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showed a normal uterine size and shape, except for a small 1 cm intramural broid. There was no evidence of adenomyosis and a normal trilaminar endometrial stripe of 8 mm at midcycle was seen. Adnexa were remarkable for a 3 cm hemorrhagic cyst on the right ovary and a 2.5 cm similar appearing cyst on the left.
Laboratory evaluation showed a normal CBC. Her anti-Mullerian hormone level was 3.4 ng/mL.
She was counseled on options for treating her dysmenorrhea and bilateral hemorrhagic cysts compatible with endometriomas. Though they were interested in fertility, her pain bothered her more. She was treated initially with a Mirena IUD. Her menses became less painful, but she complained of persistent irregular bleeding and requested removal after 3 months. She ultimately chose surgical management with a laparoscopic bilateral cystectomy and fulguration of endometriotic implants. There was no bowel involvement, and bilateral tubes were patent. Postoperative course was entirely uneventful. Follow-up exam 3 months later showed complete resolution of pain, and an ultrasound revealed bilaterally normal-appearing ovaries. Repeat AMH was stable at 3.1 ng/mL, and she was able to conceive naturally 5 months later.
Discussion
Dysmenorrhea is painful menstruation occurring with regularity and is present in 30–50% of young, reproductive-aged women [1]. When severe, it can interfere with normal daily activities and lead to frequent absenteeism from work or school. Primary dysmenorrhea is the presence of lower abdominal pain during menses without an identi able disease that attributes to the pain. It occurs more often in adolescent and younger women and is a diagnosis of exclusion, thus it requires a workup before a primary dysmenorrhea diagnosis can be made. It is often underdiagnosed and underreported. A detailed menstrual history is critical as primary dysmenorrhea often begins within 1 year of menarche. Secondary dysmenorrhea is more often found in women in their 30–40s and has identical symptoms of painful menstruation with demonstrable pathology, most commonly being benign conditions that likely develop throughout one’s late 20s and become initially symptomatic in the 30s.
At the beginning of menses, endometrial sloughing releases prostaglandins that induce uterine contractions and cause pain [2]. When contractions are particularly strong, anaerobic metabolites accumulate when intrauterine pressure exceeds arterial pressure. In addition, stretch receptors are likely activated, additively contributing to the degree of pain. The timing of pain usually begins 1–2 days before the onset of menstrual bleeding and gradually lessens over 24–72 h. It is con ned to the lower midline abdomen, but for some women the pain radiates to the back or upper thighs. When the pain is severe, gastrointestinal or neurologic symptoms such as nausea or headache often accompany the dysmenorrhea. Secondary causes of painful menstruation typically begin after age 25 and can be caused by common
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conditions such as broids, endometriosis, and adenomyosis. Given that primary dysmenorrhea is a diagnosis of exclusion, some symptoms suggestive of secondary dysmenorrhea include onset of symptoms after age 25, abnormal uterine bleeding, i.e., heavy or irregular, lateralized pain, dyspareunia, dyschezia, and absence of nausea or headaches during menstruation. Approximately 40% of women with dysmenorrhea caused by endometriosis have physical ndings on pelvic exam.
In younger women who are not sexually active, a pelvic exam is not needed when the history is highly suggestive of primary dysmenorrhea. The latter is usually not associated with any physical nding, abnormal laboratory or imaging studies, and the pelvic exam is typically normal. Tests that should be performed in sexually active individuals include cervical cultures for chlamydia/gonorrhea and a urine culture.
The only routine imaging needed to exclude a secondary cause for dysmenorrhea is a pelvic ultrasound if the clinical exam is normal, or in obese patients whose clinical exam is dif cult. Diagnostic laparoscopy is rarely indicated and only if a secondary cause is highly suspected and when routine medical treatment fails to restore adequate quality of life.
When secondary dysmenorrhea is suspected, the differential diagnosis includes endometriosis, adenomyosis, broids, ovarian cysts, chronic PID/pelvic adhesions, cervical stenosis or Mullerian anomalies, and pelvic congestion syndrome. Non- gynecologic disorders include infammatory bowel disease, irritable bowel syndrome, and psychogenic disorders.
For primary dysmenorrhea, treatment should be aimed at relief of pain and return to normal productivity. Patient education and reassurance—including the commonness of the diagnosis and low impact on future fertility—should be discussed. Heat packs and exercise are initial steps, followed by—or in combination with—NSAIDs and acetaminophen. NSAIDs inhibit prostaglandin synthesis and appear to be more effective in pain relief compared to acetaminophen [3]. The dose of NSAIDs should start at 400–600 mg every 6 h or 800 mg every 8 h with a maximum daily dose of 2400 mg/day starting with onset of menses or 24 h prior. For those at high risk of gastric ulcers, acetaminophen should be the rst-line choice. Because prostaglandins play an important role in ovulation, those trying to conceive who require pain relief beyond the tenth day of their menstrual cycle should switch over from NSAIDs to acetaminophen after the seventh day.
If rst-tier treatment with NSAIDs/acetaminophen is ineffective, then hormonal therapy is the next tier of treatment. Estrogen-progestin contraceptive agents maintain a thin endometrium, thus creating a lining with only small levels of arachidonic acid—the substrate for prostaglandin synthesis. This in turn reduces blood fow, contractility, and pain. The patient is rst screened for contraindications of combination pill use such as migraines with aura, a personal history of blood clots, or uncontrolled hypertension [4]. Estrogen doses of >35 μg vs <35 μg show a similar degree of pain relief, as do continuous vs cyclic way of administration [5]. When treating for dysmenorrhea, pill regimens with shorter placebo duration or extended length formulations (3 months of active pills/placebo week) are ideal. Oral, transdermal, and vaginal rings are all acceptable options depending on the patient’s
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comfort and choice. There has been no evidence to show decreased ef cacy of one route over another, although existing data is mostly based upon the traditional oral route.
For those who cannot take estrogen, a progesterone-only pill as an option should be discussed. Different preparation such as norethindrone 0.35 mg tablets, drospirenone 4 mg tablets, and norethindrone 5 mg tablets can be considered. Progestin- only pills are dispensed in familiar-appearing packs for those accustomed to combination oral contraceptive pills but have a higher incidence of irregular bleeding and do not inhibit ovulation as reliably as the combination pills. Injectable contraception (depot-Provera) has a 50% amenorrhea rate after 1 year of use, but there may be a delay to ovulation once discontinued. Levonorgestrel IUDs (20 μg) also reduce dysmenorrhea, and 20% of users have amenorrhea after 1 year. Implantable, single-rod etonogestrel-releasing options are also available, but less well studied for relief of dysmenorrhea. GnRH agonist treatment is another option but is typically reserved for the most refractory cases as it can increase the risk of osteopenia.
If hormonal treatment is insuf cient in relieving dysmenorrhea, the next tier in treatment is offered. Diagnostic laparoscopy to assess and excise/fulgurate endometriosis lesions or diagnose pelvic congestion syndrome is the next reasonable step. If endometriosis is found, hormonal therapy should be continued to reduce risk of recurrence. If the patient has completed her childbearing or does not wish to have children, endometrial ablation is a reasonable option, especially for those whose dysmenorrhea is associated with menorrhagia. Transcutaneous electrical nerve stimulation (TENS) are 12 weekly treatments and can be used in conjunction with NSAIDs, hormonal contraception, and heat therapy. It is hypothesized to raise the threshold for pain signals or reduce perception of pain by sending high frequency of afferent pulses to the uterus [6].
Alternative medicine options such as acupuncture or acupressure can be included in discussions and can be used in refractory cases in conjunction with the rstor second-tier agents. Level A evidence is not supportive of alternative medicine as a primary treatment for dysmenorrhea. A variety of diets/dietary supplements have also been studied with some reduction in dysmenorrhea—vegetarianism, high dairy diet, increased vitamin D3, B6, and E—in small studies that have shown limited bene t in pain reduction [7].
The goal of treatment should be to educate the patient on potential causes of dysmenorrhea and to nd the minimal effective dose of treatment needed to resume her normal daily activities. NSAIDs, acetaminophen, and heat therapy are the rst- line therapy. The second-line treatments should include hormonal options, and the third-line options are more invasive laparoscopy/hysteroscopy and TENS. Regular follow-up visits are helpful to women with dysmenorrhea to review symptoms and monitor the degree of improvement with various treatments, ensuring the patient is receiving optimal care.
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References
1.\ Klein JR, Litt IF. Epidemiology of adolescent dysmenorrhea. Pediatrics. 1981;68:661–4.
2.\ Dawood MY. Primary dysmenorrhea: advances in pathogenesis and management. Obstet Gynecol. 2006;108(2):428–41.
3.\ Armour M, Parry K, Al-Dabbas MA, et al. Self-care strategies and sources of knowledge on menstruation in 12,526 young women with dysmenorrhea: a systematic review and meta- analysis. PLoS One. 2019;14(7):e0220103.
4.\ Wong CL, Farquhar C, Roberts H, Proctor M. Oral contraceptive pill for primary dysmenorrhea. Cochrane Database Syst Rev. 2009;2009(4):CD002120.
5.\ Edelman AB, Gallo MF, Jensen JT, et al. Continuous or extended cycle vs cyclic use of combined oral contraceptives for contraception. Cochrane Database Syst Rev. 2014; 2014(3):CD004695.
6.\ Smith RP, Heltzel JA. Interrelation of analgesia and uterine activity in women with primary dysmenorrhea. A preliminary report. J Reprod Med. 1991;36(4):260–4.
7.\ Barnard ND, Scialli AR, Hurlock D, Bertron P. Diet and sex-hormone binding globulin, dysmenorrhea, and premenstrual symptoms. Obstet Gynecol. 2000;95(2):245–50.
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Chapter 8
Abnormal Uterine Bleeding
Ashley Aluko and Joshua Stewart
Case
A 34-year-old nulliparous woman presents to the of ce with irregular periods. She has been on a combined oral contraceptive pill (COC) since college. She stopped the COC approximately 6 months prior to evaluation when she and her husband began trying to conceive. She reports that she was having a regular withdrawal bleed every month while on COC. She has had two menstrual cycles since stopping the COC. The rst cycle was very heavy and lasted for approximately 8 days. The second cycle occurred approximately 90 days later, with lighter bleeding lasting for 4 days. She has been monitoring ovulation with urinary ovulation predictor kits but has become increasingly frustrated as they never turned positive.
She reports menarche at age 12 associated with normal pubertal development. Her periods were initially irregular, occurring every 30–60 days with variable amount of fow. Her cycles eventually normalized at age 14 years. Her medical history is signi cant for exercise-induced asthma for which she occasionally needs to use an albuterol inhaler, as well as anxiety which is well-controlled with psychotherapy. She has never had surgery. She has a sister with polycystic ovarian syndrome (PCOS), but otherwise denies any pertinent family history.
On physical exam, she is a well-appearing female with BMI 27 kg/m2. There is no palpable mass on her thyroid. Pelvic exam reveals normal external female genitalia, normal cervix, and a normal-sized, mobile uterus with no adnexal mass. A transvaginal ultrasound reveals a normal uterus with thin endometrial stripe (3 mm) without evidence of polyps or myomas, and normal-appearing ovaries with an antral follicle count of 13.
A. Aluko · J. Stewart (*)
Reproductive Medicine and Ob/Gyn, The Ronald Perelman and Claudia Cohen Center for Reproductive Medicine, Weill Medical College of Cornell University, New York, NY, USA e-mail: jds9013@med.cornell.edu
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