Menorrhagia is defined as menstruation at regular cycle intervals but with excessive flow and duration and is one of the most common gynecologic complaints in contemporary gynecology. See the image below.
Symptoms related by a patient with menorrhagia often can be more revealing than laboratory tests. A detailed patient history is imperative and should include inquiries about the following:
Exclusion of pregnancy (the most common cause of irregular bleeding in women of reproductive age and the first diagnosis that should be excluded before further testing or drug therapy)
Quantity and quality of bleeding
Pelvic pain and pathology
Menses pattern from menarche
Contraceptive use (intrauterine device [IUD] or hormones)
Presence of hirsutism (polycystic ovarian syndrome [PCOS])
Galactorrhea (pituitary tumor)
Systemic illnesses (hepatic or renal failure or diabetes)
Symptoms of thyroid dysfunction
Excessive bruising or known bleeding disorders
Current medications (hormones or anticoagulants)
Previous medical or surgical procedures or diagnoses
The physical examination should be tailored to the differential diagnoses suggested by the history. Initial inspection should include evaluation for the following:
Signs of severe volume depletion (eg, anemia)
Signs of androgen excess (eg, hirsutism)
General examination should include evaluation of the following:
Enlarged liver or spleen
Pelvic examination should evaluate for the following:
Presence of external genital lesions
Vaginal or cervical discharge
Uterine size, shape, and contour
Cervical motion tenderness
Adnexal tenderness or masses (especially in patients older than 40 years)
According to an international expert panel, an underlying bleeding disorder should be considered when a patient has any of the following:
Menorrhagia since menarche
Family history of bleeding disorders
Personal history of 1 or more of the following: (1) Notable bruising without known injury, (2) bleeding of the oral cavity or gastrointestinal tract without an obvious lesion, or (3) epistaxis of more than 10 minutes’ duration (possibly necessitating packing or cautery)
See Clinical Presentation for more detail.
Laboratory studies that may be useful include the following:
Complete blood count
Iron studies (total iron-binding capacity [TIBC] and total iron)
Coagulation factor studies (expensive and to be used sparingly)
Human chorionic gonadotropin (hCG) level
Thyroid function tests and prolactin level
Liver function tests (LFTs), renal function tests (blood urea nitrogen [BUN] and creatinine), or both
Hormone assays (eg, luteinizing hormone [LH], follicle-stimulating hormone [FSH], and androgen) for suspected PCOS; adrenal function tests for suspected adrenal tumors
Imaging studies and other diagnostic measures that may be helpful include the following:
Sonohysterography (saline-infusion sonography)
Papanicolaou (Pap) smear
Endometrial biopsy (EMB): Understanding EMB results is essential for any physician treating menorrhagia
See Workup for more detail.
Medical therapy should be tailored to characteristics of the patient (eg, age, coexisting medical diseases, family history, and desire for fertility). Agents used include the following:
Nonsteroidal anti-inflammatory drugs (NSAIDs): First-line medical therapy for ovulatory menorrhagia
Oral contraceptive pills (OCPs): A popular first-line therapy for women who desire contraception; dienogest−estradiol valerate has been approved by the US Food and Drug Administration (FDA) for heavy menstrual bleeding
Progestin: The most frequently prescribed medicine for menorrhagia
Levonorgestrel intrauterine system: Approved by the FDA for treatment of menorrhagia in women who use intrauterine conception; a 2-year primary care–based study of 571 women aged 25-50 years (mean, 42 years) found that a levonorgestrel intrauterine system was more effective than usual medical treatments in alleviating the adverse effects of menorrhagia on women’s lives [1, 2] ; although some fault the study for failing to adequately eliminate other possible causes of excessive bleeding before initiating treatment, the finding that 90% of the women were aged 35 years or older suggests that for the majority of the patients studied, the heavy bleeding was probably a result of age-related ovarian dysfunction 
Gonadotropin-releasing hormone (GnRH) agonists
Surgical management has been the standard of treatment in menorrhagia when the cause is organic or when medical therapy fails to alleviate symptoms. Options for surgical intervention include the following:
Dilatation and curettage: Used for diagnosis rather than treatment, typically in combination with hysteroscopy
Resectoscopic endometrial ablation: Includes transcervical resection of the endometrium (TCRE; criterion standard)),  roller-ball endometrial ablation,  and endometrial laser ablation; these techniques have largely been replaced by the nonresectoscopic procedures
Procedures for surgical excision include the following:
Menorrhagia is defined as menstruation at regular cycle intervals but with excessive flow and duration and is one of the most common gynecologic complaints in contemporary gynecology. Clinically, menorrhagia is defined as total blood loss exceeding 80 mL per cycle  or menses lasting longer than 7 days.  The World Health Organization reports that 18 million women aged 30-55 years perceive their menstrual bleeding to be exorbitant.  Reports show that only 10% of these women experience blood loss severe enough to cause anemia or be clinically defined as menorrhagia. [14, 16, 17] In practice, measuring menstrual blood loss is difficult. Thus, the diagnosis is usually based upon the patient’s history.
A normal menstrual cycle is 21-35 days in duration, with bleeding lasting an average of 7 days and flow measuring 25-80 mL. 
Menorrhagia must be distinguished clinically from other common gynecologic diagnoses. These include metrorrhagia (flow at irregular intervals), menometrorrhagia (frequent, excessive flow), polymenorrhea (bleeding at intervals < 21 d), and dysfunctional uterine bleeding (abnormal uterine bleeding without any obvious structural or systemic abnormality). 
Nearly 30% of all hysterectomies performed in the United States are performed to alleviate heavy menstrual bleeding.  Historically, definitive surgical correction has been the mainstay of treatment for menorrhagia. Modern gynecology has trended toward conservative therapy both for controlling costs and the desire of many women to preserve their uterus.
Heavy menstrual bleeding is a subjective finding, making the exact problem definition difficult. Treatment regimens must address the specific facet of the menstrual cycle the patient perceives to be abnormal, (ie, cycle length, quantity of bleeding). Finally, treatment success is usually evaluated subjectively by each patient, making positive outcome measurement difficult.
Knowledge of normal menstrual function is imperative in understanding the etiologies of menorrhagia. Four phases constitute the menstrual cycle, follicular, luteal, implantation, and menstrual.
In response to gonadotropin-releasing hormone (GnRH) from the hypothalamus, the pituitary gland synthesizes follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which induce the ovaries to produce estrogen and progesterone.
During the follicular phase, estrogen stimulation results in an increase in endometrial thickness. This also is known as the proliferative phase.
The luteal phase is intricately involved in the process of ovulation. During this phase, also known as the secretory phase, progesterone causes endometrial maturation.
If fertilization occurs, the implantation phase is maintained. Without fertilization, estrogen and progesterone withdrawal results in menstruation.
Etiologic causes are numerous and often unknown. Factors contributing to menorrhagia can be sorted into several categories, including organic, endocrinologic, anatomic, and iatrogenic.
If the bleeding workup does not provide any clues to the etiology of the menorrhagia, a patient often is given the diagnosis of dysfunctional uterine bleeding (DUB). Most cases of DUB are secondary to anovulation. Without ovulation, the corpus luteum fails to form, resulting in no progesterone secretion. Unopposed estrogen allows the endometrium to proliferate and thicken. The endometrium finally outgrows its blood supply and degenerates. The end result is asynchronous breakdown of the endometrial lining at different levels. This also is why anovulatory bleeding is heavier than normal menstrual flow.
Hemostasis of the endometrium is directly related to the functions of platelets and fibrin. Deficiencies in either of these components results in menorrhagia for patients with von Willebrand disease or thrombocytopenia. Thrombi are seen in the functional layers but are limited to the shedding surface of the tissue. These thrombi are known as “plugs” because blood can only partially flow past them. Fibrinolysis limits the fibrin deposits in the unshed layer. Following thrombin plug formation, vasoconstriction occurs and contributes to hemostasis.
Anatomic defects or growths within the uterus can alter either of the aforementioned pathways (endocrinologic/hemostatic), causing significant uterine bleeding. The clinical presentation is dependent on the location and size of the gynecologic lesion.
Organic diseases also contribute to menorrhagia in the female patient. For example, in patients with renal failure, gonadal resistance to hormones and hypothalamic-pituitary axis disturbances result in menstrual irregularities. Most women in this renal state are amenorrheic, but others also develop menorrhagia. If uremic coagulopathy ensues, it usually is due to platelet dysfunction and abnormal factor VIII function. The resulting prolonged bleeding time causes menorrhagia that can be very tenuous to treat.
Due to the overwhelming factors that can contribute to the dysfunction of either the endocrine or hematological pathways, in-depth knowledge of an existing organic disease is just as imperative as understanding the menstrual cycle itself.
Etiologies of menorrhagia are divided into 4 categories, organic, endocrinologic, anatomic, and iatrogenic.
Organic causes of menorrhagia include infection, bleeding disorders, and organ dysfunction. Consider the following:
Infections can be of any genitourinary origin. The aforementioned sexually transmitted diseases are of greater concern in the teenage and early adult population. Bleeding from the urethra or rectum always must be considered in the workup, especially in the postmenopausal woman who has negative findings after a workup for vaginal bleeding.
Coagulation disorders can evade diagnosis until menarche, when heavy menstrual bleeding presents as an unrelenting disorder. These include von Willebrand disease; factor II, V, VII, and IX deficiencies; prothrombin deficiency; idiopathic thrombocytopenia purpura (ITP); and thromboasthenia.  See more on bleeding disorders below.
Organ dysfunction causing menorrhagia includes hepatic or renal failure. Chronic liver disease impairs production of clotting factors and reduces hormone metabolism (eg, estrogen). Either of these problems may lead to heavy uterine bleeding.
Endocrine causes of menorrhagia include thyroid and adrenal gland dysfunction, pituitary tumors, anovulatory cycles, PCOS, obesity, and vasculature imbalance. Note the following:
Both hypothyroidism and hyperthyroidism result in menorrhagia. Even subclinical cases of hypothyroidism produce heavy uterine bleeding in 20% of patients. Menorrhagia usually resolves with correction of the thyroid disorder. 
Prolactin-producing pituitary tumors cause menorrhagia by disrupting (GnRH) secretion. This leads to decreased LH and FSH levels, which ultimately cause hypogonadism. Interim stages of menorrhagia result until hypogonadism manifests.
The most common etiology of heavy uterine bleeding is anovulatory cycles. The finding of menorrhagia at irregular intervals without any known organic etiology confirms the clinical diagnosis. This is most common in adolescent and perimenopausal populations.
The hallmarks of PCOS are anovulation, irregular menses, obesity, and hirsutism. Insulin resistance is common and increases androgen production by the ovaries.
Hyperinsulinemia is a direct consequence of obesity. This overproduction of insulin leads to ovarian production of androgens, as occurs in PCOS.
Vasculature imbalance is theorized to be the result of a discrepancy between the vasoconstricting and aggregating actions of prostaglandin F2 (alpha) and thromboxane A2 and the vasodilating actions of prostaglandin E2 and prostacyclin on the myometrial and endometrial vasculature.
Anatomic etiologies for menorrhagia include uterine fibroids, endometrial polyps, endometrial hyperplasia, and pregnancy. Note the following:
Fibroids and polyps are benign structures that distort the uterine wall and/or endometrium. Either may be located within the uterine lining, but fibroids may occur almost anywhere on the uterus.
The mechanism by which endometrial polyps or fibroids cause menorrhagia is not well understood. The blood supply to the fibroid or polyp is different compared to the surrounding endometrium and is thought to function independently. This blood supply is greater than the endometrial supply and may have impeded venous return, causing pooling in the areas of the fibroid. Heavy pooling is thought to weaken the endometrium in that area, and break-through bleeding ensues.
Fibroids located within the uterine wall may inhibit muscle contracture, thereby preventing normal uterine attempts at hemostasis. This also is why intramural fibroids may cause a significant amount of pain and cramping. Fibroids may enlarge to the point that they outgrow their blood supply and undergo necrosis. This also causes a great deal of pain for patients.
Endometrial hyperplasia usually results from unopposed estrogen production, regardless of the etiology. Endometrial hyperplasia can lead to endometrial cancer in 1-2% of patients with anovulatory bleeding, but it is a diagnosis of exclusion in postmenopausal bleeding (average age at menopause is 51 y). If a woman takes unopposed estrogen (without progesterone), her relative risk of endometrial cancer is 2.8 compared to nonusers. 
Iatrogenic causes of menorrhagia include IUDs, steroid hormones, chemotherapy agents, and medications (eg, anticoagulants). Consider the following:
IUDs can cause increased menstrual bleeding and cramping due to local irritation effects.
Steroid hormones and chemotherapy agents disrupt the normal menstrual cycle, which is restored easily upon cessation of the products.
Anticoagulants decrease clotting factors needed to cease any normal blood flow, including menses. This type of menorrhagia also is easily reversible.
An international expert panel including obstetrician/gynecologists and hematologists has issued guidelines to assist physicians in better recognizing bleeding disorders, such as von Willebrand disease, as a cause of menorrhagia and postpartum hemorrhage and to provide disease-specific therapy for the bleeding disorder.  Historically, a lack of awareness of underlying bleeding disorders has led to underdiagnosis in women with abnormal reproductive tract bleeding.
The panel provided expert consensus recommendations on how to identify, confirm, and manage a bleeding disorder. An underlying bleeding disorder should be considered when a patient has any of the following:
Menorrhagia since menarche
Family history of bleeding disorders
Personal history of 1 or more of the following: (1) Notable bruising without known injury; (2) bleeding of oral cavity or gastrointestinal tract without obvious lesion; and/or (3) epistaxis greater than 10 minutes duration (possibly necessitating packing or cautery)
If a bleeding disorder is suspected, consultation with a hematologist is suggested.
Although menorrhagia remains a leading reason for gynecologic office visits, only 10-20% of all menstruating women experience blood loss severe enough to be defined clinically as menorrhagia. 
Any woman of reproductive age who is menstruating may develop menorrhagia. Most patients with menorrhagia are older than 30 years.  This is because the most common cause of heavy menses in the younger population is anovulatory cycles, in which bleeding does not occur at regular intervals. 
With proper workup, diagnosis, treatment, and follow-up care, prognosis is excellent.
Infrequent episodes of menorrhagia usually do not carry severe risks to women’s general health.
Patients who lose more than 80 mL of blood, especially repetitively, are at risk for serious medical sequelae. These women are likely to develop iron-deficiency anemia as a result of their blood loss. Menorrhagia is the most common cause of anemia in premenopausal women. This usually can be remedied by simple ingestion of ferrous sulfate to replace iron stores. If the bleeding is severe enough to cause volume depletion, patients may experience shortness of breath, fatigue, palpitations, and other related symptoms. This level of anemia necessitates hospitalization for intravenous fluids and possible transfusion and/or intravenous estrogen therapy. Patients who do not respond to medical therapy may require surgical intervention to control the menorrhagia.
Other sequelae associated with menorrhagia usually are related to the etiology. For example, with hypothyroidism, patients may experience symptoms associated with a low-functioning thyroid (eg, cold intolerance, hair loss, dry skin, weight gain) in addition to the effects of significant blood loss. 
Complications of menorrhagia include the following:
Treatment of menorrhagia must be individualized to treat each patient’s specific symptoms. Cost, dosing, and patient compliance can play major roles.
If bleeding does not subside within the expected time frame, have the patient keep a menstrual calendar to better assess the resulting bleeding pattern.
If a specific treatment fails, investigate all possibilities, including noncompliance, medication dosing, diagnosis, patient age, and comorbid conditions.
Reassure patients that most bleeding stops, but not immediately. Provide literature on the treatment of choice, including expectations and adverse effects.
Many patients appreciate reassurance that they do not have cancer and are not alone in their plight.
Reassure patients who experience a treatment failure that other options are available.
Tucker ME. Levonorgestrel system eases effects of menorrhagia. Medscape Medical News. Jan 09, 2013. Available at http://www.medscape.com/viewarticle/777406. Accessed: Jan 14, 2013.
Gupta J, Kai J, Middleton L, et al. Levonorgestrel intrauterine system versus medical therapy for menorrhagia. N Engl J Med. 2013 Jan 10. 368(2):128-37. [Medline].
DeCherney A, Polan ML. Hysteroscopic management of intrauterine lesions and intractable uterine bleeding. Obstet Gynecol. 1983 Mar. 61(3):392-7. [Medline].
Chullapram T, Song JY, Fraser IS. Medium-term follow-up of women with menorrhagia treated by rollerball endometrial ablation. Obstet Gynecol. 1996 Jul. 88(1):71-6. [Medline].
Meyer WR, Walsh BW, Grainger DA, et al. Thermal balloon and rollerball ablation to treat menorrhagia: a multicenter comparison. Obstet Gynecol. 1998 Jul. 92(1):98-103. [Medline].
Garza-Leal J, Pena A, Donovan A, et al. Clinical evaluation of a third-generation thermal uterine balloon therapy system for menorrhagia coupled with curettage. J Minim Invasive Gynecol. 2010 Jan-Feb. 17(1):82-90. [Medline]. [Full Text].
Goldrath MH. Evaluation of HydroThermAblator and rollerball endometrial ablation for menorrhagia 3 years after treatment. J Am Assoc Gynecol Laparosc. 2003 Nov. 10(4):505-11. [Medline].
[Guideline] ACOG Practice Bulletin. Clinical management guidelines for obstetrician-gynecologists. Number 81, May 2007. Obstet Gynecol. 2007 May. 109(5):1233-48. [Medline].
Learman LA, Summitt RL Jr, Varner RE, et al. Hysterectomy versus expanded medical treatment for abnormal uterine bleeding: clinical outcomes in the medicine or surgery trial. Obstet Gynecol. 2004 May. 103(5 Pt 1):824-33. [Medline].
Wright RC. Hysterectomy: past, present, and future. Obstet Gynecol. 1969 Apr. 33(4):560-3. [Medline].
Showstack J, Lin F, Learman LA, et al. Randomized trial of medical treatment versus hysterectomy for abnormal uterine bleeding: resource use in the Medicine or Surgery (Ms) trial. Am J Obstet Gynecol. 2006 Feb. 194(2):332-8. [Medline].
Chen YJ, Li YT, Huang BS, Y, et al, for the Taiwan Association of Gynecology Systematic Review Group. Medical treatment for heavy menstrual bleeding. Taiwan J Obstet Gynecol. 2015 Oct. 54 (5):483-8. [Medline].
Hallberg L, Nilsson L. Determination of menstrual blood loss. Scand J Clin Lab Invest. 1964. 16:244-8. [Medline].
Goldrath MH. Hysteroscopic endometrial ablation. Obstet Gynecol Clin North Am. 1995 Sep. 22(3):559-72. [Medline].
Fraser IS, Warner P, Marantos PA. Estimating menstrual blood loss in women with normal and excessive menstrual fluid volume. Obstet Gynecol. 2001 Nov. 98(5 Pt 1):806-14. [Medline].
Warner PE, Critchley HO, Lumsden MA, Campbell-Brown M, Douglas A, Murray GD. Menorrhagia I: measured blood loss, clinical features, and outcome in women with heavy periods: a survey with follow-up data. Am J Obstet Gynecol. 2004 May. 190(5):1216-23. [Medline].
Lentz GM. Abnormal uterine bleeding. Katz VL, Lentz GM, Lobo RA, Gershenson DM, eds. Comprehensive Gynecology. 5th ed. Philadelphia, PA: Mosby; 2007. 915-32.
Glasser MH, Zimmerman JD. The HydroThermAblator system for management of menorrhagia in women with submucous myomas: 12- to 20-month follow-up. J Am Assoc Gynecol Laparosc. 2003 Nov. 10(4):521-7. [Medline].
Wilansky DL, Greisman B. Early hypothyroidism in patients with menorrhagia. Am J Obstet Gynecol. 1989 Mar. 160(3):673-7. [Medline].
Collins JA, Schlesselman JJ. Hormone replacement therapy and endometrial cancer. Lobo RA, ed. Treatment of the Postmenopausal Woman: Basic and Clinical Aspects. 2nd ed. Philadelphia, PA: Lippincott, Williams & Wilkins; 1999. 503-12.
[Guideline] James AH, Kouides PA, Abdul-Kadir R, et al. Von Willebrand disease and other bleeding disorders in women: consensus on diagnosis and management from an international expert panel. Am J Obstet Gynecol. 2009 Jul. 201(1):12.e1-8. [Medline].
Kadir RA, Economides DL, Sabin CA, et al. Frequency of inherited bleeding disorders in women with menorrhagia. Lancet. 1998 Feb 14. 351(9101):485-9. [Medline].
Dodson MG. Use of transvaginal ultrasound in diagnosing the etiology of menometrorrhagia. J Reprod Med. 1994 May. 39(5):362-72. [Medline].
Dijkhuizen FP, Mol BW, Brolmann HA, Heintz AP. The accuracy of endometrial sampling in the diagnosis of patients with endometrial carcinoma and hyperplasia: a meta-analysis. Cancer. 2000 Oct 15. 89(8):1765-72. [Medline].
Shaw RW. Assessment of medical treatments for menorrhagia. Br J Obstet Gynaecol. 1994 Jul. 101 Suppl 11:15-8. [Medline].
Jurema M, Zacur H. Menorrhagia. UpToDate. Available at http://bit.ly/fHJVtw. Accessed: March 29, 2009.
Fraser IS, McCarron G. Randomized trial of 2 hormonal and 2 prostaglandin-inhibiting agents in women with a complaint of menorrhagia. Aust N Z J Obstet Gynaecol. 1991 Feb. 31(1):66-70. [Medline].
Jensen JT, Parke S, Mellinger U, Machlitt A, Fraser IS. Effective treatment of heavy menstrual bleeding with estradiol valerate and dienogest: a randomized controlled trial. Obstet Gynecol. 2011 Apr. 117(4):777-87. [Medline].
Andersson JK, Rybo G. Levonorgestrel-releasing intrauterine device in the treatment of menorrhagia. Br J Obstet Gynaecol. 1990 Aug. 97(8):690-4. [Medline].
Rauramo I, Elo I, Istre O. Long-term treatment of menorrhagia with levonorgestrel intrauterine system versus endometrial resection. Obstet Gynecol. 2004 Dec. 104(6):1314-21. [Medline].
FDA approves intrauterine device for heavy menstrual bleeding. PR Newswire. Available at http://bit.ly/eKOVjr. 2009 Oct 01; Accessed: October 5, 2009.
Kaunitz AM, Bissonnette F, Monteiro I, Lukkari-Lax E, Muysers C, Jensen JT. Levonorgestrel-releasing intrauterine system or medroxyprogesterone for heavy menstrual bleeding: a randomized controlled trial. Obstet Gynecol. 2010 Sep. 116(3):625-32. [Medline].
Kim JY, No JH, Kim K, et al. Effect of myoma size on failure of thermal balloon ablation or levonorgestrel releasing intrauterine system treatment in women with menorrhagia. Obstet Gynecol Sci. 2013 Jan. 56(1):36-40. [Medline]. [Full Text].
Gupta JK, Daniels JP, Middleton LJ, et al. A randomised controlled trial of the clinical effectiveness and cost-effectiveness of the levonorgestrel-releasing intrauterine system in primary care against standard treatment for menorrhagia: the ECLIPSE trial. Health Technol Assess. 2015 Oct. 19 (88):1-118. [Medline].
Lukes AS, Moore KA, Muse KN, et al. Tranexamic acid treatment for heavy menstrual bleeding: a randomized controlled trial. Obstet Gynecol. 2010 Oct. 116(4):865-75. [Medline].
Ray S, Ray A. Non-surgical interventions for treating heavy menstrual bleeding (menorrhagia) in women with bleeding disorders. Cochrane Database Syst Rev. 2016 Nov 10. 11:CD010338. [Medline].
Nakamura K, Nakayama K, Sanuki K, Minamoto T, Ishibashi T, Sato E, et al. Long-term outcomes of microwave endometrial ablation for treatment of patients with menorrhagia: A retrospective cohort study. Oncol Lett. 2017 Dec. 14 (6):7783-7790. [Medline].
Nakamura K, Nakayama K, Ishikawa M, et al. Efficacy of multiple microwave endometrial ablation technique for menorrhagia resulting from adenomyosis. J Obstet Gynaecol Res. 2015 Nov. 41 (11):1769-72. [Medline].
Lethaby A, Hickey M, Garry R, Penninx J. Endometrial resection / ablation techniques for heavy menstrual bleeding. Cochrane Database Syst Rev. 2009 Oct 7. CD001501. [Medline].
Fischer F, Klapdor R, Gruessner S, Ziert Y, Hillemanns P, Hertel H. Radiofrequency endometrial ablation for the treatment of heavy menstrual bleeding among women at high surgical risk. Int J Gynaecol Obstet. 2015 Nov. 131 (2):123-8. [Medline].
Roberts TE, Tsourapas A, Middleton LJ, et al. Hysterectomy, endometrial ablation, and levonorgestrel releasing intrauterine system (Mirena) for treatment of heavy menstrual bleeding: cost effectiveness analysis. BMJ. 2011 Apr 26. 342:d2202. [Medline]. [Full Text].
Maybin JA, Critchley HO. Menstrual physiology: implications for endometrial pathology and beyond. Hum Reprod Update. 2015 Nov. 21 (6):748-61. [Medline].
Julia A Shaw, MD, MBA, FACOG Assistant Professor and Residency Program Director, Department of Obstetrics and Gynecology, Yale School of Medicine; Medical Director, Yale-New Haven Hospital Women’s Center
Julia A Shaw, MD, MBA, FACOG is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Association for Physician Leadership, Connecticut State Medical Society, AAGL, North American Menopause Society
Disclosure: Nothing to disclose.
Howard A Shaw, MD, MBA Clinical Professor of Obstetrics and Gynecology, Yale University School of Medicine; Chief Medical Officer, Medical City Denton
Howard A Shaw, MD, MBA is a member of the following medical societies: American Association for Physician Leadership, American College of Forensic Examiners Institute, American College of Healthcare Executives, American College of Obstetricians and Gynecologists
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
A David Barnes, MD, MPH, PhD, FACOG Consulting Staff, Department of Obstetrics and Gynecology, Mammoth Hospital (Mammoth Lakes, CA), Pioneer Valley Hospital (Salt Lake City, UT), Warren General Hospital (Warren, PA), and Mountain West Hospital (Tooele, UT)
A David Barnes, MD, MPH, PhD, FACOG is a member of the following medical societies: American College of Forensic Examiners Institute, American College of Obstetricians and Gynecologists, Association of Military Surgeons of the US, American Medical Association, Utah Medical Association
Disclosure: Nothing to disclose.
Michel E Rivlin, MD Former Professor, Department of Obstetrics and Gynecology, University of Mississippi School of Medicine
Michel E Rivlin, MD is a member of the following medical societies: American College of Obstetricians and Gynecologists, American Medical Association, Mississippi State Medical Association, Royal College of Surgeons of Edinburgh, Royal College of Obstetricians and Gynaecologists
Disclosure: Nothing to disclose.
Thomas Michael Price, MD Associate Professor, Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Director of Reproductive Endocrinology and Infertility Fellowship Program, Duke University Medical Center
Thomas Michael Price, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Obstetricians and Gynecologists, Phi Beta Kappa, Society for Reproductive Investigation, Society for Reproductive Endocrinology and Infertility, American Society for Reproductive Medicine
Disclosure: Received research grant from: Insigtec Inc<br/>Received consulting fee from Clinical Advisors Group for consulting; Received consulting fee from MEDA Corp Consulting for consulting; Received consulting fee from Gerson Lehrman Group Advisor for consulting; Received honoraria from ABOG for board membership.
Research & References of Menorrhagia|A&C Accounting And Tax Services