Menstrual Suppression

Read the new ACOG Clinical Consensus! – General Approaches to Medical Management of Menstrual Suppression

Why menstrual suppression?

  • As an OB/GYN that might sound like a silly question – but for our patients, this is a serious concern!

    • A holdover of understanding (even with the design of OCPs) that a “natural cycle” is necessary for health – it’s not. 

  • Goal overall is to:

    • Reduce menstrual flow, by amount and total days while

    • Find a strategy based on patients preferences and goals, balancing any risk factors.

Which method is best?

  • Combined Hormonal Contraception

    • Can achieve menstrual suppression by skipping the placebo week.

      • Some packs designed for this - 84/7 regimens, 24/4 regimens.

      • This can be done indefinitely!

        • Studies have found these extended cycle and continuous use regimens to be safe and effective

    • Patients should be counseled that over time, breakthrough bleeding is more likely to occur. In a recent RCT comparing OCPs to an LNG-IUD for menstrual suppression, folks in the OCP group had BTB:

      • 50% at pill pack 3;

      • 69% at pill pack 7;

      • 79% at pill pack 13.

    • Bleeding overall tends to decrease with successive cycles.

    • Breakthrough happens less with higher doses of estrogen (i.e., more bleeding on a 20mcg pill than a 30mcg pill).

    • BTB will decrease with each successive cycle – so it’s not unreasonable to consider monthly cycles for 3-6 months, then transition to more extended cycles. 

      • Intermittent estrogen can also be used to help prevent BTB.

    • The patch and vaginal ring can also be used for menstrual suppression, and have advantage of not requiring daily medication.

      • Patch has no difference in frequency of BTB compared to pills.

      • Ring is well tolerated for extended cycles and seems to be effective in reducing/minimizing bleeding.

  • Progestin-Only Methods

    • These can be of particular importance to patients where estrogen is contraindicated (cardiovascular disease, migraine with aura, hypertension, hypercoagulability) or undesired (trans-men, patient preference).

  • POPs

    • The mini-pill (norethindrone 0.35mg) has to be taken in a tight window, and has low rates of amenorrhea, so is generally not a great choice for menstrual suppression.

    • Norethindrone acetate 5mg can be used for menstrual suppression with better success compared to the minipill, with amenorrhea rates of up to 76% at 2 years of use.

      • However, this formulation is not approved as a contraceptive so can’t be used for this.

    • Drosperinone 4mg is a new progestin only pill on the market; data is limited, but it is likely more promising than the minipill for menstrual suppression and also has contraceptive effect. 

      • That said, likely not a first line choice for this indication specifically.

  • DMPA (depot medroxyprogesterone acetate)

    • The DMPA shot is given roughly every 3 months.

    • Amenorrhea rates are good, especially with more prolonged use – 68-71% at 2 years.

      • However, unscheduled bleeding is a common side effect.

      • Loss of bone mineral density and weight gain are other common concerns; the loss of BMD is reversible with discontinuation. 

  • LNG-IUD

    • Excellent at amenorrhea - 50% at 1 year, 60% at 5 years; highest with the 52mg varieties.

    • BTB can be managed by offering a trial of NSAIDs, POPs/OCPs, or doxycycline before discontinuing the IUD.

    • Not a good choice for patients where ovulation suppression is also desired (ie, PCOS) – the IUD has unclear/unpredictable effects on ovulation suppression.

  • Etonogestrel implant (nexplanon)

    • Can be continued up to 5 years for contraception, FDA approved for 3 years.

    • For menstrual suppression, use past 3 years may not be effective. 

    • 22% achieve amenorrhea, but breakthrough bleeding and spotting are common, especially shortly after insertion.

      • BTB can be managed with OCPs or norethindrone.

  • The ACOG document contains a very helpful but large table on the different types of hormonal contraception and their relative success, advantages, and disadvantages with menstrual suppression. Definitely worth keeping a bookmark on or a snapshot on your phone!

How do I go about selecting a method?

  • Counsel your patient with shared-decision making in mind:

    • Be aware of inequities in provision of menstrual suppression methods and your own biases

    • Share with patients realistic expectations of what each method might offer in the way of menstrual suppression

      • No method can guarantee amenorrhea

    • Take into account patient’s preferences and values

    • Be aware of medical history / medical eligibility criteria that might contraindicate certain methods

By patient population:

  • Adolescents:

    • Hormone therapies are safe for adolescents

    • Initiation of menstrual suppression is safe anytime after menarche!

      • Need to have at least one menstrual period to be certain of normal pubertal development.

    • Pelvic exam is not needed for routine prescription of contraception, unless needed for the actual insertion (i.e., IUD)

      • IUD insertion has been shown to not be any more difficult in adolescents compared to older individuals, nor more difficult in nulliparas compared to parous patients.

    • Other tenets of adolescent reproductive healthcare counseling should be applied:

      • Discuss concerns about any side effects that are common / common concerns - fertility, weight, development, bone health, STIs

      • Use the opportunity to establish healthy alignment with adolescent at the OB/GYN office to establish as a safe place for current & future care

  • Transgender / Gender Diverse Patients

    • Menstrual suppression can help reduce feelings of gender dysphoria associated with menstruation

    • Testosterone use for gender-affirming care is associated with amenorrhea, often within a few months of starting therapy.

    • GnRH is also capable of pubertal blockade and suppression of menses for gender-affirming therapy, with amenorrhea rates nearing 100%.

      • Testosterone and GnRH are not contraceptives, though - so if they are at risk of pregnancy, contraception should be discussed

      • GnRH also cannot be used long term given concerns for bone density effects.

  • Patients with physical or cognitive disabilities, or both

    • Particularly for patients with cognitive disability, menstruation is a significant source of anxiety for caregivers and is a common reason for visit for pediatric gynecology clinics, even among premenarchal patients

    • Adolescents and adults with disabilities are also often assumed (erroneously) to be asexual and do not receive sexuality and contraceptive counseling on par with their peers

      • These individuals are also at increased risk of sexual abuse and unintended pregnancy

    • Assist families with developmentally-appropriate education and family assistance with hygiene concerns, contraception, STIs, and abuse prevention

    • Menstrual suppression methods can follow the patient’s needs, preferences, and values. 

      • Consider in these patients their mobility and presence of contractures; swallowing ability for pills; and presence of other interacting drugs (i.e., antiepileptics).

      • If plan for LARC and anesthesia required, it can be considered to “bundle” together services like dental work to minimize patient exposures to anesthetics

    • If patient doesn’t have capacity to make independent decision, menstrual suppression discussions should be made with the caregiver in patient’s best insterest.

      • Ethical and prudent choice is reversible and low-risk options.

  • Populations with challenges affecting hygiene/privacy

    • Military deployment

    • Incarceration

    • Houselessness

    • Patients in war zones or difficulty with care access

    • Athletes

      • Obviously hard to think about all of the potentials here, but consider patient access to medical services, sanitary products, restrooms or private areas, in making shared-decision making on menstrual suppression

How do I manage breakthrough bleeding?

  • One of the most common challenges in menstrual suppression

  • Anticipatory counseling that this is common is helpful in reducing method discontinuation rates and improving method satisfaction, as well as reassuring that BTB is benign and common.

    • Reassure that with some methods BTB decreases or ceases after some time period of initial use

Abnormal Uterine Bleeding: The Basics

Today we talk through the varied etiologies and a basic workup for a common GYN complaint: abnormal uterine bleeding. ACOG PB 128 makes for good companion reading for women of reproductive age.

The terminology of AUB has changed quite a bit, and you may still hear older terms being used. “Dysfunctional uterine bleeding” or DUB has fallen out of favor, as have terms such as metrorrhagia or menorrhagia, yielding instead to simpler terminology such as prolonged menstrual bleeding and heavy menstrual bleeding, respectively. The terms such as oligomenorrhea (bleeding cycles > 35 days apart) and polymenorrhea (cycles < 21 days apart) are also in use to some degree.

Heavy bleeding is difficult to discern, but for research purposes has been described as >80cc blood loss per cycle. In clinical practice, this is obviously impractical, so we rely on subjective descriptions of heavy bleeding to guide care.

The biggest takeaways from this episode include the PALM-COIEN classification of bleeding by FIGO, as well as the common culprits of bleeding by age group. Remember also the criteria for working up for disorders of coagulation, which we’ve put here (though contained in the practice bulletin).

Stay tuned for future episodes about the treatments of these various etiologies, or check out our friends at The OBG Project for excellent summaries of guidelines and new literature!

ACOG PB 128

ACOG PB 128

ACOG PB 128

Progestins

Today we welcome Dr. Ben Brown, who is an assistant professor in the Division of Emergency Obstetrics and Gynecology at Women and Infants Hospital and the Warren Alpert Brown School of Medicine. Dr. Brown is also completed a fellowship in Family Planning, and thus shares with us his expertise in progestin-based contraception!

We quickly reviewed initially that progesterone naturally serves as an inhibitory feedback to luteinizing hormone during the menstrual cycle. There were also a number of downstream effects of progesterone, including cervical mucus thickening, stabilizing the endometrial lining, and down-regulating both systemic progesterone and estrogen receptors — you can review all of these again with our episode on the menstrual cycle if you missed it. These mechanisms of action underlie the way progestins work clinically. We do not cover the anti-progestins (mifepristone) and selective progesterone receptor modulators (ulipristal) today.

We then reviewed the generations of progestins. As Dr. Brown states, knowing drosperinone as a 4th generation is probably a good thing, but otherwise some of this is just good to know as a “contraception nerd.” The generations are summarized below in a nice table:

We then spoke about the delivery methods beyond the drugs — pills, injections, IUDs, implants, and more!

Side effects and contraindications are important to know for all forms of contraception. Here are a few that we review:

  • Androgenicity: more apparent in combined-hormonal methods, due to upregulation of SHBG by estrogen. Some progestins (particularly 1st generation) also competitively bind androgenic receptors — even sometimes if given without estrogen, those progestins may actually produce androgenic side effects! That said, this is quite uncommon.

  • Thrombosis: this can be very confusing and controversial:

    • Estrogen-containing methods will raise risk of both venous and arterial clots.

      • Drosperinone and other later-generation progestins has received poor press due to higher risk of thrombosis in combined formulations. The risk is overall still very low: 7-13 events per 10,000 woman years. But compared to pregnancy as a competing outcome, 20-30 events/10k woman years, and postpartum 40-60/10k woman-years!

    • Progestins alone can also raise arterial thrombus risk.

      • These are patients who you consider to have significant endovascular risk factors — longstanding poorly-controlled diabetes, coronary disease, heavy smoking, etc. This is because progestins can shift lipid profiles to a more androgenic appearance - lower HDL, higher LDL and total cholesterol.

    • The CDC’s US MEC guidelines are an excellent tool to cross-reference comorbidities against contraceptive methods.

  • Breast cancer: current or prior is a relative contraindication to hormonal contraception.

  • Severe liver disease: contraindicated due to impaired hepatic processing of steroid hormone.

  • Bariatric malabsorptive procedures: may not be great candidates for progestin-only pills due to need for consistent dosing time.

The Menstrual Cycle

On today’s episode we welcome Dr. Jay Huber. Jay is a 3rd year fellow in reproductive endocrinology and infertility at the Warren Alpert Brown School of Medicine, and today he demystifies the HPO axis, the menstrual cycle, and all of the hormonal interplay.

It’s always helpful to follow along to one of the “menstrual cycle” diagrams, one of which we include here for reference:

Wikipedia

As Dr. Huber reminds us, the ovary really runs the show due to its negative feedback effect on the hypothalamus. However, thinking top down:

  • GnRH is release from the hypothalamus in a pulsatile fashion, triggering release of FSH and/or LH, depending on the timing of the cycle.

  • In the follicular phase of the ovary, FSH stimulates development of a dominant follicle. Once the dominant follicle is large enough, it produces a high enough level of estrogen to give positive feedback to the hypothalamus. Further GnRH is released, promoting preferential LH release downstream, until an LH surge is triggered, giving us the ovulation event on day 14.

  • After this, the levels of LH and FSH decline in response to negative estrogen feedback, in the luteal phase of the ovary.

  • Simultaneously, the estrogen produced by the dominant follicle in the ovarian follicular phase above causes downstream effects on the endometrium, marking the proliferative phase here of endometrial growth in preparation for implantation.

  • Once the follicle releases the oocyte, the follicular cells become the corpus luteum, which then produces progesterone. Progesterone matures the endometrium to be ‘pro-gestational’ for implantation and the secretory phase of endometrial maturation occurs.

  • If no fertilization event occurs, the corpus luteum degenerates, and by day 23-25, progesterone withdrawal results in shedding of the endometrial lining. If a fertilization event occurs, beta-hCG prompts the corpus luteum to continue to make progesterone.

Further reading from the OBG Project:
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Managing AUB-O
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