invasion of myometrium by uterine adrenal glands. It is a rare disease and
can resemble uterine leiomyomas and endometrial carcinoma in its presentation; accordingly, diagnosis is
difficult.
Definitive diagnosis is typically accomplished by means of transvaginal ultrasonography or magnetic
resonance imaging (MRI). When the latter is used, the key finding is a thickened junctional zone (JZ line)
that is, the border between myometrium and endometrium. One paper showed that adenomyosis should be
in the differential diagnosis when a patient is treated for presumptive endometriosis and has chronic
persistent pain.[32]

Intrauterine contraceptive device

IUCDs (IUDs) may cause bladder or uterine perforation. The sooner a patient has a uterine perforation
after IUCD placement, the more likely it is that she will present with peritoneal signs. [26] Patients with bladder

perforation may have recurrent cystitis that is unresponsive to antibiotics. The IUCD must be removed
immediately to prevent further damage to the uterine or bladder walls. Abdominal radiographs may reveal
the location of an IUCD if the string is not seen in the vaginal vault. A gynecologist should be consulted
early.[26]

Premenstrual dysphoric disorder

Besides dysmenorrhea, patients with premenstrual dysphoric disorder (formerly premenstrual syndrome)
may have bloating, body aches, migraine headaches, breast tenderness, and emotional complaints. The
effects of these symptoms are occasionally debilitating. Aside from possible vaginal brownish discharge or
bleeding, pelvic examination findings are normal. It is the emergency physicians responsibility to ensure
adequate analgesia and appropriate follow-up with a gynecologist.