Principal Netter’s Obstetrics and Gynecology
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Any screen. Any time. Anywhere. Activate the eBook version of this title at no additional charge. Expert Consult eBooks give you the power to browse and find content, view enhanced images, share notes and highlights—both online and offline. Unlock your eBook today. 1 Visit expertconsult.inkling.com/redeem 2 Scan this QR code to redeem your eBook through your mobile device: Scratch off your code 3 Type code into “Enter Code” box 4 Click “Redeem” 5 Log in or Sign up 6 Go to “My Library” Place Peel Off Sticker Here It’s that easy! For technical assistance: email firstname.lastname@example.org call 1-800-401-9962 (inside the US) call +1-314-447-8200 (outside the US) Use of the current edition of the electronic version of this book (eBook) is subject to the terms of the nontransferable, limited license granted on expertconsult.inkling.com. Access to the eBook is limited to the first individual who redeems the PIN, located on the inside cover of this book, at expertconsult.inkling.com and may not be transferred to another party by resale, lending, or other means. 2015v1.0 NETTER: It’s How You Know Anatomy. Netter Collection of Medical Illustrations, 2nd Edition Entire Collection Now Available! The Netter Collection of Medical Illustrations, Dr. Frank H. Netter’s decades of work devoted to depicting each of the major body systems, has been updated and brought into modern context. The second edition of the legendary “green books” offers Netter’s timeless work, now arranged and enhanced by modern text and radiologic imaging. Contributions by field-leading doctors and teachers from world-renowned medical institutions are supplemented with new illustrations created by master artist-physician Carlos Machado and other top medical illustrators working in the Netter tradition. Netter’s Correlative Imaging Series The Netter’s Correlative Imaging series pairs classic Netter and Netter-style illustrations with imaging studies and succinct descriptions to provide you with a richer understanding of ; human anatomy. These comprehensive, normal anatomy atlases cover all major sections of the body, featuring illustrated plates side-by-side with the most common imaging modalities for each region. Shop online at elsevierhealth.com Stay current and connected in ObGyn with coverage of the latest hot topics. Comprehensive Gynecology, 7th Edition Rogerio A. Lobo, MD, David M. Gershenson, MD, Gretchen M. Lentz, MD and Fidel A. Valea, MD The primary gynecology text for over 25 years, Comprehensive Gynecology covers all of the key issues residents may encounter. This 7th edition has been fully updated with a wealth of new content, including current discussions of minimally invasive surgical approaches to gynecologic care, infertility issues and treatments, effectively managing menopausal patients, and more. Obstetrics: Normal and Problem Pregnancies, 7th Edition Steven G. Gabbe, MD, Jennifer R. Niebyl, MD, Joe Leigh Simpson, MD, Mark B. Landon, MD, Henry L. Galan, MD, Eric R. M. Jauniaux, MD, PhD, Deborah A. Driscoll, MD, Vincenzo Berghella, MD and William A. Grobman, MD Obstetrics: Normal and Problem Pregnancies remains a go-to choice for authoritative guidance on managing today’s obstetric patient. International experts put the latest knowledge in this specialty at your fingertips, with current and relevant information on everything from fetal origins of adult disease, to improving global maternal health, to important topics in day-to-day obstetrical practice. Highly readable, well-illustrated, and easy to understand, this bestselling obstetrics reference is an ideal tool for residents. Shop online at elsevierhealth.com! NETTER’S OBSTETRICS & GYNECOLOGY 3rd EDITION Roger P. Smith, MD Assistant Dean for Graduate Medical Education Professor of Clinical Biologic Sciences Charles E. Schmidt College of Medicine Florida Atlantic University Boca Raton, Florida Illustrations by Frank H. Netter, MD Contributing Illustrators Carlos A.G. Machado, MD John A. Craig, MD Kristen Wienandt Marzejon, MS, MFA Joe Chovan James A. Perkins, MS, MFA Tiffany S. DaVanzo, MA, CMI 1600 John F. Kennedy Blvd. Ste 1800 Philadelphia, PA 19103-2899 NETTER’S OBSTETRICS AND GYNECOLOGY, THIRD EDITION ISBN: 978-0-7020-7036-5 Copyright © 2018 by Elsevier, Inc. All rights reserved. Previous edition copyrighted 2009 No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Notices Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein. Library of Congress Cataloging-in-Publication Data Names: Smith, Roger P. (Roger Perry), 1949- author. | Netter, Frank H. (Frank Henry), 1906-1991, illustrator. Title: Netter’s obstetrics and gynecology / Roger P. Smith ; illustrations by Frank H. Netter ; contributing illustrators, Carlos A.G. Machado, John A. Craig, Kristen Wienandt Marzejon, Joe Chovan, James A. Perkins, Tiffany S. DaVanzo. Other titles: Obstetrics and gynecology Description: Third edition. | Philadelphia, PA : Elsevier,  | Includes bibliographical references and index. Identifiers: LCCN 2016051375 | ISBN 9780702070365 (hardcover : alk. paper) Subjects: | MESH: Genital Diseases, Female | Obstetric Surgical Procedures | Pregnancy Complications | Atlases Classification: LCC RG110 | NLM WP 17 | DDC 618.1–dc23 LC record available at https://lccn.loc.gov/2016051375 Content Strategist and Content Development Specialist: Marybeth Thiel Publishing Services Manager: Patricia Tannian Project Manager: Ted Rodgers Design Direction: Patrick Ferguson Printed in China Last digit is the print number: 9 8 7 6 5 4 3 2 1 PREFACE No student of medicine, past or present, is unaware of the extraordinary series of medical illustrations created by Dr. Frank Netter. It is an incredible body of work that has been carried forward by the talented Carlos Machado, MD, and John Craig, MD, since Dr. Netter’s passing. Older physicians have looked with envy at these images, wishing they had been available when they were learning; established physicians return to them as comfortable sources of information; young physicians seek them out for the wealth of information they contain and their ability to make clear difficult clinical concepts. This spirit of concise reference and resource is the premise of this text. This third edition maintains the same consistent format in presenting topics to facilitate rapid access—the same information is in the same location—that was so well received in the first and second editions. Chapters have been organized to provide a quick, concise resource for the diagnosis and treatment of common conditions encountered by anyone who provides care for women. In producing this third edition, more than 25 new topics have been added, including sections on embryology and anatomy, a more intuitive organization has been developed, an expanded section on commonly encountered procedures is included, new artwork has been developed, and subtle enhancements (such as indications of the level of evidence provided for references) have been made throughout the work. It is our hope that this work will be both a useful resource and a celebration of the artistic richness that is clinical medicine. Roger P. Smith, MD ABOUT THE ARTISTS FRANK H. NETTER, MD Frank H. Netter was born in 1906 in New York City. He studied art at the Art Students League and the National Academy of Design before entering medical school at New York University, where he received his MD degree in 1931. During his student years, Dr. Netter’s notebook sketches attracted the attention of the medical faculty and other physicians, allowing him to augment his income by illustrating articles and textbooks. He continued illustrating as a sideline after establishing a surgical practice in 1933, but he ultimately opted to give up his practice in favor of a full-time commitment to art. After service in the United States Army during World War II, Dr. Netter began his long collaboration with the CIBA Pharmaceutical Company (now Novartis Pharmaceuticals). This 45-year partnership resulted in the production of the extraordinary collection of medical art so familiar to physicians and other medical professionals worldwide. In 2005, Elsevier purchased the Netter Collection and all publications from Icon Learning Systems. There are now over 50 publications featuring the art of Dr. Netter available through Elsevier, Inc. (in the US: www.us.elsevierhealth.com/Netter; outside the US: www.elsevierhealth.com). Dr. Netter’s works are among the finest examples of the use of illustration in the teaching of medical concepts. The 13-book Netter Collection of Medical Illustrations, which includes the greater part of the more than 20,000 paintings created by Dr. Netter, became and remains one of the most famous medical works ever published. The Netter Atlas of Human Anatomy, first published in 1989, presents the anatomical paintings from the Netter Collection. Now translated into 16 languages, it is the anatomy atlas of choice among medical and health professions students the world over. The Netter illustrations are appreciated not only for their aesthetic qualities, but, more important, for their intellectual content. As Dr. Netter wrote in 1949, “. . . clarification of a subject is the aim and goal of illustration. No matter how beautifully painted, how delicately and subtly rendered a subject may be, it is of little value as a medical illustration if it does not serve to make clear some medical point.” Dr. Netter’s planning, conception, point of view, and approach are what inform his paintings and what make them so intellectually valuable. Frank H. Netter, MD, physician and artist, died in 1991. Learn more about the physician-artist whose work has inspired the Netter Reference collection: http://www.netterimages.com/artist/netter.htm. CARLOS MACHADO, MD Carlos Machado was chosen by Novartis to be Dr. Netter’s successor. He continues to be the main artist who contributes to the Netter collection of medical illustrations. Self-taught in medical illustration, cardiologist Carlos Machado has contributed meticulous updates to some of Dr. Netter’s original plates and has created many paintings of his own in the style of Netter as an extension of the Netter collection. Dr. Machado’s photorealistic expertise and his keen insight into the physician/ patient relationship inform his vivid and unforgettable visual style. His dedication to researching each topic and subject he paints places him among the premier medical illustrators at work today. Learn more about his background and see more of his art at: http://www.netterimages.com/artist/machado.htm. ONLINE CONTENTS Visit www.ExpertConsult.com for the following: Printable Patient Education Brochures from Ferri’s Netter Patient Advisor, 3rd Edition 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. Managing Your Anorexia Nervosa Breast Cancer: Screening and Prevention Managing Your Bulimia Managing Your Cervical Cancer Managing Your Cervical Incompetence Managing Your Cervical Polyps Managing Your Dysmenorrhea Managing Your Dysfunctional Uterine Bleeding Managing Your Endometriosis Managing Your Female Sexual Dysfunction Managing Your Fibrocystic Breast Disease Managing Your Hyperemesis Gravidarum Managing Your Infertility Kegel Exercises Strengthening Your Pelvic Floor Muscles Managing Your Lactational Mastitis Managing Your Menopause Managing Your Menorrhagia Managing Your Morning Sickness Managing Your Ovarian Cancer Managing Your Ovarian Cysts Managing Your Pelvic Inflammatory Disease Managing Your Uterine Fibroids Managing Your Vaginal Dryness Managing Your Bacterial Vaginal Infection Managing Your Miscarriage Weight Control For Women CONTENTS PART I: ANATOMY AND EMBRYOLOGY SECTION I Embryology 1 Sexual Differentiation 3 2 Upper Genital Tract Development 4 3 Lower Genital Tract Development 5 4 Development of the Breast 7 SECTION II Anatomy 27 Chronic Pelvic Pain 60 28 Constipation 62 29 Crohn Disease 64 30 Depression (Unipolar) 66 31 Diverticular Disease 68 32 Domestic Violence 69 33 Dysmenorrhea: Primary and Secondary 71 34 Dyspareunia: Deep Thrust 73 35 Dysuria 75 5 External Genitalia 11 6 Perineum 12 36 Eating Disorders: Anorexia Nervosa and Bulimia 77 7 Vagina 13 37 Fibromyalgia 79 8 Pelvic Viscera 15 38 Gallbladder Disease 82 9 Cervix, Uterus, and Adnexa 16 39 Gastritis 84 10 Ovaries 17 40 Gastroesophageal Reflux 85 11 Breast 19 41 Hair Loss 87 42 Headache: Tension and Cluster 89 43 Headache: Migraine 92 44 Hematuria 94 45 Hemorrhoids 96 46 Hyperthyroidism 97 47 Hypothyroidism 99 PART II: GYNECOLOGY AND WOMEN’S HEALTH SECTION III General Health Considerations and Counseling 12 Puberty: Normal Sequence 25 13 Health Maintenance: Ages 12–18 Years 26 14 Health Maintenance: Ages 19–39 Years 28 15 Contraception: Counseling Principles 30 16 Health Maintenance: Ages 40–64 Years 32 17 Health Maintenance: Ages 65 Years and Older 35 SECTION IV Diseases, Disorders, and Common Problems 18 Abortion 41 19 Abuse: Physical and Sexual 44 20 Acne 46 21 Alzheimer Disease 48 22 Anemia 50 23 Anorectal Fistula 52 24 Anxiety 54 25 Asthma 56 26 Cholelithiasis 58 48 Infertility: General Considerations 101 49 Irritable Bowel Syndrome 103 50 Low Back Pain 105 51 Melanoma 108 52 Myofascial Syndromes 110 53 Obesity 112 54 Osteoporosis 114 55 Pessary Therapy 117 56 Postcoital Bleeding 119 57 Premenstrual Syndrome 121 58 Pruritus Ani 123 59 Rape and Rape Trauma Syndrome 124 60 Sexual Dysfunction: Libidinal and Orgasmic Dysfunction (Anorgasmia) 127 61 Sexually Transmitted Infections: Chancroid 129 62 Sexually Transmitted Infections: Chlamydia trachomatis 131 63 Sexually Transmitted Infections: Condylomata Acuminata 133 Contents 64 Sexually Transmitted Infections: Gonorrhea 135 65 Sexually Transmitted Infections: Granuloma Inguinale (Donovanosis) 137 66 Sexually Transmitted Infections: Herpes 139 67 Sexually Transmitted Infections: Human Immunodeficiency Virus 141 68 Sexually Transmitted Infections: Human Papillomavirus 144 69 Sexually Transmitted Infections: Lymphogranuloma Venereum 147 ix 96 Vulvar Hematoma 201 97 Vulvar Lesions 203 98 Vulvar Vestibulitis (Provoked Vulvodynia) 206 SECTION VI Vaginal Disease 99 Cystocele/Urethrocele 211 100 Enterocele 212 101 Fistulae: Gastrointestinal and Urinary Tract 214 102 Rectocele 216 103 Sarcoma Botryoides 218 104 Transverse Vaginal Septum 219 105 Vaginal Cysts 221 106 Vaginal Dryness 222 107 Vaginal Lacerations 223 108 Vaginal Prolapse 225 109 Vaginitis: Atrophic 227 70 Sexually Transmitted Infections: Molluscum Contagiosum 149 71 Sexually Transmitted Infections: Parasites 150 72 Sexually Transmitted Infections: Syphilis 152 73 Sexually Transmitted Infections: Trichomonas vaginalis 155 74 Thrombophlebitis 157 75 Toxic Shock Syndrome 159 76 Ulcerative Colitis 162 110 Vaginitis: Bacterial (Nonspecific) and Bacterial Vaginosis 229 77 Urinary Incontinence: Bypass and Overflow 164 111 Vaginitis: Monilial 231 78 Urinary Incontinence: Stress 166 112 Vaginitis: Trichomonas 233 79 Urinary Incontinence: Urge 169 80 Urinary Tract Infection 171 81 Urodynamics Testing 174 82 Varicose Veins 176 SECTION V Vulvar Disease SECTION VII Cervical Disease 113 Abnormal Pap Smear: Atypical Squamous or Glandular Cells of Undetermined Origin 237 114 Abnormal Pap Smear: Low-Grade Squamous Intraepithelial Lesions and High-Grade Squamous Intraepithelial Lesions 239 115 Carcinoma in Situ (Cervix) 241 116 Cervical Cancer 243 117 Cervical Erosion 245 83 Acne Inversa (Hidradenitis Suppurativa) 181 84 Bartholin Gland: Abscess/Infection 182 85 Bartholin Gland: Cysts 118 Cervical Eversion 246 184 119 Cervical Polyps 247 86 Contact Vulvitis 186 120 Cervical Stenosis 248 87 Dyspareunia: Insertional 187 121 Cervicitis 250 88 Female Circumcision 188 122 Nabothian Cysts 252 89 Hymenal Stenosis 190 90 Hyperplastic Vulvar Dystrophy (Squamous Cell Hyperplasia, Lichen Simplex Chronicus) 192 91 Imperforate Hymen 193 92 Labial Adhesions 194 93 Lichen Planus 196 94 Lichen Sclerosus 197 95 Vulvar Cancer 199 SECTION VIII Uterine Pathology 123 Adenomyosis 255 124 Asherman Syndrome (Uterine Synechia) 256 125 Dysfunctional (Abnormal) Uterine Bleeding 258 126 Endometrial Cancer 261 127 Endometrial Hyperplasia: Simple and Complex 263 x Contents 128 Endometrial Polyps 265 168 Fibrocystic Breast Change 347 129 Endometritis 266 169 Galactocele 349 130 Hematometra 268 170 Galactorrhea 351 131 Intermenstrual Bleeding 269 171 Mammography 353 132 Irregular Menstrual Periods 271 172 Mastitis (Lactational) 355 133 Menorrhagia 274 173 Mastodynia and Mastalgia (Breast Pain) 356 134 Postmenopausal Vaginal Bleeding 276 174 Mondor Disease 358 135 Sarcoma (Uterine) 278 175 Nipple Discharge 360 136 Uterine Anomalies: Bicornuate, Septate, and Unicornuate Uterus 280 176 Paget Disease of the Breast 362 137 Uterine Leiomyomata (Fibroids, Myoma) 282 138 Uterine Prolapse 284 SECTION IX Adnexal Disease SECTION XI Reproductive, Genetic, and Endocrine Conditions 177 Abnormal Puberty 367 178 Amenorrhea: Primary 369 139 Adenofibroma 289 140 Clear Cell Carcinoma 290 179 Amenorrhea: Secondary 371 141 Dermoid Cyst 292 180 Androgen Insensitivity Syndrome 372 142 Dysgerminoma 293 181 Anovulation 374 143 Ectopic Pregnancy 295 182 Assisted Reproduction 376 144 Endometriosis 298 183 Down Syndrome 379 145 Epithelial Stromal Ovarian Tumors 301 184 Gonadal Dysgenesis 381 146 Germ Cell Tumor 303 185 Hirsutism 384 147 Granulosa Cell Tumors 304 186 Hyperprolactinemia 387 148 Hydrosalpinx (Chronic Pelvic Inflammatory Disease) 307 187 Infertility 390 149 Krukenberg Tumor 309 188 Menopause 392 150 Mucinous Ovarian Cysts 310 189 Polycystic Ovary Syndrome 395 151 Ovarian Cancer 312 190 Recurrent Pregnancy Loss 397 152 Ovarian Cysts 315 191 Sexual Ambiguity 399 153 Ovarian Fibroma 317 192 Sheehan Syndrome 401 154 Ovarian Torsion 319 193 Turner Syndrome 403 155 Pelvic Inflammatory Disease (PID) 321 194 Uterine Agenesis 405 156 Pseudomyxoma Peritonei 324 195 Vaginal Agenesis 407 157 Serous Ovarian Cysts 325 196 Virilization 408 158 Sertoli-Leydig Cell Tumor (Arrhenoblastoma) 327 159 Transitional Cell (Brenner) Tumor 329 PART III: OBSTETRICS SECTION XII Obstetrics: General Considerations SECTION X Breast Diseases and Conditions 160 Accessory Nipples (Polythelia) 333 197 Preconceptional Care and Counseling 413 161 BRCA1 and BRCA2 Mutations 334 162 Breast Cancer 336 198 Routine Prenatal Care: First Trimester 415 163 Breast Cyst 339 164 Breast Duct Ectasia 340 199 Routine Prenatal Care: Second Trimester 416 165 Breast Fat Necrosis 342 200 Routine Prenatal Care: Third Trimester 418 166 Breast Fibroadenoma 343 201 Antepartum Fetal Testing 420 167 Breast Intraductal Papilloma 345 202 Biophysical Profile 422 Contents xi 203 Contraction Stress Testing 424 243 Shoulder Dystocia 503 204 Doppler Flow Studies 425 244 Third Trimester Bleeding 505 205 Nonstress Testing 427 245 Trauma in Pregnancy 506 206 Normal Labor 429 246 Uterine Atony and Postpartum Hemorrhage 508 207 Fetal Heart Rate Testing: Bradycardia 431 247 Uterine Inversion 511 208 Fetal Heart Rate Testing: Periodic Changes 248 Uterine Rupture 513 433 209 Fetal Heart Rate Testing: Reduced Variability 435 210 Fetal Heart Rate Testing: Tachycardia 437 SECTION XIV Procedures 211 Obstetric Anesthesia/Analgesia 438 249 Amniocentesis 517 212 Normal Postpartum Changes 440 250 Aspiration of Breast Cyst 518 442 251 Bartholin Gland Cyst/Abscess Drainage 520 252 Bartholin Gland Marsupialization 521 253 Breast Biopsy: Core 523 213 Breastfeeding (Lactation) PART IV: PROCEDURES SECTION XIII Obstetric Conditions and Concerns 214 Abnormalities of Placental Implantation 447 215 Active Management of Labor 449 254 Breast Biopsy: Open 524 216 Acute Fatty Liver of Pregnancy 450 255 Cervical Cerclage 526 217 Amniotic Fluid Embolism 452 256 Cervical Conization (Cold Knife) 528 218 Breech Birth 454 257 Cervical Polypectomy 529 219 Caput Succedaneum 456 258 Cesarean Delivery 531 220 Cardiovascular Disease in Pregnancy 457 259 Chorionic Villus Sampling 534 221 Cervical Insufficiency 460 260 Circumcision (Male; Newborn and Infant) 536 222 Cholecystitis in Pregnancy 461 261 Colposcopy 539 223 Chorioamnionitis 464 262 Cervical Cryocautery 541 224 Diabetes Mellitus in Pregnancy 466 263 Cystourethroscopy 542 225 Fetal Alcohol Syndrome 468 264 Diaphragm Fitting 544 226 Gestational Trophoblastic Disease 470 265 Dilation and Curettage 546 227 Gingivitis in Pregnancy 472 266 Endometrial Biopsy 548 228 HELLP Syndrome 474 267 Forceps-Aided Delivery 550 229 Hepatitis in Pregnancy 476 230 Hyperemesis Gravidarum 478 268 Hysteroscopy: Diagnostic 552 231 Intrauterine Growth Restriction 479 232 Multiple Gestation 482 269 Hysteroscopy: Polyp and Leiomyoma Resection 554 233 Oligohydramnios 484 270 Hysteroscopic Sterilization 556 234 Placenta Previa 486 271 Intrauterine Contraceptive Device Insertion 558 235 Placental Abruption 488 272 Intrauterine Contraceptive Device Removal 560 236 Polyhydramnios 489 237 Postpartum Breast Engorgement 491 273 LEEP (Loop Electrosurgical Excision Procedure) and LLETZ (Large Loop Excision of the Transformation Zone) Conizations 562 238 Postpartum Depression 492 274 Pessary Fitting 564 239 Preeclampsia and Eclampsia 494 275 Sonohysterography 566 240 Pruritic Urticarial Papules and Plaques of Pregnancy (Puppp) 276 Subdermal Contraceptive Capsule Insertion 568 497 277 Subdermal Contraceptive Capsule Removal 570 241 Puerperal Infection 499 278 Transvaginal Ultrasonography 571 242 Rh Incompatibility 501 279 Trigger Point Injection 573 xii Contents 280 Urodynamic Testing: Complex 574 281 Urodynamic Testing: Simple 576 282 Vacuum-Assisted Delivery 578 Index 581 SECTION I Embryology 1 2 3 4 Sexual Differentiation Upper Genital Tract Development Lower Genital Tract Development Development of the Breast This page intentionally left blank 1 SEXUAL DIFFERENTIATION Genetic sex is determined by the complement and function of sex chromosomes (X and Y) that are present at the time of conception. A Y chromosome carrying specific genes is necessary for the development of testes. The testes are responsible for the organization of the sexual duct system into a male configuration and for the suppression of the paramesonephric (Müllerian) system responsible for female anatomic structures. In the absence of a Y chromosome, specifically required genes, or a functioning gonad, the development will be female. General phenotypic development of the female is viewed as a default event, although new evidence of a more complex process is emerging. Sexual differentiation genes are located on the Y chromosome, the primary of which is the SRY gene, also called the testisdetermining factor. The SRY gene is found on the short arm of the Y chromosome and influences Sertoli cell differentiation, mesonephric ridge cell development, and male architectural development of the gonad, including blood vessels and other structures of the testes. Several other genes, including those that express Paramesonephric (müllerian) duct Mesonephros Genital ridge Hindgut Chromosome 11 WT1 SF1 Mesonephric (Wolffian) duct Ureteric bud (metanephric duct) Metanephrogenic tissue Yolk sac stalk Allantois Cloaca Cloacal membrane Transcriptional activation of SRY Indifferent (undifferentiated) stage Conversion of the genital ridge into the bipotential gonad DAX1 GATA4 SRY FOG2 Chromosome Y Chromosome 17 Chromosome X Chromosome 8 Chromosomes 10 and 13 FGF9 Kidney Chromosome 1 Kidney (metanephros) Bladder FGFR2 FOXL2 Urogenital sinus proper Rectum Perineum Sertoli cells Urethra Gubernaculum Wolffian duct differentiation CH3 nt me Leydig cells Testis migration Female p velo al de gonad Testis Penis Chromosome 3 Female ent velopm Testis de Male Bipotential gonads Genital tubercle Activation SOX9 of SOX9 WNT4 + RSPO1 OH H H 21 67 H Insulin- O H like-3 Testosterone CH3 OH Masculinization of O H the genital anlage Dihydrotestosterone (DHT) Clitoris Urethra Anti-müllerian hormone (AMH or MIF) Vagina Rectum Uterus Figure 1.1 Genetics and biology of early reproductive tract development 3 4 SECTION I • Embryology steroidogenic factor-1, WT1, and DAX1, on other chromosomes, are also necessary for normal testicular development. To date, multiple mutations of the SRY gene have been reported and all are associated with sex reversals (female phenotype). As discussed earlier, genes in other locations are also important for complete male sexual differentiation. DAX1, a nuclear hormone receptor, can alter SRY activity during development by suppressing genes downstream to SRY that would normally induce testicular differentiation. A second gene, WNT4, largely confined to the adult ovary, may also serve as an “antitestis” gene. In very rare male individuals a Y chromosome may be absent, but the SRY gene may be present on another chromosome, most commonly the X chromosome, resulting in a male phenotype. It is becoming apparent that genes, such as WNT4 and DAX1, can proactively induce female gonadal development even in the presence of SRY, thereby further complicating the picture. This may account for individuals who are exceptions to the normal sexual dichotomy (eg, males with a uterus or females with an XY karyotype) or who exhibit biologic and/or behavioral characteristics of both sexes. Male gonadal development precedes female development, and the early secretion of testosterone and anti-Müllerian hormone (AMH) steers the further development of the genital tracts away from the default female phenotype. At a critical point, AMH, produced by Sertoli cells, and testosterone, secreted by Leydig cells, must be produced in sufficient amounts. AMH acts locally, thus 2 suppressing the Müllerian duct system. Testosterone acts systemically, thus causing the differentiation of the mesonephric duct system and male development of the urogenital tubercle, urogenital sinus, and urogenital folds. Enzymes involved in testosterone biosynthesis and conversion to dihydrotestosterones are regulated by genes located on autosomes. The ability to secrete AMH is a recessive trait coded on either an autosome or the X chromosome, and genes for the development of cytoplasmic receptors of androgens seem to be coded on the X chromosome. The development of the ovary occurs at approximately the 11th or 12th week of gestation, although the primordial germ cells migrate several weeks earlier to the germinal ridge. Two functional X chromosomes are necessary for the optimal development of the ovary. Thus, in 45,X and 46,XY females the ovaries are almost invariably devoid of oocytes. In contrast, germ cells in the testes do best when only one X chromosome is present; rarely do they survive in the XX or XXY condition. When non-Y-bearing oocytes enter the differentiating gonad, the primary sex cords break up and encircle the oocytes in the cortex of the gonad (in contrast to the structure of the XY gonad). This occurs at approximately 16 weeks of gestation, and the isolated cell clusters are called primordial follicles. No new oogonia form after birth and many of them degenerate well before birth. Those that remain grow and become primary follicles to be stimulated following puberty. UPPER GENITAL TRACT DEVELOPMENT Phenotypic gender is determined by a complex tissue differentiation process that begins in the medial genital thickening or ridges on the posterior surface of the embryonic body cavity. Once gonadal sexual differentiation has begun, several other events must occur for normal male or female phenotypic differentiation to occur. During the fifth week after conception, coelomic epithelium, later known as germinal epithelium, thickens in the area of the medial aspect of the mesonephros. As germinal epithelial cells proliferate, they invade the underlying mesenchyme, producing the gonadal ridge. In the sixth week after conception the primordial germ cells, which formed at approximately the fourth week after conception, in the wall of the yolk sac, migrate up the dorsal mesentery of the hindgut and enter the undifferentiated gonad. These cells will differentiate into testes or ovaries based on the gene functions noted in Chapter 1, Sexual Differentiation. Signaled by the arrival of primordial germ cells in the fifth week after conception, two sets of paired genital ducts, the mesonephric or nephric (wolffian) ducts and the paramesonephric (müllerian) ducts, develop. The mesonephric system is the precursor to the male genital system and the paramesonephric to the female reproductive structures. The mesonephros is a prominent excretory structure that consists of a series of mesonephric tubules. The tubules connect with the elongating mesonephric (wolffian) ducts as the latter extend caudally, terminating in the urogenital sinus on each side of the midline. Derived from the evagination of the coelomic epithelium, the paramesonephric ducts develop lateral to each of the mesonephric ducts. The cephalward ends of these ducts open directly into the peritoneal cavity, whereas the distal ends grow caudally, fuse in the lower midline, and form the uterovaginal primordium. They join the urogenital sinus as an elevation, known as the müllerian tubercle, which separates the urogenital area from the more posterior gut. Under the influence of the SRY gene in the prototestis the mesonephric (wolffian) ducts are maintained during development. As the developing male Sertoli cells begin to differentiate in response to SRY, they secrete a glycoprotein hormone, müllerian-inhibiting substance (MIS) or antimüllerian hormone (AMH), which causes the paramesonephric (müllerian) ducts to regress rapidly between the 8th and 10th fetal weeks. Without testosterone and AMH the mesonephric ducts degenerate and disappear, and the paramesonephric ducts develop into a uterus, fallopian tubes, and upper vagina. Leydig cells synthesize insulin-like-3 (coded by the INSL3 gene) to promote transabdominal testicular descent into the scrotum. Mutations in this gene may lead to cryp torchidism. In females a structure similar to the gubernaculum develops in the inguinal canal, giving rise to the round ligaments that suspend the uterus in the adult. Primary sex cords condense and extend to the medullary portion of the developing testes. They branch and join to form the rete testis. The testis therefore is primarily a medullary organ. Eventually the rete testis connects with the tubules of the mesonephric system and joins the developing epididymal duct. Müllerian duct remnants in the male include the appendix testis (hydatid of Morgagni) and the prostatic utricle. In females, MIS is not present, so müllerian ducts remain and the mesonephric tubules and ducts degenerate in the absence of androgens. This often results in remnant epoöphoron and paroöphoron cystic structures within the ovarian mesentery and Gartner duct cysts within the anterolateral vaginal wall. These structures are clinically important because they may develop into sizable and symptomatic cysts (see Chapter 105, Vaginal Cysts). Diaphragmatic ligament (suspensory ligament of ovary) Paramesonephric (müllerian) duct Male Ovary Testis Wolffian duct degenerates and müllerian duct persists Gonad Mesonephric tubules Mesonephric (wolffian) duct Genital cord Inguinal fold Primordium of prostate ( ) or of Skene ( ) gland Female Urogenital sinus Primordium of Cowper ( ) or of Bartholin ( ) gland Fallopian tube Gartner duct Epoöphoron Appendix vesiculosa Paroöphoron Ovary Uterus Round ligament Upper vagina Wolffian duct remnant Urethra Lower vagina Skene duct Bartholin gland Degenerating Müllerian duct Persistent Wolffian duct (vas deferens) Vas deferens Seminal vesicle Prostatic utricle Prostate gland Bulbourethral gland Vas deferens Appendix epididymidis Appendix testis Epididymis Vasa efferentia Testis Gubernaculum Figure 2.1 Homologs of the internal genitalia The process of development and loss of the müllerian and wolf fian systems begins at approximately the sixth week after conception and proceeds in a cephalad to caudal fashion. The more cephalad portions of the paramesonephric ducts, which open directly into the peritoneal cavity, form the fallopian tubes. The fused portion or uterovaginal primordium gives rise to the epithelium and glands of the uterus and cervix. Endometrial stroma and myometrium are derived from adjacent mesenchyme. Failure of the development of the paramesonephric ducts leads to agenesis of the cervix and uterus. Failure of fusion of the caudal portion of these ducts may lead to a variety of uterine anomalies, including complete duplication of the uterus and cervix or partial duplication of a variety of types (see Section VI, Chapter 136, Uterine Anomalies: Bicornuate, Septate, and Unicornuate Uterus). Peritoneal reflections in the area adjacent to the fusion of the two paramesonephric ducts give rise to the broad ligaments. Mesenchymal tissue here develops into the parametria. The remnants of the mesonephric duct in the female include a small structure called the appendix vesiculosa, a few blind tubules in the broad ligaments (the epoöphoron), and a few blind tubules adjacent to the uterus (collectively called the paroöphoron). Remnants of the mesonephric duct system are often present in the broad ligaments or may be present adjacent to the uterus and/or vagina as Gartner duct cysts. The epoöphoron or paroöphoron may develop into cysts. Cysts of the epoöphoron are known as paraovarian cysts. 6 SECTION I • Embryology Undifferentiated Genital tubercle Glans area Epithelial tag Urethral fold Urethral groove Lateral buttress (labioscrotal swelling) Anal tubercle Anal pit Female Figure 3.1 Homologs of external genitalia Urethral meatus Glans penis Body of clitoris Prepuce Glans clitoridis Prepuce Body of penis Urethral meatus Labium minus Vestibule Labium majus Vagina Perineal raphé Perianal tissues including external sphincter Anus imperforate until late in the embryonic life. However, occasionally, perforation does not completely occur (imperforate hymen). Failure of the sinovaginal bulbs to form leads to agenesis of the vagina. The precise boundary between the paramesonephric and urogenital sinus portions of the vagina has not been established. Beginning in the fourth week after conception, the genital tubercle develops at the ventral tip of the cloacal membrane, with the labioscrotal swellings and urogenital folds developing soon after on either side of the cloacal membrane. In both sexes the genital tubercle subsequently elongates to form a phallus. By the end of the sixth week, the cloacal membrane is joined by the urorectal septum. This septum separates the cloaca into the urogenital sinus ventrally and the anal canal and rectum dorsally. The point on the cloacal membrane where the urorectal septum fuses will become the site of the perineal body. The cloacal membrane, now in two parts, then ruptures, opening the vulva and anal canal. Failure of the anal membrane to rupture results in an imperforate anus. With the opening of the urogenital membrane a urethral groove forms on the undersurface of the phallus, completing the undifferentiated portion of external genital development. Differences between male Male Glans Epithelial tag Body of penis Urethral slit Urethral folds fusing Penoscrotal raphé Anal tubercle Anus Glans Epithelial tag Body of clitoris Urethral folds Urogenital slit Labioscrotal swelling Anal tubercle Anus Penoscrotal raphé Scrotum Perineal raphé Perianal tissues including external sphincter Anus and female embryos can be observed as early as the ninth week, but the distinct final forms are not found until 12 weeks of gestation. Feminization of the undifferentiated external genitalia occurs in the absence of androgenic stimulation. The embryonic phallus remains quiescent and becomes the clitoris. The urogenital folds remain unfused except in front of the anus, forming the posterior fourchette. The unfused urogenital folds form the labia minora, while the labioscrotal folds remain as the labia majora. The labioscrotal folds fuse anteriorly to form the mons pubis. A portion of the urogenital sinus between the level of the hymen and the labia develops into the vestibule of the vagina, into which the urethra, the vagina, and the ducts of Bartholin glands enter. Beyond 12 weeks of gestation, the labioscrotal folds will no longer fuse when exposed to androgens, although other manifestations of masculinization may occur. In contrast to the long-held belief that the development of the female genital was passive and occurred in the absence of androgens, the large number of estrogen receptors found in the genital tissues suggests that there is a role for maternal estrogens in the development of the female external genitalia. Female external genital structures also contain androgen receptors. The distribution of androgen receptors resembles that of the male, which explains why the female genitalia can be masculinized if exposed to high androgen levels early in gestation. The auxiliary genital glands of the female genitalia form from buds that grow out of the urethra. These buds come from the surrounding mesenchyme and form the urethral and paraurethral glands (Skene glands). These glands correspond to the prostate gland in males. Similar outgrowths of the urogenital sinus form the vestibular glands (Bartholin glands), which are homologous to the bulbourethral glands in the male. 8 SECTION I • Embryology Estrogen Childhood Progesterone Puberty Maturity Tanner Stages of Breast Development Stage 1 Elevation of papilla only Stage 2 Breast bud: elevation of breast and papilla as a small mound and enlargement of areolar diameter Figure 4.1 Developmental stages of the breast Stage 3 Stage 4 Additional enlargement Areola and papilla project of breast and areola with from surface of breast to form no separation of their secondary mound contours Stage 5 Mature stage with projection of papilla only with recession of the areola to the general contour of the breast SECTION II Anatomy 5 6 7 8 9 10 11 External Genitalia Perineum Vagina Pelvic Viscera Cervix, Uterus, and Adnexa Ovaries Breast This page intentionally left blank 5 EXTERNAL GENITALIA The perineum is bound in front by the mons veneris, behind by the buttocks, and laterally by the thighs. More deeply it is limited by the margins of the pelvic outlet; namely, the pubic symphysis and arcuate ligament, ischiopubic rami, ischial tuberosities, sacrotuberous ligaments, sacrum, and coccyx. The vulva includes the portions of the female genital tract that are externally visible in the perineal region. The mons veneris is a fatty prominence that overlies the symphysis pubis. It is covered by curly sexual (pubic) hair that functions as a dry lubricant during intercourse. From the mons veneris the labia majora extend in elliptical fashion to enclose the vulval cleft. They contain an abundance of adipose tissue and sebaceous and sweat glands and are covered by hair on their upper outer surfaces. Posteriorly a slightly raised connecting ridge, the posterior commissure or fourchette, joins them. Between the fourchette and the vaginal orifice a shallow, boat-shaped depression, the fossa navicularis, is evident. The labia minora are thin, firm, pigmented, redundant folds of skin, which split anteriorly to enclose the clitoris. Laterally, they bound the vestibule and diminish gradually as they extend posteriorly. The skin of the small labia is devoid of hair follicles, poor in sweat glands, and rich in sebaceous glands. The clitoris, a small, cylindrical, erectile organ situated at the lower border of the symphysis, is composed of two crura, a body and a glans. The crura lie deeply in close apposition with the periosteum of the ischiopubic rami. They join to form the body of the clitoris, which extends downward beneath a loose prepuce and is capped by the acorn-shaped glans. Generally, only the glans of the clitoris is externally visible between the two folds formed by the bifurcation of the labia minora. The vestibule becomes apparent on separation of the labia. Within it are found the hymen, the vaginal orifice, the urethral meatus, and the opening of Skene and Bartholin ducts. The external Pudendal, Pubic, and Inguinal Regions Pudendal cleft (groove or space between the labia majora) Prepuce of clitoris Round ligament of uterus and coverings (cut) Mons pubis Anterior commissure of labia majora Glans of clitoris External urethral orifice Superficial fatty (Camper) layer Deeper membranous (Scarpa) layer Pubic symphysis Frenulum of clitoris Superficial inguinal ring Rectus sheath (anterior layer) Suspensory ligament of clitoris Aponeurosis of external oblique muscle Anterior superior iliac spine Openings of paraurethral (Skene) ducts Labium minus Labium majus Inguinal ligament (Poupart) Pubic tubercle Saphenous opening Vestibule of vagina (cleft or space surrounded by labia minora) Fascia lata of thigh Ischiopubic ramus Superficial perineal (Colles) fascia (cut away) to open superficial perineal space Opening of greater vestibular (Bartholin) gland Ischiocavernosus muscle Perineal membrane Hymenal caruncle Vestibular fossa Frenulum of labia minora Anus Vaginal orifice Annular hymen Posterior commissure of labia majora Perineal raphe (over perineal body) Septate hymen Subcutaneous tissue Deep perineal (investing or Gallaudet) fascia (partially cut away) Ischial tuberosity Superficial perineal (Colles) fascia (cut edge turned down) Fat body of ischioanal fossa Superficial transverse perineal muscle Bulbocavernosus muscle (covers bulb of vestibule) Round ligament of uterus and coverings Superficial perineal (Colles) fascia Cribriform hymen Parous introitus Figure 5.1 External genitalia 11 urethral meatus is situated on a slight papilla-like elevation, approximately 2 cm below the clitoris. In the posterolateral aspect of the urinary orifice lie the openings of Skene ducts. They run below and parallel to the urethra for a distance of 1–1.5 cm. Bartholin ducts are visible on each side of the vestibule, in the groove between the hymen and the labia minora, at about the junction of the middle and posterior thirds of the lateral boundary of the vaginal orifice. Each duct, approximately 1.5 cm in length, passes inward and lateral to the deeply situated vulvovaginal glands. The Bartholin glands are situated posterior to the 3 and 9 o’clock locations, which is important clinically when a Bartholin gland abscess is considered in patients with labial swelling. The hymen is a thin, vascularized membrane or its remnants (the hymenal ring), which separates the vagina from the vestibule. It is covered on both sides by stratified squamous epithelium. As a rule, it shows great variation in thickness and in the size and shape of the hymenal openings (annular, septate, cribriform, crescentic, fimbriate, etc.). After tampon usage, coitus, and childbirth, the shrunken remnants of the hymen are known as carunculae hymenales or hymenal caruncles. The presence or absence of the hymen is insufficient to determine the presence or absence of past sexual activity. Anterior labial nerve (from ilioinguinal nerve) Dorsal nerve of clitoris Posterior labial nerves Superficial Branches of perineal nerve Deep Ischial tuberosity Ischial spine Produces anesthesia of pudendal and other nerves of perineal area Bulbocavernosus muscle with deep perineal (investing or Gallaudet) fascia partially removed Superficial perineal space (pouch or compartment) Ischiopubic ramus with cut edge of superficial perineal (Colles) fascia Perineal membrane Ischial tuberosity Sacrotuberous ligament Ischioanal fossa Gluteus maximus muscle Anococcygeal (ligament) body Coccyx Figure 6.1 Innervation of external genitalia and perineum Perineal branch of posterior femoral cutaneous nerve Dorsal nerve of clitoris passing superior to perineal membrane Perineal nerve Pudendal nerve in pudendal canal (Alcock)(dissected) Inferior cluneal nerves Gluteus maximus muscle (cut away) Sacrotuberous ligament Perforating cutaneous nerve Inferior anal (rectal) nerves Anococcygeal nerves Suspensory ligament of clitoris Clitoris Ischiocavernosus muscle Bulb of vestibule Perineal membrane Greater vestibular (Bartholin) gland Bulbocavernosus muscle (cut away) Superficial transverse perineal muscle Perineal body Obturator fascia Tendinous arch of levator ani muscle Inferior fascia of pelvic diaphragm (cut) Levator ani muscle External anal sphincter muscles 14 SECTION II • Anatomy Uterus (pulled up) Vaginal Wall Plane of section Round ligament of uterus Angle of view Epithelium Papilla Uterine (Fallopian) tube Internal iliac artery and vein Ligament of ovary Ovary Suspensory ligament of ovary Linea terminalis (pelvic brim) Mesovarium Broad ligament Cut edge of peritoneum forming floor of paravesical pouch Uterine vessels Cardinal (transverse cervical or Mackenrodt) ligament Nerve Blood Tendinous arch of levator ani muscle vessels ganglion Vaginal artery Ureter Uterovaginal fascia Anterior recess of ischioanal fossa Crus of clitoris Ischiocavernosus muscle Superficial perineal space Fascia lata of thigh Perineal artery Superficial perineal (Colles) fascia Bulbocavernosus muscle and deep perineal (investing or Gallaudet) fascia Vaginal wall Cervix of uterus Obturator membrane Obturator fascia Obturator internus muscle Levator ani muscle (iliococcygeus and pubococcygeus muscles) Ischiopubic ramus Compressor urethralis muscle Perineal membrane Artery of bulb of vestibule Terminal part of round ligament of uterus Labium majus Sphincter urethrovaginalis muscle Lamina propria Smooth muscle (circular and longitudinal) External fibrous layer (endopelvic fascia) Bulb of vestibule Hymenal caruncle Vagina Vestibule Labium minus Figure 7.1 Support of pelvic viscera sends more and larger papillae into the underlying connective tissue, giving the basement membrane an undulating outline. These papillae are more numerous on the posterior wall and near the vaginal orifice. Beneath the epithelium, which has a thickness of 150–200 µm, a dense connective tissue layer known as the lamina propria is supported by elastic fibers crossing from the epithelium to the underlying muscle. These elastic fibers, here and throughout the pelvis, are critical for pelvic support and function. The lamina propria becomes less dense as it approaches the muscle, and in this area, it contains a network of large, thin-walled veins, giving it the appearance of erectile tissues. The smooth muscle beneath this layer is divided into internal circular and external longitudinal groups, the latter being thicker, stronger, and continuous with superficial muscle bundles of the uterus. No dividing membrane or fascia separates these two interlacing muscle groups. The adventitial coat of the vagina is a thin, firm, fibrous layer arising from the visceral or endopelvic fascia. In this fascia and in the connective tissue between the fascia and the muscle runs another large network of veins and a rich nerve supply. In its distal extreme the vagina opens to the vulva at the hymenal ring, opening at the caudal end of the vulva, behind the opening of the urethra. When upright the vaginal tube points in an upward– backward direction with the axis of the upper portion of the vagina close to the horizontal plane and curving toward the hollow of the sacrum. In most women an angle of at least 90 degrees is formed between the vagina and uterus. The cervix is directed downward and backward to rest against the posterior vaginal wall. The spaces between the cervix and attachment of the vagina are called fornices, with the posterior fornix considerably larger than the anterior fornix. Although there is wide variation, the length of the vagina is approximately 6–9 cm (2.5–3.5 in.) along the anterior wall and 8–12 cm (3–4.5 in.) along the posterior wall. During sexual arousal, the upper portion of the vagina elongates and widens through a relative upward movement of the uterus and cervix. This is considered to facilitate capture and retention of sperm to improve the chance of conception. Throughout most of its length the vagina lies directly on top of the descending rectum, separated by the rectovaginal septum. The upper one-fourth of the vagina is separated from the rectum by the rectouterine pouch (posterior cul-de-sac). The urethra and base of the urinary bladder lie above the anterior vaginal wall, separated by the thin layers of endopelvic fascia. As they enter the bladder, the ureters pass forward and medialward close to the lateral fornices. The vagina is held in position by the surrounding endopelvic fascia and ligaments. The lower third of the vagina is surrounded and supported by the urogenital and pelvic diaphragms. The levator ani muscles and the lower portion of the cardinal ligaments support the middle third of the vagina, while the portions of the cardinal ligaments and parametria support the upper third. The vagina is supplied with an extensive anastomotic network of vessels that surround its length. The vaginal artery originates either directly from the uterine artery or as a branch of the internal iliac artery arising posterior to the origin of the uterine and inferior vesical arteries. There is an anastomosis with the descending cervical branch of the uterine artery to form the azygos arteries. Branches of the internal pudendal, inferior vesical, and middle hemorrhoidal arteries also contribute to the interconnecting network from below. These can be a significant source of bleeding with obstetric lacerations. They are also important in the development of vaginal transudate during sexual arousal, when the vagina produces lubrication to aid in penetration. 8 PELVIC VISCERA While the muscular hammock of the levator plate provides the caudal (inferior) floor for the pelvic viscera, the organs of the pelvis have their own mechanisms of support. When either or both of these two support systems fail, it can result in clinical dysfunctions, including urinary incontinence, fecal retention, and dyspareunia. The viscera contained in the female pelvis minor include the pelvic colon, urinary bladder and urethra, uterus, uterine tubes, ovaries, and vagina. The term endopelvic fascia (actually a pseudofascia) refers to the reflections of the superior fascia of the pelvic diaphragm on the pelvic viscera. At the points where these hollow organs pierce the pelvic floor, tubular fibrous investments are carried upward from the superior fascia as tightly fitting collars, which blend with and may even become inseparable from their outer muscle coat. Thus three tubes of fascia are present, encasing the urethra and bladder, the vagina and lower uterus, and the rectum. These fascial envelopes, with interwoven muscle fibers, are utilized in the repair of cystoceles and rectoceles anteriorly and posteriorly. It is also within this fibrous tube investing the lower uterine segment that the so-called intrafascial hysterectomy is performed in an effort to protect the support of the remaining vaginal cuff. The vesical, uterine, and rectal layers of endopelvic fascia are continuous with the superior fascia of the pelvic diaphragm, obturator fascia, iliac fascia, and transversalis fascia. Uterine support is maintained directly and indirectly by a number of peritoneal, ligamentous, fibrous, and fibromuscular structures. Of these the most important are the cardinal ligaments and pelvic diaphragm with its endopelvic fascial extensions. The vesicouterine peritoneal reflection is sometimes referred to as the anterior ligament of the uterus and the rectouterine peritoneal reflection as the posterior ligament. These are not true ligaments, and they provide only limited additional support. The round ligaments are flattened bands of fibromuscular tissue invested with visceral peritoneum that extend from the angles of the uterus downward, laterally, and forward, through the inguinal canal to terminate in the labia majora. These are analogous to the gubernaculum in males. The sacrouterine (uterosacral) ligaments are true ligaments of musculofascial consistency that run from the upper part of the cervix to the sides of the sacrum. At the uterine end, they merge with the adjacent posterior aspect of the cardinal ligaments and endopelvic fascial tube. The broad ligaments consist of wing-like double folds of peritoneum reflected from the lateral walls of the uterus to the lateral pelvic walls. Their superior margins encase the uterine tube and round ligaments. They then continue as the infundibulopelvic ligaments as they progress laterally and superiorly. Inferiorly the ensheathed uterine vessels and cardinal ligaments may be felt. Within the two peritoneal layers are found loose areolar tissue and fat, the fallopian tube, the round ligament, the ovarian ligament, the parametrium, the epoöphoron, paroöphoron and Gartner’s duct, the uterine and ovarian vessels, lymphatics, and nerves. The cardinal or transverse cervical ligaments (of Mackenrodt) are composed of condensed fibrous tissue and some smooth muscle fibers. They extend from the lateral aspect of the uterine isthmus in a tent-like fashion toward the pelvic wall, to become inserted, fanshaped, into the obturator and superior fasciae of the pelvic diaphragm. This triangular septum of heavy fibrous tissue includes the thick connective tissue sheath, which invests the uterine vessels. Superior view with peritoneum intact Paramedian (sagittal) dissection Median umbilical fold (urachus) Broad ligament (cut) Uterine (Fallopian) tube Ligament of ovary Ovary Ureter Vesicouterine pouch Round ligament of uterus Rectouterine pouch (of Douglas) Peritoneum (cut edge) Superior pubic ramus (cut) Rectum Urinary bladder Vesicouterine pouch Fundus of uterus Round ligament of uterus Ligament of ovary Cervix of uterus Mesosalpinx Ovary Uterine (Fallopian) tube External iliac vessels Ureter Sigmoid colon Pelvic Ischiocavernosus diaphragm muscle External anal Vagina (levator ani muscle) Labia minora sphincter muscle Labium majus Urinary bladder Inferior pubic ramus (cut) Deep transverse perineal muscle (cut) Broad ligament Deep inguinal ring Paravesical fossa Rectouterine pouch (of Douglas) Body of clitoris Body of uterus Suspensory (infundibulopelvic) ligament of ovary contains ovarian vessels Sacral promontory Median sacral vessels Abdominal aorta Ureteric fold Uterosacral ligament Pararectal fossa Figure 8.1 Paramedian dissection and super views of pelvic visera 15 Mesially and inferiorly the cardinal ligaments merge with the uterovaginal and vesical endopelvic fascial envelopes. Posteriorly, they are integrated with the uterosacral ligaments. The vesical and rectal endopelvic fasciae maintain bladder and rectum support, respectively. With the exception of the ovarian, superior hemorrhoidal, and middle sacral arteries the hypogastric divisions of the common iliac arteries supply the pelvic viscera. The uterine artery arises from the anterior division of the hypogastric artery close to or in common with the middle hemorrhoidal or vaginal artery. It courses slightly forward and medialward on the superior fascia of the levator ani muscle to the lower margin of the broad ligament. It arches over the ureter approximately 2 cm from the uterus. At the level of the isthmus, it gives off a descending cervical branch, which surrounds the cervix and anastomoses with the branches of the vaginal artery. The main uterine vessels follow a tortuous course upward along the lateral margin of the uterus, giving off spiral branches to the anterior and posterior surfaces of the uterus. The uterine artery terminates in a tubal branch within the mesosalpinx and an ovarian ramus, which anastomoses with the ovarian artery in the mesovarium. Posterior view Suspensory (infundibulopelvic) ligament of ovary Mesosalpinx Isthmus Epoöphoron Uterine (Fallopian) tube Ampulla Infundibulum Ligament of ovary Fundus of uterus Vesicular appendix (hydatid of Morgagni) Fimbriae Abdominal ostium Corpus luteum Ovary Suspensory ligament of ovary Body of uterus Ovary Mesometrium (broad ligament) Mesovarium Ureter Ligament of ovary (uteroovarian) Uterosacral ligament Rectouterine pouch (of Douglas) Frontal section Uterine (Fallopian) tube la pul Fundus of uterus Am Tubal ostium Uterine Isthmus part Body of uterus Infundibulum Folds of uterine tube Fimbriae Isthmus of uterus Ligament of ovary Endometrium Internal os Myometrium Mesometrium (broad ligament) Suspensory ligament of ovary (contains ovarian vessels) Vesicular appendix (hydatid of Morgagni) Epoöphoron Follicle (Graafian) of ovary Corpus albicans Corpus luteum Uterine vessels Cardinal (transverse cervical or Mackenrodt) ligament Vaginal fornix Cervical canal with palmate folds Vagina Cervix of uterus External os Fallopian tubes Section I Section II Section III Intramural portion Isthmus Ampulla Isthmus Ampulla Fimbria Appendix vesiculosa Figure 9.1 Uterus, ovaries, uterine, and Fallopian tubes 18 SECTION II • Anatomy Ovum Infant ovary Superficial (germinal) epithelium (cuboidal cells) Tunica albuginea Zona pellucida Corona radiata Cumulus oophorus Epithelial cord growing in Primary ova Fluid-filled follicular cavity Granulosa Theca interna Theca externa Cortex Primordial follicles Developing follicle Stages of ovum and follicle Primary follicle Epithelial cord growing in Secondary (antral) follicles Primordial follicle Superficial (germinal) epithelium (cuboidal cells) Blood vessels entering ovary Mature (graafian) follicle Visceral peritoneum of mesovarium Corpus albicans Ruptured follicle (corpus hemorrhagicum) Hilum cells Mature corpus luteum Luteal Fibrin cells Blood clot Early corpus luteum Discharged ovum Corpus luteum Aging ovary Corpus albicans Follicle in early atresia Follicular cavity (with fibrin and clot) Old atretic follicles Granulosa lutein cells Theca lutein cells Theca externa Figure 10.1 Ovarian Structures and development occurs after menarche and during adolescence. Two layers, the germinal epithelium and the tunica albuginea, constitute the surface of the prepubertal ovary. They are crowded with primordial ova that are surrounded by dark-staining cells, the origin of the future granulosa cells. As the primordial follicle develops, it sinks, with its single layer of epithelial cells, toward the center of the ovary. The attendant cells proliferate to form a layered coating of granulosa cells. A crescentic cavity forms eccentrically, in which follicular fluid accumulates. From the surrounding ovarian stroma a capsule of theca cells differentiates. The theca interna is rich in capillaries, on which the avascular theca granulosa must depend for nourishment. That stage of development is reached before menarche, while still little or no follicle-stimulating hormone is present. Before menarche, most, if not all, of these follicles develop no further but degenerate and become atretic. The mature gonad is an approximately almond-shaped structure, pitted, and scarred by the stigmata of ovulation. Spiral arteries enter at the hilus and are involved in sequential changes during the cyclic ebb and sway of follicle growth and development of corpora lutea. In the hilus are also found cells with morphologic and histochemical properties, similar to the interstitial cells of the testis, vestiges from the fetal period, before sexual differentiation occurred. Proliferation of these cells or tumor formation may result in virilization. In the ripening follicle, a dense layer of granulosa cells, the cumulus oophorus, closely protects the egg. A transparent membrane, the zona pellucida, encloses a fluid-filled perivitelline space in which the egg floats freely. The cumulus cells immediately next to the zona arrange themselves outward to form the corona radiata. The egg itself is a spherical body composed of clear protoplasm. It contains a round, dark-staining nucleus, with a definite surrounding membrane and an eccentric nucleolus. The two-layered theca envelope coats the follicle. The theca interna is composed of large epithelioid cells interspersed in connective tissue and rich in blood and lymph vessels. The theca externa Corpus luteum of pregnancy Mature corpus luteum Ovulatory cycle Mature graafian follicle Atrophy (senile or otherwise) Involuting corpus luteum Follicle growth Prepuberty Figure 10.2 Ovarian cycle is thick and dense, consisting of circularly arranged connective tissue fibers. In the follicles that do not mature but degenerate the granulosa layer first becomes disorganized. The corona loses its radial arrangement. Thereafter, the follicular cavity shrinks, and soon the egg itself loses its characteristic features. Hyaline is deposited in a wavy, concentric band. Up to this point the theca interna has continued to be a prominent layer of large, vesicular, nucleated cells. Degenerative changes rapidly progress until nothing is left except an amorphous hyaline scar. 20 SECTION II • Anatomy Anterolateral dissection Pectoralis major muscle (deep to pectoral fascia) Suspensory ligaments of breast (Cooper) Areolar glands Axillary tail (of Spence) Lymphatic drainage of breast Internal jugular vein Right lymphatic duct Serratus anterior muscle Apical axillary (subclavian) nodes Central axillary nodes Posterior axillary (subscapular) nodes Lateral axillary (humeral) nodes External oblique muscle Sagittal section Clavicle Fat Gland lobules Areola Nipple Lactiferous ducts Lactiferous sinus 2nd rib Pectoralis minor muscle Pectoralis major muscle Interpectoral (Rotter) nodes Anterior axillary (pectoral) nodes Pectoral fascia Intercostal muscles Intercostal vessels and nerve Pectoralis Suspensory ligaments major muscle of breast (Cooper) Parasternal Lactiferous duct nodes Lactiferous sinus Lung Inframammary nodes Gland lobules Fat (subcutaneous tissue layer) 6th rib Figure 11.1 Position, structure, and lymphatic drainage of the breast chest wall. From them sprout variable numbers of secondary tubules. These end in epithelial masses forming the lobules or acinar structures of the breast. The number of tubules and the size of the acinar structures vary greatly in different individuals and at different stages of life. In general, the terminal tubules and acinar structures are most numerous during the childbearing period and reach their full physiologic development only during pregnancy and lactation. These epithelial structures constitute collectively the parenchyma of the gland. The stroma is composed of a mixture of fibrous and fatty tissue, and in the absence of pregnancy and lactation the relative amounts of fatty and fibrous tissue determine the size and consistency of the breast. Fatty deposits surround and intermix with the glandular elements and make up a significant portion of the breast structure, providing much of its bulk and shape. The ratio of fatty to glandular tissue varies among individuals and with the stage of life. During menopause, the relative amount of fatty tissue increases as the glandular tissue decreases. A rich vascular and lymphatic network supplies the breasts. The sources of the abundant vascular supply of the mammary gland are the descending thoracic aorta, from which the posterior intercostal arteries branch off; the subclavian artery, from which the internal mammary artery arises; and the axillary artery, serving the mammary gland through the lateral thoracic artery and sometimes through another branch, the external mammary artery. Additional blood may be supplied by branches from the thoracodorsal artery and thoracoacromial artery, which is a short trunk that arises from the forepart of the axillary artery, its origin being generally overlapped by the upper edge of the pectoralis minor. The lymphatic distribution of the breast is complex. The mammary gland has a very rich network of lymph vessels, which is separated into two planes, the superficial or subareolar plexus of lymphatics and the deep or fascial plexus. Both originate in the interlobular spaces and in the walls of the lactiferous ducts. The 11 • Breast lymph nodes that drain the breast are not linked in a straight line; instead, they are staggered, variable, and fixed within fat pads. This arrangement complicates lymph node removal during breast cancer surgery. The sensory innervation of the breast follows the normal distribution of the dermatomes and is mainly derived from the anterolateral and anteromedial branches of the thoracic intercostal nerves T3–T5. Supraclavicular nerves from the lower fibers of the cervical plexus also provide innervation to the upper and lateral portions of the breast. Sensory enervation of the nipple is from the lateral cutaneous branch of T4. 21 Support for the breast comes from both the skin envelope and fibrous suspensory ligaments of Astley Cooper that anchor the breast to the pectoralis major fascia. The enveloping fascia of the breast is continuous with the pectoral fascia. It subdivides the glands into lobules and sends strands into the overlying skin, which in the upper hemisphere, are known as the suspensory ligaments of Cooper. Because these strands are not taut, they enable the natural motion of the breast, but result in breast ptosis as these ligaments relax with age. This page intentionally left blank SECTION III General Health Considerations and Counseling 12 Puberty: Normal Sequence 13 Health Maintenance: Ages 12–18 Years 14 Health Maintenance: Ages 19–39 Years 15 Contraception: Counseling Principles 16 Health Maintenance: Ages 40–64 Years 17 Health Maintenance: Ages 65 Years and Older This page intentionally left blank 12 PUBERTY: NORMAL SEQUENCE concerned about “being normal.” Identifying adolescents in whom the progression of sexual maturation is not normal is important so that timely evaluation and intervention may be achieved. THE CHALLENGE The onset of puberty in adolescents is a time of great emotional and physical change. By understanding the normal sequence of events and being sensitive to the presence of abnormalities, the caregiver may be able to make the most of opportunities to improve health and well-being. TACTICS Relevant Pathophysiology Hormonally, puberty involves a change from negative gonadal feedback to the establishment of the circadian and ultradian gonadal rhythms and the positive feedback controls that result in monthly cycles and fertility. It appears that three elements must be present for puberty to progress normally: adequate body mass, adequate sleep, and exposure to light. These factors appear to facilitate or allow the complex hypothalamic, pituitary, and ovarian changes that must occur. As the hypothalamus matures, there is a decrease in its sensitivity to estrogen, resulting in an increase in the production and release of gonadotropin-releasing hormone (GnRH). Consequently, follicle-stimulating hormone (FSH) levels begin to increase at approximately the 8th–10th year of life, accompanied by an increase in estrogen levels. As the sensitivity of the hypothalamus to negative feedback further decreases, FSH and luteinizing hormone (LH) levels continue to increase and acquire the rhythmic patterns necessary for normal cycling. Eventually, these hormones reach a sufficient level that the follicles can respond, initiating cyclic ovulation and menstruation. Scope of the Problem The variety of decisions, concerns, and changes confronting an adolescent are formidable, not the least of which are health issues that result from rapid growth, sexual maturation, and emerging sexuality. Puberty involves physical, emotional, and sexual changes that mark the transition from childhood to adulthood. Despite the potential need for medical education and care, teenagers have the lowest rate of physician office visits of any group. Embarrassment, an inability to pay, a lack of familiarity with healthcare delivery options, and legal obstructions to access contribute to the lack of care. Objectives of Management Understanding the normal sequence of events involved in sexual maturation is important for counseling young women who may be Female Male Higher cerebral centers “trigger” (leptin, kisspeptin, weight, nutrition) Higher cerebral centers “trigger” (leptin, kisspeptin, weight, nutrition) Axillary hair appears Pituitary gonadotropins increased Breasts develop FSH LH Uterus enlarges Menstruation begins Acne appears GnRH Acne appears Adrenal androgens increased Adrenal cortices Hair line recession begins Facial hair appears ACTH Adrenal cortices Larynx enlarges (voice deepens) Adrenal androgens increased Musculature develops Axillary hair appears Reticular zone enlarges Pubic hair appears Ovaries Reticular zone enlarges Some breast enlargement may occur Testes Pubic hair appears Estrogen increased Vaginal epithelium cornifies Body contours rounded Epiphysial union hastened Progesterone produced LH acts on theca cells to stimulate androgen production and on granulosa cells to stimulate progesterone production. FSH acts on granulosa cells to stimulate production of estrogens from androgens Estrogen produced Testosterone increased LH acts on interstitial Leydig cells to stimulate testosterone production. FSH with testosterone acts on Sertoli cells to stimulate spermatogenesis Penis, prostate, and seminal vesicles enlarge Epiphysial union hastened Figure 12.1 Hormonal events in female and male pubescence 25 Strategies The changes of puberty generally follow a predictable pattern. A growth spurt and the rounding of body curves generally herald puberty. Breast tissue begins to develop, the nipples darken, and fat is laid down in the shoulders, hips, buttocks, and in front of the pubic bone (the mons). Body hair begins to appear because of the influence of androgens made in small amounts by the ovary and adrenal glands. Height increases because of accelerated growth in the long bones of the body, capped off by the closure of the growth centers near the end of puberty. Generally, this growth spurt begins approximately 2 years before the start of menstruation itself, with growth slowing about the same time menstruation begins. Patient Education American College of Obstetricians and Gynecologists Patient Education Pamphlet AP041 (Your Changing Body - Especially for Teens), 2012. American College of Obstetricians and Gynecologists Patient Education Pamphlet AP042 (You and Your Sexuality - Especially for Teens), 2012. American College of Obstetricians and Gynecologists Patient Education Pamphlet AP049 (Your First Period - Especially for Teens), 2012. IMPLEMENTATION Special Considerations The average age of first menstruation (menarche) is approximately 11.6 years, with a normal age range of 8–16 years. These age ranges have gradually declined over the past few years and are as much as 2 years earlier for girls of African-American descent. Menarche generally occurs after the growth spurt and beginning of breast development, while changes in the pubic hair and labia are still under way. Although there is some variation in the normal progression of events, thelarche is the indication of pubertal change for most, followed by adrenarche, peak growth velocity, and ending with the onset of menstruation. This sequence generally takes 4.5 years to run its course, with a range of 1.5–6 years. REFERENCES LEVEL II McDowell MA, Brody DJ, Hughes JP. Has age at menarche changed? Results from the National Health and Nutrition Examination Survey (NHANES) 1999–2004. J Adolesc Health. 2007;40:227-231. [Epub 2007 Jan 24]. Sanchez-Garrido MA, Tena-Sempere M. Metabolic control of puberty: roles of leptin and kisspeptins. Horm Behav. 2013;64(2):187-194. LEVEL III American College of Obstetricians and Gynecologists. Menstruation in girls and adolescents: Using the menstrual cycle as a vital sign. Washington, DC: ACOG; 2009 ACOG Committee Opinion 349. American College of Obstetricians and Gynecologists. Guidelines for adolescent health care. 2nd ed. Washington, DC: ACOG; 2011. Chulani VL, Gordon LP. Adolescent growth and development. Prim Care. 2014;41(3):465-487. Neely EK, Crossen SS. Precocious puberty. Curr Opin Obstet Gynecol. 2014;26(5):332-338. Reindollar RH, McDonough PG. Pubertal aberrancy: etiology and clinical approach. J Reprod Med. 1984;29:391. 13 • Health Maintenance: Ages 12–18 Years 27 Figure 13.1 The ages of 12–18 years represent a time of extreme changes in the body, body image, personality, and personal interactions. The physician must be aware of these changes, initiate a frank and open dialogue, and assure confidentiality except in those cases where safety or bodily harm are involved. • Tobacco, alcohol, other drugs (including complementary and alternative medicines; data from the 2003 Youth Risk Behavior Surveillance Report indicate that many adolescents will begin engaging in risk-taking behaviors by the age of 13 years: 27.8% of adolescents report alcohol use before the age of 13 years) • Abuse/neglect (20%–40% of adults report abuse or sexual victimization before 18 years of age) • Sexual practices Physical • Height • Weight (body mass index) • Blood pressure • Secondary sexual characteristics (Tanner staging) • Pelvic examination (annually after 21 years of age) • Skin Laboratory (Only as Dictated by the Patient’s History) • Periodic • Pap test with high-risk human papillomavirus (HPV) cotesting (at or after 21 years of age, annually thereafter until at least three negative tests, then the interval may be increased). Note: Many patients are unaware of the difference between a Pap test and a pelvic examination for any other reason and this can be a good opportunity to discuss the difference.) • Cholesterol, high-density lipoprotein cholesterol (every 5 years) • As indicated by risk factors • Hemoglobin • Bacteriuria testing • Sexually transmitted disease testing—chlamydia and gonorrhea (if the patient has had sexual contact, screening for STIs is important but urine-based STI testing can be an efficient means for doing so without a speculum examination) • Human immunodeficiency virus (HIV) testing • Genetic testing/counseling • Rubella titer • Tuberculosis skin test • Lipid profile • Fasting glucose Imaging None indicated as routine care COUNSELING It is important to discuss issues of confidentiality with both the patient and her parent or guardian: concerns over confidentiality often are a barrier to the delivery of healthcare services, especially reproductive healthcare, for adolescents. To overcome this obstacle, a discussion of this topic at the initial visit is important along with advice about relevant state and local statutes. For example, if the patient discloses any evidence or risk of bodily harm to herself or others, confidentiality must be breached. Furthermore, state laws may mandate the reporting of physical or sexual abuse of minors. Physicians should be familiar with state and local statutes regarding the rights of minors to healthcare services and the federal and state laws that affect confidentiality. The main purpose of the initial reproductive health visit is preventive health, including educational information, rather than problemfocused care. Preventive counseling for parents or other supportive adults can include discussions about physical, sexual, and emotional development; signs and symptoms of common conditions affecting adolescents; and encouragement of lifelong healthy behaviors. • Sexuality (including topics such as prevention of pregnancy and STIs) is important because more than 85% of adolescent females will have had some form of sexual contact (vaginal, anal, oral, or same sex) by the age of 19 years; nearly one-third of all ninth graders report having had sexual intercourse, and more than 60% of all 12th graders report having had sexual intercourse. • Development • High-risk behaviors • Preventing unwanted/unintended pregnancy • Postponing sexual involvement • Contraceptive options (should also include emergency contraceptive options) • STIs • Partner selection • Barrier protection • Date rape prevention • Fitness • Hygiene (including dental); fluoride supplementation/treatment • Dietary/nutritional assessment (including eating disorders, calcium intake, and folic acid supplementation of 0.4 mg/day) • Exercise program • Psychosocial evaluation • Interpersonal/family relationships • Sexual identity • Personal goal development • Behavioral/learning disorders • Abuse/neglect • Cardiovascular risk factors • Family history • Hypertension • Dyslipidemia • Obesity • Diabetes mellitus • Health/risk behaviors • Injury prevention • Safety belts and sports or bicycle helmets • Recreational hazards • Firearms • Hearing damage • Sports • Skin exposure to ultraviolet rays • Suicide/depressive symptoms • Tobacco, alcohol, and other drugs COUNSELING RESOURCES American College of Obstetricians and Gynecologists Patient Education Pamphlet AP041 (Your Changing Body - Especially for Teens), 2012. Patient Education: American College of Obstetricians and Gynecologists Patient Education Pamphlet AP042 (You and Your Sexuality - Especially for Teens), 2015. American College of Obstetricians and Gynecologists Patient Education Pamphlet AP049 (Your First Period - Especially for Teens), 2012. American College of Obstetricians and Gynecologists. Birth control (Especially for teens). ACOG Patient Education Pamphlet AP112. Washington, DC: ACOG; 2013. American College of Obstetricians and Gynecologists. (Your first ob-gyn visit Especially for teens). ACOG Patient Education Pamphlet AP150. Washington, DC: ACOG; 2015. INTERVENTIONS: IMMUNIZATIONS If not already accomplished, HPV and hepatitis B vaccine series. Meningococcal conjugate vaccine (MCV4) is now recommended. For adolescents who have not received MCV4, the CDC now recommends vaccination before entry into high school, at approximately 15 years of age. Periodic • Tetanus-diphtheria booster (once between the ages of 14 and 16 years) High-Risk Groups • Measles, mumps, rubella (MMR) vaccine • Hepatitis B vaccine REFERENCES LEVEL II Grunbaum JA, Kann L, Kinchen S, et al. Youth risk behavior surveillance - United States, 2003 [published errata appear in MMWR Morb Mortal Wkly Rep 2004;53:536. MMWR Morb Mortal Wkly Rep. 2005;54:608]. MMWR Surveill Summ. 2004;53:1-96. Mosher WD, Chandra A, Jones J. Sexual behavior and selected health measures: men and women 15–44 years of age, United States, 2002. Adv Data. 2005;362:1-55. LEVEL III American College of Obstetricians and Gynecologists. Primary and Preventive Care. Clinical Updates in Women’s Health Care, 2007;VI(2): 1-106. American College of Obstetricians and Gynecologists. Adolescent Confidentiality and Electronic Health Records. Committee Opinion #599. Washington, DC: ACOG; 2014. American College of Obstetricians and Gynecologists. Human Papillomavirus Vaccination. Committee Opinion #641. Washington, DC: ACOG; 2015. American College of Obstetricians and Gynecologists. Guidelines for adolescent health care. 2nd ed. Washington, DC: ACOG; 2011. American College of Obstetricians and Gynecologists. Primary and preventive health care for female adolescents. In: Health Care for Adolescents. Washington, DC: ACOG; 2003:1-24. American College of Obstetricians and Gynecologists. Screening for cervical cancer. Practice Bulletin No. 131. Obstet Gynecol. 2012;120: 1222-1238. Ornstein RM, Fisher MM. Hormonal contraception in adolescents: special considerations. Paediatr Drugs. 2006;8:25-45. Zuckerbrot RA, Maxon L, Pagar D, et al. Adolescent depression screening in primary care: feasibility and acceptability. Pediatrics. 2007;119: 101-108. 14 • Health Maintenance: Ages 19–39 Years 29 Figure 14.1 During the early reproductive years, girlhood gives way to careers, motherhood, and family responsibilities with all the attendant physical and emotional changes. SCREENING History • • • • • Reason for visit Health status: medical, surgical, family Dietary/nutritional assessment Physical activity Tobacco, alcohol, and other drugs (including complementary and alternative medicines) • Abuse/neglect • Sexual practices Physical • • • • • • • • Height Weight (body mass index, BMI) Blood pressure Neck: adenopathy, thyroid Breasts Abdomen Pelvic examination Skin Laboratory • Periodic • Pap test with high-risk human papillomavirus (HPV) cotesting (physician and patient discretion after three consecutive normal tests or negative viral cotesting) • Cholesterol, high-density lipoprotein cholesterol (every five years) • As indicated by risk factors • Bacteriuria testing • Fasting glucose test or hemoglobin A1c • Genetic testing/counseling • Hemoglobin • Human immunodeficiency virus (HIV) testing • Mammography • Rubella titer • STI testing • Thyroid-stimulating hormone • Tuberculosis skin test Imaging Screening mammography may be started before the age of 40 years for patients with a strong family history of early onset breast cancer or heritable cancer syndromes. COUNSELING For those considering or at risk for pregnancy, counseling regarding preconception testing, immunization, and nutrition is always appropriate. Healthcare encounters during this period are also an excellent opportunity to discuss long-term health improvement strategies such as weight control, exercise, and nutrition. Sexuality • High-risk behaviors • Contraceptive options • Genetic counseling • Prevention of unwanted pregnancy (including emergency contraceptive options) • STIs • Partner selection • Barrier protection • Sexual function Fitness • Hygiene (including dental) • Dietary/nutritional assessment (folic acid supplementation for those at risk for or considering pregnancy; 0.4 mg/day has been shown to reduce the risk of neural tube defects) • Exercise program Psychosocial Evaluation • Interpersonal/family relationships • Domestic violence (there are more than 1.5 million cases of domestic violence each year; 20%–40% of adults report abuse or sexual victimization before the age of 18 years, and 10%–25% of wives) • Job satisfaction • Lifestyle/stress • Sleep disorders Cardiovascular Risk Factors • • • • • Family history Hypertension Dyslipidemia Obesity/diabetes mellitus Lifestyle Health/Risk Behaviors Injury Prevention • • • • • • • • • Safety belts and sports and bicycle helmets Recreational hazards Firearms Hearing Breast self-examination (while data on the efficacy of breast selfexamination is lacking, and some organizations actually discourage the practice, the possibility of detecting breast disease make this recommendation reasonable) Breast cancer chemoprophylaxis (selective estrogen receptor modulator therapy for high-risk women over the age of 35 years) Skin exposure to ultraviolet rays Suicide/depressive symptoms Tobacco, alcohol, and other drugs COUNSELING RESOURCES American College of Obstetricians and Gynecologists. Mammography and Other Screening Tests for Breast Problems. ACOG Patient Education Pamphlet AP178. Washington, DC: ACOG; 2015. American College of Obstetricians and Gynecologists. Cholesterol and Women’s Cardiovascular Health. ACOG Patient Education Pamphlet AP101. Washington, DC: ACOG; 2014. American College of Obstetricians and Gynecologists. Healthy Eating. ACOG Patient Education Pamphlet BP130. Washington, DC: ACOG; 2013. American College of Obstetricians and Gynecologists. Good Health Before Pregnancy. ACOG Patient Education Pamphlet AP056. Washington, DC: ACOG; 2015. National Cancer Institute. Breast cancer screening. Available at: <http:// www.cancer.gov/types/breast/patient/breast-screening-pdq>; accessed 12.12.2015. INTERVENTIONS: IMMUNIZATIONS If not already accomplished, HPV and hepatitis B vaccine series Periodic • Tetanus–diphtheria booster (every 10 years) High-Risk Groups • • • • Measles, mumps, rubella (MMR) vaccine Hepatitis B vaccine Influenza vaccine Pneumococcal vaccine REFERENCES LEVEL II Hahn KA, Strickland PA, Hamilton JL, et al. Hyperlipidemia guideline adherence and association with patient gender. J Womens Health (Larchmt). 2006;15(9):1009-1013. Mosher WD, Chandra A, Jones J. Sexual behavior and selected health measures: men and women 15–44 years of age, United States, 2002. Adv Data. 2005;362:1-55. LEVEL III American College of Obstetricians and Gynecologists. Breast cancer screening. Practice Bulletin No. 122. Obstet Gynecol. 2011;118: 372-382. American College of Obstetricians and Gynecologists. Primary and Preventive Care. Clinical Updates in Women’s Health Care, 2007;VI(2): 1-106. American College of Obstetricians and Gynecologists. Guidelines for women’s health care. 2nd ed. Washington, DC: ACOG; 2002. American College of Obstetricians and Gynecologists. Management of gynecologic issues in women with breast cancer. Practice Bulletin No. 126. Obstet Gyencol. 2012;119:666-682. American College of Obstetricians and Gynecologists. Screening for cervical cancer. Practice Bulletin No. 131. Obstet Gynecol. 2012;120: 1222-1238. 15 • Contraception: Counseling Principles TACTICS Relevant Pathophysiology Currently available contraceptive methods seek to prevent pregnancy by preventing the sperm and egg from uniting or by preventing implantation and growth. These goals are accomplished by preventing the development and release of the egg (oral and nonoral hormonal contraceptives and long-acting hormonal methods), preventing the union of sperm and egg by imposing a mechanical, chemical, or temporal barrier between sperm and egg (condom, diaphragm, foam, intrauterine contraceptive devices, rhythm method, withdrawal, and postcoital oral contraception), or altering the likelihood of implantation or growth (RU-486). Relative efficacy (first year failure, both real and theoretical) is shown in the accompanying table. Desire for contraception Permanent Patient Education American College of Obstetricians and Gynecologists Patient Education Booklets: • #AB020 (Birth Control, 2015) • #AP112 (Birth Control - Especially for Teens, 2013), • #AP011 (Sterilization for Women and Men, 2015) • #AP022 (Barrier Methods of Birth Control: Diaphragm, Sponge, Cervical Cap, and Condom, 2013) • #AP185 (Combined Hormonal Birth Control: Pill, Patch, and Ring, 2014) • #AP024 (Fertility Awareness-Based Methods of Family Planning, 2014) • #AP035 (Sterilization by Laparoscopy, 2013) • #AP052 (Postpartum Sterilization, 2013) • #AP114 (Emergency Contraception, 2015) • #AP180 (Hysteroscopic Sterilization, 2012) • #AP184 (Long-Acting Reversible Contraception, 2014) • #AP186 (Progestin-Only Hormonal Birth Control Methods: Pills and Injections, 2014) Sterilization, male or female Yes No Female Strategies For a couple to use a method, it must be accessible, immediately available (especially in coitally dependent or “use oriented” methods), and of reasonable cost. The impact of a method on spontaneity or the modes of sexual expression preferred by the patient and his/her partner may also be important considerations. A decision tree based on these concepts is presented in Fig. 15.1. 31 Couple Male Fertility awareness Male condom ± spermicide Combination pill Progestin pill Hormonal contraceptives Contraceptive implant Injectible medroxyprogesterone acetate Vaginal ring Patch Spermicides Female condom Barrier contraceptives Cervical cap Lea’s shield Diaphragm Progesterone IMPLEMENTATION Special Considerations Adolescent patients require reliable contraception but often have problems with adherence. Careful counseling about options (including abstinence), the risks of pregnancy and sexually transmitted infections, and the need for both contraception and disease protection must be provided. These patients may be better served by methods that rely less on the user for reliability [intrauterine contraceptive devices (IUCDs) or long-acting hormonal agents such as injections, ring, patches, and implants] than those that depend on consistent use (use-oriented methods and those that are very timesensitive such as progestin-only oral contraceptives). Contraception for breastfeeding mothers may include oral contraceptives if milk flow is well established. Long-acting progesterone contraceptives may actually result in a slight increase in breast milk production. Barrier contraceptives are not contraindicated in these patients. IUCDs, copper- or hormone-containing, may also be placed once the uterus has returned to normal or immediately postpartum following delivery of the placenta. Intrauterine contraceptives Copper T Postcoital contraceptives Figure 15.1 One of many possible decision tree approaches to the choice of contraceptive methods. Methods shown in gray have a relatively higher failure rate and should not be used if pregnancy prevention is a high priority. (Reused with permission from Beckman RB, Ling FW, Herbert WN, et al. Obstetrics and Gynecology, 7th ed. Baltimore: Williams & Wilkins; 2013.) Patients over the age of 35 years may continue to use low-dose oral contraceptives if they have no other risk factors and do not smoke. Adherence concerns are generally less in these patients, making use-oriented methods more acceptable and reliable. Longterm methods (IUCDs, long-acting progesterone contraception, or sterilization) may also be appropriate. Until menopause is confirmed by clinical or laboratory methods, contraception must be continued. Following abortion (spontaneous or induced), ovulation may occur as soon as after 2 weeks. If oral contraceptives are selected, they should be started immediately after the abortion. Contraceptive Use Among Women in the United States, 2012 Method Oral contraceptives Sterilization (female) Condom (male) Intrauterine contraceptive device Sterilization (male) Withdrawal Injectable Vaginal ring Periodic abstinence (calendar) Implant Transdermal patch Emergency contraception Other (sponge, cervical cap, female condom, etc.) Percent of Users 23.3 22.6 13.7 9.3 7.4 4.4 4.1 1.8 1.2 1.2 0.5 0.2 0.3 Perfect Use Failurea 0.3 0.5 2.0 0.1–0.6 0.1 4.0 0.05 1.8 9.0 0.05 0.3 0.2 5–26 Actual Use Failurea 8.0 0.5 15.0 0.1–0.8 0.15 27.0 3.0 2.0 25.0 0.05 8.0 0.2 16–32 a Percentage of women experiencing unintended pregnancy within first year of use Data from: The Alan Guttmacher Institute. Contraceptive Use in the United States, October 2015. Available at http://www.guttmacher.org/ pubs/fb_contr_use.html accessed on November 12, 2015. REFERENCES LEVEL III American College of Obstetricians and Gynecologists. Emergency contraception. ACOG Practice Bulletin 152. Washington, DC: ACOG; 2015. American College of Obstetricians and Gynecologists. Long-Acting Reversible Contraception: Implants and Intrauterine Devices. ACOG Practice Bulletin 121. Washington, DC: ACOG; 2011. American College of Obstetricians and Gynecologists. Noncontraceptive Uses of Hormonal Contraceptives. ACOG Practice Bulletin 110. Washington, DC: ACOG; 2010. American College of Obstetricians and Gynecologists. Use of hormonal contraception in women with coexisting medical conditions. ACOG Practice Bulletin 73. Washington, DC: ACOG; 2013. Benagiano G, Bastianelli C, Farris M. Contraception today. Ann N Y Acad Sci. 2006;1092:1-32. Deligeoroglou E, Christopoulos P, Creatsas G. Contraception in adolescence. Ann N Y Acad Sci. 2006;1092:7-90. Draper BH, Morroni C, Hoffman M, et al. Depot medroxyprogesterone versus norethisterone oenanthate for long-acting progestogenic contraception. Cochrane Database Syst Rev. 2006;(3):CD005214. Evans G, Sutton EL. Oral contraception. Med Clin North Am. 2015;99(3): 479-503. Glasier A, Gulmezoglu AM, Schmid GP, et al. Sexual and reproductive health: a matter of life and death. Lancet. 2006;368(9547):1595-1607. Hansen LB, Saseen JJ, Teal SB. Levonorgestrel-only dosing strategies for emergency contraception. Pharmacotherapy. 2007;27:278-284. Krashin J, Tang JH, Mody S, et al. Hormonal and intrauterine methods for contraception for women aged 25 years and younger. Cochrane Database Syst Rev. 2015;(8):CD009805. Kulier R, Helmerhorst FM, O’Brien P, et al. Copper containing, framed intra-uterine devices for contraception. Cochrane Database Syst Rev. 2006;(3):CD005347. McNamee K. The vaginal ring and transdermal patch: new methods of contraception. Sex Health. 2006;3:135-142. Phillips SJ, Tepper NK, Kapp N, et al. Progestogen-only contraceptive use among breastfeeding women: a systematic review. Contraception. 2015;pii: S0010-7824(15)00585-5. Practice Committee of the American Society for Reproductive Medicine. Hormonal contraception: recent advances and controversies. Fertil Steril. 2006;86(5 suppl):S229-S235. 16 • Health Maintenance: Ages 40–64 Years • Dietary/nutritional assessment • Physical activity • Tobacco, alcohol, and other drugs (including complementary and alternative medicines) • Abuse/neglect • Sexual practices • Urinary and fecal incontinence (These issues become more common with childbearing and age, but patients seldom volunteer these complaints.) Physical • • • • • • • • • Height Weight (body mass index [BMI]) Blood pressure Oral cavity Neck: adenopathy, thyroid Breasts Abdomen Pelvic and rectovaginal examination Skin Laboratory • Periodic • Pap test (physician and patient discretion after three consecutive normal tests if low risk) • Cholesterol, high-density lipoprotein cholesterol (every 5 years, starting at the age of 45 years) • Fecal occult blood test (Testing requires the collection of two to three samples of stool collected by the patient at home to be valid. A single stool sample collected at the time of digital rectal examination is not sufficient to adequately screen for colon cancer.) • Sigmoidoscopy (every 3–5 years after the age of 50 years; doublecontrast barium enema study may be substituted or a complete colonoscopy may be performed every 10 years) • As indicated by risk factors • Bacteriuria testing • Colonoscopy • Fasting glucose test • Hemoglobin • Human immunodeficiency virus (HIV) testing • Lipid profile • Mammography • Sexually transmitted disease testing • Thyroid-stimulating hormone test • Tuberculosis skin test Imaging • Mammography (every 1–2 years until the age of 50 years; annually beginning at 50 years of age) • Bone density assessment (Testing should be performed on the basis of an individual woman’s risk profile and is not indicated unless the results will influence a treatment or management decision. Testing may be recommended to postmenopausal women younger than 65 years who have risk factors for osteoporosis.) COUNSELING Healthcare encounters during this period are an excellent opportunity to discuss long-term health improvement strategies such as weight control, exercise, and nutrition. As women approach the transition from reproduction to maturity, there are often increased opportunities to rededicate to healthy lifestyles and prevention. The increasing importance of surveillance as one ages is also an important message for patients in this age group. 33 Sexuality • High-risk behaviors • Contraceptive options • Genetic counseling (for selected women in this age range) • Prevention of unwanted pregnancy (including emergency contraceptive options) • Sexually transmitted disease • Partner selection • Barrier protection • Sexual function (including sexual pain) Fitness • Hygiene (including dental) • Dietary/nutritional assessment (1000–1200 mg of calcium by diet and/or supplements; folic acid supplementation of 0.4 mg/day up to the age of 50 years) • Discussion of exercise program and the importance of remaining physically active Psychosocial Evaluation • • • • • • Interpersonal/family relationships Domestic violence Job/work satisfaction Lifestyle/stress Retirement planning Sleep disorders Cardiovascular Risk Factors • • • • • Family history Hypertension Dyslipidemia Obesity/diabetes mellitus Lifestyle Health/Risk Behaviors • Hormone replacement therapy (Data suggests that when hormone replacement is initiated within 10 years of menopause, it is not associated with some of the adverse effects reported in the Women’s Health Initiative [WHI] study and may even be associated with reductions in such things as cardiovascular disease.) • Breast cancer chemoprophylaxis (selective estrogen receptor modulator therapy for high-risk women over the age of 35 years) • Injury prevention • Safety belts • Recreational hazards • Sports involvement • Vision and hearing • Breast self-awareness • Skin exposure to ultraviolet rays • Suicide/depressive symptoms • Tobacco, alcohol, and other drugs COUNSELING RESOURCES American College of Obstetricians and Gynecologists. Cholesterol and your health. ACOG Patient Education Pamphlet AP101. Washington, DC: ACOG; 2014. American College of Obstetricians and Gynecologists. Healthy eating. ACOG Patient Education Pamphlet BP130. Washington, DC: ACOG; 2013. American College of Obstetricians and Gynecologists. Keeping Your Heart Healthy. ACOG Patient Education Pamphlet BP122. Washington, DC: ACOG; 2004. 34 SECTION III • General Health Considerations and Counseling Coronary artery disease Vaginal atrophy Breast, ovarian, and lung cancer Diabetes Osteoporosis and obesity Obstructive pulmonary disease Depression Figure 16.1 Leading causes of death and morbidity in women aged 40–64 years American College of Obstetricians and Gynecologists. Midlife Transitions: Perimenopause to Menopause. ACOG Patient Education Pamphlet AP013. Washington, DC: ACOG; 2014. American College of Obstetricians and Gynecologists. Perimenopausal Bleeding and Bleeding After Menopause. ACOG Patient Education Pamphlet AP162. Washington, DC: ACOG; 2010. American College of Obstetricians and Gynecologists. The menopause years. ACOG Patient Education Pamphlet AP047. Washington, DC: ACOG; 2015. REFERENCES INTERVENTIONS: IMMUNIZATIONS Periodic • Tetanus–diphtheria booster (every 10 years) • Influenza vaccine (annually beginning at the age of 50 years) High-Risk Groups • • • • • Measles, mumps, rubella (MMR) vaccine Hepatitis A and/or B vaccine Influenza vaccine Pneumococcal vaccine Varicella vaccine Rasgon NL, Geist CL, Kenna HA, et al. Prospective randomized trial to assess effects of continuing hormone therapy on cerebral function in postmenopausal women at risk for dementia. PLoS ONE. 2014;9(3): e89095. Manson JE, Chlebowski RT, Stefanick ML, et al. Menopausal hormone therapy and health outcomes during the intervention and extended poststopping phases of the Women’s Health Initiative randomized trials. JAMA. 2013;310(13):1353-1368. Rossouw JE, Prentice RL, Manson JE, et al. Postmenopausal hormone therapy and risk of cardiovascular disease by age and years since menopause. JAMA. 2007;297:1465-1477. LEVEL II LEVEL III Avis NE, Crawford SL, Greendale G, et al. Duration of menopausal vasomotor symptoms over the menopause transition. JAMA Intern Med. 2015;175(4):531-539. Grodstein F, Manson JE, Stampfer MJ. Hormone therapy and coronary heart disease: the role of time since menopause and age at hormone initiation. J Womens Health. 2006;15:35-44. American College of Obstetricians and Gynecologists. Care of the aging woman. Clinical Updates in Women’s Health Care, Vol VIII, No 4, October 2009 (Reaffirmed 2015). American College of Obstetricians and Gynecologists. Colorectal Cancer Screening Strategies. Committee Opinion #609. Washington, DC: ACOG; 2014. LEVEL I Americ