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Image: Schematic diagram of the female reproductive organs. Image by Lecturio.


Overview

The term dysmenorrhea is derived from three Greek words meaning “bothersome monthly flow.” Dysmenorrhea is more common during mid-to-late adolescence. It can be subdivided into primary and secondary, based on whether a pelvic pathology can be identified as the cause. Primary dysmenorrhea is more common than secondary dysmenorrhea among adolescents.

Epidemiology

Dysmenorrhea is a very common problem in adolescent girls and is the number-one gynecological cause of recurrent short-term school absenteeism in this age group. Most cases of dysmenorrhea in adolescents are reported during mid-to-late adolescence, when ovulatory menstrual cycles become established. It is less common in the early adolescent years, when most menstrual cycles are anovulatory.

The most commonly identified risk factors for primary dysmenorrhea in adolescents are early menarche and increased duration and amount of menstrual flow. Cigarette smoking is another important risk factor for primary dysmenorrhea in adolescents.

The most common cause of secondary dysmenorrhea in adolescents is endometriosis. Family history of endometriosis or bleeding disorders in an adolescent with dysmenorrhea points toward secondary rather than primary dysmenorrhea.

Pathophysiology

The pathologic process of primary dysmenorrhea is different from that of secondary dysmenorrhea, which arises from pelvic or gynecological etiologies. Primary dysmenorrhea usually occurs in adolescents with established ovulatory cycles and is very unlikely to happen with anovulatory cycles.

When ovulation occurs, omega-6 fatty acids begin building up in the phospholipids of the cell membranes of the uterus. Progesterone withdrawal right before menstruation is a normal physiologic occurrence and is responsible for the release of omega-6 fatty acids, especially arachidonic acid. The release of these fatty acids triggers the activation of prostaglandins and leukotrienes in the uterine wall, which initiates an inflammatory response. This response is responsible for the localized symptoms of dysmenorrhea such as abdominal pain and cramps. Systemic symptoms such as nausea and vomiting in addition to a headache are also common.

Prostaglandin F2-alpha activity was found to be twice as high in adolescents with dysmenorrhea compared with those who do not have any pain during menstruation. Additionally, the severity of the symptoms of dysmenorrhea was found to be positively correlated with the level of this type of prostaglandin.

Additionally, girls with primary dysmenorrhea were found to have higher levels of serum vasopressin, another potent inducer of uterine contraction during menstruation. Continued contraction of the uterine muscles leads to oxygen deprivation that induces severe cramps and pelvic pain.

The most common cause of secondary dysmenorrhea in adolescents is endometriosis. This condition is characterized by the presence and growth of uterine glands outside the uterine cavity. The most common sites for endometriosis implantation are the pelvic organs, including the ovaries and the rectum. The most likely cause of endometriosis is retrograde menstruation.

Estrogen receptors are abundant in endometriotic tissues. Additionally, aromatase is usually overly expressed in endometriotic tissues but not in the normal endometrium. Endometriotic tissues also express interleukin-1 and tumor necrosis factor alpha, both of which can influence the establishment and proliferation of the ectopic endometrial tissues.

Cycloxygenase-2 (COX-2) levels are also elevated in endometriotic tissues compared with the normal endometrium. COX-2 is responsible for the synthesis of prostaglandin F2-alpha, which is believed to be related to the pathophysiology of dysmenorrhea. Additionally, the release of prostaglandin E2 is increased in patients with endometriosis. The accumulation of prostaglandins is responsible for cyclic and non-cyclic pelvic pain in these patients. The severity of symptoms does not correlate well with the extent of the disease.

Another important cause of dysmenorrhea that is more specific to the adolescent age group is the presence of a Mullerian duct anomaly. Didelphic uterus with unilateral obstruction, imperforate hemivagina, and the presence of a vaginal septum are all possible anatomical anomalies that can lead to dysmenorrhea during the early adolescent years. Sexually active adolescents may also experience an ectopic pregnancy, which can present with acute abdominal pain and vaginal bleeding. This acute presentation should be differentiated from the recurrent abdominal cramps that are characteristic of true dysmenorrhea.

Clinical Presentation

The presentation of primary dysmenorrhea in an adolescent is characterized by low abdominal cramping. Other associated symptoms include headaches, nausea, and vomiting. The symptoms are cyclic and usually begin at the onset of the menstrual flow, lasting for 1 to 2 days.

The symptoms of secondary dysmenorrhea, however, depend on the cause and site of the pelvic abnormality. For example, adolescents with pelvic endometriosis usually present with chronic pelvic pain, mid-cycle pain, dyspareunia, and metrorrhagia. Pelvic endometriosis-associated dysmenorrhea is usually both cyclic and acyclic in the same patient. Familial history of secondary dysmenorrhea is common.

Sexually active adolescents who present with chronic pelvic pain, dysuria, and dyspareunia may have a chronic pelvic inflammatory disease. Pelvic examination can reveal cervical motion tenderness or cervical fragility, both of which are clear signs of pelvic inflammatory disease. As well, the possibility of an ectopic pregnancy should be excluded in any sexually active adolescent who presents with acute abdominal cramping pain and vaginal bleeding.

Diagnostic Work-up

Proper history taking and physical examination are usually sufficient to establish the diagnosis of dysmenorrhea, but a few points need to be taken into consideration, as the difference between primary and secondary dysmenorrhea is essential as the treatment may differ.

The first step in the diagnostic workup of dysmenorrhea is to exclude acute and life-threatening conditions such as ectopic pregnancy, when appropriate. Pregnancy should be ruled out via ultrasonography and an appropriate serum or urinary beta human chorionic globulin (HCG) test. The most common site for an ectopic pregnancy is the fallopian tube; thus, the visualization of the tubes by ultrasonography can exclude ectopic pregnancy as the cause of acute abdominal pain in a patient with vaginal bleeding.

The next step is to understand whether the dysmenorrhea is purely cyclic, acyclic, or both. Purely cyclic dysmenorrhea is very likely to be a primary condition and is unlikely to uncover any pelvic pathology. Purely acyclic chronic pelvic pain can be caused by a chronic pelvic inflammatory disease. Patients with both cyclic and acyclic dysmenorrhea most likely have endometriosis. Pelvic ultrasonography is required to confirm the diagnosis of endometriosis.

The most common sites of endometrial tissue location include the ovaries and the cul-de-sac, which can be easily visualized and examined with a proper pelvic ultrasonographic scan. Ultrasonography can also help exclude anatomical anomalies of the uterine cavity or the Mullerian ducts, which contribute to a considerable number of dysmenorrhea cases in young adolescents.

Treatment

The management of primary dysmenorrhea in adolescents can be classified into non-pharmacologic and pharmacologic treatment. Herbal preparations and acupuncture may relieve some symptoms. As well, increasing the intake of fish or other sources rich in omega-3 fatty acids tends to decrease symptoms in some patients. Most cases of primary dysmenorrhea, however, need some sort of pharmacologic intervention for adequate symptomatic relief.

The most commonly used medications for primary dysmenorrhea in adolescents are ibuprofen, naproxen, mefenamic acid, and celecoxib. These four medications belong to the non-steroidal anti-inflammatory drugs family, except for celecoxib, which is a specific COX-2 inhibitor. The efficacy, safety, and tolerability of all these medications are similar.

Oral combined contraceptive pills are also considered as first-line therapy for the management of primary dysmenorrhea in adolescents. Seasonale, Seasonique, and Lybrel have been all used with excellent results in adolescents with dysmenorrhea. The active ingredients in these medications are levonorgestrel and ethynyl estradiol.

Adolescents who do not respond to these pharmacological interventions are more likely to have secondary dysmenorrhea, and further diagnostic work-up is indicated to exclude less common causes of dysmenorrhea. Laparoscopy is indicated after 6 months of conservative management of dysmenorrhea to exclude the possibility of endometriosis.

If endometriosis implants are visualized by laparoscopy, they should be removed or obliterated by laser vaporization. Low-dose monophasic oral contraceptives can also be administered to adolescents with endometriosis in a non-cyclic fashion. Medical management of endometriosis also includes the administration of nafarelin and leuprolide, both of which are gonadotropin-releasing hormone receptor (GnRH) agonists. GnRH agonists should be avoided whenever possible, however, in young adolescent girls. Aromatase inhibitors can be also used in adolescents with endometriosis-associated dysmenorrhea, but they should be combined with a progestin to prevent the development of ovarian folliculogenesis.

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