Case Scenario - A 54-Year-Old African American Woman Reports Severe Hot Flashes (Printer-Friendly)

10/13/13
Case Scenario: A 54-Year-Old African American Woman Reports Severe Hot Flashes (printer-friendly)
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CME/CE Information
CME/CE Released: 06/13/2012; Valid for credit through 06/13/2013 This activity has expired. The accredited provider can no longer issue certificates for this activity. Medscape cannot attest to the timeliness of expired CME activities.
Target Audience
This activity is intended for primary care physicians, family practitioners, internal medicine specialists, physician assistants, nurse practitioners, nurses, menopause specialists, obstetricians/gynecologists, pharmacists, reproductive endocrinologists, and geriatricians.
Goal
The goal of this activity is to improve clinicians adoption of patient-focused dialogue in identifying and treating menopausal symptoms, including vasomotor symptoms (VMS) and vulvovaginal atrophy (VVA).
Learning Objectives
Upon completion of this activity, participants will be able to: 1. Initiate discussion about menopause-related symptoms with perimenopausal and postmenopausal women 2. Identify and rule out other potential causes of VMS or VVA menopausal symptoms that might necessitate treatment 3. Discuss the efficacy, safety, benefits, and risks of available options for the treatment of menopause-related symptoms 4. Develop culturally sensitive dialogue regarding racial, ethnic, and attitudinal differences with menopausal women about their symptoms 5. Engage in conversation about individualized treatment plans for patients experiencing menopause-related symptoms
Credits Available
Physicians - maximum of 0.75 AMA PRA Category 1 Credit(s) Nurses - 0.75 ANCC Contact Hour(s) (0.75 contact hours are in the area of pharmacology) All other healthcare professionals completing continuing education credit for this activity will be issued a certificate of participation. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Accreditation Statements
For Physicians
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The North American Menopause Society (NAMS) is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. The North American Menopause Society (NAMS) designates this enduring material for a maximum of .75 AMA PRA Category 1 Credit(s) . Physicians should claim only the credit commensurate with the extent of their participation in the activity.
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As an organization accredited by the ACCME, Medscape, LLC, requires everyone who is in a position to control the content of an education activity to disclose all relevant financial relationships with any commercial interest. The ACCME defines "relevant financial relationships" as financial relationships in any amount, occurring within the past 12 months, including financial relationships of a spouse or life partner, that could create a conflict of interest. Medscape, LLC, encourages Authors to identify investigational products or off-label uses of products regulated by the US Food and Drug Administration, at first mention and where appropriate in the content. The North American Menopause Society (NAMS) is committed to ensuring balance, independence, and objectivity in all of its educational activities. Faculty, planners, managers, and other individuals who are in a position to control the content of this activity are required to disclose any real or apparent conflict of interest they may have as related to the content of this activity. All identified conflicts of interest are thoroughly reviewed and resolved by NAMS. Complete disclosure statements are listed so that participants may evaluate the objectivity of the presentations.
CME Author(s)
Martha K. Richardson, MD, FACOG
Assistant Clinical Professor, Department of Obstetrics and Gynecology, Harvard Medical School; Director, Menopause Consultation Service, Harvard Vanguard Medical Associates, Boston, Massachusetts Disclosure: Martha K. Richardson, MD, NAMS, FACOG, has disclosed no relevant financial relationships.
Lubna L Pal, MBBS, MRCOG, MSc
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Associate Professor, Obstetrics, Gynecology, and Reproductive Sciences, Yale University School of Medicine; Director, Program for Reproductive Aging and Bone Health, Yale Reproductive Endocrinology, New Haven, Connecticut Disclosure: Lubna L. Pal, MBBS, MRCOG, MSc, has disclosed no relevant financial relationships.
Hugh S. Taylor, MD
Professor, Obstetrics, Gynecology, and Reproductive Sciences; Chief, Reproductive Endocrinology and Infertility; Director, Reproductive Endocrinology and Infertility; Yale School of Medicine, New Haven, Connecticut Disclosure: Hugh S. Taylor, MD, has disclosed no relevant financial relationships.
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Emilie McCardell
Scientific Director, Medscape, LLC Disclosure: Emilie McCardell has disclosed no relevant financial relationships.
Christin Melton
Clinical Editor, Medscape, LLC Disclosure: Christin Melton has disclosed no relevant financial relationships.
CE Reviewer
Dominique Brooks, MD
Disclosure: Dominique Brooks, MD, has disclosed no relevant financial relationships.
Nurse Planner
Laurie E. Scudder, DNP, NP
Nurse Planner, Continuing Professional Education Department, Medscape, LLC; Clinical Assistant Professor, School of Nursing and Allied Health, George Washington University, Washington, DC Disclosure: Laurie E. Scudder, DNP, NP, has disclosed no relevant financial relationships.
From Medscape Education Ob/Gyn & Women's Health
Case Scenario: A 54-Year-Old African American Woman Reports

10/13/13
Severe Hot Flashes

Lubna L. Pal, MBBS, MRCOG, MSc
Posted: 06/13/2012
Background
Ms X, a 54-year-old African American woman, says she has been having trouble sleeping and experiencing severe hot flashes. She is 5 ft 3 in tall, weighs 249 lb, and has a history of hypertension and high cholesterol. Her family history includes diabetes and cardiovascular disease (CVD) -- her mother had a venous thromboembolism at 52 years of age following a serious car accident. Her chart lists her last menstrual period as having occurred 5 years ago, and she states that she is "tired of having the hot flashes." In a discussion of Ms X's symptoms, she confirmed that the hot flashes were very uncomfortable but demurred when asked whether she was having any other symptoms. During a follow-up discussion, she was told that some women experience vaginal dryness at this time of life, and she was then asked directly, "Are you having any discomfort with intercourse?" Ms X admitted having "some" vaginal and urinary symptoms. Hot flashes, night sweats, and symptoms of urogenital atrophy (ie, vaginal dryness, dyspareunia, dysuria, and a predisposition to urinary tract infections) commonly accompany reproductive aging.[1,2] At first glance, this clinical picture is typical for menopausal syndrome. In the SWAN study, investigators are following a multiethnic cohort of reproductively aging women as they transition from premenopause into menopause. Keeping in perspective that the median age of natural menopause for the SWAN cohort is 51.4 years [3] and our patient's age and symptom spectrum, we can presume she is at the very least in late perimenopause and perhaps even in the early postmenopausal phase (Table 1).[2] Table 1. STRAW Stages of Menopause
FMP = final menstrual period; STRAW = Stages of Reproductive Aging Workshop; UAS = urogenital atrophy symptoms; VSM = vasomotor symptoms. Adapted from Harlow, et al.[2] Although the patient's urogenital symptoms seem tolerable, her vasomotor symptoms (VMS) are more severe and dominate the clinical picture. Prompt evaluation and action are warranted because the symptoms this relatively young woman has been experiencing appear to be adversely affecting her quality of life (QOL).
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In-Depth Evaluation
Lack of estrogen is appreciated as the principal pathophysiological mechanism underlying VMS and genital atrophy. Before we identify the optimal therapy for relieving our patient's symptoms, however, a more detailed evaluation is warranted to rule out processes other than estrogen deficiency that can mimic menopause-like symptoms. Clinical assessment should expand on the medical and family histories of Ms X to appreciate her unique risk profile more fully. This assessment will help quantify the net risk vs potential-for-benefit profiles of therapies that are available for symptom relief.[4] Uncontrolled thyroid dysfunction, disorders of the adrenal gland (eg, Cushing syndrome), pancreatic insufficiency (eg, poorly controlled diabetes), uncommon functional neoplasms (eg, pheochromocytoma, cortisol-secreting adrenal adenoma, carcinoid tumor) may all manifest a picture similar to menopause (Table 2).[5,6] Clinical assessment should also capture chronic infective disorders, such as HIV or hepatitis C infection, which may also manifest symptoms typically associated with menopausal syndrome.[7-9] Table 2. Testing for Conditions That May Manifest Menopausal Syndrome Symptoms Conditions Chronic diseases Cushing syndrome Thyroid disease Diabetes Mellitus Neoplasms Adrenal Carcinoid Hematologic Lung Pheochromocytoma Infections Hepatitis C HIV Tuberculosis Serology Serology PPD skin test, chest radiograph, blood quantiFERON test 24-h UFC Urinary 5HIAA CBC with differential ACTH Blood total and free metanephrines, 24-h urine VMA, 24-h urine total and free metanephrines 24-h UFC TSH Fasting blood sugar, hemoglobin A1C Screening Tests
5HIAA = 5-hydroxyindoleacetic acid; ACTH = adrenocorticotrophic hormone; CBC = complete blood count; HIV = human immunodeficiency virus; PPD = purified protein derivative; TSH = thyroid-stimulating hormone; UFC = urinefree cortisol; VMA = vanillylmandelic acid. Once we have ruled out the plausible secondary considerations, we determine that a lack of estrogen is the most likely cause of the symptoms that Ms X is experiencing. Although estrogen replacement may be the most effective of the available strategies for dealing with symptoms that emanate from estrogen deficiency, the patient's symptom burden must be weighed against her unique risk profile before deciding on a therapeutic approach. Our goal is to maximize symptom control while minimizing any potential for harm that might occur if the chosen treatment strategy were to compound the patient's innate risks (Table 3).
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Table 3. Building a Problem and Risk Profile for Ms X Obesity-Related Concerns

[10,11,12,13-16]
Hypertension and Cardiovascular Risks

[12,17,18]
Menopause-Related Concerns
[1,19]
CVD Endometrial, breast, or bowel cancer VMS Stroke Thromboembolism
CVD Lower bone mineral density Stroke
Increased bone resorption Poor QOL Urogenital atrophy and sequelae Discomfort UTI VMS
CVD = cardiovascular disease; QOL = quality-of-life; UTI = urinary tract infection; VMS = vasomotor symptoms. Our patient's body habitus, preexisting diseased vasculature, and race increase her risk for cerebrovascular accidents and cardiovascular events.[10-12] The SWAN investigators reported that African American women disproportionately experience more frequent and more severe menopausal VMS than women of other races.[3] They also found that overweight and obese women were more likely to report VMS compared with their leaner counterparts. Ms X's race and excess weight may therefore contribute to the severity of her VMS.[3,13-19,20-25] Factors such as a sedentary lifestyle and tobacco use, if applicable, could exacerbate our patient's symptoms and further escalate her risk for CVD and stroke.[13,22] An inquiry into the social history of a patient with menopausal symptoms should solicit information about modifiable health risks, including exposure to or use of tobacco, use of alcohol and recreational substances (cocaine and methadone use have been associated with bothersome VMS), and indulgence in any other toxic habits.[13,22-24] It is also important to inquire directly about issues that affect QOL, such as sleep, cognition, physical function, and sexuality, so as to quantify the overall burden of the patient's symptoms on her well-being.
Optimizing Symptom Control for Ms X

Until fairly recently, systemic oral estrogen replacement therapy was viewed as the optimal strategy for managing VMS in symptomatic women and is still considered the most effective of the available therapeutic options.[1] Prior to 2002, oral estrogen would have been considered a first-line treatment for managing bothersome VMS in patients like Ms X, particularly if the patient was deemed at risk for CVD.[25] In addition to controlling symptoms, systemic estrogen use during menopause was universally thought to confer cardioprotection; indeed, a large body of literature implied better vascular health and reduced CVD risk among menopausal women who used estrogen.[25,26] In the past decade, however, new data have redefined our perceptions and reshaped the place for hormonal therapy in menopausal medicine.[27,28] A succession of randomized controlled trials brought the potential health risks of hormonal therapy, along with its benefits, to the forefront.[28,29] As a consequence of this evolving appreciation, successful efforts were undertaken to expand the repertoire of effective nonhormonal strategies for treating common menopausal symptoms. Today's clinicians have several effective options to consider to help alleviate bothersome menopausal symptoms.[30-43]
Systemic Estrogen Replacement Therapy

Although systemic estrogen is highly effective at relieving menopausal symptoms, its benefits must be carefully balanced against its risks for each patient (Table 4).[1,28,44-46] Systemic estrogen use in menopausal women increases the risks of thromboembolism, stroke, and even CVD.[1,28,44] These vascular phenomena, although uncommon, may be particularly relevant for women who, like our patient, are obese and have preexisting diseased vasculature. A recent study by Gast and associates suggests a relationship between VMS and covert vascular dysfunction,[22] adding fuel to our concerns for Ms X's vascular health. Table 4. Benefits and Risks Associated With Menopausal Hormonal Therapy
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Benefits of HT Symptom control Reduces VMS Reduces urogenital symptoms: vaginal dryness, dyspareunia, dysuria, UTIs Improves mood Improves sexuality Other Reduces risk of vertebral and nonvertebral fractures Reduces risk of colon cancer Vascular
Risks of HT
Increases thromboembolism risk Increases stroke risk Increases risk of myocardial ischemia Cancer Increases risk of endometrial cancer (estrogen alone) Increases risk of breast cancer (especially estrogen combined with progesterone) May increase risk of lung cancer May increase risk of ovarian cancer Neurocognitive No protection against aging-related neurocognitive decline May increase risk of dementia Other Increases risk of gallstones Increased risk of incontinence
HT = hormonal therapy; UTIs = urinary tract infections; VMS = vasomotor symptoms. Data from The North American Menopause Society [1]; Rossouw JE, et al[28]; Hulley S, et al[29]; Renoux C and Suissa S[44]; Greiser CM, et al.[45,46] Although a family history of spontaneous thromboembolism could indicate an underlying genetic predisposition, a case of thromboembolism that was circumstantially provoked -- as appears to have been the case with our patient's mother -- is likely not relevant. Ms X should thus be reassured in this context. Risk quantification based on clinical assessment indicates that our patient has an enhanced risk for CVD and stroke, given her obesity, hypertension, and race. Although there is little doubt about the effectiveness of systemic estrogen therapy at relieving menopausal symptoms, this strategy's potential to cause harm to Ms X is deemed to outweigh the magnitude of benefit it might offer. In light of her innately increased risk for thromboembolism and stroke and the recognition that systemic estrogen use exacerbates these risks, menopausal hormone therapy should be considered a second- or third-line strategy for Ms X, offered only if nonhormonal therapies fail to provide significant relief of her symptoms.
Nonhormonal Therapies and Topical Estrogen

Various studies have demonstrated the efficacy of a spectrum of nonhormonal strategies against VMS (Table 5).[30] Although we can reassure the patient regarding the potential for benefit observed with multiple nonhormonal strategies, nonhormonal approaches are uniformly less effective than systemic estrogen therapy at relieving VMS. The magnitude of benefit for nonhormonal strategies may also vary between individuals. Details concerning the Ms X's overall well-being, psychological parameters, and quality and quantity of sleep will be particularly meaningful in selecting the most appropriate nonhormonal strategy. Table 5. Potentially Beneficial Nonhormonal Treatment Strategies Investigated for Managing Menopausal Symptoms
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Therapeutic Class Antidepressants SSRIs
Investigated Therapies
Citalopram, 10-30 mg/d[30,32,33] Escitalopram, 10-20 mg/d[42] Fluoxetine, 20 mg/d titrated up to 30 mg at 6 mo[30,33] Paroxetine (controlled release), 12.5-25 mg/d[30,33] SNRIs Duloxetine, 60-120 mg/d[43] Venlafaxine, 37.5-75 mg/d[30,33] Hypnotics Antiseizure Agents Antihypertensives Eszopiclone, 3 mg/d[31] Gabapentin, 100-300 mg starting dose, titrated up to 900 mg/d[30,33] Clonidine, 0.05 mg twice daily orally or 0.1 mg/d patch[30,33] Methyldopa (250 mg 3 times/d[30,33]) Stellate-ganglion blockade[41],a Acupuncture[34,39] Natural supplements (ie, herbals,[36] phytoestrogens,[36] vitamin E[37],a) Water-based lubricants and bioadhesive moisturizers Relaxation[34,38]/exercise[34,35]/yoga[38,40]
Nerve block Alternative (nonpharmaceutical) approaches
SNRIs = serotonin and norepinephrine reuptake inhibitors; SSRIs = selective serotonin reuptake inhibitors. aStudy population limited to breast cancer survivors . Selective serotonin reuptake inhibitors (SSRIs) may benefit symptomatic women with concomitant anxiety and depression. These drugs have an adverse effect on sexual ideation and performance, however, and may not be optimal for women experiencing sexual dysfunction.[47] Although selective norepinephrine reuptake inhibitors (SNRIs) are also effective at controlling menopausal symptoms, studies have associated their use with a slight increase in blood pressure, [48] a consideration that may be relevant for someone who is hypertensive like Ms X. For patients who complain of disturbed sleep, a trial of a hypnotic or an antiseizure agent may greatly improve symptom control and overall QOL.
[30,31,33]
Nonhormonal therapies do not affect vaginal tissue and hence will not improve our patient's vulvovaginal atrophy and urinary symptoms. The application of topical estrogen (ie, pessaries, tablets, creams, or rings) can reverse genital atrophy and directly improve QOL for many aging women with minimal systemic estrogen absorption.[1] Whereas systemic estrogen therapy poses risks, especially for patients who have a profile similar to that of our patient, we believe local estrogen therapy is a safe strategy for managing vulvovaginal atrophy. Given the association between excess weight and increased severity of VMS, exercise and weight reduction may help improve symptoms in obese or overweight patients like ours. Because the health burden Ms X's excess weight imposes extends well beyond her menopausal symptoms, weight reduction strategies are not only likely to mitigate the severity of her VMS, they might also reduce her lifetime morbidity and mortality risks.
Monitor Response, Revise as Needed

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If a trial of one or more nonhormonal strategies fails to provide this patient with substantial relief from bothersome VMS, systemic hormonal therapy remains an option. In recent years, studies have identified considerations that may help mitigate the risks associated with systemic hormonal therapy, such as route of administration, dose, and hormone formulation. [49-50] A reduction in the risk of thromboembolism that is associated with hormonal therapy may be achieved by administering estrogen via a transdermal route and by using lower doses of estrogen.[1] In the event that systemic estrogen therapy is deemed the most effective strategy for a patient like Ms X, one must keep in mind her innately enhanced risk for endometrial pathologies and the need to ensure adequate exposure of the endometrium to progesterone while she is receiving estrogen.[1] A trial of progesterone monotherapy, which adds only minimally to the risk of thromboembolism, may be another option for managing VMS in select patients.[51]
Summary
This vignette has provided us with an opportunity to assess menopausal symptoms systematically in a 54-year-old woman in early menopause and to undertake systematic risk assessment and quantification to arrive at a management algorithm that adheres to the principle of "Do no harm." The goal of this exercise is to guide clinicians in identifying the optimal strategies for menopause management so they can choose therapies that address a patient's symptoms yet pose minimal additive burden. The onus remains on clinicians to explore the breadth of symptoms beyond the presenting complaint so as to determine which treatment option is likely to offer the most benefit. In this obese and hypertensive individual, who has an enhanced risk of CVD and stroke, a nonhormonal strategy represents the safest first-line approach for managing her severe hot flashes. Concomitant use of topical estrogen is encouraged to help mitigate symptoms that are attributable to urogenital atrophy. Identifying ancillary symptoms (ie, issues of sleep and of sexuality [52]) and their severity will guide clinicians caring for the aging woman in determining the optimal first-line strategy for managing VMS in their patients. Clinicians must familiarize themselves with strategies to mitigate estrogen-related risks, such as using a non-oral route of administration or lowering the dose. Beyond the therapeutic interventions, lifestyle modification must be encouraged as a critical component of menopause management. In the event that nonhormonal strategies fail to improve the burden of menopausal symptoms in this relatively young woman, judicious use of systemic hormone therapy remains an option to help improve her QOL. 5HIAA = 5-hydroxyindoleacetic acid ACTH = adrenocorticotrophic hormone CBC = complete blood count CVD = cardiovascular disease FMP = final menstrual period HIV = human immunodeficiency virus HT = hormonal therapy PPD = purified protein derivative QOL = quality of life SNRI = serotonin norepinephrine reuptake inhibitor SSRI = selective serotonin reuptake inhibitor STRAW = Stages of Reproductive Aging Workshop SWAN = Study of Women's Health Across the Nation TSH = thyroid-stimulating hormone UAS = urogenital atrophy symptoms UFC = urine-free cortisol UTI = urinary tract infection VMA = vanillylmandelic acid VSM = vasomotor symptoms
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Sponsored by The North American Menopause Society (NAMS) and Medscape, LLC. Disclaimer The material presented here does not necessarily reflect the views of Medscape, LLC, or companies that support educational programming on medscape.org. These materials may discuss therapeutic products that have not been approved by the US Food and Drug Administration and off-label uses of approved products. A qualified healthcare professional should be consulted before using any therapeutic product discussed. Readers should verify all information and data before treating patients or employing any therapies described in this educational activity. Medscape Education 2012 The North American Menopause Society and Medscape, LLC Contents of Scenarios in Women's Health: Recognizing and Managing Menopausal Symptoms [/viewprogram/32506] 1. Case Scenario: A 58-Year-Old Asian American Woman With Hot Flashes, Dyspareunia, and Cystitis [/viewarticle/765071] 2. Case Scenario: A 54-Year-Old African American Woman Reports Severe Hot Flashes [/viewarticle/765072] 3. Case Scenario: A 48-Year-Old Breast Cancer Survivor With Moderate to Severe Menopausal Symptoms [/viewarticle/765074]
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Case Scenario - A 54-Year-Old African American Woman Reports Severe Hot Flashes (Printer-Friendly)

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Case Scenario - A 54-Year-Old African American Woman Reports Severe Hot Flashes (Printer-Friendly)

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10/13/13

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Disclosure: Dominique Brooks, MD, has disclosed no relevant financial relationships.

From Medscape Education Ob/Gyn & Women's Health

Case Scenario: A 54-Year-Old African American Woman Reports

Severe Hot Flashes

Table 3. Building a Problem and Risk Profile for Ms X Obesity-Related Concerns

Hypertension and Cardiovascular Risks

CVD Endometrial, breast, or bowel cancer VMS Stroke Thromboembolism

CVD Lower bone mineral density Stroke

Optimizing Symptom Control for Ms X

Systemic Estrogen Replacement Therapy

Nonhormonal Therapies and Topical Estrogen

Therapeutic Class Antidepressants SSRIs

Nerve block Alternative (nonpharmaceutical) approaches

Monitor Response, Revise as Needed

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