Dysmenorrhoea is a term used to describe low anterior pelvic pain which occurs in association with periods.
It is thought to be due to an excess or imbalance of prostaglandins and leukotrienes in the menstrual fluid, which in turn produces vasoconstriction in the uterine vessels, causing the uterine contractions which produce the pain. The prostaglandin release may also be responsible for the symptoms of diarrhoea, nausea, headache and light-headedness which may occur in association with dysmenorrhoea.
Dysmenorrhoea may be thought of as either primary or secondary.
Primary dysmenorrhoea occurs in young females with no pelvic pathology.
- It often begins with the onset of ovulatory cycles six months to one year after the menarche.
- The pain begins with the onset of the period and may last for 24-72 hours.
Secondary dysmenorrhoea occurs in association with some form of pelvic pathology:
- It is more likely to occur years after onset of menstruation.
- The pain can precede the start of the period by several days and may last throughout the period.
- There may be associated dyspareunia.
- Secondary dysmenorrhoea may occur as a result of:
- Pelvic inflammatory disease.
- Fibroids, when it is often associated with heavy menstrual bleeding.
- Developmental abnormalities.
- The copper-containing intrauterine contraception device (Cu-IUCD) may cause pelvic pain in the first few months after fitting but does not influence the severity of dysmenorrhoea in the longer term.
- Dysmenorrhoea is very common although the precise incidence is not known, as it frequently goes unreported.
- Primary dysmenorrhoea is the most commonly given reason for absence from school amongst adolescent girls and approximately 15% will complain of severe dysmenorrhoea.
- Longer duration of menses, early menarche, smoking. alcohol and obesity are all risk factors associated with dysmenorrhoea.
- Females who are depressed and/or have poor social support networks are also more likely to experience pain.
- Childbirth reduces dysmenorrhoea and its severity diminishes with age.
A presumptive diagnosis of primary dysmenorrhoea may be made on history ± abdominal examination alone in young patients who are not sexually active, and vaginal examination is not normally required in this group of patients.
Investigation of dysmenorrhoea is primarily aimed at ruling out underlying pathology and may include any or all of the following as appropriate to the individual.
- Age at menarche.
- Cycle length.
- Whether the cycle is regular.
- Duration of bleeding.
- Timing of pain in relation to period.
- Location of pain. Dysmenorrhoea is typically suprapubic but may be felt in the back of the legs or lower back
- Smoking history.
- Whether the patient is sexually active.
- Obstetric history.
- Contraceptive history.
- Any features suggestive of underlying pathology (eg, vaginal discharge, intermenstrual or postcoital bleeding, dyspareunia).
- Dyschezia and/or rectal pain or bleeding - particularly suggestive of endometriosis.
Abdominal/vaginal examinations are indicated if sexually active:
- Adenomyosis - the uterus may be enlarged and tender with a typical 'boggy' feel.
- Endometriosis - generalised tenderness in the pelvic area. The uterus may be fixed ± retroverted due to adhesions, and nodules may be palpable in the uterosacral ligaments.
- Partially imperforate hymen (rare).
- Vaginal septum (rare).
- Speculum examination to visualise the cervix.
- High vaginal swab, chlamydial swabs.
- Cervical smear, if due.
- Pelvic ultrasound - if uterine enlargement or adnexal mass is present.
- Transvaginal ultrasound.
- MRI scan.
- Laparotomy with biopsy.
Patients may be concerned about the possibility of underlying pathology and, when appropriate, reassurance and an explanation of the mechanism of menstrual pain may be helpful.
- Lifestyle changes - longitudinal studies have looked at risk factors for dysmenorrhoea and have found a clear association between smoking and dysmenorrhoea; patients should therefore be informed of this relationship and assisted in any attempts to stop smoking.
- Self-help techniques:
- There is some evidence for benefit from use of transcutaneous electrical nerve stimulation (TENS) (high-frequency) and locally applied heat.
- Anecdotally, many women find the following measures to be helpful in relieving the symptoms of dysmenorrhoea:
- Tea - regular, camomile or mint.
- Abdominal and/or back massage.
- Lying in the supine position.
- Complementary and alternative medicines - several dietary supplements and herbal remedies have been suggested but there is insufficient evidence to recommend any of them. They include calcium and magnesium, thiamine, ginger, fish oil supplements, toki-shakuyaku-san (TSS - a Japanese herbal remedy), acupuncture and acupressure. Some remedies may have adverse effects and may interact with medication.
- Non-steroidal anti-inflammatory drugs (NSAIDs) - these are the most commonly used drugs for the treatment of dysmenorrhoea due to their inhibition of prostaglandin synthesis. This is a class effect and all NSAIDs appear equally effective. Ibuprofen is most often used due to its low incidence of side-effects. Although licensed specifically for dysmenorrhoea, there are concerns that mefenamic acid is more likely to induce seizures in overdose and has a low therapeutic window increasing the risk of accidental overdose.
- Weak opioids - there is no evidence of beneficial effect and the potential for addiction means they are not recommended.
If the woman with dysmenorrhoea does not wish to conceive, offer her hormonal contraception. Ovarian suppression appears to control cyclical pelvic pain, whether or not caused by endometriosis. Adolescents and young adults who do not respond to hormonal treatment after three months should be evaluated for secondary causes of dysmenorrhoea. This is likely in approximately 10% of patients.
- Combined hormonal contraception (CHC) is often used. Despite the common use of oral CHC in the treatment of dysmenorrhoea (and guidance from the Faculty of Sexual and Reproductive Healthcare stating it can be used for this purpose from the menarche), previous evidence has been inconclusive, due to a lack of randomised control trials. However, CHC can also be used to increase cycle length by tricycling and hence reduce the frequency of the menses and therefore the symptoms.
- Oral progestogen-only contraception may also be used. In a study of 406 women with dysmenorrhoea who were given desogestrel 75 micrograms/day (Cerazette®), the pain resolved or improved considerably in 93% and, despite a high incidence of adverse effects, mainly bleeding irregularities, 90% were satisfied.
- Depo-medroxyprogesterone acetate (Depo-Provera®) is also sometimes used, as many women become amenorrhoeic within a year of starting treatment.
- The levonorgestrel-containing intrauterine system (LNG-IUS; Mirena®) has been shown to reduce the severity of dysmenorrhoea despite not being anovulatoryIt could also be considered, even in adolescents.. Neither the 52 mg LNG-IUS (Mirena®) nor the newer 13.5 mg LNG-IUS (Jaydess®) is licensed for the treatment of dysmenorrhoea; Jaydess® is less likely than Mirena®to lead to amenorrhoea.
- Danazol is rarely used now and only under specialist supervision in the treatment of severe refractory cases.
- Leuprolide acetate may be used in rare cases to suppress the menstrual cycle, but has a significant side-effect profile.
- Laparoscopic uterine nerve ablation (LUNA) has been used for the treatment of severe refractory cases; however, a Cochrane meta-analysis concluded that there is insufficient evidence of its effectiveness and it is not recommended[15, 16].
- Hysterectomy. In severe refractory cases, particularly in women who feel they have completed their families, hysterectomy may be considered.
Further reading and references
Dysmenorrhoea; NICE CKS, May 2014 (UK access only)
Marjoribanks J, Proctor ML, Farquhar C; Nonsteroidal anti-inflammatory drugs for primary dysmenorrhoea. 2010 Jan 20(1):CD001751
Proctor M, Farquhar C; Diagnosis and management of dysmenorrhoea. BMJ. 2006 May 13332(7550):1134-8.
Lindh I, Milsom I; The influence of intrauterine contraception on the prevalence and severity of dysmenorrhea: a longitudinal population study. Hum Reprod. 2013 Jul28(7):1953-60. doi: 10.1093/humrep/det101. Epub 2013 Apr 11.
Alonso C, Coe CL; Disruptions of social relationships accentuate the association between emotional distress and menstrual pain in young women. Health Psychol. 2001 Nov20(6):411-6.
Dorn LD, Negriff S, Huang B, et al; Menstrual symptoms in adolescent girls: association with smoking, depressive symptoms, and anxiety. J Adolesc Health. 2009 Mar44(3):237-43. Epub 2008 Oct 29.
Dysmenorrhoea; NICE CKS, May 2014 (UK access only)
French L; Dysmenorrhea. Am Fam Physician. 2005 Jan 1571(2):285-91.
Harel Z; Dysmenorrhea in adolescents and young adults: etiology and management. J Pediatr Adolesc Gynecol. 2006 Dec19(6):363-71.
Contraceptive Choices for Young People; Faculty of Sexual and Reproductive Healthcare (2010)
Wong CL, Farquhar C, Roberts H, et al; Oral contraceptive pill as treatment for primary dysmenorrhoea. Cochrane Database Syst Rev. 2009 Apr 15(2):CD002120.
Combined Hormonal Contraception; Faculty of Sexual and Reproductive Healthcare (2011 updated August 2012)
Ahrendt HJ, Karckt U, Pichl T, et al; The effects of an oestrogen-free, desogestrel-containing oral contraceptive in women with cyclical symptoms: results from two studies on oestrogen-related symptoms and dysmenorrhoea. Eur J Contracept Reprod Health Care. 2007 Dec12(4):354-61.
The initial management of chronic pelvic pain; Royal College of Obstetricians and Gynaecologists (May 2012)
Jaydess Levonorgestrel Intrauterine System - New Product Review; Clinical Effectiveness Unit of the Faculty of Sexual and Reproductive Healthcare, 2014
Latthe PM, Proctor ML, Farquhar CM, et al; Surgical interruption of pelvic nerve pathways in dysmenorrhea: a systematic review of effectiveness. Acta Obstet Gynecol Scand. 200786(1):4-15.
Proctor ML, Latthe PM, Farquhar CM, et al; Surgical interruption of pelvic nerve pathways for primary and secondary dysmenorrhoea. Cochrane Database Syst Rev. 2005 Oct 19(4):CD001896.