DYSMENORRHEA

INTRODUCTION: Dysmenorrhea is defined as painful menstruation. This is often sufficiently severe that it prevents a woman from performing normal activities. It may also be accompanied by other symptoms, including diarrhea, nausea, vomiting, headache, and dizziness. Dysmenorrhea may be because of a clinically identifiable cause and in that case we call it secondary dysmenorrhea, or by an excess of prostaglandins, leading to painful uterine muscle activity in which case we call it primary dysmenorrhea.

THE CASCADE OF DYSMENORRHEA: Primary and secondary dysmenorrhea are a source of recurrent disability for a significant number of women in their early reproductive years. It is uncommon for primary dysmenorrhea to occur during the first three to six menstrual cycles, when regular ovulation is not yet well established. The incidence of primary dysmenorrhea is greatest in women in their late teens to early twenties and it tends to declines with age. On the other hand, secondary dysmenorrhea becomes more common as a woman ages, because it accompanies the rising prevalence of causal factors. Childbearing does not affect the occurrence of either primary or secondary dysmenorrhea.

ETIOLOGY AND PATHOPHYSIOLOGY

Primary Dysmenorrhea: Primary dysmenorrhea is caused by excess prostaglandin F2α (PGF2α) produced in the endometrium. Prostaglandin production in the endometrium normally increases under the influence of progesterone, reaching a peak at, or soon after, the start of menstruation. With the onset of menstruation, formed prostaglandins are released from the shedding endometrium. In addition to the increase in prostaglandins from endometrial shedding, necrosis of endometrial cells provides increased substrate arachidonic acid from cell walls for prostaglandin synthesis.

Prostaglandins are potent smooth muscle stimulants that cause intense uterine contractions, resulting in intrauterine pressures to increase. PGF2α also causes contractions in smooth muscle elsewhere in the body, resulting in nausea, vomiting, and diarrhea. Besides PGF2α, prostaglandin E2 (PGE2) is also produced in the uterus. PGE2, a potent vasodilator and inhibitor of platelet aggregation, has been implicated as a cause of primary menorrhagia.

Secondary Dysmenorrhea: Secondary dysmenorrhea is caused by structural abnormalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity. Common causes of secondary dysmenorrhea include endometriosis described as; the presence of endometrial glands and stroma outside of the uterus, adenomyosis also described as; the presence of ectopic endometrial tissue within the myometrium, adhesions, pelvic inflammatory disease (PID), and leiomyomata (uterine fibroids).

DIAGNOSIS: Patients with primary dysmenorrhea present with recurrent, month-aftermonth, spasmodic lower abdominal pain that occurs on the first 1 to 3 days of menstruation. Dyspareunia is generally not found in patients with primary dysmenorrhea and, if present, should suggest a secondary cause. Symptoms In patients with primary dysmenorrhea, the pain is often diffusely located in the lower abdomen and suprapubic area, with radiation around or through to the back. The pain is described as “coming and going,” or similar to labor. This pain is frequently accompanied by moderate-to-severe nausea, vomiting, and diarrhea. Fatigue, low backache, and headache are also common.

In patients with secondary dysmenorrhea, the pain often lasts longer than the menstrual period. It may start before menstrual bleeding begins, become worse during menstruation, then persist after menstruation ends. Secondary dysmenorrhea often starts later in life than primary dysmenorrhea.

THERAPY: Patients with primary dysmenorrhea generally experience exceptional pain relief through the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which are prostaglandin synthetase inhibitors. Other useful components of therapy for primary dysmenorrhea include the application of heat; exercise; psychotherapy and reassurance; and, on occasion, endocrine therapy; that is to say, oral contraceptives to induce anovulation and pain relief.

Combined Oral Contraceptives: Combined oral contraceptives can be useful in patients who do not desire childbearing and who do not have contraindications to their use. They work by suppressing ovulation and stabilizing estrogen and progesterone levels, with a resultant decrease in endometrial prostaglandins and spontaneous uterine activity. Oral contraceptives may be taken in the traditional 28-day cycle, or in an extended fashion that increases the interval between menses. The continuous use of oral contraceptives to eliminate menses can often eliminate dysmenorrhea altogether.

Therapy for Secondary Dysmenorrhea: For secondary dysmenorrhea, when a specific diagnosis is possible, therapy directed at the underlying condition is most likely to succeed.

RELATED;

1.  Endometriosis

2.  Pelvic inflammatory disease

3.  Infertility

4.  Ectopic pregnacy

REFERENCES