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Menstrual Pain - Dysmenorrhea
Background:
Dysmenorrhea is one of the most common gynecologic complaints in
young women who present to clinicians today (Jamieson, 1996).
The term dysmenorrhea is derived from the Greek words dys,
meaning "difficult/painful/abnormal," meno, meaning "month," and
rrhea, meaning "flow." Dysmenorrhea is defined as difficult
menstrual flow or painful menstruation. The optimal management of this
symptom depends on an understanding of the underlying cause. Dysmenorrhea
is classified as primary (spasmodic) or secondary (congestive) (Dawood,
1985).
Primary dysmenorrhea is defined as menstrual pain that is not
associated with macroscopic pelvic pathology. It occurs in the first few
years after menarche (Koltz, 1995) and affects as many as 50% of
postpubescent females (Dawood, 1988).
Secondary dysmenorrhea is defined as menstrual pain that is a result of
anatomic and/or macroscopic pelvic pathology (Koltz, 1995; Dawood, 1990).
It most often is observed in women aged 30-45 years.
Several risk factors have been associated with more severe episodes of
dysmenorrhea, including the following (Harlow, 1996):
- Earlier age at menarche
- Long menstrual periods
- Heavy menstrual flow
- Smoking
- Positive family history
Obesity and alcohol consumption were found to be associated with
dysmenorrhea in some, but not all, studies (Andersch, 1982; Sundell, 1990;
Parazzini, 1994). Physical activity and the duration of the menstrual
cycle do not appear to be associated with increased menstrual pain
(Andersch, 1982).
Pathophysiology: The etiology and pathophysiology of
dysmenorrhea have not been fully elucidated. Nonetheless, the following
may be involved.
Primary dysmenorrhea
Growing evidence suggests that the pathogenesis of primary dysmenorrhea
is due to prostaglandin (PG) F2alpha (a potent myometrial stimulant and
vasoconstrictor) in the secretory endometrium (Willman, 1976). The
response to PG inhibitors in patients with dysmenorrhea supports the
assertion that dysmenorrhea is PG mediated. Substantial evidence
attributes dysmenorrhea to prolonged uterine contractions and decreased
blood flow to the myometrium. Elevated levels of PGs were found in the
endometrial fluid of dysmenorrheic women and correlated well with the
degree of pain (Helsa, 1992; Eden, 1998). A 3-fold increase in endometrial
PGs occurs from the follicular phase to the luteal phase, with a further
increase occurring during menstruation (Dambro, 1998; Speroff, 1997). The
increase in PGs in the endometrium following the fall in progesterone in
the late luteal phase results in increased myometrial tone and excessive
uterine contraction (Dawood, 1990).
Leukotrienes have been postulated to heighten the sensitivity of pain
fibers in the uterus (Helsa, 1992). Significant amounts of leukotrienes
have been demonstrated in the endometrium of women with primary
dysmenorrhea that does not respond to treatment with PG antagonists
(Demers, 1984; Rees, 1987; Chegini, 1988; Nigam, 1991; Sundell, 1990).
The posterior pituitary hormone vasopressin may be involved in
myometrial hypersensitivity, reduced uterine blood flow, and pain in
primary dysmenorrhea (Akerlund, 1979). Vasopressin's role in the
endometrium may be related to PG synthesis and release.
A neuronal hypothesis also has been advocated in the pathogenesis of
primary dysmenorrhea. Type C pain neurons are stimulated by the anaerobic
metabolites that are generated by an ischemic endometrium.
Primary dysmenorrhea also has been attributed to behavioral and
psychological factors. Although these factors have not been convincingly
demonstrated to be proven causes, they should be considered if medical
treatment fails.
Secondary dysmenorrhea
A number of factors may be involved in the pathogenesis of secondary
dysmenorrhea. Pelvic pathology including endometriosis, pelvic
inflammatory disease (PID), ovarian cysts and tumors, cervical stenosis or
occlusion, adenomyosis, fibroids, uterine polyps, intrauterine adhesions,
congenital malformations (bicornate and subseptate uterus), intrauterine
contraceptive device (IUCD), transverse vaginal septum, pelvic congestion
syndrome, and Allen-Masters syndrome can lead to secondary dysmenorrhea.
Almost any process that can affect the pelvic viscera can produce cyclic
pelvic pain (Smith, 1993).
Frequency:
- In the US: Dysmenorrhea may affect more than one
half of menstruating women. The prevalence of dysmenorrhea can be quite
variable. A survey of 113 patients in a family practice setting showed a
prevalence of dysmenorrhea of 29-44% (Sobczyk, 1978). With the
availability of oral contraceptives (OCs) and nonsteroidal
anti-inflammatory drugs (NSAIDs), both of which are effective in
relieving primary dysmenorrhea, the actual prevalence rate may be
higher.
The peak incidence of primary dysmenorrhea is in individuals in late
adolescence and the early 20s (Fraser, 1992). The incidence of
dysmenorrhea in adolescents was reported to be as high as 92% (Andersch,
1982). The incidence then falls with increasing age and with increasing
parity. The prevalence and severity of dysmenorrhea in parous women were
significantly lower (Andersch, 1982). No significant difference with
respect to prevalence and severity of dysmenorrhea was found between
nulligravid women and those in whom pregnancy had been terminated by
either spontaneous or induced abortion.
In an epidemiologic study of an adolescent population (aged 12-17 y),
Klein and Litt reported a prevalence of dysmenorrhea of 59.7%. Of those
reporting pain, 12% described it as severe, 37% as moderate, and 49% as
mild. Dysmenorrhea resulted in 14% of patients frequently missing
school. Although black adolescents reported no increased incidence of
dysmenorrhea, they were absent from school more frequently (23.6%) than
whites (12.3%), even after adjusting for socioeconomic status.
US
Frequency.
Mortality/Morbidity: Dysmenorrhea can disrupt personal
life. It is a significant public health problem that is associated with
substantial economic loss related to absence from work. Ten percent of
women with the condition have severe pain that can be incapacitating. The
economic loss has been estimated to be 600 million work hours and 2
billion dollars annually in the United States (Dawood, 1984).
Race: No data suggest that race affects the incidence
of dysmenorrhea.
Age: See Frequency.
History:
- The history is critical in establishing the diagnosis of
dysmenorrhea. It should include an assessment of the onset, duration,
type, and severity of pain. A thorough menstrual history is also
essential. This should include the age of menarche, cycle regularity,
cycle length, last menstrual period, and duration and amount of
menstrual flow.
- Determine factors that exacerbate or ameliorate the symptoms and the
degree of disruption to school, work, and social activities.
- Consider gravity and parity status, previous pelvic infections,
dyspareunia, infertility, and pelvic surgeries, injuries, and
procedures.
- Also assess symptoms such as nausea, vomiting, bloating, diarrhea,
and fatigue, which may be observed in patients with
dysmenorrhea.
- Consider sexual history, including the choice of contraceptive
methods. Establish the effect of the OC pill (OCP), if used, on
relieving or exacerbating the condition. Moreover, discuss the use of
other agents that affect dysmenorrhea pain.
- A family history may be helpful in differentiating endometriosis
from primary dysmenorrhea (Simpson, 1980; Malinak, 1980). The history
should include questions pertaining to sexual abuse because this has
been reported to be associated with dysmenorrhea and chronic pelvic pain
(Jamieson, 1997).
- In summary, a complete history should include the following:
- Menstrual frequency, length of period, estimate of the menstrual
flow, and presence or absence of intermenstrual bleeding
- Severity of pain and its relationship to the menstrual
cycle
- Impact on physical and social activity
- Progression of symptoms’ severity
- Primary dysmenorrhea should be distinguished from secondary
dysmenorrhea on the basis of clinical features.
- Primary dysmenorrhea occurs almost invariably in ovulatory cycles
and usually appears within a year after menarche. Classically, the
pain begins with the onset of menstruation or just shortly before and
persists throughout the first 1 or 2 days. The pain is described as
spasmodic and superimposed over a background of constant lower
abdominal pain, which radiates to the back or anterior and/or medial
thigh.
- Associated general symptoms, such as malaise, fatigue (85%),
nausea and vomiting (89%), diarrhea (60%), lower backache (60%), and
headache (45%), may be present with primary dysmenorrhea. Dizziness,
nervousness, and even collapse are associated with
dysmenorrhea.
- The clinical features of primary dysmenorrhea include the
following:
- Onset shortly after menarche
- Duration usually of 48-72 hours (often starting several hours
before or just after the menstrual flow)
- Cramping or laborlike pain
- Often unremarkable pelvic examination (including rectal)
- A different pattern of pain is observed with secondary
dysmenorrhea that is not limited to the onset of menses; usually this
is associated with abdominal bloating, pelvic heaviness, and back
pain. The pain usually increases progressively during the luteal phase
until it peaks around the onset of menstruation.
- The following may indicate secondary dysmenorrhea (Smith, 1993;
Smith, 1997):
- Dysmenorrhea occurring during the first 1 or 2 cycles after
menarche, which may indicate congenital outflow obstruction
- Dysmenorrhea beginning when older than 25 years
- Pelvic abnormality with physical examination (consider
endometriosis, PID, pelvic adhesions, and adenomyosis)
- Little or no response to therapy with NSAIDs, OCs, or
both
Physical:
- A pelvic examination is indicated at the initial evaluation, which
should be performed carefully to exclude uterine irregularities,
cul-de-sac tenderness, or nodularity that may suggest endometriosis,
PID, or a pelvic mass.
- Women with primary dysmenorrhea usually have normal findings on
examination.
- Pelvic pathology may be present on a pelvic examination in women
with secondary dysmenorrhea.
- However, normal findings on pelvic examination do not exclude
secondary dysmenorrhea.
- Women with endometriosis who present with secondary dysmenorrhea
have physical findings approximately 40% of the time (Barbieri, 1999;
Propst, 1998).
- Each specific pathology presenting with secondary dysmenorrhea may
have unique and specific findings on physical examination.
Causes:
- Causes of secondary dysmenorrhea include the following:
- Congenital malformation of the müllerian system
- Cervical strictures or stenosis
- Pelvic congestion syndrome
- Mittelschmerz (midcycle ovulation pain)
DIFFERENTIALS
Abortion
Ectopic Pregnancy
Endometriosis
Inflammatory
Bowel Disease
Irritable Bowel Syndrome
Ovarian Cysts
Pelvic
Inflammatory Disease
Urinary Tract Infection
Other Problems to be Considered:
The most important differential diagnosis of primary dysmenorrhea is
secondary dysmenorrhea.
Lab Studies:
- No specific diagnostic tests exist for primary dysmenorrhea. It is a
clinical diagnosis.
- The following can be performed to exclude organic causes of
dysmenorrhea:
- Cervical culture to exclude sexually transmitted
diseases
- Human chorionic gonadotropin (HCG) level to exclude ectopic
pregnancy
- Cancer antigen 125 (CA-125): This has limited clinical value in
evaluating women with dysmenorrhea due to its relatively low negative
predictive value.
Imaging Studies:
- Noninvasive studies may include abdominal and transvaginal
ultrasound. Other more invasive studies, including
hysterosalpingography, may be required
- Pelvic ultrasound scan is indicated to evaluate for situations such
as ectopic pregnancy, ovarian cysts, fibroids, and IUCD. This is a
highly sensitive test for detecting pelvic masses.
- Hysterosalpingogram is used to exclude endometrial polyps,
leiomyomas, and congenital abnormalities of the uterus.
- Intravenous pyelogram is indicated if uterine malformation is
confirmed as a cause or contributing factor for the
dysmenorrhea.
Procedures:
- Other more invasive studies, including laparoscopy, hysteroscopy,
and dilatation and curettage (D&C), may be required.
- Laparoscopic examination is the single most useful procedure. It
involves a complete diagnostic survey of the pelvis and reproductive
organs to ascertain the presence of any pathology that may account for
the clinical symptoms.
- Hysteroscopy and D&C may be indicated to evaluate intrauterine
pathology found on imaging.
- An endometrial biopsy may be indicated if endometritis is
suspected.
Medical Care:
- Grading dysmenorrhea according to severity of pain and limitation of
daily activity may help to guide the treatment strategy.
- In addition to pain relief, other mainstays of treatment are
reassurance and education.
Surgical Care:
- Surgery generally is not indicated for patients with primary
dysmenorrhea.
- In patients with secondary dysmenorrhea, treatment of the underlying
pathology may necessitate surgical intervention.
- In refractory cases of dysmenorrhea, laparoscopic presacral
neuroectomy has been studied with efficacy in some patients for as many
as 12 months after treatment (Chen, 1996, Gurgan, 1992).
Consultations: In patients with refractory symptoms, a
multidisciplinary approach may be indicated.
Diet: Both a low-fat vegetarian diet (Barnard, 2000)
and fish oil supplements (Harel, 1996) have been reported to reduce
menstrual pain in some women.
MEDICATION
Treatment of primary dysmenorrhea is
directed at providing relief from the cramping pelvic pain and associated
symptoms (eg, headache, nausea, vomiting, flushing, diarrhea) that
typically accompany or immediately precede the onset of menstrual flow.
The pelvic pain can be distressing and occasionally radiates to the back
and thighs, often necessitating prompt intervention. To date,
pharmacotherapy has been the most reliable and effective treatment for
relieving dysmenorrhea. Because the pain results from uterine
vasoconstriction, anoxia, and contractions mediated by PGs, symptomatic
relief often can be obtained from use of agents that inhibit PG synthesis
and have anti-inflammatory and analgesic properties.
NSAIDs and combination OCs are the most commonly used therapeutic
modalities for the management of primary dysmenorrhea. These agents have
different mechanisms of action and can be used adjunctively in refractory
cases. The lack of response to NSAIDs and OCs (or the combination) may
increase the suspicion of a secondary cause for dysmenorrhea. Other
therapies for dysmenorrhea have been proposed, but most are not well
studied. These include thiamine, omega3 fatty acids, magnesium,
acupuncture, herbal medicines, transdermal nitroglycerin, calcium-channel
blockers, beta-adrenergic agonists, antileukotrienes, and transcutaneous
electric nerve stimulation (TENS) units.
Treatment of secondary dysmenorrhea involves correction of the
underlying organic cause. Specific measures (medical or surgical) may be
required to treat pelvic pathology such as endometriosis and to ameliorate
the associated dysmenorrhea. Periodic use of analgesic agents as
adjunctive therapy also may be beneficial.
Drug Category: Nonsteroidal anti-inflammatory drugs
(NSAIDs) -- NSAIDs are the most commonly used treatments for
dysmenorrhea. NSAIDs decrease menstrual pain by decreasing intrauterine
pressure and lowering PG F2alpha in menstrual fluid. Because they are used
for short periods in otherwise healthy young women, they are generally
well tolerated and free of serious toxicity. GI upset is the most common
adverse effect associated with NSAIDs, but patients receiving these
medications nonetheless should be monitored for other more serious adverse
effects, including GI bleeding and renal dysfunction. Patients should also
be monitored for potential pharmacokinetic and pharmacodynamic drug
interactions and possible effects on platelet aggregation.
NSAIDs are contraindicated in patients with renal insufficiency, peptic
ulcer disease, gastritis, bleeding diatheses, and aspirin
hypersensitivity. These agents must be used on a regular basis (as-needed
use is not adequate in most patients) for several days. To avoid
inadvertent exposure to these agents during early pregnancy, NSAIDs should
be started at the onset of menstrual bleeding. While some NSAIDs have been
touted as being particularly effective for dysmenorrhea (especially the
fenamates), scientific data to support such claims are sparse and
generally weak (Zhang, 1998). Moreover, well-designed, prospective,
comparative studies are lacking. Diclofenac, ibuprofen, ketoprofen,
meclofenamate, mefenamic acid, naproxen, and rofecoxib are the NSAIDs
specifically approved by the FDA for treatment of dysmenorrhea. Aspirin
may not be as effective as other NSAIDs, and acetaminophen may be a useful
adjunct for alleviating only mild menstrual cramping pain.
NSAIDs that achieve peak serum concentrations within 30-60 minutes and
have a faster onset of action (eg, ibuprofen, naproxen, meclofenamate) may
be preferred. However, individual patient response varies, and patients
may need a trial of several agents before finding one that works. Some
NSAIDs (eg, indomethacin) should be avoided because they have a higher
incidence of adverse effects. Despite some preliminary data suggesting
efficacy in patients with primary dysmenorrhea, the newer COX-2 inhibitors
have not been demonstrated to be superior to conventional NSAIDs. However,
these agents may be used in patients unable to tolerate other NSAIDS or in
whom these agents are contraindicated. COX-2–derived prostanoids
nonetheless appear to be involved in the pathophysiology of primary
dysmenorrhea (Morrison, 1999).
NSAIDs that inhibit type I PG synthetase and suppress the production of
cyclic endoperoxides (eg, fenamates, COX-2 selective agents, propionic
acids, indole acetic acids) alleviate dysmenorrhea symptoms by decreasing
endometrial and menstrual fluid PG concentrations.
Drug Name
|
Naproxen (Naprosyn, Aleve, Anaprox)
-- For relief of mild to moderate pain; inhibits inflammatory
reactions and pain by decreasing activity of cyclooxygenase, which
results in decrease of PG synthesis.
|
| Adult Dose |
500 mg PO followed by 250 mg q6-8h;
not to exceed 1.25 g/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease; recent GI bleeding or perforation; renal
insufficiency
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effects of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of
methotrexate toxicity; phenytoin levels may be increased when
administered concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, interstitial nephritis,
hyperkalemia, hyponatremia, and renal papillary necrosis may occur;
patients with preexisting renal disease or compromised renal
perfusion risk acute renal failure; leukopenia occurs rarely, is
transient, and usually returns to normal during therapy; persistent
leukopenia, granulocytopenia, or thrombocytopenia warrants further
evaluation and may require discontinuation of drug |
Drug Name
|
Ibuprofen (Advil, Motrin, Nuprin)
-- DOC for patients with mild to moderate pain. Inhibits
inflammatory reactions and pain by decreasing PG synthesis.
|
| Adult Dose |
400 mg PO q4-6h; not to exceed 3.2
g/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease; recent GI bleeding or perforation; renal
insufficiency; high risk of bleeding
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effects of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of
methotrexate toxicity; phenytoin levels may be increased when
administered concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; caution in congestive heart failure, hypertension, and
decreased renal and hepatic function; caution in coagulation
abnormalities or during anticoagulant therapy |
Drug Name
|
Diclofenac (Cataflam, Voltaren) --
Inhibits PG synthesis by decreasing activity of enzyme
cyclooxygenase, which in turn decreases formation of PG precursors.
|
| Adult Dose |
50 mg PO tid; not to exceed 150
mg/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease; recent GI bleeding or perforation; renal
insufficiency; high risk of bleeding
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effects of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of
methotrexate toxicity; phenytoin levels may be increased when
administered concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; acute renal insufficiency, hyperkalemia, hyponatremia,
interstitial nephritis, and renal papillary necrosis may occur;
increases risk of acute renal failure in patients with preexisting
renal disease or compromised renal perfusion; low WBC counts occur
rarely and usually return to normal in ongoing therapy;
discontinuation of therapy may be necessary if persistent
leukopenia, granulocytopenia, or thrombocytopenia |
Drug Name
|
Ketoprofen (Orudis, Oruvail,
Actron) -- For relief of mild to moderate pain and inflammation.
Small dosages initially are indicated in small and elderly patients
and in those with renal or liver disease. Doses greater than 75 mg
do not increase therapeutic effects. Administer high doses with
caution and closely observe patient for response.
|
| Adult Dose |
25-50 mg PO q6-8h prn; not to
exceed 300 mg/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effects of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of
methotrexate toxicity; phenytoin levels may be increased when
administered concurrently
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; caution in congestive heart failure, hypertension, and
decreased renal and hepatic function; caution in coagulation
abnormalities or during anticoagulant therapy |
Drug Name
|
Meclofenamate sodium -- Decreases
activity of cyclooxygenase, which results in decreased formation of
PG precursors.
|
| Adult Dose |
100 mg PO tid for up to 6 d; not to
exceed 300 mg/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity; active
GI bleeding; ulcer disease
|
| Interactions |
Aspirin decreases effects;
decreases effects of diuretics; increases toxicity of warfarin and
methotrexate
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
Category D in third trimester of
pregnancy; diarrhea may occur (reduce dose or discontinue
use) |
Drug Name
|
Mefenamic acid (Ponstel) --
Inhibits inflammatory reactions and pain by decreasing PG synthesis.
|
| Adult Dose |
500 mg PO initially followed by 250
mg q6h for 2-3 d; not to exceed 1 g/d
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity; peptic
ulcer disease; recent GI bleeding or perforation; renal
insufficiency; high risk of bleeding
|
| Interactions |
Coadministration with aspirin
increases risk of inducing serious NSAID-related adverse effects;
probenecid may increase concentrations and, possibly, toxicity of
NSAIDs; may decrease effects of hydralazine, captopril, and
beta-blockers; may decrease diuretic effects of furosemide and
thiazides; may increase PT when taking anticoagulants (instruct
patients to watch for signs of bleeding); may increase risk of
methotrexate toxicity; phenytoin levels may be increased when
administered concurrently
|
| Pregnancy |
C - Safety for use during pregnancy
has not been established.
|
| Precautions |
Category D in third trimester of
pregnancy; may have adverse effects in fetus; caution in congestive
heart failure, hypertension, and decreased renal and hepatic
function; caution in anticoagulation abnormalities or during
anticoagulant therapy |
Drug Name
|
Rofecoxib (Vioxx) -- Inhibits
primarily COX-2, which is considered an inducible isoenzyme, induced
during pain and inflammatory stimuli. Inhibition of COX-1 may
contribute to NSAID GI toxicity. At therapeutic concentrations,
COX-1 isoenzyme is not inhibited, thus GI toxicity may be decreased.
Seek lowest dose for each patient.
|
| Adult Dose |
50 mg PO qd; not to exceed 50 mg/d;
tab may be taken with or without food
|
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity
|
| Interactions |
Coadministration with fluconazole
may cause increase in rofecoxib plasma concentrations because of
inhibition of rofecoxib metabolism; coadministration with rifampin
may decrease rofecoxib plasma concentrations
|
| Pregnancy |
B - Usually safe but benefits must
outweigh the risks.
|
| Precautions |
May cause fluid retention and
peripheral edema; caution in compromised cardiac function,
hypertension, and conditions predisposing to fluid retention; severe
heart failure and hyponatremia (may deteriorate circulatory
hemodynamics); NSAIDs may mask usual signs of infection; caution in
presence of existing controlled infections; evaluate symptoms and
signs suggesting liver dysfunction or in abnormal liver lab
results | Drug Category: Oral
contraceptives (OCs) -- Dysmenorrhea can be prevented
altogether in some patients by use of OCs, although these agents are not
approved by the FDA for this indication. OCs may be an appropriate
treatment choice in patients who do not wish to conceive. The combination
OCs suppress the hypothalamic-pituitary-ovarian axis and thereby inhibit
ovulation and prevent PG production in the late luteal phase. This
generally significantly reduces the amount of menstrual flow and
effectively alleviates primary dysmenorrhea in most patients.
Combination OCs and depot medroxyprogesterone acetate provide effective
pain relief and are associated with a reduced menstrual flow. The use of
NSAIDs in combination with an OC may be necessary, especially during the
first few cycles after initiation of the OC. The dose of ethinyl estradiol
generally should be less than 50 mcg. A monophasic OC containing 30 mcg of
ethinyl estradiol is a reasonable choice. To date, studies comparing the
efficacy of various OC formulations in the management of dysmenorrhea have
not been performed.
Drug Name
|
Ethinyl estradiol &
norgestimate (Ortho-Cyclen, Ortho-Prefest, Ortho Tri-Cyclen) --
Reduces secretion of LH and FSH from pituitary by decreasing amount
of gonadotropin-releasing hormones.
|
| Adult Dose |
Schedule 1 (Sunday starter): Begin
dose on first Sunday after onset of menstruation; start that Sunday
if menstrual period starts on Sunday
21-tab package: 1 tab qd
for 21 d followed by 7 d off medication; new course begins on eighth
d after taking last tab
28-tab package: 1 tab qd without
interruption
Schedule 2 (Day 1 starter): Start dose on day 1
of menstrual cycle
21-tab package: 1 tab qd for 21 d followed
by 7 d off medication; begin new course on day 8 after taking last
tab
Continue dosing cycle if 1 period missed; pregnancy test
required if 2 periods missed
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity;
endometrial and hepatic cancer; thromboembolic disorders;
undiagnosed vaginal bleeding; smokers >35 y; cardiovascular
disease
|
| Interactions |
Phenobarbital, phenytoin,
paramethadione, carbamazepine, troglitazone, rifampicin, and
griseofulvin induce enzymes that levels of contraceptive steroids;
oral anticoagulants may increase thromboembolic potential
|
| Pregnancy |
X - Contraindicated in pregnancy
|
| Precautions |
Caution in patients diagnosed with
hepatic impairment, migraine, seizure disorders, cerebrovascular
disorders, breast cancer, or thromboembolic disease | |
Drug Name
|
Ethinyl estradiol &
norethindrone (Ortho-Novum, Ovcon 50, Ortho-Novum 7/7/7, Ort --
Reduces secretion of LH and FSH from pituitary by decreasing amount
of gonadotropin-releasing hormones.
|
| Adult Dose |
Schedule 1 (Sunday starter): Begin
dose on first Sunday after onset of menstruation; start that Sunday
if menstrual period starts on Sunday
21-tab package: 1 tab qd
for 21 d followed by 7 d off medication; new course begins on eighth
d after taking last tab
28-tab package: 1 tab qd without
interruption
Schedule 2 (Day 1 starter): Start dose on day 1
of menstrual cycle
21-tab package: 1 tab qd for 21 d followed
by 7 d off medication; begin new course on day 8 after taking last
tab
Continue dosing cycle if 1 period missed; pregnancy test
required if 2 periods missed
| Pediatric Dose |
Not established
|
| Contraindications |
Documented hypersensitivity;
endometrial and hepatic cancer; thromboembolic disorders;
undiagnosed vaginal bleeding; smokers >35 y; cardiovascular
disease
|
| Interactions |
Phenobarbital, phenytoin,
paramethadione, carbamazepine, troglitazone, rifampicin, and
griseofulvin induce enzymes that levels of contraceptive steroids;
oral anticoagulants may increase thromboembolic potential
|
| Pregnancy |
X - Contraindicated in pregnancy
|
| Precautions |
Caution in patients diagnosed with
hepatic impairment, migraine, seizure disorders, cerebrovascular
disorders, breast cancer, or thromboembolic disease | |
Medical/Legal Pitfalls:
- Failure to make a diagnosis: Careful evaluation of pain is important
to avoid delay in the diagnosis of potentially life-threatening
disorders such as ectopic pregnancy or pelvic neoplasm.
- Complications of diagnostic procedures: Invasive procedures should
only be performed if clinically indicated. If complications develop
following poorly indicated procedures, the medical/legal risk is
significant.
REFERENCES
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