DYSMENORRHEA (painful periods/ menstrual cramps) one of the most common gynaecological SYMPTOM that affect the quality of life of women. the term dysmenorrhea is derived from greek words dys – painful/ abnormal; meno – month and rrhea – to flow.
Dysmenorrhea is primary when it occurs in the absence of co-existent pelvic pathology. It is due to excessive levels of prostaglandins (hormone ) which stimulates uterine contractions and vasoconstriction (the constriction/narrowing of the blood vessels) which potentiate myometrial (the middle layer of the uterus) ischemia (inadequate blood supply) causing pain.
Age at onset : 16–25 yrs
Onset of pain (spasmodic) is just prior to menstruation.
Dysmenorrhea is secondary when there is an identifiable anatomic or macroscopic pelvic pathological condition. There may be associated vaginal discharge, dysperiunia (painful sexual intercourse), menorrhagia (heavy bleeding at menstruation).
Age at onset : 30- 45 yrs
Onset of pain : Pain (congestive) increases through the luteal phase (before period starts) peaking at onset of menstruation.
Secondary dysmenorrhea may arise from a number of underlying pathological conditions.
- Pelvic Inflammatory Disease ( Infections)
- Intrauterine polyps
- Submucosal fibroids
– Congenital uterine abnormalities
– Cervical stenosis
– Asherman syndrom
– Chronic ectopic pregnancy
– Pelvic congestion syndrome
– Ovarian cysts or neoplasms
RISK FACTORS FOR DYSMENORRHEA
Young age, early menarche, heavy menstrual flow, nulliparity (state in which a woman has never carried a pregnancy), smoking, depression, anxiety, stress.
Treatment of dysmenorrhea is aimed at providing symptomatic relief as well as inhibiting the underlying processes that causes symptoms.
Primary dysmenorrhea respond to
- NSAIDs (nonsteroidal anti-inflammatory drugs, blocking production of prostaglandins) that provide analgesic (pain-killing) and anti-inflammatory effects eg: aspirin, ibuprofen and naproxen. Should be offered as first line treatment for pain relief.
- COCs (combined oral contraceptives) are commonly used as a second line therapy when NSAIDs are ineffective, poorly tolerated or contraindicated. COCs inhibit ovulation and endometrial tissue growth, thereby decreasing prostaglandin release. Contraception is the additional benefit of COCs.
Treatment of Secondary dysmenorrhea must address the underlying disease ( cyst removal/ removal of submucosal fibroids/polyps etc ). Secondary dysmenorrhea may be resistant to NSAIDs and COCs.