Abnormal (Dysfunctional) Uterine Bleeding in Emergency Medicine Medication

Updated: Dec 07, 2018
  • Author: Amir Estephan, MD; Chief Editor: Jeter (Jay) Pritchard Taylor, III, MD  more...
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Medication Summary

The goals of pharmacotherapy are to control the bleeding, reduce morbidity, and prevent complications.


Steroid hormones

Class Summary

These agents may help control bleeding. Some of them are used when bleeding is profuse and the patient is unresponsive to initial fluid management.

Ethinyl estradiol 35 μg and norethindrone 1mg (Necon 1/35, Nortrel 1/35, Ortho-Novum 1/35, Norinyl 1 + 35)

Reduces secretion of LH and FSH from pituitary by decreasing amount of GnRH.

Contraceptive pills containing estrogen and progestin have been advocated for nonsmoking patients with DUB who desire contraception. Therapy also used to treat acute hemorrhagic uterine bleeding but not as effective as other treatments perhaps because may take longer to induce endometrial proliferation when progestin is present.

Suggested mechanisms by which hormonal therapy might affect bleeding include improvement in coagulation, alterations in the microvascular circulation, and improvements in endothelial integrity. In long-term management of DUB, combination oral contraceptives are very effective.


Synthetic steroid analog, derived from ethisterone, with strong antigonadotropic activity (inhibits LH and FSH) and weak androgenic action without adverse virilizing and masculinizing effects. Increases levels of C4 component of the complement. May push the resting hematopoietic stem cells into cycle, making them more responsive to differentiation by hematopoietic growth factors. May also stimulate endogenous secretion of erythropoietin.

May impair clearance of immunoglobulin-coated platelets and decreases autoantibody production.

Certain androgenic preparations have been used historically to treat mild-to-moderate bleeding, particularly in ovulatory patients with abnormal uterine bleeding. These regimens offer no real advantage over other regimens and might cause irreversible signs of masculinization in the patient. They seldom are used for this indication today.

Use of androgens might stimulate erythropoiesis and clotting efficiency. Androgens alter endometrial tissue so that it becomes inactive and atrophic.

Estrogens, conjugated (Premarin)

Causes vasospasm of uterine arteries and initiates several coagulation-related functions, which decrease uterine bleeding. Use in pharmacologic doses also causes rapid growth of endometrial tissue over denuded and raw epithelial surface.

Medroxyprogesterone acetate (Provera)

DOC for most patients with anovulatory DUB. After acute bleeding episode controlled, can be used alone in patients with adequate amounts of endogenous estrogen to cause endometrial growth. Progestin therapy in adolescents produces regular cyclic withdrawal bleeding until positive feedback system matures. Progestins stop endometrial growth and support and organize endometrium to allow organized sloughing after their withdrawal. Bleeding ceases rapidly because of an organized slough to the basalis layer. These drugs usually do not stop acute bleeding episodes, yet produce a normal bleeding episode following their withdrawal.


Nonsteroidal Anti-inflammatory Drugs (NSAIDs)

Class Summary

These agents can decrease DUB through inhibition of prostaglandin synthesis. NSAIDs only need to be taken during menstruation.

Naproxen (Naprosyn, Aleve, Naprelan)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis.

NSAIDs decrease intraglomerular pressure and decrease proteinuria.


Gonadotropin Releasing Hormone Analog

Class Summary

These agents are generally used for short-term use to induce amenorrhea and allow the rebuilding of the red blood cell mass.

Leuprolide acetate (Lupron, Eligard)

Suppresses ovarian and testicular steroidogenesis by decreasing LH and FSH levels.

Works by reducing concentration of GnRH receptors in the pituitary via receptor down regulation and induction of postreceptor effects, which suppress gonadotropin release. After an initial gonadotropin release associated with rising estradiol levels, gonadotropin levels fall to castrate levels, with resultant hypogonadism. This form of medical castration is very effective in inducing amenorrhea, thus breaking ongoing cycle of abnormal bleeding in many anovulatory patients. Because prolonged therapy with this form of medical castration is associated with osteoporosis and other postmenopausal side effects, many practitioners add a form of low-dose hormonal replacement to the regimen. Because of the expense of these drugs, they usually are not used as a first-line approach but can be used to achieve short-term relief from a bleeding problem, particularly in patients with renal failure or blood dyscrasia.