Directions in

Directions in

Psychiatry V O L U M E

CATEGORY 1

CME

3 4

•

I N

T H I S

2 0 1 4

•

N U M B E R

3

I S S U E

An Update on New Medications for the Treatment of Major Depressive Disorder . . . . . . .159 ASIM A. SHAH, MD; AND SANJAY J. MATHEW, MD

According to the World Health Organization, unipolar depression was the third most important cause of disease worldwide in 2004. The faculty of this lesson review available treatment options, describe unmet needs, recommend augmentation strategies, and discuss some of the newer treatment options.

Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .171 DEEPIKA GOYAL, PhD, FNP; BINDU GARAPATY, PsyD; AND NANCY W. GREEN, DNP, FNP, CNM, CNL

Untreated postpartum depression (PPD) poses a threat to the maternal-child bond and the well-being of the entire family. Examine specific cultural factors and mental health help-seeking behaviors among these culturally diverse populations in an effort to improve PPD identification and treatment.

Sexual Addiction or Hypersexual Disorder: Clinical Implications for Assessment and Treatment . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .185 AVIV WEINSTEIN, PhD

Sexual addiction, which is also known as hypersexual disorder, is associated with severe psychosocial problems and risk-taking behaviors. Although sexual addiction is not included in the Diagnostic and Statistical Manual of Mental Disorders, several screening questionnaires have been developed for the diagnosis of sexual addiction or hypersexual disorder.

Confidentiality Protections Versus Collaborative Care in the Treatment of Substance Use Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .201 JENNIFER K. MANUEL, PhD; HOWARD NEWVILLE, PhD; SANDRA E. LARIOS, PhD, MPH; AND JAMES L. SORENSEN, PhD

The addition of electronic health records provides opportunity for more rapid and comprehensive communication between patients’ primary and SUD care providers while promoting a collaborative care environment. Consider how to protect your patients’ information in this era of collaborative care while maintaining rapid communication among healthcare providers.

Ebola: Clinical Progression and Clinical Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .215 AMERICAN HOSPITAL ASSOCIATION

This lesson provides readers with the clinical progression of the Ebola Virus Disease (EVD) as well as guidelines for management in the hospital setting. Readers will review the symptoms that present in the early, late, and recovery phases of the disease as well as symptom management, and guidelines for protection of healthcare providers and others who come into contact with individuals who have acquired the virus.

A HATHERLEIGH CME JOURNAL

w w w . D i r e c t i o n s I n P s y c h i a t r y . c o m

Directions in Psychiatry Senior Content Advisor Leah J. Dickstein, MD, MS Professor Emerita, University of Louisville, Psychiatriy & Behavioral Sciences, Louisville, KY; and Lecturer, Tufts University, Medical Center, Psychiatry Dept., Boston, MA

Program Advisory Board Barbaranne Branca, PhD Michigan Head Pain & Neurological Institute, Ann Arbor, MI Robert L. DuPont, MD Georgetown University, Washington, DC Richard Elliott, MD Mercer University School of Medicine, Macon, GA Joseph T. English, MD St. Vincent’s Medical, Center of New York, NY, NY Deborah I. Frank, PhD, ARNP, MFT Florida State University, College of Nursing, Tallahassee, FL Shervert Frazier, MD Psychiatrist-in-Chief, Emeritus, McLean Hospital, Belmont, MA

Wendy Packman, JD Pacific Graduate School of Psychology, San Francisco, CA

Mark S. Gold, MD University of Florida, Gainesville, FL Alison Heru, MD University of Colorado, Denver, CO

George Papakostas, MD Massachusetts General Hospital, Boston, MA

Robert M.A. Hirschfeld, MD University of Texas, Galveston, TX

Gail Erlick Robinson, MD, DPsych, FRCPC Toronto General Hospital, Toronto, Ontario

Jimmie C. Holland, MD Memorial Sloan-Kettering, Cancer Center, NY, NY

Michael A. Schwartz, MD University Hospitals of Cleveland, Cleveland, OH

Hideo Hosaki, MD Keio University, School of Medicine, Tokyo, Japan

Peter C. Whybrow, MD UCLA Department of Psychiatry and Behavioral, Sciences, Los Angeles, CA

Philip Janicak, MD Rush University, Chicago, IL.

Robert L. Williams, MD Baylor College of Medicine, Houston, TX

Carl P. Malmquist, MD University of Minnesota, Minneapolis, MN Malkah T. Notman, MD, The Cambridge Hospital, Cambridge, MA

Managing Editor Stacy M. Powell, MS

Founding Editor Frederic Flach, MD, KCHS, DFLAPA

Accreditation Statement The Hatherleigh Company, Ltd., designates this activity for a maximum of 40 AMA PRA Category 1 Credits. Physicians should only claim credit commensurate with the extent of their participation in the activity.

w w w. D i r e c t i o n s i n p s y c h i a t r y. c o m 62545 State Highway 10, Hobart, NY 13788

The Hatherleigh Company, Ltd., is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) by The Hatherleigh Company, Ltd.

Directions in Psychiatry Volume 34 • Lessons 11–15

CME Lesson 11

An Update on New Medications for the Treatment Major Depressive Disorder Page

159

Asim A Shah, MD; and Sanjay J. Mathew, MD

CME Lesson 12

Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups

Page

171

Page

185

Page

201

Page

215

Deepika Goyal, PhD, FNP; Bindu Garapaty, PsyD; and Nancy W. Green, DNP, FNP, CNM, CNI

CME Lesson 13

Sexual Addiction or Hypersexual Disorder: Clinical Implications for Assessment and Treatment Aviv Weinstein, PhD

CME Lesson 14

Confidentiality Protections Versus Collaborative Care in the Treatment of Substance Use Disorders Jennifer K. Manuel, PhD; Howard Newville, PhD; Sandra E. Larios, PhD, MPH; and James L. Sorenson, PhD

CME Lesson 15

Ebola: Clinical Progression & Clinical Evidence American Hospital Association

Conflict of Interest Faculty/Board Disclosures The authors of the lessons in this CME program are paid an honorarium to produce original manuscripts on the invited topics. The authors were selected for their expertise and, most often, on the strength of presentations made on those topics in previously published papers or symposia. Relationships are disclosed below, if they exist, between the Directions in Psychiatry faculty and their immediate family members, and commercial and/or pharmaceutical companies below. Disclosure of off-label medication usage for indications that are not approved by the FDA will be disclosed on the title page of each lesson. No commercial support was used in the development of the enclosed CME lessons.

Faculty Disclosures: Medication usage mentioned in the lessons for indications that are not approved by the FDA are listed on the title page of each lesson if they exist. Bindu Garapaty, PsyD: Deepika Goyal, PhD, FNP: Nancy W. Green, DNP, FNP, CNM, CNI: Sandra E. Larios, PhD, MPH: Jennifer K. Manuel, PhD: Sanjay J. Mathew, MD: Howard Newville, PhD: Asim A. Shah, MD: James L. Sorenson, PhD: Aviv Weinstein, PhD:

Dr. Garapaty has no conflicting interests to disclose. Dr. Goyal has no conflicting interests to disclose. Ms. Green has no conflicting interests to disclose. Dr. Larios has no conflicting interests to disclose. Dr. Manuel has no conflicting interests to disclose. Dr. Mathew has no conflicting interests to disclose. Dr. Newville has no conflicting interests to disclose. Dr. Shah has no conflicting interests to disclose. Dr. Sorenson has no conflicting interests to disclose. Dr. Weinstein has no conflicting interests to disclose.

Program Advisory Board Member Disclosures: Leah Dickstein, MD: Richard L. Elliott, MD, PhD: Deborah I. Frank, PhD, ARNP: Mark S. Gold, MD, PhD: Alison Heru, MD: Philip Janicak, MD:

George I. Papakostas, MD:

Dr. Dickstein has no conflicting interests to disclose. Dr. Elliott has no conflicting interests to disclose. Dr. Frank has no conflicting interests to disclose. Dr. Gold has no conflicting interests to disclose. Dr. Heru has no conflicting interests to disclose. Dr. Janicak has received grant/research support from: Janssen, Neuronetics, Inc., Otsuka Pharmaceutical Group; The Research Foundation for Mental Hygiene, Inc.; and has disclosed stock or other financial relationships with Lippencott, Williams & Wilkins. Dr. Papakostas has no conflicting interests to disclose.

Hatherleigh Editorial Staff: Andrew Flach, CEO: Mr. Flach has no conflicting interests to disclose. Stacy M. Powell, Managing Editor: Ms. Powell has no conflicting interests to disclose. Rick Gallub, Customer Relations Manager: Mr. Gallub has no conflicting interests to disclose.

Accreditation Standards: IOM; ACGME / ABMS Competencies Directions in Psychiatry, Vol. 34 In accordance with accreditation guidelines set forth by the ACCME, we encourage you to review the following areas of core competency and desirable physician attributes endorsed by the Institute of Medicine (IOM); The Accreditation Council for Graduate Medical Education (ACGME) / American Board of Medical Specialties (ABMS). Each CME lesson in this activity addresses at least one or more of the following attributes in each of the three areas of competency as listed below. Institute of Medicine Core Competencies: Provide Patient-Centered Care: Identify, respect, and care about patients’ differences, values, preferences, and expressed needs; relieve pain and suffering; coordinate continuous care; listen to, clearly inform, communicate with, and educate patients; share decision-making and management; and continuously advocate disease prevention, wellness, and promotion of healthy lifestyles, including a focus on population health. Work in Interdisciplinary Teams: Cooperate, collaborate, communicate, and integrate care in teams to ensure that care is continuous and reliable. Employ Evidence-Based Practice: Integrate best research with clinical expertise and patient values for optimum care, and participate in learning and research activities to the extent feasible. Apply Quality Improvement: Identify errors and hazards in care; understand and implement basic safety design principles, such as standardization and simplification; continually understand and measure quality of care in terms of structure, process, and outcomes in relation to patient and community needs; and design and test interventions to change processes and systems of care, with the objective of improving quality. Utilize Informatics: Communicate, manage, knowledge, mitigate error, and support decisionmaking using Information technology.

ACGME Competencies: Patient Care that is compassionate, appropriate, and effective for the treatment of health problems and the promotion of health. Medical Knowledge about established and evolving biomedical, clinical, and cognate (e.g. epidemiological and social-behavioral) sciences and the application of this knowledge to patient care.

Practice-Based Learning and Improvement that involves investigation and evaluation of their own patient care, appraisal and assimilation of scientific evidence, and improvements in patient care. Interpersonal and Communication Skills that result in effective information exchange and teaming with patients, their families, and other health professionals. Professionalism, as manifested through a commitment to carrying out professional responsibilities, adherence to ethical principles, and sensitivity to a diverse patient population. Systems-Based Practice, as manifested by actions that demonstrate an awareness of and responsiveness to the larger context and system of health care and the ability to effectively call on system resources to provide care that is of optimal value.

ABMS Competencies: Part I-Professional Standing: Medical specialists must hold a valid, unrestricted medical license in at least one state or jurisdiction in the USA, its territories or Canada. Part II-Lifelong Learning and Self-Assessment: Physicians participate in educational and self-assessment programs that meet specialty-specific standards that are set by their member board. Part III-Cognitive Expertise: They demonstrate, through formalized examination, that they have the fundamental, practice-related and practice environment-related knowledge to provide quality care in their specialty. Part IV-Practice Performance Assessment: They are evaluated in their clinical practice according to specialty-specific standards for patient care. They are asked to demonstrate that they can assess the quality of care they provide compared to peers and national benchmarks and then apply the best evidence or consensus recommendations to improve that care using follow-up assessments.

Directions in Psychiatry, Vol. 34 * Part 3 IOM Core Competencies

Lesson 11

Lesson 12

Lesson 13

Lesson 14

Lesson 15

X X

X X X X

X

Provide patient-centered care Work in interdisciplinary teams Employ evidence-base practice Apply quality improvement

X X

X

X X

Utilize informatics

ACGME Competencies Patient care Medical knowledge Practice-based learning and improvement

X X

X X

X X X

Interpersonal and communication skills

X X

Professionalism System-based practice

ABMS MOC Competencies

X

X X

X

X

Professional standing Commitment to lifelong learning

X X

X

X X X

Cognitive expertise Performance in practice

X

CME Information Page The objective of this continuing medical education program is to present participants with an expanded clinical skill set and raised awareness of clinically relevant issues in their profession. They will review key diagnostic criteria, cutting-edge treatment strategies, and practice points they can implement in the challenges of daily practice while providing evidence-based care to patients and clients suffering psychiatric and comorbid medical disorders. The expected outcomes include an increase in knowledge, competence, professionalism, and performance.

Target Audience: The primary target audience for this program includes, but is not limited to: psychiatrists, primary care physicians, psychiatric nurses, pharmacists, clinical psychologists, and social workers. Clinicians who have caseloads composed significantly of individuals with psychiatric disorders, and comorbid medical illnesses will find this course particularly useful. Duration of CME Status: Directions in Psychiatry begins May 1, 2014, and the preliminary expiration date is December 31, 2017. At that point, the Hatherleigh Medical Director and the editorial staff will review the CME material to determine whether the program continues to be consistent with current accreditation guidelines and standards Overall Objective: of care. A determination will be made as to whether the program can be used to earn full CME credit after that date.

Conflict of Interest Disclosure Policy Faculty members were selected for their expertise and, most often, on the strength of their presentations from previously published papers or symposia. Hatherleigh Medicial Education staff, contributing program faculty, and advisory board members, must disclose their relationships (also on behalf of their immediate family members), if they exist, with commercial and/or pharmaceutical companies prior to Hatherleigh Medical Education’s distribution and publication of their contributions to Hatherleigh Medical Education CME programs. Any aforementioned relationship that poses a potential conflict of interest will be resolved prior to publication/distribution of the CME activity, and proper notification disclosed to program participants prior to the start of the activity. Disclosure of any off-label medication usage for indications that are not currently approved by the Federal Drug Administration discussed within the CME content will be disclosed within the lesson.

Accreditation Statement * Hatherleigh’s CME Designation The Hatherleigh Company, Ltd. designates this CME journal for a maximum of 40 AMA PRA Category 1 Credits. Physicians should only claim credit commensurate with the extent of their participation in the activity. The Hatherleigh Company, Ltd. is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. This activity has been planned and implemented in accordance with the Essential Areas and Policies of the Accreditation Council for Continuing Medical Education (ACCME) by The Hatherleigh Company, Ltd.

How the Program Works * Needs Assessment * Evaluation Directions in Psychiatry includes 78 CME questions focused on key learning points within the lessons. The answers to each question must be recorded on the supplied quiz response form or via the response form at Hatherleigh’s website. All 78 questions should be answered on that form or online and submitted to Hatherleigh via the website, fax, e-mail, or regular mail for scoring. On average, participants will take up to 40 hours or more to complete this Hatherleigh CME program (i.e., reading and studying the lessons and answering the CME questions). Participants must complete and return the program assessment form which is included with each program. Participants can submit these forms with the quiz response form. Upon successful completion of the program (at least 75% correct), Hatherleigh will send participants a certificate of achievement worth 40 credit hours and a score report. This CME program was created from a learning needs assessment of participants in previous CME programs, who are virtually all physicians and other mental health clinicians. Their expressed needs were assessed by the Medical Director, the Program Advisory Board members, and editorial staff in the development of this curriculum.

About The Hatherleigh Company, Ltd. * Contact Information The Hatherleigh Company, Ltd. has published continuing medical education programs in psychiatry for more than 30 years. Dr. Frederic Flach, the company’s founder, created Directions in Psychiatry, Hatherleigh’s flagship CME program to ensure the presence of a truly independent and highly professional perspective on issues of immediate clinical import—ranging from pharmacotherapy to psychotherapy, from technical information to ethical priorities. We look forward to hearing from all subscribers via e-mail at: [email protected]. For more information about Hatherleigh CME programs, visit our website at www.hatherleigh.com, or call: 1-800-367-2550.

Directions in Psychiatry is published by The Hatherleigh Company, Ltd., 62545 State Highway 10, Hobart, NY 13788. POSTMASTER: Please send address changes to: Directions in Psychiatry, The Hatherleigh Company, Ltd., 62545 State Highway 10, Hobart, NY 13788. Copyright 2014, THE HATHERLEIGH COMPANY, LTD. All rights reserved. No part of this publication may be reproduced in any form or by any means, except as permitted under sections 107 or 108 of the United States Copyright Act, without the prior written permission of the publisher. The material in this journal is not a substitute for seeking the attention of a licensed health or medical clinician. These materials were created for professional education purposes. They may not to be duplicated or distributed or otherwise repurposed in digital or physical form in whole or in part without the express consent of the publisher. For educational use and reprints, please contact 1-800-367-2550. Statements made in its publications by contributing authors do not reflect the opinion of the company or its employees. The Hatherleigh Company, Ltd. does not endorse any product, therapeutic method, and/or treatment mentioned herein. The names of medications are typically followed by TM or ® symbols, but these symbols are not stated in this publication.

Self-assessment Pre-test

for Maintenance of Certification as Required by The American Board of Psychiatry and Neurology (ABPN) This assessment is necessary only for participants using this activity to earn credit hours to satisfy their Maintenance of Certification as required by The American Board of Psychiatry and Neurology (ABPN). Please answer and review each self-assessment question before starting your CME program. This self-assessment will not be scored by Hatherleigh.

Directions in Psychiatry, Vol. 34 * Part 3 13. Which of the following medications is approved by the FDA for adjunctive treatment of depression? A. B. C. D.

Quetiapine Aripiprazole Risperidone Both A & B

14. Are selective serotonin reuptake inhibitors (SSRIs) interchangeable? A. Yes B. No 15. Which of the following is a barrier that hinders women from diverse ethnic populations from seeking mental health services, particularly for postpartum depression? A. Strong familial support B. Acceptance and openness with health providers C. Stigma of being perceived as weak D. None of the above 16. Is sexual addiction or hypersexual disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM-5)? A. Yes B. No

Self‐Assessment Answer Key

18. What is the primary mode of transmission of the Ebola virus? A. Direct contact with blood B. Direct contact with bodily fluids such as tears, sweat, semen, urine, vomit, feces, and other C. Direct contact with contaminated objects D. All of the above 19. Early-stage symptoms in the progression of Ebola include all of the following, except: A. weakness. B. shock. C. fever greater than 101.5o F. D. hiccups. This is the end of your self-assessment test for Part 3. This self-test is for your reference only. Please do not submit these answers to Hatherleigh.

13.D, 14.B, 15.C, 16.B, 17.D, 18.D, 19.B

17. If a clinician approaches an ethically uncomfortable and challenging situation, it is best to seek guidance from: A. peers. B. counselors. C. professional associations. D. All of the above

L003333

An Update on New Medications for the Treatment of Major Depressive Disorder Asim A. Shah, MD; and Sanjay J. Mathew, MD The following medications mentioned in this lesson are not approved by the FDA for the treatment of depression, which include: alprazolam, aripiprazole, buspirone, ketamine, lithium, L-methyfolate, lurasidone, milnacipran, modafinil, olanzapine, pindolol, psychostimulants, and quetiapine. Aripiprazole and quetiapine are approved as adjuncts to antidepressants; and lurasidone is approved for bipolar depression. No commercial support was used in the development of this CME lesson.

KEY WORDS: Major Depression • Augmentation • Response • Placebo • Pharmacology LEARNING OBJECTIVES: This lesson will enable clinicians to: (1) understand that depression is the most common psychiatric disease; (2) review first-line antidepressants for treating depressive episodes in major depressive disorder; (3) discuss augmentation strategies for treating depression, and (5) utilize new treatment options for treating depression.

LESSON ABSTRACT: According to the World Health Organization, unipolar depression was the third most important cause of disease worldwide in 2004. Unipolar depression was in “eighth place in low-income countries, but at first place in middle- and high-income countries.”1 Despite it being such a common disorder, treatment options are not able to cure the disease completely, and there are numerous unmet needs in the treatment of depression. In this continuing medical education lesson, we will review the treatment options available to treat depression, describe unmet needs, recommend augmentation strategies, and discuss new treatment options.

COMPETENCY AREAS: This lesson addresses the gap in knowledge of evidence-based practices for the treatment of depression, including imminent and expert-based treatment options.

159

L003333 : An Update on New Medications for the Treatment of Major Depressive Disorder

Depression According to the World Health Organization (WHO), major depressive disorder (MDD) was the third most important cause of disease burden worldwide in 2004. Unipolar depression was in “eighth place in low-income countries, but at first place in middle- and high-income countries.”1 In a nationally representative face-to-face household survey, 6.7% of adults in the United States (US) experienced a major depressive episode in the past 12 months.2 Significantly greater percentages of lifetime major depression have been reported among women (11.7%) than men (5.6%).3 Examining ethnic differences reveals lifetime percentages of MDD of 6.5% among Caucasians, 4.6% among African Americans, and 5.2% among Hispanics.4 According to the WHO, more than 350 million people of all ages suffer from MDD globally, and about 20 million of those live in the US. Despite its prevalence and disease burden, treatment options are not curative, and there remain numerous unmet needs with respect to therapies, despite an abundance of antidepressant drug classes with varied receptor profiles. While its use has diminished in recent years in the US5 electroconvulsive therapy (ECT) is still considered a more potent and rapid option for treating acute depressive episodes in medication-refractory patients. The word placebo is derived from the Latin word placere, which literally means “to please.”6,7 As MDD is characterized by fluctuations in its course, spontaneous improvements, and features “distress” as a key symptom, it is not surprising that it is also a placebo-responsive condition.8 The mean response rates for placebo in antidepressant clinical trials ranges between 30% and 40%, 9,10 with a notable upward trend in placebo response over the past several decades. Accordingly, across Phase III registration trials performed for FDA approval, the overall effect size for the acute efficacy of antidepressant medications compared to placebo is relatively modest.6,10 While few would argue that antidepressants are beneficial in treating moderate to severe depression, arguments have been made for treating mild depression with antidepressants.11 In an article published in the Journal of the American Medical Association (JAMA)12 by Fournier et al., the magnitude of benefit of antidepressant medication compared with placebo increases with the severity of depression symptoms and may be minimal or nonexistent in patients with mild or moderate symptoms. 160

For patients with very severe depression, the benefit of medications over placebo was found to be substantial.

What Should Be Used as a First-line Treatment of Depression? Antidepressant medication has been shown to be superior to placebo in thousands of controlled clinical trials over the past five decades.13,14 The percentage of persons treated with antidepressant drugs in the US increased from 5.8% to 10.1% between 1996 and 2005; 11%– 13% of adults in the US now take these medications.15 The rate of antidepressant use increased for anxiety and adjustment disorders in addition to depressive disorders.15 Increasing use of these medications corresponded with decreasing rates of counseling and psychotherapy. Of note, antidepressants are about twice as likely to be prescribed by primary care providers (PCP) than psychiatrists. Most clinicians will agree that selective serotonin reuptake inhibitors (SSRIs) are the firstline treatment for depression today. While this may be true for PCPs, most psychiatrists will also use selective norepinephrine reuptake inhibitors (SNRIs) or bupropion (Wellbutrin, Zyban, Aplenzin) as first-line agents. In some cases, even atypical antidepressants such as mirtazapine (Remeron, Remeron soltab) are used as first-line treatments by mental health providers. When choosing an antidepressant, certain things are important to consider, such as personal and family treatment history, ease of use, tolerability and safety profile, and cost. The SSRIs have effectively replaced the tricyclic antidepressants over the past two decades because of better tolerability, convenience, and safety. All the SSRIs are now available as generics, with the exception of vilazodone (Viibryd). It is important to consider that SSRIs are not interchangeable and there are tolerability, safety, and possible efficacy differences within this class. With the recent change in FDA labeling of citalopram (Celexa; QTc warning for doses over 40 mg), there has been a new concern about its usage, especially by PCPs. Usage of paroxetine (Paxil) has dropped in females of reproductive age due to its warning about heart defects in pregnancy and the change in its FDA pregnancy risk category to D. It is not easy to track prescription data trends, but IMS Health is a leading source of prescribing information of interest to clinicians, insurance payers, and


policy-makers. This company draws information from 100,000 suppliers and includes insights from more than 45+ billion healthcare transactions processed annually. According to IMS Health National Prescription Audits, in 2009, over 469 million mental health-related prescriptions were written in the US, which increased to 519 million in 2013. Of these prescriptions, alprazolam (Niravam, Xanax) was the top psychiatric drug prescribed in the US with 45.3 million scripts written in 2009 and 49.6 million scripts written in 2013. Most of these scripts were written by non-psychiatrists. Sertraline (Zoloft), which became a generic medication in the US in June 2006, topped all antidepressant prescriptions with 34.8 million scripts written in 2009 and 41.7 million scripts written in 2013. Citalopram was the second most prescribed, with 27.3 million scripts written in 2009 and 39.5 million written in 2013 (even though we would anticipate reductions in its use following the 2012 FDA advisory). While the complete 2013 list was not available to the author, the top prescriptions for antidepressant medications in 2009 were the SSRIs escitalopram (Lexapro) and fluoxetine (Prozac), the SNRIs venlafaxine (Effexor) and duloxetine (Cymbalta), and the atypical antidepressants trazodone (Oleptro) and bupropion. As suggested by this data, psychiatrists are increasingly prescribing SNRIs as first-line treatments, perhaps due to the common perception that antidepressants that modulate norepinephrine and serotonin directly will be more effective than SSRIs by having greater effects on recovery time, remission rate, and somatic symptoms.

New Antidepressants Since 2011 Three new antidepressant medications have come to the U.S. market since 2011: vilazodone (Viibryd, 2011), levomilnacipran (Fetzima, 2013), and vortioxetine (Brintellix, 2013). Vilazodone has a unique mode of action as it selectively inhibits serotonin reuptake and partially agonizes serotonin 5-HT1A receptors. It binds with high affinity to the human serotonin (5-HT) and norepinephrine (NE) transporters (Ki = 11 and 91 nM, respectively) and potently inhibits 5-HT and NE reuptake (IC50 = 16–19 and 11 nM, respectively). Vilazodone lacks significant affinity for any other receptors, ion channels, or transporters tested in vitro, including serotonergic (5HT1-7), α- and β- adrenergic, muscarinic, or histaminergic receptors, and Ca2+, Na+, K+, or Cl- channels.

Vilazodone does not inhibit monoamine oxidase (MAO). A 3-step dose titration over several weeks is recommended to enhance tolerability and minimize gastrointestinal side effects (10 mg for one week, 20 mg for one week, and then 40 mg). Although the manufacturers of vilazodone report that the drug has a low incidence of sexual side effects, T Laughren et al. in Journal of Clinical Psychiatry16 reported in 2011 that there is no difference in its safety profile, including the sexual side effects from SSRIs. Levomilnacipran is the levo enantiomer of racemic milnacipran (Savella), and is another addition to the SNRI class, which includes venlafaxine and venlafaxine XR, duloxetine, and desvenlafaxine (Pristiq). It should be noted that milnacipran is approved as an antidepressant in Europe, but in the US, has only received regulatory approval for the treatment of fibromyalgia. Vortioxetine has multiple mechanisms related to 5HT: it selectively inhibits serotonin reuptake, antagonizes serotonin 5-HT3 receptors, and agonizes serotonin 5-HT1A receptors. Vortioxetine was developed as one of a series of compounds developed from halogenated benzenes and was intended to have combined effects on multiple 5-HT receptors and on the serotonin transporter. It has been shown in recombinant cell lines to combine 5-HT3 and 5-HT7 receptor antagonism, 5-HT1B receptor partial agonism, 5-HT1A receptor agonism, and serotonin transporter inhibition. It has an elimination half-life of over 66 hours, and data supports its efficacy in individuals with late-life depression, according to its studies on people up to 88 years of age. The short-term antidepressant efficacy of vortioxetine in patients aged 18 to 75 years was demonstrated in five 6 to 8-week, placebo-controlled studies, whereas one study showed efficacy between the ages of 64–88. Bupropion hydrochloride came back on the market as an extended release Forfivo XL 450 mg tablet in 2012; however, this formulation does not provide any therapeutic benefit over existing formulations. Bupropion hydrobromide (an alternative salt to the conventional hydrochloride) was introduced and is available as Aplenzin tablets in 174 mg, 348 mg, and 522 mg doses. Generic Budeprion was withdrawn in 2012 by FDA after a head to head study found that this drug is not equivalent to the brand name product. Venlafaxine modified release or extended release 225 mg has also been available in a single-tablet formulation for the last 161


several years. Finally, trazodone, was reformulated as a once a day extended release antidepressant in 150 mg and 300 mg doses, but prescription data doesn’t show many prescriptions of this agent, perhaps due to its cost of about $175 for a month’s supply and the availability of generic trazodone. Table 1: Antidepressant Medications Within This Lesson Generic

Trade Name

Alprazolam

Niravam, Xanax

Aripiprazole

Abilify

Bupropion

Wellbutrin, Zyban, Aplenzin

Citalopram

Celexa

Desvenlafaxine

Pristiq

Duloxetine

Cymbalta

Escitalopram

Lexapro

Fluoxetine

Prozac

Ketamine

—

Levomilnacipran

Fetzima

L-methylfolate

Deplin

Lurasidone

Latuda

Milnacipran

Savella

Mirtazapine

Remeron, Remeron soltab

Olanzapine

Zyprexa

Paroxetine

Paxil

S-adenosyl-methionine

SAMe

Sertraline

Zoloft

Trazodone

Oleptro

Venlafaxine

Effexor

Vilazodone

Viibryd

Vortioxetine

Brintellix

162

Augmentation Strategies for Treating Depression Treatment-resistant depression (TRD) refers to depression with inadequate clinical response after taking a therapeutic dose of antidepressant therapy for an adequate duration (generally 6–8 weeks). Traditionally, the concept of treatment resistance has focused on non-response (i.e., patients who do not experience at least a 50% reduction of symptoms). However, inadequate response is increasingly viewed as a lack of symptom remission.17,18 It is increasingly common to use adjunctive medications while treating depression, especially when adequate results are not achieved by monotherapy. Numerous drug combinations have been used as augmentation strategies for difficult-to-treat depression. SSRIs have been combined with bupropion, tricyclics, and mirtazapine. In the past when SNRI’s were not available, clinicians used to combine desipramine (Norpramin) with fluoxetine to make their own SNRI. They would use fluoxetine in the daytime and low-dose desipramine at night. The other common combinations for augmentation are with venlafaxine. It has been commonly combined with mirtazapine and also with bupropion. Some have used all three, i.e., venlafaxine, bupropion, and mirtazapine together and achieved good results. It should be noted that the Food and Drug Administration (FDA) has not approved any traditional antidepressant medication for augmentation, and only mirtazapine has two positive studies on its augmentation effects. Atypical antipsychotics are also used extensively for augmentation purposes. Aripiprazole (Abilify) and quetiapine XR are FDA-approved as adjunctive treatments for patients who have inadequately responded to antidepressant monotherapy. Olanzapine (Zyprexa), in combination with fluoxetine, is FDA-approved for TRD as well as bipolar depression; in addition, quetiapine and quetiapine XR and lurasidone (Latuda) are also FDA-approved to treat bipolar depression as monotherapy. The efficacy of lithium as an augmenting agent for depression dates back to the 1980s when lithium was typically tested at divided doses of 600 mg/ day. Improvement of depression resistant to tricyclic


antidepressants (TCAs) has usually followed. Lithium has been tested for antidepressant augmentation in 11 double-blind placebo-controlled trials.19-39 A meta-analysis performed by Bauer and Dopfmer40 revealed that the lithium-augmentation group displayed a 45% response rate compared with 18% in the placebo group. Lithium augmentation has not been particularly effective when added to SSRIs or SNRIs.36,40,42 Augmentation with thyroid hormone,43 buspirone,44 pindolol,45 psychostimulants,46-52 and modafinil53 has been common clinical practice. Recently, with the marketing of the folate supplement, usage of folate has increased, especially methyltetrahydrofolate and S-adenosylmethionine (SAMe), which might have antidepressant effects.54-55 An open-label trial of methyfolate (up to 30 mg/day) in SSRI-refractory patients suggested its usefulness as an adjunct.56 A randomized trial of 127 patients that compared 0.5 mg/day of folic acid and fluoxetine to fluoxetine and a placebo found that depressive symptoms improved significantly better in the folate group in women but not in men.57 Recent open-label studies report potentiation effects of SAMe as an augmenting agent in SSRI-refractory patients with MDD.58-59 L-methylfolate (Deplin) is approved by the FDA as a medicinal food for patients with an inadequate response to antidepressants and low RBC folate.

conclusion. Ketamine has demonstrated efficacy and safety as a rapidly-acting antidepressant when administered intravenously. However, the antidepressant effect is time-limited, typically lasting between a week and a month. The critical next step in future research will be to determine the best strategy for maintenance of efficacy. This will require experimentation with varying multiple infusion schedules and different methods of administering ketamine in an attempt to prolong the antidepressant effects and minimize dissociative or potential addictive side effects. Multiple options to prolong the antidepressant effects of ketamine have been proposed. Although ketamine does have significant abuse potential, the small doses used to treat bipolar and unipolar depression have not demonstrated negative effects in study participants so far. This promising treatment, when used carefully and at low doses, has great potential as a rapidly-acting antidepressant. However, essential information on safety and efficacy in long-term use, which is necessary to justify these alternatives as viable clinical treatments, are currently insufficient for ketamine and completely lacking for the other glutamatergic compounds. Further research can help to elucidate whether these treatment options are effective.60

The Role of Ketamine

Depression can be a very devastating and crippling disease, and in most cases complete remission is not possible. While numerous medicinal options are available, monotherapy may not always be sufficient, and combinations are used in these cases. In the last decade, no new breakthrough treatments have made it to the market, and the bulk of the treatment options depend on SSRI and SNRI-related drugs. Further research is needed on drugs that target glutamate, especially ketamine.

Antidepressant treatments that target the glutamate system hold high promise as novel, efficacious, and rapidly-acting treatments for MDD. Ketamine, a glutamate N-methyl-D-aspartate (NMDA) receptor antagonist, has shown rapid antidepressant effects, but small study groups and inadequate control conditions in prior studies have precluded a definitive

Conclusion

About the Faculty Asim A. Shah, MD: Dr. Shah is Associate Professor, Menninger Department of Psychiatry, Baylor College of Medicine, Houston, TX; and Chief of Psychiatry for Ben Taub Hospital and Harris Health System. Sanjay J. Mathew, MD: Dr. Mathew is Associate Professor, Menninger Department of Psychiatry, Baylor College of Medicine, Houston, TX.

163


References 1.

World Health Organization. The Global Burden of Disease: 2004 Update. Geneva, Switzerland: WHO Press, 2008.

2. Kessler RC, Chiu WT, Demler O, Merikangas KR, Walters EE. Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the National Comorbidity Survey Replication. Arch Gen Psychiatry. 2005;62:617–627. 3. Ford DE, Erlinger TP. Depression and C-reactive protein in US adults: Data from the third National Health and Nutrition Survey. Arch Intern Med. 2004;164:1010–1014. 4.

Oquendo MA, Lizardi D, Greenwald S, Weissman MM, Mann JJ. Rates of lifetime suicide attempt and rates of lifetime major depression in different ethnic groups in the United States. Acta Psychiat Scand. 2004;110:446–451.

5.

Case BG, Bertollo DN, Laska EM, Price LH, Siegel CE, Olfson M, Marcus SC. Declining use of electroconvulsive therapy in United States general hospitals. Biol Psychiatry. 2013;15;73(2):119-26. doi: 10.1016/j.biopsych.2012.09.005. Epub 2012 Oct 8.

6.

Dago PL., Quitkin FM. Role of the placebo in depressive disorders. CNS Drugs. 1995;4:335–340.

7.

Shapiro AK. A historic and heuristic definition of the placebo. Psychiatry. 1964;27:52–58

8. Khan A., Brown WA. The placebo enigma in antidepressant clinical trials. J Clin Psychopharmacol. 2001;21:123–125. 9.

Brown WA. Placebo as a treatment for depression. Neuropsychopharmacology. 1994;10:265–269

10. Trivedi MH, Rush H. Does a placebo run-in or a placebo treatment cell affect the efficacy of antidepressant medications? Neuropsychopharmacology. 1994;11:33–43 11. Kirsch I, Deacon BF, Huedo-Medina TB, Scoboria A, Moore TJ, Johnson BT. Initial severity and antidepressant benefits: a meta-analysis of data submitted to the Food and Drug Administration. PLoS Med. 2008;5:e45 12. Fournier JC, DeRubeis RJ, Hollon SD, Dimidjian S, Amsterdam JD, Shelton RC, Fawcett J. “Antidepressant Drug Effects and Depression Severity: A Patient-Level Meta-analysis” JAMA. 2010;303(1):47-53. doi:10.1001/jama.2009.1943 13. Mulrow CD, Williams JW Jr, Trivedi M, et al. Treatment of Depression: Newer Pharmacotherapies [AHCPR publication No. 99-E014]. 14. Depression in Primary Care: Vol 2, Treatment of Major Depression [Clinical Practice Guideline No. 5; AHCPR Publication No. 93-0551]. Depression Guideline Panel. Rockville, MD: US Dept of Health and Human Services; 1993 15. Olfson M, Marcus SC. National patterns in antidepressant medication treatments.” Arch Gen Psychiatry. 2009;66(8):848-856. 16. Laughren TP, Gobburu J, Temple RJ, Unger EF, Bhattaram A, Dinh PV, et al. Vilazodone: clinical basis for the US food and drug administration’s approval of a new antidepressant. J Clin Psychiatry. 2011;72(9):1166-1173-10.4088/JCP.11r06984. 17. Keller MB. Remission versus response: the new gold standard of antidepressant care. J Clin Psychiatry. 2004;65(Suppl. 4):53–59. 18. Thase ME. Evaluating antidepressant therapies: remission as the optimal outcome. J Clin Psychiatry. 2003;64(Suppl. 13): 18–25. 19. Fava M. Diagnosis and definition of treatment-resistant depression. Biological Psychiatry. 2003;53:649–659. 20. Thase ME, Greenhouse JB, Frank E et al. Treatment of major depression with psychotherapy or psychotherapy–pharmacotherapy combinations. Arch Gen Psychiatry. 1997;54:1009–1015. 21. Elhwuegi AS. Central monoamines and their role in major depression. Progress in Neuropsychopharmacology and Biological Psychiatry. 2004;28:435–451 22. Hansen RA, Gartlehner G, Lohr KN, Gaynes BN, Carey TS. Efficacy and safety of second-generation antidepressants in the treatment of major depressive disorder. Annals of Internal Medicine. 2005;143:415–426. 23. Bauer M, Whybrow PC, Angst J, Versiani M, Moller HJ. World federation of societies of biological psychiatry (WFSBP) guidelines for biological treatment of unipolar depressive disorders, Part 1: acute and continuation treatment of major depressive disorder. World Journal of Biological Psychiatry. 2002;3:5–43. 24. Mischoulon D, Nierenberg AA, Kizilbash L, Rosenbaum JF, Fava M. Strategies for managing depression refractory to selective serotonin reuptake inhibitor treatment: a survey of clinicians. Canadian Journal of Psychiatry. 2000;45:476–481. 25. Fredman SJ, Fava M, Kienke AS, White CN, Nierenberg AA, Rosenbaum JF. Partial response, nonresponse, and relapse with selective serotonin reuptake inhibitors in major depression: a survey of current “next-step” practices. J Clin Psychiatry. 2000;61:403–408. 26. Nelson JC. Treatment of antidepressant nonresponders: augmentation or switch? J Clin Psychiatry. 1998;59(Suppl. 15):35–41. 27. Ros S, Agüera L, De La Gándara J, Rojo JE, De Pedro JM. Potentiation strategies for treatment-resistant depression. Acta Psychiatrica Scandinavica. 2005;112(Suppl. 428):14–24. 28. Fava M, Rush AJ. Current status of augmentation and combination treatments for major depressive disorder: a literature review and a proposal for a novel approach to improve practice. Psychotherapy and Psychosomatics. 2006;75:139–153. 29. Heninger GR, Charney DS, Sternberg DE. Lithium carbonate augmentation of antidepressant treatment. An effective prescription for treatment-refractory depression. Arch Gen Psychiatry. 1983;40:1335–1342. 30. Kantor D, McNevin S, Leichner P, Harper D, Krenn M. The benefit of lithium carbonate adjunct in refractory depression – fact or fiction? Canadian Journal of Psychiatry. 1986;31:416–418. 31. Zusky PM, Biederman J, Rosenbaum JF, Manschreck TC, Gross CC, Weilberg JB, Gastfriend DR. Adjunct low dose lithium carbonate in treatment-resistant depression: a placebo-controlled study. Journal of Clinical Psychopharmacology. 1988;8:120–124. 32. Schopf J, Baumann P, Lemarchand T, Rey M. Treatment of endogenous depressions resistant to tricyclic antidepressants or related drugs by lithium addition. Results of a placebo-controlled double-blind study. Pharmacopsychiatry. 1989;22;183–187. 33. Browne M, Lapierre YD, Hrdina PD, Horn E. Lithium as an adjunct in the treatment of major depression. International Clinical Psychopharmacology. 1990;5:103–110.

165


34. Joffe RT, Singer W, Levitt AJ, MacDonald C. A placebo-controlled comparison of lithium and triiodothyronine augmentation of tricyclic antidepressants in unipolar refractory depression. Archives of General Psychiatry. 1993;50:387–393 35. Stein G, Bernadt M. Lithium augmentation therapy in tricyclic-resistant depression. A controlled trial using lithium in low and normal doses. British Journal of Psychiatry. 1993;162;634–640. 36. Katona CL, Bou-Saleh MT, Harrison DA et al. Placebo-controlled trial of lithium augmentation of fluoxetine and lofepramine. British Journal of Psychiatry. 1995;166:80–86. 37. Baumann P, Nil R, Souche A et al. A double-blind, placebo-controlled study of citalopram with and without lithium in the treatment of therapy-resistant depressive patients: a clinical, pharmacokinetic, and pharmacogenetic investigation. J Clin Psychopharmacol. 1996;16:307–314. 38. Januel D, Poirier MF, D’alche-Biree F, Dib M, Olie JP. Multicenter double-blind randomized parallel-group clinical trial of efficacy of the combination clomipramine (150 mg/day) plus lithium carbonate (750 mg/day) versus clomipramine (150 mg/day) plus placebo in the treatment of unipolar major depression. Journal of Affective Disorders. 2003;76:191–200. 39. Bauer M, Bschor T, Kunz D, Berghofer A, Strohle A, Muller-Oerlinghausen B. Double-blind, placebo-controlled trial of the use of lithium to augment antidepressant medication in continuation treatment of unipolar major depression. American Journal of Psychiatry. 2000;157:1429–1435. 40. Bauer M, Dopfmer S. Lithium augmentation in treatment-resistant depression: meta-analysis of placebo-controlled studies. J Clin Psychopharmacol. 1999;19:427–434. 41. Fava M, Rosenbaum JF, McGrath PJ, Stewart JW, Amsterdam JD, Quitkin FM. Lithium and tricyclic augmentation of fluoxetine treatment for resistant major depression: a double-blind, controlled study. American Journal of Psychiatry. 1994;151:1372–1374. 42. Fava M, Alpert J, Nierenberg A et al. Double-blind study of high-dose fluoxetine versus lithium or desipramine augmentation of fluoxetine in partial responders and nonresponders to fluoxetine. J Clin Psychopharmacol. 2002;22:379–387. 43. Aronson R, Offman HJ, Joffe RT, Naylor CD. Triiodothyronine augmentation in the treatment of refractory depression. A meta-analysis. Arch Gen Psychiatry. 1996;53:842–848. 44. Blier P, Ward NM. Is there a role for 5-HT1A agonists in the treatment of depression? Biological Psychiatry. 2003;53:193–203. 45. Ballesteros J, Callado LF. Effectiveness of pindolol plus serotonin uptake inhibitors in depression: a meta-analysis of early and late outcomes from randomised controlled trials. J Affect Disord. 2004;79:137–147. 46. Fawcett J, Kravitz HM, Zajecka JM, Schaff MR. CNS stimulant potentiation of monoamine oxidase inhibitors in treatment-refractory depression. J Clin Psychopharmacol. 1991;11:127–132. 47. Feighner JP, Herbstein J, Damlouji N. Combined MAOI, TCA, and direct stimulant therapy of treatment-resistant depression. Journal of Clinical Psychiatry. 1985;46:206–209. 48. Linet LS. Treatment of a refractory depression with a combination of fluoxetine and d-amphetamine. Am J Psychiatry. 1989;146:803–804. 49. Masand PS, Anand VS, Tanquary JF. Psychostimulant augmentation of second generation antidepressants: a case series. Depress Anxiety. 1998;7:89–91. 50. Metz A, Shader RI. Combination of fluoxetine with pemoline in the treatment of major depressive disorder. Int Clin Psychopharmacol. 1991;6:93–96. 51. Stoll AL, Pillay SS, Diamond L, Workum SB, Cole JO. Methylphenidate augmentation of serotonin selective reuptake inhibitors: a case series. Journal of Clinical Psychiatry. 1996;57:72–76. 52. Wharton RN, Perel JM, Dayton PG, Malitz S. A potential clinical use for methylphenidate with tricyclic antidepressants. Am J Psychiatry. 1971;127:1619–1625. 53. Menza MA, Kaufman KR, Castellanos A. Modafinil augmentation of antidepressant treatment in depression. Journal of Clinical Psychiatry. 2000;61:378–381. 54. Abalan F. Primer in folic acid: folates and neuropsychiatry. Nutrition. 1999;15:595–598. 55. Alpert JE, Mischoulon D, Nierenberg AA, Fava M. Nutrition and depression: focus on folate. Nutrition. 2000;16:544–546. 56. Alpert JE, Mischoulon D, Rubenstein GE, Bottonari K, Nierenberg AA, Fava M. Folinic acid (Leucovorin) as an adjunctive treatment for SSRI-refractory depression. Ann Clin Psychiatry. 2002;14:33–38. 57. Coppen A, Bailey J. Enhancement of the antidepressant action of fluoxetine by folic acid: a randomised, placebo controlled trial. J Affect Disord. 2000;60:121–130. 58. Rosenbaum JF, Fava M, Falk WE, Pollack MH, Cohen LS, Cohen BM, Zubenko GS. The antidepressant potential of oral S-adenosyl-l-methionine. Acta Psychiatrica Scandinavica. 1990;81:432–436. 59 Alpert JE, Papakostas G, Mischoulon D et al. S-adenosyl-L-methionine (SAMe) as an adjunct for resistant major depressive disorder: an open trial following partial or nonresponse to selective serotonin reuptake inhibitors or venlafaxine. J Clin Psychopharmacol. 2004;24:661–664. 60. Murrough JW, Iosifescu DV, Chang LC, Al Jurdi RK, Green CE, Perez AM, et al. “Antidepressant efficacy of ketamine in treatment-resistant major depression: a two-site randomized controlled trial.” Am J Psychiatry. 2013;1;170(10):1134-42. doi:10.1176/appi.ajp. 2013.13030392.

166


L003333

Multiple-Choice Questions 41. According to the World Health Organization (WHO), major depressive disorder (MDD) was the most important cause of disease burden worldwide in 2004. A. First B. Third C. Fourth D. Tenth

42. The mean response rates for placebo in antidepressant clinical trials range between: A. 30% to 40% B. 10% to 20% C. 50% D. 0% to 5%

43. The most common antidepressant medications used are: A. Selective norepinephrine reuptake inhibitors B. Selective serotonin reuptake inhibitors C. Tricyclic antidepressants D. Monoamine oxidase inhibitors

44. Ketamine is a: A. GABA antagonist B. NMDA receptor antagonist C. Selective norepinephrine reuptake inhibitors D. Opioid antagonist

167

Best Practices in CME An Update on New Medications for the Treatment of Major Depressive Disorder By Asim A. Shah, MD; and Sanjay J. Mathew, MD ID#: L003333

This valuable take-home reference translates evidence-based, continuing medical education research and theory, acquired from reading the associated CME lesson, into a stepwise approach that reviews key learning points for easy assimilation into your armamentarium of knowledge and daily practice.

CME Lesson Overview The information in this lesson will be helpful to general practitioners, psychiatrists, and family physicians who require information on treating patients with depression by using antidepressant as monotherapy and using some adjunctive agents. According to the World Health Organization, major depressive disorder (MDD) was the third most important cause of disease burden worldwide in 2004. Unipolar depression was in “eighth place in low-income countries, but at first place in middle- and high-income countries.”

Key Point 1: Prevalence of the Disease Depression affects more than 20 million people in United States. Primary care physicians (PCPs) are potential gatekeepers and thus, should understand the disease and start early treatment. This lesson will help them to comfortably start treatment with antidepressants.

Key Point 2: Meeting Unmet Needs In spite of depression being such a common disorder, treatment options are not able to cure the disease completely, and there are numerous unmet patient needs. Available options include medications, psychotherapy, ECT,TMS, etc.

Key Point 3: What Should be Used as the First-line Treatment of Depression? Antidepressant medication has been shown to be superior to placebo in thousands of controlled clinical trials over the past five decades.The most common first-line treatment of depression includes SSRIs such as: sertraline, fluoxetine, paroxetine, citalopram, and escitalopram.

Key Point 4: New Options Available This lesson discusses the direction of depression treatment whether it is ketamine or glutamate receptors and the newer treatment options that are being investigated.

The information presented herein is based upon the content in the associated CME lesson. If you have comments or feedback about this page, please send your feedback via email to: [email protected] and reference the ID number under the title to which you are referring. We will review your commentary, which may be used for publication. The material in this journal is not a substitute for seeking the attention of a licensed health or medical clinician. These materials were created for professional education purposes only and are not the express opinion of The Hatherleigh Company, Ltd.

Notes

L003334

Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups Deepika Goyal, PhD, FNP; Bindu Garapaty, PsyD; and Nancy W. Green, DNP, FNP, CNM, CNL No commercial support was used in the development of this CME lesson.

KEY WORDS: Postpartum Depression • Asian American • African American • Hispanic • Latina LEARNING OBJECTIVES: This lesson will review postpartum depression among diverse populations, including African American, Asian American, and Hispanic/Latina women. Cultural factors, mental health help-seeking behavior, identification, and treatment will be explored. Upon completion of this lesson, clinicians will be better informed to (1) describe cultural factors related to postpartum depression health and help seeking among diverse populations, (2) identify available screening tools for postpartum depression assessment among diverse populations, and (3) describe current referral and treatment guidelines for postpartum depression.

LESSON ABSTRACT: Untreated postpartum depression (PPD) poses a threat to the maternal-child bond and the well-being of the entire family. With timely identification, women from diverse racial and ethnic backgrounds are easily treated, including those of African American, Asian American, and Hispanic/Latina descent, who are less likely to self-report depressive symptoms, thus delaying treatment. This lesson examines specific cultural factors and mental health help-seeking behaviors among these culturally diverse populations in an effort to improve PPD identification and treatment. Evidence-based PPD screening questionnaires and treatment options will also be discussed. COMPETENCY AREAS: This lesson helps clinicians to provide better patient-centered care to women by helping them identify, respect, and care about patients’ differences, values, preferences, and expressed needs; relieve pain and suffering; coordinate continuous care; listen to, clearly inform, communicate with, and educate patients; share decision making and management; and continuously advocate disease prevention, wellness, and promotion of healthy lifestyles, including a focus on population health.

171

L003334 : Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups

Introduction Societal expectations often dictate that the birth of a new baby should be a time of great joy and excitement for new parents. However, the experiences of some parents may not conform to such societal expectations. Parents are often blindsided by the development of postpartum mood disorders, including postpartum baby or maternity blues, postpartum depression (PPD), and postpartum psychosis. Each of these affective mood disorders has a unique presentation, a specific constellation of symptoms, and suggested treatment methodologies. Of the three postpartum affective mood disorders, maternity blues is the most common, affecting up to 84% of new mothers.1,2 Self-limiting in nature, the symptoms including tearfulness, anxiety, and irritability, present within the first 4–7 days postpartum and often resolve without treatment.1 Symptoms that persist longer than 2 weeks or increase in severity are red flags and reasons for prompt referral and further evaluation. The rarest of the postpartum mood disorders, postpartum psychosis, affects 1/1000 women.3 Symptoms include mood fluctuation, delusions, auditory hallucinations, and insomnia, which present rapidly after the infant’s birth.4 Postpartum psychosis requires immediate inpatient psychiatric evaluation and treatment because this disorder may lead to suicide and infanticide.5 Defined as a depressive episode occurring between 2 weeks and 12 months after childbirth, PPD affects 1 in 7 new mothers.6 The multiple risks to the mother, infant, and whole family have been well documented. When PPD is left untreated, the more serious risks include disruption of the mother-infant bond,7 child maltreatment,8 and infanticide.5 Although all postpartum mood disorders require diligent clinical assessment and intervention, the focus of this lesson is on identifying and treating PPD. According to 2013 United States (U.S.) Census data,9 63% of the U.S. population self-identifies as white, 17% as Hispanic or Latino, 13% as African American, and 5.3% as Asian American. Given these statistics, it is not surprising that the majority of PPD research in the United States to date has focused on PPD among Caucasian women, with a lesser focus on minority women, such as African American, Asian American, 172

and Hispanic/Latino women. In order for clinicians to provide culturally sensitive care for all women, it is imperative to understand the nuances related to mental health help-seeking behavior, as well as the identification and treatment of PPD in diverse racial and ethnic groups. The following sections will discuss childbearing among African American, Asian American, and Hispanic/Latino populations regarding the following: (1) cultural factors influencing mental health help-seeking behavior, (2) PPD screening tools for use in culturally diverse populations, (3) DSM-V guidelines and when to refer patients, and (4) PPD treatment among culturally diverse populations.

Cultural Factors and Mental Health Help-Seeking Discussing and recognizing the importance of specific cultural nuances and practices is imperative for understanding effective treatment interventions. Terms such as “normal” are often defined by certain cultural assumptions. However, these cultural assumptions mirror the values of the mainstream culture.10 An ethnocentric treatment model can serve as a barrier to understanding the experiences of people in different ethnic demographics. Cultural understanding is the first step toward providing effective interventions in various ethnic groups. Historical knowledge of ethnic groups’ struggles, challenges, and cultural definitions are significant factors in working successfully with ethnic minority persons.10 The next step involves an increased level of awareness of the clinician’s stereotypes and biases toward motherhood and mental health. For example, there is distrust in the African American community of healthcare providers in general because of limited cultural exposure to mental health services. Therefore, when working with the African American population, it is important to enlist the support of the maternal figurehead, which may include the help of faith leaders, as well as informal support networks and community organizations, in treatment interventions.11 The Model Minority, a term created by Petersen (1966),12 was used to describe the success of ethnic minorities despite their marginalization, which led to the myth that potentially ALL minorities could be successful. This myth has served as a barrier and has contributed to the lack of the provider’s cultural understanding of the


Table 1: Shifting the Multicultural Lens African American

Asian

Hispanic

Black

Korean, Japanese, Chinese, Indian, Vietnamese, Filipino

Chicana/Latina

Psychosocial structure

collective family structure

collective family structure, value of time

collective family structure

Family hierarchy and values

women at the “center” of the household

patriarchal, education is important, plays a role, respect for elders is key

Cultural and familial history is important, mother plays a large role in family, religion, enjoy present activities, respect for elderly, parents, and males

Ideologies of health and healing

cultural mistrust of healthcare providers’ racism and microaggressions

alternative practices, yoga, meditation, karmic philosophies

indigenous healing practices, feelings before facts

Emotional support

emotional support may be provided by community organizations

keep feelings private, work hard, stay focused

folk healing practices, spiritual healers

Adapted from: Ponterotto et al, Handbook of Multicultural Counseling

cultural traditions, practices, and behaviors that define healthy behavior, which could affect the quality of care. Moreover, the levels of acculturation and assimilation can affect the degree of stigma associated with help-seeking behaviors. Because of the diversity represented, clinicians can benefit from having a general understanding of the culture and creating a relationship with the patient that ensures a safe environment for asking questions and sharing information.

Postpartum Depression among Diverse Race and Ethnic Groups Among diverse racial and ethnic groups, cultural factors, societal beliefs, and stigma contribute to maternal mental health help-seeking behavior. An additional barrier, social shame, may affect those who self-identify as needing help because of the perception that depression is caused by personal weakness and is a “family problem” rather than an illness.13,14 Although minority women are not well represented in the literature as Caucasians are, the findings of existing research on minority women and PPD are alarming. Similar across all three racial and ethnic groups, the findings indicate that minority women are at a greater risk for developing PPD, compared with Caucasian women, with rates up to

60%.15,16,17 Common barriers to mental health treatment and care across all three groups include stigma,13,18-20 access to mental health care,21 and several barriers related to socioeconomic status, finances, transportation, and childcare issues.21,22 African American women may shy away from actively seeking mental health care because the disclosure of mental health symptoms may be perceived as a sign of weakness.23 Additionally, African American women are socialized to handle stressful events, as illustrated in the cultural theme of “dealing with it” and staying strong.24 African American women are more likely to delay seeking professional help, and they first try to manage depressive symptoms on their own, relying on their faith and upholding the image of “being strong.”24 They are also more likely to rely on their support network (family, friends) and spiritual guidance from clergy.11 The U.S. Asian population, including persons of Chinese, Filipino, Indian, Japanese, Korean, and Vietnamese descent, is expected to increase to 34 million by 2050.25 As community members, Asian Americans are less self-oriented and more family-oriented compared with the Western perspective of individual autonomy.26 Goyal, Wang, Shen, Wong, and Palaniappan (2012) found that Asian American women were significantly 173


less likely to be diagnosed with PPD, compared with Caucasian women.27 The term “Hispanic” includes individuals whose ancestry originates in Mexico, Puerto Rico, Cuba, El Salvador, the Dominican Republic, and other Latin American countries. Similar to African American women, Hispanic women also seek advice from their family, friends, and informal sources before seeking professional medical care.19,28,29 Moreover, when Hispanic women do seek care for PPD, they are less likely to refill their prescriptions or receive follow-up treatment for PPD, compared with non-Hispanic women.30

Postpartum Depression: Screening and Referral The effect of untreated PPD on the growth, development, and physical health of infants and children has been well documented.31,32 Screening new mothers for depressive symptoms has been shown to be cost-effective in providing timely referral, diagnosis, and treatment, all of which minimize the long-term effects of delayed/ undetected PPD.33 Given the detrimental effects of

untreated PPD on the infant, the American Academy of Pediatrics (AAP) recommends universal screening using the Edinburgh Postnatal Depression Scale (EPDS) at the infant’s 1-, 2-, and 4-month visits.34 The EPDS is the most often used and cited PPD screening questionnaire, worldwide. More recently, the Patient Health Questionnaire-9 (PHQ-9)35 has been strongly suggested as another option for PPD screening since it is the most widely used depression questionnaire by mental health and primary health-care providers. The use of a depression questionnaire, familiar to all disciplines, will likely decrease barriers to screening. The EPDS and the PHQ-9 assess the severity of depressive symptoms, are self-report Likert questionnaires, and are free for use in the public domain. They are available and validated for use in several languages, written at the thirdgrade reading level (below the recommended sixth-grade reading level), and are easily completed in 5-10 minutes (see Table 2). The 10-item EPDS has been validated for use in pregnant and postpartum women.36 Scores can range between 0 and 27; scores ≥10 indicate a high risk of developing depression, warranting prompt referral for

Table 2: Commonly Used Postpartum Depression Questionnaires Characteristics

EPDS

PHQ-9

General purpose

designed specifically for pregnant and postpartum women

designed for use in all adults in primary care settings

Number of items

10 items

9 items

Symptom timeframe

previous week

previous 2 weeks

Validated for pregnant and postpartum populations

yes, both

yes, both

Range of scores

0-30

0-27

Translated in languages other than English

27

27

Cut off scores

>10

>9

Screens for suicidal thought

yes

yes

Screens for anxiety

yes

yes

EPDS = Edinburgh Postnatal Depression Scale; PHQ-9 = Patient Health Questionnaire-9

174


further evaluation and treatment.37 The 9-item PHQ-9 has also been validated for use in pregnant and postpartum populations.38 The EPDS and PHQ-9 are validated for depression screening and are not diagnostic. Therefore, immediate referral to a mental health professional is strongly advised for the diagnosis and treatment of any patient scoring at or above the established cut-off points and those with suicidal or homicidal ideation. The Institute of Medicine39 and Mental Health America (MHA)40 both suggest that depression screening is the most effective in a setting where immediate professional mental health follow-up is available (e.g., psychologists, psychiatrists, and counseling resources). This may include models for care delivery, such as colocated mental health services within primary care settings or telemental health services for rural areas. Although the EPDS and the PHQ-9 are recommended as first-line screening for PPD, they may not always be feasible. For example, in ethnic populations or populations with low health literacy, clinician-administered screening or using a visual scale may be preferred.41 Alternatively, the 2-item Patient Health Questionnaire-2 (PHQ-2)42,43,44 or the 2-item EPDS,44 similar to the PHQ-2, may also be used. These questionnaires screen for general depressive symptoms. They can be administered verbally, and a positive screen is determined by a “yes” answer to either of the following questions: 1. Over the past 2 weeks, have you ever felt down, depressed, or hopeless? Hopelessness could be an indication of suicidal ideation, and the patient should be referred to a psychiatrist. 2. Over the past 2 weeks, have you felt little interest or pleasure in doing things? Anhedonia or loss of pleasure in usual activities is also an indication of depression, and the patient should be referred to a psychiatrist.

These 2-item questionnaires have the advantage of brevity; however, they may have lower validity in detecting depression in diverse populations. This disadvantage can be mitigated by using a 2-step process in which screening is first performed with a 2-item questionnaire followed by the full EPDS or the PHQ-9, based on the patient’s answers.42

Postpartum Depression Referral and Treatment Contrary to the research findings, the American Psychiatric Association’s (APA)45 Diagnostic and Statistical Manual of Mental Disorders (DSM) maintains that the diagnosis of PPD is the same as that of major depressive disorder (MMD), “with postpartum onset defined as the onset within four weeks of childbirth” (DSM-IV). The new fifth edition (DSM-5) notes a significant change from the earlier version45; the DSM-5 now defines “with peripartum onset” as the most recent episode of depression occurring during pregnancy, as well as within the 4 weeks following delivery. Whether the onset of MMD occurs during or after the pregnancy is not as critical as the timely referral for further evaluation and treatment, which is imperative in mitigating the adverse effects of untreated PPD on the entire family. Currently, the Structured Clinical Interview (SCID) is considered the “gold standard” for MMD diagnosis.46 However, the SCID may not always be feasible, and screening questionnaires such as the EPDS and PHQ-9 provide a relatively quick “snapshot” of the severity of a patient’s depressive symptoms. Referral for further evaluation and treatment should be made (a) when patients score at or above the designated cut-off point for each questionnaire, (b) when suicidal or infanticidal thoughts are present or verbalized, and (c) whenever the clinician feels further evaluation is warranted. Stigma renders mental health treatment among diverse populations very challenging for clinicians because although the rate of antidepressant use in the United States has increased by 400% over the past 20 years,47 Asian Americans, African Americans, and Hispanic/Latinos are less likely to use or be prescribed antidepressant drugs, compared with whites.47,48 Similar findings relate to seeking treatment for mental health in the form of therapy. The diverse populations discussed in this lesson are less likely to seek or continue therapy for mental illness, compared with Caucasians. Primary care physicians (PCPs) are often the first point of contact for individuals’ medical needs and may very well be first to encounter presenting psychiatric symptoms. The disparity in healthcare among certain ethnic groups contributes to fewer individuals seeing a PCP or being diagnosed with PPD. Prescribing clinicians

175


should consider the possible need to adjust medication dosages as the metabolic rate and other biological factors may differ between ethnic minority groups compared with Caucasians.49 Since antidepressant and therapy-based interventions are common first-line treatment modalities for PPD, where feasible, clinicians should consider alternative methods, such as yoga,50,51,52 which has been associated with improved maternal mental health outcomes. Strategies for promoting adequate sleep53,54 and a robust social support network55 should also be discussed with patients since the lack of both is also associated with PPD.

2. The NP must also assess for suicidal or infanticidal ideation.

Case Study 1

4. Since poor sleep is a known risk factor for developing PPD, the NP should inquire about Nina’s intake of caffeine or alcohol as well as use of any over the counter medications or Ayurvedic herbal treatments. The NP should also include screening for sleep disturbance, such as the General Sleep Disturbance Scale.56

Nina is a 28-year-old Southeast Asian female who presents to the clinic 6 weeks after the uncomplicated vaginal birth of her first baby, a healthy infant girl. Nina and her husband migrated to the United States from India 4 years ago after they married. Nina works as a medical assistant in a doctor’s office; she is on maternity leave and due back in 2 weeks. She is breastfeeding and is at the obstetric nurse practitioner’s office for her 6-week postpartum checkup. When asked how she is feeling, Nina states that she is having a significant number of anxious thoughts about going back to work and that she is having a lot of difficulty sleeping, even when the baby is sleeping. Further questioning by the nurse practitioner reveals that Nina is feeling overwhelmed and isolated because her friends, who she states are her main support system, are back in India. Nina states she has few friends here and feels worried all the time, especially about leaving her new infant in daycare when she goes back to work. The postpartum physical exam is without complications. What other assessment(s) should the nurse practitioner (NP) perform at this time? Answers 1. The NP should assess the presence of depressive symptoms using a validated questionnaire, such as the EPDS or PHQ-9*.

176

3. Although Nina verbalizes no current thoughts of harm to herself or others, her EPDS score is 12/30 (cut-off score ≥10), indicating that she has a high risk of developing PPD. The NP will refer Nina to a psychiatrist/psychologist for further evaluation and treatment. The NP will also obtain routine lab tests to rule out anemia and hypothyroidism, which may also contribute to depressive symptoms.

Case Study 2 Shaundra is a 20-year-old African American woman who presents to the postpartum clinic for her postpartum check-up at 8 weeks because she was not able to keep a 6-week appointment. She had a spontaneous vaginal birth at 28 weeks gestation because of severe pre-eclampsia and preterm labor. Her infant weighed 2 pounds and 11 ounces at birth because of intrauterine growth restriction from poorly controlled pre-eclampsia. The infant boy is formula-fed and has been transferred to a tertiary care center 4 hours from Shaundra’s home in rural Georgia. He was hospitalized until 38 days of life and has experienced many health problems during his neonatal course, including 2 readmissions to the local hospital after initial discharge. Shaundra works at a fast food restaurant, has a high school education, and is covered by Medicaid insurance. She lives with her mother, grandmother, and 4 younger siblings. She has returned to work and has arranged that


her grandmother care for her infant. During her visit, the certified nurse midwife (CNM) observes that Shaundra’s physical exam and labs are normal, but when asked about her infant, she begins to cry. She says that she just simply cannot take care of this baby with all of his problems and that she wants to run away. The CNM administers the EPDS. Shaundra scores 16/30. Shaundra denies thoughts of self-harm or harm to others. She reports that she cannot focus at work and has had three occupational injuries since returning to work. The nearest Medicaid-approved mental health services provider is an hour away with no appointments available for 8 weeks. Which of the following are assessments or interventions that may help the CNM care for Shaundra? 1. Obtain thyroid stimulating hormone (TSH), Free T4, T3, and complete blood count (CBC) levels. 2. The CNM should assess for suicidal or infanticidal ideation.

3. The CNM should consult with her supervising physician to develop a treatment and follow-up plan for Shaundra. 4. An emergency referral for immediate psychiatric evaluation and treatment must be made since Shaundra has verbalized inability to take care of her infant and wanting to “run away.” 5. Consider the use of telemental health services for follow-up psychiatric appointments given Shaundra’s distance from the clinic and the limited availability of in-person mental health appointments. 6. Patient health counseling should focus on self-care, including obtaining daily exercise, getting enough sleep, and taking prescribed medications (vitamins). Shaundra should also be encouraged to enlist the help of her social support network to lessen her depressive symptoms. Answer: All of the above.

About the Faculty Deepika Goyal, PhD, FNP: Dr. Goyal is a Professor of Nursing, College of Applied Sciences and Arts, The Valley Foundation School of Nursing, San Jose State University, San Jose, CA. Bindu Garapaty, PsyD: Dr. Garapaty is a leader in the Maternal Child Health arena with more than 10 years of experience within healthcare and academia. Nancy W. Green, DNP, FNP, CNM, CNL: Dr. Green is an Assistant Professor of Nursing, School of Nursing and Health Professions, University of San Francisco, San Francisco, CA.

177


References 1.

Gaynes BN, Gavin N, Meltzer-Brody S, et al. Perinatal depression: prevalence, screening accuracy, and screening outcomes. [Meta-Analysis Review]. Evidence Report/ Technology Assessment (Summ). 2005;119: 1-8.

2.

Vesga-Lopez O, Blanco C, Keyes K, Olfson M, Grant BF, Hasin DS. Psychiatric disorders in pregnant and postpartum women in the United States. Archives of General Psychiatry. 2008;65(7):805-815. doi:10.1001/archpsyc.65.7.805

3.

Sit D, Rothschild AJ, Wisner KL. A review of postpartum psychosis. [Research Support, Non-U.S. Gov’t Review]. Journal of Women’s Health (Larchmt). 2006;15(4):352368. doi:10.1089/jwh.2006.15.352

4.

Wisner KL, Peindl KS, Hanusa BH. Effects of childbearing on the natural history of panic disorder with comorbid mood disorder. J Affect Disord. 1996;41(3):173-180.

5.

Spinelli, M. G. (2004). Maternal infanticide associated with mental illness: prevention and the promise of saved lives. Am J Psychiatry. 2002;161(9):1548-1557.

6.

Wisner KL, Sit DK, McShea MC, et al. Onset timing, thoughts of self-harm, and diagnoses in postpartum women with screen-positive depression findings. JAMA Psychiatry. 2013;1-9. doi: 10.1001/jamapsychiatry.2013.87

7.

Beck CT. Postpartum depressed mothers’ experiences interacting with their children. Nursing Research. 1996;45(2): 98-104.

8.

Reijneveld SA, van der Wal MF, Brugman E, Hira Sing RA, Verloove-Vanhorick SP. [Prevalence of parental behaviour to diminish the crying of infants that may lead to abuse]. Nederlands Tijdschrift voor Geneeskunde. 2004;148(45): 2227-2230.

9.

US Census Bureau. State and County Quickfacts. 2013. http://quickfacts.census.gov/qfd/states/00000.html.

10. Sue DW, Sue D. Counseling the culturally different: Theory and practice. 2nd ed. Oxford, England: John Wiley & Sons; 1990. 11. Scholle SH, Kelleher K. Preferences for depression advice among low-income women. Journal of Maternal Child Health. 2003;7(2): 95-102. 12. Petersen W. Success story, Japanese-American style. New York Times. January 9, 1966. 13. Cook TM, WangJ. Causation beliefs and stigma against depression: Results from a population-based study. J Affect Disord. 2011:133 (1-2): 86 t-92. doi:10.1016/j. jad.2011.03.030 14. Teng L, Robertson-Blackmore E, Stewart DE. Healthcare worker’s perceptions of barriers to care by immigrant women with postpartum depression: An exploratory qualitative study. Archives of Women’s Mental Health. 2007;10(3):93-101. 15. Goyal D, Murphy SO, Cohen J. Immigrant Asian Indian women and postpartum depression. [Research]. Journal of Obstetric, Gynecologic, and Neonatal Nursing. 2006; 35(1):98-104. 16. Liu CH, Tronick E. Rates and predictors of postpartum depression by race and ethnicity: Results from the 2004 to 2007 New York City PRAMS Survey (Pregnancy Risk Assessment Monitoring System). Journal of Maternal Child Health. 2013; doi: 10.1007/s10995-012-1171-z 17. Shellman L, Beckstrand RL, Callister LC, Luthy KE. Freeborn D. Postpartum depression in immigrant Hispanic women: A comparative community sample. J Am Assoc Nurse Pract. 2014;26(9), 488-497. doi:10.1002/2327-6924.12088 18. Alvidrez J, Snowden LR, Kaiser DM. The experience of stigma among Black mental health consumers. [Research Support, N.I.H., Extramural]. Journal of Health Care for the Poor and Underserved. 2008:9(3):874-893. doi:10.1353/hpu.0.0058 19. Callister LC, Beckstrand, RL, Corbett C. Postpartum depression and help-seeking behaviors in immigrant Hispanic women. [Research Support, Non-U.S. Gov’t]. Journal of Obstetric, Gynecologic, and Neonatal Nursing. 2011;40(4):440-449. doi: 10.1111/j.1552-6909.2011.01254.x 20. Fogel J, Ford DE. Stigma beliefs of Asian Americans with depression in an internet sample. [Research Support, U.S. Gov’t, P.H.S.]. Can J Psychiatry. 2005;50(8): 470-478. 21. Jesse DE, Dolbier CL, Blanchard A. Barriers to seeking help and treatment suggestions for prenatal depressive symptoms: Focus groups with rural low-income women. Issues Ment Health Nurs. 2008;29(1):3-19. doi:10.1080/01612840701748664 22. Sobey WS. Barriers to postpartum depression prevention and treatment: A policy analysis. Journal of Midwifery & Women’s Health. 2002;47(5): 331-336. 23. Brown S, Lumley J. Physical health problems after childbirth and maternal depression at six to seven months postpartum. BJOG, An International Journal of Obstetrics & Gynaecology. 2000;107(10):1194-1201. 24. Amankwaa LC. Postpartum depression among African American women. Issues in Mental Health Nursing. 2003;24(3): 297-316. 25. US Census Bureau. The Asian Population. 2010. http://www.census.gov/prod/cen2010/briefs/c2010br-11.pdf 26. Tewari N, Inman A, Sandhu, DS. South Asian Americans: Culture, concerns and therapeutic strategies. In: Iwamasa JMG, ed. Culturally Diverse Mental Health: The Challenges of Research and Resistance (pp. 191-209). New York: Taylor & Francis Inc.; 2003. 27. Goyal D, Wang EJ, Shen J, Wong EC, Palaniappan, LP. Clinically identified postpartum depression in Asian American mothers. Journal of Obstetric, Gynecologic, and Neonatal Nursing. 2012;41(3):408-416. doi:10.1111/j.1552-6909.2012.01352.x 28. Cabassa LJ, Zayas LH. Latino immigrants’ intentions to seek depression care. [Research Support, N.I.H., Extramural]. The American Journal of Orthopsychiatry. 2007;77(2):231-242. doi:10.1037/0002-9432.77.2.231 29. Garces IC, Scarinci IC, Harrison L. An examination of sociocultural factors associated with health and health care seeking among Latina immigrants. J Immigr Minor Health. 2006;8(4):377-385. doi:10.1007/s10903-006-9008-8 30. Kozhimannil KB, Trinacty CM, Busch, AB, Huskamp HA, Adams AS. Racial and ethnic disparities in postpartum depression care among low-income women. Psychiatric Services. 2011;62(6):619-625. doi:10.1176/appi.ps.62.6.619 31. Halligan SL, Murray L, Martins C, Cooper, PJ. Maternal depression and psychiatric outcomes in adolescent offspring: A 13-year longitudinal study. [Research Support, Non-U.S. Gov’t]. J Affect Disord. 2007;97(1-3):145-154. doi:10.1016/j.jad. 2006.06.010

179


32. Siegenthaler E, Munder T, Egger M. Effect of preventive interventions in mentally ill parents on the mental health of the offspring: Systematic review and meta-analysis. [Meta-Analysis Review]. Journal of the American Academy of Child & Adolescent Psychiatry. 2012;51(1): 8-17 e18. doi:10.1016/j.jaac.2011.10.018 33. Milgrom J, Mendelsohn J, Gemmill AW. Does postnatal depression screening work? Throwing out the bathwater, keeping the baby. J Affect Disord. 2011;132(3): 301-310. doi:10.1016/j.jad.2010.09.031 34. Earls MF. Incorporating recognition and management of perinatal and postpartum depression into pediatric practice. Pediatrics. 2010; 126(5):1032-1039. doi:10.1542/ peds.2010-2348 35. Kroenke K, Spitzer RL, Williams JB. The PHQ-9: Validity of a brief depression severity measure. [Research Support, Non-U.S. Gov’t Validation Studies]. Journal of General Internal Medicine. 2001;16(9):606-613. 36. Zubaran C, Schumacher M, Roxo MR, Foresti K. Screening tools for postpartum depression: Validity and cultural dimensions. African Journal of Psychiatry (Johannesbg). 2010;13(5):357-365. 37. Cox JL, Holden JM, Sagovsky R. Detection of postnatal depression. Development of the 10-item Edinburgh Postnatal Depression Scale. British Journal of Psychiatry. 1987;150:782-786. 38. Sidebottom AC, Harrison PA, Godecker A, Kim H. Validation of the patient health questionnaire (PHQ)-9 for prenatal depression screening. [Research Support, U.S. Gov’t, P.H.S. Validation Studies]. Archives of Women’s Mental Health. 2012;15(5):367-374. doi:10.1007/s00737-012-0295-x 39. National Research Council and Institute of Medicine. Depression in parents, parenting, and children: Opportunities to improve identification, treatment, and prevention. Washington, DC: The National Academies Press; 2009. http://www.nap.edu/catalog. php?record_id=12565&utm_expid=4418042-5.krRTDpXJQISoXLpdo-1Ynw.0&utm_referrer=http%3A%2F%2Fwww.nap.edu%2Fopenbook.php%3Frecord_id%3D12565%26page%3DR2. 40. Mental Health America. Position #49: Perinatal Mental Health. http://www.mentalhealthamerica.net/issues/position-statement-49-perinatal-mental-health. Accessed October 12, 2014 41. Downe SM, Butler E, Hinder S. Screening tools for depressed mood after childbirth in UK-based South Asian women: a systematic review. [Review]. J Adv Nurs. 2007;57(6):565-583. doi:10.1111/j.1365-2648.2006.04028.x 42. Gjerdingen D, Crow S, McGovern P, Miner M, Center B. Postpartum depression screening at well-child visits: Validity of a 2-question screen and the PHQ-9. Annals of Family Medicine. 2009;7(1):63-70. doi:10.1370/afm.933 43. Kroenke K, Spitzer RL, Williams JB. The Patient Health Questionnaire-2: Validity of a two-item depression screener. [Comparative Study Evaluation Studies Research Support, Non-U.S. Gov’t]. Medical Care. 2003;41(11):1284-1292. doi:10.1097/01.MLR. 0000093487. 78664.3C 44. Venkatesh KK, Zlotnick C, Triche EW, Ware C, Phipps MG. Accuracy of brief screening tools for identifying postpartum depression among adolescent mothers. Pediatrics. 2014;133(1):e45-53. doi:10.1542/peds.2013-1628 45. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA, American Psychiatric Association, 2013. 46. First MB, Spitzer RL, Williams JB, Gibbon M. Structured Clinical Interview for DSM-IV (SCID). Washington, DC: American Psychiatric Association: 1995. 47. Pratt LA, Brody S, Gu Q. Antidepressant use in persons aged 12 and over United States, 2005-2008. NCHS Data Brief. 2011;76. www.cdc.gov/nchs/data/databriefs/db76. pdf 48. Gonzalez HM, Tarraf W, West BT, Chan D, Miranda PY, Leong FT. Research article. Antidepressant use among Asians in the United States. Depress Anxiety. 201027(1):4655. doi:10.1002/da.20636 49. Murphy E, McMahon FJ. Pharmacogenetics of antidepressants, mood stabilizers, and antipsychotics in diverse human populations. Discovery Medicine. 2013;16(87):113-122. 50. Bershadsky S, Trumpfheller L, Kimble HB, Pipaloff D, Yim IS. The effect of prenatal Hatha yoga on affect, cortisol and depressive symptoms. Complementary Therapies in Clinical Practice. 2014;20(2):106-113. doi:10.1016/j.ctcp.2014.01.002 51. Marc I, Toureche N, Ernst E, Hodnett ED, Blanchet C, Dodin S. Njoya MM. Mind-body interventions during pregnancy for preventing or treating women’s anxiety. Cochrane Database Syst Rev. 2011;7: CD007559. doi:10.1002/14651858.CD007559.pub2 52. Muzik M, Hamilton SE, Rosenblum LK, Waxler E, Hadi Z. Mindfulness yoga during pregnancy for psychiatrically at-risk women: Preliminary results from a pilot feasibility study. Complementary Therapies in Clinical Practice. 2012;18(4):235-240. doi:10.1016/ j.ctcp.2012.06.006 53. Goyal D, Gay C, Lee K. Fragmented maternal sleep is more strongly correlated with depressive symptoms than infant temperament at three months postpartum. Archives of Women’s Mental Health. 2009;12(4):229-237. doi:10.1007/s00737-009-0070-9 54. Goyal D, Gay CL, Lee KA. Patterns of sleep disruption and depressive symptoms in new mothers. [Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov’t]. The Journal of Perinatal & Neonatal Nursing. 2007;21(2):123-129. doi:10.1097/01. JPN. 0000270629.58746.96 55. Beck CT. Predictors of postpartum depression: An update. Nurs Res. 2001;50(5): 275-285. 56. Lee KA, Gay CL. Can modifications to the bedroom environment improve the sleep of new parents? Two randomized controlled trials. [Randomized Controlled Trial Research Support, N.I.H., Extramural]. Research in Nursing and Health. 2011; 34(1):7-19. doi:10.1002/ nur.20413

180

L003334 : Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups

L003334 : Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups

L003334

L003334

Multiple-Choice Questions

Multiple-Choice Questions

45. Which of the following statements are correct regarding the selection of a postpartum depression screening tool for diverse populations?

45. Which of the following statements are correct regarding the selection of a postpartum depression screening tool for diverse populations?

A. Neither the EPDS nor the PHQ9 is validated for use in diverse populations.

A. Neither the EPDS nor the PHQ9 is validated for use in diverse populations.

B. The EPDS and the PHQ9 are validated for use in diverse populations.

B. The EPDS and the PHQ9 are validated for use in diverse populations.

C. The EPDS is validated for use only in postpartum populations.

C. The EPDS is validated for use only in postpartum populations.

D. The PHQ9 is validated for use only in pregnant populations.

D. The PHQ9 is validated for use only in pregnant populations.

46. When should a patient be referred for a further mental health evaluation?

46. When should a patient be referred for a further mental health evaluation?

A. When a patient scores above the established cut-off point on a questionnaire

A. When a patient scores above the established cut-off point on a questionnaire

B. When a patient verbalizes suicidal ideation

B. When a patient verbalizes suicidal ideation

C. When the clinician feels that further evaluation is appropriate

C. When the clinician feels that further evaluation is appropriate

D. All of the above

D. All of the above

47. What cut-off score on the (GLQEXUJK3RVWQDWDO'HSUHVVLRQ6FDOH would prompt you to refer your patient for further evaluation?

47. What cut-off score on the (GLQEXUJK3RVWQDWDO'HSUHVVLRQ6FDOH would prompt you to refer your patient for further evaluation?

A. 6

A. 6

B. 4

B. 4

C. 11

C. 11

D. 8

D. 8

:KDWDUHWKHGLDJQRVWLFJXLGHOLQHVIRU33'EDVHGRQWKHQHZ'LDJQRVWLFDQG6WDWLVWLFDO0DQXDO of Mental Disorders (DSM-5)"'LDJQRVLVVKRXOGEHEDVHGRQZKLFKRIWKHIROORZLQJ"

:KDWDUHWKHGLDJQRVWLFJXLGHOLQHVIRU33'EDVHGRQWKHQHZ'LDJQRVWLFDQG6WDWLVWLFDO0DQXDO of Mental Disorders (DSM-5)"'LDJQRVLVVKRXOGEHEDVHGRQZKLFKRIWKHIROORZLQJ"

A. Symptom onset within 4 weeks of childbirth

A. Symptom onset within 4 weeks of childbirth

B. Symptom onset during the pregnancy as well as in the 4 weeks following delivery

B. Symptom onset during the pregnancy as well as in the 4 weeks following delivery

C. Symptom onset 18 months after childbirth

C. Symptom onset 18 months after childbirth

D. All of the above

D. All of the above

181

181

Best Practices in CME Postpartum Depression Identification, Referral, and Treatment among Diverse Racial and Ethnic Groups By Deepika Goyal, PhD, FNP; Bindu Garapaty, PsyD; and Nancy W. Green, DNP, FNP, CNM, CNL ID#: L003334

This valuable take-home reference translates evidence-based, continuing medical education research and theory, which is acquired from reading the associated CME lesson, into a stepwise approach that reviews key learning points for easy assimilation into your armamentarium of knowledge and daily practice.

CME Lesson Overview Easily treated with timely identification, women from diverse racial and ethnic backgrounds, including those of African American, Asian American, and Hispanic/Latino descent, are less likely to self-report depressive symptoms delaying treatment. This lesson examines specific cultural factors and mental health help-seeking behaviors among culturally diverse populations in an effort to improve the identification and treatment of postpartum depression.

Key Point 1: Prevalence of Postpartum Depression Minority women are at an increased risk of developing PPD.

Key Point 2: Barriers to Seeking Treatment The common cultural barrier to mentalhealth help-seeking across all three race/ ethnic groups is stigma associated with mental illness and treatment.

Key Point 3: Cultural Considerations in Treatment

Key Point 4: The Need for Patient Education Screening and education regarding PPD should occur for all new mothers during the postpartum period and at all well baby visits.

Key Point 5: The Role of the Family Cultural values play a significant role in access to mental health care, and the entire family should be involved in treatment decisions.

Clinicians must consider cultural values versus labeling patients “non-compliant.”


Notes

L003335

Sexual Addiction or Hypersexual Disorder: Clinical Implications for Assessment and Treatment Aviv Weinstein, PhD Medications mentioned in this lesson are not approved by the FDA for the treatment of sexual addiction or hypersexual disorder. No commercial support was used in the development of this CME lesson.

KEY WORDS: Sexual Addiction • Hypersexual Disorder • Compulsive Sexual Behavior • Impulsivity LEARNING OBJECTIVES: Clinicians will review recent evidence for the assessment and the psychobiological basis and treatment of sexual addiction, including diagnosis, comorbidity with other psychiatric disorders, and treatment studies. Instruments for assessing sexual addiction are discussed, as well as data on the neuropsychological and biological basis of this disorder. LESSON ABSTRACT: Sexual addiction, which is also known as hypersexual disorder, is associated with severe psychosocial problems and risk-taking behaviors. People who suffer from sexual addiction or hypersexual disorder have reported having obsessive thoughts, fantasies, and problematic behaviors, including excessive masturbation, cybersex, pornography use, sexual behavior with consenting adults, telephone sex, and strip club visitation. Sexual addiction is not included in the Diagnostic and Statistical Manual of Mental Disorders. Several screening questionnaires have been developed over the years for the diagnosis of sexual addiction or hypersexual disorder. Prevalence rates of sexual addiction range from 3% to 6%. There is a co-occurrence of sexual addiction with other addictions and psychiatric disorders such as anxiety disorders, posttraumatic stress disorder (PTSD), alcohol and drug abuse, pathological gambling, and attention deficit hyperactivity disorder (ADHD). Several treatment studies have shown the efficacy of the combination of pharmacological treatment with cognitive-behavior therapy.

COMPETENCY AREAS: This lesson addresses the gap in learning in the area of sexual addiction or hypersexual disorder, including diagnosis, assessment, prevalence, comorbidity, cognitive-behavioral and neurobiological mechanisms, and psychological and pharmacological treatment. Many clinicians lack understanding of how to adequately diagnose and treat sexual addiction or hypersexual disorder, which often goes underreported by patients. Pharmacological treatment with SSRIs together with cognitive-behavior therapy may be useful for treating sexual addiction. Upon the conclusion of this lesson, readers will have a better understanding of sexual addiction or hypersexual disorder and its diagnosis and treatment.

185

L003335 : Sexual Addiction or Hypersexual Disorder: Clinical Implications for Assessment and Treatment

Introduction History of Sexual Addiction and Its Treatment: Sexual addiction, which is also known as hypersexual disorder, is associated with severe psychosocial problems and risk-taking behaviors.1-3 Various terms have been used to name the condition, including sexual compulsivity, sexual impulsivity,4 out-of-control sexual behavior,5 sexual addiction, and hypersexual behavior.6-7 In 1812, U.S. physician Benjamin Rush documented in his book Medical Inquiries and Observations Upon the Diseases of the Mind the case of a person with “excessive” sexual appetite which caused him great psychological distress.8 In 1886, German psychiatrist Dr. Richard von Krafft-Ebbing argued that “pathological sexuality” is a psychiatric illness that results in an impulsive series of sexual enjoyment resulting in legal, moral, and psychological problems.9 In the mid-1970s, British psychologist Dr. Jim Orford suggested that hypersexuality should be included in the spectrum of addictive disorders. He argued that hypersexuality is similar to excessive drinking and gambling in that hypersexuality is an excessive appetitive behavior that does not have psychoactive drugs as an object.10 He described the behavior as a maladaptive pattern of use and impaired control of a behavior that was associated with adverse consequences.10 Several problems with the dependence model of sex were discussed by Orford and Carnes,10-11 notably that it is difficult to separate normal and abnormal sexual behavior, it is difficult to determine when loss of control occurs, and it is difficult to assess the role of culture in this model. In his 2001 best-selling book, Out of the Shadows: Understanding Sexual Addiction, Carnes described sexual addiction as a psychopathological condition of excessive sexual behavior.12 A distinct approach was proposed by Mick and Hollander, who argued that sexual addiction can be conceptualized as a disorder on the impulsive-compulsive spectrum.4 According to this view, impulsivity and compulsivity coexist. First, an impulsive component (pleasure, arousal, or gratification) initiates the cycle, and then a compulsive component leads to the persistence of the behavior.4 186

Sexual addiction, or hypersexual disorder, is not recognized as a disorder in the Diagnostic and Statistical Manual of Mental Disorders (DSM). The DSM3-R13 referred to sexual addiction as a sexual disorder “not otherwise specified.” The two versions of the DSM-4 omitted sexual addiction. However, the Work Group on Sexual and Gender Identity Disorders proposed diagnostic criteria for hypersexual disorder to be considered for inclusion in the DSM-5.7 Empirical research on sexual addiction has increased in recent years,7,14-15 which has led to considerable interest in developing measures that assess sexual addiction and hypersexual disorder.16 Recently, the American Psychiatric Association Board of Trustees rejected several proposals for the new disorder, and therefore, hypersexual disorder does not appear in the new DSM-5. Even though clinicians have been treating the disorder, the Board of Trustees estimated that there was not enough research to consider adding the disorder to Section 3 (disorders that require further research) of the DSM-5.17 Given the variation in definitions, conceptualizations, and assessments of sexual addiction or hypersexual disorder and its rejection by the DSM-5, the purpose of the current review is to emphasize the assessment, diagnosis, clinical, and neurobiological characteristics of the disorder and to provide clinicians with a detailed description of treatment options available.

Diagnosis and Assessment Criteria: In recent years, claims have emerged against the inclusion of the condition in the DSM-5. Authors have argued that this diagnosis was unnecessary and would be harmful to patients, whereas others suggested that the disorder does not exist.18-19 In the 1990s, Goodman replaced the term “substance” in the DSM-4’s definition of “substance dependence” with “sexual behavior”20 (see Table 1). Kafka21 proposed to use the term “hypersexual disorder,” and the diagnostic criteria for hypersexual disorder showed good external validity with measures of impulsivity, emotional dysregulation, and stress proneness, as well as good internal consistency. Writing on behalf of the Work Group on Sexual and Gender Identity Disorders, Kafka21 proposed the diagnosis of hypersexual disorder (see Table 2). The diagnosis did not require dependence, tolerance,


and withdrawal—Kafka’s criteria incorporated other key aspects of addiction such as unsuccessful efforts to cut down, greater use than intended, and serious social and occupational consequences. Ultimately, the DSM-5 committee decided that there was not enough research to include hypersexual disorder as a diagnosis in the DSM-5.

Assessment of Sexual Addiction In recent years, research on sexual addiction has increased, and screening instruments have been developed to diagnose or quantify the disorder.3,22-25 Currently, 22 questionnaires assess sexual addiction. These questionnaires assess symptoms of sexual addiction and/

Table 1: Goodman’s Proposed Sexual Addiction Diagnostic Criteria20 A maladaptive pattern of sexual behavior leading to clinically significant impairment or distress as manifested by 3 (or more) of the following and occurring at any time in the same 12-month period: 1. Tolerance, as defined by either of the following: (a) A need for a markedly increased amount or intensity of sexual behavior to achieve the desired effect. (b) Markedly diminished effect with continued involvement in sexual behavior at the same level of intensity. 2. Withdrawal, as manifested by either of the following: (a) Characteristic psychophysiological withdrawal syndromes of physiologically described changes and/or psychologically described changes upon discontinuation of the sexual behavior. (b) The same (or a closely related) sexual behavior is engaged in to relieve or avoid withdrawal symptoms. 3. The sexual behavior is often engaged in over a longer period, in greater quantity, or at a higher level of intensity than was intended. 4. There is a persistent desire or unsuccessful effort to cut down or control the sexual behavior. 5. A great deal of time is spent in activities necessary to prepare for the sexual behavior, to engage in the behavior, or to recover from its effects. 6. Important social, occupational, or recreational activities are given up or reduced because of the sexual behavior. 7. The sexual behavior continues despite knowledge of a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by the behavior.

Table 2: Kafka’s Proposed Hypersexual Disorder Diagnostic Criteria21 A. Over a period of at least 6 consecutive months, recurrent and intense sexual fantasies, sexual urges, or sexual behaviors in association with 4 or more of the following 5 criteria: 1. Excessive time consumed by sexual fantasies and urges and by planning for and engaging in sexual behavior. 2. Repetitively engaging in these sexual fantasies, urges, and behavior in response to dysphoric mood states (e.g., anxiety, depression, boredom, irritability). 3. Repetitively engaging in sexual fantasies, urges, or behaviors in response to stressful life events. 4. Repetitive but unsuccessful efforts to control or significantly reduce the sexual fantasies, urges, and behaviors. 5. Repetitively engaging in sexual behaviors while disregarding the risk for physical or emotional harm to self or others. B. There is clinically significant personal distress or impairment in social occupational or other important areas of functioning associated with the frequency and intensity of the sexual fantasies, urges, and behaviors. C. These sexual fantasies, urges, and behaviors are not due to direct physiological effects of exogenous substances (e.g., abuse of drugs or medications) or to manic episodes. D. The person is at least 18 years of age. Specify if: masturbation, pornography, sexual behavior with consenting adults, cybersex, telephone sex, strip clubs. Specify if in remission: no distress, impairment, or recurring behavior and in an uncontrolled environment, and state duration of remission in months in a controlled environment.

187


or the adverse consequences of the disorder. The psychometric qualities of the existing measures are generally low, and further validation studies are required. The primary concerns for and limitations regarding the existing measures include (a) the absence of valid cut-off criteria to identify sexual addiction; (b) a lack of generalizability (e.g., some instruments have been used only in very specific samples, such as men who have sex with men); and (c) variance in reliability, response format (dimensional versus categorical responses), and factorial structures.3 Carnes created one of the first instruments for assessing sexual addiction—the Sexual Addiction Screening Test (SAST).26 The SAST is composed of 25 items that measure symptoms of sexual addiction, mostly geared toward heterosexual men. The Cronbach’s alpha coefficients for the total score of the SAST range from 0.85 to 0.95. The SAST discriminated between male sex addicts and non-addicts,26 and it was related to other measures of sexual addiction.27-28 Carnes has also developed two other versions: the WSAST (the SAST for women)29 and the GSAST (the SAST for men who have sex with men [MSM]).30 A new version of the SAST, the SAST-R,31 was developed, and it applies to heterosexual men and women and MSM. Recently, Carnes and colleagues also created the PATHOS, a short instrument that assesses sexual addiction. The PATHOS has 6 items to preoccupation, shame, treatment-seeking, hurting others, outof-control behavior, and sadness.32 Kalichman and Rompa developed the Sexual Compulsivity Scale (SCS), which is a 10-item questionnaire that assesses sexual compulsive behavior, sexual preoccupations, and intrusive sexual-related thoughts.33 A cut-off score of 24 or higher has been used to indicate problems with sexual addiction. The SCS displays good psychometric properties with Cronbach’s alpha coefficients ranging from 0.59 to 0.92.26 The SCS has a good convergent validity and relates to other measures of sexual addiction.33 The SCS also has good discriminant validity, and is unrelated to ethnicity,34-35 education, and income.34 Miner et al reported that the SCS predicted the practice of engaging in unprotected sex, a large number of sexual partners, the use of cocaine in HIV-positive men, and high frequency of sex-seeking behavior on the Internet.36

188

Prevalence Rates To date, no large epidemiological studies of sexual addiction have been conducted using standardized diagnostic criteria.7,37 However, some studies have estimated the prevalence of sexual addiction to be between 3% and 6% of the general population.38-41 The occurrence rates of sexual addiction vary in the literature depending on characteristics examined such as gender, sexual orientation, age, and the diagnostic criteria implemented in the study. The prevalence of sexual addiction-related disorders ranges from 3% to 16.8%.42-45 In a Swedish sample of 2,450 participants from the general population, Langström and Hanson estimated that 12% of men and 6.8% of women present with hypersexuality.46 The researchers found that 5% to 10% of the most sexually active respondents reported higher levels of co-occurring addictions, risk-taking behaviors, distress, and psychiatric symptoms, suggesting a subgroup of the most sexually active who may have psychosocial impairments.46 Traeen et al47 specifically investigated pornography dependence in the adult Norwegian male population, and found that 1% of their sample masturbated to ejaculation twice or more per day while viewing pornography. Laumann et al48 reported that 7.6% of American men (n = 1320; ages 18–59) engaged in partnered sex 4 or more times/week for at least 1 year, and 1.2% of the men masturbated more than once/day during the year leading up to the survey. Higher rates have been suggested in specific populations, such as sexual offenders, patients with HIV,49 and people with hypersexual disorders and paraphilias.50 The evidence suggests that men have a higher prevalence of sexual addictions than women; the estimated ratio of sexual addictions is between 3 and 5 men for every 1 woman.51-53 The dissimilar prevalence rates reported can at least partially be attributed to the use of different classification criteria along with the use of different screening instruments and/or cut-off criteria.

Psychiatric Comorbidity The adverse consequences of sexual addiction are similar to the consequences of other addictive disorders.54 Other direct risks are associated with unprotected and anonymous sexual encounters, such as HIV/AIDS,


other sexually transmitted diseases, and unwanted pregnancy.12,51-52 Hypersexual men and women also engage in tobacco use, alcohol, and illicit drug abuse.55-56 Among men, gambling is prevalent.7 Other psychiatric comorbidities include mood disorders, depression, anxiety,55,57 social anxiety, dysthymia, attention deficit hyperactivity disorder,4,37,58 affect dysregulation,59 and posttraumatic stress disorder.60 Finally, some studies find that sexual addiction is associated with or in response to dysphoric affects or stressful life events.61-64 The co-occurrence of sexual addiction and other addictions suggest that these disorders share etiological mechanisms, such as neurobiological and psychosocial factors (e.g., personality traits, cognitive deficits, or bias).65 Carnes66 reported that the majority of a sample of 1603 sex addicts reported a lifetime prevalence of other addictive and abusive behaviors such as substance abuse, gambling, or eating disorders. Finally, a study of pathological gamblers67 found that 19.6% of the subjects also met the criteria for compulsive sexual behavior (CSB). The majority of the subjects who met the criteria for both disorders reported that CSB had preceded their gambling problems.

Behavioral Characteristics of Sexual Addiction Sexual addiction or hypersexual disorder includes various types of problematic behaviors.37,54,68 Coleman and colleagues classified seven subtypes of impulsive-compulsive sexual behavior: compulsive cruising and multiple partners, compulsive fixation on an unattainable partner, compulsive masturbation, compulsive use of erotica, compulsive use of the Internet for sexual purposes, multiple compulsive love relationships, and compulsive sexuality in a relationship.69 Behavioral symptoms may also include engaging in risky sexual activities, paying for sexual services, and resisting behavioral changes to avert HIV risk.69-72 Bancroft57 suggested that 2 types of sexual behavior are especially likely to become out of control: masturbation and the new and exceedingly important development of the sexual use of the Internet. A growing number of men and women use the Internet for sexual purposes.

Men are more likely to access sexually explicit material online, while women are more likely to use the Internet for interactions and cybersex.5 According to Kafka, the various proposed subtypes of hypersexual disorder are excessive masturbation, which is the most common sexual outlet for single and married individuals over the life course,73 cybersex, pornography use, sexual behavior with consenting adults, telephone sex, strip club visitation, and other behaviors.7

Cognitive, Social, and Emotional Factors: More than 90% of people who are categorized as having sexual addiction or hypersexual disorder reported having obsessive thoughts and behaviors or sexual fantasies.74 Hypersexual men and women were more likely to be younger and to have been separated from their parents during childhood.46 These subjects initiated sexual behaviors at an earlier age, had a higher frequency of sexual behaviors, and had experienced more diverse sexual experiences than subjects who were not hypersexual. The most important gender difference was the link between sexual addiction and a history of sexual abuse for women.46 Sexual abuse was linked to promiscuous or risky sexual behavior.75-76 Dysfunctional attachment during childhood is a major risk factor for sexual addiction. Early negative childhood attachment experiences may negatively impact individuals’ affective, cognitive, and behavioral development and favor the development and maintenance of sexual addiction.39,77-79 Sexual addiction can be defined as a clinical syndrome characterized by the experience of sexual urges, fantasies, and behaviors that are recurrent and intense and cause a distressful interference in one’s daily functioning.80 Sexual addiction has also been associated with impulsivity,81-82 loneliness,83 low self-worth, insecure attachment styles,84-85 personal distress,86-87 and self-hatred and shame.55,88-89 More than 70% of sexual addiction patients report withdrawal symptoms between sexual episodes. Withdrawal symptoms include nervousness, insomnia, sweating, nausea, increased heart rate, shortness of breath, and fatigue.39,90-91 Men are less likely to feel satisfied with their sexual life, have more relationship-associated problems, and are more likely to have consulted professional help for their sexual problems.51 189


Associated Psychobiological Mechanisms The sexual addictive process is described by Goodman as an interaction of impairments in three functional systems: motivation-reward, affect regulation, and behavioral inhibition.65 Brain imaging studies of human sexual behavior in normal subjects and subjects with sexual disorders used positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) to identify brain mechanisms that underlie responses to visual sexual stimuli. These studies have demonstrated that visual sexual stimuli are associated with the activation of the brain’s reward mechanisms, including the limbic and paralimbic regions (the anterior cingulate gyrus and the orbitofrontal cortex) and the striatum (the head of the caudate nucleus and putamen). These regions contain dopaminergic (DA) projections that are an important part of the brain reward network. Gender effects were found, with men showing significantly greater amygdala activation, which perhaps reflects differences in how men and women process sexual signals.92 Amygdala activation in men characterizes the “appetitive” phase of sexual behavior, whereas ejaculation, which characterizes the “consummatory” phase of sexual behavior in men, is associated with a decrease in amygdala activity.93 Further brain imaging studies of human subjects during sexual arousal suggest that the frontal areas of the brain may exert control and exercise reason over the posterior reward centers.94-95 Brain scan studies of sexual dimorphism may help us understand the differences between men and women, particularly when it comes to sexual acting-out. For instance, a sexual activity-related PET study demonstrated that male arousal was more often associated with activation of the visual cortices of the brain—even when the subjects’ eyes were closed.96 Female arousal was associated with stronger activity in the left dorsal frontoparietal regions, including the premotor and posterior parietal areas.97 During orgasm, male and female brain functioning appears similar with activation in the anterior lobe of the cerebellar vermis and deep cerebellar nuclei and deactivations in the left ventromedial and orbitofrontal cortex. Although promising and intriguing, today’s PET and fMRI studies do not yet provide any clinical guidance in treating sexual addiction.2 190

The comorbidity between sexual addiction and pathological gambling (PG) could be explained by common neurobiological mechanisms. Grant and Steinberg68 found that compulsive sexual behavior occurred in 19.6% of patients with PG. In 70.5% of those with co-occurring disorders, compulsive sexual behavior predated pathological gambling. Furthermore, patients treated with dopaminergic agents for idiopathic Parkinsonism sometimes developed PG and sexual compulsivity.98 In addition, patients with PG and sexual addiction were treated with naltrexone, an opiate antagonist commonly used to treat opiate and alcohol addiction.98 Genetic data may also explain abnormalities in sexual desire. In humans, the heritability of sexually promiscuous behavior in both genders has been evaluated in twin studies.99 Human sexuality may be associated with genes that mediate dopamine transmission, specifically the D4 dopamine receptor, which is associated with novelty seeking.100-103 Long alleles of the D4 dopamine receptor (7 repeats of the allele or more) were associated with disinhibition and impulsivity,104 initiating sexual activity,105 and having had a “one-night stand,” but not in overall sexual infidelity.106

Treatment Pharmacological Treatment: Currently, there is a lack of consensus and empirical research on sexual addiction/hypersexual disorders, and clear diagnostic criteria are needed to test the efficacy of psychological and pharmacological treatments in controlled studies. However, similar to other behavioral addictions (e.g., pathological gambling and compulsive buying), the appropriate treatment of sexual addiction should include a combination of pharmacological and psychological approaches.3,107 Pharmacological treatments have limited evidence of success. To date, no large double-blind clinical trials have been conducted in patients with sexual addiction/ hypersexual disorders. One small, 12-week randomized trial showed an effect of selective serotonin reuptake inhibitors (SSRIs; escitalopram 20–60 mg) on sexual desire, sexual drive, frequency of masturbation, and pornography use.108 Escitalopram (Lexapro) has


demonstrated a moderate and significant decrease in masturbation and pornography use.109 Open-label trials and anecdotal reports support the use of SSRIs such as fluoxetine to reduce desire, arousal, and orgasm.110-111 Finally, naltrexone (Revia, Vivitrol) is commonly used to treat opiate and alcohol addiction, has been reported to be effective in reducing problem gambling, and may be effective for some patients with sexual addiction. Open-label studies and case reports of naltrexone112 and topiramate (Topamax)113 showed promise in decreasing the frequency of excessive sexual behavior. In a retrospective review of 19 adult men treated with naltrexone for compulsive sexual behavior, 89% indicated a decrease in compulsive sexual behavior symptoms.114

Psychological Treatment: Motivational interviewing, cognitive-behavior therapy, and couples and family therapy have been shown to be efficient for treating several forms of drug and behavioral addiction.115-117 Behavioral therapies may be associated with reductions in substance use and may have effects on cognitive control, impulsivity, motivation, and attention and related brain mechanisms.118 Group-based treatments can also be used.119 Although Sex Addicts Anonymous is not affiliated with any other organization, the basic principles of the group are found in the 12 steps and 12 traditions of Alcoholics Anonymous. Treatment consists of approaches that have been used for substance addiction such as group and individual therapy, motivational interviewing, cognitive-behavioral techniques, relapse prevention, insight-oriented therapy, and family therapy. In the United States, numerous inpatient and outpatient treatment centers use an addiction model to treat sexual compulsivity and addiction. Carnes has developed a task-centered approach program with a series of operationalized workbooks appropriate for treating sexual addiction patients.120

Conclusion Sexual addiction or hypersexual disorder involves powerful sexual urges together with lack of control of these urges and preoccupation or an obsession with sexual behavior. Sexually addicted patients lack control of this activity, which has long-term harmful consequences functionally and socially, as well as economically. Several screening questionnaires have been created specifically to assess the proposed diagnostic criteria for hypersexual disorder and are likely to be the best choice of measures if the researcher or clinician is looking for a brief instrument. According to Womack,25 a thorough assessment of hypersexual behavior includes (a) a self-report measure of general symptoms, (b) a self-report measure of consequences, (c) a clinical interview, and (d) an objective assessment of sexual behavior. The neurobiological and psychological mechanisms of sexual addiction are under investigation, and currently, there is no validated pharmacological or psychological treatment for this disorder. The absence of validated treatment is at least partly because sexual addiction is not clearly defined and diagnosed as a clinical disorder; instead, it is a construct that covers many different types of problematic sexual behaviors. Due to this diversity, Kor et al.121 concluded that despite many similarities between the features of hypersexual behavior and substance-related disorders, the research on hypersexual disorder at this time is in its infancy and much remains to be learned before it can be definitively characterized as an addiction. Rosenberg et al.2 anticipated that as psychiatric research improves our understanding, studies will support the existence of sexual addiction and related disorders as painful and serious disorders. Hopefully, future research will be able to integrate the different types of problematic sexual behavior into a clinically defined disorder.

About the Faculty Aviv Weinstein, PhD: Dr. Weinstein is a senior lecturer at the Department of Behavioral Science at the University of Ariel and a senior psychologist at the Department of Nuclear Medicine at the Tel Aviv Sourasky Medical Center in Israel.

191


References 1. Quadland MC. Compulsive sexual behavior: definition of a problem and an approach to treatment. J Sex Marital Ther. 1985;11(2):121-132. 2.

Rosenberg KP, O’Connor S, Carnes P. Sexual addiction: An Overview. In Rosenberg, KP, Feder LC. (Eds.) “Behavioral Addictions: Criteria, Evidence and Treatment” Elsevier Science: Burlington USA. 2014.

3. Karila L, Wéry A, Weinstein A, Cottencin O, Reynaud M, Billieux J. Sexual addiction orhypersexual disorder: Different terms for the same problem? A review of the literature. In “New Behaviors, New Drugs: The Modern Landscape of Addiction” Current Pharmaceutical Design. 2014. 4. Mick TM, Hollander E. Impulsive-compulsive sexual behavior. CNS Spectr. 2006;11(12):944-955. 5. Bancroft J. Sexual behavior that is “out of control”: a theoretical conceptual approach. Psychiatr Clin North Am. 2008;31(4):593-601. 6. Gilliland R, South M, Carpenter BN, Hardy S. The roles of shame and guilt in hypersexual behavior. Sex Addict Compulsivity. 2011;(18):12-29. 7. Kafka MP. Hypersexual disorder: A proposed diagnosis for DSM-V. Arch Sex Behav. 2010;39(2):377-400. 8. Rush B. Medical inquiries and observations upon the diseases of the mind. Birmingham, AL: Gryphon Editions Ltd. 1979. 9. Krafft-Ebing, R. von. Psychopathia sexualis. New York: G. P. Putnam’s Sons (Original work published 1886), Neuroscience Biobehavior Rev. 1965;19:261–277. 10. Orford J. Hypersexuality: Implications for a theory of dependence. Brit J Addict. 1978;73:299-310. 11. Carnes PJ. Contrary to Love: Helping the Sexual Addict. Center City, MN: Hazelden. 1994. 12. Carnes P. Out of the Shadows: Understanding Sexual Addiction. Hazelden Information & Educational Services; Édition : 3rd Revised edition. 2001. 13. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Third Edition, revised (DSM-III-R) Arlington, VA. American Psychiatric Association, 1987. 14. Krueger RB, Kaplan MS. The paraphilic and hypersexual disorders: an overview. J Psychiatr Pract. 2001;(6):391-403. 15. Levine SB. What is sexual addiction? J Sex Marital Ther. 2010;36(3):261-275. 16. Womack S, Hook J, Ramos M, Davis D, Penberthy K. Measuring Hypersexual Behavior. Sex Addict Compulsivity. 2013;20(1-2):65-78. 17. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA, American Psychiatric Association, 2013. 18. Reid RC, Carpenter BN, Spackman M, Willes DL. Alexithymia, emotional instability, and vulnerability to stress proneness in patients seeking help for hypersexual behavior. J Sex Marital Ther. 2008;34:133-149. 19. Raymond NC, Coleman E, Miner MH. Psychiatric comorbidity and compulsive/impulsive traits in compulsive sexual behavior. Compr Psychiat. 2003;44(5): 370-380. 20. Goodman A. Sexual addiction: designation and treatment. J Sex Marital Ther. 1992;18(4):303-314. 21. Kafka MP. Hypersexual disorder: A proposed diagnosis for DSM-V. Arc Sex Behav. 2010;39(2):377–400. 22. Marshall LE, Briken P. Assessment, diagnosis, and management of hypersexual disorders. Curr Opin Psychiatry. 2010;23(6):570-573. 23. Reid RC, Carpenter BN, Hook JN, Garos S, Manning JC, Gilliland R, et al. Report of findings in a DSM-5 field trial for hypersexual disorder. J Sex Med. 2012; 9(11):2868-77. 24. Hook JN, Hook JP, Davis DE, Worthington EL, Jr., Penberthy JK. Measuring sexual addiction and compulsivity: a critical review of instruments. J Sex Marital Ther. 2010;36(3):227-260. 25. Womack SD, Hook JN, Ramos M, Davis DE, Penberthy JN. Measuring Hypersexual Behavior. Sex Addict & Compulsivity. 2013;20:65–78. 26. Carnes P. Sexual addiction screening test. Tenn Nurse. 1991;54(3):29. 27. Delmonico DL, Bubenzer DL, West JD. Assessing sexual addiction with the Sexual Dependency Inventory—Revised. Sex Addict & Compulsivity. 1998;5:179-187. 28. Delmonico DL, Miller JA. The Internet Sex Screening Test: A comparison of sexual compulsives versus non-sexual compulsives. Sex and Relationship Ther. 2003;18:261–276. 29. Garos S, Stock WA. Measuring disorders of sexual frequency and control: The Garos Sexual Behavior Index. Sex Addict and Compulsivity. 1998;5:159–177. 30. Carnes P, O’Hara S. The Women’s Sexual Addiction Screening Test. Unpublished measures, Wickenburg, AZ. 2000. 30. Carnes P, Weiss R. The Sexual Addiction Screening Test for Gay Men. Unpublished measures, Wickenburg, AZ. 2002. 31. Carnes P, Green B, Carnes S. The Same Yet Different: Refocusing the Sexual Addiction Screening Test (SAST) to Reflect Orientation and Gender. Sex Addict Compulsivity. 2010;17(1):7-30. 32. Carnes PJ, Green BA, Merlo LJ, Polles A, Carnes S, Gold MS. PATHOS: a brief screening application for assessing sexual addiction. J Addict Med. 2012;6(1): 29-34. 33. Kalichman SC, Johnson JR, Adair V, Rompa D, Multhauf K, Kelley JA. Sexual sensation seeking: Scale development and predicting AIDS-risk behavior among homosexually active men. J Personal Assessment. 1994;62:385–397. 34. Benotsch EG, Kalichman SC, Kelly JA. Sexual compulsivity and substance use in HIV-seropositive men who have sex with men: prevalence and predictors of highrisk behaviors. Addict Behav. 1999;24(6):857-868. 35. O’Leary A, Fisher HH, Purcell DW, Spikes PS, Gomez CA. Correlates of risk patterns and race/ethnicity among HIV-positive men wh have sex with men. AIDS and Behav. 2007;11:706-715. 36. Miner MH, Coleman E, Center BA, Ross M, Rosser BR. The compulsive sexual behavior inventory: psychometric properties. Arch Sex Behav. 2007; 36(4): 579-587. 37. Garcia FD, Thibaut F. Sexual addictions. Am J Drug Alc Abuse. 2010;36(5):254-260.

193


38. Sussman S, Lisha N, Griffiths M. Prevalence of the addictions: a problem of the majority or the minority? Evaluation Health Prof. 2011;34(1):3-56. 39. Carnes PJ. Don’t Call it Love: Recovering from Sexual Addiction. New York: Bantam Books. 1991. 40. Freimuth M, Waddell M, Stannard J, Kelley S, Kipper A, Richardson A, et al. Expanding the scope of dual diagnosis and co-addictions: Behavioral addictions. J Groups Addict Recovery. 2008;3:137-160. 41. Kuzma JM, Black DW. Epidemiology, prevalence, and natural history of compulsive sexual behavior. Psychiatr Clin North Am. 2008;31(4):603-611. 42. Cooper A, Morahan-Martin J, Mathy RM, Maheu M. Toward an increased understanding of user demographics in online sexual activities. J Sex Marital Ther. 2002;28:105-129. 43. Cook DR. Self-identified addictions and emotional disturbances in a sample of college students. Psychol Addict Behav. 1987;1:55-61. 44. MacLaren VV, Best LA. Multiple addictive behaviors in young adults: student norms for the shorter PROMIS questionnaire. Addict Behav. 2010;35:252-255. 45. Seegers JA. The Prevalence of Sexual Addiction Symptoms on the College Campus. Sex Addict Compulsivity. 2003;10:247-258. 46. Langstrom N, Hanson RK. High rates of sexual behavior in the general population: correlates and predictors. Arch Sex Behav. 2006;35(1):37-52. 47. Træen B, Spitznogle K, Beverfjord A. Attitudes and use of pornography in the Norwegian population 2002. J Sex Res. 2004;41:193–200. 48. Laumann EO, Gagnon JH, Michael RT, Michaels S. The social organization of sexuality: sexual practices in the United States. Chicago: University of Chicago Press. 1994. 49. Marshall L, Marshall W. Sexual addiction in incarcerated sexual offenders. Sex Addict Compulsivity. 2006;13:377-390. 50. Kafka MP, Prentky R. A comparative study of nonparaphilic sexual addictions and paraphilias in men. J Clin Psychiatry. 1992;53(10):345-350. 51. Carnes PJ. Sexual addiction and compulsion: recognition, treatment, and recovery. CNS Spectr. 2000;5(10):63-72. 52. Black DW. The epidemiology and phenomenology of compulsive sexual behavior. CNS Spectr. 2000;5(1):26-72. 53. Black DW, Kehrberg LL, Flumerfelt DL, Schlosser SS. Characteristics of 36 subjects reporting compulsive sexual behavior. Am J Psychiat. 1997;154(2): 243-249. 54. Gold SN, Heffner CL. Sexual addiction: many conceptions, minimal data. Clin Psychol Rev. 1998;18(3):367-381. 55. Kaplan MS, Krueger RB. Diagnosis, assessment, and treatment of hypersexuality. J Sex Res. 2010;47(2–3):181–198. 56. Sussman S. Sexual addiction among teens: A review. Sex Addict Compulsivity. 2007;14:257–278. 57. Bancroft J. Human Sexuality and Its Problems (3rd ed.). New York: Elsevier. 2009. 58. Semaille P. The new types of addiction. Rev Med Brux. 2009;30(4):335-357. 59. Samenow CP. Classifying problematic sexual behaviors—It’s all in the name. Sex Addict Compulsivity. 2010;17:3–6. 60. Carnes P. Don’t Call It Love. New York, NY: Bantam Books. 1991. 61. Reid RC. Assessing readiness to change among clients seeking help for hypersexual behavior. Sex Addict Compulsivity. 2007;14:167–186. 62. Reid RC, Carpenter BN, Spackman M, Willes DL. Alexithymia, emotional instability, and vulnerability to stress proneness in patients seeking help for hypersexual behavior. J Sex Marital Ther. 2008;34:133-149. 63. Raymond NC, Coleman E, Miner MH. Psychiatric comorbidity and compulsive/impulsive traits in compulsive sexual behavior. Compr Psychiat. 2003;44(5): 370-380. 64. Reid RC, Carpenter BN. Exploring relationships of psychopathology in hypersexual patients using the MMPI-2. J Sex Marital Ther. 2009;35(4):294-310. 65. Goodman A. Neurobiology of addiction. An integrative review. Biochem Pharmacol. 2008;75(1):266-322. 66. Carnes P, Murray R, Charpentier L. Bargains with chaos: Sex addicts and addiction interaction disorder. Sexual Addict Compulsivity. 2005;12:79–120. 68. Grant JE, Steinberg MA. Compulsive sexual behavior and pathological gambling. Sex Addict Compulsivity. 2005;12:235–244. 69. Goodman A. Diagnosis and treatment of sexual addiction. J Sex Marital Ther. 1993; 19(3): 225-251. 70. Coleman E, Raymond N, McBean A. Assessment and treatment of compulsive sexual behavior. Minn Med. 2003;86(7):42-47. 71. Coleman-Kennedy C, Pendley A. Assessment and diagnosis of sexual addiction. J Am Psychiat Nurses Assoc. 2002;8(5):143-151. 72. Kalichman SC, Rompa D. Sexual sensation seeking and sexual compulsivity scales: Reliability, validity, and predicting HIV risk behavior. J Personal Assess. 1995;65:586-601. 73. Kafka MP, Prentky RA. Compulsive sexual behavior characteristics. Am J Psychiat. 1997;154(11):1632. 74. Stein DJ. Classifying hypersexual disorders: compulsive, impulsive, and addictive models. Psychiatr Clin North Am. 2008;31(4): 587-591. 75. Bensley LS, Van Eenwyk J, Simmons KW. Self-reported childhood sexual and physical abuse and adult HIV-risk behaviors and heavy drinking. Am J Prev Med. 2000;18(2):151-158. 76. Shrier LA, Pierce JD, Emans SJ, DuRant RH. Gender differences in risk behaviors associated with forced or pressured sex. Arch Pediatr Adolesc Med. 1998; 152(1):57-63. 77. Earle R, Crow G. Lonely all the time: recognizing, understanding, and overcoming sexual addiction of addicts and co-dependents. New York: Pocket Books. 1998. 78. Mellody P. Facing love addiction: giving yourself the power to change the way you love. Harper: San Francisco. 1992. 79. Katehakis A. Affective neuroscience and the treatment of sexual addiction. Sex Addict Compulsivity. 2009;16:1-31.

194


80. Storholm ED, Fisher DG, Napper LE, Reynolds GL, Halkitis PN. Proposing a tentative cut point for the Compulsive Sexual Behavior Inventory. Arch Sex Behav. 2011;40(6):1301-1308. 81. Miner MH, Raymond N, Mueller BA, Lloyd M, Lim KO. Preliminary investigation of the impulsive and neuroanatomical characteristics of compulsive sexual behavior. Psychiat Res Neuroimaging. 2009;174:146–151. 82. Raymond NC, Coleman E, Miner MH. Psychiatric comorbidity and compulsive-impulsive traits in compulsive sexual behavior. Comp Psychiat. 2003; 44:370–380. 83. Yoder VC, Virden TB, Amin K. Internet pornography and loneliness: An association? Sex Addict Compulsivity. 2005;12:19–44. 84. Earle RH, Earle MR. Sexual addiction: Case studies and management. New York:Brunner/Mazel. 1995. 85. Zapf JL, Greiner J, Carroll J. Attachment styles and male sexual addiction. Sex Addict Compulsivity. 2008;15:158–175. 86. Kafka MP, & Hennen J. The paraphilia-related disorders: An empirical investigation of nonparaphilic hypersexuality disorders in outpatients males. J Sex Marital Ther. 1999;25:305–319. 87. Kingston DA, Firestone P. Problematic hypersexuality: A review of conceptualization and diagnosis. Sex Addict Compulsivity. 2008;15:284–310. 88. Kort J. Covert cultural sexual abuse of gay male teenagers contributing to etiology of sexual addiction. Sex Addict Compulsivity. 2004;11:287–300. 89. Reid RC, Harper JM, Anderson EH. Coping strategies used by hypersexual patients to defend against the painful effects of shame. Clin Psychol Psychotherapy. 2009;16:125–138. 90. Carnes P, Schneider JP. Recognition and management of addictive sexual disorders: guide for the primary care clinician. Lippincotts Prim Care Pract. 2000; 4(3):302-318. 91. Nakken C. The Addictive Personality: Understanding the Addictive Process and Compulsive Behavior, 2nd ed. Center City, MN: Hazelden. 1996. 92. Hamann S, Herman RA, Nolan CL, Wallen K. Men and women differ in amygdala response to visual sexual stimuli. Nat Neurosci. 2004;7(4):411-6. 93. Holstege G, Georgiadis JR, Paans AM, Meiners LC, van der Graaf FH, Reinders AA. Brain activation during human male ejaculation. J Neurosci. 2003;23(27): 9185-9193. 94. Georgiadis JR. Doing it... wild? On the role of the cerebral cortex in human sexual activity. Socioaffective Neurosci Psychol. 2012;2:17337. 95. Sescousse G, Redouté J, Dreher JC. The architecture of reward value coding in the human orbitofrontal cortex. J Neurosci. 2010;30:13095–13104. 96. Georgiadis JR, Farrell M, Boessen R, Denton D, Gavrilescu M, Kortekaas R, et al. Dynamic subcortical blood flow during male sexual activity with ecological validity: A perfusion fMRI study. Neuroimage. 2010;50:208-216. 97. Georgiadis JR, Reinders AA, Paans AM, Renken R, Kortekaas R. Men versus women on sexual brain function: Prominent differences during tactile genital stimulation, but not during orgasm. Human Brain Map. 2009;30:3089-3101. 98. Bostwick JM, Hecksel KA, Stevens SR, Bower JH, Ahlskog JE. Frequency of new-onset pathologic compulsive gambling or hypersexuality after drug treatment of idiopathic Parkinson Disease. Mayo Clin Proc. 2009;84(4):310–316. 99. Zietsch BP, Verweij KJH, Bailey JM, Wright MJ, Martin NG. Genetics and environmental influences on risky sexual behaviour and its relationship with personality. Behavior Gen. 2010;40(1):12–21. 100. Chen CS, Burton M, Greenberger E, Dmitrieva J. Population migration and the variation of dopamine D4 receptor (DRD4) allele frequencies around the globe. Evolut Hum Behav. 1999;20:309–324. 101. Ding Y, Chi H, Grady DL, Morishima A, Kidd JR, Kidd KK, et al. Evidence of positive selection acting at the human dopamine receptor D4 gene locus. PNAS. 2002;99:309–314. 102. Harpending H, Cochran G. In our genes. PNAS. 2002;99:10–12. 103. Wang E, Ding Y, Flodman P, Kidd JR, Kidd KK, Grady DL, et al. The genetic architecture of selection at the human dopamine receptor D4 (DRD4) gene locus. Am J Human Gen. 2004;74(5):931–944. 104. Congdon E, Lesch KP, Canli T. Analysis of DRD4 and DAT polymorphisms and behavioral inhibition in healthy adults: Implication for impulsivity. Am J Med Gen Part B: Neuropsychiatric Genetics. 2008;147B: 27–32. 105. Eisenberg DT A, Campbell B, MacKillop J, Modi M, Dang D, Lum JK. et al. Polymorphisms in the dopamine D4 and D2 receptor genes and reproductive and sexual behaviors. Evol Psychol. 2007;5(4):696–715. 106. Garcia JR, MacKillop J, Aller EL, Merriwether AM, Wilson DS, Lum JK. Associations between dopamine D4 receptor gene variation with both infidelity and sexual promiscuity. PLoS One. 2010;5(11). 107. Dawson GN, Warren DE. Evaluating and treating sexual addiction. Am Fam Physician. 2012;86(1):74-76. 108. Wainberg M, Muenc F, Morgenstern J, Hollander E, Irwin T, Parsons J, et al. A double-blind study of citalopram versus placebo in the treatment of compulsive sexual behaviors in gay and bisexual men. J Clin Psychiat. 2006;67(12):1968–1973. 109. Tosto G, Talarico G, Lenzi GL, Bruno G. Effect of citalopram in treating hypersexuality in an Alzheimer’s disease case. Neurol Sci. 2008;29:269–270. 110. Kafka MP, Prentky R. Fluoxetine treatment of nonparaphilic sexual addictions and paraphilias in men. J Clin Psychiat. 1992;53(10):351-358. 111. Stein DJ, Hollander E, Anthony DT, Schneier FR, Fallon BA, Liebowitz MR, et al. Serotonergic medications for sexual obsessions, sexual addictions, and paraphilias. J Clin Psychiat. 1992; 53(8):267-271. 112. Bostwick JM, Bucci JA. Internet sexual addiction treated with naltrexone. Mayo Clin Proc. 2008;83(2):226-230. 113. Khazaal Y, Zullino DF. Topiramate in the treatment of compulsive sexual behavior: case report. BMC Psychiat. 2006;6:22. 114. Raymond NC, Grant JE, Coleman E. Augmentation with naltrexone to treat compulsive sexual behavior: A case series. Ann Clin Psychiat. 2010;22(1):56–62. 115. Carroll KM, Onken LS. Behavioral therapies for drug abuse. Am J Psychiat. 2005;162(8):1452-1460.

195


116. Orzack MH, Voluse AC, Wolf D, Hennen J. An ongoing study of group treatment for men involved in problematic Internet-enabled sexual behavior. Cyberpsychol Behav. 2006; 9(3): 348-360. 117. Young KS. Cognitive behavior therapy with Internet addicts: treatment outcomes and implications. Cyberpsychol Behav. 2007;10(5):671-679. 118. DeVito EE, Worhunsky PD, Carroll KM, Rounsaville BJ, Kober H, Potenza MN. A preliminary study of the neural effects of behavioral therapy for substance use disorders. Drug Alc Depen. 2012;122(3):228-235. 119. Southern S. Treatment of compulsive cybersex behavior. Psychiatr Clin North Am. 2008;31(4):697-712. 120. Carnes PJ. Sexual Addiction: Chapter 18.4. In Sadock S. (Ed.) “Comprehensive Textbook of Psychiatry” Vol. 1. Lippincott, Williams & Wilkins: Philadelphia, PA. 2005. 121. Kor A, Fogel YA, Reid RC, Potenza MN. Should Hypersexual Disorder be Classified as an Addiction? Sex Addict Compulsivity. 2013;20:27–47.

196


L003335

Multiple-Choice Questions 49. According to the lesson, all of the following statements regarding sexual addiction or hypersexual disorder are true, except: A. Sexual addiction, or hypersexual disorder, is often associated with risk-taking behavior and psychosocial problems. B. The proposed diagnosis of hypersexual disorder requires the presence of dependence, tolerance, and withdrawal. C. Hypersexual disorder has been associated with compulsivity, impulsivity, emotional dysregulation, and stress proneness. D. Hypersexual disorder is repetitively engaging in sexual fantasies, urges, and behavior in response to dysphoric mood states (e.g., anxiety, depression, boredom, irritability).

50. Which of the following psychiatric disorders has not been frequently described as related to hypersexual disorder? A. Depression B. Anxiety C. Attention and hyperactivity disorder D. Schizophrenia

51. Hypersexual disorder has been shown to be related to all of the following, except: A. increased activity of the dopamine reward areas to visual sexual stimuli. B. increased impulsivity and risk-taking behavior. C. shared comorbidity with pathological gambling. D. there is higher prevalence of hypersexual disorder in women than men.

52. Which of the following medications has not been shown to be useful in treatment for hypersexual disorder? A. Escitalopram, a selective serotonin reuptake inhibitor B. Naltrexone, an opiate antagonist C. Topiramate, an anticonvulsant medication D. Risperidol, an antipsychotic 197

Best Practices in CME Sexual Addiction or Hypersexual Disorder: Clinical Implications for Assessment and Treatment By Aviv Weinstein, PhD

ID#: L003335

This valuable take-home reference translates evidence-based, continuing medical education research and theory acquired from reading the associated CME lesson into a stepwise approach that reviews key learning points for easy assimilation into your armamentarium of knowledge and daily practice.

CME Lesson Overview Clinicians will review recent evidence for the assessment, the psychobiological basis, and treatment of sexual addiction, including diagnosis, comorbidity with other psychiatric disorders, and treatment studies.

Key Point 1: Diagnosis Diagnose the disorder using valid instruments.

Key Point 2: Assessment Assess psychiatric comorbidity using psychiatric questionnaires.

Key Point 3: Identify Circumstances

Key Point 4: Identify Physical and Social Effects Assess physical and cognitive effects of the disorder using health questionnaires.

Key Point 5: Treatment Discuss psychological and pharmacological treatments such as CBT and SSRIs.

Identify social, behavioral, and emotional circumstances.


Notes

L903336

Confidentiality Protections Versus Collaborative Care in the Treatment of Substance Use Disorders Jennifer K. Manuel, PhD; Howard Newville, PhD; Sandra E. Larios, PhD, MPH; and James L. Sorensen, PhD No commercial support was used in the development of this CME lesson.

KEY WORDS: Electronic Health Records • Substance Use Disorders Treatment • Patient Confidentiality LEARNING OBJECTIVES: Clinicians will review the current policies regarding patient confidentiality issues and substance use disorder (SUD) treatment. Readers will consider how to protect their patients in this era of collaborative care while maintaining rapid communication among healthcare providers. As this lesson discusses substance use disorders, the implications can be considered among other medical conditions.

LESSON ABSTRACT: Practitioners in federally-assisted substance use disorder (SUD) treatment programs are faced with increasingly complex decisions when addressing patient confidentiality issues. Recent policy changes, intended to make treatment more available and accessible, are having an impact on delivery of SUD treatment in the United States. The addition of electronic health records provides opportunity for more rapid and comprehensive communication between patients’ primary and SUD care providers while promoting a collaborative care environment. This shift toward collaborative care is complicated by the special protections that SUD documentation receives in SUD treatment programs, which vary depending on what care is provided and the setting where the patient is treated. This lesson explores the special protections for substance abuse documentation, discrepancies in treatment documentation, ways to deal with these issues in clinical practice, and the need for more knowledge about how to harmonize treatment in the SUD and primary care systems.

COMPETENCY AREAS: This lesson addresses the issue of ethical decision making for clinicians working in substance use disorder treatment programs. With the recent changes in policies that make substance use disorder treatment more available and the rise in the use of electronic health records to facilitate collaboration, clinicians often face questions regarding the protections for substance use disorder documentation, the involvement of the legal system, and the involvement of other parties in the treatment program. Upon completion of this lesson, readers will have a better understanding of the recent policy changes regarding substance use disorder treatment and will provide clinicians with a better understanding of ethical practice regarding collaboration and consultation.

201

L903336 : Confidentiality Protections Versus Collaborative Care in the Treatment of Substance Use Disorders

Introduction Increasingly, substance use assessment and treatment is occurring in health care settings such as primary care clinics, emergency departments, and trauma units. Furthermore, many health care settings have adopted or plan to adopt the use of electronic health records (EHRs), a change that can facilitate the integration of substance use disorder (SUD) treatment with other forms of health care. Thus, the landscape of SUD treatment has shifted in recent years. At the same time, current regulations for SUD treatment confidentiality have not been updated, despite the number of changes in how and where SUD is delivered. In this paper, the authors provide a summary of recent legislative and policy changes, the reasons for confidentiality protections, review the degree that substance abuse treatment documentation is protected in different environments, and suggest several directions for maintaining confidentiality while promoting coordination of care.

The Advance of Electronic Health Records Systems: The American Recovery and Reinvestment Act of 2009 (ARRA), also known as the “economic stimulus package,” provided $19.2 billion for the modernization of electronic health records.1 The Health Information Technology for Economic and Clinical Health (HITECH Act), contained within the ARRA, also codified into law an executive order by President Bush from 2004 that created the Office of the National Coordinator for Health Information Technology (ONC) as part of the Department of Health and Human Services, which is charged with ensuring that all patients have a certified electronic health record by 2014. In addition, health care providers and hospitals who adopt a “meaningful” use of EHR will be eligible for incentive payments.2 During this period of reform the Substance Abuse Mental Health Services Administration (SAMHSA), the agency of the Department of Health and Human Services (DHHS) responsible for the prevention and treatment of substance use disorders, has provided support for the coordination and integration of SUD treatment and healthcare. SAMHSA lists as core consensus principles in health reform to “eradicate fragmentation by requiring coordination and integration of care for physical, 202

mental, and substance use conditions” and “adopt and fully utilize health information technology.”3p4 In sum, these legislative and policy developments will increase accessibility to behavioral health services and facilitate the coordination of care for patients in health care settings with the goal of improving care for patients in the United States. Given the under-detection and under-treatment of SUDs, coordinated care environments, such as practitioners in health care settings who screen for and treat individuals who are engaging in risky or problematic substance use, can increase the detection and treatment of SUDs among patients who may not otherwise present for specialty SUD treatment.4

Why Confidentiality Laws? 42 CFR Part 2 The federal regulations, 42 CFR Part

2,5,6 were developed during a time of independent SUD treatment programs, to increase treatment engagement and reduce the discrimination associated with SUD treatment. The regulations have since been updated but their purpose has remained intact: to prevent law enforcement from using substance abuse treatment patient records as a means of arresting patients.7 Congress, wishing to make substance abuse treatment more accessible stated, “The conferees wish to stress their conviction that the strictest adherence to. . . [confidentiality] is absolutely essential to the success of all drug abuse prevention programs. Every patient and former patient must be assured that his right to privacy will be protected. Without that assurance, fear of public disclosure of drug abuse or of records that will attach for life will discourage thousands from seeking the treatment they must have if this tragic national problem is to be overcome.”8p33 42 CFR Part 25,6 applies confidentiality regulations to federally-assisted SUD programs, defined as an individual, entity, or unit within a general medical facility who offers or provides substance use diagnosis, treatment or referral to treatment or medical staff in a general medical care setting “whose primary function is the provision of alcohol or drug abuse diagnosis, treatment or referral for treatment.”6; 2.11 To be consistent with the 42 CFR Part 2 language, substance use providers and settings, who meet the above criteria, will be referred to as “SUD programs” throughout our discussions of privacy laws in SUD care. “Patient” refers to “any individual who has applied for or been given diagnosis or


treatment for alcohol or drug abuse at a federally assisted program and includes any individual who, after arrest on a criminal charge, is identified as an alcohol or drug abuser in order to determine that individual’s eligibility to participate in a program.”6; 2.11 42 CFR Part 2 stipulates that the “records of the identity, diagnosis, prognosis, or treatment of any patient which are maintained in connection with the performance of any drug abuse prevention function conducted, regulated, or directly or indirectly assisted by any department or agency of the United States” 6; 2.1 may not be disclosed to others unless the patient gives prior written consent for the release of his/ her information. Thus, programs meeting the 42 CFR Part 2 criteria may not share any information relating to the patient without specific patient consent. Patient consent is required for each disclosure (no blanket waivers of consent are permitted), and re-disclosure is forbidden unless a provider receives patient consent. While the general rule is no disclosure without patient consent, the confidentiality regulations have boundaries. Disclosures to medical personnel are allowed without specific patient authorization for medical emergencies if there is an immediate threat; however this information must be documented in the patient’s records. Suspected child abuse or neglect may be reported, but restrictions still apply to the original patient records of the SUD program; in other words a report is allowed but disclosure that the patient is in a SUD program is not permitted. With the patient’s consent disclosure is authorized to a qualified service organization (QSO): This is an organization that has a written agreement (Qualified Service Organization Agreement or “QSOA”) with the SUD treatment program, stating that the QSO will be governed by the confidentiality regulations, with no disclosure without consent, and will resist judicial efforts to obtain patient records. In recent years (2010–2011) SAMSHA set forth two sets of Frequently Asked Questions (FAQs) to further clarify how the existing legislation is applicable with the current technological advances. “Applying the Substance Abuse Confidentiality Regulations to Health Information Exchange” and “Applying the Substance Abuse Confidentiality Regulations 42 CFR Part 2” describe a variety of issues including the limitations of consent, the role of HIPPA, and the relationship between 42 CFR part 2 and state laws.9 These FAQs are intended

to clarify the 42 CFR Part 2 guidelines, however many questions remain about how to interpret the guidelines in coordinated care environments and in the context of an ever-changing digital era. Furthermore, while there has been considerable improvement in the technology for documenting treatment and the integration of SUD treatment with medical care, our current privacy laws regarding substances use disorders remain largely unchanged.

HIPAA Regulations: As years passed, additional legislation was adopted to further ensure patient privacy. In 1996, the United States Congress passed the Health Information Portability and Accountability Act (HIPAA), which contains a privacy rule that restricts the spread of Protected Health Information (PHI). HIPAA regulates PHI held by “covered entities,” such as health plans, health care clearinghouses, and health care providers. HIPAA was written for direct transfers of electronic information between providers, rather than networks streamlining information.10 Some view HIPAA as restricting the necessary transfer of data and needing improvements to facilitate smoother communication10-12 whereas others suggest that the HIPAA Privacy Rule should be augmented with new federal regulations.13 Modifications have been proposed to address some of the privacy issues with 42 CFR Part 2 and HIPAA. For example, the Patient Protection Coalition, a group aiming to reform 42 CFR Part 2, has suggested permitting disclosures of demographic information, diagnosis, medications, laboratory results, and current and past treatment providers to ensure patient safety. Additionally, they support enhancing patient protections regarding discrimination based on having received SUD treatment and strengthening legal ramifications for unauthorized disclosures of information.14 Federal privacy laws are further complicated with the advent of electronic medical records.15 Federal privacy laws were written before the development of electronic medical records, when all records were kept in paper form, rendering some parts of these laws obsolete and other parts in opposition to the electronic changeover.16 Various groups insist on maintaining the strict protections in 42 CFR Part 217 whereas others argue for a reform of the current confidentiality protections.18 203


Integration of SUD Treatment and Healthcare: Increasingly, substance use treatment services are being offered in health care settings at the urging of groups such as the Institute of Medicine.19 This shift reflects the realization that many individuals drinking or using drugs at risky levels will present for care in mainstream health care settings rather than specialty SUD programs. These patients may be in need of SUD treatment but may be unwilling or unable to seek specialty substance use care. Integrating “medically harmful substance use” information into EHRs can improve patient safety and provide better care to patients.20 Efforts, such as the Screening and Brief Intervention and Referral to Treatment initiative funded by SAHMSA, encourage the assessment and treatment of substance use disorders in healthcare settings21 and have been successful in reducing patients’ alcohol and drug use.22 The integration of SUD treatment and healthcare settings can be an effective way of assessing and treating patients who may not have pursued specialty SUD care and in providing a greater continuity of care for those patients who are receiving specialty SUD treatment. However, combining these services is complicated, in part due to the greater protections offered to patients in certain settings with substance use disorders. When general health care providers assess for and provide a brief intervention in a general health care setting, the documentation of the pertinent substance use information does not fall under the SUD confidentiality regulations.23 However, if a patient in a federally-funded healthcare setting is seen or treated by a specialty substance abuse provider whose primary job responsibility is to assess for and treat substance use patients, this patient-provider information does merit protection under the 42 CFR Part 2 confidentiality regulations. At this point, providers must document only essential information within the medical record. As Miller et al.23 note, “The problem here is determining what is essential for primary care providers to know. Primary care providers themselves may argue that they need to know everything in order to provide the best care to the patient.”p.294 There is ambiguity about the documentation of integrated substance abuse information in healthcare settings, with no uniform method of recording this material. For instance, when SUD treatment services 204

were implemented into a university associated primary care clinic in New Mexico, Ernst, Miller, and Rollnick24 reported on the lack of clarity regarding confidential protections in a primary care setting. After seeking legal counsel, the authors decided to adhere to the regulations because “the services were specific to substance abuse, and psychotherapy was provided to some patients”24p3 The integration of SUD treatment and health care raises questions about what integration means for SUD documentation in health care settings. Integration also highlights possibly discordant regulations regarding the treatment of SUDs in substance use and health care settings. If the SUD confidentiality regulations do not apply to a general medical doctor prescribing naltrexone in a primary care setting or talking to a patient about the risks of drinking while pregnant what is the rationale for the discrepancy in protections? In Table 1 we highlight the discrepancy between the documentation of SUD information by SUD in federally assisted SUD-focused programs versus general medical providers in non-SUD settings.

Confidentiality Protections in Current Practice: Practitioners ask as we move toward an era where medications are increasingly being prescribed for SUD, are the current protections potentially harmful to patients? Providers of patients who are prescribed naltrexone, buprenorphine, or methadone may need this information in order to accurately treat their patients. While the 42 CFR Part 2 guidelines indicate that patient information may be disclosed in medical emergency situations, preventing a potentially fatal drug interaction does not necessitate a disclosure if there is not an immediate medical emergency.25 A study by Walley et al.26 found that 59% of the opioid patients on methadone maintenance therapy (MMT) were also prescribed medications with a potentially harmful interaction with their MMT. In fact, 19% of the patients were prescribed three or more medications that could potentially interact with MMT. Currently, the patient must serve as the intermediary between their SUD and healthcare providers or sign an authorization of release of information for each of their particular providers. As a result “failure to share patient-specific information across providers promotes uncoordinated and sometimes unsafe care.”27, p716


Table 1: SUD Documentation in Specialty and General Medical Setting Specialty SUD Provider in Federally-assisted SUD Program

Documentation and Explanation

• Patient schedules an appointment with a SUD clinic because he is concerned about his alcohol use.

The SUD counselor documents the details of the patient’s visit in the SUD clinic notes. These notes are protected by 42 CFR • Patient completes a brief assessment interview and then meets with Part 2 and are therefore not accessible to others outside the program (in particular the patient’s primary care provider), his counselor. without a specific release of information from the patient • Patient and his counselor discuss the patient’s goals for treatment, unless there is a qualifying medical emergency or an established and patient is encouraged to attend weekly SUD sessions. Patient is not QSOA exists. actively withdrawing from alcohol, so counselor decides that patient does not to attend a detoxification center. • Patient asks if there are medications to help him deal with cravings, but counselor indicates he does not have prescription privileges. Patient is encouraged to ask his primary care provider about the use of naltrexone. Medical Provider in Emergency Room

Documentation

• Patient is asked about his alcohol and drug use as part of a visit to an emergency room for a traumatic injury. Patient indicates his injury occurred while intoxicated and voices concern about drinking.

Provider documents the details of the patient’s visit, including the patient’s SUD diagnosis and history of drinking. This information is not protected by 42 CFR Part 2 because the provider’s primary function did not include the provision of substance use services nor did the interaction take place in an identified substance-focused unit.

• Provider (general medical provider) assesses substance use history and diagnoses the Patient with alcohol dependence.

Nonetheless, in a recent national survey, adults have expressed some concerns about the potential for shared health information. In this survey, 42% of participants indicated that they would feel uncomfortable if their private health information was shared with other organizations, even if any identifying information was excluded. Furthermore, 15% of participants reported that they would hide information and 33% indicated that they may hide information from their doctor if he/she shared information through an HER.28 Patients with substance use disorders or risky substance use may be more likely to hide substance use information out of privacy concerns and fears of stigmatization.

Solving a Clinical Conundrum: Maintaining Confidentiality in a Coordinated Care Environment: In 2010 an article in Alcoholism &Drug Abuse Weekly7 asked, “Can electronic medical records and patient confidentiality coexist?” The answer appears to be “Yes, but they need to be harmonized.” People involved in this tuning process will include legislators, judges, attorneys, and insurance adjusters, but a major place where these issues will be acted out is in human service programs treating people with SUD. With that in mind, we provide some

suggested actions that staff in SUD treatment programs can take to cope with these controversies.

Keep Context in Mind For all providers and other healthcare personnel, it is vital to understand the reasons why the confidentiality laws exist and also why the context is changing. Gaining an understanding in the principles, laws, and guidelines is important. Then when the question arises about protection of confidentiality, ethical principles such as respect for persons, autonomy, justice, beneficence, and non-maleficence can be part of the decision-making process.29 The federal confidentiality statutes need to be followed, as well as various guidelines from legislation like HIPAA and applicable state and municipal regulations. Guidelines are available from several valuable resources. CSAT/SAMHSA has developed over 50 written Treatment Improvement Protocols. These are available online at http://www.ncbi.nlm.nih.gov/books/ NBK14119/ and were written for staff in a wide variety of SUD treatment programs. CSAT has also published a number of Technical Assistance Publications (TAPS), including TAP 13, Confidentiality of patient records for 205


alcohol and drug treatment.30 TIP 40, Clinical guidelines for the use of buprenorphine in the treatment of opioid addiction,

has specific information on the confidentiality requirements for physicians who are providing office-based opioid addiction treatment. The TIP also includes a sample consent form to release information protected by 42 CFR Part 2.31 Additionally the Legal Action Center (LAC) can be an excellent resource, available online at http://www. lac.org/. LAC is a non-profit law and policy organization that seeks to fight discrimination against individuals with addictions, HIV/AIDS or criminal records. They provide on-line courses available both in basic and advanced issues concerning confidentiality, as well as brochures, sample forms for physicians and treatment programs, and policy analyses, including a paper on confidentiality of alcohol and drug records in the 21st Century.

Consider State Laws State laws may institute additional protections on patients’ privacy, so it is important to remain informed about state confidential protections. While states may require additional protections, they may not authorize a program to disclose information that is protected by 42 CFR Part 2. Thus, state laws may provide additional protections but they may not undermine the federal protections.

Seek Guidance When a provider approaches an uncomfortable situation it is wise to seek guidance. Counselors, peers, clinical supervisors, physicians, and licensed professionals at the SUD treatment program are essential for support, and professional associations can be helpful. For example the NAADAC, the National Association for Addiction Professionals (http://www.naadac.org/), offers webinar trainings, one of which is Compliance with Ethical Standards for Drug, Alcohol and Addictions Counselors. We stress that the specific guidelines may be changing constantly as new information emerges. For example, earlier in this paper we mentioned that in July 2010 CSAT released a “Frequently Asked Questions” paper (http://www.samhsa.gov/HealthPrivacy/docs /EHRFAQs.pdf). The paper was initially drafted by the LAC. Enos32 documents the many points of controversy about this document, and a month later SAMHSA sponsored a stakeholders meeting to air different viewpoints and clarify the “FAQs.” We also emphasize the importance of 206

seeking legal guidance, which is a vital step in situations where rules may be changing, and new legal precedents may be emerging. A treatment counselor is likely to need both clear and authoritative guidance from a legal professional.

Implement At the clinic level, update guidelines for your patients, staff, and referral sources, and if guidelines do not exist, it may be wise to develop them. Examples of such guidelines are available from the CSAT TIPS and TAPS mentioned above, or they may be available locally or through the single state agency that is responsible for SUD treatment.

Seek Feedback Obtaining feedback from those affected is an obvious suggestion, but feedback often happens only when something has gone wrong. Encourage quality assurance studies to understand what is working and why. Encourage research to understand how serious specific issues are in your setting. As an example of the utility of research, Salomon et al.33 surveyed psychiatric clinicians who had recently switched to an electronic health record system and found the majority opinion was that open therapeutic communications were not interfered with. On the other hand, once they were using the electronic health record system the majority was less willing to record highly confidential information. In short, the clinicians indicated that the system worked but they were more cautious than before about recording sensitive information.

Keep Learning At the individual level, keep up to date as guidelines change. A 2009 CSAT TIP entitled Clinical Supervision and Professional Development of the Substance Abuse Counselor may be helpful (TIP 52).21 At the program and

system levels attend to the needs for training among those in your system. In addition, as the ethical standards continue to evolve in substance abuse treatment, it is essential that providers remain up to date on the latest ethical guidelines.

Conclusions This [lesson] explored protecting confidentiality in SUD treatment programs in the light of changes that have occurred recently in the policies and regulations.


Legislation has been enacted to make SUD treatment more affordable and accessible to patients in need. Treatments are increasingly being offered in health care settings such as primary care clinics, emergency, and trauma units. Technological development has fostered the development and proliferation electronic health records rather than paper charts. In this context we acknowledge the difficulty of maintaining patient confidentiality versus sharing vital information with providers in a collaborative care setting. In this paper the authors provide a summary of recent legislative and policy changes, the reasons for confidentiality protections, review the degree that substance abuse documentation is protected in different environments, and suggest several directions for maintaining confidentiality while promoting coordination of care. The field of substance abuse treatment has changed drastically since the time when the privacy laws were first developed. SUD treatment is more widely available, provided by a broad range of health care providers, and is often treated by medications. The integration of SUD care has reached patients who may not have otherwise sought treatment. Our paper provides guidance and advice to staff in SUD treatment programs regarding how to negotiate confidentiality issues in treatment programs. The issues are changing, and the ethical principles of good health care and professional practice will be increasingly relevant in this time when the field is undergoing significant change in its clientele, location of services, and its technology. Until the field stabilizes again it will be the helping professionals in the human service settings who make the most important decisions about what is best for their clientele.

This analysis is limited by several factors that can be informed through further research. There is a need for clear ethical analyses that explore the advantages and drawbacks of topics such as protecting patient confidentiality versus promoting integrated care. It would be helpful to understand more about the extent of stigmatization of SUD and whether, over time the stigma has diminished or increased. This information can inform guidance about the extent to which confidentiality protections are needed by those receiving treatment for SUD. Additional research needs to provide information about what are the most frequently occurring and most troubling ethical confidentiality and privacy issues facing various actors in SUD treatment and prevention. In addition we need to know how these issues are being resolved in the field. Further there is a need for concerted organizational attention to resolve an increasingly acrimonious debate about the need to keep versus revise the federal confidentiality regulations that will soon have been enacted fully 50 years ago. Our current confidentiality regulations for SUD treatment have not been updated, despite the number of changes in location and context of care programs. It may be that federal confidentiality guidelines will be rewritten to reflect the changing times, or like the U.S. Constitution, the field may look to these as enduring adages that need to be interpreted to provide more clear guidance to a rapidly evolving field. In either case, there is a need for the national action to enact administrative mechanisms that will air the many facets of the issue and then come to a resolution. With clarity at the federal level the state and local agencies will be able to attune their regulations and guidelines so that a national approach to these issues can develop.

About the Faculty Jennifer K. Manuel, PhD: Dr. Manuel is a Postdoctoral Fellow, San Francisco General Hospital Department of Psychiatry, University of California, San Francisco. Howard Newville, PhD: Dr. Newville is a research scientist at St. Luke’s-Roosevelt Hospital, Behavioral Science Research Unit, New York, NY; and a Postdoctoral Fellow, San Francisco General Hospital Department of Psychiatry, University of California, San Francisco. Sandra E. Larios, PhD, MPH: Dr. Larios is a Postdoctoral Fellow, San Francisco General Hospital Department of Psychiatry, University of California, San Francisco. James L. Sorensen, PhD: Dr. Sorensen is Professor, Department of Psychiatry, University of San Francisco, San Francisco.

207


References 1.

Steinbrook R. Health care and the American Recovery and Reinvestment Act. N Engl J Med. 2009;360:1057–1106. doi: 10.1056/ NEJMp0900665.

2.

Department of Health and Human Services. EHR Incentives and Certification: How to Attain Meaningful Use. Accessed from http://www.healthit.gov/providers-professionals/ how-attain-meaningful-use.

3.

Hutchings GP, King K. Ensuring U.S. Health Reform Includes Prevention and Treatment of Mental and Substance Use Disorders – A Framework for Discussion: Core Consensus Principles for Reform from the Mental Health and Substance Abuse Community. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2009.

4.

Tai B, Wu W, Clark HW. Electronic health records: essential tools in integrating substance abuse treatment with primary care. Substance Abuse and Rehabilitation. 2012;3:1–8.

5.

US Department of Health Education and Welfare. Confidentiality of alcohol and drug use patient records - PHS. Final rule of Fed Register. 1987;52(110):21796–21814.

6.

US Department of Health and Human Services. Confidentiality of alcohol and drug use patient records. Fed Register. 1975;40(91):20522–20542.

7.

Author. Can electronic medical records and patient confidentiality coexist? Alcoholism & Drug Abuse Weekly. 2010;22(4):1–3.

8.

H.R. Rep. No. 92_920, 92d Cong., 2d Sess., p. 33. U.S. Code Cong. & Admin. News; 1972. p. 2072.

9.

Substance Abuse Mental Health Service Agency. Applying the Substance Abuse Confidentiality Regulations 42 CFR Part 2. 2011. Downloaded from http://www. integration.samhsa.gov/operations-administration/confidentiality on May 9, 2013.

10. Greenberg MD, Ridgely MS, Hillestad RJ. Crossed wires: How yesterday’s privacy rules might undercut tomorrow’s nationwide health information network. Heal Aff. 2009;28:450–452. doi: 10.1377/hlthaff.28.2.450. 11. Gostin LO, Nass S. Reforming the HIPAA privacy rule. JAMA. 2009;301:1373–1375. doi: 10.1001/jama.2009.424. 12. McGraw D, Dempsey JX, Harris L, Goldman J. Privacy as an enabler, not an impediment: Building trust into health information exchange. Heal Aff. 2009;28:416–427. doi: 10.1377/hlthaff.28.2.416. 13. McDonald C. Protecting patients in health information exchange: A defense of the HIPAA Privacy Rule. Heal Aff. 2009;28:447–449. doi: 10.1377/hlthaff.28.2.447. 14. Patient Protection Coalition. A proposal to promote coordination of care and to strengthen patient protections under the federal alcohol and drug abuse confidentiality law. 2010. Available at http://www.law.virginia.edu/pdf/faculty/bonnie_patientprotection.pdf, accessed (December 18, 2012) 15. McCarty D, McConnell KJ, Schmidt LA. Priorities for policy research on treatments for alcohol and drug use disorders. J Subst Abus Treat. 2010;39(2):87–95. doi: 10.1016/j.jsat.2010.05.003. 16. Connors B, Leipold J. The 42 CFR Part 2 and NHIN Conundrum. Behavioral Healthcare. 2009;29(7):52–53. 17. Legal Action Center. Confidentiality of alcohol and drug records in the 21st century. 2010. Available at http://www.lac.org/doc_library/lac/publications/Confidentiality_ of_Alcohol_and_Drug_Records_in_the_21st_Century-1-20-10.pdf, Accessed on December 18, 2012. 18. Popovits, R.M. Confidentiality law: time for change? Behavioral Healthcare. 2010. Accessed http://www.behavioral.net/article/ confidentiality-law-time-change December 19, 2012. 19. Donaldson MS, Yordy KD, Lohr KN, Vanselow NA, Institute of Medicine, Committee on the Future of Primary Care. Primary Care: America’s Health in a New Era Washington. DC: Institute of Medicine; 1996. Available at http://www.nap.edu/readingroom/ books/primary/summary.html, accessed (December 18, 2012) 20. Tai B, McLellan AT. Integrating information on substance use disorders into electronic health record systems. J Subst Abus Treat. 2012;43(1):12–19. doi: 10.1016/j. jsat.2011.10.010. 21. Center for Substance Abuse Treatment. Clinical Supervision and Professional Development of the Substance Abuse Counselor. Treatment Improvement Protocol (TIP) Series 52. DHHS Publication No. (SMA) 09–4435. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2009. 22. Madras BK, Compton WM, Avula D, Stegbauer T, Stein JB, Clark HW. Screening, brief interventions, referral to treatment (SBIRT) for illicit drug and alcohol use at multiple healthcare sites: Comparison at intake and six months. Drug Alcohol Depend. 2009;99(1–3):280–295. 23. Miller WR, Baca C, Compton WM, Ernst DE, Manuel JK, Pringle B, Schermer CR, Weiss RD, Willenbring ML, Zweben A. Addressing substance abuse in health care settings. Alcoholism: Clinical and Experimental Resarch. 2006;30(2):292–302. doi: 10.1111/j.1530-0277.2006.00027.x. 24. Ernst D, Miller WR, Rollnick S. Treating substance abuse in primary care: a demonstration project. Int J Integrated Care. 2007;7(10):1–8. 25. Substance Abuse Mental Health Service Agency. Applying the Substance Abuse Confidentiality Regulations to Health Information Exchange. 2010. Downloaded from http://www.integration.samhsa.gov/operations-administration/confidentiality on May 9, 2013. 26. Walley AY, Alperen JK, Cheng DM, Botticelli M, Castro-Donlan C, Samet JH, Alford DP. Office-based management of opioid dependence with buprenorphine: Clinical practices and barriers. J Gen Intern Med. 2008;23:1393–1398. doi: 10.1007/s11606-008-0686-x. 27. Pincus HA, Page AE, Druss B, Appelbaum PS, Gottlieb G, England M. Can psychiatry cross the quality chasm? Improving the quality of health care for mental and substance use conditions. Am J Psychiatry. 2007;164(5):712–719. doi: 10.1176/appi.ajp.164.5.712. 28. Undem T. Consumers and health information technology: A national survey. 2010. Accessed http://www.chcf.org/~/media/MEDIA%20LIBRARY%20Files/PDF/C/ PDF%20ConsumersHealthInfoTechnologyNationalSurvey.pdf on December 18, 2012. 29. King TE, Jr, Wheeler MB. Medical management of underserved patients: Principles, practice, and populations. New York: McGraw-Hill; 2007. 30. Center for Substance Abuse Treatment. Confidentiality of patient records for alcohol and other drug programs. Technical Assistance Protocol (TAP) Series 16. NCADI Inventory Number BKD156. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2006.

209


31. Center for Substance Abuse Treatment. Clinical guidelines for the use of buprenorphine in the treatment of opioid addiction. Treatment Improvement Protocol (TIP) Series 40. DHHS Publication No. (SMA) 04–3939. Rockville, MD: Substance Abuse and Mental Health Services Administration; 2004. 32. Enos G. SAMHSA document on confidentiality regulations raises further questions. 2010. Available at http://www.jointogether.org/news/ features/2010/samhsadocument-on.html, accessed March 8, 2011. 33. Salomon RM, Blackford JU, Rosenbloom ST, Seidel S, Clayton EW, Dilts DM, Finder SG. Openness of patients’ reporting with use of electronic records: Psychiatric clinicians’ views. JAmerican Med Inf Assoc. 2009;17:54–60

Hatherleigh’s Note: Additional typeface treatment was added to text for emphasis along with title page information, CME, and Best Practices which were not part of the original article. Competing interests The authors declare that they have no competing interests. Authors’ contributions JKM drafted Confidentiality protections in current practice, Integration of SUD treatment and healthcare, and edited the manuscript. Together, JKM and SEL drafted Table 1. HN drafted parts of The advance of electronic health records, Why confidentiality laws and HIPAA regulations. SEL drafted parts of The advance of electronic health records, Why confidentiality laws and HIPAA regulations. JLS drafted Why Confidentiality Laws, Solving a clinical conundrum and Conclusions and edited the manuscript. All authors read and approved the final manuscript. Acknowledgements Supported in part by NIH/NIDA and NIH/NIMH Grants P50DA09253 (PI=Joseph Guydish; joseph.guydish@ ucsf.edu), U10DA015815 (PI=James Sorensen; [email protected]), R01DA020781 (PI=Carmen Masson; [email protected]), R21DA020369 (PI=James Sorensen), T32DA07250 (PI=James Sorensen), T32MH018261 (PI Patricia Arean; patricia. [email protected]), F32DA0324465 (PI=Howard Newville; [email protected]) and the Robert Wood Johnson Foundation (Dr. Sorensen). The authors acknowledge and support the above funding sources we recognize that the views presented in this manuscript are that of the authors and not of the funding sources. Authors’ contributions JKM drafted Confidentiality protections in current practice, Integration of SUD treatment and healthcare, and edited the manuscript. Together, JKM and SEL drafted Table 1. HN drafted parts of The advance of electronic health records, Why confidentiality laws and HIPAA regulations. SEL drafted parts of The advance of electronic health records, Why confidentiality laws and HIPAA regulations. JLS drafted Why Confidentiality Laws, Solving a clinical conundrum and Conclusions and edited the manuscript. All authors read and approved the final manuscript. Acknowledgements Supported in part by NIH/NIDA and NIH/NIMH Grants P50DA09253 (PI=Joseph Guydish; joseph.guydish @ucsf.edu), U10DA015815 (PI=James Sorensen; [email protected]), R01DA020781 (PI=Carmen Masson; [email protected]), R21DA020369 (PI=James Sorensen), T32DA07250 (PI=James Sorensen), T32MH018261 (PI Patricia Arean; patricia. [email protected]), F32DA0324465 (PI=Howard Newville; [email protected]) and the Robert Wood Johnson Foundation (Dr. Sorensen). The authors acknowledge and support the above funding sources we recognize that the views presented in this manuscript are that of the authors and not of the funding sources. Copyright © 2013 Manuel et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

210


L903336

Multiple-Choice Questions 53. The increase in the use of electronic medical records is due in large part to: A. the invention and increased use of mobile computing technology, allowing doctors to send records with greater ease. B. expectations on the part of the patient that doctors should be able to access all information in their medical history quickly and efficiently. C. increased funding in the 2009 economic stimulus package providing for the modernization of electronic health record-keeping systems. D. the need for doctors to have easier access to information so that patients can be seen at a faster rate, compensating for increased demand.

54. What is the purpose of the confidentiality laws detailed in 42 CRF Part Two? A. To provide patients seeking mental health care protections above and beyond HIPAA B. To prevent police from using medical records to arrest patients seeking help for substance abuse C. To remind clinicians of their ethical responsibilities regarding confidentiality D. To aid law enforcement in the event a criminal defendant makes a mental health-related defense

55. According to a study by Walley et al., what percentage of patients on methadone maintenance therapy were prescribed a drug with a potentially harmful interaction? A. 59% B. 32% C. 6% D. 79%

56. According to the lesson, why is it important to understand why the confidentiality laws exist and why the context of these laws is changing? A. To protect the patient autonomy B. To be able to reconcile one’s ethical concerns within the boundaries of the law C. To be certain about what information is protected by confidentiality D. All of the above 211

Best Practices in CME Confidentiality Protections Versus Collaborative Care in the Treatment of Substance Use Disorders By Jennifer K. Manuel, PhD; Howard Newville, PhD; Sandra E. Larios, PhD, MPH; and James L. Sorensen, PhD ID#: L903336

This valuable take-home reference translates evidence-based, continuing medical education research and theory, acquired from reading the associated CME lesson, into a stepwise approach that reviews key learning points for easy assimilation into your armamentarium of knowledge and daily practice.

CME Lesson Overview This lesson is designed to help clinicians understand the impact of electronic health records on patients and ethical questions in substance use disorder treatment settings.

Key Point 1: Introduction

The American Recovery and Reinvestment Act of 2009 (ARRA), also known as the “economic stimulus package,” provided $19.2 billion for the modernization of electronic health records.

Key Point 2: Extra Protections for Patients in Recovery from Substance Abuse

42 CFR Part 25,6 applies confidentiality regulations to federally-assisted SUD programs, defined as an individual, entity, or unit within a general medical facility who offers or provides substance use diagnosis, treatment, or referral to treatment or medical staff in a general medical care setting “whose primary function is the provision of alcohol or drug abuse diagnosis, treatment or referral for treatment.”

Key Point 3: Be Mindful of Context

For all providers and other healthcare personnel, it is vital to understand why the confidentiality laws exist and why the context is changing. Gaining an understanding of the principles, laws, and guidelines is

important. Then when the question arises about protection of confidentiality, ethical principles such as respect for persons, autonomy, justice, beneficence, and nonmaleficence can be part of the decision-making process.29 The federal confidentiality statutes must be followed, as well as various guidelines from legislation such as HIPAA and applicable state and municipal regulations.

Key Point 4: Implement Guidelines

At the clinic level, update guidelines for your patients, staff, and referral sources. If guidelines do not exist, it is wise to develop them.

Key Point 5: Seek Guidance and Feedback in Ethical Confounding Situations

When a provider approaches an uncomfortable situation, clinicians should seek guidance. Treating clinicians, peers, clinical supervisors, physicians, and licensed professionals at the SUD treatment program are essential for support, and professional associations can be helpful.


Notes

L903337

Ebola Facts: Clinical Progression & Clinical Evidence American Hospital Association Compiled by the American Hospital Association (AHA), the Accreditation Council for Continuing Medical Education (ACCME) has disseminated this information to all continuing medical education providers and encouraged providers to share this information in their CME series.a

KEY WORDS: Ebola Virus • Early Stages • Pathophysiology • ZMapp LEARNING OBJECTIVES: This lesson provides readers with the clinical progression of the Ebola Virus Disease (EVD) as well as guidelines for management in the hospital setting. Readers will review the symptoms that present in the early, late, and recovery phases of the disease as well as symptom management, and guidelines for protection of healthcare providers and others who come into contact with individuals who have acquired the virus.

LESSON ABSTRACT: In response to the Ebola public health emergency, the American Hospital Association (AHA) has provided an Ebola education package for CME providers. This package contains information that the American Hospital Association believes would be useful to healthcare providers and institutions right now, including this FAQ. For more recent updates, readers should refer to the Centers for Disease Control and Prevention (CDC) or other cited sources on the day they access this information to get the most current information or version that may now be available.a

COMPETENCY AREAS: This lesson provides healthcare providers with current information released by the American Hospital Association regarding the presentation of the Ebola virus and how to manage presenting symptoms. This lesson also provides informatics for systematic controls in the hospital setting.

a

For more information, please visit: accme.org

215

L903337 : Ebola Facts: Clinical Progression & Clinical Evidence

Table 1: DISEASE PROGRESSION

Table 2: CLINICAL EVIDENCE CARE COMPONENT

CLINICAL MANAGEMENT

Disease Pathophysiology4

Research suggests the virus first infects dendritic cells, disabling immune system, and then attacks the vascular system, causing hemorrhage, hypotension and shock. The virus also affects the liver (impacting coagulation proteins), the adrenal gland (affecting steroid synthesis for blood pressure stabilization) and the gastrointestinal tract (diarrhea).

Hemodynamic Support1,2,5-7

Hypotension/Shock: Aggressive IV fluid resuscitation resembling the approach to the septic shock patient is identified by the CDC as one of three interventions that impact mortality through observation and case series. Base fluid selection (Lactated Ringers or Normal Saline) on patient electrolyte status. One animal study examined supplemental fluid resuscitation of infected, hypotensive rhesus macaques, which resulted in improved renal parameters. Hydrocortisone may be considered to support viral disruption in steroid synthesis.

Hypotension/shock, hemorrhage/DIC

Hemorrhage/DIC: Management of hemorrhage is inconsistent in literature. Literature around previous outbreak transfusion strategies includes various blood products, antifibrinolytics, and clotting factors. One recent report suggests the use of melatonin to combat endothelial disruption, disseminated intravascular coagulation (DIC) and multiple organ hemorrhage due to potential benefit, high safety profile, and limited alternative therapies. Respiratory Support1,2,8-10 Oxygen therapy, ventilation

216

Maintain adequate oxygenation (titrate to SpO2 >90%). To protect the airway and/or treat multisystem organ failure, standard mechanical ventilation practices should be followed with the addition of HEPA filtration of airflow gases. Methods of non-invasive ventilation are not ideal due to increased potential for aspiration and infection transmission. Additional measures including placement of ventilated patients in a negative pressure room, use of video/optical laryngoscopy for intubation, use of rapid sequence intubation with neuromuscular blockade, and use of a ventilator-patient monitoring system interface to minimize entry into the patient room should be considered.1-2,6-8


Table 3: CLINICAL EVIDENCE CARE COMPONENT

CLINICAL MANAGEMENT

Infection Suppor t1,2,6,11 Fever, secondar y infection, malaise, plasma transfusion, antivirals

Treat fever with acetaminophen (avoid aspirin and NSAIDs due to antiplatelet activity). Identify any additional sources of infection and treat with appropriate empiric antimicrobials. If sepsis develops, administer broad-spectrum IV antibiotics within 1 hour and follow Sur viving Sepsis Early Goal Directed Therapy (EGDT). Antiviral and antimalarial agents are not efficacious for Zaire Ebola virus. Consider passive immunotherapy early in disease course by transfusing whole blood or plasma donated from a convalescent patient.

Renal/Hepatic Suppor t1,2,4,6,12,13

Renal: Advanced stage may lead to impaired kidney function, increased creatinine and BUN, and decreased urine output. Renal failure has been repor ted in fatal cases. Patients may experience persistent oliguria, hematuria and proteinuria despite IV fluid resuscitation. Repor ts of peritoneal and hemodialysis show no consistent correlation on sur vivability, and transmission risk to healthcare workers should be considered. Hepatic: Patients demonstrate impaired liver function, hepatomegaly and elevated liver enzymes (ALT/AST), but severity is lower than that seen in hepatitis A/B or yellow fever. One study showed AST was several times higher than ALT in fatal cases.

Pain Management2,14-16

Treat mild pain with acetaminophen and moderate to severe pain with opioids. Avoid diclofenac, ibuprofen and other NSAIDS due to antiplatelet activity; avoid tramadol due to seizure activity. The management of pain resembling the approach to a critically ill patient with potential multi-organ failure should be followed due to high risk of renal and hepatic failure.

Neurologic Suppor t1,6 Anxiety, Confusion, Seizures

Monitor the patient for confusion, anxiety and seizures. Treat anxiety and seizures with benzodiazepines. Avoid the use of other medications that may reduce seizure threshold. Late in the disease progression, monitor neurologic status for increased intracranial pressure and intracranial hemorrhage.

Gastrointestinal Suppor t1,10 Nutrition, Nausea/ Vomiting, Diarrhea

Provide rehydration therapy to prevent volume depletion. Correct abnormal electrolytes. Proton pump inhibitors should be administered for dyspepsia and gastrointestinal bleed prophylaxis. Administer antiemetics for nausea/vomiting. Monitor for dehydration.

Sur vivability2,3

Dependent upon access to basic care and patient immune status. Current West Africa Ebola strain has repor ted 70% mor tality rate (October 14, 2014).

Recover y2,13

Recover y (weeks to months) is highly dependent on suppor tive care and immunologic response of patient. Men can still transmit Ebola virus through semen for up to 3 months so abstinence is encouraged during this time. Once fully recovered, patients are no longer able to transmit the virus. Development of antibodies last at least 10 years but it is unknown if this confers lifelong immunity or if infection with other strains is possible. Acute complications include: generalized weakness, weight loss, headache, sensor y distor tion, migrator y ar thralgias, skin sloughing, alopecia, and persistent anemia. Uveitis and orchitis can occur weeks after illness, and virus can persist in aqueous humor and semen.

Experimental Therapies2,4

No experimental vaccines or antiviral medications have been fully tested for safety or efficacy. ZMapp (Mapp Biopharmaceutical, Inc.), is an experimental treatment of three monoclonal antibodies that bind to viral protein. All available doses have been distributed at this time. Several experimental vaccines and treatments in animal models show promise.

217


References and Evidence Classification 1.

Clinical management of patients with viral haemorrhagic fever: a pocket guide for the front-line health worker. World Health Organization. World Health Organization , 2014. April 2014. Level 3

2.

Ebola (Ebola Virus Disease). Centers for Disease Control and Prevention website http://www.cdc.gov/vhf/ebola/. Updated October 3, 2014. Accessed October 16, 2014.

3.

WHO finds 70 percent Ebola mortality rate. Aljazeera.com Aljazeera America, 15 Oct 2014. Web. 16 Oct 2014.

4.

Ansari AA. Clinical features and pathobiology of Ebola virusinfection J Autoimmun 2014 Sep 23. Doi: 10.1016/j.jaut/2014.09.001. [Epub ahead of print] Level 3

5.

Kortepeter MG, Salwer JV, Hensley LE, et al. Real-time monitoring of cardiovascular function in rhesus macaques infected with Zaire ebolavirus. J Infect Dis 2011 Nov;204 Suppl 3:S1000-10. Animal study

Level 3

6.

Clark DV, Jahrling PB, Lawler JV. Clinical management of filovirus-infected patients. Viruses. 2012; 4, 1668-1686. Level 3

7.

Tan DX, Korkmaz A, Reiter RG, Manchester LC. Ebola virus disease: potential use of melatonin as treatment. J Pineal Res. 2014 Sep 27. doi: 10.1111/jpi.12186. [Epub ahead of print] Level 3

8.

Ebola Clinical Care Guidelines: a guide for clinicians in Canada. http://www.ammi.ca/media/69846/Ebola%20Clinical%20Care%20Guidelines %202%20Sep%202014. pdf. Updated August 29, 2014. Accessed October 16, 2014. Level 3

9.

Feldmann H, Geisbert TW. Ebola haemorrhagic fever. The Lancet. 2011;377(9768):849-62. Level 3

10.

Fowler RA, Fletcher T, Fischer WA, 2nd, Lamontagne F, Jacob S, Brett-Major D, et al. Caring for critically ill patients with ebola virus disease. Perspectives from west Africa. Am J Respir Crit Care Med. 2014;190(7):733-7. Level 3

11.

Mupapa K, Massamba M, Kibadi K, Kuvala K, Bwaka, et al. Treatment of ebola hemorrhagic fever with blood transfusion from convalescent patients. J Infect Dis. 1999; 179(Suppl 1):S18-23. Level 2

12.

Roddy P, Colebunders R, Jeffs B, et al. Filovirus hemorrhagic fever outbreak case management: a review of current and future treatment options. Infect Disease. 2011; 204: S791-S795. Level 3

13.

Kortepeter MG, Bausch DG, Bray M. Basic clinical and laboratory features of filoviral hemorrhagic fever. Infect Disease. 2011; 204: S810-S816. Level 3

14.

WHO: IMAI District Clinician Manual: Hospital Care for Adolescents and Adults- Guidelines for the Management of Common Illnesses with Limited Resources, 2011. Available at http://apps.who.int/iris/bitstream/10665/ 77751/1/9789241548281_ Vol1_eng.pdf. Level 3

15.

Sprecher A. Filovirus haemorrhagic fever guidelines. Médecins Sans Frontières Belgium 2013. (in draft) Level 3

16.

Barr J, Fraser GL, Puntillo K, et al. Clinical practice guidelines for the management of pain, agitation, and delirium in adult patients in the intensive care unit. Crit Care Med 2013; 41:263. Level 3

219


L903337

Multiple-Choice Questions 57. What is the first part of one’s body attacked by the Ebola virus? A. The adrenal system B. Vascular system causing hemorrhage C. Immune system by infecting dendritic cells D. Gastrointestinal tract causing diarrhea

58. To manage pain in patients with Ebola Virus Disease (EVD), clinicians should: A. administer NSAIDS such as ibuprofen. B. avoid tramadol due to potential seizure activity. C. administer aspirin. D. None of the above

59. Which of the following medications is recommended to provide neurological support to patients with EVD who experience anxiety, confusion, and seizures? A. Benzodiazepines B. Opioids C. Selective serotonin reuptake inhibitors D. Selective norepinephrine reuptake inhibitors

60. For patients who fully recover from the Ebola viral infection: A. patients have immunity to all known strains of the Ebola virus. B. individuals develop antibodies for a lifetime. C. men can still transmit the virus through semen for up to 3 months. D. None of the above

221

Best Practices in CME Safe Management of Patients with Ebola Virus Disease (EVD) in U.S. Hospitals By the American Hospital Association ID#: L903337

This valuable take-home reference translates evidence-based, continuing medical education research and theory, which is acquired from reading the associated CME lesson, into a stepwise approach that reviews key learning points for easy assimilation into your armamentarium of knowledge and daily practice.

CME Lesson Overview In lieu of the Best Practice Key Points, we are inserting this valuable Frequently Asked Questions page which also reviews the lesson material.

Safe Management of Patients with Ebola Virus Disease (EVD) in U.S. Hospitals Frequently Asked Questions The recent EVD outbreak in West Africa has increased the possibility of patients traveling from the impacted countries to the United States. Additionally, two American citizens with EVD were medically evacuated to the United States to receive care at Emory University Hospital in Atlanta. The following are answers to frequently asked questions about the safety of this medical evacuation and the necessary infection control procedures to protect patients and healthcare providers in U.S. hospitals.

Are U.S. hospitals ready to care for patients with Ebola virus disease (EVD)? Yes – any U.S. hospital that is following CDC’s infection control recommendations and can isolate a patient in a private room is capable of safely managing a patient with EVD. CDC recommends that U.S. hospitals isolate the patient in a private room and implement standard, contact, and droplet precautions.



What should U.S. hospitals do if they have a patient with suspect EVD? Early recognition is critical for infection control. Healthcare providers should be alert for and evaluate any patients suspected of having EVD who have (see EVD case definition): 1. A fever of greater than 38.6 degrees Celsius or 101.5 degrees Fahrenheit, and additional symptoms such as severe headache, muscle pain, vomiting, diarrhea, abdominal pain, or unexplained hemorrhage; AND 2. Risk factors within the past 3 weeks before the onset of symptoms, such as contact with blood or other body fluids of a patient known to have or suspected to have EVD; residence in—or travel to—an area where EVD transmission is active; or direct handling of bats or nonhuman primates from disease-endemic areas. Malaria diagnostics should also be a part of initial testing because it is the most common cause of febrile illness in persons with a travel history to the affected countries.

When should patients with suspected EVD in U.S. hospitals be tested? CDC recommends testing for all persons with onset of fever within 21 days of having a high-risk exposure such as (See CDC’s laboratory testing guidance): • percutaneous or mucous membrane exposure or direct skin contact with body fluids of a person with a confirmed or suspected case of EVD without appropriate personal protective equipment (PPE), • laboratory processing of body fluids of suspected or confirmed EVD cases without appropriate PPE or standard biosafety precautions, or • participation in funeral rites or other direct exposure to human remains in the geographic area where the outbreak is occurring without appropriate PPE. For persons with a high-risk exposure but without a fever, testing is recommended only if there are other compatible clinical symptoms present and blood work findings are abnormal (i.e., thrombocytopenia

Directions in

Directions in

Suggest Documents

INGREDIENTS INGREDIENTS DIRECTIONS DIRECTIONS

Directions

Directions

New Directions in Cryptography

Postcolonial Directions in Education

Directions in

New Directions in Touch

Postcolonial Directions in Education

Part One Directions: Part Two Directions: Part Three Directions ...

Angles and Directions Angles and Directions Angles and Directions ...

Biotechnology - new directions in medicine

Future directions in asthma management

New directions in fracture characterization

eGovernment in Sweden: New Directions

New Directions In Cellular Automata

Flat directions in susy guts

Future Directions in Software Engineering

Future Directions in Astronomy Visualisation

Future Directions in Software Engineering

Directions in Software Development and

New Directions in Conservation Medicine

Future Directions in Tele-Robotics

STRATEGIC DIRECTIONS IN VERIFICATION ... - CiteSeerX

Future directions in speech production