Dysmenorrhea, commonly known as painful periods, is lower abdominal pain experienced during menstruation. Further categorized as primary and secondary dysmenorrhea, it is one of the most frequently reported complaints among women of reproductive age, with a prevalence of 80% in adolescents. Severe dysmenorrhea can affect mental health, impair activities of daily living (ADLs), and cause absenteeism from work and school in 12% of cases.
What are the risk factors & etiology?
Primary dysmenorrhea is defined as menstrual pain without any identifiable cause. It is related to anovulatory cycles and manifests 6-12 months after the start of menses (menarche).
Secondary dysmenorrhea refers to menstrual pain in the presence of organic pathology. It usually presents 12 months after menarche and is often accompanied by progressive mid-cycle/acyclic pain, irregular/heavy menstrual bleeding, and chronic pelvic pain.
Associated risk factors are:
- Age: primary dysmenorrhea is commoner in younger women (peri-menarche); secondary dysmenorrhea usually affects women >25 years of age.
- Smoking
- Higher BMI/obesity
- Family history of dysmenorrhea
- Stress
- Depression/anxiety
- Nulliparity
- Heavy menstrual bleeding
- Earlier age at menarche
In pre-menopausal women, endometriosis and adenomyosis are recognized as the commonest etiologies of secondary dysmenorrhea. Several other etiologies exist, including:
- Uterine abnormalities – Endometriosis, fibroids, adenomyosis, endometrial polyps
- Pelvic inflammatory disease
- Genital outflow tract obstructive anomalies – Uterine Agenesis/Hypoplasia, unicornuate, bicornuate, septate, didelphys, arcuate uterus, imperforate hymen, diethylstilbestrol related anomalies
- IUCD use
Pathophysiology
Dysmenorrhea results from vasoconstriction and inflammatory changes that are catalyzed by prostaglandins, leukotrienes, and vasopressin. Premenstrual drop in progesterone levels results in an increased secretion of prostaglandins from the shedding endometrium. Prostaglandin F (PGF) is the main culprit responsible for intense uterine contractions. Similarly, vasopressin increases uterine contractility resulting in vasoconstriction and blood flow restriction. This further leads to anaerobic metabolite formation that triggers the pain receptors.
History, physical examination & evaluation
Apart from lower abdominopelvic pain, patients often present with headaches, nausea/vomiting, indigestion, constipation/diarrhea, bloating, fatigue, and sometimes urinary symptoms.
Physical examination for primary dysmenorrhea is usually unremarkable, and a pelvic exam is unnecessary in such cases. Pelvic examination should be performed when there is suspicion of a secondary cause of dysmenorrhea, in sexually active adolescents and women and those non-responsive to treatment.
The presence of the following suggests secondary dysmenorrhea:
- Foul smelling or discolored vaginal discharge with associated symptoms (swelling, itching, pain) – Pelvic inflammatory disease
- Infertility, adnexal masses, pelvic tenderness, dyspareunia, dysuria, dyschezia – Endometriosis
- Evenly-shaped uterus with abnormal bleeding – Adenomyosis
- Uneven uterus with abnormal bleeding – Fibroids
- Bulging bluish mass at introitus with a history of cyclic pain in the absence of menses – Imperforate hymen
Ultrasound helps determine the causes of secondary dysmenorrhea, such as genital tract outflow obstruction, congenital anomalies, and uterine/adnexal tumors (fibroids, endometriosis, and adenomyosis).
A b-hCG pregnancy test is performed in those with suspected pregnancy (to rule out ectopic pregnancy).
High vaginal and endocervical swabs are taken in those with abnormal vaginal discharge. Similarly, cervical cytology/biopsy may be required in those with malignancy suspicion.
Doppler ultrasound and MRI are recommended in suspected cases of torsion, deep pelvic endometriosis, and adenomyosis, and where transvaginal ultrasound is indecisive.
What are the complications?
Associated complications with primary and secondary dysmenorrhea include ADL impairment and mental health deterioration. Infertility, heavy menstrual bleeding, anemia, and prolapse have been associated with secondary dysmenorrhea (depending on the etiology).
Management
Non-steroidal anti-inflammatory drugs (NSAIDs) are the recommended first line of treatment and are more effective than other analgesics. 27-35% improvement has been documented with regular use. Mefenamic acid and Ibuprofen are the preferred choices due to safety and efficacy. COX-2 inhibitors are usually recommended for those experiencing significant gastrointestinal or neurological side effects.
Combined oral contraceptive pills (COCPs) are prescribed in non-responsive cases and those wanting contraception. COCPs counter dysmenorrhea by ovulation inhibition, decreasing prostaglandin formation, endometrial proliferation, and menstrual volume. Progestin-only pills are advised for those with secondary dysmenorrhea or who have contraindications to COCP’s use. Furthermore, studies suggest primary and secondary dysmenorrhea improvement with Levonorgestrel-releasing intrauterine systems (considered safe in both adolescents and nulliparous women).
Diet rich in vitamins and minerals with regular exercise seem to reduce dysmenorrhea. Some studies have found heat to be as effective as NSAIDs. Additionally, the efficacy of ginger has also been documented, especially when used during the initial 3-4 days of menses. Acupuncture, herbal therapy, and transcutaneous electrical nerve stimulation (TENS) may prove beneficial in certain situations, but more supportive evidence is required to advocate these.
An insight from mamahood
Dysmenorrhea is not just a nuisance; it can interfere with social functioning and affect daily life. Mamas, you are not alone; 16-91% of reproductive-age women experience dysmenorrhea at some point in their lives. Therefore, we recommend regular gynecological visits, medication compliance, and dietary and lifestyle changes to overcome this debilitating condition.
